David Boothman A research from UT Southwestern Medical Center claims that a natural protein, altering development factor beta1 (TGF-ß1), which could usually curb the development of cancer cells apparently causes a rebound effect following an extended exposure. Cancer cells supposedly get into an overdrive and become even more hostile and probably spread.

The method for this turnaround is unidentified but researchers believe that cancerous cells could trigger a cover mechanism in reaction to the deadly protein. This procedure apparently switches on a flow of cancer-promoting genes. But clinicians could use this rebound for enhanced treatments.

Dr. David Boothman, co-senior author of the research, professor of radiation oncology and pharmacology and associate director of translational research in the Harold C. Simmons Comprehensive Cancer Center at UT Southwestern, commented, “These genetic changes would start prior to metastases, so if we detect them early, we might be able to tailor treatment in anticipation of a more aggressive cancer.”

The research was presumably performed on cells from mice and in samples from women with metastatic breast cancer.

TGF-ß1 seemingly manages several cellular functions, counting cell growth, cell proliferation and normal cell death. It could also work to repress tumors and avert cancers from scattering.

The researchers, counting co-senior colleague Dr. Lindsey Mayo from the Indiana University School of Medicine, apparently analyzed a surge of biochemical responses in cells uncovered to TGF-ß1. They assumed that lengthened exposure could switch on a specific cancer-causing gene, which in turn, could generate other cancer-supporting reactions.

In tissue from women with metastatic breast cancer, around 60 percent of the patients apparently exhibited both TGF-ß1 action and elevated levels of the cancer-causing gene. The team also observed nutlin3, a protein that could obstruct the act of the cancer-causing gene. They discovered that nutlin3 apparently obstructs the cancer-boosting effects of lasting TGF-ß1 exposure, thereby averting metastasis and destroying cancer cells.

Additional research could be required to verify whether nutlin3 might be worth developing more as an anti-cancer drug.

The research would appear in the Journal of Clinical Investigation.