Home / Deep Research / Primary Cutaneous Aggressive Epidermotropic CD8+ T-cell Lymphoma

Primary Cutaneous Aggressive Epidermotropic CD8+ T-cell Lymphoma

1. Disease Information

2026-05-07
Falcon MONDO:0015811 Model: Edison Scientific Literature 30 citations

1. Disease Information

1.1 Overview / definition (current understanding)

The entity is recognized within modern cutaneous lymphoma classifications as a distinct clinicopathologic syndrome of epidermotropic CD8+ cytotoxic T cells with aggressive behavior and poor outcomes. (deenen2019pitfallsindiagnosing pages 1-2, geller2018nktcelllymphomanasal pages 1-3)

In the WHO–EORTC 2018 update, it is listed explicitly as “Primary cutaneous aggressive epidermotropic CD8-positive T-cell lymphoma (provisional)” and summarized as presenting with ulcerating plaques, nodules, and tumors, with a typical immunophenotype CD3+, CD4−, CD8+, cytotoxic proteins positive, CD56−, and EBV−. (willemze2019the2018update pages 13-16, willemze2019the2018update media 461b18ed)

1.2 Key identifiers / ontology codes

Within the retrieved full texts, no MONDO, Orphanet (ORPHA), MeSH, ICD-10/ICD-11, or OMIM identifiers were provided for this specific disease name, including in the WHO–EORTC update excerpts and multiple case reports/reviews. (willemze2019the2018update pages 13-16, loya2023probableprimarycutaneous pages 4-4, sundram2019cutaneouslymphoproliferativedisorders pages 1-2)

1.3 Synonyms and alternative names

Nomenclature varies across clinical, dermatopathology, and molecular literature (e.g., “PCAETCL,” “pcAECyTCL,” and inclusion of “cytotoxic”). A harmonized list of name variants observed in the retrieved sources is provided below.

