Materiały źródłowe

• #1 Non-Hodgkin Lymphoma – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK559328/

  Non-Hodgkin lymphoma is a group of malignant neoplasms originating from lymphoid tissues, mainly the lymph nodes. These tumors may result from chromosomal translocation, various toxins, infections, and chronic inflammation. […] Non-Hodgkin lymphoma (NHL) is a neoplasm of the lymphoid tissues originating from B cell precursors, mature B cells, T cell precursors, and mature T cells. NHL comprises various subtypes, each with different epidemiologies, etiologies, immunophenotypic, genetic, clinical features, and response to therapy. It can be divided into 2 groups, 'indolent’ and 'aggressive,’ based on the disease’s prognosis. […] NHL may be associated with various factors, including infections, environmental factors, immunodeficiency states, and chronic inflammation. Various infectious agents have been attributed to different types of NHL.

• #2 Non-Hodgkin Lymphoma (NHL): Practice Essentials, Background, Pathophysiology

  https://emedicine.medscape.com/article/203399-overview

  NHLs are tumors originating from lymphoid tissues, mainly of lymph nodes. These tumors may result from chromosomal translocations, infections, environmental factors, immunodeficiency states, and chronic inflammation. […] NHL represents a progressive clonal expansion of B cells or T cells and/or NK cells arising from an accumulation of lesions affecting proto-oncogenes or tumor suppressor genes, resulting in cell immortalization. These oncogenes can be activated by chromosomal translocations (ie, the genetic hallmark of lymphoid malignancies), or tumor suppressor loci can be inactivated by chromosomal deletion or mutation. In addition, the genome of certain lymphoma subtypes can be altered with the introduction of exogenous genes by various oncogenic viruses. Several cytogenetic lesions are associated with specific NHLs, reflecting the presence of specific markers of diagnostic significance in subclassifying various NHL subtypes.

• #3 The molecular pathogenesis of B‐cell non‐Hodgkin lymphoma

  https://ouci.dntb.gov.ua/en/works/45WK5qO9/

  The B‐cell non‐Hodgkin lymphomas (B‐NHL) are a diverse group of haematological malignancies which arise from the mature B‐lymphocyte compartment. Recently, our understanding of the molecular pathogenesis of these disorders has greatly increased due to technological advances such as high‐throughput DNA sequencing techniques. A paradigm of B‐NHL pathogenesis has emerged where the normal genetic processes that are central to generating B‐cell receptor diversity (somatic hypermutation and class switch/VDJ recombination) also drive the genesis of large‐scale, chromosomal‐level genetic lesions and smaller‐scale gene‐level mutations to produce the malignant phenotypes observed. […] This review covers the current understanding of the causative genetic processes of B‐NHL, the associated driving molecular lesions and the implications of these findings for the treatment of this group of disorders.

• #4 Non-Hodgkin Lymphoma – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK559328/

  Epstein-Barr virus, a DNA virus, is associated with the causation of certain types of NHL, including an endemic variant of Burkitt lymphoma. […] Human T-cell leukemia virus type 1 (HTLV-1) causes adult T-cell lymphoma. It induces chronic antigenic stimulation and cytokine dysregulation, resulting in uncontrolled B- or T-cell stimulation and proliferation. […] Hepatitis C virus (HCV) results in clonal B-cell expansions. Splenic marginal zone lymphoma and diffuse large B-cell lymphoma are some subtypes of NHL caused by HCV. […] NHL arises from B, T, or natural killer cells due to chromosomal translocation or mutation/deletion. Proto-oncogenes are activated by chromosomal translocation and tumor suppressor genes are inactivated by chromosomal deletion or mutation. The t (14;18) translocation is NHL’s most common chromosomal abnormality. This translocation is most common in follicular lymphoma. The t (11;14) translocation is associated with mantle cell lymphoma. This results in the overexpression of cyclin D1, a cell cycle regulator. The t (8;14) translocation of c-myc (8) and heavy chain Ig (14) is associated with Burkitt lymphoma. Alteration in BCL-2 and BCL-6 is associated with diffuse large B-cell lymphoma. Primary CNS lymphoma is mostly associated with HIV/AIDS.

