Materiały źródłowe

• #1 Salivary gland tumor pathophysiology – wikidoc

  https://www.wikidoc.org/index.php/Salivary_gland_tumor_pathophysiology

  The pathophysiology of salivary gland tumors depends on the histological subtype. […] The parotid gland is the most frequent site of salivary gland tumors which accounts for approximately 80 to 85 percent of these tumors. […] About 75 percent of parotid lesions are benign and approximately 25 percent are malignant. […] Overall approximately 80% of all parotid masses are benign.

• #2 Parotid neoplasms: analysis of 600 patients attended at a single institution | Brazilian Journal of Otorhinolaryngology

  https://www.elsevier.es/en-revista-brazilian-journal-otorhinolaryngology-english-edition–497-articulo-parotid-neoplasms-analysis-600-patients-S1808869415304869

  Salivary gland neoplasms are a rare group of tumors; the annual incidence rate is 1 in 100,000 individual, comprising about 3% of all head and neck neoplasms. The mean age of patients with salivary gland tumors is 45 years, peaking in the sixth and seventh decades of life. Benign salivary gland tumors occur more frequently in females, while malignant tumors are slightly more frequent in males. […] The parotid gland is the most frequent site about 70% of cases. About 80% of parotid tumors are benign, the most common being the pleomorphic adenoma (60% of parotid tumors), followed by Warthin’s tumor (10% of parotid tumors). […] The most common salivary gland malignancy is the mucoepidermoid carcinoma, which involves mostly the parotid gland, followed by the minor, submandibulary and sublingual salivary glands. The cystic adenoid carcinoma is the second most frequent malignancy in this area; other parotid tumors are acinar cell carcinomas, adenocarcinoma NOS, and the carcinoma ex pleomorphic adenoma.

• #3 Parotid Cancer – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK538340/

  Salivary gland neoplasms may be benign or malignant, and malignant tumors can be primary or metastatic. Due to the epithelial and the non-epithelial histology of the affected organ, many histological types of parotid tumors are possible, although some are rare. […] There are two main theories of how salivary gland tumors arise, but the consensus is with the multicellular theory, that each tumor type forms from a specific differentiated cell of origin within the salivary gland unit. Excretory stem cells give rise to mucoepidermoid and squamous cell carcinomas, while intercalated stem cells can lead to pleomorphic adenomas, adenoid cystic carcinomas, oncocytomas, adenocarcinomas, and acinic cell carcinomas. […] Several oncogenes have been implicated in salivary gland tumors. Mutations of P53, MDM2, Bcl-2, and ras have been found in both benign and malignant lesions.

• #4 Pathogenesis of salivary gland neoplasms: The concepts of histogenesis and morphogenesis – Journal of Global Oral Health

  https://jglobaloralhealth.org/pathogenesis-of-salivary-gland-neoplasms-the-concepts-of-histogenesis-and-morphogenesis/

  The differences in pathogenesis give rise to variations in the histopathological morphology of the SGNs. […] The present review aims to elaborate on the classification of SGNs based on the concepts of histogenesis and morphogenesis. […] The etiological factors of human SGNs remain obscure except for radiation and certain viruses. […] The histogenic concept of salivary gland tumors has usually relied on histologic observations of the fetal salivary gland and the cellular differentiation involved in particular segments of the duct system. […] Over the years, several theories involving the histogenesis concept in SGNs have been put forth. […] The theory suggests that the differentiated luminal and abluminal cells of the mature salivary glands are capable of proliferating into neoplasms.

• #5 Pathogenesis of salivary gland neoplasms: The concepts of histogenesis and morphogenesis – Journal of Global Oral Health

  https://jglobaloralhealth.org/pathogenesis-of-salivary-gland-neoplasms-the-concepts-of-histogenesis-and-morphogenesis/

  The morphogenetic approach focuses on tumor differentiation and other cellular processes that critically influence histomorphology. […] The presence or absence of luminal and abluminal cells, myoepithelial cells, and extracellular matrix (ECM) consisting of proteoglycans, laminin, and elastin, form the basis of the morphogenic concept of SGN pathogenesis. […] The advent of IHC has confirmed much of the assumptions on which the histogenic and morphogenic concepts of SGN pathogenesis were based. […] The present review elucidates the pathogenesis of the salivary gland tumor to understand the resulting histopathology, tumor morphology, and cellular differentiation of the tumor which reflect the parent cell.

