Abstract

The objective of this proposal is to identify new dominant gene defects in thyroid tumors, and to clarify the role of some of the mutations already discovered on the clinical behavior of thyroid neoplasms.
The specific aims are to: 1) Determine the prognostic value of ras mutations in thyroid neoplasms: the hypothesis that point mutations and/or gene amplification of ras may predispose follicular or papillary carcinomas to undergo further transformation to a more aggressive phenotype will be tested; 2) Identify chromosomal locl affected by gene amplification in thyroid neoplasms; 3) Identify rapid turnover mRNAs overexpressed in human thyroid tumors; 4) Identify transforming cDNAs from human thyroid cancers by using a modified expression cloning strategy to isolate growth-promoting genes from thyroid cancer specimens.

  Funding Agency

Agency
National Institute of Health (NIH)
Institute
National Cancer Institute (NCI)
Type
Research Project (R01)
Project #
5R01CA050706-09
Application #
2712633
Study Section
Endocrinology Study Section (END)
Program Officer
Mohla, Suresh
Project Start
1989-08-01
Project End
2000-05-31
Budget Start
1998-06-01
Budget End
1999-05-31
Support Year
9
Fiscal Year
1998
Total Cost
Indirect Cost

  Institution

Name
University of Cincinnati
Department
Internal Medicine/Medicine
Type
Schools of Medicine
DUNS #
City
Cincinnati
State
OH
Country
United States
Zip Code
45221

  Publications

Bellelli, Roberto; Vitagliano, Donata; Federico, Giorgia et al. (2018) Oncogene-induced senescence and its evasion in a mouse model of thyroid neoplasia. Mol Cell Endocrinol 460:24-35
Krishnamoorthy, Gnana P; Davidson, Natalie R; Leach, Steven D et al. (2018) EIF1AX and RAS mutations cooperate to drive thyroid tumorigenesis through ATF4 and c-MYC. Cancer Discov :
Untch, Brian R; Dos Anjos, Vanessa; Garcia-Rendueles, Maria E R et al. (2018) Tipifarnib Inhibits HRAS-Driven Dedifferentiated Thyroid Cancers. Cancer Res 78:4642-4657
Azouzi, Naïma; Cailloux, Jérémy; Cazarin, Juliana M et al. (2017) NADPH Oxidase NOX4 Is a Critical Mediator of BRAFV600E-Induced Downregulation of the Sodium/Iodide Symporter in Papillary Thyroid Carcinomas. Antioxid Redox Signal 26:864-877
Ibrahimpasic, Tihana; Xu, Bin; Landa, Iñigo et al. (2017) Genomic Alterations in Fatal Forms of Non-Anaplastic Thyroid Cancer: Identification of MED12 and RBM10 as Novel Thyroid Cancer Genes Associated with Tumor Virulence. Clin Cancer Res 23:5970-5980
Montero-Conde, Cristina; Leandro-Garcia, Luis J; Chen, Xu et al. (2017) Transposon mutagenesis identifies chromatin modifiers cooperating with Ras in thyroid tumorigenesis and detects ATXN7 as a cancer gene. Proc Natl Acad Sci U S A 114:E4951-E4960
Fagin, James A; Wells Jr, Samuel A (2016) Biologic and Clinical Perspectives on Thyroid Cancer. N Engl J Med 375:1054-67
Dogan, Snjezana; Wang, Lu; Ptashkin, Ryan N et al. (2016) Mammary analog secretory carcinoma of the thyroid gland: A primary thyroid adenocarcinoma harboring ETV6-NTRK3 fusion. Mod Pathol 29:985-95
Landa, Iñigo; Ibrahimpasic, Tihana; Boucai, Laura et al. (2016) Genomic and transcriptomic hallmarks of poorly differentiated and anaplastic thyroid cancers. J Clin Invest 126:1052-66
Nagarajah, James; Le, Mina; Knauf, Jeffrey A et al. (2016) Sustained ERK inhibition maximizes responses of BrafV600E thyroid cancers to radioiodine. J Clin Invest 126:4119-4124

Showing the most recent 10 out of 42 publications