2 results match your criteria: "Brigham and Women's Hospital and Dana-Faber Cancer Institute[Affiliation]"

Pivotal role of augmented αB-crystallin in tumor development induced by deficient TSC1/2 complex.

Oncogene

August 2014

State Key Laboratory of Medical Molecular Biology, Department of Physiology and Pathophysiology, Institute of Basic Medical Sciences and School of Basic Medicine, Graduate School of Peking Union Medical College, Peking Union Medical College and Chinese Academy of Medical Sciences, Beijing, China.

Tuberous sclerosis complex 1 (TSC1) and TSC2 are suppressors of mechanistic target of rapamycin (mTOR). mTOR is the major component of two protein complexes: mTOR complex 1 (mTORC1) and mTORC2. Inactive mutation of either TSC1 or TSC2 unleashes mTOR signaling and consequently causes TSC, a benign tumor syndrome affecting multiple organs.

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Background: Use of 5 mg/day finasteride (Proscar) for benign prostatic hyperplasia is known to affect serum concentrations of prostate-specific antigen (PSA). When men taking this treatment undergo screening for prostate cancer, a compensatory adjustment of the PSA concentration (to multiply the value by two) is recommended. Whether this recommendation should apply to men taking 1 mg/day finasteride (Propecia) for the treatment of androgenic alopecia is unknown.

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