Primary cutaneous CD8-positive aggressive epidermotropic cytotoxic T-cell lymphoma

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Haematolymphoid Tumours (WHO Classification, 5th ed.)

(General Instructions – The focus of these pages is the clinically significant genetic alterations in each disease type. This is based on up-to-date knowledge from multiple resources such as PubMed and the WHO classification books. The CCGA is meant to be a supplemental resource to the WHO classification books; the CCGA captures in a continually updated wiki-stye manner the current genetics/genomics knowledge of each disease, which evolves more rapidly than books can be revised and published. If the same disease is described in multiple WHO classification books, the genetics-related information for that disease will be consolidated into a single main page that has this template (other pages would only contain a link to this main page). 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); to add (or move) a row or column in a table, click nearby within the table and select the > symbol that appears. 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)*

Ahmed Eladely, MBBCh. Andrew Siref, MD.

Creighton University, Omaha, NE.

WHO Classification of Disease

Structure Disease
Book 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(s) Primary cutaneous CD8-positive aggressive epidermotropic cytotoxic T-cell lymphoma

WHO Essential and Desirable Genetic Diagnostic Criteria

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WHO Essential Criteria (Genetics)*
WHO Desirable Criteria (Genetics)*
Other Classification

*Note: These are only the genetic/genomic criteria. Additional diagnostic criteria can be found in the WHO Classification of Tumours.

Related Terminology

(Instructions: The table will have the related terminology from the WHO autocompleted.)

Acceptable
Not Recommended

Gene Rearrangements

Driver Gene Fusion(s) and Common Partner Genes Molecular Pathogenesis Typical Chromosomal Alteration(s) Prevalence -Common >20%, Recurrent 5-20% or Rare <5% (Disease) Diagnostic, Prognostic, and Therapeutic Significance - D, P, T Established Clinical Significance Per Guidelines - Yes or No (Source) Clinical Relevance Details/Other Notes
EXAMPLE: ABL1 EXAMPLE: BCR::ABL1 EXAMPLE: The pathogenic derivative is the der(22) resulting in fusion of 5’ BCR and 3’ABL1. EXAMPLE: t(9;22)(q34;q11.2) EXAMPLE: Common (CML) EXAMPLE: D, P, T EXAMPLE: Yes (WHO, NCCN) 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). BCR::ABL1 is generally favorable in CML (add reference).

EXAMPLE: CIC EXAMPLE: CIC::DUX4 EXAMPLE: Typically, the last exon of CIC is fused to DUX4. The fusion breakpoint in CIC is usually intra-exonic and removes an inhibitory sequence, upregulating PEA3 genes downstream of CIC including ETV1, ETV4, and ETV5. EXAMPLE: t(4;19)(q25;q13) EXAMPLE: Common (CIC-rearranged sarcoma) EXAMPLE: D EXAMPLE:

DUX4 has many homologous genes; an alternate translocation in a minority of cases is t(10;19), but this is usually indistinguishable from t(4;19) by short-read sequencing (add references).

EXAMPLE: ALK EXAMPLE: ELM4::ALK


Other fusion partners include KIF5B, NPM1, STRN, TFG, TPM3, CLTC, KLC1

EXAMPLE: Fusions result in constitutive activation of the ALK tyrosine kinase. The most common ALK fusion is EML4::ALK, with breakpoints in intron 19 of ALK. At the transcript level, a variable (5’) partner gene is fused to 3’ ALK at exon 20. Rarely, ALK fusions contain exon 19 due to breakpoints in intron 18. EXAMPLE: N/A EXAMPLE: Rare (Lung adenocarcinoma) EXAMPLE: T EXAMPLE:

Both balanced and unbalanced forms are observed by FISH (add references).

