The DF/HCC Lung Cancer Program will continue to generate new discoveries in host susceptibility, exposure to pulmonary carcinogens, epidemiology, and pathogenesis of lung cancer, and will apply this information to develop novel prevention and therapeutic strategies to prevent lung cancer and improve the therapies of patients at risk or with lung cancer. The Lung Cancer Program was approved at the time of the last CCSG review in 2005 and was awarded a merit score of excellent to outstanding. The Lung Cancer Program has 60 members representing ten departments of HMS and'HSPH and six member institutions. Members have a broad range of expertise in epidemiology, molecular epidemiology, genetics, cancer biology, clinical trials and outcomes analyses. Program members have had nearly 692 publications in the last five years. Of these 692, 30% are intra-programmatic, 47% are inter-programmatic and 33% are inter-institutional peer-reviewed manuscripts. DF/HCC provides a mechanism for these Lung Cancer Program investigators to develop an interconnected program of population, basic and clinical scientists based on overiapping and interactive areas of expertise. The Lung Cancer Program has nearly $13 million in external support, including more than $6 million in NCI funding and $2.3 million in other peer-reviewed support.
The specific aims for the next five years are to: 1) Identify germline polymorphisms and determine their role in the susceptibility, pathogenesis and response to therapy and survival in lung cancer;2) Define pathogenic mechanisms underlying the development of lung cancer;and 3) Exploit the discoveries in pathogenesis to develop novel therapeutic approaches to thoracic malignancies.
Lung cancer is the leading cause of cancer deaths in the United States. The delineation of the pathogenesis has helped identify driving mutations of lung cancer. The studies proposed in this application will continue to define host susceptibility, the steps involved in the development of cancer and the ability to inhibit these crucial steps to develop clinically effective targeted treatments for individual patients'tumors.
|Hu, Yanhui; Comjean, Aram; Roesel, Charles et al. (2016) FlyRNAi.org-the database of the Drosophila RNAi screening center and transgenic RNAi project: 2017 update. Nucleic Acids Res :|
|Hong, Theodore S; Wo, Jennifer Y; Yeap, Beow Y et al. (2016) Multi-Institutional Phase II Study of High-Dose Hypofractionated Proton Beam Therapy in Patients With Localized, Unresectable Hepatocellular Carcinoma and Intrahepatic Cholangiocarcinoma. J Clin Oncol 34:460-8|
|Freedman, Rachel A; Gelman, Rebecca S; Wefel, Jeffrey S et al. (2016) Translational Breast Cancer Research Consortium (TBCRC) 022: A Phase II Trial of Neratinib for Patients With Human Epidermal Growth Factor Receptor 2-Positive Breast Cancer and Brain Metastases. J Clin Oncol 34:945-52|
|Mohr, Stephanie E; Hu, Yanhui; Ewen-Campen, Benjamin et al. (2016) CRISPR guide RNA design for research applications. FEBS J 283:3232-8|
|Brunner, Andrew M; Li, Shuli; Fathi, Amir T et al. (2016) Haematopoietic cell transplantation with and without sorafenib maintenance for patients with FLT3-ITD acute myeloid leukaemia in first complete remission. Br J Haematol 175:496-504|
|Cox, Andrew G; Hwang, Katie L; Brown, Kristin K et al. (2016) Yap reprograms glutamine metabolism to increase nucleotide biosynthesis and enable liver growth. Nat Cell Biol 18:886-96|
|McKay, Tina B; Hjortdal, Jesper; Sejersen, Henrik et al. (2016) Endocrine and Metabolic Pathways Linked to Keratoconus: Implications for the Role of Hormones in the Stromal Microenvironment. Sci Rep 6:25534|
|Nelms, Bradlee D; Waldron, Levi; Barrera, Luis A et al. (2016) CellMapper: rapid and accurate inference of gene expression in difficult-to-isolate cell types. Genome Biol 17:201|
|Tan, Justin L; Fogley, Rachel D; Flynn, Ryan A et al. (2016) Stress from Nucleotide Depletion Activates the Transcriptional Regulator HEXIM1 to Suppress Melanoma. Mol Cell 62:34-46|
|Johnson, Shawn F; Cruz, Cristina; Greifenberg, Ann Katrin et al. (2016) CDK12 Inhibition Reverses De Novo and Acquired PARP Inhibitor Resistance in BRCA Wild-Type and Mutated Models of Triple-Negative Breast Cancer. Cell Rep 17:2367-2381|
Showing the most recent 10 out of 303 publications