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Kinase expression and chromosomal rearrangements in papillary thyroid cancer tissues: investigations at the molecular and microscopic levels

Weier, H.-U. G. and Kwan, J. and Lu, C.-M. and Ito, Y. and Wang, M. and Baumgartner, A. and Hayward, S. W. and Weier, J. F. and Zitzelsberger, H. F. (2009) Kinase expression and chromosomal rearrangements in papillary thyroid cancer tissues: investigations at the molecular and microscopic levels. Journal of Physiology and Pharmacology, 60 (Suppl.). pp. 47-55. ISSN 0867-5910 . https://resolver.caltech.edu/CaltechAUTHORS:20100316-134010153

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Abstract

Structural chromosome aberrations are known hallmarks of many solid tumors. In the papillary form of thyroid cancer (PTC), for example, activation of the receptor tyrosine kinase (RTK) genes, ret or the neurotrophic tyrosine kinase receptor type I (NTRK1) by intra- or interchromosomal rearrangements have been suggested as a cause of the disease. The 1986 accident at the nuclear power plant in Chernobyl, Ukraine, led to the uncontrolled release of high levels of radioisotopes. Ten years later, the incidence of childhood papillary thyroid cancer (chPTC) near Chernobyl had risen by two orders of magnitude. Tumors removed from some of these patients showed aberrant expression of the ret RTK gene due to a ret/PTC1 or ret/PTC3 rearrangement involving chromosome 10. However, many cultured chPTC cells show a normal G-banded karyotype and no ret rearrangement. We hypothesize that the "ret-negative" tumors inappropriately express a different oncogene or have lost function of a tumor suppressor as a result of chromosomal rearrangements, and decided to apply molecular and cytogenetic methods to search for potentially oncogenic chromosomal rearrangements in Chernobyl chPTC cases. Knowledge of the kind of genetic alterations may facilitate the early detection and staging of chPTC as well as provide guidance for therapeutic intervention.


Item Type:Article
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URLURL TypeDescription
http://www.jpp.krakow.pl/PublisherUNSPECIFIED
Additional Information:© 2009 Polish Physiological Society. Received : August 5, 2009. Accepted : September 10, 2009. This work was supported in parts by NIH grants CA80792, CA88258, CA123370, and HD45736, and a grant from the Director, Office of Energy Research, Office of Health and Environmental Research, U.S. Department of Energy, under contract DE-AC02-05CH11231. JFW was supported in part by NIH grant HD41425 and a grant from the UC Discovery Program, which also supported AB. We gratefully acknowledge the support from staff and students at LBNL and the Helmholtz Zentrum Muenchen. We also like to express our thanks to the scientists at the Human Genome Center, California Institute of Technology, Pasadena, and the Wellcome Trust Sanger Institute, Cambridge, UK, especially the Chromosome 9 Mapping Group, whose generosity made these studies possible. Parts of this work have been presented at the 13th Congress of the International Federation of Societies for Histochemistry and Cytochemistry (ICHC2008), Medical University of Gdansk, Poland, August 27-30, 2008. Disclaimer: This document was prepared as an account of work sponsored by the United States Government. While this document is believed to contain correct information, neither the United States Government nor any agency thereof, nor The Regents of the University of California, nor any of their employees, makes any warranty, express or implied, or assumes any legal responsibility for the accuracy, completeness, or usefulness of any information, apparatus, product, or process disclosed, or represents that its use would not infringe privately owned rights. Reference herein to any specific commercial product, process, or service by its trade name, trademark, manufacturer, or otherwise, does not necessarily constitute or imply its endorsement, recommendation, or favoring by the United States Government or any agency thereof, or The Regents of the University of California. The views and opinions of authors expressed herein do not necessarily state or reflect those of the United States Government or any agency thereof, or The Regents of the University of California.
Funders:
Funding AgencyGrant Number
NIHCA80792
NIHCA88258
NIHCA123370
NIHHD45736
Director, Office of Energy Research, Office of Health and Environmental Research, U.S. Department of EnergyDE-AC02-05CH11231
NIHHD41425
UC Discovery ProgramUNSPECIFIED
Subject Keywords:thyroid cancer, radiation, Chernobyl, gene expression, chromosome aberration, translocation
Issue or Number:Suppl.
Record Number:CaltechAUTHORS:20100316-134010153
Persistent URL:https://resolver.caltech.edu/CaltechAUTHORS:20100316-134010153
Usage Policy:No commercial reproduction, distribution, display or performance rights in this work are provided.
ID Code:17757
Collection:CaltechAUTHORS
Deposited By: Tony Diaz
Deposited On:22 Mar 2010 04:00
Last Modified:03 Oct 2019 01:33

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