The Tumor Microenvironment and Metastasis (TMM) Program is the newest Program at the IU Simon Cancer Center (IUSCC);it arose from our strategic plan and from existing collaborations in a working group originally based in the HMI Program, where interactive investigators looked at solid tumors and metastatic processes. The research goals of TMM are to: 1) advance our basic understanding of the role of cancer cell stromal interactions in cancer initiation, progression and metastasis, 2) evaluate the functions of the metastatic niche, and 3) translate discoveries of the pathobiology of solid tumors, the tumor microenvironment, and the metastatic niche into new cancer targets and novel therapies. The ultimate programmatic goal of TMM is to translate discoveries of the tumor microenvironment's pathophysiology into new cancer targets and appropriately targeted therapies for treating metastatic cancers. Two central themes encompass these goals: 1) Cancer cell-stroma interactions and 2) The metastatic niche. Despite its relatively recent establishment in late 2009, TMM is highly productive and collaborative in its basic and translational approaches to understanding the pathobiology of solid tumors, cancer cell-stroma interactions, the tumor microenvironment, and the metastatic niche. TMM has 25 full and 9 associate members from over 14 departments/divisions on the campuses of Indiana University School of Medicine, lU-Bloomington, and Notre Dame, including: Endocrinology, Dermatology, Biochemistry and Molecular Biology, Division of Hem/Onc (Adult and Peds), Pathology and Laboratory Medicine, Radiology, Anatomy and Cell Biology, Neonatal-Perinatal Medicine, Cellular and Integrative Physiology, Clinical Pharmacology, Medical and Molecular Genetics, OB/GYN, and Chemistry/Biochemistry (Notre Dame). Over this funding period, TMM members have published a total of 453 papers, of which 31.2% represent intra-programmatic collaborations, 35.7% represent interprogrammatic collaborations, and 24.7% represent inter-institutional collaborations. The Program has a total of $8.5M in current peer reviewed funding, with $4.3M from the NCI, $$2.6M from other NIH branches, $1.2M from the Department of Defense, $180K from the ACS, and $250K in other peer-reviewed funding.

National Institute of Health (NIH)
National Cancer Institute (NCI)
Center Core Grants (P30)
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Subcommittee G - Education (NCI)
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Indiana University-Purdue University at Indianapolis
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Kedage, Vivekananda; Selvaraj, Nagarathinam; Nicholas, Taylor R et al. (2016) An Interaction with Ewing's Sarcoma Breakpoint Protein EWS Defines a Specific Oncogenic Mechanism of ETS Factors Rearranged in Prostate Cancer. Cell Rep 17:1289-1301
Nudelman, Kelly N H; McDonald, Brenna C; Wang, Yang et al. (2016) Cerebral Perfusion and Gray Matter Changes Associated With Chemotherapy-Induced Peripheral Neuropathy. J Clin Oncol 34:677-83
Hoggatt, Jonathan; Hoggatt, Amber F; Tate, Tiffany A et al. (2016) Bleeding the laboratory mouse: Not all methods are equal. Exp Hematol 44:132-137.e1
Haley, James; Tomar, Sunil; Pulliam, Nicholas et al. (2016) Functional characterization of a panel of high-grade serous ovarian cancer cell lines as representative experimental models of the disease. Oncotarget 7:32810-20
Radovich, Milan; Solzak, Jeffrey P; Hancock, Bradley A et al. (2016) A large microRNA cluster on chromosome 19 is a transcriptional hallmark of WHO type A and AB thymomas. Br J Cancer 114:477-84
Li, Wei; Liu, Liangyi; Gomez, Aurelie et al. (2016) Proteomics analysis reveals a Th17-prone cell population in presymptomatic graft-versus-host disease. JCI Insight 1:
Champion, Victoria L; Rawl, Susan M; Bourff, Sara A et al. (2016) Randomized trial of DVD, telephone, and usual care for increasing mammography adherence. J Health Psychol 21:916-26
Meijome, Tomas E; Baughman, Jenna T; Hooker, R Adam et al. (2016) C-Mpl Is Expressed on Osteoblasts and Osteoclasts and Is Important in Regulating Skeletal Homeostasis. J Cell Biochem 117:959-69
Richine, B M; Virts, E L; Bowling, J D et al. (2016) Syk kinase and Shp2 phosphatase inhibition cooperate to reduce FLT3-ITD-induced STAT5 activation and proliferation of acute myeloid leukemia. Leukemia 30:2094-2097
Masters, Andrea R; Gufford, Brandon T; Lu, Jessica Bo Li et al. (2016) Chiral Plasma Pharmacokinetics and Urinary Excretion of Bupropion and Metabolites in Healthy Volunteers. J Pharmacol Exp Ther 358:230-8

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