Materiały źródłowe

• #1 Bowen’s Disease

  https://pmc.ncbi.nlm.nih.gov/articles/PMC8917478/

  Bowen’s disease (BD) is an in-situ squamous cell carcinoma of epidermis. The etiology of BD is multifactorial with high incidence among Caucasians. The major etiological factors of BD include ultraviolet light exposure, immunosuppression, and Human Papilloma Virus (HPV) infections. The cumulative exposure to ultraviolet light radiation produces DNA damage and immunosuppression facilitating the clonal expansion of underlying p53 mutation. The patients with allogeneic organ transplantation on immunosuppressive drugs such as systemic corticosteroids, azathioprine, and cyclosporine may activate different pathways resulting in induction and promotion of skin malignancies. In immunosuppressed patients, Merkel cell polyomavirus has been associated. The BD arising secondary to arsenic exposure is known to occur after several decades. Arsenic exposures produce oxidative stress and deplete antioxidants. It causes immune dysregulation, impaired DNA repair, genotoxicity, and disorganized signal transduction. In BD, several subtypes of Human Papilloma Virus such as HPV 16, 18, 31, 33, 35, 54, 58, 61, 62, and 73 have been detected. A strong association with HPV 16 had been reported with vulvar BD. HPV DNA is observed in 31% of the extragenital BD. BD is also known to arise following ionizing radiation, thermal skin injury, inflammatory dermatoses such as chronic lupus erythematosus, lupus vulgaris, and following Psoralens and Ultraviolet-A radiation. The incidence of aneuploidy and DNA instability is high in lesional skin of BD. The development of invasive SCC is due to destruction of basement membrane mediated by metalloproteinases. The development of invasive carcinomas is more common among elderly people and immunocompromised individuals. The clinical signs suggestive of malignant transformation are ulceration, bleeding, and nodule formation. According to few retrospective studies, the risk of malignant transformation is around 3% in case of extra-genital BD and 10% in EQ. The invasive SCC of genitals tends to be more aggressive and metastatic. Around 16% of the invasive SCC of penis arises from EQ, while almost 100% of the invasive SCCs arising from photo-exposed areas are from underlying BD.

• #2 Bowen’s Disease – PubMed

  https://pubmed.ncbi.nlm.nih.gov/35287414/

  Bowen’s disease (BD) is an in-situ squamous cell carcinoma of epidermis. […] The etiology of BD is multifactorial with high incidence among Caucasians. […] BD is considered as the „lull before the storm,” which precedes an overt squamous cell carcinoma. […] Histopathology is the gold standard diagnostic modality to confirm the diagnosis. […] Immunohistochemistry, dermoscopy, and reflectance confocal microscopy are the adjuvant modalities used in the diagnosis of BD. […] The available therapeutic modalities include topical chemotherapy, surgical modalities, light-based modalities, and destructive therapies. […] It requires a combined effort of dermatologist, oncosurgeon, and plastic surgeon to plan and execute the management in various presentations of BD.

• #3 Bowen’s Disease – PubMed

  https://pubmed.ncbi.nlm.nih.gov/35287414/

  Bowen’s disease (BD) is an in-situ squamous cell carcinoma of epidermis. […] The etiology of BD is multifactorial with high incidence among Caucasians. […] BD is considered as the „lull before the storm,” which precedes an overt squamous cell carcinoma. […] Histopathology is the gold standard diagnostic modality to confirm the diagnosis. […] Immunohistochemistry, dermoscopy, and reflectance confocal microscopy are the adjuvant modalities used in the diagnosis of BD. […] The available therapeutic modalities include topical chemotherapy, surgical modalities, light-based modalities, and destructive therapies. […] It requires a combined effort of dermatologist, oncosurgeon, and plastic surgeon to plan and execute the management in various presentations of BD.

• #4 Intraepidermal squamous cell carcinoma, intraepidermal SCC, Bowen’s disease

  https://dermnetnz.org/topics/intraepidermal-squamous-cell-carcinoma

  Ultraviolet radiation (UV) is the main cause of intraepidermal SCC. It damages the skin cell nucleic acids (DNA), resulting in a mutant clone of the gene p53, setting off uncontrolled growth of the skin cells. UV also suppresses the immune response, preventing recovery from damage. […] Human papillomavirus (HPV) is another major cause of intraepidermal SCC. Oncogenic strains of HPV are the main cause of squamous intraepithelial lesions (SIL), that is, squamous cell carcinoma in situ in mucosal tissue.

• #5 Bowen Disease: Practice Essentials, Pathophysiology, Etiology

  https://emedicine.medscape.com/article/1100113-overview

  Bowen disease is a form of intraepidermal carcinoma, a malignant tumor of keratinocytes. Bowen disease may ultimately progress to an invasive squamous cell carcinoma. […] Chronic UV radiation exposure: The age and sun-exposed body distribution of Bowen disease suggests the importance of chronic sun damage as a factor in the carcinogenesis of Bowen disease. […] The literature supports an association between Bowen disease and arsenic exposure, often occurring after a time lag of 10 years. […] Human papillomavirus type 16 is by far the most common subtype isolated from lesions of Bowen disease, although other subtypes, such as HPV 2, 18, 31, 33, 54, 56, 61, 62, and 73 also have been found. […] Immunosuppressed patients with Bowen disease are more likely to have multiple tumors and more aggressive tumors. […] Other possible causes include genetic factors, trauma, other chemical carcinogens, and x-ray radiation.

• #6 Pathology Outlines – Squamous cell carcinoma in situ / Bowen disease

  https://www.pathologyoutlines.com/topic/skintumornonmelanocyticcisgeneral.html

  Pathophysiology […] Poorly characterized […] May often relate to TP53 mutations, which are present in 7 – 45% of SCCIS cases (Biomedicines 2021;9:171) […] […] […] Etiology […] Multifactorial […] Ultraviolet radiation damages the skin cell nucleic acids, leading to the mutation and cloning of the p53 gene (StatPearls: Intraepidermal Carcinoma [Accessed 9 October 2024]) […] Diseases or drugs capable of suppressing immune responses to skin damage also can trigger the mutation of squamous cells […] Arsenic exposure causes oxidative stress, antioxidant depletion, immune dysfunction, genotoxicity, impaired DNA repair and disrupted signal transduction (Toxicol Appl Pharmacol 2023;479:116730) […] HPV in predominantly genital and periungual lesions but it is also reported in extragenital cases […] HPV16 as the most prevalent subtype (Int J Cancer 1983;32:563)

• #7 Pathology Outlines – Squamous cell carcinoma in situ / Bowen disease

  https://www.pathologyoutlines.com/topic/skintumornonmelanocyticcisgeneral.html

  Pathophysiology […] Poorly characterized […] May often relate to TP53 mutations, which are present in 7 – 45% of SCCIS cases (Biomedicines 2021;9:171) […] […] […] Etiology […] Multifactorial […] Ultraviolet radiation damages the skin cell nucleic acids, leading to the mutation and cloning of the p53 gene (StatPearls: Intraepidermal Carcinoma [Accessed 9 October 2024]) […] Diseases or drugs capable of suppressing immune responses to skin damage also can trigger the mutation of squamous cells […] Arsenic exposure causes oxidative stress, antioxidant depletion, immune dysfunction, genotoxicity, impaired DNA repair and disrupted signal transduction (Toxicol Appl Pharmacol 2023;479:116730) […] HPV in predominantly genital and periungual lesions but it is also reported in extragenital cases […] HPV16 as the most prevalent subtype (Int J Cancer 1983;32:563)

• #8 Cutaneous squamous-cell carcinoma – Wikipedia

  https://en.wikipedia.org/wiki/Cutaneous_squamous-cell_carcinoma

  Compared to basal cell carcinoma, cSCC is more likely to spread to distant areas. […] When confined to the epidermis, the outermost layer of the skin, the pre-invasive or in situ form of cSCC is termed Bowen’s disease. […] The condition originates from squamous cells located in the skin’s upper layers. […] Research, both in vivo and in vitro, indicates a crucial role for the upregulation of FGFR2, part of the fibroblast growth factor receptor immunoglobin family, in cSCC cell progression. […] Mutations in the TPL2 gene leads to overexpression of FGFR2, which activates the mTORC1 and AKT pathways in primary and metastatic cSCC cell lines. […] A significant proportion of cSCC and its precursor lesions carry UV-induced p53 mutations. […] In fact, these mutations are present in up to 90% of cSCC cases. The detection of p53 mutations in precursor lesions indicates that this could be an early event in the development of squamous cell carcinoma.

• #9 Intraepidermal squamous cell carcinoma, intraepidermal SCC, Bowen’s disease

  https://dermnetnz.org/topics/intraepidermal-squamous-cell-carcinoma

  Ultraviolet radiation (UV) is the main cause of intraepidermal SCC. It damages the skin cell nucleic acids (DNA), resulting in a mutant clone of the gene p53, setting off uncontrolled growth of the skin cells. UV also suppresses the immune response, preventing recovery from damage. […] Human papillomavirus (HPV) is another major cause of intraepidermal SCC. Oncogenic strains of HPV are the main cause of squamous intraepithelial lesions (SIL), that is, squamous cell carcinoma in situ in mucosal tissue.

• #10 Bowen Disease: Practice Essentials, Pathophysiology, Etiology

  https://emedicine.medscape.com/article/1100113-overview

  Bowen disease is a form of intraepidermal carcinoma, a malignant tumor of keratinocytes. Bowen disease may ultimately progress to an invasive squamous cell carcinoma. […] Chronic UV radiation exposure: The age and sun-exposed body distribution of Bowen disease suggests the importance of chronic sun damage as a factor in the carcinogenesis of Bowen disease. […] The literature supports an association between Bowen disease and arsenic exposure, often occurring after a time lag of 10 years. […] Human papillomavirus type 16 is by far the most common subtype isolated from lesions of Bowen disease, although other subtypes, such as HPV 2, 18, 31, 33, 54, 56, 61, 62, and 73 also have been found. […] Immunosuppressed patients with Bowen disease are more likely to have multiple tumors and more aggressive tumors. […] Other possible causes include genetic factors, trauma, other chemical carcinogens, and x-ray radiation.

• #11 Pathology Outlines – Squamous cell carcinoma in situ / Bowen disease

  https://www.pathologyoutlines.com/topic/skintumornonmelanocyticcisgeneral.html

  Pathophysiology […] Poorly characterized […] May often relate to TP53 mutations, which are present in 7 – 45% of SCCIS cases (Biomedicines 2021;9:171) […] […] […] Etiology […] Multifactorial […] Ultraviolet radiation damages the skin cell nucleic acids, leading to the mutation and cloning of the p53 gene (StatPearls: Intraepidermal Carcinoma [Accessed 9 October 2024]) […] Diseases or drugs capable of suppressing immune responses to skin damage also can trigger the mutation of squamous cells […] Arsenic exposure causes oxidative stress, antioxidant depletion, immune dysfunction, genotoxicity, impaired DNA repair and disrupted signal transduction (Toxicol Appl Pharmacol 2023;479:116730) […] HPV in predominantly genital and periungual lesions but it is also reported in extragenital cases […] HPV16 as the most prevalent subtype (Int J Cancer 1983;32:563)

• #12 Bowen’s Disease

  https://pmc.ncbi.nlm.nih.gov/articles/PMC8917478/

  Bowen’s disease (BD) is an in-situ squamous cell carcinoma of epidermis. The etiology of BD is multifactorial with high incidence among Caucasians. The major etiological factors of BD include ultraviolet light exposure, immunosuppression, and Human Papilloma Virus (HPV) infections. The cumulative exposure to ultraviolet light radiation produces DNA damage and immunosuppression facilitating the clonal expansion of underlying p53 mutation. The patients with allogeneic organ transplantation on immunosuppressive drugs such as systemic corticosteroids, azathioprine, and cyclosporine may activate different pathways resulting in induction and promotion of skin malignancies. In immunosuppressed patients, Merkel cell polyomavirus has been associated. The BD arising secondary to arsenic exposure is known to occur after several decades. Arsenic exposures produce oxidative stress and deplete antioxidants. It causes immune dysregulation, impaired DNA repair, genotoxicity, and disorganized signal transduction. In BD, several subtypes of Human Papilloma Virus such as HPV 16, 18, 31, 33, 35, 54, 58, 61, 62, and 73 have been detected. A strong association with HPV 16 had been reported with vulvar BD. HPV DNA is observed in 31% of the extragenital BD. BD is also known to arise following ionizing radiation, thermal skin injury, inflammatory dermatoses such as chronic lupus erythematosus, lupus vulgaris, and following Psoralens and Ultraviolet-A radiation. The incidence of aneuploidy and DNA instability is high in lesional skin of BD. The development of invasive SCC is due to destruction of basement membrane mediated by metalloproteinases. The development of invasive carcinomas is more common among elderly people and immunocompromised individuals. The clinical signs suggestive of malignant transformation are ulceration, bleeding, and nodule formation. According to few retrospective studies, the risk of malignant transformation is around 3% in case of extra-genital BD and 10% in EQ. The invasive SCC of genitals tends to be more aggressive and metastatic. Around 16% of the invasive SCC of penis arises from EQ, while almost 100% of the invasive SCCs arising from photo-exposed areas are from underlying BD.

