Phase I study of an oral histone deacetylase inhibitor, suberoylanilide hydroxamic acid, in patients with advanced cancer.

By W. Kelly, O. O'Connor, M. Krug, J. Chiao, M. Heaney, Tracy, Curley, Barbara MacGregore-Cortelli, W. Tong, J. Secrist and 8 more. Journal of Clinical Oncology, 2005

913 citations recorded by the source corpus.

Subfields: Cancer Research, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/e9097e4e33ba58a34f1fbeab6bddc2e26969f23c

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Citations in the corpus

Discovery and development of SAHA as an anticancer agent (2007, background): “SAHA showed activity in hematologic malignancies including Hodgkin's disease, nonHodgkin's lymphomas and cutaneous T-cell lymphoma (CTCL) and in patients with solid tumors including thyroid, renal cell, mesothelioma, laryngeal and urothelial carcinomas ( Table 3 ) (”
Phase IIb multicenter trial of vorinostat in patients with persistent, progressive, or treatment refractory cutaneous T-cell lymphoma. (2007, background): “In phase I studies, vorinostat has been generally well-tolerated with dose-limiting toxicities of anorexia, dehydration, diarrhea, fatigue, nausea, vomiting, and thrombocytopenia.(7,15-18) In these trials, activity was observed in patients with solid and hematologic malignancies, including CTCL.”
Histone Deacetylase Inhibitors: Overview and Perspectives (2007, neutral): “(66) and orally administered drug (67).”
Phase 2 trial of oral vorinostat (suberoylanilide hydroxamic acid, SAHA) for refractory cutaneous T-cell lymphoma (CTCL). (2007, neutral): “Thrombocytopenia 20 (54) 10 (27) 3 (8) 4 (11) 3 (8)”
Dimethyl sulfoxide to vorinostat: development of this histone deacetylase inhibitor as an anticancer drug (2007, background): “In phase 1/2 clinical trials, SAHA has shown significant anticancer activity in both hematologic and solid tumors at doses well tolerated by patient”
Histone Deacetylase Inhibitors in Clinical Studies as Templates for New Anticancer Agents (2015, background): “For hematological malignancies, vorinostat can be given orally with a maximum tolerated dose of 400 mg once daily or 200 mg twice daily, but the dose level can be increased up to 600 mg in solid tumors [36].”
Histone deacetylase inhibitors and the promise of epigenetic (and more) treatments for cancer (2006, background): “, should serve as indicators of effectiveness, but these need to be validated clinically and do not always seem to correlate strictly with pharmacokinetic profile”