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


{{CMG}}; {{AE}}  
{{CMG}}; {{AE}} {{Preeti}}
==Overview==
==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==
==Pathophysiology==
*Non-Hodgkin's lymphoma is a group of heterogeneous tumors with varied clinical presentation and histological appearance.
*[[Lymphoma|Lymphomas]] can arise from different stages of [[B cell|B cell development]]:
*These lymphoid tumors are derived from B lymphocytes, T lymphocytes, or natural killer cells which are the main immune cells in the body.<ref name="pmid21261680">{{cite journal| author=Farrell K, Jarrett RF| title=The molecular pathogenesis of Hodgkin lymphoma. | journal=Histopathology | year= 2011 | volume= 58 | issue= 1 | pages= 15-25 | pmid=21261680 | doi=10.1111/j.1365-2559.2010.03705.x | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=21261680  }}</ref>
*[[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]]).
*The 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>
*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.
** Burkitt lymphoma
*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]].
** Diffuse large B cell lymphoma
*Both of these processes require  rapid cell turnover and multiple double stranded [[DNA]] breaks, which is error-prone.
** Mantle cell lymphoma
*Somatically acquired genetic alterations ( mainly [[Chromosomal translocation|translocations]]) of these processes is probably the underlying cause of lymphomagenesis.
** Small lymphocytic lymphoma
** Follicular lymphoma
** Extranodal marginal zone lymphoma
** Splenic marginal zone lymphoma
** Lymphoplasmacytic lymphoma


=== Pathogenesis ===
* The major subtypes of non-hodgkin lymphoma (NHL) include the following:
* The main pathogenesis mechanism of NHL is genetic mutations of the proto-oncogenes and tumor suppressor genes. It is activation of proto-oncogenes or inactivation of the tumor suppressor genes. 
** Mature B-cell neoplasms:
* Unlike the solid tumors, the lymphomas do not have have microsatellite instability which is a DNA mismatch repair defect. Microsatellite instability is incorporated in the pathogenesis of many solid tumors. 
*** [[Diffuse large B cell lymphoma]]
* In NHL, there is mostly single or few chromosomal abnormalities in the genes causing lymphoma and it is caused by chromosomal translocation. The unbalanced translocations has been shown to be the cause of the disease progression.<ref name="pmid7579360">{{cite journal| author=Johansson B, Mertens F, Mitelman F| title=Cytogenetic evolution patterns in non-Hodgkin's lymphoma. | journal=Blood | year= 1995 | volume= 86 | issue= 10 | pages= 3905-14 | pmid=7579360 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=7579360  }}</ref>
*** [[Follicular lymphoma]]
*
*** [[Burkitt's lymphoma|Burkitt lymphoma]]
* Different genetic alteration related to lymphoma:<ref name="pmid22216861">{{cite journal| author=Couronné L, Bastard C, Bernard OA| title=TET2 and DNMT3A mutations in human T-cell lymphoma. | journal=N Engl J Med | year= 2012 | volume= 366 | issue= 1 | pages= 95-6 | pmid=22216861 | doi=10.1056/NEJMc1111708 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22216861  }}</ref>
*** [[Mantle cell lymphoma]]
** Point mutation which result in changes in control of transcription genes as TET and DNMT3A mutations.
*** [[Hairy cell leukemia]]
** Spliceosome mutations altering the process of translation.
*** Extranodal marginal zone lymphoma
* Deletion of p53 tumor suppresor gene is related to specific types of NHL as late stages of follicular lymphoma, CLL/SLL, and mantle cell lymphoma.<ref name="pmid2052620">{{cite journal| author=Gaidano G, Ballerini P, Gong JZ, Inghirami G, Neri A, Newcomb EW et al.| title=p53 mutations in human lymphoid malignancies: association with Burkitt lymphoma and chronic lymphocytic leukemia. | journal=Proc Natl Acad Sci U S A | year= 1991 | volume= 88 | issue= 12 | pages= 5413-7 | pmid=2052620 | doi= | pmc=51883 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=2052620  }}</ref>
*** [[Splenic marginal zone lymphoma]]
* The p53 gene inactivation is caused by point mutation in one allele and may be associated with consequent deletion of the second allele "second hit hypothesis". The deletion of the chromosome 6q is the frequent chromosomal deletion associated with lymphomas.<ref name="pmid1356511">{{cite journal| author=Gaidano G, Hauptschein RS, Parsa NZ, Offit K, Rao PH, Lenoir G et al.| title=Deletions involving two distinct regions of 6q in B-cell non-Hodgkin lymphoma. | journal=Blood | year= 1992 | volume= 80 | issue= 7 | pages= 1781-7 | pmid=1356511 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=1356511  }}</ref>
*** [[Multiple myeloma|Plasma cell myeloma]]
** Mature T and NK neoplasms:
*** [[Adult T-cell leukemia|Adult T-cell lymphoma]]
*** [[Mycosis fungoides]]
*** [[Sezary syndrome]]
*** [[Peripheral T cell lymphoma]]


==== Chromosomal translocation ====
*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.
*[[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>
*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>
*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 />


==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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