A latest research by Moores Cancer Center at the University of California, San Diego, claims that a molecular signature may assist in accounting for the aggressive behavior of different cancers like pancreatic, breast and melanoma. It may also envisage the probability of successful treatment with a particular anti-cancer drug. The findings could result in a personalized approach to treatment for various solid tumors that may be at present resistant to therapies.
Researchers have found that a receptor sitting on the surface of certain aggressive tumor cells may apparently stimulate a key enzyme, src-kinase, which could assist tumor cells in becoming more aggressive in the body. This enzyme is apparently the aim of the anticancer drug dasatinib, which may obstruct its activity and supposedly at present accepted for treating chronic myelogenous leukemia (CML). The scientists claim that the receptor, a protein known as integrin alpha-v beta-3 on some of the more regular solid tumors such as breast, colon, lung and pancreas may aid in identifying individuals with many other types of cancer, that are also likely to respond to the drug.
David Cheresh, PhD, professor and vice chair of pathology at the UC San Diego School of Medicine and the Moores UCSD Cancer Center, who led the work, commented, “These results could enable us to identify the subpopulation of cancer patients who are likely to respond to treatment with dasatinib. Rather than treat all patients with a given tumor type the same way, by identifying a specific molecular signature consisting of the receptor and its activated enzyme, we can customize the treatment in such a way that we impact the patients most likely to be sensitive to a drug.”
The growth properties of pancreatic and breast cancer cells that supposedly expressed the alpha-v beta-3 receptor was compared by the researchers to those that did not. This led to the detection of a molecular pathway that apparently accounted for the increased tumor.
Cheresh mentioned, “Once we identified the pathway, we immediately realized that the drug dasatinib, which targets this pathway, would be a logical choice to use against these cancers.”
Cheresh stated that when the pathway was identified, it was instantly understood that the drug dasatinib which apparently aims this pathway could be a rational option to use against these cancers. Cheresh pointed to pancreatic cancer tumors, about 60 percent of which apparently carry the marker on the tumor cell surface. But it was apparently seen that tumors lacking the marker seem to be resistant to the drug.
Cheresh remarked, “We would argue that pancreatic cancer patients with alpha-v beta-3 would respond to dasatinib.”
Observing that the marker may be recognized by a biopsy, Cheresh commented, “We discovered an unexpected pathway that accounts for increased malignancy in a population of some of the most dangerous cancers. There are features of the findings that allow us to implicate dasatinib not just for a single tumor type, but for all tumors with the malignant signature.”
These findings have apparently resulted in discussions about the potential design of a clinical trial.
Barbara Parker, MD, medical director of oncology services at the Moores UCSD Cancer Center, mentioned that these observations suggest a strategy for testing the effectiveness of dasatinib in breast cancer patients who are positive for the alpha-v beta-3 receptor.
This research was published in the online edition of Nature Medicine.