Partnership to Test Genome-Driven Breast Cancer Therapies

(National Cancer Institute)

15 May 2014. Researchers at Indiana University’s medical school in Indianapolis and Paradigm, a genomic sequencing company in Ann Arbor, Michigan are enrolling patients in a clinical study testing the ability of genomic sequencing to find optimal treatments for an aggressive type of breast cancer. The study covers women with triple-negative breast cancer, a form of the disease that does not respond to some of the more frequently used drugs, and where patients are at high risk of relapse after chemotherapy and surgery.

The trial aims to test the ability of genomic sequencing to more precisely identify mutations in the genomic composition of the patients’ tumors, and use those findings to tailor the treatments prescribed for patients. Milan Radovich, a professor of surgery and genetics at Indiana, and one of the study leaders, says in a university statement the trial “will use our understanding of genomics to identify the gas pedal for each woman’s specific cancer and see if we can find a drug that will block the gas pedal in a way that is better than non-specific chemotherapies.”

Paradigm will perform genomic sequencing of the DNA and associated RNA — ribonucleic acid, the molecules that direct the expression of genes — from the tumors following chemotherapy. Sequencing the DNA and RNA of the tumors identifies specific mutations and expression of genes that generate proteins influencing the tumors’ growth.

Half of the patients in the study will receive therapies based on the analysis of the DNA and RNA sequencing, while the other half of the group will receive the usual standard of cancer care. The main measure of efficacy in the trial is two-year disease-free survival rate, but the researchers are also tracking adverse effects of the therapies, toxicity rates from the treatments, and clinical and demographic characteristics of tumor samples.

“If the mutation is taking place in a certain gene or protein that controls a certain function, and if the mutation has caused damage in that pathway,” says Bryan Schneider, professor of medicine at Indiana and co-leader of the study, “one can intuitively pick a drug that may also be interacting in that very same pathway to either try to stop or shut down an overly activated pathway.”

In the following video, Radovich and Schneider tell more about the study.

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