Table (click to expand)
Canonical name Common abbreviations Synonyms/variants in literature Classification status notes (WHO/WHO-EORTC provisional/definitive as supported) External identifiers (MONDO/Orphanet/MeSH/ICD) Key supporting citations with PMID/DOI/URL if available
Primary cutaneous aggressive epidermotropic CD8-positive T-cell lymphoma CD8+ AECTCL; PCAETCL; PCAE-TCL; pcAECyTCL Primary cutaneous CD8+ aggressive epidermotropic cytotoxic T-cell lymphoma; Primary cutaneous aggressive epidermotropic cytotoxic CD8 positive T cell lymphoma; Primary cutaneous CD8+ aggressive epidermotropic T-cell lymphoma; Aggressive epidermotropic cutaneous CD8+ lymphoma; Primary cutaneous aggressive epidermotropic CD8+ cytotoxic T-cell lymphoma Listed as a provisional entity in WHO-EORTC 2018 / recent cutaneous lymphoma classifications; described as a rare subtype of cutaneous T-cell lymphoma (CTCL) / primary cutaneous peripheral T-cell lymphoma. WHO-EORTC table lists frequency <1% and 5-year DSS 31%. (willemze2019the2018update pages 13-16, kempf2019cutaneouslymphomas—anupdate pages 1-3, sundram2019cutaneouslymphoproliferativedisorders pages 1-2, willemze2019the2018update media 461b18ed) MONDO/Orphanet/MeSH/ICD: not found in retrieved sources. Retrieved texts explicitly did not provide controlled-vocabulary identifiers. (willemze2019the2018update pages 13-16, loya2023probableprimarycutaneous pages 4-4, lupu2018anunusualpresentation pages 6-6, sundram2019cutaneouslymphoproliferativedisorders pages 1-2) Willemze et al., Blood 2019. DOI: 10.1182/blood-2018-11-881268. URL: https://doi.org/10.1182/blood-2018-11-881268 (willemze2019the2018update pages 13-16, willemze2019the2018update media 461b18ed)
Primary cutaneous CD8+ aggressive epidermotropic cytotoxic T-cell lymphoma PCAECTCL; PCAETL Primary cutaneous aggressive epidermotropic CD8+ T-cell lymphoma; Primary cutaneous CD8+ aggressive epidermotropic cytotoxic T-cell lymphoma Used in reviews/case reports as the same disease label; described as provisional in WHO-EORTC-based classification discussions. (deenen2019pitfallsindiagnosing pages 1-2, geller2018nktcelllymphomanasal pages 1-3, sundram2019cutaneouslymphoproliferativedisorders pages 1-2) MONDO/Orphanet/MeSH/ICD: not found in retrieved sources. (loya2023probableprimarycutaneous pages 4-4, sundram2019cutaneouslymphoproliferativedisorders pages 1-2) Deenen et al., Br J Dermatol 2019. DOI: 10.1111/bjd.17252. URL: https://doi.org/10.1111/bjd.17252; Geller et al., Semin Cutan Med Surg 2018. DOI: 10.12788/j.sder.2018.020. URL: https://doi.org/10.12788/j.sder.2018.020 (deenen2019pitfallsindiagnosing pages 1-2, geller2018nktcelllymphomanasal pages 1-3)
Primary cutaneous CD8+ aggressive epidermotropic cytotoxic T-cell lymphoma (molecular-study nomenclature) pcAECyTCL pcAETCL; primary cutaneous aggressive epidermotropic T-cell lymphoma Molecular/genomic study uses this wording for the same rare aggressive CTCL entity; supports disease definition and biology, but retrieved context does not alter its provisional classification status from WHO-EORTC sources. (torres2021deregulationofjak2 pages 1-2, gallardo2022geneticsabnormalitieswith pages 1-2) MONDO/Orphanet/MeSH/ICD: not found in retrieved sources. (willemze2019the2018update pages 13-16, loya2023probableprimarycutaneous pages 4-4) Torres et al., Haematologica 2021. DOI: 10.3324/haematol.2020.274506. URL: https://doi.org/10.3324/haematol.2020.274506 (torres2021deregulationofjak2 pages 1-2, torres2021deregulationofjak2 pages 3-5, torres2021deregulationofjak2 pages 5-7)

Table: This table compiles the main disease names, abbreviations, classification notes, and the absence of standardized external identifiers in the retrieved sources for primary cutaneous aggressive epidermotropic CD8+ T-cell lymphoma. It is useful for harmonizing terminology across pathology, clinical, and molecular literature.

1.4 Source type of information

Evidence in the retrieved corpus is predominantly aggregated disease-level classification/registry summaries (WHO–EORTC) plus small case series and case reports; prospective interventional data are scarce and repeatedly described as limited for this disease. (willemze2019the2018update pages 13-16, stuver2024throughthickand pages 1-2, cyrenne2018transplantationinthe pages 4-5)

2. Etiology

2.1 Disease causal factors

Primary driver biology (current evidence): JAK2/JAK–STAT pathway deregulation. A whole-genome and RNA-sequencing study provides evidence that structural and mutational alterations converging on JAK2 signaling are central in this lymphoma, including recurrent JAK2 fusions and loss of negative regulation via SH2B3. (torres2021deregulationofjak2 pages 1-2, torres2021deregulationofjak2 pages 3-5)

Direct quote (abstract evidence): “we show that mutually exclusive structural alterations involving JAK2 and SH2B3 predominantly underlie pcAECyTCL… Functional studies confirmed oncogenicity of JAK2 fusions… and their sensitivity to JAK inhibitor treatment.” (Haematologica; published online 2021; DOI https://doi.org/10.3324/haematol.2020.274506). (torres2021deregulationofjak2 pages 1-2)

