In order to evaluate the relevance of basic science discoveries to human lung cancer, it has been and will continue to be necessary to obtain and analyze human tissues. The purpose of the Tissue Banks Core (TBC) ia to provide to SPORE investigators a large number of well preserved and well characterized tumors, dysplastic lesions, benign tissues, cell lines and cell and tissue fractions as well as relevant clinical information for laboratory study. Fixed, frozen and cultured tissue, serum, peripheral blood cells (PBC), urine and sputum from patients with lung cancer or at risk for lung cancer are collected through tissue procurement protocols of SPORE-affiliated institutions and the Southwest Oncology Group (SWOG). Tissue and cellular specimens are characterized as to cell type and cytogenetic and immunohistochemical marker expression by pathologists and technicians of the TBC. Microdissection and in vitro culture techniques are used to isolate and purify tumor cells and preneoplastic epithelium from contaminating stromal cells. DNA and RNA are extracted from tissue homogenates and purified cell populations and aliquoted for PCR-based procedures and blotting techniques. Inventories of tissues and cells and products prepared from these are maintained at storage sites both at Grand Junction St. Mary's Cancer Research Institute and the UCHSC. Clinical data regarding potential causative, hereditary and prognostic factors are linked in a centralized database to specimens characterized and prepared by the TBC and are available for correlation with information regarding specific specimens obtained in basic science programs. Both prospectively and retrospectively collected tissue samples and clinical information are tracked by the TBC. Tissue from invasive tumors and adjacent non- neoplastic lung tissue, pretreatment plasma and PBC from patients with these tumors are collected and processed from patients treated surgically at SPORE affiliated institutions. The TBC constitutes a unique national source of uniformly typed, staged, treated and observed tumors and preneoplastic lesions. The C permits the most efficient possible use of limited amounts of tissue available from patients with lung cancer. Materials collected by the TBC are available to SPORE and other approved and funded investigators on the basis of scientific review.

Agency
National Institute of Health (NIH)
Institute
National Cancer Institute (NCI)
Type
Specialized Center (P50)
Project #
5P50CA058187-07
Application #
6102827
Study Section
Project Start
1999-05-01
Project End
2000-04-30
Budget Start
1998-10-01
Budget End
1999-09-30
Support Year
7
Fiscal Year
1999
Total Cost
Indirect Cost
Name
University of Colorado Denver
Department
Type
DUNS #
065391526
City
Aurora
State
CO
Country
United States
Zip Code
80045
Patil, Tejas; Smith, Derek E; Bunn, Paul A et al. (2018) The Incidence of Brain Metastases in Stage IV ROS1-Rearranged Non-Small Cell Lung Cancer and Rate of Central Nervous System Progression on Crizotinib. J Thorac Oncol 13:1717-1726
Suda, Kenichi; Kim, Jihye; Murakami, Isao et al. (2018) Innate Genetic Evolution of Lung Cancers and Spatial Heterogeneity: Analysis of Treatment-Naïve Lesions. J Thorac Oncol 13:1496-1507
Helfrich, Barbara A; Gao, Dexiang; Bunn Jr, Paul A (2018) Eribulin inhibits the growth of small cell lung cancer cell lines alone and with radiotherapy. Lung Cancer 118:148-154
Kleczko, Emily K; Heasley, Lynn E (2018) Mechanisms of rapid cancer cell reprogramming initiated by targeted receptor tyrosine kinase inhibitors and inherent therapeutic vulnerabilities. Mol Cancer 17:60
McCoach, Caroline E; Le, Anh T; Gowan, Katherine et al. (2018) Resistance Mechanisms to Targeted Therapies in ROS1+ and ALK+ Non-small Cell Lung Cancer. Clin Cancer Res 24:3334-3347
Drilon, Alexander; Laetsch, Theodore W; Kummar, Shivaani et al. (2018) Efficacy of Larotrectinib in TRK Fusion-Positive Cancers in Adults and Children. N Engl J Med 378:731-739
Pilling, Amanda B; Kim, Jihye; Estrada-Bernal, Adriana et al. (2018) ALK is a critical regulator of the MYC-signaling axis in ALK positive lung cancer. Oncotarget 9:8823-8835
Kwak, Jeff W; Laskowski, Jennifer; Li, Howard Y et al. (2018) Complement Activation via a C3a Receptor Pathway Alters CD4+ T Lymphocytes and Mediates Lung Cancer Progression. Cancer Res 78:143-156
Sakamoto, Mandy R; Honce, Justin M; Lindquist, Deborah L et al. (2018) Lorlatinib Salvages CNS Relapse in an ALK-Positive Non-Small-Cell Lung Cancer Patient Previously Treated With Crizotinib and High-Dose Brigatinib. Clin Lung Cancer :
McCoach, Caroline E; Blakely, Collin M; Banks, Kimberly C et al. (2018) Clinical Utility of Cell-Free DNA for the Detection of ALK Fusions and Genomic Mechanisms of ALK Inhibitor Resistance in Non-Small Cell Lung Cancer. Clin Cancer Res 24:2758-2770

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