The principal objectives of the SPORE Lung Cancer Screening and Tissue Procurement CORE are to: (1) screen high risk smoker and ex-smoker patients identified through community and institutionally-based pulmonologists with sputum cytology to identify subjects with moderate or severe dysplasia; (2) obtain, classify, and bank sputum samples from the above; (3) support SPORE clinical investigations by obtaining bronchoscopy, serum, and urine specimens as required; and (4) maintain a registry of demographic data on all above patients. The CORE will create an archive of specimens, clinical, and demographic data for use in longitudinal investigations to evaluate hypotheses concerning the biological basis of lung carcinogenesis. The high risk population will be patients with airflow obstruction who have smoking histories of 40 or more pack years. This patient group has been selected because the risk for lung cancer has been found to increase in proportion to degree of airflow obstruction within smoking populations. The total accrual goal for the three year SPORE grant is 4,000 subjects. From prior experience, it is estimated that about 20% of these will have moderate or severe dysplasia. To enroll and instruct subjects on the selected method for sputum collection (i.e., early morning, spontaneous cough technique), the Lung Cancer Institute of Colorado's consortium of community and institutionally- based pulmonologists will be employed. Sputa collected from subjects will be processed and examined at the cytology laboratories of the following institutions: University of Colorado Health Sciences Center, Denver Veterans Administration Medical Center, Presbyterian Denver Hospital, and St. Mary's Medical Center, Grand Junction. Cytologic examinations will be performed by the SPORE pathologist panel to identify dysplastic patients for subsequent participation (if consent is obtained) in SPORE clinical studies.

Agency
National Institute of Health (NIH)
Institute
National Cancer Institute (NCI)
Type
Specialized Center (P50)
Project #
1P50CA058187-01
Application #
3796274
Study Section
Project Start
Project End
Budget Start
Budget End
Support Year
1
Fiscal Year
1992
Total Cost
Indirect Cost
Name
University of Colorado Denver
Department
Type
DUNS #
065391526
City
Aurora
State
CO
Country
United States
Zip Code
80045
McDaniel, Nellie K; Cummings, Christopher T; Iida, Mari et al. (2018) MERTK Mediates Intrinsic and Adaptive Resistance to AXL-targeting Agents. Mol Cancer Ther 17:2297-2308
Ghosh, Moumita; Miller, York E; Vandivier, R William et al. (2018) Reply to Sohal: Airway Basal Cell Reprogramming and Epithelial-Mesenchymal Transition: A Potential Key to Understanding Early Chronic Obstructive Pulmonary Disease. Am J Respir Crit Care Med 197:1645-1646
Ghosh, Moumita; Miller, York E; Nakachi, Ichiro et al. (2018) Exhaustion of Airway Basal Progenitor Cells in Early and Established Chronic Obstructive Pulmonary Disease. Am J Respir Crit Care Med 197:885-896
Farago, Anna F; Taylor, Martin S; Doebele, Robert C et al. (2018) Clinicopathologic Features of Non-Small-Cell Lung Cancer Harboring an NTRK Gene Fusion. JCO Precis Oncol 2018:
He, Yayi; Liu, Sangtian; Mattei, Jane et al. (2018) The combination of anti-KIR monoclonal antibodies with anti-PD-1/PD-L1 monoclonal antibodies could be a critical breakthrough in overcoming tumor immune escape in NSCLC. Drug Des Devel Ther 12:981-986
Genova, Carlo; Socinski, Mark A; Hozak, Rebecca R et al. (2018) EGFR Gene Copy Number by FISH May Predict Outcome of Necitumumab in Squamous Lung Carcinomas: Analysis from the SQUIRE Study. J Thorac Oncol 13:228-236
Merrick, Daniel T; Edwards, Michael G; Franklin, Wilbur A et al. (2018) Altered Cell-Cycle Control, Inflammation, and Adhesion in High-Risk Persistent Bronchial Dysplasia. Cancer Res 78:4971-4983
Li, Howard Y; McSharry, Maria; Walker, Deandra et al. (2018) Targeted overexpression of prostacyclin synthase inhibits lung tumor progression by recruiting CD4+ T lymphocytes in tumors that express MHC class II. Oncoimmunology 7:e1423182
Ravichandran, Kameswaran; Holditch, Sara; Brown, Carolyn N et al. (2018) IL-33 deficiency slows cancer growth but does not protect against cisplatin-induced AKI in mice with cancer. Am J Physiol Renal Physiol 314:F356-F366
Hilberg, Frank; Tontsch-Grunt, Ulrike; Baum, Anke et al. (2018) Triple Angiokinase Inhibitor Nintedanib Directly Inhibits Tumor Cell Growth and Induces Tumor Shrinkage via Blocking Oncogenic Receptor Tyrosine Kinases. J Pharmacol Exp Ther 364:494-503

Showing the most recent 10 out of 435 publications