2.2 Risk factors

No validated environmental, infectious, or inherited germline predisposition factors were identified in the retrieved sources. The current literature base is dominated by somatic tumor profiling and clinicopathologic case descriptions. (torres2021deregulationofjak2 pages 1-2, deenen2019pitfallsindiagnosing pages 1-2)

2.3 Protective factors / gene–environment interactions

No protective factors or gene–environment interaction evidence was identified in the retrieved sources. (willemze2019the2018update pages 13-16)

3. Phenotypes

3.1 Clinical phenotypes (signs/symptoms)

Common presentation includes rapidly progressive papules/plaques/nodules/tumors, often ulcerated or necrotic, with potential extracutaneous spread (reported sites include lung, testis, CNS, oral mucosa in case-based literature). (loya2023probableprimarycutaneous pages 3-4, kempf2021cutaneoust‐celllymphomas—an pages 1-2)

In WHO–EORTC tabulations, the typical presentation is ulcerating plaques, nodules and tumors. (willemze2019the2018update media 461b18ed)

3.2 Age of onset, severity, and progression

This is generally described as aggressive and rapidly progressive, with poor survival. (kempf2021cutaneoust‐celllymphomas—an pages 1-2, loya2023probableprimarycutaneous pages 3-4)

3.3 Differential diagnosis / diagnostic pitfalls

It can clinically and histologically mimic inflammatory or indolent lymphoproliferative disorders; a documented pitfall is resemblance to pyoderma gangrenosum or lymphomatoid papulosis (LyP) type D, necessitating close clinicopathologic correlation and appropriate immunophenotyping. (deenen2019pitfallsindiagnosing pages 1-2)

3.4 Suggested HPO terms (for knowledge base annotation; not exhaustive)

(These are ontology suggestions; the retrieved sources support the underlying clinical concepts but do not provide HPO mappings.) (loya2023probableprimarycutaneous pages 3-4, willemze2019the2018update media 461b18ed)

4. Genetic / Molecular Information

4.1 Recurrent somatic alterations (primary literature)

High-resolution genomics (WGS/RNA-seq; n=12 tumors) identified: (i) recurrent JAK2 fusions (e.g., PCM1::JAK2, KHDRBS1::JAK2, TFG::JAK2) and (ii) mutually exclusive focal inactivation of SH2B3, a negative regulator of JAK2 signaling. Together, alterations affecting the JAK2–SH2B3 axis predominated. (torres2021deregulationofjak2 pages 5-7, torres2021deregulationofjak2 pages 2-3)

Mechanistically, JAK2 fusion architecture is consistent with constitutive activation: the fusions join the JAK2 kinase domain to partner oligomerization domains, predicted to “self-oligo/dimerize and become activated without the need of cytokine-mediated receptor stimulation.” (torres2021deregulationofjak2 pages 3-5)

Additional recurrent cooperating lesions reported include frequent disruption of CDKN2A/B (9p21) and deletions of chromatin regulators (e.g., ARID1A, EED), consistent with cell-cycle checkpoint loss and chromatin dysregulation as cooperating hallmarks. (torres2021deregulationofjak2 pages 3-5, torres2021deregulationofjak2 pages 2-3)

A review summarizing genetic abnormalities across primary cutaneous lymphomas also reports recurrent targetable fusions in this entity, including CAPRIN1::JAK2 and SELENOI::ABL1, reinforcing the theme of kinase-fusion-driven oncogenic signaling. (gallardo2022geneticsabnormalitieswith pages 7-9)

4.2 Functional consequences and therapeutic implications

Functional assays showed JAK2 fusions to be oncogenic and sensitive to JAK inhibition, supporting biomarker-driven consideration of JAK inhibitors (e.g., ruxolitinib) when an activated JAK2 axis is detected. (torres2021deregulationofjak2 pages 1-2, torres2021deregulationofjak2 pages 5-7)

