The mission of the Lung Cancer SPORE Career Development Program is to stimulate basic, translational and clinical research in lung cancer by recruiting new and established investigators in the area of lung cancer. The Career Development Program within the SPORE provides financial support for this mission, while the SPORE itself provides a nurturing and stimulating environment for those who are being initiated into lung cancer research. The Career Development Program has the following objectives: 1) To recruit ohysicians, scientist, and physician-scientist to direct their research efforts to the field of lung cancer;2) To train and guide these investigators through the process of developing into outstanding investigators in the translational areas of lung cancer research, including laboratory, clinical, and population science. The faculty within the SPORE has a long-standing record in mentoring postdoctoral fellows, new independent nvestigators, and physician-scientists for careers in translational research. In the first grant period, we designed the Career Development Program with two components: support of new Faculty Members and support of both beginning and advanced Post-Doctoral Fellows. This plan was given a highly meritorious rating by the SPORE peer review panel in 2000. During the ensuing five years, SPORE guidelines have changed and Career Development Awards to Post-Doctoral Fellows are restricted to those who are very close to a faculty appointment. We have designed a new Career Development plan in the renewal to accommodate this change in the guidelines, focusing only on Faculty Members and Fellows or Research Associates who are near to a faculty appointment. The SPORE Career Development Program will consider candidates identified through a well-defined recruitment process, and will especially seek to support women and minority candidates.

Agency
National Institute of Health (NIH)
Institute
National Cancer Institute (NCI)
Type
Specialized Center (P50)
Project #
5P50CA090440-09
Application #
7843716
Study Section
Special Emphasis Panel (ZCA1)
Project Start
Project End
Budget Start
2009-05-01
Budget End
2010-04-30
Support Year
9
Fiscal Year
2009
Total Cost
$108,785
Indirect Cost
Name
University of Pittsburgh
Department
Type
DUNS #
004514360
City
Pittsburgh
State
PA
Country
United States
Zip Code
15213
Leng, Shuguang; Diergaarde, Brenda; Picchi, Maria A et al. (2018) Gene Promoter Hypermethylation Detected in Sputum Predicts FEV1 Decline and All-Cause Mortality in Smokers. Am J Respir Crit Care Med 198:187-196
Rothenberger, Natalie J; Somasundaram, Ashwin; Stabile, Laura P (2018) The Role of the Estrogen Pathway in the Tumor Microenvironment. Int J Mol Sci 19:
Yochum, Zachary A; Cades, Jessica; Wang, Hailun et al. (2018) Targeting the EMT transcription factor TWIST1 overcomes resistance to EGFR inhibitors in EGFR-mutant non-small-cell lung cancer. Oncogene :
Stabile, Laura P; Farooqui, Mariya; Kanterewicz, Beatriz et al. (2018) Preclinical Evidence for Combined Use of Aromatase Inhibitors and NSAIDs as Preventive Agents of Tobacco-Induced Lung Cancer. J Thorac Oncol 13:399-412
Volonte, Daniela; Vyas, Avani R; Chen, Chen et al. (2018) Caveolin-1 promotes the tumor suppressor properties of oncogene-induced cellular senescence. J Biol Chem 293:1794-1809
Yochum, Zachary A; Cades, Jessica; Mazzacurati, Lucia et al. (2017) A First-in-Class TWIST1 Inhibitor with Activity in Oncogene-Driven Lung Cancer. Mol Cancer Res 15:1764-1776
Chatterjee, Suman; Huang, Eric H-B; Christie, Ian et al. (2017) Acquired Resistance to the Hsp90 Inhibitor, Ganetespib, in KRAS-Mutant NSCLC Is Mediated via Reactivation of the ERK-p90RSK-mTOR Signaling Network. Mol Cancer Ther 16:793-804
Moiseeva, Tatiana; Hood, Brian; Schamus, Sandy et al. (2017) ATR kinase inhibition induces unscheduled origin firing through a Cdc7-dependent association between GINS and And-1. Nat Commun 8:1392
Sun, Fan; Xiao, Gutian; Qu, Zhaoxia (2017) Murine Bronchoalveolar Lavage. Bio Protoc 7:
Zhou, Jingjiao; Qu, Zhaoxia; Sun, Fan et al. (2017) Myeloid STAT3 Promotes Lung Tumorigenesis by Transforming Tumor Immunosurveillance into Tumor-Promoting Inflammation. Cancer Immunol Res 5:257-268

Showing the most recent 10 out of 191 publications