Exciting New Research Presented at the ASCO GU Symposium on Modified Citrus Pectin!

Published: February 8, 2018 | By Better Health Publishing

Modified Citrus Pectin Shows Significant Benefits in Biochemically Relapsed Prostate Cancer

Research Presented at the American Society of Clinical Oncology Genitourinary Cancer Conference Found Seventy-Nine Percent of Study Participants Experienced a Slowing or No Growth in the Progression of Their Disease; Most Experienced No Growth

(San Francisco, CA – February 8, 2018) Research presented at the American Society of Clinical Oncology (ASCO) Genitourinary Cancer Conference February 8, 2018 showed that 79 percent of study participants whose prostate cancer was progressing experienced results indicating slower or no growth of the disease when taking modified citrus pectin (P-MCP).

“With more than 60 percent of patients in the trial showing no evidence of disease progression, the results imply improvement over historical cohort data. No patient discontinued therapy because of side effects,” said Daniel Keizman, M.D., lead investigator of the multicenter trial study and head of the Genitourinary Oncology Service at Meir Medical Center in Kfar-Saba, Israel.

Of the first 34 patients completing six months of treatment, 27 (79%) showed lengthening of prostate specific antigen (PSA) doubling times, which is a measure of the progression of the disease. These results indicated that P-MCP may be controlling their cancer progression. Twenty-one patients (62%) showed improvement or stabilization of disease, without any progression. In 13 patients (38%), disease progression was seen, with 10 patients (29%) progressing only by PSA and only 3 patients (9%) progressing on bone or CT scans. In addition, P-MCP produced no significant side effects during the study period.

“Following surgery and/or radiation, about 30 percent of prostate cancer patients relapse biochemically with rising PSA levels. The benefit of androgen deprivation therapy, the typical treatment used in this situation, has not been demonstrated and may be offset by significant toxicities,” said Dr. Keizman.

The clinical trial is looking into the effects of P-MCP, which is a form of soluble, dietary fiber. Normal pectin contains long-branched carbohydrate molecules that cannot be absorbed by the gastrointestinal tract. P-MCP is a low molecular weight pectin with shorter fibers, providing greater bioavailability and therapeutic value. In addition, P-MCP has been shown to be active against galectin-3, an inflammatory protein overexpressed in cancer cells and linked to tumorigenesis and metastasis.

In the study, patients with biochemically relapsed prostate cancer, with progressively rising PSA levels in three or more tests, were enrolled in the prospective trial. Participants received 4.8 grams of P-MCP, three times a day, for six months. Since all patients demonstrated progression before the study on consecutive PSA tests, the reduction of PSA doubling time is a promising result.

This research builds on two previous clinical trials showing P-MCP consistently slows PSA level increases. A final analysis of this six-month study is planned for late 2018. Patients who did not progress clinically at six months are being treated for another 12 months. A full report, including 18-month data and correlative analysis, will be released once the data is complete.

“We are happy with the current results suggesting that P-MCP therapy may be active and safe in this setting. We are planning a future phase III randomized trial to assess the clinical benefit of P-MCP treatment in this setting,” says Dr. Keizman.

Source: Effect of PectaSol-C modified citrus pectin (P-MCP) treatment (tx) on PSA dynamics in patients (pts) with nonmetastatic, biochemically relapsed prostate cancer (BRPC): Results of the interim analysis of a prospective phase II study.

Daniel Keizman, Moshe A. Frenkel, Todd Michael Edwards, Eli Rosenbaum, David Margel, David Sarid, Victoria Neiman, Maya Gottfried, Natalie Maimon, Ilan Leibovitch, Hadas Dresler, and Isaac Eliaz. Journal of Clinical Oncology 2017 35:15_suppl, e16588-e16588

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