• #5 The molecular pathogenesis of B‐cell non‐Hodgkin lymphoma

  https://ouci.dntb.gov.ua/en/works/45WK5qO9/

  Genetic and molecular alterations are not only critical for lymphomagenesis but also largely responsible for differing therapeutic response in these neoplasms. In recent years, advanced molecular tools have provided a deeper understanding regarding these oncogenic drives for predicting progression as well as refractory behavior in these diseases. […] Chromosomal translocations are the main etiological factor of hematologic malignancies. These translocations are generally the consequence of aberrant DNA double-strand break (DSB) repair. DSBs arise either exogenously or endogenously in cells and are repaired by major pathways, including non-homologous end-joining (NHEJ), homologous recombination (HR), and other minor pathways such as alternative end-joining (A-EJ). Therefore, defective NHEJ, HR, or A-EJ pathways force hematopoietic cells toward tumorigenesis.

• #6 Non-Hodgkin Lymphoma (NHL): Practice Essentials, Background, Pathophysiology

  https://emedicine.medscape.com/article/203399-overview

  Chromosomal translocations and molecular rearrangements play an important role in the pathogenesis of many lymphomas and correlate with histology and immunophenotype. […] The t(14;18)(q32;q21) translocation is the most common chromosomal abnormality associated with NHL. This translocation occurs in 85% of follicular lymphomas and 28% of higher-grade NHLs. This translocation results in the juxtaposition of the bcl -2 apoptotic inhibitor oncogene at chromosome band 18q21 to the heavy chain region of the immunoglobulin (Ig) locus within chromosome band 14q32. […] Some viruses are implicated in the pathogenesis of NHL, probably because of their ability to induce chronic antigenic stimulation and cytokine dysregulation, which leads to uncontrolled B- or T-cell stimulation, proliferation, and lymphomagenesis. Epstein-Barr virus (EBV) is a DNA virus that is associated with Burkitt lymphoma (especially the endemic form in Africa), Hodgkin disease, lymphomas in immunocompromised patients (eg, from HIV infection, organ transplantation), and sinonasal lymphoma.

• #7 Non-Hodgkin lymphoma pathophysiology – wikidoc

  https://www.wikidoc.org/index.php/Non-Hodgkin_lymphoma_pathophysiology

  BCL-2 is an anti-apoptotic protein, and the t(14;18)(q32;q21) translocation results in markedly elevated expression of BCL-2, which blocks the healthy germinal center default program of apoptotic cell death and represents a defining pathogenic feature of follicular lymphoma. […] Similarly, mantle cell lymphoma is characterised by the t(11;14)(q13;q32) translocation, which leads to the deregulated expression of cyclin D1. […] Moreover, burkitt lymphoma overexpresses MYC as a result of the t(8;14)(q24;q32) translocation or variants. […] Recurrent translocations are less common in peripheral T-cell lymphomas than in other types of lymphoma, and examples include the characteristic t(2;5) (p23;q35) translocation seen in anaplastic lymphoma kinase (ALK)-positive anaplastic T-cell lymphoma and the t(5;9)(q33;q22) translocation associated with follicular T-cell lymphoma. […] Recurrent translocations including t(6;7) (p25;q32) and recurrent gene fusions involving the tumour-suppressor gene TP63 are characteristic of ALK-negative anaplastic T-cell lymphoma.

• #8 Non-Hodgkin’s and Hodgkin’s Lymphoma | Basicmedical Key

  https://basicmedicalkey.com/non-hodgkins-and-hodgkins-lymphoma/

  This results in the overexpression of BCL2, a protein that renders cells resistant to programmed cell death (apoptosis). […] The fact that this translocation exists in a large fraction of healthy adults is evidence that further mutagenic events are crucial for lymphomagenesis. […] Genetic errors involving BCL6 (a transcription factor), BCL2 (an antiapoptotic protein) and FAS (CD95, a TNF-family receptor), are often linked to the development and behavior of DLBCL. […] However, individual lesions fail to explain the pathologic and clinical heterogeneity of DLBCL. […] These lymphomas usually have a translocation between chromosomes 2 and 5, causing markedly increased ALK expression and altered intracellular signaling involved in disease pathogenesis. […] Myc deregulation is observed in more than 90% of cases to be due to a translocation between chromosome 8 (containing the c-myc gene) and one of various partner chromosomes, most commonly chromosome 14.

