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Research Brief

Analyses of patients with advanced breast cancer resistant to orthosteric PI3Kα inhibitors revealed that secondary resistance mutations in PIK3CA alter the inhibitor binding pocket, which can be overcome by use of the allosteric PI3Kα inhibitor RLY-2608.

Research Articles

The most prevalent oncogenic mutants of PIK3CA can be selectively targeted by RLY-2608, providing a clinical opportunity to overcome toxicities associated with current treatments.

Continuous and obligatory mutagenesis in patients with germline DNA replication-repair deficient refractory glioblastoma allows for sustained immune-surveillance and prolonged survival following synergistic immune-directed combinations.

As part of Cohort A of the plasmaMATCH trial, baseline ESR1 mutations were found to be predictive of response to fulvestrant, and ESR1 F404 mutations that occur in cis with classical activating ESR1 mutations promote resistance.

MHC-I heterogeneity drives anti-PD-L1 resistance in triple negative breast cancer tumors and enhances NK cell infiltration, and combination of anti-PD-L1 therapy with anti-NKGA2A, which suppresses NK cell function, restores response.

Targeting KRAS in lung cancer cells promotes differentiation into a KRAS inhibitor-resistant cell state with alveolar identity, which represents a novel target for overcoming resistance to KRAS inhibition.

Genetic depletion or small molecule inhibition of RIPK2-sensitized pancreatic ductal adenocarcinoma to anti-PD-1 therapy via an increase in MHC-I surface levels by negating NBR1-mediated autophagy-lysosomal degradation.

Pancreatic ductal adenocarcinoma explant models reveal that malignant epithelial cells induce Hedgehog signaling in fibroblasts that leads to inhibition of noncanonical WNT signaling and VEGFR2-dependent endothelial hypersprouting.

Evaluation of a large panel of human cancer cells revealed that gain-of-function effects of mutant TP53 are not required for tumor growth and therapy resistance, whereas loss of wild-type TP53 functions is essential for these phenotypes.

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