EXAMPLE: ABL1 EXAMPLE: N/A EXAMPLE: Intragenic deletion of exons 2–7 in EGFR removes the ligand-binding domain, resulting in a constitutively active tyrosine kinase with downstream activation of multiple oncogenic pathways. EXAMPLE: N/A EXAMPLE: Recurrent (IDH-wildtype Glioblastoma) EXAMPLE: D, P, T

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.[1]

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.[1]
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.[1]
ABL1 fusion[2] 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.[3]
BAZ1A rearrangement[1] None specified None specified 2 of 12 patients No Unknown No
PTPRC rearrangement[1] None specified None specified 2 of 12 patients No Unknown No
RB1 rearrangement[1] None specified None specified 2 of 12 patients No Unknown No
MTAP rearrangement[1] None specified None specified 3 of 12 patients No Unknown No
SH2B3 rearrangement[1] None specified None specified 2 of 12 patients No Unknown No
CLEC16A rearrangement[1] None specified None specified 2 of 12 patients No Unknown No
PIP4K2A rearrangement[1] None specified None specified 2 of 12 patients No Unknown No
DLEU1 rearrangement[1] None specified None specified 2 of 12 patients No Unknown No
SLC24A2 rearrangement[1] None specified None specified 2 of 12 patients No Unknown No
ABR rearrangement[1] None specified None specified 2 of 12 patients No Unknown No
GNA14 rearrangement[1] None specified None specified 2 of 12 patients No Unknown No
RHCE rearrangement[1] None specified None specified 2 of 12 patients No Unknown No
RHD rearrangement[1] None specified None specified 2 of 12 patients No Unknown No
DLG2 rearrangement[1] None specified None specified 2 of 12 patients No Unknown No
FRMD4A rearrangement[1] None specified None specified 2 of 12 patients No Unknown No

Individual Region Genomic Gain/Loss/LOH

Put your text here and fill in the table (Instructions: Includes aberrations not involving gene rearrangements. Details on clinical significance such as prognosis and other important information can be provided in the notes section. Can refer to CGC workgroup tables as linked on the homepage if applicable. Please include references throughout the table. Do not delete the table.)

Chr # Gain, Loss, Amp, LOH Minimal Region Cytoband and/or Genomic Coordinates [Genome Build; Size] Relevant Gene(s) Diagnostic, Prognostic, and Therapeutic Significance - D, P, T Established Clinical Significance Per Guidelines - Yes or No (Source) Clinical Relevance Details/Other Notes
EXAMPLE:

7

EXAMPLE: Loss EXAMPLE:

chr7

EXAMPLE:

Unknown

EXAMPLE: D, P EXAMPLE: 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 references).

EXAMPLE:

8

EXAMPLE: Gain EXAMPLE:

chr8

EXAMPLE:

Unknown

EXAMPLE: D, P EXAMPLE:

Common recurrent secondary finding for t(8;21) (add references).

EXAMPLE:

17

EXAMPLE: Amp EXAMPLE:

17q12; chr17:39,700,064-39,728,658 [hg38; 28.6 kb]

EXAMPLE:

ERBB2

EXAMPLE: D, P, T EXAMPLE:

Amplification of ERBB2 is associated with HER2 overexpression in HER2 positive breast cancer (add references). Add criteria for how amplification is defined.

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

Characteristic Chromosomal or Other Global Mutational 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.[4]

Chromosomal Pattern Molecular Pathogenesis Prevalence -

Common >20%, Recurrent 5-20% or Rare <5% (Disease)

Diagnostic, Prognostic, and Therapeutic Significance - D, P, T Established Clinical Significance Per Guidelines - Yes or No (Source) Clinical Relevance Details/Other Notes


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 or common as well either disease defining and/or clinically significant. If a gene has multiple mechanisms depending on the type or site of the alteration, add multiple entries 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. Details on clinical significance such as prognosis and other important information such as concomitant and mutually exclusive mutations can be provided in the notes section. Please include references throughout the table. Do not delete the table.)