• #13 Bowen’s Disease

  https://pmc.ncbi.nlm.nih.gov/articles/PMC8917478/

  Bowen’s disease (BD) is an in-situ squamous cell carcinoma of epidermis. The etiology of BD is multifactorial with high incidence among Caucasians. The major etiological factors of BD include ultraviolet light exposure, immunosuppression, and Human Papilloma Virus (HPV) infections. The cumulative exposure to ultraviolet light radiation produces DNA damage and immunosuppression facilitating the clonal expansion of underlying p53 mutation. The patients with allogeneic organ transplantation on immunosuppressive drugs such as systemic corticosteroids, azathioprine, and cyclosporine may activate different pathways resulting in induction and promotion of skin malignancies. In immunosuppressed patients, Merkel cell polyomavirus has been associated. The BD arising secondary to arsenic exposure is known to occur after several decades. Arsenic exposures produce oxidative stress and deplete antioxidants. It causes immune dysregulation, impaired DNA repair, genotoxicity, and disorganized signal transduction. In BD, several subtypes of Human Papilloma Virus such as HPV 16, 18, 31, 33, 35, 54, 58, 61, 62, and 73 have been detected. A strong association with HPV 16 had been reported with vulvar BD. HPV DNA is observed in 31% of the extragenital BD. BD is also known to arise following ionizing radiation, thermal skin injury, inflammatory dermatoses such as chronic lupus erythematosus, lupus vulgaris, and following Psoralens and Ultraviolet-A radiation. The incidence of aneuploidy and DNA instability is high in lesional skin of BD. The development of invasive SCC is due to destruction of basement membrane mediated by metalloproteinases. The development of invasive carcinomas is more common among elderly people and immunocompromised individuals. The clinical signs suggestive of malignant transformation are ulceration, bleeding, and nodule formation. According to few retrospective studies, the risk of malignant transformation is around 3% in case of extra-genital BD and 10% in EQ. The invasive SCC of genitals tends to be more aggressive and metastatic. Around 16% of the invasive SCC of penis arises from EQ, while almost 100% of the invasive SCCs arising from photo-exposed areas are from underlying BD.

• #14 Intraepidermal squamous cell carcinoma, intraepidermal SCC, Bowen’s disease

  https://dermnetnz.org/topics/intraepidermal-squamous-cell-carcinoma

  Ultraviolet radiation (UV) is the main cause of intraepidermal SCC. It damages the skin cell nucleic acids (DNA), resulting in a mutant clone of the gene p53, setting off uncontrolled growth of the skin cells. UV also suppresses the immune response, preventing recovery from damage. […] Human papillomavirus (HPV) is another major cause of intraepidermal SCC. Oncogenic strains of HPV are the main cause of squamous intraepithelial lesions (SIL), that is, squamous cell carcinoma in situ in mucosal tissue.

• #15 Bowen’s disease (Squamous Cell Carcinoma In Situ; erythroplasia of Queyrat; Squamous Cell Carcinoma In Situ of the Penis) – Dermatology Advisor

  https://www.dermatologyadvisor.com/home/decision-support-in-medicine/dermatology/bowens-disease-squamous-cell-carcinoma-in-situ-erythroplasia-of-queyrat-squamous-cell-carcinoma-in-situ-of-the-penis/

  Bowens disease may evolve de novo or from a preexisting actinic keratosis. […] Erythroplasia of Queyrat involves the mucocutaneous surface of the penis and is usually seen in uncircumcised males with chronic inflammation and/or viral infection leading to keratinocyte dysplasia. […] Both involve the malignant transformation of the epidermal layer of the skin without invasion through the epidermal-dermal junction. If atypical keratinocytes infiltrate the dermis, then the lesion has progressed to an invasive SCC. […] HPV DNA has been detected in 40% to 80% of cases of penile SCC. The most common associated HPV types reported are HPV type 8 and coinfection with types 16, 39, and 51. Erythroplasia of Queyrat has been found to have a strong association with HPV 16, which is a high-risk oncogenic virus type. In periungual Bowens disease, HPV type 16 has been found to play an important role in carcinogenesis.

• #16 Bowen’s disease (Squamous Cell Carcinoma In Situ; erythroplasia of Queyrat; Squamous Cell Carcinoma In Situ of the Penis) – Dermatology Advisor

  https://www.dermatologyadvisor.com/home/decision-support-in-medicine/dermatology/bowens-disease-squamous-cell-carcinoma-in-situ-erythroplasia-of-queyrat-squamous-cell-carcinoma-in-situ-of-the-penis/

  Bowens disease may evolve de novo or from a preexisting actinic keratosis. […] Erythroplasia of Queyrat involves the mucocutaneous surface of the penis and is usually seen in uncircumcised males with chronic inflammation and/or viral infection leading to keratinocyte dysplasia. […] Both involve the malignant transformation of the epidermal layer of the skin without invasion through the epidermal-dermal junction. If atypical keratinocytes infiltrate the dermis, then the lesion has progressed to an invasive SCC. […] HPV DNA has been detected in 40% to 80% of cases of penile SCC. The most common associated HPV types reported are HPV type 8 and coinfection with types 16, 39, and 51. Erythroplasia of Queyrat has been found to have a strong association with HPV 16, which is a high-risk oncogenic virus type. In periungual Bowens disease, HPV type 16 has been found to play an important role in carcinogenesis.

• #17

  https://journals.lww.com/idoj/fulltext/2022/13020/bowen_s_disease.2.aspx

  Bowen’s disease (BD) is an in-situ squamous cell carcinoma of epidermis. The etiology of BD is multifactorial. The major etiological factors of BD include ultraviolet light exposure, immunosuppression, and Human Papilloma Virus (HPV) infections. The cumulative exposure to ultraviolet light radiation produces DNA damage and immunosuppression facilitating the clonal expansion of underlying p53 mutation. The patients with allogeneic organ transplantation on immunosuppressive drugs such as systemic corticosteroids, azathioprine, and cyclosporine may activate different pathways resulting in induction and promotion of skin malignancies. In immunosuppressed patients, Merkel cell polyomavirus has been associated. The BD arising secondary to arsenic exposure is known to occur after several decades. Arsenic exposures produce oxidative stress and deplete antioxidants. It causes immune dysregulation, impaired DNA repair, genotoxicity, and disorganized signal transduction. In BD, several subtypes of Human Papilloma Virus such as HPV 16, 18, 31, 33, 35, 54, 58, 61, 62, and 73 have been detected. A strong association with HPV 16 had been reported with vulvar BD. HPV DNA is observed in 31% of the extragenital BD. BD is also known to arise following ionizing radiation, thermal skin injury, inflammatory dermatoses such as chronic lupus erythematosus, lupus vulgaris, and following Psoralens and Ultraviolet-A radiation. The incidence of aneuploidy and DNA instability is high in lesional skin of BD. The development of invasive SCC is due to destruction of basement membrane mediated by metalloproteinases. The development of invasive carcinomas is more common among elderly people and immunocompromised individuals. The clinical signs suggestive of malignant transformation are ulceration, bleeding, and nodule formation. According to few retrospective studies, the risk of malignant transformation is around 3% in case of extra-genital BD and 10% in EQ. The invasive SCC of genitals tends to be more aggressive and metastatic. Around 16% of the invasive SCC of penis arises from EQ, while almost 100% of the invasive SCCs arising from photo-exposed areas are from underlying BD.

• #18 Bowen’s Disease

  https://pmc.ncbi.nlm.nih.gov/articles/PMC8917478/

  Bowen’s disease (BD) is an in-situ squamous cell carcinoma of epidermis. The etiology of BD is multifactorial with high incidence among Caucasians. The major etiological factors of BD include ultraviolet light exposure, immunosuppression, and Human Papilloma Virus (HPV) infections. The cumulative exposure to ultraviolet light radiation produces DNA damage and immunosuppression facilitating the clonal expansion of underlying p53 mutation. The patients with allogeneic organ transplantation on immunosuppressive drugs such as systemic corticosteroids, azathioprine, and cyclosporine may activate different pathways resulting in induction and promotion of skin malignancies. In immunosuppressed patients, Merkel cell polyomavirus has been associated. The BD arising secondary to arsenic exposure is known to occur after several decades. Arsenic exposures produce oxidative stress and deplete antioxidants. It causes immune dysregulation, impaired DNA repair, genotoxicity, and disorganized signal transduction. In BD, several subtypes of Human Papilloma Virus such as HPV 16, 18, 31, 33, 35, 54, 58, 61, 62, and 73 have been detected. A strong association with HPV 16 had been reported with vulvar BD. HPV DNA is observed in 31% of the extragenital BD. BD is also known to arise following ionizing radiation, thermal skin injury, inflammatory dermatoses such as chronic lupus erythematosus, lupus vulgaris, and following Psoralens and Ultraviolet-A radiation. The incidence of aneuploidy and DNA instability is high in lesional skin of BD. The development of invasive SCC is due to destruction of basement membrane mediated by metalloproteinases. The development of invasive carcinomas is more common among elderly people and immunocompromised individuals. The clinical signs suggestive of malignant transformation are ulceration, bleeding, and nodule formation. According to few retrospective studies, the risk of malignant transformation is around 3% in case of extra-genital BD and 10% in EQ. The invasive SCC of genitals tends to be more aggressive and metastatic. Around 16% of the invasive SCC of penis arises from EQ, while almost 100% of the invasive SCCs arising from photo-exposed areas are from underlying BD.

• #19

  https://journals.lww.com/idoj/fulltext/2022/13020/bowen_s_disease.2.aspx

  Bowen’s disease (BD) is an in-situ squamous cell carcinoma of epidermis. The etiology of BD is multifactorial. The major etiological factors of BD include ultraviolet light exposure, immunosuppression, and Human Papilloma Virus (HPV) infections. The cumulative exposure to ultraviolet light radiation produces DNA damage and immunosuppression facilitating the clonal expansion of underlying p53 mutation. The patients with allogeneic organ transplantation on immunosuppressive drugs such as systemic corticosteroids, azathioprine, and cyclosporine may activate different pathways resulting in induction and promotion of skin malignancies. In immunosuppressed patients, Merkel cell polyomavirus has been associated. The BD arising secondary to arsenic exposure is known to occur after several decades. Arsenic exposures produce oxidative stress and deplete antioxidants. It causes immune dysregulation, impaired DNA repair, genotoxicity, and disorganized signal transduction. In BD, several subtypes of Human Papilloma Virus such as HPV 16, 18, 31, 33, 35, 54, 58, 61, 62, and 73 have been detected. A strong association with HPV 16 had been reported with vulvar BD. HPV DNA is observed in 31% of the extragenital BD. BD is also known to arise following ionizing radiation, thermal skin injury, inflammatory dermatoses such as chronic lupus erythematosus, lupus vulgaris, and following Psoralens and Ultraviolet-A radiation. The incidence of aneuploidy and DNA instability is high in lesional skin of BD. The development of invasive SCC is due to destruction of basement membrane mediated by metalloproteinases. The development of invasive carcinomas is more common among elderly people and immunocompromised individuals. The clinical signs suggestive of malignant transformation are ulceration, bleeding, and nodule formation. According to few retrospective studies, the risk of malignant transformation is around 3% in case of extra-genital BD and 10% in EQ. The invasive SCC of genitals tends to be more aggressive and metastatic. Around 16% of the invasive SCC of penis arises from EQ, while almost 100% of the invasive SCCs arising from photo-exposed areas are from underlying BD.

• #20 Pathology Outlines – Squamous cell carcinoma in situ / Bowen disease

  https://www.pathologyoutlines.com/topic/skintumornonmelanocyticcisgeneral.html

  Pathophysiology […] Poorly characterized […] May often relate to TP53 mutations, which are present in 7 – 45% of SCCIS cases (Biomedicines 2021;9:171) […] […] […] Etiology […] Multifactorial […] Ultraviolet radiation damages the skin cell nucleic acids, leading to the mutation and cloning of the p53 gene (StatPearls: Intraepidermal Carcinoma [Accessed 9 October 2024]) […] Diseases or drugs capable of suppressing immune responses to skin damage also can trigger the mutation of squamous cells […] Arsenic exposure causes oxidative stress, antioxidant depletion, immune dysfunction, genotoxicity, impaired DNA repair and disrupted signal transduction (Toxicol Appl Pharmacol 2023;479:116730) […] HPV in predominantly genital and periungual lesions but it is also reported in extragenital cases […] HPV16 as the most prevalent subtype (Int J Cancer 1983;32:563)

• #21 Bowen Disease: Practice Essentials, Pathophysiology, Etiology

  https://emedicine.medscape.com/article/1100113-overview

  Bowen disease is a form of intraepidermal carcinoma, a malignant tumor of keratinocytes. Bowen disease may ultimately progress to an invasive squamous cell carcinoma. […] Chronic UV radiation exposure: The age and sun-exposed body distribution of Bowen disease suggests the importance of chronic sun damage as a factor in the carcinogenesis of Bowen disease. […] The literature supports an association between Bowen disease and arsenic exposure, often occurring after a time lag of 10 years. […] Human papillomavirus type 16 is by far the most common subtype isolated from lesions of Bowen disease, although other subtypes, such as HPV 2, 18, 31, 33, 54, 56, 61, 62, and 73 also have been found. […] Immunosuppressed patients with Bowen disease are more likely to have multiple tumors and more aggressive tumors. […] Other possible causes include genetic factors, trauma, other chemical carcinogens, and x-ray radiation.

