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Two Classes of FOXA1 Mutations Drive Prostate Cancer Initiation and Treatment Resistance

Researchers now have preclinical models replicating FOXA1 mutation–driven prostate cancers for testing targeted therapies

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Overview

  • The University of Michigan Rogel Health Cancer Center study used genetically engineered mouse models and was published in Science
  • Class 1 FOXA1 mutations cooperate with TP53 loss to trigger aggressive, androgen-dependent tumors that respond to androgen deprivation therapy
  • Class 2 FOXA1 mutations reprogram cellular lineage identity in metastatic tumors, enabling resistance to conventional hormone treatments
  • FOXA1 alterations are found in 10–40% of hormone-dependent prostate cancers and play a direct causal role in both tumor initiation and therapy resistance
  • The new models offer a platform for developing FOXA1 mutation–specific therapeutic strategies aimed at blocking tumor growth or overcoming resistance