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Genomic Analysis of Cutaneous CD30-Positive Lymphoproliferative Disorders.

Farah R Abdulla1, Weiwei Zhang2, Xiwei Wu3

  • 1Department of Surgery, City of Hope National Medical Center, Duarte, California, USA.

JID Innovations : Skin Science From Molecules to Population Health
|January 3, 2022
PubMed
Summary

Genomic analysis reveals shared epigenetic alterations in lymphomatoid papulosis (LyP) and primary cutaneous anaplastic large cell lymphoma (C-ALCL), alongside unique mutations in C-ALCL. These findings offer insights into the development of these CD30+ T-cell lymphomas.

Keywords:
BI-ALCL, breast implant‒associated anaplastic large cell lymphomaC-ALCL, cutaneous anaplastic large cell lymphomaCD30+LPD, CD30+ lymphoproliferative disorderCN, copy numberCTCL, cutaneous T-cell lymphomaFFPE, formalin-fixed, paraffin-embeddedIHC, immunohistochemistryLyP, lymphomatoid papulosisMF, mycosis fungoidesSTAT, signal transducer and activator of transcriptionsALCL, systemic anaplastic large cell lymphoma

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Area of Science:

  • Oncology
  • Genetics
  • Dermatology

Background:

  • Primary cutaneous CD30+ T-cell lymphoproliferative disorders, including lymphomatoid papulosis (LyP) and primary cutaneous anaplastic large cell lymphoma (C-ALCL), are common skin lymphomas.
  • While sharing histology, LyP and C-ALCL exhibit distinct clinical behaviors and prognoses, suggesting underlying molecular differences.
  • Understanding the genomic landscape is crucial for elucidating the pathogenesis of these related yet distinct conditions.

Purpose of the Study:

  • To identify oncogenic genomic variants driving the development of LyP and C-ALCL.
  • To compare the molecular profiles of LyP and C-ALCL to understand shared and unique pathogenic mechanisms.
  • To investigate the role of epigenetic modifications and signaling pathways in lymphomagenesis.

Main Methods:

  • Whole-exome sequencing was performed on specimens from six LyP and five C-ALCL cases.
  • Clinical information, pathology, and immunohistochemistry were reviewed to confirm diagnoses.
  • Genomic alterations in epigenetic modifying genes and signaling pathways were analyzed.

Main Results:

  • Both LyP and C-ALCL showed recurrent alterations in epigenetic modifying genes (e.g., SETD2, KMT2A, KMT2D, CREBBP).
  • C-ALCL uniquely harbored mutations in STAT3 and EOMES, involved in immune signaling and lymphocyte development.
  • Genomic characterization confirmed the involvement of multiple pathways in the pathogenesis of these lymphomas.

Conclusions:

  • Shared aberrations in epigenetic modifying genes suggest common lymphomagenesis mechanisms between LyP and C-ALCL.
  • Distinct mutations in C-ALCL may explain the differences in clinical course and prognosis compared to LyP.
  • These findings advance the understanding of the molecular basis of CD30+ T-cell lymphomas.