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{{Non-Hodgkin lymphoma}}
{{Non-Hodgkin lymphoma}}


{{CMG}}; {{AE}}  
{{CMG}}; {{AE}} {{Preeti}}
==Overview==
==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.
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. These aberrations are mainly seen in form of chromosomal translocation. About 85% of NHL's are of B-cell origin and only 15% are derived from T/NK cells. Two specific lymphomas, follicular lymphoma and diffuse large B cell lymphoma, account for about 65% of all non-Hodgkin lymphomas.
 


==Pathophysiology==
==Pathophysiology==
 
*[[Lymphoma|Lymphomas]] can arise from different stages of [[B cell|B cell development]]:
===Pathogenesis==
*[[B cell|B cell development]] starts in the primary lymphoid tissue, the [[bone marrow]] and subsequent maturation takes place in secondary [[Lymphatic system|lymphoid tissue]] ([[spleen]] and [[Lymph node|lymph nodes]]).
 
*At the [[germinal centers]] of secondary lymphoid tissue [[B cell|B cells]] encounter antigens via [[T cell|T cells]] and then undergo [[affinity maturation]] to produce [[Antibody|immunoglobulins]] of high affinity.
*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 [[Class switching|immunoglobulin class switching]].
*It supports rapid B-cell proliferation for [[immunoglobulin]] affinity maturation and production of antibody diversity through two processes know as [[somatic hypermutation]] (SHM) and [[Class switching|immunoglobulin class switching]].
*Both of these processes require  rapid cell turnover and multiple double stranded [[DNA]] breaks, which is error-prone.
*Both of these processes require  rapid cell turnover and multiple double stranded [[DNA]] breaks, which is error-prone.
*Somatically acquired genetic alterations ( mainly [[Chromosomal translocation|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><ref name="pmid10648419">{{cite journal |vauthors=Nardini E, Aiello A, Giardini R, Colnaghi MI, Ménard S, Balsari A |title=Detection of aberrant isotype switch recombination in low-grade and high-grade gastric MALT lymphomas |journal=Blood |volume=95 |issue=3 |pages=1032–8 |date=February 2000 |pmid=10648419 |doi= |url=}}</ref><ref name="pmid18097447">{{cite journal |vauthors=Klein U, Dalla-Favera R |title=Germinal centres: role in B-cell physiology and malignancy |journal=Nat. Rev. Immunol. |volume=8 |issue=1 |pages=22–33 |date=January 2008 |pmid=18097447 |doi=10.1038/nri2217 |url=}}</ref>
*Somatically acquired genetic alterations ( mainly [[Chromosomal translocation|translocations]]) of these processes is probably the underlying cause of lymphomagenesis.


* The major subtypes of non-hodgkin lymphoma include the following:<ref name="pmid21261684">{{cite journal| author=Coupland SE| title=The challenge of the microenvironment in B-cell lymphomas. | journal=Histopathology | year= 2011 | volume= 58 | issue= 1 | pages= 69-80 | pmid=21261684 | doi=10.1111/j.1365-2559.2010.03706.x | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=21261684  }}</ref><ref>{{cite journal|doi=10.1182/blood-2016- 01-643569}}</ref>
* The major subtypes of non-hodgkin lymphoma (NHL) include the following:
** Mature B-cell neoplasms:
** Mature B-cell neoplasms:
*** Burkitt lymphoma  
*** [[Diffuse large B cell lymphoma]]
*** Diffuse large B cell lymphoma  
*** [[Follicular lymphoma]]
*** Mantle cell lymphoma
*** [[Burkitt's lymphoma|Burkitt lymphoma]]
*** Small lymphocytic lymphoma
*** [[Mantle cell lymphoma]]
*** Follicular lymphoma
*** [[Hairy cell leukemia]]
*** Extranodal marginal zone lymphoma
*** Extranodal marginal zone lymphoma
*** Splenic marginal zone lymphoma
*** [[Splenic marginal zone lymphoma]]
*** Lymphoplasmacytic lymphoma
*** [[Multiple myeloma|Plasma cell myeloma]]
** Mature T and NK neoplasms:
** Mature T and NK neoplasms:
*** Adult T-cell lymphoma
*** [[Adult T-cell leukemia|Adult T-cell lymphoma]]
*** Mycosis fungoides
*** [[Mycosis fungoides]]
*** Sezary syndrome
*** [[Sezary syndrome]]
*** Peripheral T cell lymphoma
*** [[Peripheral T cell lymphoma]]
 
