Difference between revisions of "HAEM5:Adult T-cell leukaemia/lymphoma"

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This page was converted to the new template on 2023-12-07. The original page can be found at HAEM4:Adult T-cell Leukemia/Lymphoma.

(General Instructions – The main focus of these pages is the clinically significant genetic alterations in each disease type. Use HUGO-approved gene names and symbols (italicized when appropriate), HGVS-based nomenclature for variants, as well as generic names of drugs and testing platforms or assays if applicable. Please complete tables whenever possible and do not delete them (add N/A if not applicable in the table and delete the examples). Please do not delete or alter the section headings. The use of bullet points alongside short blocks of text rather than only large paragraphs is encouraged. Additional instructions below in italicized blue text should not be included in the final page content. Please also see Author_Instructions and FAQs as well as contact your Associate Editor or Technical Support)

Primary Author(s)*

Prasad R. Kopparapu, PhD and Ferrin C. Wheeler, PhD, FACMG

Vanderbilt University Medical Center

Cancer Category / Type

Mature T- and NK-Cell Neoplasms

Cancer Sub-Classification / Subtype

Adult T-Cell Leukemia/lymphoma (ATLL)

Definition / Description of Disease

Adult T-cell Leukemia/Lymphoma (ATLL) is a systemic, aggressive T-cell malignancy cause by chronic infection of human T lymphotropic virus 1 (HTLV-1) with poor prognosis^[1].

Synonyms / Terminology

Adult T-cell leukemia, Adult T-cell lymphoma, HTLV-1 associated adult T-cell leukemia-lymphoma.

Epidemiology / Prevalence

ATLL is endemic in many parts of Southwestern Japan, the Caribbean basin, Sub-Saharan Africa, South America, Romania, Northern Iran, parts of the Middle East and Australo-Melanesia^[2]^[3].

ATLL occurs only in adults between 30 to 90 years of age with an average age of 58 years. The male-to-female ratio is 1.5:1^[4].

Transmission occurs through breast milk, sexual fluids, peripheral blood and blood products^[2].

Clinical Features

Put your text here and fill in the table (Instruction: Can include references in the table)

Signs and Symptoms	EXAMPLE Asymptomatic (incidental finding on complete blood counts) EXAMPLE B-symptoms (weight loss, fever, night sweats) EXAMPLE Fatigue EXAMPLE Lymphadenopathy (uncommon)
Laboratory Findings	EXAMPLE Cytopenias EXAMPLE Lymphocytosis (low level)

editv4:Clinical Features

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ATLL is classified into four clinical subtypes: Acute, Lymphoma, Chronic and Smoldering^[5].
Acute: Most common type (65% of patients) with elevated WBC count, skin rash and generalized lymphadenopathy, hypercalcemia, hepatosplenomegaly, elevated LDH and frequent opportunistic infections like pneumocystis jirovecii pneumonia and strongyloidiasis.
Lymphoma: The lymphomatous variant is characterized by lymphadenopathy, absence of lymphocytosis, possible extranodal lesions with minimal peripheral blood involvement and less frequent hypercalcemia.
Chronic: The chronic variant can progress to acute or lymphomatous subtype. This variant manifests with lymphocytosis and exfoliative skin lesions. Atypical lymphocytes are fewer in number in peripheral blood. There can be mild hepatosplenomegaly and lymphadenopathy. Hypercalcemia is not observed, and no involvement of CNS, bone and gastrointestinal tract, and neither ascites nor pleural effusion.
Smoldering: This variant may also progress to the acute subtype upon long duration. This variant may present with skin or lung lesions. More than 5% circulating abnormal T-cell lymphocytes can be found in the absence of leukocytosis. No manifestation of hypercalcemia, hepatosplenomegaly or lymphadenopathy.

Sites of Involvement

In addition to lymph node involvement, there is involvement in extranodal sites like spleen, skin, lung, liver, gastrointestinal tract and CNS, making this a systemic disease with peripheral blood involvement^[6].