4.3 Suggested GO biological process terms (mechanism annotation)

4.4 Suggested cell types (Cell Ontology; mechanism annotation)

(These are ontology suggestions aligned to the immunophenotype and lineage reported in WHO–EORTC tables and molecular studies.) (willemze2019the2018update media 461b18ed, willemze2019the2018update pages 13-16)

5. Environmental Information

No specific environmental, lifestyle, occupational, or infectious triggers were identified in the retrieved sources for this entity. (willemze2019the2018update pages 13-16)

6. Mechanism / Pathophysiology

6.1 Causal chain (integrated model)

  1. Initiating oncogenic lesions: recurrent JAK2 gene fusions or loss of negative regulation via SH2B3 produce persistent JAK2 signaling. (torres2021deregulationofjak2 pages 3-5, torres2021deregulationofjak2 pages 5-7)
  2. Signal transduction and transcriptional programs: transcriptome analysis shows upregulation of JAK2 signaling, cell-cycle programs, and TNF-α/NF-κB signaling, plus a high inflammatory response signature. (torres2021deregulationofjak2 pages 1-2, torres2021deregulationofjak2 pages 5-7)
  3. Tumor expansion and tissue phenotype: malignant CD8+ cytotoxic T cells infiltrate the epidermis (marked epidermotropism), producing clinically aggressive ulcerating plaques/tumors with capacity for extracutaneous dissemination. (willemze2019the2018update media 461b18ed, loya2023probableprimarycutaneous pages 3-4)

6.2 Molecular profiling technologies

The most disease-specific mechanistic evidence in the retrieved set comes from whole-genome sequencing and RNA sequencing in pcAECyTCL tumors. (torres2021deregulationofjak2 pages 1-2, torres2021deregulationofjak2 pages 2-3)

7. Anatomical Structures Affected

7.1 Organ/tissue level

  • Primary site: skin (cutaneous lymphoma by definition; no extracutaneous disease at diagnosis in classification frameworks). (willemze2019the2018update pages 13-16)
  • Clinical morphology: ulcerating plaques/nodules/tumors. (willemze2019the2018update media 461b18ed)

7.2 Suggested UBERON terms

8. Temporal Development

8.1 Onset and progression

The disease is described as having rapid onset of necrotic/ulcerated plaques and tumors and an aggressive course. (kempf2021cutaneoust‐celllymphomas—an pages 1-2)

9. Inheritance and Population

9.1 Epidemiology (rarity)

WHO–EORTC tabulated frequency is <1% among primary cutaneous lymphomas in registry-based summaries. (willemze2019the2018update media 461b18ed)

A 2023 case report summarizes the rarity as “about 1% of cutaneous T-cell lymphomas” and notes that “slightly more than 30 cases” had been reported in the literature at that time (case-report-level secondary summary). (loya2023probableprimarycutaneous pages 3-4)

9.2 Inheritance

No germline inheritance pattern was identified in the retrieved sources; available evidence supports a predominantly somatic oncogenic process (e.g., JAK2 fusions, SH2B3 deletions). (torres2021deregulationofjak2 pages 3-5)

10. Diagnostics

10.1 Diagnostic approach (clinicopathologic)

Diagnosis relies on combined clinical and histopathologic evaluation because of overlap with other CD8+ cutaneous lymphomas and inflammatory mimics. (lupu2018anunusualpresentation pages 6-6, deenen2019pitfallsindiagnosing pages 1-2)

WHO–EORTC immunophenotype snapshot (Table data): CD3+, CD4−, CD8+, cytotoxic proteins positive, CD56−, EBV−, lineage αβ T-cell. (willemze2019the2018update media 461b18ed)

10.2 Biomarkers and molecular tests

Given the recurrent JAK2 fusions and SH2B3 alterations, contemporary molecular profiling (e.g., RNA-seq fusion detection and/or DNA-based profiling) can identify actionable lesions and support classification in challenging cases. (torres2021deregulationofjak2 pages 5-7, gallardo2022geneticsabnormalitieswith pages 7-9)

