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The Tumor Microenvironment02:17

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Every normal cell or tissue is embedded in a complex local environment called stroma, consisting of different cell types, a basal membrane, and blood vessels. As normal cells mutate and develop into cancer cells, their local environment also changes to allow cancer progression. The tumor microenvironment (TME) consists of a complex cellular matrix of stromal cells and the developing tumor. The cross-talk between cancer cells and surrounding stromal cells is critical to disrupt normal tissue...
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STAT6 mutations enriched at diffuse large B-cell lymphoma relapse reshape the tumor microenvironment.

Alexandre Benoit1,2, Madelyn J Abraham1,2, Sheena Li1

  • 1Lady Davis Institute, Jewish General Hospital, 3755 Côte Sainte-Catherine Road, Montreal, QC, H3T 1E2, Canada.

International Journal of Hematology
|January 29, 2024
PubMed
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STAT6 mutations in diffuse large B-cell lymphoma (DLBCL) promote cell survival and alter the tumor microenvironment, contributing to therapeutic resistance. These findings highlight a potential new target for DLBCL treatment.

Keywords:
DLBCLSTAT6Tumor microenvironment

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Area of Science:

  • Oncology
  • Immunology
  • Molecular Biology

Background:

  • Diffuse large B-cell lymphoma (DLBCL) frequently relapses after initial treatment, with approximately 40% of patients experiencing recurrence.
  • Signal transducer and activator of transcription 6 (STAT6) mutations, specifically D419, are found more often in relapsed/refractory DLBCL (rrDLBCL), suggesting a role in treatment resistance.
  • The JAK/STAT signaling pathway is implicated in therapeutic resistance in DLBCL.

Purpose of the Study:

  • To investigate the functional role of STAT6 D419 mutations in DLBCL cell survival and microenvironment reprogramming.
  • To understand how STAT6 D419 mutations sustain STAT6 activation and influence DLBCL progression.
  • To determine the impact of STAT6 D419 mutations on gene expression and tumor-infiltrating immune cells.

Main Methods:

  • Comparative analysis of phospho-STAT6 D419N and wild-type (WT) STAT6 nuclear retention and DNA-binding specificity following IL-4 stimulation.
  • Assessment of gene expression profiles induced by STAT6 D419N versus STAT6 WT upon IL-4 stimulation.
  • Quantification of CD4+ T-cell infiltration in DLBCL tumors based on phospho-STAT6 status.

Main Results:

  • Phospho-STAT6 D419N exhibited prolonged nuclear retention and recognized a more restricted DNA-binding sequence compared to phospho-STAT6 WT.
  • STAT6 D419N expression induced a greater magnitude of gene expression changes, with a more selective target gene list, including those involved in cell survival, proliferation, migration, and chemotaxis.
  • CCL17 (TARC) was a significantly upregulated gene induced by STAT6 D419N, known to attract CD4+ T-cells.
  • DLBCL tumors with phospho-STAT6+ cells showed a higher proportion of infiltrating CD4+ T-cells compared to phospho-STAT6- tumors.

Conclusions:

  • STAT6 D419 mutations in DLBCL contribute to cell-autonomous alterations and enhanced signaling pathways.
  • These mutations promote the secretion of chemokines like CCL17, which modifies the tumor microenvironment by increasing CD4+ T-cell infiltration.
  • The altered tumor microenvironment and enhanced signaling driven by STAT6 D419 mutations may play a significant role in DLBCL therapeutic resistance and progression.