• #22 Bowen’s Disease: Causes, Symptoms, and Treatment

  https://patient.info/doctor/bowens-disease-pro

  Bowen’s disease is a form of intraepidermal (in situ) squamous cell carcinoma (SCC) of the skin. […] Bowen’s disease arises in the outer layers of the epidermis and the risk of progression to invasive SCC is relatively low at about 3% for typical cases. […] There is a strong association with human papillomavirus (HPV), particularly in genital and perianal lesions and in lesions on the hands and feet. […] Malignant and premalignant skin tumours are more common in patients who have received organ transplants. […] Bowen’s disease should be seen as a risk marker for other non-melanoma skin cancer (NMSC); a third of patients will have another NMSC at the time of diagnosis and patients with Bowen’s disease are 4.3 times more likely to develop NMSC in the future, most likely due to the common aetiology of ultraviolet (UV) light.

• #23 Bowen’s Disease: Causes, Symptoms, and Treatment

  https://patient.info/doctor/bowens-disease-pro

  Bowen’s disease is a form of intraepidermal (in situ) squamous cell carcinoma (SCC) of the skin. […] Bowen’s disease arises in the outer layers of the epidermis and the risk of progression to invasive SCC is relatively low at about 3% for typical cases. […] There is a strong association with human papillomavirus (HPV), particularly in genital and perianal lesions and in lesions on the hands and feet. […] Malignant and premalignant skin tumours are more common in patients who have received organ transplants. […] Bowen’s disease should be seen as a risk marker for other non-melanoma skin cancer (NMSC); a third of patients will have another NMSC at the time of diagnosis and patients with Bowen’s disease are 4.3 times more likely to develop NMSC in the future, most likely due to the common aetiology of ultraviolet (UV) light.

• #24 Bowen Disease: Practice Essentials, Pathophysiology, Etiology

  https://emedicine.medscape.com/article/1100113-overview

  Bowen disease is a form of intraepidermal carcinoma, a malignant tumor of keratinocytes. Bowen disease may ultimately progress to an invasive squamous cell carcinoma. […] Chronic UV radiation exposure: The age and sun-exposed body distribution of Bowen disease suggests the importance of chronic sun damage as a factor in the carcinogenesis of Bowen disease. […] The literature supports an association between Bowen disease and arsenic exposure, often occurring after a time lag of 10 years. […] Human papillomavirus type 16 is by far the most common subtype isolated from lesions of Bowen disease, although other subtypes, such as HPV 2, 18, 31, 33, 54, 56, 61, 62, and 73 also have been found. […] Immunosuppressed patients with Bowen disease are more likely to have multiple tumors and more aggressive tumors. […] Other possible causes include genetic factors, trauma, other chemical carcinogens, and x-ray radiation.

• #25 Pathology Outlines – Squamous cell carcinoma in situ / Bowen disease

  https://www.pathologyoutlines.com/topic/skintumornonmelanocyticcisgeneral.html

  Pathophysiology […] Poorly characterized […] May often relate to TP53 mutations, which are present in 7 – 45% of SCCIS cases (Biomedicines 2021;9:171) […] […] […] Etiology […] Multifactorial […] Ultraviolet radiation damages the skin cell nucleic acids, leading to the mutation and cloning of the p53 gene (StatPearls: Intraepidermal Carcinoma [Accessed 9 October 2024]) […] Diseases or drugs capable of suppressing immune responses to skin damage also can trigger the mutation of squamous cells […] Arsenic exposure causes oxidative stress, antioxidant depletion, immune dysfunction, genotoxicity, impaired DNA repair and disrupted signal transduction (Toxicol Appl Pharmacol 2023;479:116730) […] HPV in predominantly genital and periungual lesions but it is also reported in extragenital cases […] HPV16 as the most prevalent subtype (Int J Cancer 1983;32:563)

• #26 Azthena logo with the word Azthena

  https://www.news-medical.net/health/Bowens-Disease-Causes.aspx

  Bowen’s disease, also called squamous cell carcinoma (SCC) in situ, is a primitive kind of skin cancer. It occurs due to aberrant growth, division, and accretion of cells present in the epidermis of the skin (outer layer of skin). […] Risk of Bowen’s disease generally arises due to higher exposure of the skin to ultraviolet radiation. […] Chronic exposure to ultraviolet (UV) rays from the sun, which may be work-related exposure, is primarily responsible for developing SCC in situ. On exposure, UV radiation involves in mechanisms such as inactivation of p53 suppressing genes, which in turn cause aggressive development of skin malignancies like Bowen’s disease. […] The sexually transmitted human papilloma virus (HPV) is found to be one of the causes of Bowen’s disease. […] Malignancy on skin is very common in immunocompromised patients. […] Consumption of arsenic-contaminated food and water results in arsenic poisoning, and chronic exposure to it may lead to skin malignancies such as Bowen’s disease and basal cell carcinoma. […] In the 20th century, ionizing radiation was also stated to be an inducing agent of Bowen’s disease.

• #27 Bowen disease | EBSCO Research Starters

  https://www.ebsco.com/research-starters/health-and-medicine/bowen-disease

  Bowen disease originates from the overproliferation of squamous cells, the flat superficial cells that make up the upper layer of the skin (epidermis). […] Triggers of this overproliferation include ultraviolet light from chronic sun exposure and exposure to HPV-16. Both can damage or alter cellular deoxyribonucleic acid (DNA) and the cellular controls regulating cell division. […] Arsenic has been hypothesized to enhance the carcinogenic properties of ultraviolet irradiation, as it has a propensity to accumulate in the skin as well as the lungs, bladder, kidney, and liver.

• #28

  https://journals.lww.com/idoj/fulltext/2022/13020/bowen_s_disease.2.aspx

  Bowen’s disease (BD) is an in-situ squamous cell carcinoma of epidermis. The etiology of BD is multifactorial. The major etiological factors of BD include ultraviolet light exposure, immunosuppression, and Human Papilloma Virus (HPV) infections. The cumulative exposure to ultraviolet light radiation produces DNA damage and immunosuppression facilitating the clonal expansion of underlying p53 mutation. The patients with allogeneic organ transplantation on immunosuppressive drugs such as systemic corticosteroids, azathioprine, and cyclosporine may activate different pathways resulting in induction and promotion of skin malignancies. In immunosuppressed patients, Merkel cell polyomavirus has been associated. The BD arising secondary to arsenic exposure is known to occur after several decades. Arsenic exposures produce oxidative stress and deplete antioxidants. It causes immune dysregulation, impaired DNA repair, genotoxicity, and disorganized signal transduction. In BD, several subtypes of Human Papilloma Virus such as HPV 16, 18, 31, 33, 35, 54, 58, 61, 62, and 73 have been detected. A strong association with HPV 16 had been reported with vulvar BD. HPV DNA is observed in 31% of the extragenital BD. BD is also known to arise following ionizing radiation, thermal skin injury, inflammatory dermatoses such as chronic lupus erythematosus, lupus vulgaris, and following Psoralens and Ultraviolet-A radiation. The incidence of aneuploidy and DNA instability is high in lesional skin of BD. The development of invasive SCC is due to destruction of basement membrane mediated by metalloproteinases. The development of invasive carcinomas is more common among elderly people and immunocompromised individuals. The clinical signs suggestive of malignant transformation are ulceration, bleeding, and nodule formation. According to few retrospective studies, the risk of malignant transformation is around 3% in case of extra-genital BD and 10% in EQ. The invasive SCC of genitals tends to be more aggressive and metastatic. Around 16% of the invasive SCC of penis arises from EQ, while almost 100% of the invasive SCCs arising from photo-exposed areas are from underlying BD.

• #29 Azthena logo with the word Azthena

  https://www.news-medical.net/health/Bowens-Disease-Causes.aspx

  Bowen’s disease, also called squamous cell carcinoma (SCC) in situ, is a primitive kind of skin cancer. It occurs due to aberrant growth, division, and accretion of cells present in the epidermis of the skin (outer layer of skin). […] Risk of Bowen’s disease generally arises due to higher exposure of the skin to ultraviolet radiation. […] Chronic exposure to ultraviolet (UV) rays from the sun, which may be work-related exposure, is primarily responsible for developing SCC in situ. On exposure, UV radiation involves in mechanisms such as inactivation of p53 suppressing genes, which in turn cause aggressive development of skin malignancies like Bowen’s disease. […] The sexually transmitted human papilloma virus (HPV) is found to be one of the causes of Bowen’s disease. […] Malignancy on skin is very common in immunocompromised patients. […] Consumption of arsenic-contaminated food and water results in arsenic poisoning, and chronic exposure to it may lead to skin malignancies such as Bowen’s disease and basal cell carcinoma. […] In the 20th century, ionizing radiation was also stated to be an inducing agent of Bowen’s disease.

• #30 A case of Bowen’s disease possibly attributed to chronic stimulation by a metal wristwatch | Anais Brasileiros de Dermatologia

  https://www.anaisdedermatologia.org.br/en-a-case-bowens-disease-possibly-articulo-S0365059622002720

  Bowens disease, Squamous Cell Carcinoma (SCC) in situ, is a common skin cancer in elderly people, and its causal factors include sun exposure, irradiation, arsenic exposure, burn, scar, injury, Human Papillomavirus (HPV), and immunosuppressive status. […] The patient had Bowens disease that may have been caused by chronic stimulation as a result of repetitive contact or friction with the case back of his metal wristwatch. […] Chronic stimulation leads to chronic wounds and scars, which can develop into squamous cell carcinoma. […] This mechanism may be associated with the development of Bowens disease. […] In the present case, we speculate that superficial damage may have been induced by chronic stimulation/friction with a metal wristwatch, leading to the development of Bowens disease during the repetitive repair process. […] Further studies are needed to clarify the causative mechanisms of Bowens disease.

• #31 Bowen Disease: Practice Essentials, Pathophysiology, Etiology

  https://emedicine.medscape.com/article/1100113-overview

  Bowen disease is a form of intraepidermal carcinoma, a malignant tumor of keratinocytes. Bowen disease may ultimately progress to an invasive squamous cell carcinoma. […] Chronic UV radiation exposure: The age and sun-exposed body distribution of Bowen disease suggests the importance of chronic sun damage as a factor in the carcinogenesis of Bowen disease. […] The literature supports an association between Bowen disease and arsenic exposure, often occurring after a time lag of 10 years. […] Human papillomavirus type 16 is by far the most common subtype isolated from lesions of Bowen disease, although other subtypes, such as HPV 2, 18, 31, 33, 54, 56, 61, 62, and 73 also have been found. […] Immunosuppressed patients with Bowen disease are more likely to have multiple tumors and more aggressive tumors. […] Other possible causes include genetic factors, trauma, other chemical carcinogens, and x-ray radiation.

• #32 Bowen Disease Workup: Histologic Findings

  https://emedicine.medscape.com/article/1100113-workup

  Bowen disease is a full-thickness anaplasia of the epidermis, with loss of the normal maturation of its components. Keratinocytes are atypical and disorderly, often described as having a windblown appearance. […] Genetically, an increased expression and mutation of TP53 has been observed. In addition, lesions have been reported to have one or more deletions in the 9q markers.

• #33 Bowen disease | EBSCO Research Starters

  https://www.ebsco.com/research-starters/health-and-medicine/bowen-disease

  Bowen disease originates from the overproliferation of squamous cells, the flat superficial cells that make up the upper layer of the skin (epidermis). […] Triggers of this overproliferation include ultraviolet light from chronic sun exposure and exposure to HPV-16. Both can damage or alter cellular deoxyribonucleic acid (DNA) and the cellular controls regulating cell division. […] Arsenic has been hypothesized to enhance the carcinogenic properties of ultraviolet irradiation, as it has a propensity to accumulate in the skin as well as the lungs, bladder, kidney, and liver.

• #34 Bowen disease | EBSCO Research Starters

  https://www.ebsco.com/research-starters/health-and-medicine/bowen-disease

  Bowen disease originates from the overproliferation of squamous cells, the flat superficial cells that make up the upper layer of the skin (epidermis). […] Triggers of this overproliferation include ultraviolet light from chronic sun exposure and exposure to HPV-16. Both can damage or alter cellular deoxyribonucleic acid (DNA) and the cellular controls regulating cell division. […] Arsenic has been hypothesized to enhance the carcinogenic properties of ultraviolet irradiation, as it has a propensity to accumulate in the skin as well as the lungs, bladder, kidney, and liver.

• #35 Bowen’s disease – wikidoc

  https://www.wikidoc.org/index.php/Bowen%27s_disease

  Cells in Bowen’s disease are extremely unusual or atypical under the microscope. […] In many cases, cells look worse under the microscope than the cells of many outright and invading squamous cell carcinomas. […] Degree of atypia (strangeness, unusualness) seen under the microscope best tells how cells may behave (should they invade another portion of the body). […] Bowen’s disease can also occur as a part of Borst-Jadassohn phenomenon which is a heterogeneous group of following intraepithelial lesions. […] Common causes include solar damage, aging, arsenic, immunosuppression (after organ transplant, AIDS), HPV, Merkel cell polyomavirus, irradiation (UV irradiation, photochemotherapy, radiotherapy), chronic skin injury, dermatoses, and Sjogren’s syndrome. […] Histopathology shows unusual or atypical cells.

