:: Posted by American Biotechnologist on 04-19-2013
Researchers at UT Southwestern Medical Center have found that alternative splicing – a process that allows a single gene to code for multiple proteins – appears to be a new potential target for anti-telomerase cancer therapy.
The enzyme telomerase is overexpressed in almost all cancer cells, and previous research efforts have failed to identify good telomerase inhibitors. The study by Dr. Woodring Wright and UT Southwestern colleagues in the April 4 issue of Cell Reports identifies a new approach for inhibiting telomerase, which is an enzyme that drives uncontrolled division and replication of cancer cells.
:: Posted by American Biotechnologist on 03-14-2013
Researchers have discovered a unique monoclonal antibody that can effectively reach inside a cancer cell, a key goal for these important anticancer agents, since most proteins that cause cancer or are associated with cancer are buried inside cancer cells. Scientists from Memorial Sloan-Kettering Cancer Center and Eureka Therapeutics have collaborated to create the new human monoclonal antibody, which targets a protein associated with many types of cancer and is of great interest to cancer researchers.
Unlike other human therapeutic monoclonal antibodies, which can target only proteins that remain on the outside of cancer cells, the new monoclonal antibody, called ESK1, targets a protein that resides on the inside of the cell.
:: Posted by American Biotechnologist on 01-09-2013
First he discovered the double helix, now he hopes to find a cure for cancer. In what has been billed as his “most important work since the double helix,” James Watson recently elaborated upon the dual role of reactive oxygen species (ROS) as both an elixer of life and a deadly force behind incurable mesenchymal cancers.
Although antioxidants have been popularly promoted as important health food choices, Dr. Watson writes that they can be quite harmful in late stage cancer, often causing rapid progression of the disease.
According to Watson, cancers that become resistant to chemotherapeutic treatment, simultaneously become resistant to ionizing radiotherapy due to the action of ROS to induce apoptosis. Therefore, the key to curing cancer will largely depend upon discovering new ways of reducing antioxidant levels.
:: Posted by American Biotechnologist on 10-09-2012
Although tumor metastasis causes about 90 percent of cancer deaths, the exact mechanism that allows cancer cells to spread from one part of the body to another is not well understood. One key question is how tumor cells detach from the structural elements that normally hold tissues in place, then reattach themselves in a new site.
A new study from MIT cancer researchers reveals some of the cellular adhesion molecules that are critical to this process. The findings, published Oct. 9 in Nature Communications, offer potential new cancer drug targets, says Sangeeta Bhatia, the John and Dorothy Wilson Professor of Health Sciences and Technology and Electrical Engineering and Computer Science, and leader of the research team.
:: Posted by American Biotechnologist on 08-14-2012
To survive, tumors need blood supply to provide them with nutrients and oxygen. To get that supply, cancer cells stimulate new blood vessel growth—a process called tumor angiogenesis. Many attempts have been made to inhibit this process as a means to choke off tumors. But tumor angiogenesis can be sloppy, resulting in immature and malformed blood vessels. Since anti-cancer drugs are carried to tumors by the bloodstream, abnormal blood vessel development also hampers delivery. What if, rather than putting a stop to angiogenesis, we could help tumor blood vessels mature more completely, so tumor-killing therapies could more effectively reach their targets? This counterintuitive concept was proposed several years ago, but researchers lacked a way to do it. Now, in a paper published August 14 in the journal Cancer Cell, Sanford-Burnham researchers found a molecule that promotes the tumor vessel maturation process—a discovery that might provide a method for improving cancer drug delivery.
“Our finding suggests that an ability to regulate this molecule could allow us to solve various problems caused by blood vessel abnormalities, including inefficient drug delivery to tumors,” said Masanobu Komatsu, Ph.D., associate professor at Sanford-Burnham and senior author of the study.