• #9 Non-Hodgkin’s Lymphoma (NHL).ppt

  https://www.slideshare.net/slideshow/nonhodgkins-lymphoma-nhlppt/252167927

  Non-Hodgkin’s lymphomas arise from monoclonal expansion of malignant B or T cells. […] Progressive clonal expansion of mature B-cells or T-cells arising from activated oncogenes or inactivated tumor suppressor genes 85% of NHLs are of B-cell origin. […] May result from chromosomal translocations, infections, environmental factors, immunocompromised states, and chronic inflammation. […] Chromosomal translocations Burkitt lymphoma t(8;14) translocation of c-myc and heavy-chain Ig. […] Diffuse large B-cell lymphoma expression of Bcl-2 and Bcl-6 levels of Bcl-2 inhibits apoptosis. […] Follicular lymphoma t(14;18) translocation of heavy-chain Ig and BCL-2. […] Mantle cell lymphoma t(11;14) translocation of cyclin D1 and heavy-chain Ig. […] Marginal zone lymphoma t(11;18) translocation of API2 and MALT1 promotes the continuous activation of the transcription factor NF-B.

• #10 SciELO Brazil – Pathophysiology and molecular aspects of diffuse large B-cell lymphoma Pathophysiology and molecular aspects of diffuse large B-cell lymphoma

  https://www.scielo.br/j/rbhh/a/yY6ZnSWrQ9LRTDMrkyfWPcS/

  Diffuse large B-Cell lymphoma is the most common subtype of non-Hodgkin lymphoma in the West. […] As for other cancers, non-Hodgkin lymphoma involves patterns of multi factorial pathogenesis with environmental factors, as well as genetic, occupational and dietary factors, contributing to its development. […] Multiple lesions involving molecular pathways of B-cell proliferation and differentiation may result in the activation of oncogenes such as the BCL2, BCL6,and MYC genes and the inactivation of tumor suppressor genes such as p53 and INK4, as well as other important transcription factors such as OCT-1 and OCT-2. […] Thus, it is important to know and understand the key factors and molecular pathways involved in the pathogenesis of diffuse large B-Cell lymphoma. […] Proto-oncogenes are important to control cell proliferation. However, when inappropriately activated by genetic abnormalities such as chromosomal translocations, gene mutations or amplification, the cells may acquire a malignant transformation.

• #11 Non-Hodgkin lymphoma – Symptoms and causes – Mayo Clinic

  https://www.mayoclinic.org/diseases-conditions/non-hodgkins-lymphoma/symptoms-causes/syc-20375680

  Non-Hodgkin lymphoma is a type of cancer that affects the lymphatic system. The cause of non-Hodgkin lymphoma often isn’t known. This cancer starts when germ-fighting white blood cells called lymphocytes develop changes in their DNA. A cell’s DNA holds the instructions that tell the cell what to do. […] In non-Hodgkin lymphoma, the cancer cells often build up in the lymph nodes. They also can build up in other parts of the lymphatic system. […] Non-Hodgkin lymphoma most often begins in the: B cells. B cells are a type of lymphocyte that fights infection. B cells make antibodies against foreign invaders. Most non-Hodgkin lymphoma arises from B cells. […] The DNA changes tell the cancer cells to make more cells quickly. Cancer cells can keep living when healthy cells would die. This causes too many cells.

• #12 Pathogenesis – NHL Strive

  https://strive-nhl.com/clinician-portal/pathogenesis/

  Most NHL cancers are associated with chromosomal abnormalities, originating within a single cell, with subsequent cells carrying the identical variation. As such, lymphomas arise at different stages of B-cell differentiation. Specific recombination events lead to the development of chromosomal aberrations. The germinal center is surrounded by a mantle zone of naive B cells, most of which express the CD5 marker which might comprise a distinct B-cell subset. Recombination activating gene 1 (RAG1)-dependent and RAG2-dependent V(D)J recombination takes place in the bone marrow. The potentially resulting t(14;18) and t(11;14) represent critical first steps in lymphomagenesis of different lymphoma subtypes. After antigen contact, the stimulated B cells migrate to the lymph node and form the germinal center after upregulation of BCL6. The events during the germinal center reaction include activation-induced cytidine deaminase (AID) –mediated somatic hypermutation and class-switch recombination, which are critical events for lymphoma evolution. The germinal center reaction is terminated by the differentiation of B cells into plasma cells. XBP1 and Blimp-1 are key regulators for plasmacytic differentiation.

