Chemotherapy kills tumor cells, but it also causes very serious damage to the rest of the body. A team of researchers led by Igor? A team of researchers led by Roninson at the University of South Carolina School of Pharmacy has just published research finding a new class of drugs that can reduce the adverse effects of chemotherapy on cells. Traditional anti-cancer drugs, while currently the mainstay of cancer treatment, have side effects that can damage healthy cells and cause the growth of surviving cancer cells. Conventional drugs cause cancer to resurface, in part because they damage both tumor cells and the patient’s normal tissues, leading to many changes including aging in cells damaged by the drugs. Cellular senescence or aging can result and can also be induced by conventional anti-cancer drugs and other factors that cause DNA damage. Senescent cells and other damaged cells have been shown to be a class of cells associated with the production of cancer as well as other diseases such as Alzheimer’s and arthritis. Recent studies have convincingly demonstrated the importance of the secretion of bioactive factors by these senescent cells, but there is no practical way to stop this pattern from arising. In this latest study, a series of chemicals inhibited the senescence of damaged cells and their secretion patterns. This inhibition is key to reducing the cancer-promoting effects of chemotherapy. University of Athens (Greece) co-author Hippokratis Kiaris performed the usual anti-cancer drug treatment in mice that recovered from this treatment after both drug-treated and untreated mice were injected with cancer cells. Strikingly, the tumors of the mice pretreated with anticancer drugs were more effective than those of the untreated mice. In addition, the anti-cancer drug pretreated mice had higher levels of proteins in their blood that stimulated tumor cell growth. However, tumor growth and production of tumor-supporting growth factors were inhibited after the mice were given a drug called Senexin A. Also Senexin A improved the antitumor efficacy of conventional drugs. The protein of action of Senexin A is CDK8 (cell cycle protein-dependent kinase 8). Senexin A is the first selective inhibitor of CDK8, which, unlike other known CDK family kinases, does not play a role in cell division, although it is involved in the regulation of gene expression. Previous studies have confirmed that CDK8 plays an important role in cancer types such as colon cancer and melanoma. The team found a strong association between CDK8 gene expression and the duration of non-recurrence survival in patients with breast and ovarian cancer. The results of this latest study confirm that CDK8 is associated with injury and aging-induced carcinogenesis supporting protein production, and that new drugs in the CDK8 inhibitory class have the potential to provide therapeutic benefits for different types of cancer.