June 28 (UPI) — A drug being tested for use against several cancers was found to be effective at reversing drug resistance in head and neck skin cancers, according to a study.
Researchers at the University of Queensland in Australia found the protein E2F7 was controlling drug resistance in the affected cells. The researchers, who published their findings Wednesday in the journal Science Translational Medicine, added selinexor to an existing anthracycline chemotherapy treatment and found that squamous cell cancers started to respond to treatment.
In April, the U.S. Food and Drug Administration gave fast-track designation to Karyopharm Therapeutics for the drug to be used with patients with multiple myeloma and who received at least three prior lines of therapy. The drug, which is available in oral form, has also been tested with in patients with gynecological malignancies, glioblastoma, head and neck squamous cell carcinomas, libosarcomas and lymphoma.
Head and neck cancer occurs when abnormal cells grow from the squamous cells in the the skin’s outermost layer, the epidermis. These cancers are in the mouth, nose, throat, larynx, sinuses or salivary glands.
An estimated 13,740 people — 10,250 men and 3,490 women — will die from head and neck cancers this year, with the two most significant risk factors for the diseases being alcohol and tobacco use.
The overall five-year survival rate for head and neck cancers is 56 percent in white people and 34 percent in African Americans, according to the ModernMedicine Network, but researchers say that if they can improve the efficacy of treatments this could improve.
“The drugs used to treat squamous cell carcinomas that have spread to other parts of the body only work for a small fraction of patients,” Dr. Nicholas Saunders, associate professor of the Queensland Diamantina Institute, said in a press release.
He notes the disease is only curable if diagnosed early, but finding a defect in the cell protein will help improve the number of people whose treatment is effective and their post-treatment survival — and more than 80 percent the researchers looked at had the defect.
“We discovered that in most squamous carcinomas E2F7 is pumped out of the nucleus, meaning it can no longer stop drug resistance occurring,” Saunders said. “By administering a drug that helps to keep E2F7 in the nucleus, the cancer cells become sensitive to existing chemotherapeutics.”