• #36 Bowen’s disease – wikidoc

  https://www.wikidoc.org/index.php/Bowen%27s_disease

  Cells in Bowen’s disease are extremely unusual or atypical under the microscope. […] In many cases, cells look worse under the microscope than the cells of many outright and invading squamous cell carcinomas. […] Degree of atypia (strangeness, unusualness) seen under the microscope best tells how cells may behave (should they invade another portion of the body). […] Bowen’s disease can also occur as a part of Borst-Jadassohn phenomenon which is a heterogeneous group of following intraepithelial lesions. […] Common causes include solar damage, aging, arsenic, immunosuppression (after organ transplant, AIDS), HPV, Merkel cell polyomavirus, irradiation (UV irradiation, photochemotherapy, radiotherapy), chronic skin injury, dermatoses, and Sjogren’s syndrome. […] Histopathology shows unusual or atypical cells.

• #37 Bowen’s disease – wikidoc

  https://www.wikidoc.org/index.php/Bowen%27s_disease

  Cells in Bowen’s disease are extremely unusual or atypical under the microscope. […] In many cases, cells look worse under the microscope than the cells of many outright and invading squamous cell carcinomas. […] Degree of atypia (strangeness, unusualness) seen under the microscope best tells how cells may behave (should they invade another portion of the body). […] Bowen’s disease can also occur as a part of Borst-Jadassohn phenomenon which is a heterogeneous group of following intraepithelial lesions. […] Common causes include solar damage, aging, arsenic, immunosuppression (after organ transplant, AIDS), HPV, Merkel cell polyomavirus, irradiation (UV irradiation, photochemotherapy, radiotherapy), chronic skin injury, dermatoses, and Sjogren’s syndrome. […] Histopathology shows unusual or atypical cells.

• #38 Bowen’s disease of the nipple and areola | CCID

  https://www.dovepress.com/bowens-disease-of-the-nipple-and-areola-case-report-and-literature-rev-peer-reviewed-fulltext-article-CCID

  Bowens disease (BD) is a type of non-melanocytic intraepidermal malignancy, firstly described by John Templeton Bowen in 1912. It usually presents as a gradually enlarging well-demarcated erythematous plaque with an irregular border and crusting or scaling surface. To our best knowledge, BD usually develops on sun-exposed areas such as head, neck and extremities, with rare cases showed lesions involving palms, soles or breast. […] BD is firstly recognized as an intraepidermal or in situ malignant neoplasm precursor in 1912. Most cases of BD present with lesions on body parts that have been exposed to ultraviolet light, such as hand, head, and neck, with a few cases presenting with lesions on the nipples. […] The histological characteristics included thickening of the epithelium, parakeratosis, epithelial mitoses, pleomorphic nuclei with full-thickness epidermal atypia, and sparing of the basal layer. The other histological features included abnormal keratinocytes throughout a thickened epidermis, as well as involvement of acrotrichia, with or without hyperpigmentation of basal keratinocytes and/or melanophages in the dermis.

• #39 Bowen Disease Workup: Histologic Findings

  https://emedicine.medscape.com/article/1100113-workup

  Bowen disease is a full-thickness anaplasia of the epidermis, with loss of the normal maturation of its components. Keratinocytes are atypical and disorderly, often described as having a windblown appearance. […] Genetically, an increased expression and mutation of TP53 has been observed. In addition, lesions have been reported to have one or more deletions in the 9q markers.

• #40 Bowen’s Disease

  https://pmc.ncbi.nlm.nih.gov/articles/PMC8917478/

  Bowen’s disease (BD) is an in-situ squamous cell carcinoma of epidermis. The etiology of BD is multifactorial with high incidence among Caucasians. The major etiological factors of BD include ultraviolet light exposure, immunosuppression, and Human Papilloma Virus (HPV) infections. The cumulative exposure to ultraviolet light radiation produces DNA damage and immunosuppression facilitating the clonal expansion of underlying p53 mutation. The patients with allogeneic organ transplantation on immunosuppressive drugs such as systemic corticosteroids, azathioprine, and cyclosporine may activate different pathways resulting in induction and promotion of skin malignancies. In immunosuppressed patients, Merkel cell polyomavirus has been associated. The BD arising secondary to arsenic exposure is known to occur after several decades. Arsenic exposures produce oxidative stress and deplete antioxidants. It causes immune dysregulation, impaired DNA repair, genotoxicity, and disorganized signal transduction. In BD, several subtypes of Human Papilloma Virus such as HPV 16, 18, 31, 33, 35, 54, 58, 61, 62, and 73 have been detected. A strong association with HPV 16 had been reported with vulvar BD. HPV DNA is observed in 31% of the extragenital BD. BD is also known to arise following ionizing radiation, thermal skin injury, inflammatory dermatoses such as chronic lupus erythematosus, lupus vulgaris, and following Psoralens and Ultraviolet-A radiation. The incidence of aneuploidy and DNA instability is high in lesional skin of BD. The development of invasive SCC is due to destruction of basement membrane mediated by metalloproteinases. The development of invasive carcinomas is more common among elderly people and immunocompromised individuals. The clinical signs suggestive of malignant transformation are ulceration, bleeding, and nodule formation. According to few retrospective studies, the risk of malignant transformation is around 3% in case of extra-genital BD and 10% in EQ. The invasive SCC of genitals tends to be more aggressive and metastatic. Around 16% of the invasive SCC of penis arises from EQ, while almost 100% of the invasive SCCs arising from photo-exposed areas are from underlying BD.

• #41

  https://journals.lww.com/idoj/fulltext/2022/13020/bowen_s_disease.2.aspx

  Bowen’s disease (BD) is an in-situ squamous cell carcinoma of epidermis. The etiology of BD is multifactorial. The major etiological factors of BD include ultraviolet light exposure, immunosuppression, and Human Papilloma Virus (HPV) infections. The cumulative exposure to ultraviolet light radiation produces DNA damage and immunosuppression facilitating the clonal expansion of underlying p53 mutation. The patients with allogeneic organ transplantation on immunosuppressive drugs such as systemic corticosteroids, azathioprine, and cyclosporine may activate different pathways resulting in induction and promotion of skin malignancies. In immunosuppressed patients, Merkel cell polyomavirus has been associated. The BD arising secondary to arsenic exposure is known to occur after several decades. Arsenic exposures produce oxidative stress and deplete antioxidants. It causes immune dysregulation, impaired DNA repair, genotoxicity, and disorganized signal transduction. In BD, several subtypes of Human Papilloma Virus such as HPV 16, 18, 31, 33, 35, 54, 58, 61, 62, and 73 have been detected. A strong association with HPV 16 had been reported with vulvar BD. HPV DNA is observed in 31% of the extragenital BD. BD is also known to arise following ionizing radiation, thermal skin injury, inflammatory dermatoses such as chronic lupus erythematosus, lupus vulgaris, and following Psoralens and Ultraviolet-A radiation. The incidence of aneuploidy and DNA instability is high in lesional skin of BD. The development of invasive SCC is due to destruction of basement membrane mediated by metalloproteinases. The development of invasive carcinomas is more common among elderly people and immunocompromised individuals. The clinical signs suggestive of malignant transformation are ulceration, bleeding, and nodule formation. According to few retrospective studies, the risk of malignant transformation is around 3% in case of extra-genital BD and 10% in EQ. The invasive SCC of genitals tends to be more aggressive and metastatic. Around 16% of the invasive SCC of penis arises from EQ, while almost 100% of the invasive SCCs arising from photo-exposed areas are from underlying BD.

• #42 Bowen’s Disease Symptoms, Causes, Diagnosis, and Treatment

  https://www.healthline.com/health/skin-cancer/bowens-disease

  Bowens disease is an early form of squamous cell carcinoma (SCC), a type of skin cancer. […] The specific cause of Bowens disease is currently unknown. But there are certain factors associated with the disease. […] Prolonged exposure to ultraviolet (UV) radiation is a major contributor to Bowens disease. […] Over time, UV radiation damages the DNA in your skin. This can lead to cancerous conditions like Bowens disease. […] A mutation of the p53 gene can lead to various forms of tumors, including those involved in skin cancer. […] A weakened immune system can increase the expression of a p53 mutation. This may cause Bowens disease. […] A human papillomavirus (HPV) infection is another potential cause of Bowens disease. Several types of HPV may be associated with the disease. […] Chronic arsenic exposure can lead to Bowens disease. It takes about 10 years to develop after your first exposure.

• #43 Bowen’s Disease Symptoms, Causes, Diagnosis, and Treatment

  https://www.healthline.com/health/skin-cancer/bowens-disease

  Bowens disease is an early form of squamous cell carcinoma (SCC), a type of skin cancer. […] The specific cause of Bowens disease is currently unknown. But there are certain factors associated with the disease. […] Prolonged exposure to ultraviolet (UV) radiation is a major contributor to Bowens disease. […] Over time, UV radiation damages the DNA in your skin. This can lead to cancerous conditions like Bowens disease. […] A mutation of the p53 gene can lead to various forms of tumors, including those involved in skin cancer. […] A weakened immune system can increase the expression of a p53 mutation. This may cause Bowens disease. […] A human papillomavirus (HPV) infection is another potential cause of Bowens disease. Several types of HPV may be associated with the disease. […] Chronic arsenic exposure can lead to Bowens disease. It takes about 10 years to develop after your first exposure.

• #44 Cutaneous squamous-cell carcinoma – Wikipedia

  https://en.wikipedia.org/wiki/Cutaneous_squamous-cell_carcinoma

  Compared to basal cell carcinoma, cSCC is more likely to spread to distant areas. […] When confined to the epidermis, the outermost layer of the skin, the pre-invasive or in situ form of cSCC is termed Bowen’s disease. […] The condition originates from squamous cells located in the skin’s upper layers. […] Research, both in vivo and in vitro, indicates a crucial role for the upregulation of FGFR2, part of the fibroblast growth factor receptor immunoglobin family, in cSCC cell progression. […] Mutations in the TPL2 gene leads to overexpression of FGFR2, which activates the mTORC1 and AKT pathways in primary and metastatic cSCC cell lines. […] A significant proportion of cSCC and its precursor lesions carry UV-induced p53 mutations. […] In fact, these mutations are present in up to 90% of cSCC cases. The detection of p53 mutations in precursor lesions indicates that this could be an early event in the development of squamous cell carcinoma.

• #45 Bowen’s Disease

  https://pmc.ncbi.nlm.nih.gov/articles/PMC8917478/

  Bowen’s disease (BD) is an in-situ squamous cell carcinoma of epidermis. The etiology of BD is multifactorial with high incidence among Caucasians. The major etiological factors of BD include ultraviolet light exposure, immunosuppression, and Human Papilloma Virus (HPV) infections. The cumulative exposure to ultraviolet light radiation produces DNA damage and immunosuppression facilitating the clonal expansion of underlying p53 mutation. The patients with allogeneic organ transplantation on immunosuppressive drugs such as systemic corticosteroids, azathioprine, and cyclosporine may activate different pathways resulting in induction and promotion of skin malignancies. In immunosuppressed patients, Merkel cell polyomavirus has been associated. The BD arising secondary to arsenic exposure is known to occur after several decades. Arsenic exposures produce oxidative stress and deplete antioxidants. It causes immune dysregulation, impaired DNA repair, genotoxicity, and disorganized signal transduction. In BD, several subtypes of Human Papilloma Virus such as HPV 16, 18, 31, 33, 35, 54, 58, 61, 62, and 73 have been detected. A strong association with HPV 16 had been reported with vulvar BD. HPV DNA is observed in 31% of the extragenital BD. BD is also known to arise following ionizing radiation, thermal skin injury, inflammatory dermatoses such as chronic lupus erythematosus, lupus vulgaris, and following Psoralens and Ultraviolet-A radiation. The incidence of aneuploidy and DNA instability is high in lesional skin of BD. The development of invasive SCC is due to destruction of basement membrane mediated by metalloproteinases. The development of invasive carcinomas is more common among elderly people and immunocompromised individuals. The clinical signs suggestive of malignant transformation are ulceration, bleeding, and nodule formation. According to few retrospective studies, the risk of malignant transformation is around 3% in case of extra-genital BD and 10% in EQ. The invasive SCC of genitals tends to be more aggressive and metastatic. Around 16% of the invasive SCC of penis arises from EQ, while almost 100% of the invasive SCCs arising from photo-exposed areas are from underlying BD.