Morphologic Features

The morphological features of ATLL in skin include erythema, papules, and nodules based on macroscopic examination and perivascular infiltration of atypical lymphoid cells, diffuse infiltration of medium to large sized atypical lymphoid cells and infiltration of large atypical lymphoid cell as per histopathological observations.

Lymph node lesions present as pleomorphic small, medium and large cell types, anaplastic and an angioimmunoblastic T-cell lymphoma type.

Infiltration of atypical lymphoid cells with irregular or round nuclei is seen in the bone marrow cavity with detection of hypercalcemia.

In liver, infiltration of atypical medium to large sized lymphoid cells with irregular nuclei is seen.

Diffuse, pleomorphic and anaplastic type cells can infiltrate the stomach destroying the gastric glands.

In peripheral blood, “flower like” cells that have multilobed nucleus with basophilic cytoplasm can be observed by Giemsa staining^[7].

Immunophenotype

In most patients, tumor cells exhibit phenotype of mature CD4+ T cells by expressing CD2, CD3, CD5, CD25, CD45RO, CD29, T-cell receptor αβ, FOXP3, CD52, and HLA-DR^[8]^[9].

Most cases are CD4+CD8-, but rarely, cases can be CD4-CD8+ or CD4+CD8+. A typical immunophenotype for ATLL is: CD2+, CD3+, CD4+, CD7-, CD8-, CD25+, CD30+/-, TCR αβ+^[10].

Immunophenotypic characterization of CD3, CD4, CD7 , CD8, and CD25 are the minimum requirement for an ATLL diagnosis.

Finding	Marker
Positive (universal)	CD2, CD3, CD5, CD4, CCD4
Positive (subset)	CD8, CD4, CD30, FOXP3
Negative (universal)	CD7, CD8, TdT, TCL1, ALK1, B cell antigens, cytotoxic molecules
Negative (subset)	CD4,CD8, ALK

Chromosomal Rearrangements (Gene Fusions)

Put your text here and fill in the table

Chromosomal Rearrangement	Genes in Fusion (5’ or 3’ Segments)	Pathogenic Derivative	Prevalence	Diagnostic Significance (Yes, No or Unknown)	Prognostic Significance (Yes, No or Unknown)	Therapeutic Significance (Yes, No or Unknown)	Notes
EXAMPLE t(9;22)(q34;q11.2)	EXAMPLE 3'ABL1 / 5'BCR	EXAMPLE der(22)	EXAMPLE 20% (COSMIC) EXAMPLE 30% (add reference)	Yes	No	Yes	EXAMPLE The t(9;22) is diagnostic of CML in the appropriate morphology and clinical context (add reference). This fusion is responsive to targeted therapy such as Imatinib (Gleevec) (add reference).

editv4:Chromosomal Rearrangements (Gene Fusions)

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Tandem duplications of 2q33.2 segments cause formation of CTLA4-CD28 and ICOS-CD28 fusion products that render prolonged co-stimulatory signals^[11].

Chromosomal Rearrangement Genes in Fusion (5’ or 3’ Segments) Pathogenic Derivative Prevalence

2q33.2 (Tandem Duplication) 5’ CTLA/3’CD28 der(2) 7%

2q33.2 (Tandem Duplication) 5’ICOS/3’CD28 der(2) 7%

editv4:Clinical Significance (Diagnosis, Prognosis and Therapeutic Implications).

Please incorporate this section into the relevant tables found in:
Chromosomal Rearrangements (Gene Fusions)

Individual Region Genomic Gain/Loss/LOH

Characteristic Chromosomal Patterns

Gene Mutations (SNV/INDEL)

