Difference between revisions of "HAEM5:Primary cutaneous CD8-positive aggressive epidermotropic cytotoxic T-cell lymphoma"

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Primary Author(s)*

Ahmed Eladely, MBBCh. Andrew Siref, MD.

Creighton University, Omaha, NE.

Cancer Category / Type

Book	WHO Classification of Disease - Haematolymphoid Tumours (5th ed.)
Category	T-cell and NK-cell lymphoid proliferations and lymphomas
Family	Mature T-cell and NK-cell neoplasms
Type	Primary cutaneous T-cell lymphoid proliferations and lymphomas
Subtype	Primary cutaneous CD8-positive aggressive epidermotropic cytotoxic T-cell lymphoma

Cancer Sub-Classification / Subtype

None

Definition / Description of Disease

Primary cutaneous CD8-positive aggressive epidermotropic cytotoxic T-cell lymphoma (PCAETL) is a rare and poorly characterized neoplastic proliferation of T lymphocytes with CD8 and cytotoxic molecule expression. PCAETL is marked by epidermal necrosis, a high proliferation index, and aggressive clinical behavior. It should be distinguished from other rare epidermotropic subtypes of cutaneous gamma-delta T-cell lymphomas (such as gamma-delta mycosis fungoides), CD8+ mycosis fungoides, localized pagetoid reticulosis, and type D lymphomatoid papulosis.^[1]^[2]^[3]

Synonyms / Terminology

Berti lymphoma

Disseminated pagetoid reticulosis, Ketron–Goodman type (obsolete)

Epidemiology / Prevalence

PCAETL is rare, comprising less than 1% of all cutaneous T-cell lymphomas. It typically occurs in adults and shows a predilection for males.^[1]^[3]

Clinical Features

Signs and Symptoms	Diffusely distributed papules (common) Localized papules (less common) Ulcerated nodules, tumors, and plaques Erosion or central necrosis Preceded by chronic, poorly defined patches (subset) Disseminated to visceral sites (lungs, testes, CNS) Lymph nodes spared No association with immunosuppression ^[1]^[2]^[3]
Laboratory Findings	None

Sites of Involvement

PCAETL can present with either localized or generalized skin lesions and may affect the oral mucosa.^[4]

Morphologic Features

Pagetoid epithelial involvement (epidermal and adnexal) is typically observed; however, the infiltrate may involve the entire dermis.^[3]^[5] Lymphocyte morphology ranges from monomorphic to pleomorphic. Rimming of subcutaneous fat spaces has been reported. Spongiosis can result in blister formation.^[6]

The tumor cells typically consist of atypical small to large lymphocytes with indented nuclei, minimal cytoplasm, and occasional immunoblastic features. Histological signs of cytotoxicity are evident, including epidermal necrosis or ulceration, dermal necrosis, karyorrhexis, and rare angiocentric destruction.^[2]^[3]^[6] Ulceration can resemble pyoderma gangrenosum.^[7] There is often pronounced pagetoid epidermotropism, particularly in cases with widespread lesions.^[1]^[8]

Immunophenotype

Finding	Marker
Positive	CD3, TIA1, granzyme B, perforin, CCR4
CD4/CD8	CD8+/CD4-; rare cases of double positivity or double negativity have been reported
CD2/CD5/CD7	CD2(+/-), CD5(-), CD7(-/+)
TCR	TCR-βF1+, rarely TCRγδ+; rare cases of double positive and null type have been reported
Ki67 %	>75%
Negative	EBER, CD1a, CD30, CD25, ALK1, EMA
Variable	CD45RA(+/-), CD15(-/+) ^[9]^[10]^[11]

Chromosomal Rearrangements (Gene Fusions)

In PCAETL, recurrent genomic events affecting genes involved in the cell cycle, chromatin regulation, and the JAK/STAT pathway have been reported, including complex genomic rearrangements and diverse JAK2 fusions. Upregulated JAK2 signaling is a consistent finding in nearly all cases, distinguishing PCAETL from other cytotoxic cutaneous T-cell lymphomas. Cases without JAK2 fusions often exhibit gain-of-function mutations in JAK2, STAT3, and STAT5B, alongside loss of negative regulators of the JAK/STAT pathway, particularly SH2B3.^[11]