• #6 Parotid tumors – Symptoms and causes – Mayo Clinic

  https://www.mayoclinic.org/diseases-conditions/parotid-tumor/symptoms-causes/syc-20578986

  Parotid tumors are growths of cells that start in the parotid glands. […] It’s not clear what causes parotid tumors. These tumors start as a growth of cells in the parotid glands. Parotid tumors happen when cells in the parotid glands develop changes in their DNA. A cell’s DNA holds the instructions that tell the cell what to do. In healthy cells, the DNA gives instructions to grow and multiply at a set rate. The instructions tell the cells to die at a set time. In tumor cells, the DNA changes give different instructions. The changes tell the tumor cells to grow and multiply quickly. Tumor cells can keep living when healthy cells would die. This causes too many cells. […] Sometimes the changes in the DNA turn the cells into cancer cells. Cancer cells can invade and destroy healthy body tissue. In time, cancer cells can break away and spread to other parts of the body. When cancer spreads, it’s called metastatic cancer.

• #7 Salivary gland tumors – Symptoms and causes – Mayo Clinic

  https://www.mayoclinic.org/diseases-conditions/salivary-gland-cancer/symptoms-causes/syc-20354151

  Salivary gland tumors happen when cells in a salivary gland develop changes in their DNA. A cell’s DNA holds the instructions that tell the cell what to do. In healthy cells, the DNA gives instructions to grow and multiply at a set rate. The instructions also tell the cells to die at a set time. In tumor cells, the changes give different instructions. The changes tell the tumor cells to make many more cells quickly. Tumor cells can keep living when healthy cells would die. This causes too many cells. […] Sometimes the changes in the DNA turn the cells into cancer cells. Cancer cells can invade and destroy healthy body tissue. In time, cancer cells can break away and spread to other parts of the body. When cancer spreads, it’s called metastatic cancer.

• #8 Salivary Gland Neoplasms: Practice Essentials, Epidemiology, Etiology

  https://emedicine.medscape.com/article/852373-overview

  As with most cancers, the exact molecular mechanism by which tumorigenesis occurs in salivary gland neoplasms is incompletely understood. Multiple pathways and oncogenes have been implicated, including oncogenes that are known to be associated with a wide variety of human cancers. These include p53, Bcl-2, PI3K/Akt, MDM2, and ras. […] Mutation in p53 have been found in both benign and malignant salivary gland neoplasms and some evidence suggests that the presence of p53 mutations correlates with a higher rate of tumor recurrence. RAS is a G protein involved in growth signal transduction, and derangements in ras signalling are implicated in a wide variety of solid tumors. H-Ras mutations have been shown in a significant proportion of pleomorphic adenomas, adenocarcinomas, and mucoepidermoid carcinomas.

• #9 Salivary Gland Neoplasms: Practice Essentials, Epidemiology, Etiology

  https://emedicine.medscape.com/article/852373-overview

  Studies that look at the neovascularization in salivary gland neoplasms have revealed factors that increase angiogenesis and are important in the progression of salivary gland neoplasms. Vascular endothelial growth factor (VEGF) is expressed by over half of salivary gland carcinomas tested and is correlated with clinical stage, recurrence, metastasis, and survival. […] Seventy percent of pleomorphic adenomas have associated chromosomal rearrangements. The most common is a rearrangement of 8q12, occurring in 39% of pleomorphic adenomas. The target gene at this locus is PLAG1, which encodes a zinc finger transcription factor. The other target gene is HMGA2, which encodes a nonhistone chromosomal high mobility group protein that is involved in structural regulation of the chromosome and transcription. This gene is located at 12q13-15. Because these rearrangements are unique to pleomorphic adenomas amongst salivary gland neoplasms, interrogation of these rearrangements by RT-PCR or FISH may aid in diagnosis.