ATLL diagnosis can be made based on seropositivity for HTLV-1 and histologically and/or cytologically proven peripheral T cell lymphoma (PTCL). Diagnosis can also be made by quantifying proviral DNA loads (PVLs) in peripheral blood mononuclear cells using real time PCR. PVL of an infected person can range from 0.01 to 50% or higher. Other diagnostic criteria includes appropriate patient demographic information, hypercalcemia, skin lesions and a leukemic phase.
The prognosis of ATLL is largely dependent on the subtype. The acute and lymphomatous subtypes are aggressive, with a median survival of 6.2 months and 10.2 months, respectively. The less-aggressive chronic and smoldering subtypes have a median survival of approximately 4.5 years^[5]. Prognostic factors include clinical variant, age, serum calcium and LDH levels as well as detection of opportunistic infections of parasitic or viral types and p16 gene deletion and p53 mutation.
As ATLL is resistant to most chemotherapy, there is no standard chemotherapy regimen. High dose combination chemotherapy and bone marrow transplantation have been tried previously^[12]. Monoclonal antibody-based therapies against IL-2R (anti-Tac), CCR4 (mogamulizumab) and CD52 (alemtuzumab) have also been attempted along with arsenic trioxide, interferon α and zidovudine^[13].

Individual Region Genomic Gain / Loss / LOH

Put your text here and fill in the table (Instructions: Includes aberrations not involving gene fusions. Can include references in the table. Can refer to CGC workgroup tables as linked on the homepage if applicable.)

Chr #	Gain / Loss / Amp / LOH	Minimal Region Genomic Coordinates [Genome Build]	Minimal Region Cytoband	Diagnostic Significance (Yes, No or Unknown)	Prognostic Significance (Yes, No or Unknown)	Therapeutic Significance (Yes, No or Unknown)	Notes
EXAMPLE 7	EXAMPLE Loss	EXAMPLE chr7:1- 159,335,973 [hg38]	EXAMPLE chr7	Yes	Yes	No	EXAMPLE Presence of monosomy 7 (or 7q deletion) is sufficient for a diagnosis of AML with MDS-related changes when there is ≥20% blasts and no prior therapy (add reference). Monosomy 7/7q deletion is associated with a poor prognosis in AML (add reference).
EXAMPLE 8	EXAMPLE Gain	EXAMPLE chr8:1-145,138,636 [hg38]	EXAMPLE chr8	No	No	No	EXAMPLE Common recurrent secondary finding for t(8;21) (add reference).

editv4:Genomic Gain/Loss/LOH

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ATLL with high number of chromosomal imbalances is associated with poor survival^[14]^[15]^[16]^[17].

Chromosome Number Gain/Loss/Amp/LOH Region

1 Gain 1q

2 Gain 2p

3 Gain 3p

4 Gain 4q

6 Loss 6q

7 Gain 7p, 7q

9 Amp 9p

10 Loss 10p

13 Loss 13q

14 Gain 14q

16 Loss 16q

18 Loss 18p

Characteristic Chromosomal Patterns

Put your text here (EXAMPLE PATTERNS: hyperdiploid; gain of odd number chromosomes including typically chromosome 1, 3, 5, 7, 11, and 17; co-deletion of 1p and 19q; complex karyotypes without characteristic genetic findings; chromothripsis)

Chromosomal Pattern	Diagnostic Significance (Yes, No or Unknown)	Prognostic Significance (Yes, No or Unknown)	Therapeutic Significance (Yes, No or Unknown)	Notes
EXAMPLE Co-deletion of 1p and 18q	Yes	No	No	EXAMPLE: See chromosomal rearrangements table as this pattern is due to an unbalanced derivative translocation associated with oligodendroglioma (add reference).

editv4:Characteristic Chromosomal Aberrations / Patterns

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Cytogenetic studies show that ATLL often has a complex abnormal karyotype without a single distinct abnormality. Observed recurrent abnormalities include trisomy for 3, 7 or 21 and monosomy for X as well as deletion of Y and abnormalities of chromosome 6 and 14. Chromosome 14 rearrangements involving TCRA and TCRD at 14q11 and TCL1 at 14q32 have been documented^[18]. Frequent deletions in known fragile sites have been detected in over 500 patients^[11].