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
JAK2 fusion	KHDRBS1-JAK2 PCM1-JAK2 TFG-JAK2	Self-oligo/dimerization of JAK2	3 of 12 patients	No	Unknown	Yes	Potential therapeutic target with JAK inhibitors.^[11]
MYC fusion	ACTB-MYC NPM1-MYC	Chimeric MYC proteins with altered cell cycle regulation.	2 of 12 patients	No	Unknown	No	Both patients had JAK2 fusions.^[11]
ABL1 fusion^[9]	SELENO1-ABL1	Retained its catalytic tyrosine kinase domain but lost its N-terminal SH2 and SH3 regulatory domains	1 of 6 patients	No	Unknown	Yes	Potential therapeutic target with Imatinib.^[12]
BAZ1A rearrangement^[11]	None specified	None specified	2 of 12 patients	No	Unknown	No
PTPRC rearrangement^[11]	None specified	None specified	2 of 12 patients	No	Unknown	No
RB1 rearrangement^[11]	None specified	None specified	2 of 12 patients	No	Unknown	No
MTAP rearrangement^[11]	None specified	None specified	3 of 12 patients	No	Unknown	No
SH2B3 rearrangement^[11]	None specified	None specified	2 of 12 patients	No	Unknown	No
CLEC16A rearrangement^[11]	None specified	None specified	2 of 12 patients	No	Unknown	No
PIP4K2A rearrangement^[11]	None specified	None specified	2 of 12 patients	No	Unknown	No
DLEU1 rearrangement^[11]	None specified	None specified	2 of 12 patients	No	Unknown	No
SLC24A2 rearrangement^[11]	None specified	None specified	2 of 12 patients	No	Unknown	No
ABR rearrangement^[11]	None specified	None specified	2 of 12 patients	No	Unknown	No
GNA14 rearrangement^[11]	None specified	None specified	2 of 12 patients	No	Unknown	No
RHCE rearrangement^[11]	None specified	None specified	2 of 12 patients	No	Unknown	No
RHD rearrangement^[11]	None specified	None specified	2 of 12 patients	No	Unknown	No
DLG2 rearrangement^[11]	None specified	None specified	2 of 12 patients	No	Unknown	No
FRMD4A rearrangement^[11]	None specified	None specified	2 of 12 patients	No	Unknown	No

Individual Region Genomic Gain / Loss / LOH

Chr #	Gain / Loss / Amp / LOH	Minimal Region Cytoband	Diagnostic Significance (Yes, No or Unknown)	Prognostic Significance (Yes, No or Unknown)	Therapeutic Significance (Yes, No or Unknown)	Notes
1	Loss	p36.11^[10]^[11]	No	No	No
1	Loss	1p36.22^[11]	No	No	No
1	Loss	1p36.32-p36.33^[10]^[11]	No	No	No
2	Loss	q37.3^[10]	No	No	No
4	Loss	q13.2^[11]
7	Gain	q21.11-q22.3^[10]	No	No	No
7	Gain	q22.1^[11]	No	No	No
7	Gain	q32.1-q36.1^[10]	No	No	No
7	Gain	q35^[11]	No		No
7	Gain	q36.1-q36.3^[10]^[11]	No	No	No
7	Loss	p14.1^[11]	No	No	No
7	Loss	q34^[10]^[11]	No	No	No
8	Loss	p12^[10]	No	No	No
8	Gain	q24.3^[10]	No	No	No
9	Loss	p21.3^[10]^[11]	No	No	No	The most frequently affected locus, shows losses in the MTAP, CDKN2A, and CDKN2B regions (12/20 patients).^[10] It was also the most common in another study (10/12 patients).^[11]
10	Loss	p11.22^[11]	No	No	No
11	Loss	q23.2^[11]	No	No	No
12	Loss	q24.12	No	No	No
13	Loss	q14.11^[10]^[11]	No	No	No
14	Loss	q11.2^[10]^[11]	No	No	No
16	Loss	p13.13^[11]	No	No	No
17	Loss	p13.2^[10]	No	No	No
17	Loss	p13.3^[11]	No	No	No	No cancer genes.^[11]
17	Gain	q21.31^[10]	No	No	No
17	Gain	q21.33-q22^[10]^[11]	No	No	No
17	Gain	q22^[11]	No	No	No
17	Gain	q25.3^[10]	No	No	No
19	Loss	p13.3^[11]	No	No	No
21	Gain	q22.12^[10]	No	No	No
X	Gain	p11.23-p11.22^[10]	No	No	No
X	Gain	q28^[10]	No	No	No

