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MEK1/2

Intermittent Treatment of BRAFV600E Melanoma Cells Delays Resistance by Adaptive Resensitization to Drug Rechallenge

[Proceedings of the National Academy of Sciences of the United States of America] Investigators showed that intermittent treatment with the BRAFV600E inhibitor, LGX818/encorafenib, suppressed growth compared with continuous treatment in human melanoma cells engineered to express BRAFV600E, p61-BRAFV600E, or MEK2C125 oncogenes.

Selumetinib: A Selective MEK1 Inhibitor for Solid Tumor Treatment

[Clinical and Experimental Medicine] The efficacy of selumetinib in various solid tumors such as colorectal cancer, lung cancer, neurofibroma, and melanoma is investigated.

STRAP is a Critical Mediator of APC Mutation-Induced Intestinal Tumorigenesis through a Feed-Forward Mechanism

[Gastroenterology] The authors generated Strap intestinal epithelial knockout mice by crossing mice containing floxed alleles of Strap with Villin-Cre mice. They used human colon cancer cell lines and human and mouse colon tumor-derived organoids for STRAP knockdown/knockout and overexpression experiments.

RASAL2 Confers Collateral MEK/EGFR Dependency in Chemoresistant Triple-Negative Breast Cancer

[Clinical Cancer Research] Scientists performed transcriptional profiling of tumors from a Phase II clinical trial of platinum chemotherapy for advanced TNBC, revealing a gene expression signature that identified de novo chemorefractory tumors.

Implication of Human Endogenous Retrovirus W Family Envelope in Hepatocellular Carcinoma Promotes MEK/ERK-Mediated Metastatic Invasiveness and Doxorubicin Resistance

[Cell Death Discovery] There is no report on the expression pattern and potential mechanism of Syncytin-1 in hepatocellular carcinoma (HCC). Functional experiments in vitro and in vivo demonstrated that Syncytin-1 enhanced cell proliferation, metastasis, and tumorigenicity in HCC.

Probing the Signaling Requirements for Naive Human Pluripotency by High-Throughput Chemical Screening

[Cell Reports] The authors reported that MEK1/2 inhibitors could be replaced during maintenance of naive human pluripotency by inhibitors targeting either upstream or downstream kinases. Naive human ESCs maintained under these alternative conditions displayed elevated levels of ERK phosphorylation but retained genome-wide DNA hypomethylation and a transcriptional identity of the pre-implantation epiblast.

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