Gene Mutations (SNV / INDEL)

Put your text here and fill in the table (Instructions: This table is not meant to be an exhaustive list; please include only genes/alterations that are recurrent and common as well either disease defining and/or clinically significant. Can include references in the table. For clinical significance, denote associations with FDA-approved therapy (not an extensive list of applicable drugs) and NCCN or other national guidelines if applicable; Can also refer to CGC workgroup tables as linked on the homepage if applicable as well as any high impact papers or reviews of gene mutations in this entity.)

Gene; Genetic Alteration	Presumed Mechanism (Tumor Suppressor Gene [TSG] / Oncogene / Other)	Prevalence (COSMIC / TCGA / Other)	Concomitant Mutations	Mutually Exclusive Mutations	Diagnostic Significance (Yes, No or Unknown)	Prognostic Significance (Yes, No or Unknown)	Therapeutic Significance (Yes, No or Unknown)	Notes
EXAMPLE: TP53; Variable LOF mutations EXAMPLE: EGFR; Exon 20 mutations EXAMPLE: BRAF; Activating mutations	EXAMPLE: TSG	EXAMPLE: 20% (COSMIC) EXAMPLE: 30% (add Reference)	EXAMPLE: IDH1 R123H	EXAMPLE: EGFR amplification				EXAMPLE: Excludes hairy cell leukemia (HCL) (add reference).

Note: A more extensive list of mutations can be found in cBioportal (https://www.cbioportal.org/), COSMIC (https://cancer.sanger.ac.uk/cosmic), ICGC (https://dcc.icgc.org/) and/or other databases. When applicable, gene-specific pages within the CCGA site directly link to pertinent external content.

editv4:Gene Mutations (SNV/INDEL)

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Over 10% of ATLL cases harbor mostly gain of function mutations. ATLL harbors multiple recurrent mutations in genes involved in the TCR-NF-κB pathway, tumor suppressors, transcription factors involved in cell growth and proliferation, apoptosis, and immune surveillance^[19]^[17]^[20].

Gene Mutation Oncogene/Tumor Suppressor/Other Presumed Mechanism (LOF/GOF/Other; Driver/Passenger) Prevalence (COSMIC/TCGA/Other)

PLCG1 TCR – NF-κB Signaling GOF

PKCB TCR – NF-κB Signaling GOF

CARD11 TCR – NF-κB Signaling GOF

VAV1 TCR – NF-κB Signaling GOF

CD237 TCR – NF-κB Signaling GOF

RHOA RAS-RAF-ERK pathway GOF

IRF4 Transcription Factor GOF

NOTCH1 Transcription Factor GOF

FBXW7 Transcription Factor GOF

STAT3 Transcription Factor GOF

TNFAIP3/A20 TCR – NF-κB Signaling LOF

NFKBIA/IκBα TCR – NF-κB Signaling LOF

TRAF3 TCR – NF-κB Signaling LOF

CBLB TCR – NF-κB Signaling LOF

TP53 Tumor Suppressor LOF

CDKN2 Tumor Suppressor LOF

GATA3 Transcription Factor LOF

EP300 Transcription Factor LOF

FAS Apoptosis LOF

WWOX Apoptosis LOF

HLA-B Immune Surveillance LOF

B2M Immune Surveillance LOF

PD-L1 Immune Surveillance Amplification

Other Mutations

Type Gene/Region/Other

Concomitant Mutations EXAMPLE IDH1 R123H

Secondary Mutations EXAMPLE Trisomy 7

Mutually Exclusive EXAMPLE EGFR Amplification

Epigenomic Alterations

Epigenetic alterations also result in dysregulated TCR/NF-κB signaling in ATLL. DNA hypermethylation of CpG islands is detected in 1/3^rd of all ATLL patients. As a result, genes involved in Cys2-His2 (C2H2) zinc finger genes and those encoding MHC class I molecules are silenced^[11].

ATLL patients have high expression of polycomb repressive complex (PRC) 2 components like EZH2, its homolog EZH1 and H3K27 methylase causing accumulation of trimethylation of H3K27 and altering the expression of over half of the genes. The severity of the disease is linked to continued down regulation of genes^[21].

