Cancer is commonly referred to as a ?cell biological problem? in which genetic abnormalities or environmental insults induce profound changes in basic cellular functions such as gene regulation, cell division, cell adhesion, receptor signaling and trafficking, and differentiation. The central goal of the Mayo Clinic Cancer Center (MCCC) Cell Biology Program is to define the molecular genetic and cellular basis of neoplastic transformation, growth, and metastasis while providing insights into cell growth and senescence, organ development, chromatin dynamics, and genomic alterations. The MCCC Cell Biology Program includes 34 members from 16 different departments that collectively bring in substantial cancer-based NIH funding ($4.5M directs with 56% from the NCI). These members conduct research across a broad spectrum of cancers, which is focused in 4 specific aims: 1) To investigate the fundamental genetic and epigenetic mechanisms regulating the cell cycle and transcription control in normal, senescent, and neoplastic cells; 2) To elucidate the mechanisms through which cell signaling pathways and receptor endocytic activity promote uncontrolled cell growth; 3) To determine how the crosstalk between cancer cells and their microenvironment promotes cancer growth by regulating neo-angiogenesis, inflammation, immune evasion, and fibrosis; and 4) To understand how cells attach to substrates and to each other, and how these attachments are altered as a cell initiates migration and invasion. The Cell Biology Program studies cellular processes relevant to the development or prevention of a broad spectrum of human cancers and broadly interfaces with other MCCC Programs. In addition to conducting innovative and cutting-edge cancer-relevant research, the Cell Biology Program organizes and sponsors many interactive scientific gatherings, including national and international meetings, and provides a central hub for basic cancer biology at Mayo Clinic. Of the 483 cancer-relevant papers published by our members between 2013 and 2017, 66 were intraprogrammatic and 235 were interprogrammatic, underscoring the high value added by the Program to the Cancer Center.

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Yu, Jia; Qin, Bo; Moyer, Ann M et al. (2018) DNA methyltransferase expression in triple-negative breast cancer predicts sensitivity to decitabine. J Clin Invest 128:2376-2388
Sugihara, Takaaki; Werneburg, Nathan W; Hernandez, Matthew C et al. (2018) YAP Tyrosine Phosphorylation and Nuclear Localization in Cholangiocarcinoma Cells Are Regulated by LCK and Independent of LATS Activity. Mol Cancer Res 16:1556-1567
Natanzon, Yanina; Goode, Ellen L; Cunningham, Julie M (2018) Epigenetics in ovarian cancer. Semin Cancer Biol 51:160-169
Kleinstern, Geffen; Camp, Nicola J; Goldin, Lynn R et al. (2018) Association of polygenic risk score with the risk of chronic lymphocytic leukemia and monoclonal B-cell lymphocytosis. Blood 131:2541-2551
Liu, Gang; Mukherjee, Bhramar; Lee, Seunggeun et al. (2018) Robust Tests for Additive Gene-Environment Interaction in Case-Control Studies Using Gene-Environment Independence. Am J Epidemiol 187:366-377
Ong, Jue-Sheng; Hwang, Liang-Dar; Cuellar-Partida, Gabriel et al. (2018) Assessment of moderate coffee consumption and risk of epithelial ovarian cancer: a Mendelian randomization study. Int J Epidemiol 47:450-459
Kumar, Shaji K; Buadi, Francis K; LaPlant, Betsy et al. (2018) Phase 1/2 trial of ixazomib, cyclophosphamide and dexamethasone in patients with previously untreated symptomatic multiple myeloma. Blood Cancer J 8:70
Schafer, Eric S; Rau, Rachel E; Berg, Stacey et al. (2018) A phase 1 study of eribulin mesylate (E7389), a novel microtubule-targeting chemotherapeutic agent, in children with refractory or recurrent solid tumors: A Children's Oncology Group Phase 1 Consortium study (ADVL1314). Pediatr Blood Cancer 65:e27066
Kalli, Kimberly R; Block, Matthew S; Kasi, Pashtoon M et al. (2018) Folate Receptor Alpha Peptide Vaccine Generates Immunity in Breast and Ovarian Cancer Patients. Clin Cancer Res 24:3014-3025
Wang, Sophia S; Carrington, Mary; Berndt, Sonja I et al. (2018) HLA Class I and II Diversity Contributes to the Etiologic Heterogeneity of Non-Hodgkin Lymphoma Subtypes. Cancer Res 78:4086-4096

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