• #46

  https://journals.lww.com/idoj/fulltext/2022/13020/bowen_s_disease.2.aspx

  Bowen’s disease (BD) is an in-situ squamous cell carcinoma of epidermis. The etiology of BD is multifactorial. The major etiological factors of BD include ultraviolet light exposure, immunosuppression, and Human Papilloma Virus (HPV) infections. The cumulative exposure to ultraviolet light radiation produces DNA damage and immunosuppression facilitating the clonal expansion of underlying p53 mutation. The patients with allogeneic organ transplantation on immunosuppressive drugs such as systemic corticosteroids, azathioprine, and cyclosporine may activate different pathways resulting in induction and promotion of skin malignancies. In immunosuppressed patients, Merkel cell polyomavirus has been associated. The BD arising secondary to arsenic exposure is known to occur after several decades. Arsenic exposures produce oxidative stress and deplete antioxidants. It causes immune dysregulation, impaired DNA repair, genotoxicity, and disorganized signal transduction. In BD, several subtypes of Human Papilloma Virus such as HPV 16, 18, 31, 33, 35, 54, 58, 61, 62, and 73 have been detected. A strong association with HPV 16 had been reported with vulvar BD. HPV DNA is observed in 31% of the extragenital BD. BD is also known to arise following ionizing radiation, thermal skin injury, inflammatory dermatoses such as chronic lupus erythematosus, lupus vulgaris, and following Psoralens and Ultraviolet-A radiation. The incidence of aneuploidy and DNA instability is high in lesional skin of BD. The development of invasive SCC is due to destruction of basement membrane mediated by metalloproteinases. The development of invasive carcinomas is more common among elderly people and immunocompromised individuals. The clinical signs suggestive of malignant transformation are ulceration, bleeding, and nodule formation. According to few retrospective studies, the risk of malignant transformation is around 3% in case of extra-genital BD and 10% in EQ. The invasive SCC of genitals tends to be more aggressive and metastatic. Around 16% of the invasive SCC of penis arises from EQ, while almost 100% of the invasive SCCs arising from photo-exposed areas are from underlying BD.

• #47 From Bowen disease to cutaneous squamous cell carcinoma: eight markers were verified from transcriptomic and proteomic analyses | Journal of Translational Medicine | Full Text

  https://translational-medicine.biomedcentral.com/articles/10.1186/s12967-022-03622-1

  This study highlights that eight proteins, TNC, FSCN1, SERPINB1, ACTN1, RAB31, COL3A1, COL1A1, CD36, were significantly associated with the mechanisms of invasion and metastasis in Bowens disease. […] The exact mechanisms by which BD progresses to CSCC are complicated and merits more attention. […] Therefore, these significantly DEPs may play essential roles in the pathogenesis of malignant biological behaviors in CSCC. […] The results indicated the higher-regulation of COL3A1 and COL1A1 could suppressed CSCC progression, which may be involved in the etiology of altered cell adhesion process. […] Our study confirmed that up-regulation of RAB31 in CSCC relative to Bowen disease and RAB31 may play a crucial role in CSCC invasion, metastasis process. […] Our study revealed that higher expression of SERPINB1 in CSCC relative to Bowen disease. This results may indicated the SERPINB1could as a novel therapeutic target to manage CSCC. […] The results suggested that SERPINB1 knockdown could significantly inhibits CSCC cell migration and invasion.

• #48 From Bowen disease to cutaneous squamous cell carcinoma: eight markers were verified from transcriptomic and proteomic analyses | Journal of Translational Medicine | Full Text

  https://translational-medicine.biomedcentral.com/articles/10.1186/s12967-022-03622-1

  Bowen’s disease is a cutaneous squamous cell carcinoma (CSCC) in situ. If left untreated, BD may progress to invasive CSCC. […] However, the mechanisms of invasion and metastasis from Bowens disease to CSCC is complicated and still unclear. […] The aim of this study was to explore the biomarkers and molecular alterations in Bowens disease development process via analyzing the proteomics changes in tissues of CSCC, Bowen disease and healthy skin. […] A total of 501 proteins were differentially expressed between the CSCC and healthy skin tissues, with 332 up-regulated and 169 down-regulated at least 1.5-fold with a P value0.05. […] These proteins were mainly involved in multiple pathways, including Focal adhesion, ECM-receptor interaction, Human papillomavirus infection, PI3K-Akt signaling pathway, PPAR signaling pathway, AMPK signaling pathway and others.

• #49 From Bowen disease to cutaneous squamous cell carcinoma: eight markers were verified from transcriptomic and proteomic analyses | Journal of Translational Medicine | Full Text

  https://translational-medicine.biomedcentral.com/articles/10.1186/s12967-022-03622-1

  This study highlights that eight proteins, TNC, FSCN1, SERPINB1, ACTN1, RAB31, COL3A1, COL1A1, CD36, were significantly associated with the mechanisms of invasion and metastasis in Bowens disease. […] The exact mechanisms by which BD progresses to CSCC are complicated and merits more attention. […] Therefore, these significantly DEPs may play essential roles in the pathogenesis of malignant biological behaviors in CSCC. […] The results indicated the higher-regulation of COL3A1 and COL1A1 could suppressed CSCC progression, which may be involved in the etiology of altered cell adhesion process. […] Our study confirmed that up-regulation of RAB31 in CSCC relative to Bowen disease and RAB31 may play a crucial role in CSCC invasion, metastasis process. […] Our study revealed that higher expression of SERPINB1 in CSCC relative to Bowen disease. This results may indicated the SERPINB1could as a novel therapeutic target to manage CSCC. […] The results suggested that SERPINB1 knockdown could significantly inhibits CSCC cell migration and invasion.

• #50

  https://link.springer.com/article/10.1007/BF00784349

  We investigated the dermal inflammatory infiltrate and the expression of HLA-DR and 2-microglobulin on the tumour cells in 8 Bowen’s disease (BD) using a series of monoclonal antibodies. The inflammatory infiltrate was classified as mild, moderate or heavy. The infiltrate in all cases consisted mainly of T cells (55-21%) and where the T helper (T H) subset predominated over the T suppressor/cytotoxic (T s/c) subset (T H/T s/c ratio of 2.4-1.0). […] We concluded that there is evidence for a T cell-mediated anti-tumour immune response which may account for the infrequent invasive growth in BD.

• #51

  https://link.springer.com/article/10.1007/BF00784349

  We investigated the dermal inflammatory infiltrate and the expression of HLA-DR and 2-microglobulin on the tumour cells in 8 Bowen’s disease (BD) using a series of monoclonal antibodies. The inflammatory infiltrate was classified as mild, moderate or heavy. The infiltrate in all cases consisted mainly of T cells (55-21%) and where the T helper (T H) subset predominated over the T suppressor/cytotoxic (T s/c) subset (T H/T s/c ratio of 2.4-1.0). […] We concluded that there is evidence for a T cell-mediated anti-tumour immune response which may account for the infrequent invasive growth in BD.

• #52 Bowen’s disease | Better Health Channel

  https://www.betterhealth.vic.gov.au/health/conditionsandtreatments/bowens-disease

  Bowens disease is an early form of skin cancer that appears as a persistent, slow-growing, red and scaly skin patch. In Bowens disease, the skin cancer is located only in the epidermis, the uppermost layer of the skin. […] Rarely, the skin cancer can invade into the dermis and then it is called an invasive squamous cell carcinoma. Only invasive squamous cell carcinoma can metastasise to other parts of the body and become a life-threatening skin cancer. […] In most cases, Bowens disease remains confined to the upper layer of the skin (epidermis). However, if left untreated, the affected cells may migrate deeper into the skin layers. If a patch of Bowens disease becomes raised, tender or is bleeding, then it will need immediate medical attention. […] The cause of Bowens disease is often unknown, but known risk factors include: […] Viral infection infections with certain subtypes of the human papilloma virus (wart virus) can predispose to Bowens disease. This is especially relevant for genital Bowens disease.

• #53 Bowen’s disease | Better Health Channel

  https://www.betterhealth.vic.gov.au/health/conditionsandtreatments/bowens-disease

  Bowens disease is an early form of skin cancer that appears as a persistent, slow-growing, red and scaly skin patch. In Bowens disease, the skin cancer is located only in the epidermis, the uppermost layer of the skin. […] Rarely, the skin cancer can invade into the dermis and then it is called an invasive squamous cell carcinoma. Only invasive squamous cell carcinoma can metastasise to other parts of the body and become a life-threatening skin cancer. […] In most cases, Bowens disease remains confined to the upper layer of the skin (epidermis). However, if left untreated, the affected cells may migrate deeper into the skin layers. If a patch of Bowens disease becomes raised, tender or is bleeding, then it will need immediate medical attention. […] The cause of Bowens disease is often unknown, but known risk factors include: […] Viral infection infections with certain subtypes of the human papilloma virus (wart virus) can predispose to Bowens disease. This is especially relevant for genital Bowens disease.

• #54 Bowen’s Disease of the Eyelid: a Teaching Case Report | The Journal of Optometric Education

  https://journal.opted.org/article/bowens-disease-of-the-eyelid-a-teaching-case-report/

  BD is a precancerous lesion that may have delayed diagnosis due to its slow-growing nature. Lesions frequently arise between the sixth and ninth decade of life on areas of sun-exposed skin. Co-management between eyecare professionals and dermatologists is imperative to successfully diagnose and treat BD as well as monitor patients for recurrence. BD appears similar to other skin lesions and thus requires biopsy for a definitive diagnosis. Lesions are typically treated surgically with excision but can also be managed topically with antineoplastic agents. BD has a favorable prognosis with a low risk of progression to SCC.

• #55 Squamous Cell Carcinoma In Situ—The Importance of Early Diagnosis in Bowen Disease, Vulvar Intraepithelial Neoplasia, Penile Intraepithelial Neoplasia, and Erythroplasia of Queyrat

  https://www.mdpi.com/2075-4418/14/16/1799

  Bowen’s disease represents an in situ cSCC, with a 3–5% risk of progressing into invasive SCC. […] The primary etiological factors of BD are exposure to ultraviolet light, immunosuppression, and human papillomavirus (HPV) infections. […] Cumulative exposure to ultraviolet (UV) light radiation causes DNA damage and immunosuppression, which promotes the clonal expansion of cells with p53 mutations. […] Furthermore, exposure to certain toxic substances, such as arsenic, and infection with oncogenic strains of HPV also contribute to the development of BD. […] Histopathology remains the gold standard for diagnosis, revealing hyperkeratosis, parakeratosis, acanthosis with elongation and thickening of rete ridges, absence of the granular layer, and full-thickness keratinocyte atypia without breaching the dermo–epidermal junction.

• #56 Bowen’s Disease of the Eyelid: a Teaching Case Report | The Journal of Optometric Education

  https://journal.opted.org/article/bowens-disease-of-the-eyelid-a-teaching-case-report/

  Topical interventions include photodynamic therapy (PDT) and antineoplastic agents. With PDT, a cream specific to cancer cells is applied to a lesion and exposed to laser, releasing toxic material thereby destroying abnormal cells. Antineoplastic agents are medications used to treat cancer by inhibiting cell division. Two specific antineoplastic medications used in BD are imiquimod and 5-fluorouracil. Imiquimod stimulates the immune system and is thought to increase the presence of lymphocytes, macrophages and dendritic cells within a BD lesion. 5-fluorouracil interferes with DNA synthesis to reduce cell proliferation and has a cure rate of about 80%. […] Overall, BD has a favorable prognosis with a risk of conversion to SCC of 3-4%. After treatment, there is a 10% chance of BD reocurrence. Optometrists should counsel their patients on preventative measures including the use of broad-spectrum sunscreen, wide-brimmed hats, UV400 sunglasses, avoiding chronic sun exposure, refraining from tanning bed use, and actively self-examining their skin for new or developing lesions. Patients should be educated on abnormal characteristics of a lesion such as sclerosis, hemorrhaging, allodynia, growth and/or change in pigmentation. Patients with a history of skin cancer should also have a screening with their primary care physician or dermatologist every 6-12 months.

• #57 Bowen’s Disease

  https://pmc.ncbi.nlm.nih.gov/articles/PMC8917478/

  Bowen’s disease (BD) is an in-situ squamous cell carcinoma of epidermis. The etiology of BD is multifactorial with high incidence among Caucasians. The major etiological factors of BD include ultraviolet light exposure, immunosuppression, and Human Papilloma Virus (HPV) infections. The cumulative exposure to ultraviolet light radiation produces DNA damage and immunosuppression facilitating the clonal expansion of underlying p53 mutation. The patients with allogeneic organ transplantation on immunosuppressive drugs such as systemic corticosteroids, azathioprine, and cyclosporine may activate different pathways resulting in induction and promotion of skin malignancies. In immunosuppressed patients, Merkel cell polyomavirus has been associated. The BD arising secondary to arsenic exposure is known to occur after several decades. Arsenic exposures produce oxidative stress and deplete antioxidants. It causes immune dysregulation, impaired DNA repair, genotoxicity, and disorganized signal transduction. In BD, several subtypes of Human Papilloma Virus such as HPV 16, 18, 31, 33, 35, 54, 58, 61, 62, and 73 have been detected. A strong association with HPV 16 had been reported with vulvar BD. HPV DNA is observed in 31% of the extragenital BD. BD is also known to arise following ionizing radiation, thermal skin injury, inflammatory dermatoses such as chronic lupus erythematosus, lupus vulgaris, and following Psoralens and Ultraviolet-A radiation. The incidence of aneuploidy and DNA instability is high in lesional skin of BD. The development of invasive SCC is due to destruction of basement membrane mediated by metalloproteinases. The development of invasive carcinomas is more common among elderly people and immunocompromised individuals. The clinical signs suggestive of malignant transformation are ulceration, bleeding, and nodule formation. According to few retrospective studies, the risk of malignant transformation is around 3% in case of extra-genital BD and 10% in EQ. The invasive SCC of genitals tends to be more aggressive and metastatic. Around 16% of the invasive SCC of penis arises from EQ, while almost 100% of the invasive SCCs arising from photo-exposed areas are from underlying BD.