• #10 Salivary Gland Neoplasms: Practice Essentials, Epidemiology, Etiology

  https://emedicine.medscape.com/article/852373-overview

  In mucoepidermoid carcinoma, the t(11;19)(q21;p13) chromosomal translocation has be identified in up to 70% of cases. This translocation creates a MECT1-MAML2 fusion protein that disrupts the Notch signaling pathway. This fusion protein is expressed by all cell types of mucoepidermoid when the translocation is present. Interestingly, fusion-positive tumors appear to be much less aggressive than fusion-negative tumors. Fusion-positive patients have significantly longer median survival and lower rates of local recurrence and distant metastasis. […] CD117 or c-kit is a tyrosine kinase receptor that is found in adenoid cystic carcinoma, myoepithelial carcinoma, and lymphoepitheliomalike carcinoma. CD117 expression is able to reliably differentiate ACC from polymorphous low-grade adenocarcinoma, and small molecule inhibitors of this receptor are currently being studied as a potential therapeutic agent.

• #11 Salivary Gland Neoplasms: Practice Essentials, Epidemiology, Etiology

  https://emedicine.medscape.com/article/852373-overview

  Other salivary gland neoplasms have been associated with overexpressed beta-catenin through abnormal Wnt signaling. Adenoid cystic carcinoma with mutations in CTNNB1 (b-catenin gene), AXIN1 (axis inhibition protein 1), and APC (adenomatosis polyposis coli tumor suppressor) show tumorigenesis via this process. Promoter methylation is known to develop tumors by inactivating tumor suppressor genes. Mutations that cause hypermethylation and downregulation of 14-3-3, a target gene for p53 in the Gap2/mitosis (G2/M) cell cycle checkpoint, was found to be extensive in adenoid cystic carcinoma (ACC). The methylation of genes that control apoptosis and DNA repair were also found in ACC, especially in high-grade tumors. […] Chromosomal loss has been found to be an important cause of mutations and tumorigenesis in salivary gland tumors. Allelic loss of chromosomal arm 19q has been reported to occur commonly in adenoid cystic carcinoma. Mucoepidermoid carcinomas also show the loss of chromosomal arms 2q, 5p, 12p, and 16q more than 50% of the time.

• #12 Head and Neck: Salivary gland tumors: an overview

  https://atlasgeneticsoncology.org/solid-tumor/5328/head-and-neck-salivary-gland-tumors-an-overview

  Histogenesis: PA has been shown to be of monoclonal origin. A common single cell may give rise to epithelial and modified myoepithelial cells, as well as mesenchymal elements. The two components may share a common origin from a single uncommitted cell (e.g. pluripotent intercalated duct cell) that may differentiate along epithelial and mesenchymal cell lines. Alternatively, PA could develop from committed progenitor cells, e.g. epithelial basal ductal cells. Upon neoplastic transformation, some of those cells may undergo divergent differentiation and acquire a mesenchymal phenotype. […] PLAG1 is a developmentally regulated zinc finger gene that maps to 8q12. It is not expressed in normal salivary gland parenchyma. The gene product is a nuclear protein that functions as a DNA-binding transcription factor. Potential PLAG1 binding sites have been found in promoter 3 of the IGF-II (insulin-like growth factor II) gene. It was shown that PLAG1 bound IGF-II promoter 3 and stimulated its activity. IGF-II was highly expressed in PAs with up-regulated PLAG1 gene. Conversely, IGF-II up-regulation was neither detected in PAs without abnormal PLAG1 expression, nor in normal salivary gland parenchyma. Thus, IGF-II is a potential PLAG1 target gene. PLAG1 may play a role in PA pathogenesis by inducing growth factor production, hence cell proliferation.

