IBA researchers discovered a new function of the well-established tumor suppressor p16INK4A in cervical carcinoma cells. Somehow counter-intuitively, depletion of the tumor suppressor protein p16INK4A  was shown to inhibit the proliferation of HeLa cervical carcinoma cells and to send these cells into cellular senescence. Researchers of the Jansen-Dürr group further identified a new molecular mechanism underlying this seemingly paradoxical effect, by demonstrating that p16INK4A is required to maintain high-level expression of the human papillomavirus E7 oncogene which is known as an essential driver of cervical carcinogenesis. Together these findings provide new insight into molecular pathways driving cervical carcinoma and may explain the well-known fact that p16INK4A, although acting as tumor suppressor in other cancers, is highly expressed in most if not all cervical carcinomas.