Non-Hodgkin lymphoma pathophysiology: Difference between revisions
Preeti Singh (talk | contribs) |
Preeti Singh (talk | contribs) No edit summary |
||
| Line 8: | Line 8: | ||
==Pathophysiology== | ==Pathophysiology== | ||
===Pathogenesis== | ===Pathogenesis== | ||
* | |||
*Lymphomas can arise from different stages of B cell devevlopment: | |||
* | * [[B cell development]] starts in the primary lymphoid tissue, the bone marrow and subsequent maturation takes place in secondary lymphoid tissue (spleen and lymph nodes). | ||
*[ | *At the [[germinal centers]] of secondary lymphoid tissue B cells encounter antigens via T cells and then undergo affinity maturation to produce immunoglobulins of high affinity. | ||
* | *It supports rapid B-cell proliferation for [[immunoglobulin]] affinity maturation and production of antibody diversity through two processes know as [[somatic hypermutation]] (SHM) and [[immunoglobulin class-switch]]. | ||
*Both of these processes require rapid cell turnover and multiple double stranded [[DNA]] breaks, which is error-prone. | |||
* | *Somatically acquired genetic alterations ( mainly translocations) of these processes is probably the underlying cause of lymphomagenesis.<ref name="pmid25712152">{{cite journal |vauthors=Basso K, Dalla-Favera R |title=Germinal centres and B cell lymphomagenesis |journal=Nat. Rev. Immunol. |volume=15 |issue=3 |pages=172–84 |date=March 2015 |pmid=25712152 |doi=10.1038/nri3814 |url=}}</ref> | ||
* | |||
==Genetics== | ==Genetics== | ||
Revision as of 19:28, 12 December 2018
|
Non-Hodgkin lymphoma Microchapters |
|
Differentiating Non-Hodgkin's Lymphoma |
|---|
|
Treatment |
|
Case Studies |
|
Non-Hodgkin lymphoma pathophysiology On the Web |
|
American Roentgen Ray Society Images of Non-Hodgkin lymphoma pathophysiology |
|
Risk calculators and risk factors for Non-Hodgkin lymphoma pathophysiology |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief:
Overview
Non Hodgkin's Lymphoma 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. These aberrations are mainly seen in form of chromosomal translocation.
Pathophysiology
=Pathogenesis
- Lymphomas can arise from different stages of B cell devevlopment:
- B cell development starts in the primary lymphoid tissue, the bone marrow and subsequent maturation takes place in secondary lymphoid tissue (spleen and lymph nodes).
- At the germinal centers of secondary lymphoid tissue B cells encounter antigens via T cells and then undergo affinity maturation to produce immunoglobulins of high affinity.
- It supports rapid B-cell proliferation for immunoglobulin affinity maturation and production of antibody diversity through two processes know as somatic hypermutation (SHM) and immunoglobulin class-switch.
- Both of these processes require rapid cell turnover and multiple double stranded DNA breaks, which is error-prone.
- Somatically acquired genetic alterations ( mainly translocations) of these processes is probably the underlying cause of lymphomagenesis.[1]
Genetics
[Disease name] is transmitted in [mode of genetic transmission] pattern.
OR
Genes involved in the pathogenesis of [disease name] include:
- [Gene1]
- [Gene2]
- [Gene3]
OR
The development of [disease name] is the result of multiple genetic mutations such as:
- [Mutation 1]
- [Mutation 2]
- [Mutation 3]
Associated Conditions
Conditions associated with [disease name] include:
- [Condition 1]
- [Condition 2]
- [Condition 3]
Gross Pathology
On gross pathology, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].
Microscopic Pathology
On microscopic histopathological analysis, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].
References
- ↑ Basso K, Dalla-Favera R (March 2015). "Germinal centres and B cell lymphomagenesis". Nat. Rev. Immunol. 15 (3): 172–84. doi:10.1038/nri3814. PMID 25712152.
Genetics
The development of Non-Hodgkin lymphoma is the result of multiple genetic mutations such as:[1][2]
- Mutations of the B-cell receptor genes and NFKB pathway
- RNA splicing mutations in the small lymphocytic lymphoma
- Genetic mutations in histone formation:[3]
- MLL2
- MEF2B
- EZH2
- CREBBP
- EP300
- MLL2
Gross Pathology
On gross pathology, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].
Microscopic Pathology
On microscopic histopathological analysis, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].
References
- ↑ Pasqualucci L, Trifonov V, Fabbri G, Ma J, Rossi D, Chiarenza A; et al. (2011). "Analysis of the coding genome of diffuse large B-cell lymphoma". Nat Genet. 43 (9): 830–7. doi:10.1038/ng.892. PMC 3297422. PMID 21804550.
- ↑ Lohr JG, Stojanov P, Lawrence MS, Auclair D, Chapuy B, Sougnez C; et al. (2012). "Discovery and prioritization of somatic mutations in diffuse large B-cell lymphoma (DLBCL) by whole-exome sequencing". Proc Natl Acad Sci U S A. 109 (10): 3879–84. doi:10.1073/pnas.1121343109. PMC 3309757. PMID 22343534.
- ↑ Green MR, Gentles AJ, Nair RV, Irish JM, Kihira S, Liu CL; et al. (2013). "Hierarchy in somatic mutations arising during genomic evolution and progression of follicular lymphoma". Blood. 121 (9): 1604–11. doi:10.1182/blood-2012-09-457283. PMC 3587323. PMID 23297126.