Genes and Main Pathways Involved

Put your text here and fill in the table (Instructions: Can include references in the table.)

Gene; Genetic Alteration	Pathway	Pathophysiologic Outcome
EXAMPLE: BRAF and MAP2K1; Activating mutations	EXAMPLE: MAPK signaling	EXAMPLE: Increased cell growth and proliferation
EXAMPLE: CDKN2A; Inactivating mutations	EXAMPLE: Cell cycle regulation	EXAMPLE: Unregulated cell division
EXAMPLE: KMT2C and ARID1A; Inactivating mutations	EXAMPLE: Histone modification, chromatin remodeling	EXAMPLE: Abnormal gene expression program

editv4:Genes and Main Pathways Involved

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The most important genes involved in the development and progress of ATLL are the Tax and HBZ contributed by the HTLV-1 virus and genes listed in gene mutations table (above) from the host. The main pathways involved are TCR-NF-κB signaling by gain of function and amplifications in PLCG1, VAV1 and FYN, CD28, PRKCB, CARD11, IRF4 and RHOA; and loss of function mutations or deletions in CBLB, TRAF, TNFAIP3 and CSNK1A1^[11].
Genes involving the immune surveillance program are also heavy altered to evade the immune response either by deletions in MHC class1 molecules, CD58, FAS or constitutive activation of PD-L1.
Genes involved in the Lymphocyte activation and differentiation(IRF4, GATA3, IKZF2) are also altered.
Chemokine receptors including CCR4 and CCR7 are responsible for the infiltration of neoplastic cells into other organs along with activation of PI3K/AKT signaling.
The epigenetic mechanism is also exploited to alter gene expression and promote ATLL progression as explained above.

Genetic Diagnostic Testing Methods

Initial diagnosis of ATLL should include a comprehensive physical exam with skin evaluation and CT scans of the chest, abdomen and pelvis. The laboratory evaluation should include: a complete blood count (CBC), metabolic panel (serum electrolyte levels, calcium, creatinine and blood urea nitrogen) and serum LDH levels. Testing methods including PCR, Flow Cytometry, ELISA, serology, and immunohistochemistry in addition to morphologic studies may be employed to diagnose ATLL^[10].

Familial Forms

Put your text here (Instructions: Include associated hereditary conditions/syndromes that cause this entity or are caused by this entity.)

Additional Information

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Links

Put your text placeholder here (or anywhere appropriate on the page) and use the "Link" icon at the top of the page (Instructions: Once you have a text placeholder entered to which you want to add a link, highlight that text, select the "Link" icon at the top of the page, and search the name of the internal page to which you want to link this text, or enter an external internet address including the "http://www." portion.)

References

(use the "Cite" icon at the top of the page) (Instructions: Add each reference into the text above by clicking on where you want to insert the reference, selecting the “Cite” icon at the top of the page, and using the “Automatic” tab option to search such as by PMID to select the reference to insert. The reference list in this section will be automatically generated and sorted. If a PMID is not available, such as for a book, please use the “Cite” icon, select “Manual” and then “Basic Form”, and include the entire reference.)

