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PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
1998-4-9
pubmed:abstractText
Malignant tumors of the thyroid gland vary considerably in aggressiveness, ranging from a well-differentiated, clinically indolent, to an undifferentiated, often lethal phenotype. Undifferentiated (anaplastic) thyroid tumors are supposed to be derived, through a process of progression, from previously differentiated neoplasms. A common genetic alteration in thyroid tumors is the rearrangement of the tyrosine kinase-encoding RET proto-oncogene, leading to the generation of chimeric RET/PTC oncogenes. To define the characteristics of the thyroid tumor subset with RET rearrangements, we have investigated its activation by a combined immunohistochemistry and reverse transcription-PCR approach in a series of 316 well-characterized thyroid tumors representative of the main diagnostic groups. RET activation was detected in 81 of 201 (40.3%) papillary carcinomas. It correlated with tumors exhibiting the "classic" morphological features of papillary cancer or with the microcarcinoma subtype (P = 0.017). RET activation in papillary carcinoma was not associated with clinical markers (such as large tumor size, extrathyroidal extension, or metastases) of increased morbidity. Follicular-type neoplasms (61 adenomas and 22 carcinomas), as well as the aggressive poorly differentiated (15 cases) or undifferentiated (anaplastic) carcinomas (17 cases), were negative. This study demonstrates that all thyroid carcinomas harboring activating RET rearrangements exhibit a well-differentiated phenotype, that of papillary carcinoma, and indicates that the subset of RET/PTC-positive papillary carcinomas do not progress to more aggressive, less differentiated tumor phenotypes.
pubmed:commentsCorrections
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
1078-0432
pubmed:author
pubmed:issnType
Print
pubmed:volume
4
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
287-94
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed-meshheading:9516913-Adolescent, pubmed-meshheading:9516913-Adult, pubmed-meshheading:9516913-Age Factors, pubmed-meshheading:9516913-Carcinoma, Papillary, pubmed-meshheading:9516913-Cell Differentiation, pubmed-meshheading:9516913-Child, pubmed-meshheading:9516913-Child, Preschool, pubmed-meshheading:9516913-Disease Progression, pubmed-meshheading:9516913-Drosophila Proteins, pubmed-meshheading:9516913-Female, pubmed-meshheading:9516913-Gene Expression Regulation, Neoplastic, pubmed-meshheading:9516913-Gene Rearrangement, pubmed-meshheading:9516913-Humans, pubmed-meshheading:9516913-Immunohistochemistry, pubmed-meshheading:9516913-Infant, pubmed-meshheading:9516913-Isomerism, pubmed-meshheading:9516913-Male, pubmed-meshheading:9516913-Phenotype, pubmed-meshheading:9516913-Proto-Oncogene Proteins, pubmed-meshheading:9516913-Proto-Oncogene Proteins c-ret, pubmed-meshheading:9516913-Receptor Protein-Tyrosine Kinases, pubmed-meshheading:9516913-Risk Factors, pubmed-meshheading:9516913-Thyroid Neoplasms
pubmed:year
1998
pubmed:articleTitle
RET/PTC oncogene activation defines a subset of papillary thyroid carcinomas lacking evidence of progression to poorly differentiated or undifferentiated tumor phenotypes.
pubmed:affiliation
Department of Pathology, Yale University School of Medicine, New Haven, Connecticut 06510, USA. giovanni.tallini@yale.edu
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't