• #13

  https://step2.medbullets.com/oncology/120408/pleomorphic-adenoma

  tumor has both epithelial and connective tissue origin may undergo malignant transformation tumor lacks a true capsule and may have microscopic extensions results in a high risk of recurrence in cases treated with surgical resections performed with inadequate surgical margins […] Recurrence of tumor after surgical resection associated factors incomplete capsule extension of tumor nodules beyond the capsule tumor rupture during surgical resection […] Malignant transformation incidence 2-7% of cases associated factors multiple tumor recurrences deep lobe tumors male gender increased age

• #14 Salivary Gland Tumors – Ear, Nose, and Throat Disorders – MSD Manual Professional Edition

  https://www.msdmanuals.com/professional/ear-nose-and-throat-disorders/tumors-of-the-head-and-neck/salivary-gland-tumors

  Most salivary gland tumors are benign and occur in the parotid glands. […] About 85% of salivary gland tumors occur in the parotid glands, followed by the submandibular and minor salivary glands, and about 1% occur in the sublingual glands. […] Pleomorphic adenomas (mixed-type tumors) can undergo malignant transformation, but this transformation usually occurs only after the benign tumor has been present for 15 to 20 years. Once malignant degeneration of a pleomorphic adenoma occurs, it is known as carcinoma ex pleomorphic adenoma. […] Mucoepidermoid carcinoma is the most common salivary gland cancer, typically occurring in people in their 20s to 50s. It can manifest in any salivary gland, most commonly in the parotid gland but also in the submandibular gland or a minor salivary gland of the palate.

• #15 Pathogenesis of Warthin’s tumors in: Interventional Medicine and Applied Science Volume 8 Issue 2 (2016)

  https://akjournals.com/view/journals/1646/8/2/article-p41.xml

  Warthins tumor, also known as papillary cystadenoma lymphomatosum, monomorphic adenoma, or adenolymphoma, is a benign cystic tumor of the salivary glands containing abundant lymphocytes and lymph node-like stroma. […] The aim of this study is to analyze the pathogenesis of Warthins tumor. […] This study indicates that the Warthin tumor is a consequence of inflammatory etiology. […] There is no consensus regarding the origin of this tumor. However, the studies by Kotwall, Pinkston and Cole, and Yoo et al. have demonstrated that these tumors are associated with cigarette smoking, which may be due to the irritation of the ductal epithelium by tobacco smoke that initiates the tumorigenesis. […] Studies conducted among atomic bomb survivors suggest that radiation may also be implicated in the Warthins tumorigenesis.

• #16 Head and Neck: Salivary gland tumors: an overview

  https://atlasgeneticsoncology.org/solid-tumor/5328/head-and-neck-salivary-gland-tumors-an-overview

  The etiology of SGTs is so far unknown. Putative risk factors include cigarette smoking, genetic predisposition, viral infections, rubber manufacturing, plumbing, some types of woodworking, as well as asbestos mining, exposure to nickel compounds, and cellular phone use. The only well-established risk factor is ionizing radiation. Atomic bomb survivors and cancer patients treated by radiation present with a substantially higher risk of developing SGTs. However, there is a strong association between Warthin tumor (WT) and cigarette smoking, with WT occurring 8 times more often in smokers than in non-smokers. Irritants in tobacco smoke may cause metaplasia in the parotid gland. The association with tobacco use may explain the higher incidence of WT in males. […] A growing number of both benign and malignant SGTs are characterized by recurrent genetic alterations, particularly chromosome translocations. Specific chromosomal rearrangements are commonly found in malignant hematopoietic proliferations as well as in sarcomas, but less than 1% of all epithelial cancers are characterized by such distinct, recurrent genomic anomalies. Those anomalies may serve as diagnostic, prognostic and/or predictive markers in SGTs and their identification may complement the morphologic evaluation. Chromosome translocations in SGTs result in pathogenetically relevant fusion oncogenes. Those genes encode novel fusion proteins as well as ectopically expressed normal or truncated proteins that may play a role in tumor initiation and/or progression.

• #17 Pathogenesis of Warthin’s tumors in: Interventional Medicine and Applied Science Volume 8 Issue 2 (2016)

  https://akjournals.com/view/journals/1646/8/2/article-p41.xml

  There is also an earlier view by Santucci et al. of the strong association of the Epstein-Barr virus in the etiology of Warthins tumors. […] Histopathological analysis of the stroma and parenchyma revealed balanced distribution of epithelial and stromal component. Epithelial component of the Warthins tumor is the trigger for the tumor process. […] The immunostaining of stromal component with Ki-67 markers showed lymphocytic proliferation in the stromal cells of the tumor with predominantly type B-plasmacytoid (CD79A immunostained).