10.3 Differential diagnosis (examples supported in retrieved sources)

  • Pyoderma gangrenosum (clinical mimic)
  • Lymphomatoid papulosis type D
  • CD8+ mycosis fungoides
  • Cutaneous γδ T-cell lymphoma
  • Primary cutaneous peripheral T-cell lymphoma, NOS

(deenen2019pitfallsindiagnosing pages 1-2, loya2023probableprimarycutaneous pages 3-4)

11. Outcome / Prognosis

11.1 Registry-level survival statistics

WHO–EORTC table data report 5-year disease-specific survival (DSS) ~31% for this provisional entity. (willemze2019the2018update media 461b18ed)

11.2 Case-based prognosis estimates

A 2023 case report states a “survival time of 32 months from the commencement of skin lesions” (secondary summary of prior literature). (loya2023probableprimarycutaneous pages 3-4)

12. Treatment

12.1 Current practice patterns and real-world implementations

Because prospective trials are scarce, real-world management often follows aggressive lymphoma paradigms and institutional experience.

Systemic chemotherapy and radiation: A multi-institution case series reported use of multiagent regimens (e.g., CHOP, EPOCH, gemcitabine-based regimens, ICE/DHAP), plus radiotherapy including localized XRT and total skin electron beam therapy (TSEBT). (cyrenne2018transplantationinthe pages 4-5, cyrenne2018transplantationinthe pages 7-9)

Transplantation: The same series emphasizes that durable responses were observed mainly with allogeneic stem cell transplantation (allo-SCT) or brentuximab vedotin in selected settings. (cyrenne2018transplantationinthe pages 4-5)

Targeted / biomarker-driven therapy: Genomic evidence supporting JAK2 pathway targeting has enabled off-label or investigational use of JAK inhibitors (e.g., ruxolitinib), including use after relapse post-transplant in a 2023 case report. (sopena2023hematopoieticstemcell pages 2-3, torres2021deregulationofjak2 pages 1-2)

12.2 Expert opinion (2023–2024 priority)

A 2024 ASH Hematology expert review stresses that PCAETCL has “few prospective studies to guide treatment,” and that “recent genomic insights… such as the presence of JAK2 fusions in PCAETCL… have created options for new biomarker-driven strategies.” (Hematology; Dec 2024; DOI https://doi.org/10.1182/hematology.2024000529). (stuver2024throughthickand pages 1-2)

12.3 Treatment outcomes and statistics (available)

In the 2018 case series, outcomes included multiple complete responses in individuals receiving allo-SCT and brentuximab; at last follow-up, transplanted patients were alive, with median follow-up around 40 months (range reported). (cyrenne2018transplantationinthe pages 4-5)

A 2023 case report reiterates poor baseline prognosis (“5-year survival rate of less than 40%”) and describes multi-line therapy culminating in allo-HSCT, followed by relapse treated with ruxolitinib. (sopena2023hematopoieticstemcell pages 1-2, sopena2023hematopoieticstemcell pages 2-3)

12.4 MAXO terms (treatment action ontology; suggested)

  • Chemotherapy (MAXO:0000058)
  • Radiation therapy (MAXO:0000014)
  • Allogeneic hematopoietic stem cell transplantation (MAXO term; concept supported by clinical text)
  • Janus kinase inhibitor therapy (MAXO concept)

(These are ontology suggestions; supporting evidence for modalities is in cited clinical series/case reports.) (cyrenne2018transplantationinthe pages 7-9, sopena2023hematopoieticstemcell pages 2-3)

12.5 Ongoing clinical trials / registries (not disease-specific but relevant to cytotoxic/T-cell lymphoma populations)

13. Prevention

No primary prevention strategy is supported in the retrieved sources. Secondary prevention is limited to early recognition and accurate diagnosis, given frequent diagnostic pitfalls and aggressive progression. (deenen2019pitfallsindiagnosing pages 1-2, lupu2018anunusualpresentation pages 6-6)

