The following tidbit may have greater significance for scientists attempting to introduce novel cancer treatments. Investigators from the University of Colorado Cancer Center claim that a class of drugs thought to kill cancer cells block ‘cross talk’ between the cancer cell and normal immune cells that results in a decline of cancer growth as well as spread. The study findings can probably alter the way cancer drugs are developed.
Endothelin-A receptor antagonist drugs are apparently capable of only halting the start of cancer spread to other organs, not treating large, established primary-or distant-site tumors. Scientists believe that these drugs block the ‘tumor host interactions’ at sites of metastasis that declines tumor growth at these locations. It is known that endothelin-A receptor antagonist medications hinder the action of the endothelin 1 [ET-1] protein. This protein is possibly involved in stimulating cancer cell growth and spread.
Dan Theodorescu, MD, PhD, director of the University of Colorado Cancer Center and professor of surgery and pharmacology at the University of Colorado School of Medicine, lead investigator, shared, “Had we known this before the trials, we wouldn’t have used them to try to reduce large, established tumors. We would have used them to try to suppress the appearance of metastasis. This new information has important implications for how we test drugs for effectiveness before human use and then on how we select patients in clinical trials with these agents, especially since many types of cancer secrete ET-1.”
During the research, scientists found that ET-1 attracts immune cells called macrophages to cancer cells lodged in the lungs. The macrophages seemingly start making factors that stimulate the cancer cells in the lungs to grow termed as metastatic colonization. It is assumed that metastatic colonization decreases the patient’s chance of survival considerably. Two endothelin-A receptor antagonist drugs Abbott’s atrasentan and AstraZeneca’s zibotentan supposedly had complications in large phase 3 clinical trials.