• #18 Pathogenesis of Warthin’s Tumor: Neoplastic or Non-Neoplastic?

  https://www.mdpi.com/2072-6694/16/5/912

  Warthin’s tumor is a well-known and frequent tumor in the salivary gland, but its pathogenesis is not fully understood. […] The pathogenesis of Warthin’s tumor is not fully understood, and several hypotheses have been proposed. […] Recently, it has been reported that chronic inflammation and aging cells promote the growth of Warthin’s tumor. […] Several reports regarding the origin of the tumor have suggested that (1) Warthin’s tumor is an IgG4-related disease, (2) epithelial cells that compose Warthin’s tumor accumulate mitochondria, and (3) Warthin’s tumor is a metaplastic lesion in the lymph nodes. […] It is possible that the pathogenesis of Warthin’s tumor includes mitochondrial metabolic abnormalities, accumulation of aged cells, chronic inflammation, and senescence-associated secretory phenotype (SASP).

• #19 Pathogenesis of Warthin’s Tumor: Neoplastic or Non-Neoplastic?

  https://www.mdpi.com/2072-6694/16/5/912

  In this short review, we propose that DNA damage, metabolic dysfunction of mitochondria, senescent cells, SASP, human papillomavirus, and IgG4 may be involved in the development of Warthin’s tumor. […] Various possible pathogeneses and risk factors have been described. […] However, based on our previous studies, we believe that mitochondrial metabolic abnormalities, senescent cell accumulation, chronic inflammation, SASP, and HPV infection may be involved in the pathogenesis of Warthin’s tumor. […] Morphologically, the cytoplasm of Warthin’s tumor reflects a state of mitochondrial overaccumulation called oncocytosis, which is caused by abnormal mitochondrial metabolism and involves damage to the mitochondrial genome. […] Whether Warthin’s tumor is a true neoplasm that occurs as a clonal growth or non-neoplastic developmental malformation remains controversial.

• #20 Are Multiple Tumors of the Parotid Gland Uncommon or Underestimated? | Anticancer Research

  https://ar.iiarjournals.org/content/37/9/5263

  Parotid gland tumors are mostly solitary tumors of the salivary gland tissue. […] Similarly, there are no established theories on their genesis and why certain histological types more commonly result in multiple tumors than others. […] The discussion over their pathogenesis remains inconclusive, as current genetic investigations support a 1950’s hypothesis that the nature of Warthin tumors is not neoplastic and results from immunological interaction between epithelium and lymphoid stroma, resulting in hyperplasia of the lymphoid components, and non-clonal proliferation of its epithelial components, and that Warthin tumors should rather be classified as a tumor-like lesion and not as a benign tumor. […] Other parotid tumors that have a tendency to develop multiple lesions are also derived from lymphatic tissue.

• #21 Head and Neck: Salivary gland tumors: Warthins tumors

  https://atlasgeneticsoncology.org/solid-tumor/5424/head-and-neck-salivary-gland-tumors-warthins-tumors

  The details of the pathogenesis of Warthins tumor are still unclear. However, because of the arguments against a true neoplastic origin of this tumor, the author favour a hypothesis combining immunological interactions between tumor cells and lymphocytic infiltrations with heterotopia. […] In the WHO classification of salivary gland tumors, certain diseases of the salivary glands are considered tumor-like lesions. Warthins tumor may therefore also be classified in the group of tumor-like lesions, since both the epithelial and lymphoid tumor components are polyclonal in origin. […] Several studies showed that a significant number of patients suffering from Warthins tumor are smokers, in contrast to patients with other salivary gland tumors. […] Warthins tumor consists of oncocytic cells containing numerous mitochondria frequently showing structural abnormalities and reduced metabolic function.

