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It is demonstrated that uveal melanoma progression reflects an integrated CN-transcriptional ecosystem extending beyond chromosome 3 loss, with cytoband-level genomic evolution shaping malignant fitness and therapeutic response.
It is shown that KRAS targeting with MRTX1133 or Daraxonrasib specifically synergizes with anti-CTLA4, but not other immune checkpoint inhibitors, in inducing tertiary lymphoid structures and promoting anti-tumor immune responses in preclinical pancreatic cancer models.
Mediator complex kinase CDK8 is identified as a driver of resistance towards KRASG12D inhibition in pancreatic ductal adenocarcinoma (PDAC), promoting stromal remodeling and immunosuppression and CDK8 inhibition in resistant tumors re-primes PDAC to anti-CTLA-4 immunotherapy efficacy.
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