All the genes found in these regions are implicated in several pathways associated with lymphoma and tumor development, including T-cell signaling, DNA damage response, the JAK-STAT pathway, and epigenetic modifications.^[10]

Characteristic Chromosomal Patterns

Although PCAETL exhibit multiple copy number alterations (CNAs), they lack a distinct signature or genomic profile, as their recurrent CNAs partially or entirely overlap with those found in other aggressive cutaneous T cell lymphomas.^[10]

Gene Mutations (SNV / INDEL)

Gene; Genetic Alteration	Presumed Mechanism (Tumor Suppressor Gene [TSG] / Oncogene / 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
JAK3; p.R657W, p.M511I	Oncogene	None specified	None specified	No	Unknown	No	Gain-of-function mutations
JAK2; p.L393V	Oncogene	None specified	None specified	No	Unknown	No	Germline SNV renders JAK2 hypersensitive to cytokine stimulation
STAT3; p.H19R, p.G604A	Oncogene	JAK2 fusions, SH2B3 deletions	None specified	No	Unknown	No	Gain-of-function mutations
STAT5B; p.N642H, p.P702S, p.Y665F, p.S434L	Oncogene	SH2B3 deletions	None specified	No	Unknown	No	Gain-of-function mutations
SH2B3; p.L201Sfs78, p.V35Afs154	Tumor Suppressor Gene (TSG)	STAT5B mutations, JAK or STAT gene mutations	JAK2 fusions	No	Unknown	No	Frameshift mutations leading to loss of function
SOCS1; p.S71Rfs*14	Tumor Suppressor Gene (TSG)	JAK or STAT gene mutations	None specified	No	Unknown	No	Frameshift mutation leading to a premature stop codon^[11]

Many SNVs and deletions in other genes are also detected and are predicted to be deleterious.^[11]

Epigenomic Alterations

Alteration in LIN28, ARID1A, PARP10, MLL3, and MLL5 have been described and may play a role in the pathogenesis.^[10]

Genes and Main Pathways Involved

Gene; Genetic Alteration	Pathway	Pathophysiologic Outcome
JAK2; Fusion	JAK-STAT	Constitutive activation leading to cytokine-independent cell survival and proliferation. Overactivation of signaling pathways due to self-oligo/dimerization of the chimeric proteins.
SH2B3; Deletion	JAK-STAT	Loss of negative feedback regulation on JAK2 signaling, resulting in enhanced JAK2 pathway activation.
PTPRC; Deletion	JAK-STAT	Disruption of negative regulation of the JAK-STAT pathway, contributing to overactivation of JAK2 signaling.
STAT3; SNV	JAK-STAT	Gain-of-function mutations resulting in enhanced signaling and cell survival.
STAT5; SNV	JAK-STAT	Gain-of-function mutations leading to overactivation of the pathway, promoting cell proliferation.
MYC; Fusions	Cell Cycle Regulation	Dysregulation of cell cycle processes, contributing to uncontrolled cell proliferation.
CDKN2A/B; Deletions	Cell Cycle Regulation	Inactivation of tumor suppressor genes leading to disruptions in cell cycle control.
TP53; Truncating Mutations (nonsense, frameshift)	Cell Cycle Regulation	Loss of p53 function leading to impaired DNA repair and increased genomic instability.
ARID1A; Deletions	Chromatin Regulation	Loss of chromatin remodeling activity affecting gene expression and cell growth regulation.
KMT2D; Truncating Mutations	Chromatin Regulation	Disruption in histone methylation, affecting gene expression and cell differentiation.
NCOR1; Truncating Mutations	Chromatin Regulation	Loss of corepressor function, leading to altered gene expression and potentially contributing to oncogenesis.^[11]

Genetic Diagnostic Testing Methods

Fluorescence In Situ Hybridization (FISH): Detects chromosomal rearrangements and specific gene fusions, such as JAK2 fusions.