• #22 Malignant Transformation in a Parotid Warthin

  https://www.jscimedcentral.com/jounal-article-info/Journal-of-Cancer-Biology-and-Research/Malignant-Transformation-in-a–Parotid-Warthin%E2%80%99s-Tumor%3A-Clinical–Features-and-Histopathological–Examination-5849

  Warthins tumor is a salivary gland tumor consisting of epithelial and lymphoid components. […] The malignant transformation of Warthins tumor is extremely rare and occurs in about 0.3% of cases. The transformation of the lymphoid component to a malignant lymphoma appears to occur more frequently than an epithelial malignant transformation, which is extremely rare. […] Pathogenesis of malignant transformation of Warthins tumor is unknown. […] Malignant diagnosis requires evidence of stromal invasion, local invasion or lymph node metastasis. […] Therefore, we suggest that the physicians should thoroughly investigate the cervical lymph nodes when the patient had a malignant Warthins tumor and consider prophylactic neck. […] The malignant transformation of Warthins tumor is rare. Diagnosis is based on histopathology and immunohistochemistry.

• #23 An overview of the rare parotid gland cancer | Head & Neck Oncology | Full Text

  https://headandneckoncology.biomedcentral.com/articles/10.1186/1758-3284-3-40

  Cancer of the parotid gland is relatively rare, but carries poor prognosis owing to its prevailing distant metastases. […] we review some current discoveries of its tumorigenesis molecular mechanism. […] The mechanism behind the development of parotid gland cancer is not fully understood. One theory involves vacuolar protein sorting-associated protein 4B homolog (VPS4B). This protein is responsible for vesicular trafficking and the maturation of autophagosomes in mammalian cells. […] Given the essential role for VPS4B in MVB maturation, it is speculated that loss of VPS4 function might promote tumorigenesis through its effect of prolonging the duration of EGFR signaling. […] Although increased levels of EGFR expression are observed in a variety of cancers, including head and neck, ovary, cervix, bladder, esophagus, stomach, brain, breast, colon, and lung, and frequently confer an adverse prognosis, but many cancers exhibited EGFR over-expression in the absence of EGFR gene amplification. It is therefore postulated that the widespread phenomenon of EGFR over-expression in human cancers occurs, at least in part, as a consequence of common pathological events, other than genomic changes, associated with solid tumors.

• #24 Salivary Gland Neoplasms: Practice Essentials, Epidemiology, Etiology

  https://emedicine.medscape.com/article/852373-overview

  Multiple other genes are being investigated in the tumorigenesis of salivary gland neoplasms. Hepatocyte growth factor (HGF), a protein that causes morphogenesis and dispersion of epithelial cells, has been found to increase adenoid cystic carcinoma scattering and perhaps invasiveness. Expression of proliferating cell nuclear antigen (PCNA) was found in the 2 most common malignant salivary tumors, mucoepidermoid carcinomas and adenoid cystic carcinomas, with higher expression in submandibular gland-derived malignancies. Overexpression of fibroblast growth factor 8b has been shown to lead to salivary gland tumors in transgenic mice. […] Newer research in salivary gland neoplasms is focusing on factors that increase tumor invasion and spread. Matrix metalloproteinase-1, tenascin-C, and beta-6 integrin have been found to be associated with benign tumor expansion and tissue invasion by malignant tumors. In adenoid cystic carcinoma, increased immunoreactivity for nerve growth factor and tyrosine kinase A has been correlated with perineural invasion.

• #25 Can the height of the parotid tumor be a predictor of malignancy? – Huh – Gland Surgery

  https://gs.amegroups.org/article/view/63170/html

  Malignant tumors of the parotid gland tend to locate at the superior part of the gland compared to benign tumors. […] Height of the tumor in the parotid gland should be deliberately considered during the first encounter of the patient, which in turn could curate the next step in the diagnostic approach and treatment planning. […] Our study demonstrates for the first time that malignant parotid tumors tend to locate at a higher level (cephalad) in the parotid gland compared to benign tumors. […] The main finding of this study is that tumor location in the parotid gland can provide information that can distinguish malignant from benign tumors. […] If the tumor is located at the superior portion of the parotid gland, the degree of alertness for the possibility of malignancy should be maintained, even if benign is more likely on other studies.

