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PMID: 16858683 Published · ppublish English Journal Article Research Support, Non-U.S. Gov't

Association of aberrant methylation of tumor suppressor genes with tumor aggressiveness and BRAF mutation in papillary thyroid cancer.

International journal of cancer ·Vol. 119 ·No. 10 ·2006-11-15 ·Pages 2322-9

Hu S, Liu D, Tufano RP, Carson KA, Rosenbaum E, Cohen Y, Holt EH, Kiseljak-Vassiliades K, Rhoden KJ, Tolaney S, Condouris S, Tallini G, Westra WH, Umbricht CB, Zeiger MA, Califano JA, Vasko V, Xing M

Abstract

The role of aberrant tumor suppressor gene methylation in the aggressiveness of papillary thyroid cancer (PTC) has not been documented. By showing promoter methylation-induced gene silencing in PTC-derived cell lines, we first demonstrated the functional consequence of methylation of several recently identified tumor suppressor genes, including those for tissue inhibitor of metalloproteinase-3 (TIMP3), SLC5A8, death-associated protein kinase (DAPK) and retinoic acid receptor beta2 (RARbeta2). We then investigated the role of methylation of these genes in the aggressiveness of PTC by examining the relationship of their aberrant methylation to clinicopathological characteristics and BRAF mutation in 231 primary PTC tumors. Methylation of TIMP3, SLC5A8 and DAPK was significantly associated with several aggressive features of PTC, including extrathyroidal invasion, lymph node metastasis, multifocality and advanced tumor stages. Methylation of these genes was also significantly associated with BRAF mutation in PTC, either individually or collectively in various combinations. Methylation of these genes, either individually or collectively, occurred more frequently in more aggressive classical and tall-cell PTC subtypes than in less aggressive follicular-variant PTC, with the latter known to infrequently harbor BRAF mutation. Several other tumor suppressor genes investigated were not methylated. These results suggest that aberrant methylation and hence silencing of TIMP3, SLC5A8, DAPK and RARbeta2, in association with BRAF mutation, may be an important step in PTC tumorigenesis and progression.

MeSH Terms
Apoptosis Regulatory Proteins/genetics Calcium-Calmodulin-Dependent Protein Kinases/genetics Carcinoma, Papillary/genetics,pathology Cation Transport Proteins/genetics Cell Line, Tumor DNA Methylation DNA, Neoplasm/metabolism Death-Associated Protein Kinases Disease Progression Gene Silencing Genes, Tumor Suppressor Humans Monocarboxylic Acid Transporters Mutation Proto-Oncogene Proteins B-raf/genetics Receptors, Retinoic Acid/genetics Reverse Transcriptase Polymerase Chain Reaction Thyroid Neoplasms/genetics,pathology Tissue Inhibitor of Metalloproteinase-3/genetics
Chemicals
Apoptosis Regulatory Proteins Cation Transport Proteins DNA, Neoplasm Monocarboxylic Acid Transporters Receptors, Retinoic Acid SLC5A8 protein, human TIMP3 protein, human Tissue Inhibitor of Metalloproteinase-3 retinoic acid receptor beta BRAF protein, human Death-Associated Protein Kinases Proto-Oncogene Proteins B-raf Calcium-Calmodulin-Dependent Protein Kinases
Authors & Affiliations
18 authors, click to expand affiliations / ORCID
Hu Shuiying
Department of Medicine, Division of Endocrinology and Metabolism, The Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA.
Liu Dingxie
Tufano Ralph P
Carson Kathryn A
Rosenbaum Eli
Cohen Yoram
Holt Elizabeth H
Kiseljak-Vassiliades Katja
Rhoden Kerry J
Tolaney Sara
Condouris Stephen
Tallini Giovanni
Westra William H
Umbricht Christopher B
Zeiger Martha A
Califano Joseph A
Vasko Vasily
Xing Mingzhao
Article Info
Journal
International journal of cancer
Abbr.
Int J Cancer
ISSN
0020-7136
Published
2006-11-15
Pages
2322-9
Language
English
Region
United States
NLM ID
0042124
Subset
IM
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