Polymerase Chain Reaction (PCR): Amplifies specific regions of DNA to identify genetic alterations, including gene fusions and specific mutations.

Next-Generation Sequencing (NGS): Identifies pathogenic small-scale mutations (SNVs and INDELs) and structural alterations. NGS can analyze multiple genes and pathways simultaneously, which is useful for comprehensive genetic profiling.^[11]

Familial Forms

Unknown

Additional Information

PCAETL has an aggressive clinical course, with a median survival time of 12 months. The prognosis is similar regardless of whether the morphology is small or large cell, or whether the lesions are localized or diffuse.^[2]

Links

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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.)

↑ ^1.0 ^1.1 ^1.2 ^1.3 Berti, E.; et al. (1999-08). "Primary cutaneous CD8-positive epidermotropic cytotoxic T cell lymphomas. A distinct clinicopathological entity with an aggressive clinical behavior". The American Journal of Pathology. 155 (2): 483–492. doi:10.1016/S0002-9440(10)65144-9. ISSN 0002-9440. PMC 1866866. PMID 10433941. Check date values in: |date= (help)
↑ ^2.0 ^2.1 ^2.2 ^2.3 Guitart, Joan; et al. (2017-05). "Primary cutaneous aggressive epidermotropic cytotoxic T-cell lymphomas: reappraisal of a provisional entity in the 2016 WHO classification of cutaneous lymphomas". Modern Pathology: An Official Journal of the United States and Canadian Academy of Pathology, Inc. 30 (5): 761–772. doi:10.1038/modpathol.2016.240. ISSN 1530-0285. PMC 5413429. PMID 28128277. Check date values in: |date= (help)
↑ ^3.0 ^3.1 ^3.2 ^3.3 ^3.4 Robson, Alistair; et al. (2015-10). "Aggressive epidermotropic cutaneous CD8+ lymphoma: a cutaneous lymphoma with distinct clinical and pathological features. Report of an EORTC Cutaneous Lymphoma Task Force Workshop". Histopathology. 67 (4): 425–441. doi:10.1111/his.12371. ISSN 1365-2559. PMID 24438036. Check date values in: |date= (help)
↑ Travassos, Daphine Caxias; et al. (2022-06). "Primary cutaneous CD8+ cytotoxic T-cell lymphoma of the face with intraoral involvement, resulting in facial nerve palsy after chemotherapy". Journal of Cutaneous Pathology. 49 (6): 560–564. doi:10.1111/cup.14199. ISSN 1600-0560. PMID 35001425 Check |pmid= value (help). Check date values in: |date= (help)
↑ Saruta, Hiroshi; et al. (2017-09). "Hematopoietic stem cell transplantation in advanced cutaneous T-cell lymphoma". The Journal of Dermatology. 44 (9): 1038–1042. doi:10.1111/1346-8138.13848. ISSN 1346-8138. PMID 28391645. Check date values in: |date= (help)
↑ ^6.0 ^6.1 Nofal, Ahmad; et al. (2012-10). "Primary cutaneous aggressive epidermotropic CD8+ T-cell lymphoma: proposed diagnostic criteria and therapeutic evaluation". Journal of the American Academy of Dermatology. 67 (4): 748–759. doi:10.1016/j.jaad.2011.07.043. ISSN 1097-6787. PMID 22226429. Check date values in: |date= (help)
↑ Deenen, N. J.; et al. (2019-02). "Pitfalls in diagnosing primary cutaneous aggressive epidermotropic CD8+ T-cell lymphoma". The British Journal of Dermatology. 180 (2): 411–412. doi:10.1111/bjd.17252. ISSN 1365-2133. PMID 30259963. Check date values in: |date= (help)
↑ Willemze, Rein; et al. (2005-05-15). "WHO-EORTC classification for cutaneous lymphomas". Blood. 105 (10): 3768–3785. doi:10.1182/blood-2004-09-3502. ISSN 0006-4971. PMID 15692063.
↑ ^9.0 ^9.1 Lee, Katie; et al. (2021-12-09). "Primary cytotoxic T-cell lymphomas harbor recurrent targetable alterations in the JAK-STAT pathway". Blood. 138 (23): 2435–2440. doi:10.1182/blood.2021012536. ISSN 1528-0020. PMC 8662071 Check |pmc= value (help). PMID 34432866 Check |pmid= value (help).
↑ ^10.00 ^10.01 ^10.02 ^10.03 ^10.04 ^10.05 ^10.06 ^10.07 ^10.08 ^10.09 ^10.10 ^10.11 ^10.12 ^10.13 ^10.14 ^10.15 ^10.16 ^10.17 ^10.18 ^10.19 ^10.20 ^10.21 ^10.22 ^10.23 Fanoni, Daniele; et al. (2018-12). "Array-based CGH of primary cutaneous CD8+ aggressive EPIDERMO-tropic cytotoxic T-cell lymphoma". Genes, Chromosomes & Cancer. 57 (12): 622–629. doi:10.1002/gcc.22673. ISSN 1098-2264. PMID 30307677. Check date values in: |date= (help)
↑ ^11.00 ^11.01 ^11.02 ^11.03 ^11.04 ^11.05 ^11.06 ^11.07 ^11.08 ^11.09 ^11.10 ^11.11 ^11.12 ^11.13 ^11.14 ^11.15 ^11.16 ^11.17 ^11.18 ^11.19 ^11.20 ^11.21 ^11.22 ^11.23 ^11.24 ^11.25 ^11.26 ^11.27 ^11.28 ^11.29 ^11.30 ^11.31 ^11.32 ^11.33 ^11.34 ^11.35 ^11.36 ^11.37 ^11.38 ^11.39 ^11.40 ^11.41 ^11.42 ^11.43 Bastidas Torres, Armando N.; et al. (2022-03-01). "Deregulation of JAK2 signaling underlies primary cutaneous CD8+ aggressive epidermotropic cytotoxic T-cell lymphoma". Haematologica. 107 (3): 702–714. doi:10.3324/haematol.2020.274506. ISSN 1592-8721. PMC 8883537 Check |pmc= value (help). PMID 33792220 Check |pmid= value (help).
↑ Buus, Terkild B.; et al. (2021-12-09). "Oncogenic fusions JAK up CD8+ cytotoxic CTCL". Blood. 138 (23): 2311–2312. doi:10.1182/blood.2021013619. ISSN 0006-4971.

