Matthew G. Rees

This study identifies CDK8 inhibition as a therapeutic strategy for alveolar rhabdomyosarcoma by inducing myogenic differentiation and impairing tumor growth through a mechanism involving the Mediator kinase module, SAGA complex, and SIX4.

This study identifies RAS(ON) inhibitors effective against NRAS-mutated melanoma and reveals resistance mechanisms through Ppia and Map2k1 mutations.

The paper identifies 25% of 7,264 non-canonical open reading frames (ncORFs) as producing translated gene products, supported by over 3,000 peptides from 3.8 billion mass spectra.

This paper develops a small molecule, BRD8833, that induces BCR-ABL phosphorylation to disrupt its active site electric field, leading to loss of hyperactivity and apoptosis in BCR-ABL-dependent cancer cells.

This study shows that degrading p300/CBP in prostate cancer suppresses tumor growth more effectively than inhibiting their activity, highlighting their role in maintaining the active AR enhanceosome.

This study identifies P-glycoprotein as a mediator of Rapaprotin resistance and shows that co-treatment with tariquidar restores its efficacy in colorectal cancer cells.

This study shows CDK11 is critical for cancer cell survival and identifies 1p36 deletions as a biomarker for CDK11 inhibitor sensitivity, but on-target toxicity limits therapeutic efficacy.

This study identifies DNA hypomethylation, not DNA damage, as the primary mechanism of azacytidine and decitabine anti-cancer activity, linking it to chromatin regulators like USP48.

This study shows that CDK9 degradation with KI-CDK9d-32 is more effective than inhibition in disrupting MYC transcriptional networks and causes MYC downregulation and nucleolar destabilization.

The paper identifies genetic vulnerabilities linked to transcription factor activities in cancer cell lines using CRISPR knockout data and validates targets associated with TEAD1.