The Gastrointestinal Cancer (GI) Program of the Mayo Clinic Cancer Center (MCCC) continues to make significant contributions in the areas of basic, translational, and clinical research by using a multidisciplinary and interactive team approach. The primary objective of the GI Program is to use novel observations, mechanistic insights and research outcomes to benefit patients with GI cancers or at risk for GI malignancies, including those from our catchment area. This work is accomplished through robust intra- and interprogrammatic interactions focused on 4 Aims: 1) application of early detection approaches, 2) identification and evaluation of predictive or prognostic biomarkers, 3) role of the tumor microenvironment and microbiome in cancer development and progression, and 4) individualized therapeutic strategies.
Aim 3 is a new and evolving effort that builds upon an existing base of NCI-funded investigators in these fields of research, and interacts with the Microbiome Program within the Mayo Clinic Center for Individualized Medicine to expand the existing germ-free mouse facility and a metabolomics core lab. The GI Program consists of 54 members from 17 departments. Our GI Program developed a SPORE grant in Pancreatic Cancer where major contributions and interactions continue. The GI Program also developed a Hepatobiliary (HB) SPORE proposal that received a highly competitive score with a funding decision expected in mid-2018. As a result of this score, the MCCC was awarded a CCSG supplement of $750K from the NCI with an aim to maintain the infrastructure for liver cancer research. Our NIH-funded research platform and portfolio of innovative clinical trials is expanding and benefits from interactions across the 3 MCCC sites and with other multi-institutional networks; these interactions are enhancing accrual. The GI research program is supported by total direct funding of $10.2M ($5.1M peer-reviewed, with 69% from NCI). Since 2013, Program members have contributed more than 871 publications to the literature, of which 28% represent intraprogrammatic and 31% reflect interprogrammatic collaborations; 21% are in journals with an impact factor ?10. These publications reflect numerous scientific accomplishments and discoveries, several of which have been practice changing. Formal mentoring of junior faculty continues with an increased effort to provide pilot grant funding to our investigators.
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|Geller, James I; Fox, Elizabeth; Turpin, Brian K et al. (2018) A study of axitinib, a VEGF receptor tyrosine kinase inhibitor, in children and adolescents with recurrent or refractory solid tumors: A Children's Oncology Group phase 1 and pilot consortium trial (ADVL1315). Cancer 124:4548-4555|
|Luchtel, Rebecca A; Dasari, Surendra; Oishi, Naoki et al. (2018) Molecular profiling reveals immunogenic cues in anaplastic large cell lymphomas with DUSP22 rearrangements. Blood 132:1386-1398|
|Oishi, Naoki; Brody, Garry S; Ketterling, Rhett P et al. (2018) Genetic subtyping of breast implant-associated anaplastic large cell lymphoma. Blood 132:544-547|
|DuBois, Steven G; Mosse, Yael P; Fox, Elizabeth et al. (2018) Phase II Trial of Alisertib in Combination with Irinotecan and Temozolomide for Patients with Relapsed or Refractory Neuroblastoma. Clin Cancer Res 24:6142-6149|
|Farber, Benjamin A; Lalazar, Gadi; Simon, Elana P et al. (2018) Non coding RNA analysis in fibrolamellar hepatocellular carcinoma. Oncotarget 9:10211-10227|
|Lu, Yingchang; Beeghly-Fadiel, Alicia; Wu, Lang et al. (2018) A Transcriptome-Wide Association Study Among 97,898 Women to Identify Candidate Susceptibility Genes for Epithelial Ovarian Cancer Risk. Cancer Res 78:5419-5430|
|Dasari, Surendra; Newsom, Sean A; Ehrlicher, Sarah E et al. (2018) Remodeling of skeletal muscle mitochondrial proteome with high-fat diet involves greater changes to ?-oxidation than electron transfer proteins in mice. Am J Physiol Endocrinol Metab 315:E425-E434|
|Nowsheen, Somaira; Aziz, Khaled; Aziz, Asef et al. (2018) L3MBTL2 orchestrates ubiquitin signalling by dictating the sequential recruitment of RNF8 and RNF168 after DNA damage. Nat Cell Biol 20:455-464|
|Razidlo, Gina L; Burton, Kevin M; McNiven, Mark A (2018) Interleukin-6 promotes pancreatic cancer cell migration by rapidly activating the small GTPase CDC42. J Biol Chem 293:11143-11153|
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