EXAMPLE Book

Arber DA, et al., (2017). Acute myeloid leukaemia with recurrent genetic abnormalities, 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, p129-171.

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: “Primary cutaneous CD8-positive aggressive epidermotropic cytotoxic T-cell lymphoma”. Compendium of Cancer Genome Aberrations (CCGA), Cancer Genomics Consortium (CGC), updated 08/2/2024, https://ccga.io/index.php/HAEM5:Primary_cutaneous_CD8-positive_aggressive_epidermotropic_cytotoxic_T-cell_lymphoma.

[:02-1] 1.0 ^1.1 ^1.2 ^1.3 Berti, E.; et al. (1999-08). "Primary cutaneous CD8-positive epidermotropic cytotoxic T cell lymphomas. A distinct clinicopathological entity with an aggressive clinical behavior". The American Journal of Pathology. 155 (2): 483–492. doi:10.1016/S0002-9440(10)65144-9. ISSN 0002-9440. PMC 1866866. PMID 10433941. Check date values in: |date= (help)

[:12-2] 2.0 ^2.1 ^2.2 ^2.3 Guitart, Joan; et al. (2017-05). "Primary cutaneous aggressive epidermotropic cytotoxic T-cell lymphomas: reappraisal of a provisional entity in the 2016 WHO classification of cutaneous lymphomas". Modern Pathology: An Official Journal of the United States and Canadian Academy of Pathology, Inc. 30 (5): 761–772. doi:10.1038/modpathol.2016.240. ISSN 1530-0285. PMC 5413429. PMID 28128277. Check date values in: |date= (help)

[:22-3] 3.0 ^3.1 ^3.2 ^3.3 ^3.4 Robson, Alistair; et al. (2015-10). "Aggressive epidermotropic cutaneous CD8+ lymphoma: a cutaneous lymphoma with distinct clinical and pathological features. Report of an EORTC Cutaneous Lymphoma Task Force Workshop". Histopathology. 67 (4): 425–441. doi:10.1111/his.12371. ISSN 1365-2559. PMID 24438036. Check date values in: |date= (help)