• #13

  https://journals.lww.com/jfmpc/fulltext/2020/09040/non_hodgkin_s_lymphoma__a_review.12.aspx

  Chronic antigenic stimulation increases B-cell proliferation, which in turn increases the probability of a random genetic mistake, particularly related to immunoglobulin gene rearrangements. […] In cases in which a virus acts as the foreign stimulant, the virus itself may infect a normal cell and integrate viral DNA into the host genome, thereby transforming the cell into a malignant cell capable of self-replication. […] Chromosomal translocations, usually balanced reciprocal recombinations, are the genetic hallmark of lymphoid malignancies; their presence has been confirmed in up to 90% of NHL cases. […] At a molecular level, these translocations with or without additional chromosomal deletions and mutations may precipitate oncogene activation or tumor suppressor gene inactivation.

• #14 SciELO Brazil – Pathophysiology and molecular aspects of diffuse large B-cell lymphoma Pathophysiology and molecular aspects of diffuse large B-cell lymphoma

  https://www.scielo.br/j/rbhh/a/yY6ZnSWrQ9LRTDMrkyfWPcS/

  Similar to other cancers, the pathogenesis of DLBCL occurs in multiple steps that results in the development of the disease. […] The BCL6 gene is one of the most frequently affected in DLBCL. […] The role of the BCL6 gene in the pathogenesis of DLBCL was recently elucidated. […] The p53 gene is located on chromosome 17, encoding a nuclear phosphoprotein p53. […] Patients with absent or mutated p53 present more aggressive disease and worse prognosis. […] MYC gene mutations may occur in regions of exons and introns. […] The differentiation and proliferation of B-cells are controlled by transcription factors. […] Recent studies have demonstrated, through the RNA interference technique, that OCT factors influence the survival of cells in lymphomas with the t(14; 18).

• #15 Non-Hodgkin lymphoma – Wikipedia

  https://en.wikipedia.org/wiki/Non-Hodgkin_lymphoma

  Lymphomas are types of cancer that develop from lymphocytes, a type of white blood cell. Risk factors include poor immune function, autoimmune diseases, Helicobacter pylori infection, hepatitis C, obesity, and Epstein-Barr virus infection. The many different forms of lymphoma probably have different causes. These possible causes and associations with at least some forms of NHL include: […] Epstein-Barr virus: associated with Burkitt’s lymphoma, follicular dendritic cell sarcoma, extranodal NK-T-cell lymphoma and diffuse large B-cell lymphoma. […] Immune suppression rather than HIV itself is implicated in the pathogenesis of this malignancy, with a clear correlation between the degree of immune suppression and the risk of developing NHL.

• #16 Hepatitis B Virus Linked to Non-Hodgkin Lymphoma – Focus on Follicular Lymphoma

  https://www.medpagetoday.com/resource-centers/focus-follicular-lymphoma/hepatitis-b-virus-linked-non-hodgkin-lymphoma/2398

  While the induction of lymphomagenesis by lymphotropic viruses such as EBV and HTLV has shed some light on the viral pathogen-NHL link, less is known about the extent of the impact and mechanistic underpinnings of indirect mechanisms of NHL development mediated by non-lymphotropic viruses. […] Dalia said that while the cumulative data from this and other meta-analyses suggest that in individuals with a history of HBV there is a higher risk of developing NHL, prospective studies are really needed to confirm the causal relationship between HBV exposure and NHL risk. […] Lymphomagenesis occurs upon direct or indirect transformation of mature lymphocytes. […] Given that HBV-specific sequences are detectable in PBMNCs and in hemopoietic tumor cells in HBV-positive patients, it is possible that similar mechanisms may be invoked in lymphoid cells to initiate and promote lymphomagenesis.