Gene Genetic Alteration Tumor Suppressor Gene, Oncogene, Other Prevalence -

Common >20%, Recurrent 5-20% or Rare <5% (Disease)

Diagnostic, Prognostic, and Therapeutic Significance - D, P, T   Established Clinical Significance Per Guidelines - Yes or No (Source) Clinical Relevance Details/Other Notes
EXAMPLE:EGFR


EXAMPLE: Exon 18-21 activating mutations EXAMPLE: Oncogene EXAMPLE: Common (lung cancer) EXAMPLE: T EXAMPLE: Yes (NCCN) EXAMPLE: Exons 18, 19, and 21 mutations are targetable for therapy. Exon 20 T790M variants cause resistance to first generation TKI therapy and are targetable by second and third generation TKIs (add references).
EXAMPLE: TP53; Variable LOF mutations


EXAMPLE: Variable LOF mutations EXAMPLE: Tumor Supressor Gene EXAMPLE: Common (breast cancer) EXAMPLE: P EXAMPLE: >90% are somatic; rare germline alterations associated with Li-Fraumeni syndrome (add reference). Denotes a poor prognosis in breast cancer.
EXAMPLE: BRAF; Activating mutations EXAMPLE: Activating mutations EXAMPLE: Oncogene EXAMPLE: Common (melanoma) EXAMPLE: T

Note: A more extensive list of mutations can be found in cBioportal, COSMIC, and/or other databases. When applicable, gene-specific pages within the CCGA site directly link to pertinent external content.

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[1]

Many SNVs and deletions in other genes are also detected and are predicted to be deleterious.[1]

Epigenomic Alterations

Alteration in LIN28, ARID1A, PARP10, MLL3, and MLL5 have been described and may play a role in the pathogenesis.[4]

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.[1]

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.[1]

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.[5]

This disease is defined/characterized as detailed below:

  • 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.[6][5][7]

The epidemiology/prevalence of this disease is detailed below:

  • PCAETL is rare, comprising less than 1% of all cutaneous T-cell lymphomas. It typically occurs in adults and shows a predilection for males.[6][7]

The clinical features of this disease are detailed below:

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 [6][5][7]

Laboratory findings - None

The sites of involvement of this disease are detailed below:

  • PCAETL can present with either localized or generalized skin lesions and may affect the oral mucosa.[8]

The morphologic features of this disease are detailed below:

  • Pagetoid epithelial involvement (epidermal and adnexal) is typically observed; however, the infiltrate may involve the entire dermis.[7][9] Lymphocyte morphology ranges from monomorphic to pleomorphic. Rimming of subcutaneous fat spaces has been reported. Spongiosis can result in blister formation.[10]
  • 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.[5][7][10] Ulceration can resemble pyoderma gangrenosum.[11] There is often pronounced pagetoid epidermotropism, particularly in cases with widespread lesions.[6][12]

The immunophenotype of this disease is detailed below:

  • 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(-/+) [2][4][1]

Links

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References

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Notes

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Prior Author(s):


*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 02/19/2025, https://ccga.io/index.php/HAEM5:Primary_cutaneous_CD8-positive_aggressive_epidermotropic_cytotoxic_T-cell_lymphoma.

  1. ↑ Jump up to: 1.00 1.01 1.02 1.03 1.04 1.05 1.06 1.07 1.08 1.09 1.10 1.11 1.12 1.13 1.14 1.15 1.16 1.17 1.18 1.19 1.20 1.21 1.22 1.23 1.24 1.25 1.26 1.27 1.28 1.29 1.30 1.31 1.32 1.33 1.34 1.35 1.36 1.37 1.38 1.39 1.40 1.41 1.42 1.43 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).
  2. ↑ Jump up to: 2.0 2.1 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).
  3. ↑ 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.
  4. ↑ Jump up to: 4.00 4.01 4.02 4.03 4.04 4.05 4.06 4.07 4.08 4.09 4.10 4.11 4.12 4.13 4.14 4.15 4.16 4.17 4.18 4.19 4.20 4.21 4.22 4.23 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)
  5. ↑ Jump up to: 5.0 5.1 5.2 5.3 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)
  6. ↑ Jump up to: 6.0 6.1 6.2 6.3 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)
  7. ↑ Jump up to: 7.0 7.1 7.2 7.3 7.4 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)
  8. ↑ 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)
  9. ↑ 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)
  10. ↑ Jump up to: 10.0 10.1 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)
  11. ↑ 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)
  12. ↑ 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.
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