• #58

  https://journals.lww.com/idoj/fulltext/2022/13020/bowen_s_disease.2.aspx

  Bowen’s disease (BD) is an in-situ squamous cell carcinoma of epidermis. The etiology of BD is multifactorial. The major etiological factors of BD include ultraviolet light exposure, immunosuppression, and Human Papilloma Virus (HPV) infections. The cumulative exposure to ultraviolet light radiation produces DNA damage and immunosuppression facilitating the clonal expansion of underlying p53 mutation. The patients with allogeneic organ transplantation on immunosuppressive drugs such as systemic corticosteroids, azathioprine, and cyclosporine may activate different pathways resulting in induction and promotion of skin malignancies. In immunosuppressed patients, Merkel cell polyomavirus has been associated. The BD arising secondary to arsenic exposure is known to occur after several decades. Arsenic exposures produce oxidative stress and deplete antioxidants. It causes immune dysregulation, impaired DNA repair, genotoxicity, and disorganized signal transduction. In BD, several subtypes of Human Papilloma Virus such as HPV 16, 18, 31, 33, 35, 54, 58, 61, 62, and 73 have been detected. A strong association with HPV 16 had been reported with vulvar BD. HPV DNA is observed in 31% of the extragenital BD. BD is also known to arise following ionizing radiation, thermal skin injury, inflammatory dermatoses such as chronic lupus erythematosus, lupus vulgaris, and following Psoralens and Ultraviolet-A radiation. The incidence of aneuploidy and DNA instability is high in lesional skin of BD. The development of invasive SCC is due to destruction of basement membrane mediated by metalloproteinases. The development of invasive carcinomas is more common among elderly people and immunocompromised individuals. The clinical signs suggestive of malignant transformation are ulceration, bleeding, and nodule formation. According to few retrospective studies, the risk of malignant transformation is around 3% in case of extra-genital BD and 10% in EQ. The invasive SCC of genitals tends to be more aggressive and metastatic. Around 16% of the invasive SCC of penis arises from EQ, while almost 100% of the invasive SCCs arising from photo-exposed areas are from underlying BD.

• #59 Bowen’s Disease

  https://pmc.ncbi.nlm.nih.gov/articles/PMC8917478/

  Bowen’s disease (BD) is an in-situ squamous cell carcinoma of epidermis. The etiology of BD is multifactorial with high incidence among Caucasians. The major etiological factors of BD include ultraviolet light exposure, immunosuppression, and Human Papilloma Virus (HPV) infections. The cumulative exposure to ultraviolet light radiation produces DNA damage and immunosuppression facilitating the clonal expansion of underlying p53 mutation. The patients with allogeneic organ transplantation on immunosuppressive drugs such as systemic corticosteroids, azathioprine, and cyclosporine may activate different pathways resulting in induction and promotion of skin malignancies. In immunosuppressed patients, Merkel cell polyomavirus has been associated. The BD arising secondary to arsenic exposure is known to occur after several decades. Arsenic exposures produce oxidative stress and deplete antioxidants. It causes immune dysregulation, impaired DNA repair, genotoxicity, and disorganized signal transduction. In BD, several subtypes of Human Papilloma Virus such as HPV 16, 18, 31, 33, 35, 54, 58, 61, 62, and 73 have been detected. A strong association with HPV 16 had been reported with vulvar BD. HPV DNA is observed in 31% of the extragenital BD. BD is also known to arise following ionizing radiation, thermal skin injury, inflammatory dermatoses such as chronic lupus erythematosus, lupus vulgaris, and following Psoralens and Ultraviolet-A radiation. The incidence of aneuploidy and DNA instability is high in lesional skin of BD. The development of invasive SCC is due to destruction of basement membrane mediated by metalloproteinases. The development of invasive carcinomas is more common among elderly people and immunocompromised individuals. The clinical signs suggestive of malignant transformation are ulceration, bleeding, and nodule formation. According to few retrospective studies, the risk of malignant transformation is around 3% in case of extra-genital BD and 10% in EQ. The invasive SCC of genitals tends to be more aggressive and metastatic. Around 16% of the invasive SCC of penis arises from EQ, while almost 100% of the invasive SCCs arising from photo-exposed areas are from underlying BD.

• #60

  https://journals.lww.com/idoj/fulltext/2022/13020/bowen_s_disease.2.aspx

  Bowen’s disease (BD) is an in-situ squamous cell carcinoma of epidermis. The etiology of BD is multifactorial. The major etiological factors of BD include ultraviolet light exposure, immunosuppression, and Human Papilloma Virus (HPV) infections. The cumulative exposure to ultraviolet light radiation produces DNA damage and immunosuppression facilitating the clonal expansion of underlying p53 mutation. The patients with allogeneic organ transplantation on immunosuppressive drugs such as systemic corticosteroids, azathioprine, and cyclosporine may activate different pathways resulting in induction and promotion of skin malignancies. In immunosuppressed patients, Merkel cell polyomavirus has been associated. The BD arising secondary to arsenic exposure is known to occur after several decades. Arsenic exposures produce oxidative stress and deplete antioxidants. It causes immune dysregulation, impaired DNA repair, genotoxicity, and disorganized signal transduction. In BD, several subtypes of Human Papilloma Virus such as HPV 16, 18, 31, 33, 35, 54, 58, 61, 62, and 73 have been detected. A strong association with HPV 16 had been reported with vulvar BD. HPV DNA is observed in 31% of the extragenital BD. BD is also known to arise following ionizing radiation, thermal skin injury, inflammatory dermatoses such as chronic lupus erythematosus, lupus vulgaris, and following Psoralens and Ultraviolet-A radiation. The incidence of aneuploidy and DNA instability is high in lesional skin of BD. The development of invasive SCC is due to destruction of basement membrane mediated by metalloproteinases. The development of invasive carcinomas is more common among elderly people and immunocompromised individuals. The clinical signs suggestive of malignant transformation are ulceration, bleeding, and nodule formation. According to few retrospective studies, the risk of malignant transformation is around 3% in case of extra-genital BD and 10% in EQ. The invasive SCC of genitals tends to be more aggressive and metastatic. Around 16% of the invasive SCC of penis arises from EQ, while almost 100% of the invasive SCCs arising from photo-exposed areas are from underlying BD.

• #61 Bowen’s Disease

  https://pmc.ncbi.nlm.nih.gov/articles/PMC8917478/

  Bowen’s disease (BD) is an in-situ squamous cell carcinoma of epidermis. The etiology of BD is multifactorial with high incidence among Caucasians. The major etiological factors of BD include ultraviolet light exposure, immunosuppression, and Human Papilloma Virus (HPV) infections. The cumulative exposure to ultraviolet light radiation produces DNA damage and immunosuppression facilitating the clonal expansion of underlying p53 mutation. The patients with allogeneic organ transplantation on immunosuppressive drugs such as systemic corticosteroids, azathioprine, and cyclosporine may activate different pathways resulting in induction and promotion of skin malignancies. In immunosuppressed patients, Merkel cell polyomavirus has been associated. The BD arising secondary to arsenic exposure is known to occur after several decades. Arsenic exposures produce oxidative stress and deplete antioxidants. It causes immune dysregulation, impaired DNA repair, genotoxicity, and disorganized signal transduction. In BD, several subtypes of Human Papilloma Virus such as HPV 16, 18, 31, 33, 35, 54, 58, 61, 62, and 73 have been detected. A strong association with HPV 16 had been reported with vulvar BD. HPV DNA is observed in 31% of the extragenital BD. BD is also known to arise following ionizing radiation, thermal skin injury, inflammatory dermatoses such as chronic lupus erythematosus, lupus vulgaris, and following Psoralens and Ultraviolet-A radiation. The incidence of aneuploidy and DNA instability is high in lesional skin of BD. The development of invasive SCC is due to destruction of basement membrane mediated by metalloproteinases. The development of invasive carcinomas is more common among elderly people and immunocompromised individuals. The clinical signs suggestive of malignant transformation are ulceration, bleeding, and nodule formation. According to few retrospective studies, the risk of malignant transformation is around 3% in case of extra-genital BD and 10% in EQ. The invasive SCC of genitals tends to be more aggressive and metastatic. Around 16% of the invasive SCC of penis arises from EQ, while almost 100% of the invasive SCCs arising from photo-exposed areas are from underlying BD.

• #62

  https://journals.lww.com/idoj/fulltext/2022/13020/bowen_s_disease.2.aspx

  Bowen’s disease (BD) is an in-situ squamous cell carcinoma of epidermis. The etiology of BD is multifactorial. The major etiological factors of BD include ultraviolet light exposure, immunosuppression, and Human Papilloma Virus (HPV) infections. The cumulative exposure to ultraviolet light radiation produces DNA damage and immunosuppression facilitating the clonal expansion of underlying p53 mutation. The patients with allogeneic organ transplantation on immunosuppressive drugs such as systemic corticosteroids, azathioprine, and cyclosporine may activate different pathways resulting in induction and promotion of skin malignancies. In immunosuppressed patients, Merkel cell polyomavirus has been associated. The BD arising secondary to arsenic exposure is known to occur after several decades. Arsenic exposures produce oxidative stress and deplete antioxidants. It causes immune dysregulation, impaired DNA repair, genotoxicity, and disorganized signal transduction. In BD, several subtypes of Human Papilloma Virus such as HPV 16, 18, 31, 33, 35, 54, 58, 61, 62, and 73 have been detected. A strong association with HPV 16 had been reported with vulvar BD. HPV DNA is observed in 31% of the extragenital BD. BD is also known to arise following ionizing radiation, thermal skin injury, inflammatory dermatoses such as chronic lupus erythematosus, lupus vulgaris, and following Psoralens and Ultraviolet-A radiation. The incidence of aneuploidy and DNA instability is high in lesional skin of BD. The development of invasive SCC is due to destruction of basement membrane mediated by metalloproteinases. The development of invasive carcinomas is more common among elderly people and immunocompromised individuals. The clinical signs suggestive of malignant transformation are ulceration, bleeding, and nodule formation. According to few retrospective studies, the risk of malignant transformation is around 3% in case of extra-genital BD and 10% in EQ. The invasive SCC of genitals tends to be more aggressive and metastatic. Around 16% of the invasive SCC of penis arises from EQ, while almost 100% of the invasive SCCs arising from photo-exposed areas are from underlying BD.

• #63 Bowen’s Disease

  https://pmc.ncbi.nlm.nih.gov/articles/PMC8917478/

  Bowen’s disease (BD) is an in-situ squamous cell carcinoma of epidermis. The etiology of BD is multifactorial with high incidence among Caucasians. The major etiological factors of BD include ultraviolet light exposure, immunosuppression, and Human Papilloma Virus (HPV) infections. The cumulative exposure to ultraviolet light radiation produces DNA damage and immunosuppression facilitating the clonal expansion of underlying p53 mutation. The patients with allogeneic organ transplantation on immunosuppressive drugs such as systemic corticosteroids, azathioprine, and cyclosporine may activate different pathways resulting in induction and promotion of skin malignancies. In immunosuppressed patients, Merkel cell polyomavirus has been associated. The BD arising secondary to arsenic exposure is known to occur after several decades. Arsenic exposures produce oxidative stress and deplete antioxidants. It causes immune dysregulation, impaired DNA repair, genotoxicity, and disorganized signal transduction. In BD, several subtypes of Human Papilloma Virus such as HPV 16, 18, 31, 33, 35, 54, 58, 61, 62, and 73 have been detected. A strong association with HPV 16 had been reported with vulvar BD. HPV DNA is observed in 31% of the extragenital BD. BD is also known to arise following ionizing radiation, thermal skin injury, inflammatory dermatoses such as chronic lupus erythematosus, lupus vulgaris, and following Psoralens and Ultraviolet-A radiation. The incidence of aneuploidy and DNA instability is high in lesional skin of BD. The development of invasive SCC is due to destruction of basement membrane mediated by metalloproteinases. The development of invasive carcinomas is more common among elderly people and immunocompromised individuals. The clinical signs suggestive of malignant transformation are ulceration, bleeding, and nodule formation. According to few retrospective studies, the risk of malignant transformation is around 3% in case of extra-genital BD and 10% in EQ. The invasive SCC of genitals tends to be more aggressive and metastatic. Around 16% of the invasive SCC of penis arises from EQ, while almost 100% of the invasive SCCs arising from photo-exposed areas are from underlying BD.

• #64

  https://journals.lww.com/idoj/fulltext/2022/13020/bowen_s_disease.2.aspx

  Bowen’s disease (BD) is an in-situ squamous cell carcinoma of epidermis. The etiology of BD is multifactorial. The major etiological factors of BD include ultraviolet light exposure, immunosuppression, and Human Papilloma Virus (HPV) infections. The cumulative exposure to ultraviolet light radiation produces DNA damage and immunosuppression facilitating the clonal expansion of underlying p53 mutation. The patients with allogeneic organ transplantation on immunosuppressive drugs such as systemic corticosteroids, azathioprine, and cyclosporine may activate different pathways resulting in induction and promotion of skin malignancies. In immunosuppressed patients, Merkel cell polyomavirus has been associated. The BD arising secondary to arsenic exposure is known to occur after several decades. Arsenic exposures produce oxidative stress and deplete antioxidants. It causes immune dysregulation, impaired DNA repair, genotoxicity, and disorganized signal transduction. In BD, several subtypes of Human Papilloma Virus such as HPV 16, 18, 31, 33, 35, 54, 58, 61, 62, and 73 have been detected. A strong association with HPV 16 had been reported with vulvar BD. HPV DNA is observed in 31% of the extragenital BD. BD is also known to arise following ionizing radiation, thermal skin injury, inflammatory dermatoses such as chronic lupus erythematosus, lupus vulgaris, and following Psoralens and Ultraviolet-A radiation. The incidence of aneuploidy and DNA instability is high in lesional skin of BD. The development of invasive SCC is due to destruction of basement membrane mediated by metalloproteinases. The development of invasive carcinomas is more common among elderly people and immunocompromised individuals. The clinical signs suggestive of malignant transformation are ulceration, bleeding, and nodule formation. According to few retrospective studies, the risk of malignant transformation is around 3% in case of extra-genital BD and 10% in EQ. The invasive SCC of genitals tends to be more aggressive and metastatic. Around 16% of the invasive SCC of penis arises from EQ, while almost 100% of the invasive SCCs arising from photo-exposed areas are from underlying BD.

