Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2008-3-14
pubmed:abstractText
Connexin26 (Cx26), a component of GAP junctions and until recently believed to be a tumor suppressor gene, has been shown to play an important role in lymphatic invasion as well as lymph node and distant metastases in squamous lung cancer and breast cancer. In the study presented here, we investigated Cx26 expression in human papillary thyroid cancer (PTC) and follicular thyroid cancer (FTC) and its relationship with various clinicopathological parameters. Of 69 PTCs, 33 were positive for Cx26 (47.8%), as were five of 11 FTCs (45.5%), all follicular thyroid adenomas (n=22) and normal thyroid tissues (n=20) were negative for Cx26. A statistically significant association was observed between Cx26 expression and large tumor size (p=0.028 for PTC) and lymph node metastases (p=0.053 (marginally significant) for PTC and p=0.035 for FTC). Presence of intra-glandular dissemination of tumor cells was significantly (p=0.048) more frequent in Cx26-positive (30.3%) than Cx26-negative PTCs (11.1%). Lymphatic vessel invasion was more frequent in Cx26-positive PTCs (6.1%) than in Cx26-negative PTCs (0%) though the difference was not statistically significant. These results suggest that Cx26 may be implicated in the pathogenesis of PTC and FTC and is associated with the biologically aggressive phenotypes of these tumors.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
0304-3835
pubmed:author
pubmed:issnType
Print
pubmed:day
18
pubmed:volume
262
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
248-56
pubmed:meshHeading
pubmed:year
2008
pubmed:articleTitle
Connexin26 expression is associated with aggressive phenotype in human papillary and follicular thyroid cancers.
pubmed:affiliation
Department of Breast and Endocrine Surgery, Osaka University Graduate School of Medicine, 2-2 Yamadaoka, Suita-shi, Osaka 567-0871, Japan.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't