==Genetics==
{| class="wikitable"
|+
!NHL Subtype
!Translocations
!Genes involves
|-
|Burkitt lymphoma
|t(8;14)
 
|c-myc, IgH (Ig heavy chain)
|-
|Diffuse large B cell lymphoma
|t(3;16)(q27;p11)


t(11;14)(q13;q32)
*About 85% of NHLs are of B-cell origin and only 15% are derived from T/NK cells.<ref name="pmid15992695">{{cite journal| author=Morton LM, Zheng T, Holford TR, Holly EA, Chiu BC, Costantini AS et al.| title=Alcohol consumption and risk of non-Hodgkin lymphoma: a pooled analysis. | journal=Lancet Oncol | year= 2005 | volume= 6 | issue= 7 | pages= 469-76 | pmid=15992695 | doi=10.1016/S1470-2045(05)70214-X | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15992695  }} </ref>
|
*The small remainder stems from [[macrophages]].  
|-
*These [[tumors]] are characterized by the level of [[differentiation]], the size of the [[cell]] of origin, the origin cell's rate of [[proliferation]], and the histological pattern of growth.
|Mantle cell lymphoma
*[[Lymphomas]] of small [[lymphocytes]] generally have a more indolent course than those of large [[lymphocytes]], which may have intermediate-grade or high-grade aggressiveness.
|
*Two specific lymphomas, [[follicular lymphoma]] and [[diffuse large B cell lymphoma]], account for about 65% of all non-Hodgkin lymphomas.
|
*The gene-expression profiles of almost all non-Hodgkin lymphomas are a reflection of the equivalent healthy cell of origin from which the [[lymphoma]] is derived.<ref name="pmid15992695">{{cite journal| author=Morton LM, Zheng T, Holford TR, Holly EA, Chiu BC, Costantini AS et al.| title=Alcohol consumption and risk of non-Hodgkin lymphoma: a pooled analysis. | journal=Lancet Oncol | year= 2005 | volume= 6 | issue= 7 | pages= 469-76 | pmid=15992695 | doi=10.1016/S1470-2045(05)70214-X | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15992695  }} </ref>
|-
*[[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.<ref name="pmid25174027">{{cite journal| author=Wang SS, Flowers CR, Kadin ME, Chang ET, Hughes AM, Ansell SM et al.| title=Medical history, lifestyle, family history, and occupational risk factors for peripheral T-cell lymphomas: the InterLymph Non-Hodgkin Lymphoma Subtypes Project. | journal=J Natl Cancer Inst Monogr | year= 2014 | volume= 2014 | issue= 48 | pages= 66-75 | pmid=25174027 | doi=10.1093/jncimonographs/lgu012 | pmc=4155466 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=25174027  }} </ref>
|Small lymphocytic lymphoma
