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ELYS, a multifunctional protein with critical roles in the cell cycle, is essential for the vigorous proliferation and survival of difficult-to-treat cancers carrying mutations in the KRAS oncogene, making it a compelling target for novel drug treatments.

Cancer cells driven by mutations in KRAS or EGFR are dependent on DUSP6 to prevent ERK-induced cell death, creating a novel vulnerability for targeted therapy.

Environmental cues, not oncogene-induced senescence, may stop melanocytes with an activating mutation in the BRAF gene from turning into melanoma.

The tumor suppressor p53 prevents tumor cell growth by employing a small RNA called miR-139-5p to inhibit the activity of an tumorigenic protein, cAMP-specific phosphodiesterase 4D.

Loss-of-function screening identified transglutaminase 2 (TGM2) as a putative tumor suppressor in the TP53 pathway and revealed that TGM2-mediated autophagy and CDKN1A-mediated cell cycle arrest are two critical barriers that prevent oncogenic transformation.

A functional ovarian-specific PAX8-centric regulon is susceptible to FDA-approved HDAC inhibitors, providing the rationale to target human cancers driven by lineage-survival oncogenes with epigenetic therapeutics perturbing the enhancer topology.

BRD9 provides the first actionable therapeutic target in synovial sarcoma tumours that is both biochemically and functionally linked to the SS18-SSX fusion protein which drives disease development.

The protein IFI6 regulates DNA replication via the transcription factor E2F2, which is necessary for transformation and growth of melanomas induced by the NRASQ61K mutant oncogene product.

ST recruitment of STRIPAK facilitates PP2A-mediated dephosphorylation of MAP4K4 and induces cell transformation highlighting that STRIPAK complex plays a key role in defining PP2A specificity and activity.

Overexpression of inhibitor of Bruton's tyrosine kinase contributes to the process of tumorigenesis by amplifying translation, represents a promising target for anti-cancer therapies.