Thoughts on this. True or BS.

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DCA Dichloroacetate Breakthrough Anticancer Agent

Mary, an old patient in my office, called in last week to ask for advice about her husband, Jim. He had been quite healthy for many years, and recently noticed back pain. His primary care doctor ordered a CAT scan which showed a large lung mass (Red Arrow Above image) and destructive lesions in the spine. Biopsies confirmed the lung mass was indeed cancer, with metastatic spread to the thoracic vertebral bodies. Jim was referred to the local oncologist who started radiation and chemotherapy. Above Header Image CAT scan of lung cancer mass (Red Arrow) in left lung courtesy of wikimedia commons…

After a week of chemotherapy, Jim was miserable from the adverse effects of nausea, and vomiting, and loss of appetite. Jim felt so bad, he declined any further chemotherapy treatment. Mary asked if I had any suggestions.

Professor Varda Shoshan-Barmatz of the Department of Life Sciences and the founding Director of the NIBN, in collaboration with Dr. Jay Chung of the NIH, have successfully demonstrated that the mitochondrial protein VDAC1 is critical for the release of mitochondrial DNA (mtDNA) associated with the lupus disease.

They demonstrated that restricting of VDAC1 with a newly developed molecule resulted in substantial improvement in pathological aspects of the disease.

“When VDAC1 is over-expressed, as found in several diseases, a large pore composed of several VDAC1 units is formed, allowing the release of pro-cell death factors and mtDNA,” BGU explained in a statement.

Last November, CHIPSA Hospital hosted a unique, first-of-its-kind event celebrating the lives of 22 late stage cancer survivors who, according to doctors, shouldn’t even be alive. Surrounded by world-renowned doctors, scientists, and researchers, these patients shared their inspiring stories of how they healed their terminal disease when conventional treatment had failed them.

CHIPSA is not an ordinary hospital. For one, we take patients who are typically told they have no other treatment options left. We then offer those patients innovative immunotherapies that aren’t available anywhere in the United States.

Our collaborative event highlighted the patients who have benefited from those types of therapies, featuring people on all ends of the treatment spectrum: the researchers who developed them, the doctors who administered them, and the patients who received them.

Antibiotic-resistant bacteria are increasingly the source of deadly infections. A team of scientists from the Technical University of Munich (TUM) and the Helmholtz Center for Infection Research (HZI) in Braunschweig have now modified an approved cancer drug to develop an active agent against multidrug-resistant pathogens.

The methicillin-resistant Staphylococcus aureus (MRSA) is the source of severe and persistent infections. Some strains are even resistant to multiple antibiotics. There is consequently an urgent need for new drugs effective against MRSA infections.

“The industrial development of new antibiotics is stalling and not keeping pace with the spread of antibiotic resistance. We urgently need innovative approaches to meet the need for new infection therapies that do not lead directly to renewed resistance,” says Prof. Eva Medina, director of the HZI Infection Immunology Research Group.

Mount Sinai researchers have designed an innovative experimental therapy that may be able to stop the growth of triple-negative breast cancer, the deadliest type of breast cancer, which has few effective treatment options, according to a study published in Nature Chemical Biology in December.

The therapy is known is MS1943. In a cancer cell line and mouse models, it degraded a protein called EZH2 that drives the growth of triple-negative breast cancer.

Research teams led by Jian Jin, Ph.D., Director of the Mount Sinai Center for Therapeutics Discovery, and Ramon Parsons, MD, Ph.D., Director of The Tisch Cancer Institute at Mount Sinai, developed MS1943 as a first-in-class small-molecule agent that selectively degrades EZH2. They also showed that agents that inhibit the enzymatic activity of EZH2 but do not degrade EZH2 did not work in triple-negative breast cancer.