*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]].<ref name="pmid25174027">{{cite journal| author=Wang SS, Flowers CR, Kadin ME, Chang ET, Hughes AM, Ansell SM et al.| title=Medical history, lifestyle, family history, and occupational risk factors for peripheral T-cell lymphomas: the InterLymph Non-Hodgkin Lymphoma Subtypes Project. | journal=J Natl Cancer Inst Monogr | year= 2014 | volume= 2014 | issue= 48 | pages= 66-75 | pmid=25174027 | doi=10.1093/jncimonographs/lgu012 | pmc=4155466 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=25174027  }} </ref><ref name="pmid25174034">{{cite journal| author=Morton LM, Slager SL, Cerhan JR, Wang SS, Vajdic CM, Skibola CF et al.| title=Etiologic heterogeneity among non-Hodgkin lymphoma subtypes: the InterLymph Non-Hodgkin Lymphoma Subtypes Project. | journal=J Natl Cancer Inst Monogr | year= 2014 | volume= 2014 | issue= 48 | pages= 130-44 | pmid=25174034 | doi=10.1093/jncimonographs/lgu013 | pmc=4155467 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=25174034  }} </ref>
|
*Similarly, [[mantle cell lymphoma]] is characterised by the t(11;14)(q13;q32) translocation, which leads to the deregulated expression of [[cyclin D1]].<ref name="pmid28978864">{{cite journal| author=Tamaru JI| title=2016 revision of the WHO classification of lymphoid neoplasms. | journal=Rinsho Ketsueki | year= 2017 | volume= 58 | issue= 10 | pages= 2188-2193 | pmid=28978864 | doi=10.11406/rinketsu.58.2188 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=28978864  }} </ref>
|
*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 lymphoma|follicular T-cell lymphoma]].<ref name="pmid26980727">{{cite journal| author=Swerdlow SH, Campo E, Pileri SA, Harris NL, Stein H, Siebert R et al.| title=The 2016 revision of the World Health Organization classification of lymphoid neoplasms. | journal=Blood | year= 2016 | volume= 127 | issue= 20 | pages= 2375-90 | pmid=26980727 | doi=10.1182/blood-2016-01-643569 | pmc=4874220 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=26980727  }} </ref>
|Follicular 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]].<ref name="pmid26980727">{{cite journal| author=Swerdlow SH, Campo E, Pileri SA, Harris NL, Stein H, Siebert R et al.| title=The 2016 revision of the World Health Organization classification of lymphoid neoplasms. | journal=Blood | year= 2016 | volume= 127 | issue= 20 | pages= 2375-90 | pmid=26980727 | doi=10.1182/blood-2016-01-643569 | pmc=4874220 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=26980727  }} </ref><ref name="pmid29741263">{{cite journal| author=Matutes E| title=The 2017 WHO update on mature T- and natural killer (NK) cell neoplasms. | journal=Int J Lab Hematol | year= 2018 | volume= 40 Suppl 1 | issue=  | pages= 97-103 | pmid=29741263 | doi=10.1111/ijlh.12817 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=29741263  }} </ref><br />
|
|
|-
|Extranodal marginal zone lymphoma
|
|
|-
|Splenic marginal zone lymphoma
|
|
|-
|Lymphoplasmacytic lymphoma
|
|
|}
[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==
{{Reflist|2}}
 