• #17 Non-Hodgkin Lymphomas – Hematology and Oncology – Merck Manual Professional Edition

  https://www.merckmanuals.com/professional/hematology-and-oncology/lymphomas/non-hodgkin-lymphomas

  Most non-Hodgkin lymphomas arise from B lymphocytes; the remainder arise from T lymphocytes or natural killer cells. The stage of lymphocyte differentiation at which the oncogenic event occurs determines the disease presentation and outcome. […] The cause of non-Hodgkin lymphoma is unknown, although, as with the leukemias, substantial evidence suggests a viral cause (eg, human T-cell leukemia-lymphoma virus, Epstein-Barr virus, hepatitis B virus, hepatitis C virus, HIV, human herpesvirus 8) in some cases. […] Genetic factors appear to play a role. Certain single nucleotide polymorphisms increase the risk of lymphoma. Patients with a first-degree relative with Hodgkin or non-Hodgkin lymphoma have an increased risk of non-Hodgkin lymphoma. […] Hypogammaglobulinemia caused by a progressive decrease in immunoglobulin production is present in 15% of patients at diagnosis. Hypogammaglobulinemia increases the risk of serious bacterial infection, and patients may require IV immune globulin to replace deficient immunoglobulins.

• #18 Hepatitis B Virus Linked to Non-Hodgkin Lymphoma – Focus on Follicular Lymphoma

  https://www.medpagetoday.com/resource-centers/focus-follicular-lymphoma/hepatitis-b-virus-linked-non-hodgkin-lymphoma/2398

  Hepatitis B virus (HBV) exposure, indicated by the presence of surface antigen (sAg) or DNA, is associated with non-Hodgkin lymphoma (NHL) development, according to a recent meta-analysis of 58 studies published in English and Chinese peer-reviewed journals. […] Viral infection-mediated oncogenesis has been identified as a molecular mechanism of pathogenesis in many neoplasms, including hepatocellular carcinoma and non-Hodgkin lymphoma (NHL). […] HBV infection was more strongly associated with risk of developing B-cell NHL than T-cell NHL, with a significant HBV-NHL development risk association in diffuse large B-cell lymphoma and follicular lymphoma. […] In addition to host genetics, autoimmune disorders, environmental exposures, and modifiable risk factors, viral infections have been identified as risk factors for NHL.

• #19 Hepatitis B Virus Linked to Non-Hodgkin Lymphoma – Focus on Follicular Lymphoma

  https://www.medpagetoday.com/resource-centers/focus-follicular-lymphoma/hepatitis-b-virus-linked-non-hodgkin-lymphoma/2398

  HBV-mediated NHL development may also be driven by “an immunologic response to chronic immunogenic stimulation.” […] Future studies aimed at the mechanisms of HBV-mediated malignant transformation and the overlap between HBV-mediated processes in increasing the risk of HCC and NHL, if any, would be of great interest.

• #20 Lymphomas: pathogenesis, clinical features and diagnosis – The Pharmaceutical Journal

  https://pharmaceutical-journal.com/article/ld/lymphomas-pathogenesis-clinical-features-and-diagnosis

  The lymphomas are a heterogenous group of blood cancers caused by the clonal proliferation of B or T lymphocytes. […] There is a strong association between immunodeficiency, such as HIV infection, and risk of developing non-Hodgkin lymphoma. Recipients of organ transplantation who are receiving immunosuppressants such as ciclosporin or tacrolimus are at risk of developing post-transplant lymphoproliferative disease (PTLD), a proliferation of B cells caused by the Epstein-Barr virus that, if untreated, can progress to non-Hodgkin lymphoma. […] The Epstein-Barr virus is implicated in the development of Burkitt’s lymphoma, although its overall importance as a risk factor is much less than for Hodgkin lymphoma. […] Helicobacter pylori infection is strongly associated with mucosa-associated lymphoid tissue (MALT) lymphoma, a form of non-Hodgkin lymphoma that occurs in the stomach. Other risk factors for non-Hodgkin lymphoma include hepatitis B and hepatitis C, working in rubber production and exposure to chemicals such as benzene and ethylene oxide.