• #65 Bowen’s Disease

  https://pmc.ncbi.nlm.nih.gov/articles/PMC8917478/

  Bowen’s disease (BD) is an in-situ squamous cell carcinoma of epidermis. The etiology of BD is multifactorial with high incidence among Caucasians. The major etiological factors of BD include ultraviolet light exposure, immunosuppression, and Human Papilloma Virus (HPV) infections. The cumulative exposure to ultraviolet light radiation produces DNA damage and immunosuppression facilitating the clonal expansion of underlying p53 mutation. The patients with allogeneic organ transplantation on immunosuppressive drugs such as systemic corticosteroids, azathioprine, and cyclosporine may activate different pathways resulting in induction and promotion of skin malignancies. In immunosuppressed patients, Merkel cell polyomavirus has been associated. The BD arising secondary to arsenic exposure is known to occur after several decades. Arsenic exposures produce oxidative stress and deplete antioxidants. It causes immune dysregulation, impaired DNA repair, genotoxicity, and disorganized signal transduction. In BD, several subtypes of Human Papilloma Virus such as HPV 16, 18, 31, 33, 35, 54, 58, 61, 62, and 73 have been detected. A strong association with HPV 16 had been reported with vulvar BD. HPV DNA is observed in 31% of the extragenital BD. BD is also known to arise following ionizing radiation, thermal skin injury, inflammatory dermatoses such as chronic lupus erythematosus, lupus vulgaris, and following Psoralens and Ultraviolet-A radiation. The incidence of aneuploidy and DNA instability is high in lesional skin of BD. The development of invasive SCC is due to destruction of basement membrane mediated by metalloproteinases. The development of invasive carcinomas is more common among elderly people and immunocompromised individuals. The clinical signs suggestive of malignant transformation are ulceration, bleeding, and nodule formation. According to few retrospective studies, the risk of malignant transformation is around 3% in case of extra-genital BD and 10% in EQ. The invasive SCC of genitals tends to be more aggressive and metastatic. Around 16% of the invasive SCC of penis arises from EQ, while almost 100% of the invasive SCCs arising from photo-exposed areas are from underlying BD.

• #66

  https://journals.lww.com/idoj/fulltext/2022/13020/bowen_s_disease.2.aspx

  Bowen’s disease (BD) is an in-situ squamous cell carcinoma of epidermis. The etiology of BD is multifactorial. The major etiological factors of BD include ultraviolet light exposure, immunosuppression, and Human Papilloma Virus (HPV) infections. The cumulative exposure to ultraviolet light radiation produces DNA damage and immunosuppression facilitating the clonal expansion of underlying p53 mutation. The patients with allogeneic organ transplantation on immunosuppressive drugs such as systemic corticosteroids, azathioprine, and cyclosporine may activate different pathways resulting in induction and promotion of skin malignancies. In immunosuppressed patients, Merkel cell polyomavirus has been associated. The BD arising secondary to arsenic exposure is known to occur after several decades. Arsenic exposures produce oxidative stress and deplete antioxidants. It causes immune dysregulation, impaired DNA repair, genotoxicity, and disorganized signal transduction. In BD, several subtypes of Human Papilloma Virus such as HPV 16, 18, 31, 33, 35, 54, 58, 61, 62, and 73 have been detected. A strong association with HPV 16 had been reported with vulvar BD. HPV DNA is observed in 31% of the extragenital BD. BD is also known to arise following ionizing radiation, thermal skin injury, inflammatory dermatoses such as chronic lupus erythematosus, lupus vulgaris, and following Psoralens and Ultraviolet-A radiation. The incidence of aneuploidy and DNA instability is high in lesional skin of BD. The development of invasive SCC is due to destruction of basement membrane mediated by metalloproteinases. The development of invasive carcinomas is more common among elderly people and immunocompromised individuals. The clinical signs suggestive of malignant transformation are ulceration, bleeding, and nodule formation. According to few retrospective studies, the risk of malignant transformation is around 3% in case of extra-genital BD and 10% in EQ. The invasive SCC of genitals tends to be more aggressive and metastatic. Around 16% of the invasive SCC of penis arises from EQ, while almost 100% of the invasive SCCs arising from photo-exposed areas are from underlying BD.

• #67 Bowen’s Disease: Causes, Treatment, Prognosis and More

  https://www.verywellhealth.com/bowen-s-disease-overview-and-more-5197049

  Bowens disease (also called squamous cell carcinoma in situ) is a non-invasive early form of skin cancer, characterized by slow-growing patches of red, scaly skin. It affects the squamous cells in the outermost layer of the skin. […] The exact cause of Bowens disease is not known, but several risk factors for the condition have been identified, including: Chronic sun exposure or exposure from indoor tanning beds, A weakened immune system, Previous radiotherapy treatment, Human papillomavirus (HPV). […] Chronic exposure to arsenic might also be a contributing risk factor for Bowens disease. Research suggests that Bowens disease may appear roughly 10 years after initial exposure to arsenic. […] In some cases, undiagnosed or untreated Bowens disease can develop into a more invasive form of skin cancer called squamous cell skin cancer. Estimates suggest the progression occurs in one in 20 to one in 30 people with untreated Bowens disease.

• #68 Squamous Cell Carcinoma In Situ—The Importance of Early Diagnosis in Bowen Disease, Vulvar Intraepithelial Neoplasia, Penile Intraepithelial Neoplasia, and Erythroplasia of Queyrat

  https://www.mdpi.com/2075-4418/14/16/1799

  BD is characterized by distinct immunohistochemical profiles that aid in its differentiation from other dermatological conditions. […] The early diagnosis of BD, VIN, and PeIN is crucial due to their potential for malignant transformation and significant impact on patient outcomes. Detecting these early SCCs at an initial stage enables timely and effective treatment, reducing the risk of progression to invasive SCC.

• #69 Squamous Cell Carcinoma In Situ—The Importance of Early Diagnosis in Bowen Disease, Vulvar Intraepithelial Neoplasia, Penile Intraepithelial Neoplasia, and Erythroplasia of Queyrat

  https://www.mdpi.com/2075-4418/14/16/1799

  BD is characterized by distinct immunohistochemical profiles that aid in its differentiation from other dermatological conditions. […] The early diagnosis of BD, VIN, and PeIN is crucial due to their potential for malignant transformation and significant impact on patient outcomes. Detecting these early SCCs at an initial stage enables timely and effective treatment, reducing the risk of progression to invasive SCC.

• #70 Squamous cell carcinoma of the skin – Symptoms and causes – Mayo Clinic

  https://www.mayoclinic.org/diseases-conditions/squamous-cell-carcinoma/symptoms-causes/syc-20352480

  Squamous cell carcinoma of the skin occurs when the squamous cells in the skin get changes in their DNA. […] The changes tell the squamous cells to multiply quickly. The cells continue living when healthy cells would die as part of their natural life cycle. […] Ultraviolet (UV) radiation causes most of the DNA changes in skin cells. UV radiation can come from sunlight, tanning lamps and tanning beds.

• #71 Squamous cell carcinoma of the skin – Symptoms and causes – Mayo Clinic

  https://www.mayoclinic.org/diseases-conditions/squamous-cell-carcinoma/symptoms-causes/syc-20352480

  Squamous cell carcinoma of the skin occurs when the squamous cells in the skin get changes in their DNA. […] The changes tell the squamous cells to multiply quickly. The cells continue living when healthy cells would die as part of their natural life cycle. […] Ultraviolet (UV) radiation causes most of the DNA changes in skin cells. UV radiation can come from sunlight, tanning lamps and tanning beds.

• #72 Bowen’s Disease Symptoms, Causes, Diagnosis, and Treatment

  https://www.healthline.com/health/skin-cancer/bowens-disease

  Bowens disease is an early form of squamous cell carcinoma (SCC), a type of skin cancer. […] The specific cause of Bowens disease is currently unknown. But there are certain factors associated with the disease. […] Prolonged exposure to ultraviolet (UV) radiation is a major contributor to Bowens disease. […] Over time, UV radiation damages the DNA in your skin. This can lead to cancerous conditions like Bowens disease. […] A mutation of the p53 gene can lead to various forms of tumors, including those involved in skin cancer. […] A weakened immune system can increase the expression of a p53 mutation. This may cause Bowens disease. […] A human papillomavirus (HPV) infection is another potential cause of Bowens disease. Several types of HPV may be associated with the disease. […] Chronic arsenic exposure can lead to Bowens disease. It takes about 10 years to develop after your first exposure.

• #73 Bowen’s disease of the anal canal treated with radiation therapy: A case report

  https://www.oatext.com/bowens-disease-of-the-anal-canal-treated-with-radiation-therapy-a-case-report.php

  Bowens disease, also known as intraepithelial neoplasia, is a very slow-growing carcinoma in situ. In Bowens disease, surgical resection is the standard of treatment. […] HPV infection is most commonly responsible for etiology. Up to 80 percent of AIN cases are believed to develop from infections from the Human Papilloma Virus (HPV) 16 and 18. HPV E6 and E7 gene products inactivate the mitotic regulator proteins of tumor suppressor genes (p53 and Rb), thereby permitting malignant transformation. […] Because of the morbidity and the high recurrence rates associated with surgical resection of Bowens disease, several treatment modalities have been applied, including imiquimod, external fluorouracil, laser therapy, radiotherapy and, photodynamic therapy. […] Of these, radiation therapy is appropriate for larger and recurrent lesions with good functional and cosmetic results.

• #74 Human papillomavirus infection and p16 expression in the immunocompetent patients with extragenital/extraungual Bowen’s disease | Diagnostic Pathology | Full Text

  https://diagnosticpathology.biomedcentral.com/articles/10.1186/s13000-016-0505-3

  The role of human papillomaviruses (HPV) in the development of squamous cell carcinoma (SCC) has been established for anogenital lesions but still remains controversial for carcinomas in other sites. […] The aim of this study was to determine the -HPV and -HPV prevalence and their association with p16 expression, sun exposure, and clinicopathological findings in patients with Bowens disease (BD). […] HPV may play an etiological role at least in some SCC in situ arising in extragenital sites. […] The presence of the p16-expression, papillomatosis or koilocyte-like change is not a reliable marker of HPV infection in SCC in situ. […] The mechanisms responsible for HPV driven malignant transformation of cutaneous keratinocytes are not yet fully understood and further investigation in that matter is warranted.

• #75 Human papillomavirus infection and p16 expression in the immunocompetent patients with extragenital/extraungual Bowen’s disease | Diagnostic Pathology | Full Text

  https://diagnosticpathology.biomedcentral.com/articles/10.1186/s13000-016-0505-3

  The role of human papillomaviruses (HPV) in the development of squamous cell carcinoma (SCC) has been established for anogenital lesions but still remains controversial for carcinomas in other sites. […] The aim of this study was to determine the -HPV and -HPV prevalence and their association with p16 expression, sun exposure, and clinicopathological findings in patients with Bowens disease (BD). […] HPV may play an etiological role at least in some SCC in situ arising in extragenital sites. […] The presence of the p16-expression, papillomatosis or koilocyte-like change is not a reliable marker of HPV infection in SCC in situ. […] The mechanisms responsible for HPV driven malignant transformation of cutaneous keratinocytes are not yet fully understood and further investigation in that matter is warranted.

• #76 Human papillomavirus infection and p16 expression in the immunocompetent patients with extragenital/extraungual Bowen’s disease | Diagnostic Pathology | Full Text

  https://diagnosticpathology.biomedcentral.com/articles/10.1186/s13000-016-0505-3

  The role of human papillomaviruses (HPV) in the development of squamous cell carcinoma (SCC) has been established for anogenital lesions but still remains controversial for carcinomas in other sites. […] The aim of this study was to determine the -HPV and -HPV prevalence and their association with p16 expression, sun exposure, and clinicopathological findings in patients with Bowens disease (BD). […] HPV may play an etiological role at least in some SCC in situ arising in extragenital sites. […] The presence of the p16-expression, papillomatosis or koilocyte-like change is not a reliable marker of HPV infection in SCC in situ. […] The mechanisms responsible for HPV driven malignant transformation of cutaneous keratinocytes are not yet fully understood and further investigation in that matter is warranted.