{{WH}}
{{WS}}
[[Category: (name of the system)]]


==Genetics==
==Genetics==
The development of Non-Hodgkin lymphoma is the result of multiple genetic mutations such as:<ref name="pmid21804550">{{cite journal| author=Pasqualucci L, Trifonov V, Fabbri G, Ma J, Rossi D, Chiarenza A et al.| title=Analysis of the coding genome of diffuse large B-cell lymphoma. | journal=Nat Genet | year= 2011 | volume= 43 | issue= 9 | pages= 830-7 | pmid=21804550 | doi=10.1038/ng.892 | pmc=3297422 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=21804550  }}</ref><ref name="pmid22343534">{{cite journal| author=Lohr JG, Stojanov P, Lawrence MS, Auclair D, Chapuy B, Sougnez C et al.| title=Discovery and prioritization of somatic mutations in diffuse large B-cell lymphoma (DLBCL) by whole-exome sequencing. | journal=Proc Natl Acad Sci U S A | year= 2012 | volume= 109 | issue= 10 | pages= 3879-84 | pmid=22343534 | doi=10.1073/pnas.1121343109 | pmc=3309757 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22343534  }}</ref>
The development of non-Hodgkin lymphoma is the result of multiple genetic mutations such as:<ref name="pmid21804550">{{cite journal| author=Pasqualucci L, Trifonov V, Fabbri G, Ma J, Rossi D, Chiarenza A et al.| title=Analysis of the coding genome of diffuse large B-cell lymphoma. | journal=Nat Genet | year= 2011 | volume= 43 | issue= 9 | pages= 830-7 | pmid=21804550 | doi=10.1038/ng.892 | pmc=3297422 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=21804550  }}</ref><ref name="pmid22343534">{{cite journal| author=Lohr JG, Stojanov P, Lawrence MS, Auclair D, Chapuy B, Sougnez C et al.| title=Discovery and prioritization of somatic mutations in diffuse large B-cell lymphoma (DLBCL) by whole-exome sequencing. | journal=Proc Natl Acad Sci U S A | year= 2012 | volume= 109 | issue= 10 | pages= 3879-84 | pmid=22343534 | doi=10.1073/pnas.1121343109 | pmc=3309757 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22343534  }}</ref>
*[[Mutations]] of the [[B-cell]] receptor genes and [[NFKB]] pathway.
*[[RNA splicing]] [[mutations]] in the [[small lymphocytic lymphoma]].
*[[Genetic mutations]] in histone formation:<ref name="pmid23297126">{{cite journal| author=Green MR, Gentles AJ, Nair RV, Irish JM, Kihira S, Liu CL et al.| title=Hierarchy in somatic mutations arising during genomic evolution and progression of follicular lymphoma. | journal=Blood | year= 2013 | volume= 121 | issue= 9 | pages= 1604-11 | pmid=23297126 | doi=10.1182/blood-2012-09-457283 | pmc=3587323 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23297126  }}</ref>
**[[MLL2]]
**[[MEF2B]]
**[[EZH2]]
**CREBBP
**[[EP300]]
**[[MLL2]]
**[[KMT2D]]
*Mutations in [[CDKN2A]] alters cell cycle control and affects JAK–STAT signalling.
*Upregulation of key signalling pathways such as [[CD79B]], [[MYD88]], [[CARD11]].
*Block to terminal differentiation such as [[BCL6]] translocations and loss of [[PRDM1]].


*Mutations of the B-cell receptor genes and NFKB pathway
== Associated Conditions ==
*RNA splicing mutations in the small lymphocytic lymphoma
* Several conditions are associated with non-Hodgkin's lymphoma depending on the type. However, [[Epstein Barr virus]], [[Human Immunodeficiency Virus|human immunodeficiency virus]], and [[hepatitis C]] infection are commonly present.
*Genetic mutations in histone formation:<ref name="pmid23297126">{{cite journal| author=Green MR, Gentles AJ, Nair RV, Irish JM, Kihira S, Liu CL et al.| title=Hierarchy in somatic mutations arising during genomic evolution and progression of follicular lymphoma. | journal=Blood | year= 2013 | volume= 121 | issue= 9 | pages= 1604-11 | pmid=23297126 | doi=10.1182/blood-2012-09-457283 | pmc=3587323 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23297126  }}</ref>
**MLL2
**MEF2B
**EZH2
**CREBBP
**EP300
**MLL2


==Gross Pathology==
== Gross Pathology ==
On gross pathology, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].
*For information on gross pathology findings of [[Follicular lymphoma]], [[Follicular lymphoma pathophysiology#Gross Pathology|click here]].
*For information on gross pathology findings of [[Mantle cell lymphoma]], [[Mantel cell lymphoma pathophysiology#Gross Pathology|click here]].
*For information on gross pathology findings of [[Hairy cell leukemia]], [[hairy cell leukemia pathophysiology#Gross Pathology|click here]].
*For information on gross pathology findings of [[Splenic marginal zone lymphoma]], [[Splenic marginal zone lymphoma pathophysiology#Gross Pathology|click here]].
*For information on gross pathology findings of [[Mycosis fungoides]], [[Mycosis fungoides pathophysiology#Gross Pathology|click here]].
*For information on gross pathology findings of [[Peripheral T cell lymphoma]], [[Peripheral T cell lymphoma pathophysiology#Gross Pathology|click here]].


