Author Manuscript Published OnlineFirst on July 8, 2020; DOI: 10.1158/0008-5472.CAN-20-0108 Author manuscripts have been peer reviewed and accepted for publication but have not yet been edited. Cellular senescence promotes skin carcinogenesis through p38MAPK and p44/p42 MAPK signaling Fatouma Alimirah1, Tanya Pulido1, Alexis Valdovinos1, Sena Alptekin1,2, Emily Chang1, Elijah Jones1, Diego A. Diaz1, Jose Flores1, Michael C. Velarde1,3, Marco Demaria1,4, Albert R. Davalos1, Christopher D. Wiley1, Chandani Limbad1, Pierre-Yves Desprez1, and Judith Campisi1,5* 1Buck Institute for Research on Aging, Novato, CA 94945, USA 2Dokuz Eylul University School of Medicine, Izmir 35340, Turkey 3Institute of Biology, University of the Philippines Diliman, College of Science, Quezon City 1101, Philippines 4European Research Institute for the Biology of Ageing, University Medical Center Groningen, Groningen, the Netherlands 5Biosciences Division, Lawrence Berkeley National Laboratory, Berkeley, CA 94720, USA *Lead Contact: Judith Campisi, Buck Institute for Research on Aging, 8001 Redwood Boulevard, Novato, CA 94945, USA; Email:
[email protected] or
[email protected]. Telephone: 1-415-209-2066; Fax: 1-415-493-3640 Running title: Senescence and skin carcinogenesis Key words: doxorubicin, senescence-associated secretory phenotype, squamous cell carcinoma, microenvironment, inflammation, transgenic mice, tumorspheres Conflict of Interests JC is a co-founder of Unity Biotechnology and MD owns equity in Unity Biotechnology. All other authors declare no competing financial interests. Downloaded from cancerres.aacrjournals.org on September 25, 2021. © 2020 American Association for Cancer Research. Author Manuscript Published OnlineFirst on July 8, 2020; DOI: 10.1158/0008-5472.CAN-20-0108 Author manuscripts have been peer reviewed and accepted for publication but have not yet been edited.