↑ Thiele, J. et al., (2017). Adult T-cell leukemia/lymphoma, in World Health Organization Classification of Tumours of Haematopoietic and Lymphoid Tissues, Revised 4th edition. Swerdlow SH, Campo E, Harris NL, Jaffe ES, Pileri SA, Stein H, Thiele J, Arber DA, Hasserjian RP, Le Beau MM, Orazi A, and Siebert R, Editors. IARC Press: Lyon, France, p363-367
↑ ^2.0 ^2.1 Gessain, Antoine; et al. (2012). "Epidemiological Aspects and World Distribution of HTLV-1 Infection". Frontiers in Microbiology. 3: 388. doi:10.3389/fmicb.2012.00388. ISSN 1664-302X. PMC 3498738. PMID 23162541.
↑ Mehta-Shah, Neha; et al. (08 2017). "Adult T-Cell Leukemia/Lymphoma". Journal of Oncology Practice. 13 (8): 487–492. doi:10.1200/JOP.2017.021907. ISSN 1935-469X. PMC 6366298. PMID 28796966. Check date values in: |date= (help)
↑ Rocquain, Julien; et al. (2010-08-02). "Combined mutations of ASXL1, CBL, FLT3, IDH1, IDH2, JAK2, KRAS, NPM1, NRAS, RUNX1, TET2 and WT1 genes in myelodysplastic syndromes and acute myeloid leukemias". BMC cancer. 10: 401. doi:10.1186/1471-2407-10-401. ISSN 1471-2407. PMC 2923633. PMID 20678218.
↑ ^5.0 ^5.1 Shimoyama, M. (1991-11). "Diagnostic criteria and classification of clinical subtypes of adult T-cell leukaemia-lymphoma. A report from the Lymphoma Study Group (1984-87)". British Journal of Haematology. 79 (3): 428–437. doi:10.1111/j.1365-2141.1991.tb08051.x. ISSN 0007-1048. PMID 1751370. Check date values in: |date= (help)
↑ Bunn, P. A.; et al. (1983-08-04). "Clinical course of retrovirus-associated adult T-cell lymphoma in the United States". The New England Journal of Medicine. 309 (5): 257–264. doi:10.1056/NEJM198308043090501. ISSN 0028-4793. PMID 6602943.
↑ Ohshima, Koichi (2007-06). "Pathological features of diseases associated with human T-cell leukemia virus type I". Cancer Science. 98 (6): 772–778. doi:10.1111/j.1349-7006.2007.00456.x. ISSN 1347-9032. PMID 17388788. Check date values in: |date= (help)
↑ Roncador, G.; et al. (2005-12). "FOXP3, a selective marker for a subset of adult T-cell leukaemia/lymphoma". Leukemia. 19 (12): 2247–2253. doi:10.1038/sj.leu.2403965. ISSN 0887-6924. PMID 16193085. Check date values in: |date= (help)
↑ Ishida, Takashi; et al. (2003-09-01). "Clinical significance of CCR4 expression in adult T-cell leukemia/lymphoma: its close association with skin involvement and unfavorable outcome". Clinical Cancer Research: An Official Journal of the American Association for Cancer Research. 9 (10 Pt 1): 3625–3634. ISSN 1078-0432. PMID 14506150.
↑ ^10.0 ^10.1 NCCN Clinical Practice Guidelines in Oncology, T-Cell Lymphomas, Version 1.2021. Available at NCCN.org.
↑ ^11.0 ^11.1 ^11.2 ^11.3 Kataoka, Keisuke; et al. (2015-11). "Integrated molecular analysis of adult T cell leukemia/lymphoma". Nature Genetics. 47 (11): 1304–1315. doi:10.1038/ng.3415. ISSN 1546-1718. PMID 26437031. Check date values in: |date= (help)
↑ Hishizawa, Masakatsu; et al. (2010-08-26). "Transplantation of allogeneic hematopoietic stem cells for adult T-cell leukemia: a nationwide retrospective study". Blood. 116 (8): 1369–1376. doi:10.1182/blood-2009-10-247510. ISSN 1528-0020. PMID 20479287.
↑ Hermine, Olivier; et al. (02 2018). "A Review of New Findings in Adult T-cell Leukemia-Lymphoma: A Focus on Current and Emerging Treatment Strategies". Advances in Therapy. 35 (2): 135–152. doi:10.1007/s12325-018-0658-4. ISSN 1865-8652. PMC 5818559. PMID 29411267. Check date values in: |date= (help)
↑ Itoyama, T.; et al. (2001-06-01). "Cytogenetic analysis and clinical significance in adult T-cell leukemia/lymphoma: a study of 50 cases from the human T-cell leukemia virus type-1 endemic area, Nagasaki". Blood. 97 (11): 3612–3620. doi:10.1182/blood.v97.11.3612. ISSN 0006-4971. PMID 11369658.
↑ Tsukasaki, K.; et al. (2001-06-15). "Comparative genomic hybridization analysis in adult T-cell leukemia/lymphoma: correlation with clinical course". Blood. 97 (12): 3875–3881. doi:10.1182/blood.v97.12.3875. ISSN 0006-4971. PMID 11389029.
↑ Oshiro, Aya; et al. (2006-06-01). "Identification of subtype-specific genomic alterations in aggressive adult T-cell leukemia/lymphoma". Blood. 107 (11): 4500–4507. doi:10.1182/blood-2005-09-3801. ISSN 0006-4971. PMID 16484591.
↑ ^17.0 ^17.1 Kataoka, Keisuke; et al. (01 11, 2018). "Prognostic relevance of integrated genetic profiling in adult T-cell leukemia/lymphoma". Blood. 131 (2): 215–225. doi:10.1182/blood-2017-01-761874. ISSN 1528-0020. PMC 5757690. PMID 29084771. Check date values in: |date= (help)
↑ "Correlation of chromosome abnormalities with histologic and immunologic characteristics in non-Hodgkin's lymphoma and adult T cell leukemia-lymphoma. Fifth International Workshop on Chromosomes in Leukemia-Lymphoma". Blood. 70 (5): 1554–1564. 1987-11. ISSN 0006-4971. PMID 2889485. Check date values in: |date= (help)
↑ Kogure, Yasunori; et al. (2017-09). "Genetic alterations in adult T-cell leukemia/lymphoma". Cancer Science. 108 (9): 1719–1725. doi:10.1111/cas.13303. ISSN 1349-7006. PMC 5581529. PMID 28627735. Check date values in: |date= (help)
↑ Kataoka, Keisuke; et al. (2015-11). "Integrated molecular analysis of adult T cell leukemia/lymphoma". Nature Genetics. 47 (11): 1304–1315. doi:10.1038/ng.3415. ISSN 1546-1718. PMID 26437031. Check date values in: |date= (help)
↑ Fujikawa, Dai; et al. (2016-04-07). "Polycomb-dependent epigenetic landscape in adult T-cell leukemia". Blood. 127 (14): 1790–1802. doi:10.1182/blood-2015-08-662593. ISSN 1528-0020. PMID 26773042.