[4] Travassos, Daphine Caxias; et al. (2022-06). "Primary cutaneous CD8+ cytotoxic T-cell lymphoma of the face with intraoral involvement, resulting in facial nerve palsy after chemotherapy". Journal of Cutaneous Pathology. 49 (6): 560–564. doi:10.1111/cup.14199. ISSN 1600-0560. PMID 35001425 Check |pmid= value (help). Check date values in: |date= (help)

[5] Saruta, Hiroshi; et al. (2017-09). "Hematopoietic stem cell transplantation in advanced cutaneous T-cell lymphoma". The Journal of Dermatology. 44 (9): 1038–1042. doi:10.1111/1346-8138.13848. ISSN 1346-8138. PMID 28391645. Check date values in: |date= (help)

[:0-6] 6.0 ^6.1 Nofal, Ahmad; et al. (2012-10). "Primary cutaneous aggressive epidermotropic CD8+ T-cell lymphoma: proposed diagnostic criteria and therapeutic evaluation". Journal of the American Academy of Dermatology. 67 (4): 748–759. doi:10.1016/j.jaad.2011.07.043. ISSN 1097-6787. PMID 22226429. Check date values in: |date= (help)

[7] Deenen, N. J.; et al. (2019-02). "Pitfalls in diagnosing primary cutaneous aggressive epidermotropic CD8+ T-cell lymphoma". The British Journal of Dermatology. 180 (2): 411–412. doi:10.1111/bjd.17252. ISSN 1365-2133. PMID 30259963. Check date values in: |date= (help)

[8] Willemze, Rein; et al. (2005-05-15). "WHO-EORTC classification for cutaneous lymphomas". Blood. 105 (10): 3768–3785. doi:10.1182/blood-2004-09-3502. ISSN 0006-4971. PMID 15692063.

[:5-9] 9.0 ^9.1 Lee, Katie; et al. (2021-12-09). "Primary cytotoxic T-cell lymphomas harbor recurrent targetable alterations in the JAK-STAT pathway". Blood. 138 (23): 2435–2440. doi:10.1182/blood.2021012536. ISSN 1528-0020. PMC 8662071 Check |pmc= value (help). PMID 34432866 Check |pmid= value (help).

[:6-10] 10.00 ^10.01 ^10.02 ^10.03 ^10.04 ^10.05 ^10.06 ^10.07 ^10.08 ^10.09 ^10.10 ^10.11 ^10.12 ^10.13 ^10.14 ^10.15 ^10.16 ^10.17 ^10.18 ^10.19 ^10.20 ^10.21 ^10.22 ^10.23 Fanoni, Daniele; et al. (2018-12). "Array-based CGH of primary cutaneous CD8+ aggressive EPIDERMO-tropic cytotoxic T-cell lymphoma". Genes, Chromosomes & Cancer. 57 (12): 622–629. doi:10.1002/gcc.22673. ISSN 1098-2264. PMID 30307677. Check date values in: |date= (help)

[:3-11] 11.00 ^11.01 ^11.02 ^11.03 ^11.04 ^11.05 ^11.06 ^11.07 ^11.08 ^11.09 ^11.10 ^11.11 ^11.12 ^11.13 ^11.14 ^11.15 ^11.16 ^11.17 ^11.18 ^11.19 ^11.20 ^11.21 ^11.22 ^11.23 ^11.24 ^11.25 ^11.26 ^11.27 ^11.28 ^11.29 ^11.30 ^11.31 ^11.32 ^11.33 ^11.34 ^11.35 ^11.36 ^11.37 ^11.38 ^11.39 ^11.40 ^11.41 ^11.42 ^11.43 Bastidas Torres, Armando N.; et al. (2022-03-01). "Deregulation of JAK2 signaling underlies primary cutaneous CD8+ aggressive epidermotropic cytotoxic T-cell lymphoma". Haematologica. 107 (3): 702–714. doi:10.3324/haematol.2020.274506. ISSN 1592-8721. PMC 8883537 Check |pmc= value (help). PMID 33792220 Check |pmid= value (help).

[12] Buus, Terkild B.; et al. (2021-12-09). "Oncogenic fusions JAK up CD8+ cytotoxic CTCL". Blood. 138 (23): 2311–2312. doi:10.1182/blood.2021013619. ISSN 0006-4971.

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