Modified Citrus Pectin Shows Potential in Relapsed Prostate Cancer Patients, Study Suggests

Modified Citrus Pectin Shows Potential in Relapsed Prostate Cancer Patients, Study Suggests
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Treament with modified citrus pectin (MCP), a nutritional supplement, led to promising results in men with recurrent prostate cancer, according to preliminary results from a Phase 2b trial.

The study with the results, “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,” was published in the Journal of Clinical Oncology in conjunction with the 2017 ASCO (American Society of Clinical Oncology) Annual Meeting in Chicago.

The protein PSA (prostate specific antigen) is made only by the prostate gland. Although the increase in PSA production is not exclusive to prostate cancer, its measurement is a valuable tool in cancer screening. Therefore, assessing the PSA doubling time (PSADT) is a viable measure of tumor growth in patients whose prostate has been targeted with surgery and/or radiation. The PSADT reflects the time taken by the number of tumor cells to duplicate.

Current treatment options for patients with biochemically relapsed prostate cancer (BRPC; rising PSA levels), such as androgen deprivation therapy, have significant toxicity concerns. That’s why new non-toxic therapies are being investigated.

Pectin is extracted from the pith of citrus fruit peels and is subjected to a modification process to ease its entrance in the bloodstream. PectaSol-C MCP (or P-MCP) inhibits galectin-3, a carbohydrate-binding protein, which is involved in cancer development and inflammation.

Preliminary data indicates that P-MCP is active in prostate cancer. But its safety and effect on PSA dynamics in patients with BRPC had not been tested.

The clinical trial performed at Meir Medical Center in Kfar-Saba, Israel, included 35 patients from multiple cancer centers with non-metastatic biochemical relapse. Patients had a median age of 74 years. P-MCP was given orally three times per day. Patients who did not show disease worsening either clinically, biochemically (PSA), or radiologically at six months were treated for another 12 months.

Results at six months of treatment showed that P-MCP slowed PSA doubling time in 79 percent of non-metastatic patients and halted growth or induced a decrease in size in 62 percent of patients. Final results of the clinical trial are expected at 18 months of treatment.

“This study confirmed the results seen in two previous smaller studies,” Moshe Frenkel, MD, co-investigator of the trial and clinical associate professor at the University of Texas Medical Branch, said in a press release.

“We are constantly looking for natural options that affect cancer progression with minimal side effects. Based on the intermediary findings of the study, MCP has the potential to fall into this category with patients affected by prostate cancer,” added Frenkel, who is also the director of the Complementary and Integrative Medicine Unit in the Institute of Oncology at Meir Medical Center.

José is a science news writer with a PhD in Neuroscience from Universidade of Porto, in Portugal. He has also studied Biochemistry at Universidade do Porto and was a postdoctoral associate at Weill Cornell Medicine, in New York, and at The University of Western Ontario in London, Ontario, Canada. His work has ranged from the association of central cardiovascular and pain control to the neurobiological basis of hypertension, and the molecular pathways driving Alzheimer’s disease.
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José is a science news writer with a PhD in Neuroscience from Universidade of Porto, in Portugal. He has also studied Biochemistry at Universidade do Porto and was a postdoctoral associate at Weill Cornell Medicine, in New York, and at The University of Western Ontario in London, Ontario, Canada. His work has ranged from the association of central cardiovascular and pain control to the neurobiological basis of hypertension, and the molecular pathways driving Alzheimer’s disease.
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