Notes

*Primary authors will typically be those that initially create and complete the content of a page. If a subsequent user modifies the content and feels the effort put forth is of high enough significance to warrant listing in the authorship section, please contact the CCGA coordinators (contact information provided on the homepage). Additional global feedback or concerns are also welcome. *Citation of this Page: “Adult T-cell leukaemia/lymphoma”. Compendium of Cancer Genome Aberrations (CCGA), Cancer Genomics Consortium (CGC), updated 09/6/2024, https://ccga.io/index.php/HAEM5:Adult_T-cell_leukaemia/lymphoma.

[1] Thiele, J. et al., (2017). Adult T-cell leukemia/lymphoma, in World Health Organization Classification of Tumours of Haematopoietic and Lymphoid Tissues, Revised 4th edition. Swerdlow SH, Campo E, Harris NL, Jaffe ES, Pileri SA, Stein H, Thiele J, Arber DA, Hasserjian RP, Le Beau MM, Orazi A, and Siebert R, Editors. IARC Press: Lyon, France, p363-367

[:0-2] 2.0 ^2.1 Gessain, Antoine; et al. (2012). "Epidemiological Aspects and World Distribution of HTLV-1 Infection". Frontiers in Microbiology. 3: 388. doi:10.3389/fmicb.2012.00388. ISSN 1664-302X. PMC 3498738. PMID 23162541.