14. Other Species / Natural Disease

No naturally occurring veterinary/other-species analog was identified in the retrieved sources. (willemze2019the2018update pages 13-16)

15. Model Organisms

No dedicated in vivo model organism systems were identified in the retrieved sources. Mechanistic functional work in the key molecular study used cell-based assays to validate oncogenicity of JAK2 fusions and their inhibitor sensitivity. (torres2021deregulationofjak2 pages 5-7)

Notes on evidence gaps

  1. Standard identifiers (MONDO/Orphanet/ICD/MeSH) were not present in the retrieved full-text excerpts; mapping will require dedicated queries to those ontology resources using the synonyms listed. (willemze2019the2018update pages 13-16, loya2023probableprimarycutaneous pages 4-4)
  2. Many clinical outcome statistics remain based on registry summaries and small case series, reflecting the rarity and the limited prospective trial evidence base. (stuver2024throughthickand pages 1-2, cyrenne2018transplantationinthe pages 4-5)

References

  1. (deenen2019pitfallsindiagnosing pages 1-2): N. J. Deenen, L. Koens, E. H. Jaspars, M. Vermeer, R. Willemze, M. D. de Rie, and M. Bekkenk. Pitfalls in diagnosing primary cutaneous aggressive epidermotropic cd8+ t‐cell lymphoma. British Journal of Dermatology, 180:411-412, Oct 2019. URL: https://doi.org/10.1111/bjd.17252, doi:10.1111/bjd.17252. This article has 13 citations and is from a highest quality peer-reviewed journal.

  2. (geller2018nktcelllymphomanasal pages 1-3): Shamir Geller, Patricia L Myskowski, and Melissa Pulitzer. Nk/t-cell lymphoma, nasal type, γδ t-cell lymphoma, and cd8-positive epidermotropic t-cell lymphoma—clinical and histopathologic features, differential diagnosis, and treatment. Seminars in Cutaneous Medicine and Surgery, 37:30-38, Mar 2018. URL: https://doi.org/10.12788/j.sder.2018.020, doi:10.12788/j.sder.2018.020. This article has 53 citations and is from a peer-reviewed journal.

  3. (willemze2019the2018update pages 13-16): Rein Willemze, Lorenzo Cerroni, Werner Kempf, Emilio Berti, Fabio Facchetti, Steven H. Swerdlow, and Elaine S. Jaffe. The 2018 update of the who-eortc classification for primary cutaneous lymphomas. Blood, 133 16:1703-1714, Apr 2019. URL: https://doi.org/10.1182/blood-2018-11-881268, doi:10.1182/blood-2018-11-881268. This article has 1674 citations and is from a highest quality peer-reviewed journal.

  4. (willemze2019the2018update media 461b18ed): Rein Willemze, Lorenzo Cerroni, Werner Kempf, Emilio Berti, Fabio Facchetti, Steven H. Swerdlow, and Elaine S. Jaffe. The 2018 update of the who-eortc classification for primary cutaneous lymphomas. Blood, 133 16:1703-1714, Apr 2019. URL: https://doi.org/10.1182/blood-2018-11-881268, doi:10.1182/blood-2018-11-881268. This article has 1674 citations and is from a highest quality peer-reviewed journal.

  5. (loya2023probableprimarycutaneous pages 4-4): Marcela Velarde Loya, Monica G Millan Reza, Mariana Olaya Cordova, and Zaira D Chavéz López. Probable primary cutaneous cd8+ aggressive epidermotropic cytotoxic t-cell lymphoma: a case report of a diagnostic challenge. Cureus, Aug 2023. URL: https://doi.org/10.7759/cureus.44375, doi:10.7759/cureus.44375. This article has 1 citations.

