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• W2806087519 abstract "Breast cancer is the most commonly diagnosed malignancy in women. Analysis of breast cancer genomic DNA indicates frequent loss-of-function mutations in components of the cJUN NH2-terminal kinase (JNK) signaling pathway. Since JNK signaling can promote cell proliferation by activating the AP1 transcription factor, this apparent association of reduced JNK signaling with tumor development was unexpected. We examined the effect of JNK deficiency in the murine breast epithelium. Loss of JNK signaling caused genomic instability and the development of breast cancer. Moreover, JNK deficiency caused widespread early neoplasia and rapid tumor formation in a murine model of breast cancer. This tumor suppressive function was not mediated by a role of JNK in the growth of established tumors, but by a requirement of JNK to prevent tumor initiation. Together, these data identify JNK pathway defects as ‘driver’ mutations that promote genome instability and tumor initiation." @default.
• W2806087519 created "2018-06-13" @default.
• W2806087519 creator A5013989394 @default.
• W2806087519 creator A5020468831 @default.
• W2806087519 creator A5033012006 @default.
• W2806087519 creator A5084904672 @default.
• W2806087519 date "2018-06-01" @default.
• W2806087519 modified "2023-10-02" @default.
• W2806087519 title "The cJUN NH2-terminal kinase (JNK) signaling pathway promotes genome stability and prevents tumor initiation" @default.
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• W2806087519 doi "https://doi.org/10.7554/elife.36389" @default.
• W2806087519 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/5984035" @default.
• W2806087519 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/29856313" @default.
• W2806087519 hasPublicationYear "2018" @default.
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