[3] Mehta-Shah, Neha; et al. (08 2017). "Adult T-Cell Leukemia/Lymphoma". Journal of Oncology Practice. 13 (8): 487–492. doi:10.1200/JOP.2017.021907. ISSN 1935-469X. PMC 6366298. PMID 28796966. Check date values in: |date= (help)

[4] Rocquain, Julien; et al. (2010-08-02). "Combined mutations of ASXL1, CBL, FLT3, IDH1, IDH2, JAK2, KRAS, NPM1, NRAS, RUNX1, TET2 and WT1 genes in myelodysplastic syndromes and acute myeloid leukemias". BMC cancer. 10: 401. doi:10.1186/1471-2407-10-401. ISSN 1471-2407. PMC 2923633. PMID 20678218.

[:3-5] 5.0 ^5.1 Shimoyama, M. (1991-11). "Diagnostic criteria and classification of clinical subtypes of adult T-cell leukaemia-lymphoma. A report from the Lymphoma Study Group (1984-87)". British Journal of Haematology. 79 (3): 428–437. doi:10.1111/j.1365-2141.1991.tb08051.x. ISSN 0007-1048. PMID 1751370. Check date values in: |date= (help)

[6] Bunn, P. A.; et al. (1983-08-04). "Clinical course of retrovirus-associated adult T-cell lymphoma in the United States". The New England Journal of Medicine. 309 (5): 257–264. doi:10.1056/NEJM198308043090501. ISSN 0028-4793. PMID 6602943.

[7] Ohshima, Koichi (2007-06). "Pathological features of diseases associated with human T-cell leukemia virus type I". Cancer Science. 98 (6): 772–778. doi:10.1111/j.1349-7006.2007.00456.x. ISSN 1347-9032. PMID 17388788. Check date values in: |date= (help)

[8] Roncador, G.; et al. (2005-12). "FOXP3, a selective marker for a subset of adult T-cell leukaemia/lymphoma". Leukemia. 19 (12): 2247–2253. doi:10.1038/sj.leu.2403965. ISSN 0887-6924. PMID 16193085. Check date values in: |date= (help)

[9] Ishida, Takashi; et al. (2003-09-01). "Clinical significance of CCR4 expression in adult T-cell leukemia/lymphoma: its close association with skin involvement and unfavorable outcome". Clinical Cancer Research: An Official Journal of the American Association for Cancer Research. 9 (10 Pt 1): 3625–3634. ISSN 1078-0432. PMID 14506150.

[:4-10] 10.0 ^10.1 NCCN Clinical Practice Guidelines in Oncology, T-Cell Lymphomas, Version 1.2021. Available at NCCN.org.

[:1-11] 11.0 ^11.1 ^11.2 ^11.3 Kataoka, Keisuke; et al. (2015-11). "Integrated molecular analysis of adult T cell leukemia/lymphoma". Nature Genetics. 47 (11): 1304–1315. doi:10.1038/ng.3415. ISSN 1546-1718. PMID 26437031. Check date values in: |date= (help)

[12] Hishizawa, Masakatsu; et al. (2010-08-26). "Transplantation of allogeneic hematopoietic stem cells for adult T-cell leukemia: a nationwide retrospective study". Blood. 116 (8): 1369–1376. doi:10.1182/blood-2009-10-247510. ISSN 1528-0020. PMID 20479287.

[13] Hermine, Olivier; et al. (02 2018). "A Review of New Findings in Adult T-cell Leukemia-Lymphoma: A Focus on Current and Emerging Treatment Strategies". Advances in Therapy. 35 (2): 135–152. doi:10.1007/s12325-018-0658-4. ISSN 1865-8652. PMC 5818559. PMID 29411267. Check date values in: |date= (help)

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[19] Kogure, Yasunori; et al. (2017-09). "Genetic alterations in adult T-cell leukemia/lymphoma". Cancer Science. 108 (9): 1719–1725. doi:10.1111/cas.13303. ISSN 1349-7006. PMC 5581529. PMID 28627735. Check date values in: |date= (help)

[20] Kataoka, Keisuke; et al. (2015-11). "Integrated molecular analysis of adult T cell leukemia/lymphoma". Nature Genetics. 47 (11): 1304–1315. doi:10.1038/ng.3415. ISSN 1546-1718. PMID 26437031. Check date values in: |date= (help)

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