  6. (sundram2019cutaneouslymphoproliferativedisorders pages 1-2): Uma Sundram. Cutaneous lymphoproliferative disorders: what’s new in the revised 4th edition of the world health organization (who) classification of lymphoid neoplasms. Advances in Anatomic Pathology, 26:93-113, Mar 2019. URL: https://doi.org/10.1097/pap.0000000000000208, doi:10.1097/pap.0000000000000208. This article has 21 citations and is from a domain leading peer-reviewed journal.

  7. (kempf2019cutaneouslymphomas—anupdate pages 1-3): Werner Kempf, Anne‐Katrin Zimmermann, and Christina Mitteldorf. Cutaneous lymphomas—an update 2019. Hematological Oncology, 37:43-47, Jun 2019. URL: https://doi.org/10.1002/hon.2584, doi:10.1002/hon.2584. This article has 110 citations and is from a peer-reviewed journal.

  8. (lupu2018anunusualpresentation pages 6-6): M Lupu, V Voiculescu, and L Papagheorghe. An unusual presentation of primary cutaneous aggressive epidermotropic cd8+ t cell lymphoma. Unknown journal, 2018.

  9. (torres2021deregulationofjak2 pages 1-2): Armando N. Bastidas Torres, Davy Cats, Jacoba J. Out-Luiting, Daniele Fanoni, Hailiang Mei, Luigia Venegoni, Rein Willemze, Maarten H. Vermeer, Emilio Berti, and Cornelis P. Tensen. Deregulation of jak2 signaling underlies primary cutaneous cd8+ aggressive epidermotropic cytotoxic t-cell lymphoma. Haematologica, 107:702-714, Apr 2021. URL: https://doi.org/10.3324/haematol.2020.274506, doi:10.3324/haematol.2020.274506. This article has 61 citations.

  10. (gallardo2022geneticsabnormalitieswith pages 1-2): Fernando Gallardo and Ramon M. Pujol. Genetics abnormalities with clinical impact in primary cutaneous lymphomas. Cancers, 14:4972, Oct 2022. URL: https://doi.org/10.3390/cancers14204972, doi:10.3390/cancers14204972. This article has 22 citations.

  11. (torres2021deregulationofjak2 pages 3-5): Armando N. Bastidas Torres, Davy Cats, Jacoba J. Out-Luiting, Daniele Fanoni, Hailiang Mei, Luigia Venegoni, Rein Willemze, Maarten H. Vermeer, Emilio Berti, and Cornelis P. Tensen. Deregulation of jak2 signaling underlies primary cutaneous cd8+ aggressive epidermotropic cytotoxic t-cell lymphoma. Haematologica, 107:702-714, Apr 2021. URL: https://doi.org/10.3324/haematol.2020.274506, doi:10.3324/haematol.2020.274506. This article has 61 citations.

  12. (torres2021deregulationofjak2 pages 5-7): Armando N. Bastidas Torres, Davy Cats, Jacoba J. Out-Luiting, Daniele Fanoni, Hailiang Mei, Luigia Venegoni, Rein Willemze, Maarten H. Vermeer, Emilio Berti, and Cornelis P. Tensen. Deregulation of jak2 signaling underlies primary cutaneous cd8+ aggressive epidermotropic cytotoxic t-cell lymphoma. Haematologica, 107:702-714, Apr 2021. URL: https://doi.org/10.3324/haematol.2020.274506, doi:10.3324/haematol.2020.274506. This article has 61 citations.

  13. (stuver2024throughthickand pages 1-2): Robert Stuver and Steven M. Horwitz. Through thick and thin: confronting the aggressive cutaneous t-cell lymphomas. Hematology, 2024:62-68, Dec 2024. URL: https://doi.org/10.1182/hematology.2024000529, doi:10.1182/hematology.2024000529. This article has 0 citations and is from a peer-reviewed journal.