• #21

  https://journals.lww.com/jfmpc/fulltext/2020/09040/non_hodgkin_s_lymphoma__a_review.12.aspx

  Lymphomas constitute the third most common neoplasm in head and neck region arising from the lymphoreticular system. […] This review describes the pathogenesis of NHL and explains some of the important NHL (Marginal zone B-cell Lymphoma, follicular lymphoma, mantle cell lymphoma). […] Central pathogenetic mechanisms include immunosuppression, especially in relation to T-cell function and loss of control of latent EBV infection, and chronic antigen stimulation. […] Immunosuppression in a variety of medical conditions increases the risk of NHL. The most well-established risk factors for malignant lymphomas are characterized by dysregulation or suppression of T-cell function (HIV/AIDS, organ transplantation) that allows for Epstein-Barr virus (EBV) driven B-cell proliferation and transformation.

• #22 Non-Hodgkin Lymphoma (NHL): Practice Essentials, Background, Pathophysiology

  https://emedicine.medscape.com/article/203399-overview

  Environmental factors linked to the development of NHL include chemicals (eg, pesticides, herbicides, solvents, organic chemicals, wood preservatives, dusts, hair dye), chemotherapy, and radiation exposure. […] Chronic inflammation observed in patients with autoimmune disorders, such as Sjgren syndrome and Hashimoto thyroiditis, promotes the development of MALT and predisposes patients to subsequent lymphoid malignancies. Hashimoto thyroiditis is a preexisting condition in 23-56% of patients with primary thyroid lymphomas.

• #23 Non-Hodgkin’s and Hodgkin’s Lymphoma | Basicmedical Key

  https://basicmedicalkey.com/non-hodgkins-and-hodgkins-lymphoma/

  Expression of the viruss genetic program by cell machinery (as occurs in chronic Epstein-Barr virus infection) contributes to the pathogenesis of HLs and lymphoproliferative disorders in immunosuppressed patients following organ transplant. […] Such stimulation can also follow immune attack on self-antigens, possibly explaining the link between some lymphomas and autoimmune conditions such as rheumatoid arthritis and systemic lupus erythematosis. […] The interaction among these etiologic factors, and in particular the cellular interactions among immune and tumor cells (in the tumor microenvironment), are important topics of research in lymphoma pathogenesis and therapy. […] In follicular lymphoma, the classic genetic lesion is the translocation between chromosomes 14 and 18 t(14;18), seen in the majority of cases (70%).

• #24 The role of novel immunotherapies in non-Hodgkin lymphoma – Pishko – Translational Cancer Research

  https://tcr.amegroups.org/article/view/11958/html

  Immunotherapy is an evolving modality in the treatment of non-Hodgkin lymphoma. […] The power of the immune system to fight hematologic malignancies is seen in allogeneic stem cell transplant, where donor T cells attack residual malignant cells in the recipient. […] Among the first therapies to demonstrate the power of the immune system was allogeneic stem cell transplant for hematologic malignancy. […] To utilize the power of the immune system without the adverse effects of GVHD, work has been ongoing for 20 years in vaccinations against specific tumor antigens to bolster the immune system. […] Given the limited salvage options, non-Hodgkin lymphoma would benefit from the further application of immunotherapy. Adoptive cellular therapies, immune-checkpoint inhibitors, and novel antibody therapies have all demonstrated efficacy in both aggressive and indolent non-Hodgkin lymphoma.

• #25 The role of novel immunotherapies in non-Hodgkin lymphoma – Pishko – Translational Cancer Research

  https://tcr.amegroups.org/article/view/11958/html

  CAR T cells are autologous T lymphocytes genetically engineered to bind to specific antigens expressed on malignant cells. […] Through the CAR T cell binding to the malignant cell, the signaling domains stimulate T-cell proliferation, cytolysis, and cytokine secretion to eliminate the tumor cell. […] Studies suggest some cases remain resistant to CAR T cells. Resistance may in part be due to the inability of the CAR T-cell to overcome the inhibition produced by the tumor cells expression of T-cell inhibitory ligands. […] Tumor cells abrogate the immune system by mimicking strategies used by the healthy immune system to regulate response and allow for self-tolerance. […] Monoclonal antibodies targeting CTLA-4 and PD-1 are now developed to decrease the down-regulation of T-cell response against tumor cells.

