Eisenman Lab

Fred Hutchinson Cancer Center

Seattle · United States

NIH-funded
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NIH R01 · 2024

Investigating Max as a tumor suppressor gene in small cell lung cancer and other neuroendocrine tumors

SUMMARY Dysregulated expression of the MYC family of transcriptional regulators is a common denominator in a wide spectrum of human cancers, including small cell lung carcinoma (SCLC), a highly aggressive neuroendocrine- type tumor that is among the leading causes of US cancer mortality. MYC family proteins specifically heterodimerize with MAX in order to bind genomic DNA and stimulate widespread transcription. Surprisingly, recent reports show that MAX is inactivated through deletions and truncating mutations in a significant subset of SCLC and other neuroendocrine cancers. The paradox that MAX may act as a tumor suppressor, but yet be crucial for MYC oncogenicity in SCLC, has important…

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