Survival signals and targets for therapy in breast implant-associated ALK--anaplastic large cell lymphoma

Clin Cancer Res. 2012 Sep 1;18(17):4549-59. doi: 10.1158/1078-0432.CCR-12-0101. Epub 2012 Jul 12.

Abstract

Purpose: Anaplastic lymphoma kinase (ALK)-negative, T-cell, anaplastic, non-Hodgkin lymphoma (T-ALCL) in patients with textured saline and silicone breast implants is a recently recognized clinical entity for which the etiology and optimal treatment remain unknown.

Experimental design: Using three newly established model cell lines from patient biopsy specimens, designated T-cell breast lymphoma (TLBR)-1 to -3, we characterized the phenotype and function of these tumors to identify mechanisms of cell survival and potential therapeutic targets.

Results: Cytogenetics revealed chromosomal atypia with partial or complete trisomy and absence of the NPM-ALK (2;5) translocation. Phenotypic characterization showed strong positivity for CD30, CD71, T-cell CD2/5/7, and antigen presentation (HLA-DR, CD80, CD86) markers, and interleukin (IL)-2 (CD25, CD122) and IL-6 receptors. Studies of these model cell lines showed strong activation of STAT3 signaling, likely related to autocrine production of IL-6 and decreased SHP-1. STAT3 inhibition, directly or by recovery of SHP-1, and cyclophosphamide-Adriamycin-vincristine-prednisone (CHOP) chemotherapy reagents, effectively kill cells of all three TLBR models in vitro and may be pursued as therapies for patients with breast implant-associated T-ALCLs.

Conclusions: The TLBR cell lines closely resemble the primary breast implant-associated lymphomas from which they were derived and as such provide valuable preclinical models to study their unique biology.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Anaplastic Lymphoma Kinase
  • Antineoplastic Agents / pharmacology
  • Apoptosis / drug effects
  • Breast Implantation / adverse effects
  • Female
  • Humans
  • Interleukin-6* / metabolism
  • Lymphoma, Large-Cell, Anaplastic* / metabolism
  • Lymphoma, Large-Cell, Anaplastic* / pathology
  • Lymphoma, Large-Cell, Anaplastic* / therapy
  • Molecular Targeted Therapy
  • Protein Tyrosine Phosphatase, Non-Receptor Type 6* / antagonists & inhibitors
  • Protein Tyrosine Phosphatase, Non-Receptor Type 6* / metabolism
  • Receptor Protein-Tyrosine Kinases / metabolism
  • STAT3 Transcription Factor* / antagonists & inhibitors
  • STAT3 Transcription Factor* / metabolism
  • Signal Transduction / drug effects
  • Tumor Cells, Cultured

Substances

  • Antineoplastic Agents
  • Interleukin-6
  • STAT3 Transcription Factor
  • STAT3 protein, human
  • ALK protein, human
  • Anaplastic Lymphoma Kinase
  • Receptor Protein-Tyrosine Kinases
  • PTPN6 protein, human
  • Protein Tyrosine Phosphatase, Non-Receptor Type 6