• #26 Updates on Molecular Pathogenesis of Non-Hodgkin’s Lymphoma | SpringerLink

  https://link.springer.com/chapter/10.1007/16833_2023_146

  Recent advances in molecular characterization of different types of cancers improved refining the diagnostic criteria, prediction of prognosis, and identification of correct targets for drug development. […] Considering the board functional heterogenicity and property to transform in lymphoid malignancies, varied pathogenic mechanisms have been proposed underlying B cell, T cell, or lineage negative lymphomas. […] These current pieces of evidence show that although intrinsic genetic variations, epigenetic alterations, oncogenic viruses, and microenvironmental interactions are implicated in all subtypes of lymphomas, unique subtypes present accumulation for particular recurrent aberrations targeting specific pathways.

• #27 The role of novel immunotherapies in non-Hodgkin lymphoma – Pishko – Translational Cancer Research

  https://tcr.amegroups.org/article/view/11958/html

  Immune-checkpoint inhibitors antibodies are currently approved for treatment in a variety of malignancies, and have gained remarkable successes. […] Recent studies have added non-Hodgkin lymphoma to the rapidly expanding list of malignancies with remarkable response to immunotherapies in both indolent and aggressive subtypes.

• #28 Pathogenesis of non-Hodgkin’s lymphoma – PubMed

  https://pubmed.ncbi.nlm.nih.gov/21483013/

  The understanding of the molecular pathogenesis of non-Hodgkin’s lymphomas (NHL) has significantly improved in recent years. Advances in molecular biology and genetics lead to the identification and characterization of several oncogenic pathways involved in lymphomagenesis. This knowledge will ultimately lead to improved diagnostic and therapeutic strategies for patients with NHL. This review summarizes current concepts of the molecular pathogenesis of the most common NHL subtypes, with a special emphasis on diffuse large B-cell lymphoma, the most common lymphoma subtype.

• #29

  https://haematologica.org/article/view/717

  Despite a common origin from mature lymphoid cells, non-Hodgkin lymphomas (NHL) represent a surprisingly heterogeneous group of lymphoid malignancies whose classification is continuously being remodeled. […] In this respect, knowledge of the molecular pathogenesis of NHL, which is based upon genetic lesions leading to activation of proto-oncogenes (e.g. BCL-1, BCL-2, BCL-6, c-MYC) or disruption of tumor suppressor genes (e.g. p53), is becoming increasingly relevant for the clinician. […] These lesions combine into multiple molecular pathways which are selectively associated with distinct NHL types. […] Thus, for example, rearrangements of BCL-1, BCL-2, BCL-6, and c-MYC are the genetic hallmarks of mantle cell, follicular, diffuse large cell, and Burkitt’s lymphoma, respectively. […] Overall, from clinical perspective, NHL genetic lesions serve three purposes: a) they assist and complement histologic diagnosis; b) they provide a molecular marker with prognostic relevance; c) they allow evaluation of minimal residual disease through highly specific and highly sensitive technologies.

• #30 Non-Hodgkin lymphoma pathophysiology – wikidoc

  https://www.wikidoc.org/index.php/Non-Hodgkin_lymphoma_pathophysiology

  Non Hodgkin’s Lymphoma (NHL) represents a heterogeneous group of diseases with varied clinical presentation and histological appearance. It arises from cell of the lymphoid system, tumors are mainly derived from B lymphocytes, but are also from T lymphocytes, or natural killer cells. Lymphomas rise from different stages of B and T cell differentiation. Aberrations in the tightly controlled steps of B cell development can lead to oncogenesis. […] Somatically acquired genetic alterations (mainly translocations) of these processes is probably the underlying cause of lymphomagenesis. […] Follicular lymphoma most commonly results from the t(14;18)(q32;q21) translocation; this translocation places BCL2 (which encodes B-cell CLL/lymphoma 2) under control of the IGH enhancer element, leading to constitutive BCL2 expression.

• #31 Pulsenotes | Non-Hodgkin lymphoma notes

  https://app.pulsenotes.com/medicine/haematology/notes/non-hodgkin-lymphoma

  Follicular lymphoma is the second most common form of NHL. […] The exact pathogenesis is not understood. Around 85% have a translocation between chromosomes 14 and 18, t(14;18), however this is a non-specific change that may be seen in many without lymphoma. […] It is caused by mutation to c-myc proto-oncogene. This most commonly occurs due to a translocation between chromosomes 8 and 14, t(8;14)(q24;q32).

