Dear Colleagues,

More than half a century ago, in 1969, somatic cell hybrid studies by Henry Harris, George Klein, and colleagues provided evidence that cellular factors could regulate the activity of oncogenes in a dominant manner. In 1971, Alfred Knudson proposed that retinoblastomas were caused by two mutational events. It took another dozen years before, in 1983, Webster Cavenee, Ray White, and colleagues provided experimental proof for this “two hit” theory. Two years later, in 1985, Eric Stanbridge proposed naming this newly emerging class of cancer-associated genes “tumor suppressors”. After initial evidence placed tumor protein P53 in the oncogene category, in 1989, Arnold Levine and Bert Vogelstein et al. provided clear evidence that P53 has tumor suppressive activity. Tumor suppressor gene mutations are often associated with familial cancer syndromes. As a result of this new knowledge, the 1990s saw the identification of a number of tumor suppressor genes including APC, NF-1 and -2, VHL, BRCA1 and 2, PTCH, and PTEN. To date, more than 40 tumor suppressor genes have been cloned. Over the past four decades, we have come to understand that tumor suppressors are key regulators of many fundamental cellular processes and that the mutation or dysregulation of one or more tumor suppressors is a key event in the pathogenesis of most human cancers. This Special Issue of Cancers celebrates the long and rich history of tumor suppressor biology and highlights the importance of this class of genes in understanding and addressing current obstacles in cancer treatment. We invite submissions focused on the basic biology or clinical and therapeutic implications of tumor suppressors. Related reviews are also welcome.

Prof. Dr. Kristi L. Neufeld
Dr. Shane Stecklein
Guest Editors

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• tumor suppressor
• cancer