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Cancer-Critical Genes I: Proto-oncogenes01:33

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Genes usually encode proteins necessary for the proper functioning of a healthy cell. Mutations can often cause changes to the gene expression pattern, thereby altering the phenotype.
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Tumor progression is a phenomenon where the pre-formed tumor acquires successive mutations to become clinically more aggressive and malignant. In the 1950s, Foulds first described the stepwise progression of cancer cells through successive stages.
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FOXA1 Alterations in Prostate Cancer: Expression, Mutation Classes, and Copy Number Changes.

Steven Lehrer1, Peter Rheinstein2

  • 1Department of Radiation Oncology, Icahn School of Medicine at Mount Sinai, New York, NY, U.S.A.; stevenlehrer@hotmail.com.

In Vivo (Athens, Greece)
|January 2, 2026
PubMed
Summary

Forkhead box A1 (FOXA1) alterations represent a key driver in prostate cancer, distinct from TMPRSS2-ERG fusions. These mutations influence therapy resistance and tumor progression, marking FOXA1 as a potential therapeutic target.

Keywords:
FOXA1PROX1TMPRSS2-ERG fusionlineage plasticityprostate cancer

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Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Prostate cancer exhibits significant transcriptional dysregulation in the androgen receptor (AR) signaling pathway.
  • The pioneer factor FOXA1, crucial for AR binding to chromatin, is altered in 10-40% of prostate tumors.
  • FOXA1 mutations are classified into Class 1 (enhancing tumorigenesis) and Class 2 (promoting plasticity and resistance).

Purpose of the Study:

  • To investigate the role of FOXA1 alterations in prostate cancer.
  • To understand the interplay between FOXA1, TMPRSS2-ERG fusions, and PROX1.
  • To assess the association of FOXA1 status with genomic instability.

Main Methods:

  • Analysis of The Cancer Genome Atlas (TCGA) Prostate Adenocarcinoma (PRAD) cohort (n=492) using UCSC Xena and cBioPortal.
  • Categorization of FOXA1 mutations and assessment of copy number variations.
  • Evaluation of mutual exclusivity, co-occurrence, and association with genomic instability (Fraction Genome Altered - FGA).

Main Results:

  • FOXA1 mutations were categorized into Wing 2 (Class 1) and C-terminal truncations (Class 2).
  • FOXA1 alterations were mutually exclusive with TMPRSS2-ERG fusions.
  • A moderate correlation was observed between FOXA1 alterations and genomic instability.

Conclusions:

  • FOXA1 constitutes a major oncogenic axis in prostate cancer, independent of TMPRSS2-ERG and PROX1.
  • FOXA1 mutations drive distinct transcriptional programs associated with therapy resistance.
  • FOXA1 is a critical biomarker and potential therapeutic target for chromatin-directed interventions in prostate cancer.