• #32 Pathogenesis of Non-Hodgkin’s Lymphoma | CoLab

  https://colab.ws/articles/10.1200%2Fjco.2010.33.3252

  The understanding of the molecular pathogenesis of non-Hodgkin’s lymphomas (NHL) has significantly improved in recent years. Advances in molecular biology and genetics lead to the identification and characterization of several oncogenic pathways involved in lymphomagenesis. […] This knowledge will ultimately lead to improved diagnostic and therapeutic strategies for patients with NHL. […] This review summarizes current concepts of the molecular pathogenesis of the most common NHL subtypes, with a special emphasis on diffuse large B-cell lymphoma, the most common lymphoma subtype.

• #33 Non-Hodgkin Lymphoma (NHL) – Oxford Medical Education

  https://oxfordmedicaleducation.com/haematology/non-hodgkin-lymphoma-nhl/

  Many subtypes of lymphoma have characteristic genetic changes, causing overexpression of particular genes which drive proliferation or promote survival. Many involve translocations with genes highly expressed in lymphocytes, such as immunoglobulin heavy chain. […] Follicular lymphoma is associated with BCL2 overexpression due to a translocation t(14:18) between the BCL2 gene on chr. 18 and the Ig heavy chain chain on chr. 14. […] Mantle cell lymphoma is associated with t(11:14) between the cyclin D1 gene (chr. 11) and the Ig heavy chain gene (chr. 14), which upregulates cyclin D1 expression. […] Lymphoplasmacytic lymphoma is associated with Myd88 overexpression due to an activating point mutation. […] Burkitt lymphoma has a rearrangement which causes overexpression of the oncogene MYC on chr. 8. The most common is t(8:14) between the Ig heavy chain gene on chr. 8, but t(2:8) is also seen, with the kappa light chain gene, as is t(8:22) with the lambda light chain gene. […] Diffuse large B cell lymphoma is associated with overexpression of BCL6, though there are a number of mechanisms, both isolated mutations and chromosomal rearrangements, underlying this.

• #34 Azthena logo with the word Azthena

  https://www.news-medical.net/health/What-is-Non-Hodgkin-Lymphoma.aspx

  Non-Hodgkin lymphomas arise by a multistep accumulation of genetic aberrations that result in a growth advantage of the malignant clone. […] Recurrent translocations during lymphocyte differentiation that lead to deregulated expression of oncogenes often represent an initial step, but secondary genetic alterations are a prerequisite for complete malignant transformation. […] The condition has been associated with chronic autoimmune or inflammatory illnesses such as Hashimotos thyroiditis, rheumatoid arthritis or Sjgren syndrome. Chronic infection is also linked with its pathogenesis; for example, primary gastric non-Hodgkin lymphoma of mucosa-associated lymphoid tissue (MALT-NHL) has shown strong correlation with Helicobacter pylori infection. […] Immune suppression is a known risk factor for non-Hodgkin lymphoma. In patients who underwent solid organ transplantation, the risk of the disease has been specifically associated with the duration of immunosuppression and the type of drugs used. Furthermore, this lymphoma is a common complication in patients with human immunodeficiency virus infection that most frequently affects the gastrointestinal tract.

• #35 Pathogenesis – NHL Strive

  https://strive-nhl.com/clinician-portal/pathogenesis/

  Various recurrent genomic and molecular biomarkers are involved in B-cell lymphomas, with prognostic effects related to various genetic abnormalities in proteins including MYC, BCL2, BCL6, TP53, etc. Additionally, development of unique anti-CD antibodies for treatment of specific lymphomas is possible due to specific biomarker expression at each stage of B-cell development and differentiation. […] Taking CD20 expression as an example, it is largely restricted to B-cells and certain stages of their development; pro-B cells, differentiated plasmablasts or plasma cells do not express CD20. Furthermore, CD-20 is detected in approximately 95% of all B-cell malignanices.

• #36 Molecular genetics related to non-Hodgkin lymphoma

  https://www.degruyter.com/document/doi/10.1515/biol-2016-0011/html?lang=en

  This article will give you a new insight into classification of NHL from specific genetic changes, which may be helpful with prediction of outcome and guidance of therapy. […] All of these phenomenon play crucial roles in the progression, pathogenesis and prognosis of cancer. Difference in roles of each molecular genetic component also provides for us more information about the classification of NHL and guidance for therapeutic decision-making.

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