• #26 Can the height of the parotid tumor be a predictor of malignancy? – Huh – Gland Surgery

  https://gs.amegroups.org/article/view/63170/html

  According to our study, the cutoff heights from each reference points were most significant at 22.5 mm inferior from the superior surface of the hard palate, and 51.5 mm inferior from the condylar head. […] The findings of this study may not provide a conclusive diagnosis. However, it offers considerable information in the diagnostic process, especially concerning the relevant value of its false negative rate. Therefore, evaluation of parotid tumor by its location among the parotid gland should be considered to indicate possible malignant lesion, which may lead to confirmation studies such as core-needle biopsy or intra-operative frozen biopsy, or even suggesting an en bloc resection as a surgical plan.

• #27 Are Multiple Tumors of the Parotid Gland Uncommon or Underestimated? | Anticancer Research

  https://ar.iiarjournals.org/content/37/9/5263

  Most parotid gland lymph nodes are located in the superficial part of the parotoid gland and this may explain why multifocal tumors were mainly found superficially. […] The vast majority (96%, 89 of 93 cases) of multifocal parotid tumors were of lymphatic origin: Warthin tumors, parotid lymphoma, inflammatory pseudotumors and metastatic lesions. […] Today, the actual significance of multiple tumors is even higher because Warthin tumors have become by far the most important tumor entity among neoplasms of the parotid gland over the last two decades.

• #28 Synchronous multiple unilateral parotid gland tumors of benign and malignant histological types: case report and literature review | Brazilian Journal of Otorhinolaryngology

  https://www.elsevier.es/en-revista-brazilian-journal-otorhinolaryngology-english-edition–497-articulo-synchronous-multiple-unilateral-parotid-gland-S1808869416300337

  Synchronous benign and malignant ipsilateral parotid tumors are an extremely rare phenomenon. It was described for the first time by Tanaka in 1953 as mucoepidermoid carcinoma associated with Warthin tumor. […] This paper is the first one to present an in-depth study of a rare case of Warthin tumor coexisting with carcinoma ex pleomorphic adenoma in the same salivary gland. […] The etiology of carcinoma ex pleomorphic adenoma is associated with the accumulation of genetic instabilities in long-standing pleomorphic adenomas, hence in the present case, the primary tumor was present for many years, what is important for process of malignization. […] Although there are some data about the incidence of multiple parotid tumors after radiotherapy, our patient had no history of radiation before.

• #29 Molecular Pathogenesis of Parotid Gland Tumors: Insights and Implications

  https://www.hilarispublisher.com/open-access/molecular-pathogenesis-of-parotid-gland-tumors-insights-and-implications-108197.html

  The tumor microenvironment, comprising stromal cells, immune cells and extracellular matrix components, plays a critical role in tumor progression. Interactions between tumor cells and the microenvironment can influence tumor behavior and response to therapy. […] The molecular characterization of parotid gland tumors has significantly improved diagnostic accuracy. Techniques such as fluorescence in situ hybridization (FISH) and next-generation sequencing (NGS) allow for the detection of specific genetic alterations, aiding in the differentiation between benign and malignant tumors. […] Understanding the molecular pathways involved in parotid gland tumors has paved the way for targeted therapies. Inhibitors of RTKs, such as cetuximab and trastuzumab, have shown efficacy in preclinical models.

• #30 Molecular Pathogenesis of Parotid Gland Tumors: Insights and Implications

  https://www.hilarispublisher.com/open-access/molecular-pathogenesis-of-parotid-gland-tumors-insights-and-implications-108197.html

  Molecular markers can also provide prognostic information, helping to predict disease progression and patient outcomes. For instance, the presence of the CRTC1-MAML2 fusion gene in mucoepidermoid carcinoma is associated with a better prognosis, while MYB-NFIB fusion in adenoid cystic carcinoma is linked to a more aggressive clinical course. […] The study of the molecular pathogenesis of parotid gland tumors is still evolving. Future research should focus on the identification of novel genetic and epigenetic alterations, the development of more effective targeted therapies and the exploration of the tumor microenvironment. […] The molecular pathogenesis of parotid gland tumors involves a complex interplay of genetic, epigenetic and microenvironmental factors. Advances in molecular diagnostics and targeted therapies hold promise for improving the diagnosis, treatment and prognosis of these tumors.