  14. (cyrenne2018transplantationinthe pages 4-5): Benoit M. Cyrenne, Juliet Fraser Gibson, Antonio Subtil, Michael Girardi, Iris Isufi, Stuart Seropian, and Francine Foss. Transplantation in the treatment of primary cutaneous aggressive epidermotropic cytotoxic cd8‐positive t‐cell lymphoma. Clinical Lymphoma, Myeloma & Leukemia, 18:e85–e93, Jan 2018. URL: https://doi.org/10.1016/j.clml.2017.11.004, doi:10.1016/j.clml.2017.11.004. This article has 21 citations.

  15. (loya2023probableprimarycutaneous pages 3-4): Marcela Velarde Loya, Monica G Millan Reza, Mariana Olaya Cordova, and Zaira D Chavéz López. Probable primary cutaneous cd8+ aggressive epidermotropic cytotoxic t-cell lymphoma: a case report of a diagnostic challenge. Cureus, Aug 2023. URL: https://doi.org/10.7759/cureus.44375, doi:10.7759/cureus.44375. This article has 1 citations.

  16. (kempf2021cutaneoust‐celllymphomas—an pages 1-2): Werner Kempf and Christina Mitteldorf. Cutaneous t‐cell lymphomas—an update 2021. Hematological Oncology, 39:46-51, Jun 2021. URL: https://doi.org/10.1002/hon.2850, doi:10.1002/hon.2850. This article has 106 citations and is from a peer-reviewed journal.

  17. (torres2021deregulationofjak2 pages 2-3): Armando N. Bastidas Torres, Davy Cats, Jacoba J. Out-Luiting, Daniele Fanoni, Hailiang Mei, Luigia Venegoni, Rein Willemze, Maarten H. Vermeer, Emilio Berti, and Cornelis P. Tensen. Deregulation of jak2 signaling underlies primary cutaneous cd8+ aggressive epidermotropic cytotoxic t-cell lymphoma. Haematologica, 107:702-714, Apr 2021. URL: https://doi.org/10.3324/haematol.2020.274506, doi:10.3324/haematol.2020.274506. This article has 61 citations.

  18. (gallardo2022geneticsabnormalitieswith pages 7-9): Fernando Gallardo and Ramon M. Pujol. Genetics abnormalities with clinical impact in primary cutaneous lymphomas. Cancers, 14:4972, Oct 2022. URL: https://doi.org/10.3390/cancers14204972, doi:10.3390/cancers14204972. This article has 22 citations.

  19. (cyrenne2018transplantationinthe pages 7-9): Benoit M. Cyrenne, Juliet Fraser Gibson, Antonio Subtil, Michael Girardi, Iris Isufi, Stuart Seropian, and Francine Foss. Transplantation in the treatment of primary cutaneous aggressive epidermotropic cytotoxic cd8‐positive t‐cell lymphoma. Clinical Lymphoma, Myeloma & Leukemia, 18:e85–e93, Jan 2018. URL: https://doi.org/10.1016/j.clml.2017.11.004, doi:10.1016/j.clml.2017.11.004. This article has 21 citations.

  20. (sopena2023hematopoieticstemcell pages 2-3): L Sopena, M Merchante, MA Alcácera, and I Varela. Hematopoietic stem cell transplantation in primary cutaneous aggressive epidermotropic cd8+ t-cell lymphoma: a case report. Journal of Clinical Images and Medical Case Reports, Oct 2023. URL: https://doi.org/10.52768/2766-7820/2646, doi:10.52768/2766-7820/2646. This article has 0 citations.

  21. (sopena2023hematopoieticstemcell pages 1-2): L Sopena, M Merchante, MA Alcácera, and I Varela. Hematopoietic stem cell transplantation in primary cutaneous aggressive epidermotropic cd8+ t-cell lymphoma: a case report. Journal of Clinical Images and Medical Case Reports, Oct 2023. URL: https://doi.org/10.52768/2766-7820/2646, doi:10.52768/2766-7820/2646. This article has 0 citations.