• #77 Human papillomavirus infection and p16 expression in the immunocompetent patients with extragenital/extraungual Bowen’s disease | Diagnostic Pathology | Full Text

  https://diagnosticpathology.biomedcentral.com/articles/10.1186/s13000-016-0505-3

  Nevertheless, the epidemiological and experimental evidence suggests the role of combined effects of ultraviolet radiation, immunosuppression and -papillomavirus infection. […] Our study further supports the hypothesis that HPV infection might serve as an important co-factor in the carcinogenesis of BD and cSCC and identifies HPV 9 as a possibly significant -HPV genotype with respect to mixed -HPV infections and keratinocyte carcinogenesis.

• #78 SciELO Brazil – Pigmented Bowen’s disease: a case report of an unusual variant Pigmented Bowen’s disease: a case report of an unusual variant

  https://www.scielo.br/j/jbpml/a/ZKy3FRmPVy9jb4Z59bfY8sq/

  Bowen’s disease is a squamous cell carcinoma in situ with the potential to turn into invasive carcinoma. […] The pigmented BD is a rare variant that accounts for less than 2% of BD cases, and is considered difficult to diagnose. […] It is characterized by the typical alterations of BD and by melanin increase in the epidermis and dermis. […] Risk factors are the same as BD’s: exposure to sunlight, radiotherapy, arsenic, trauma, and infection with human papillomavirus (HPV). […] Little is known about the mechanism of pigmentation of BD, and several theories attempt to explain its origin. […] The theory of „colonization” asserts that the pigment occurs due to the presence of an increased number of melanocytic hyperplasia with hypertrophic dendritic processes dispersed through the tumor.

• #79 SciELO Brazil – Pigmented Bowen’s disease: a case report of an unusual variant Pigmented Bowen’s disease: a case report of an unusual variant

  https://www.scielo.br/j/jbpml/a/ZKy3FRmPVy9jb4Z59bfY8sq/

  Bowen’s disease is a squamous cell carcinoma in situ with the potential to turn into invasive carcinoma. […] The pigmented BD is a rare variant that accounts for less than 2% of BD cases, and is considered difficult to diagnose. […] It is characterized by the typical alterations of BD and by melanin increase in the epidermis and dermis. […] Risk factors are the same as BD’s: exposure to sunlight, radiotherapy, arsenic, trauma, and infection with human papillomavirus (HPV). […] Little is known about the mechanism of pigmentation of BD, and several theories attempt to explain its origin. […] The theory of „colonization” asserts that the pigment occurs due to the presence of an increased number of melanocytic hyperplasia with hypertrophic dendritic processes dispersed through the tumor.

• #80 SciELO Brazil – Pigmented Bowen’s disease: a case report of an unusual variant Pigmented Bowen’s disease: a case report of an unusual variant

  https://www.scielo.br/j/jbpml/a/ZKy3FRmPVy9jb4Z59bfY8sq/

  Bowen’s disease is a squamous cell carcinoma in situ with the potential to turn into invasive carcinoma. […] The pigmented BD is a rare variant that accounts for less than 2% of BD cases, and is considered difficult to diagnose. […] It is characterized by the typical alterations of BD and by melanin increase in the epidermis and dermis. […] Risk factors are the same as BD’s: exposure to sunlight, radiotherapy, arsenic, trauma, and infection with human papillomavirus (HPV). […] Little is known about the mechanism of pigmentation of BD, and several theories attempt to explain its origin. […] The theory of „colonization” asserts that the pigment occurs due to the presence of an increased number of melanocytic hyperplasia with hypertrophic dendritic processes dispersed through the tumor.

• #81 SciELO Brazil – Pigmented Bowen’s disease: a case report of an unusual variant Pigmented Bowen’s disease: a case report of an unusual variant

  https://www.scielo.br/j/jbpml/a/ZKy3FRmPVy9jb4Z59bfY8sq/

  Another theory suggests that, in pigmented BD case without scaling and keratosis signals, atypical keratinocytes are still in a well-differentiated stage, having, therefore, melanin. […] A third hypothesis suggests that specific growth factors or cytokines produced by cancer cells may stimulate the proliferation of melanocytes and melanin production.

• #82 SciELO Brazil – Pigmented Bowen’s disease: a case report of an unusual variant Pigmented Bowen’s disease: a case report of an unusual variant

  https://www.scielo.br/j/jbpml/a/ZKy3FRmPVy9jb4Z59bfY8sq/

  Another theory suggests that, in pigmented BD case without scaling and keratosis signals, atypical keratinocytes are still in a well-differentiated stage, having, therefore, melanin. […] A third hypothesis suggests that specific growth factors or cytokines produced by cancer cells may stimulate the proliferation of melanocytes and melanin production.

• #83 Bowen’s Disease – PubMed

  https://pubmed.ncbi.nlm.nih.gov/35287414/

  Bowen’s disease (BD) is an in-situ squamous cell carcinoma of epidermis. […] The etiology of BD is multifactorial with high incidence among Caucasians. […] BD is considered as the „lull before the storm,” which precedes an overt squamous cell carcinoma. […] Histopathology is the gold standard diagnostic modality to confirm the diagnosis. […] Immunohistochemistry, dermoscopy, and reflectance confocal microscopy are the adjuvant modalities used in the diagnosis of BD. […] The available therapeutic modalities include topical chemotherapy, surgical modalities, light-based modalities, and destructive therapies. […] It requires a combined effort of dermatologist, oncosurgeon, and plastic surgeon to plan and execute the management in various presentations of BD.

• #84 Bowen’s Disease of the Penis | Consultant360

  https://www.consultant360.com/articles/bowen-s-disease-penis

  Bowens disease is a superficial squamous cell carcinoma in which cancer cells are confined to all layers of the epidermis but have not yet invaded the dermis. […] The exact etiology is unknown, but several studies have linked this disorder to human papillomavirus infection. […] Imiquimod is an immune response modulator that acts on the toll-like receptor (TLR) 7. It is thought that TLR-7 induces interferon-, which enhances Th1 cell-mediated antitumor activity, macrophages, and cytokines.

• #85 Bowen’s Disease Treatment |Skin Cancer and Reconstructive Surgery Center

  https://scarscenter.com/bowens-disease/

  Bowens disease or squamous cell carcinoma in situ is a cutaneous neoplasm with a 3-5% risk of invasive carcinoma. […] Sun exposure is one of the causes of Bowens carcinoma, but over of cases have detectable oncogenic HPV types 16 and 18. The implication is that HPV-induced Bowens disease should be responsive to agents with antitumor and antiviral effect. […] Topical and destructive therapies have the potential to partially clear the lesion creating noncontiguous skip tumors. Aggressive surgical treatment would be required to achieve cure then. There is an additional risk to non-surgical treatments that must be considered areas of invasive carcinoma within squamous cell carcinoma in situ.

• #86 Bowen’s disease of the anal canal treated with radiation therapy: A case report

  https://www.oatext.com/bowens-disease-of-the-anal-canal-treated-with-radiation-therapy-a-case-report.php

  Bowens disease, also known as intraepithelial neoplasia, is a very slow-growing carcinoma in situ. In Bowens disease, surgical resection is the standard of treatment. […] HPV infection is most commonly responsible for etiology. Up to 80 percent of AIN cases are believed to develop from infections from the Human Papilloma Virus (HPV) 16 and 18. HPV E6 and E7 gene products inactivate the mitotic regulator proteins of tumor suppressor genes (p53 and Rb), thereby permitting malignant transformation. […] Because of the morbidity and the high recurrence rates associated with surgical resection of Bowens disease, several treatment modalities have been applied, including imiquimod, external fluorouracil, laser therapy, radiotherapy and, photodynamic therapy. […] Of these, radiation therapy is appropriate for larger and recurrent lesions with good functional and cosmetic results.

• #87 Non-surgical management of actinic keratosis, Bowen’s disease and non-melanoma skin cancer | The PMFA Journal

  https://www.thepmfajournal.com/features/post/non-surgical-management-of-actinic-keratosis-bowen-s-disease-and-non-melanoma-skin-cancer

  Bowens disease (BD) is histologically characterised as SCC in situ. […] Several aetiological factors of BD have been described; ultraviolet (UV) radiation, radiotherapy, arsenic ingestion, immunosuppression and human papillomavirus infection are associated with increased risks of developing BD. […] Development of a lump or ulcer, pain or bleeding within BD may indicate progression to SCC, which occurs in about 3-5% of cases. […] PDT is often considered an effective first-line treatment choice for the treatment of AK and BD. Clinical clearance rates of BD treated by PDT were reported to be 88% at three months. […] Compared to cryotherapy, 5-FU or imiquimod, PDT is probably more appropriate and better tolerated as a treatment for larger lesions (3cm diameter), with two treatments of MAL-PDT, scheduled one week apart, clearing 96% of larger BD lesions at three months.

• #88 Bowenoid Papulosis and Invasive Bowen’s Disease: A Multidisciplinary Approach | HTML | Acta Dermato-Venereologica

  https://www.medicaljournals.se/acta/content/html/10.2340/00015555-1328

  According to some studies, women who continue to smoke after treatment are 30 times more likely to have persistent vulvar disease. […] Several pathways have been proposed to explain how retinoids can control viral replication. They can down-regulate the expression of HPV messenger-RNA or indirectly induce transforming growth factor-, which inhibits cell proliferation and transcription of E6/E7 genes in cervical epithelial cells. […] We speculated that brachytherapy in combination with isotretinoin could cooperate to clear the bowenoid field and prevent recurrences, and in our patient this was accentually the case.

• #89 Bowenoid Papulosis and Invasive Bowen’s Disease: A Multidisciplinary Approach | HTML | Acta Dermato-Venereologica

  https://www.medicaljournals.se/acta/content/html/10.2340/00015555-1328

  According to some studies, women who continue to smoke after treatment are 30 times more likely to have persistent vulvar disease. […] Several pathways have been proposed to explain how retinoids can control viral replication. They can down-regulate the expression of HPV messenger-RNA or indirectly induce transforming growth factor-, which inhibits cell proliferation and transcription of E6/E7 genes in cervical epithelial cells. […] We speculated that brachytherapy in combination with isotretinoin could cooperate to clear the bowenoid field and prevent recurrences, and in our patient this was accentually the case.

• #90 Secondary Localized Cutaneous Amyloidosis is not Rare in Bowen’s Disease and Bowenoid Papulosis – Turkish Journal of Pathology

  https://turkjpath.org/text.php?id=1969

  Secondary localized cutaneous amyloidosis is a histopathological finding seen in the dermis, in various benign, premalignant, and malignant skin conditions, without clinical significance. […] Although the occurrence of secondary localized cutaneous amyloidosis in epithelial tumors is a well-known phenomenon, its incidence has not been previously reported in Bowens disease and Bowenoid papulosis. […] Moreover, in three of six cases, we histologically observed areas of regression with a marked prominence of amyloid deposition. Remarkably, two of these patients had a history of topical application of destructive agents which reveals a possible etiologic relationship between secondary localized cutaneous amyloidosis and cellular apoptosis/necrosis induced by these external agents. […] The mechanism of amyloid deposition in PLCA and SLCA has been postulated to be similar. Literature findings suggest that amyloid is derived from degenerated epidermal cells and keratin released from apoptotic basal keratinocytes or colloid bodies is the precursor protein.

• #91 Secondary Localized Cutaneous Amyloidosis is not Rare in Bowen’s Disease and Bowenoid Papulosis – Turkish Journal of Pathology

  https://turkjpath.org/text.php?id=1969

  Secondary localized cutaneous amyloidosis is a histopathological finding seen in the dermis, in various benign, premalignant, and malignant skin conditions, without clinical significance. […] Although the occurrence of secondary localized cutaneous amyloidosis in epithelial tumors is a well-known phenomenon, its incidence has not been previously reported in Bowens disease and Bowenoid papulosis. […] Moreover, in three of six cases, we histologically observed areas of regression with a marked prominence of amyloid deposition. Remarkably, two of these patients had a history of topical application of destructive agents which reveals a possible etiologic relationship between secondary localized cutaneous amyloidosis and cellular apoptosis/necrosis induced by these external agents. […] The mechanism of amyloid deposition in PLCA and SLCA has been postulated to be similar. Literature findings suggest that amyloid is derived from degenerated epidermal cells and keratin released from apoptotic basal keratinocytes or colloid bodies is the precursor protein.

• #92 Secondary Localized Cutaneous Amyloidosis is not Rare in Bowen’s Disease and Bowenoid Papulosis – Turkish Journal of Pathology

  https://turkjpath.org/text.php?id=1969

  Secondary localized cutaneous amyloidosis is a histopathological finding seen in the dermis, in various benign, premalignant, and malignant skin conditions, without clinical significance. […] Although the occurrence of secondary localized cutaneous amyloidosis in epithelial tumors is a well-known phenomenon, its incidence has not been previously reported in Bowens disease and Bowenoid papulosis. […] Moreover, in three of six cases, we histologically observed areas of regression with a marked prominence of amyloid deposition. Remarkably, two of these patients had a history of topical application of destructive agents which reveals a possible etiologic relationship between secondary localized cutaneous amyloidosis and cellular apoptosis/necrosis induced by these external agents. […] The mechanism of amyloid deposition in PLCA and SLCA has been postulated to be similar. Literature findings suggest that amyloid is derived from degenerated epidermal cells and keratin released from apoptotic basal keratinocytes or colloid bodies is the precursor protein.

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