Functional Tumor Cell Profiling (FTCP)

Doctor offers new test to find best personal cancer treatments
A California based cancer physician is offering a new test that could tell which cancer drugs will be most effective on an individual patient’s cancer. This approach could lead to improved treatment of mesothelioma in the future.

Dr. Larry Weisenthal's new series of tests, called Functional Tumor Cell Profiling (FTCP), is a process that takes live cancer cells from a patient and exposes them to a series of anti-cancer drugs to see which will work and which won’t. FTCP could save patients and doctors time and money, while avoiding painful and ineffective treatments.

FTCP incubates cancer cells (a gram being the recommended amount) over a 96 hour period. During this time, the sample is exposed to more than twenty different anti-cancer drugs, and in some cases, combinations of drugs. After each drug is used on the sample in multiple doses (to ensure accuracy), three different methods are used to measure the effectiveness of the drug. The results are then compared to the Weisenthal Cancer Group index database. Using this information, Dr. Weisenthal rules out which cancer treatments won’t work, and recommends which show promise.

Weisenthal, evaluates all the samples himself, spending 6-8 hours on each one. For Dr. Weisenthal and his team to use FTCP, they must receive a live cancer specimen, preferably a solid mass, although malignant effusions are often useable as well. The cost of the procedure is around $5000. Medicare covers the process, as do most insurers. For more information, visit weisenthalcancer.com

Stopping cancer regrowth
Scientists have long been perplexed by the ability of cancerous tumors to regenerate so quickly after chemotherapy. This is one reason mesothelioma is such a tough disease. New research with mice subjects indicate that the body’s own defense mechanisms help the tumors rebound. The University of Toronto researches who conducted the study also believe their work points to a new set of drugs that could minimize this unwanted side effect of chemotherapy.

"Chemotherapy remains the most commonly employed form of systemic cancer treatment. However, although partial or complete shrinkage of tumor mass is frequently induced in chemotherapy-responsive tumors, survival benefits of such responses can be compromised by rapid regrowth of the drug-treated tumors," says senior study author Dr. Robert S. Kerbel of the Sunnybrook Health Sciences Centre in Toronto.

Kerbel and his team found that many chemotherapeutic treatments not only attack the cancer in a patient, but the blood vessels around the site that supply the tissue with nutrients and oxygen. In theory this would be beneficial—as a way to cut off the cancer’s supply lines—but in reality the body reacts in a way that actually makes sure the tumor receives more of the body’s resources after chemotherapy is over.

As a defense mechanism, the body directs “circulating endothelial progenitor" (CEP) cells to the damaged blood vessels around the tumor. CEP cells are blood vessel precursors, and they repopulate the area and enable the tumor to receive the blood and oxygen it needs to regrow.

The process of sending CEP cells to the site begins with a cellular growth factor called SDF-1alpha. Anti-angiogenic drugs that block the formation of blood vessels or a compound that specifically targeted SDF-1alpha, used in concert with chemotherapy, could reduce the chances of cancer regrowth.

"We view this as a yin-yang, action-reaction situation," Kerbel said. "The primary action is the effect of the drug on the tumor. The reaction is the host response, which compromises part of the action, and you want to blunt that with an antiangiogenic drug and/or something targeting this [protein] SDF-1. That's what this paper is all about."

The new research could help explain why some antiangiogenic drugs work well with chemotherapy, while others do not. "Several hypotheses have been proposed to explain how antiangiogenic drugs enhance the treatment efficacy of cytotoxic chemotherapy, including impairing the ability of chemotherapy-responsive tumors to regrow after therapy," explained co- author Dr. Yuval Shaked.

The new research helps scientists understand the process that the antiangiogenic drugs are trying to correct, thereby helping to explain why some combinations of chemotherapy and antiangiogenic drugs are more effective than others.

“Our findings provide a potential explanation of why not all chemotherapy drugs will necessarily have their efficacy enhanced by the addition of an antiangiogenic agent when the mechanism involves blunting CEP mobilization acutely induced by the chemotherapy drug," Kerbel said.

The research appeared in the Sept. 9, 2008 edition of the Journal Cancer Cell.