• #31 Parotid neoplasms: analysis of 600 patients attended at a single institution | Brazilian Journal of Otorhinolaryngology

  https://www.elsevier.es/en-revista-brazilian-journal-otorhinolaryngology-english-edition–497-articulo-parotid-neoplasms-analysis-600-patients-S1808869415304869

  The treatment of choice for benign and malignant parotid tumors is partial or total parotidectomy, according to the extent of the tumor. Radiotherapy may be useful in malignancies as adjuvant therapy; chemotherapy is rarely used. Local, regional and distance recurrence rates are 40%, 15% and 11% each, and worsened the prognosis. […] The treatment of choice for benign tumors of the parotid gland is parotidectomy, preserving the facial nerve. Generally, partial parotidectomy is done in tumors limited to the superficial lobe, which is fully resected. Removal of the whole parotid lobe aims to attain adequate surgical margins and avoid rupture of the capsule, which reduces the recurrence rate. Total parotidectomy in benign tumors is done when the deep lobe of the parotid is involved. Rupture of the capsule during surgical resection and positive microscopic margins may lead to recurrences. […] Adjuvant radiotherapy has been shown to be effective for improving local control and increased survival. Local, regional and distance recurrence rates for parotid malignant tumors are about 40%, 15% and 11% each; in these cases, the prognosis is worse.

• #32

  https://link.springer.com/article/10.1007/s12070-023-03906-y

  Pleomorphic adenoma (PA) is the most common salivary gland neoplasm, followed by Warthins tumor (WT). […] Immune escape is a carcinogenesis mechanism of tumors to avoid the host immune system by producing PD-L1. […] Therefore, PD-L1 is one of the PA pathways to transform into CXPA through immune escape. […] WT expressed PD-L1 in the cytoplasm and lymphoid stroma but not on the cell membrane. It is interpreted as positive constitutive, which may have the function of increasing tumor cell growth, while overexpressed PD-L1 in lymphoid stroma is thought to be associated with a poor prognosis of the tumor and is suspected to transform into malignancy, such as B-cell Lymphoma.

• #33 Childhood Salivary Gland Tumors – NCI

  https://www.cancer.gov/types/head-and-neck/patient/child/salivary-gland-treatment-pdq

  Targeted therapy (entrectinib or larotrectinib) may be used to treat recurrent childhood salivary gland cancer. Recurrent salivary gland cancer is cancer that has come back after it has been treated. Targeted therapy uses drugs or other substances to block the action of specific enzymes, proteins, or other molecules involved in the growth and spread of cancer cells. The doctor may suggest biomarker tests to help predict your child’s response to certain targeted therapy drugs.

• #34 Parotid Gland Tumors: Symptoms, Causes & Treatment

  https://my.clevelandclinic.org/health/diseases/parotid-tumor

  Abnormal masses or tumors that develop on your parotid gland may be benign (non-cancerous) or malignant (cancerous). […] Experts arent sure exactly what causes these cancerous and noncancerous tumors. Research suggests some common possible causes include using tobacco or having radiation therapy for head and neck cancer. […] Treatment typically involves surgery to remove the tumor. Surgery cures noncancerous tumors and may cure cancerous ones, as well. But cancerous parotid gland tumors can come back (recur). […] Parotidectomy, which is surgery to remove part or all of your parotid gland, is the most common treatment for cancerous and noncancerous tumors. People with cancerous tumors also receive radiation therapy after surgery. […] Survival rates are estimates of the percentage of people with this condition who were alive five years after diagnosis. Rates vary widely depending on factors like tumor subtype, tumor stage, and tumor grade. […] Mucoepidermoid carcinoma (MEC) is the most common subtype of cancerous parotid gland tumor. The survival rate ranges from 86% for low-grade tumors to 22% for high-grade tumors.

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