Clinical Research Papers:
Combination epigenetic therapy in metastatic colorectal cancer (mCRC) with subcutaneous 5-azacitidine and entinostat: a phase 2 consortium/stand Up 2 cancer study
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Abstract
Nilofer S. Azad1, Anthony el-Khoueiry2, Jun Yin3, Ann L. Oberg3, Patrick Flynn4, Douglas Adkins5, Anup Sharma1, Daniel J. Weisenberger2, Thomas Brown1, Prakriti Medvari1, Peter A. Jones6, Hariharan Easwaran1, Ihab Kamel1, Nathan Bahary7, George Kim8, Joel Picus9, Henry C. Pitot3, Charles Erlichman3, Ross Donehower1, Hui Shen6, Peter W. Laird6, Richard Piekarz9, Stephen Baylin1 and Nita Ahuja1
1 Johns Hopkins University, Baltimore, MD, USA
2 University of Southern California, Los Angeles, CA, USA
3 Mayo Clinic, Rochestor, MN, USA
4 Metro-Minnesota CCOP, Minneapolis, MN, USA
5 Washington University, St. Louis, MO, USA
6 Van Andel Research Institute, Grand Rapids, MI, USA
7 University of Pittsburgh, Pittsburgh, PA, USA
8 Mayo Clinic, Jacksonville, FL, USA
9 Washington University, St. Louis, MO, USA
10 Cancer Therapy Evaluation Program, National Cancer Institute, Bethesda, MD, USA
Correspondence to:
Nilofer S. Azad, email:
Keywords: epigenetics, colorectal cancer, DNA methyltransferases inhibitors, histone deacetylase inhibitors
Received: August 11, 2016 Accepted: October 25, 2016 Published: February 05, 2017
Abstract
Purpose: Therapy with demethylating agent 5-azacitidine and histone deacetylase inhibitor entinostat shows synergistic re-expression of tumor-suppressor genes and growth inhibition in colorectal (CRC) cell lines and in vivo studies.
Experimental Design: We conducted a phase II, multi-institutional study of the combination in metastatic CRC patients. Subcutaneous azacitidine was administered at 40 mg/m2 days 1-5 and 8-10 and entinostat was given 7 mg orally on days 3 and 10. An interim analysis indicated toxicity crossed the pre-specified safety boundary but was secondary to disease. A 2nd cohort with added eligibility restrictions was accrued: prior therapies were limited to no more than 2 or 3 (KRAS-mutated and KRAS-wildtype cancers, respectively) and <30% of liver involvement. The primary endpoint was RECIST response. Serial biopsies were performed at baseline and after 2 cycles of therapy.
Results: Forty-seven patients were enrolled (24:Cohort 1, 23:Cohort 2). Patients were heavily pre-treated (median prior therapies 4: Cohort 1 and 2.5: cohort 2). No responses were observed. Median progression-free survival was 1.9 months; overall survival was 5.6 and 8.3 months in Cohorts 1 and 2, respectively. Toxicity was tolerable and as expected. Unsupervised cluster analysis of serial tumor biopsies suggested greater DNA demethylation in patients with PFS above the median.
Conclusion: In this first trial of CRC patients with combination epigenetic therapy, we show tolerable therapy without significant clinical activity as determined by RECIST responses. Reversal of hypermethylation was seen in a subset of patients and correlated with improved PFS.
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