==Microscopic Pathology==
== Microscopy Pathology ==
On microscopic histopathological analysis, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].
*For information on microscopic pathology findings of [[Follicular lymphoma]], [[Follicular lymphoma pathophysiology#Microscopic Pathology|click here]].
*For information on microscopic pathology findings of [[Mantle cell lymphoma]], [[Mantel cell lymphoma pathophysiology#Microscopic Pathology|click here]].
*For information on microscopic pathology findings of [[Hairy cell leukemia]], [[hairy cell leukemia pathophysiology#Microscopic Pathology|click here]].
*For information on microscopic pathology findings of [[Splenic marginal zone lymphoma]], [[Splenic marginal zone lymphoma pathophysiology#Microscopic Pathology|click here]].
*For information on microscopic pathology findings of [[Mycosis fungoides]], [[Mycosis fungoides pathophysiology#Microscopic Pathology|click here]].
*For information on microscopic pathology findings of [[Peripheral T cell lymphoma]], [[Peripheral T cell lymphoma pathophysiology#Microscopic Pathology|click here]].


==References==
==References==

Latest revision as of 20:27, 21 January 2019

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Preeti Singh, M.B.B.S.[2]

Overview

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. These aberrations are mainly seen in form of chromosomal translocation. About 85% of NHL's are of B-cell origin and only 15% are derived from T/NK cells. Two specific lymphomas, follicular lymphoma and diffuse large B cell lymphoma, account for about 65% of all non-Hodgkin lymphomas.

Pathophysiology

Genetics

The development of non-Hodgkin lymphoma is the result of multiple genetic mutations such as:[7][8]

Associated Conditions

Gross Pathology

Microscopy Pathology

References

  1. ↑ 1.0 1.1 Morton LM, Zheng T, Holford TR, Holly EA, Chiu BC, Costantini AS; et al. (2005). "Alcohol consumption and risk of non-Hodgkin lymphoma: a pooled analysis". Lancet Oncol. 6 (7): 469–76. doi:10.1016/S1470-2045(05)70214-X. PMID 15992695.
  2. ↑ 2.0 2.1 Wang SS, Flowers CR, Kadin ME, Chang ET, Hughes AM, Ansell SM; et al. (2014). "Medical history, lifestyle, family history, and occupational risk factors for peripheral T-cell lymphomas: the InterLymph Non-Hodgkin Lymphoma Subtypes Project". J Natl Cancer Inst Monogr. 2014 (48): 66–75. doi:10.1093/jncimonographs/lgu012. PMC 4155466. PMID 25174027.
  3. ↑ Morton LM, Slager SL, Cerhan JR, Wang SS, Vajdic CM, Skibola CF; et al. (2014). "Etiologic heterogeneity among non-Hodgkin lymphoma subtypes: the InterLymph Non-Hodgkin Lymphoma Subtypes Project". J Natl Cancer Inst Monogr. 2014 (48): 130–44. doi:10.1093/jncimonographs/lgu013. PMC 4155467. PMID 25174034.
  4. ↑ Tamaru JI (2017). "2016 revision of the WHO classification of lymphoid neoplasms". Rinsho Ketsueki. 58 (10): 2188–2193. doi:10.11406/rinketsu.58.2188. PMID 28978864.
  5. ↑ 5.0 5.1 Swerdlow SH, Campo E, Pileri SA, Harris NL, Stein H, Siebert R; et al. (2016). "The 2016 revision of the World Health Organization classification of lymphoid neoplasms". Blood. 127 (20): 2375–90. doi:10.1182/blood-2016-01-643569. PMC 4874220. PMID 26980727.
  6. ↑ Matutes E (2018). "The 2017 WHO update on mature T- and natural killer (NK) cell neoplasms". Int J Lab Hematol. 40 Suppl 1: 97–103. doi:10.1111/ijlh.12817. PMID 29741263.
  7. ↑ 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.
  8. ↑ 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.
  9. ↑ 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.


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