HCQ and Prostate Cancer ? Profncampbell's Blog

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Sub-category:

Prostate Cancer

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Category:

Genitourinary Cancer

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Meeting:

2011 Genitourinary Cancers Symposium

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Session Type and Session Title:

General Poster Session B: Prostate Cancer

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Abstract No:

164

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Citation:

J Clin Oncol 29: 2011 (suppl 7; abstr 164)

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Author(s):

T. McCarthy, T. M. Mayer, M. N. Stein, M. Anand, F. Collins, C. Jeyamohan, D. Metzger, D. Moore, E. White, R. S. DiPaola; Robert Wood Johnson Medical School, Piscataway, NJ; The Cancer Institute of New Jersey/University of Medicine and Dentistry of New Jersey, New Brunswick, NJ

Abstract Disclosures

Abstracts that were granted an exception in accordance with ASCO?s Conflict of Interest Policy are designated with a caret symbol (^) here and in the printed Proceedings.

Abstract:

Background: Autophagy is conserved, genetically controlled catabolic response to starvation and stress whereby cells self- digest intracellular proteins and organelles by targeting them for degradation in lysosomes to generate energy and mitigate damage, thereby supporting cancer cell survival. We hypothesized that HCQ, by blocking autophagy, would slow PC growth. Methods: Pts had rising PSA after primary therapy for PC, no radiographic evidence of metastasis, no (neo)adjuvant ADT within 3 months of enrollment and testosterone > 150 ng/dL. HCQ was dosed at 400 mg/day (cohort 1) or 600 mg/day (cohort 2). Endpoints were PSA response (defined as a change in slope of PSA rise by at least 25%, when log (PSA) is plotted vs. time) and assessment of safety and tolerability. Levels of p62 (which accumulates upon autophagy inhibition) and accumulation of autophagosomes (measured by EM) were assessed in blood mononuclear cells. Results: 38 pts (35 cohort 1; 3 cohort 2) of planned 64 pts with median age 65 (52-81), Gleason scores: 5 (5%), 6 (18%), 7 (55%), 8 (8%), 9 (13%) have been accrued. 30 pts have completed 6 cycles of therapy and 2 pts have completed 4 cycles of HCQ. 14/32 (44%) pts included in the analysis had a decrease in doubling time after treatment. 2 (6%) had declining PSA. Treatment was well tolerated, with grade 1 rash (10%), grade 1 nausea (10%) and grade 1 diarrhea (20%) being the predominant side effects noted. 3 pts had grade 2 toxicities (rash and diarrhea). There were no grade 3/4 toxicities. EM and p62 was assessed in 12 and 20 pts, respectively, and showed evidence of mitochondrial dysfunction and p62 accumulation. Conclusions: HCQ 400 mg/day appears to have some activity in PSA progression after localized therapy with minimal toxicity. Evaluation with higher doses of HCQ is ongoing. Assessing markers of autophagy including EM and p62 are feasible in pts and will require further validation in larger trials.

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Source: http://profncampbell.wordpress.com/2012/02/24/hcq-and-prostate-cancer/

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