Expressions of Id-1 and Id-2 in Hyperplastic Thyroid Tissue and Thyroid Carcinoma
Korean Journal of Pathology
;
: 60-65, 2006.
Article
in English
| WPRIM
| ID: wpr-229097
ABSTRACT
BACKGROUND:
Id proteins are a family of helix-loop-helix proteins and are regarded to be negative regulators of cell differentiation. In general, Id-1 and Id-2 expressions are upregulated during tumor development and progression in a variety of neoplasms, and these expressions may be associated with aggressive tumor behavior. However, little is known about the roles of Id-1 and Id-2 in thyroid neoplasms.METHODS:
The expressions of Id-1 and Id-2 were assessed immunohistochemically in 310 normal, hyperplastic, and neoplastic thyroid tissues using tissue microarrays.RESULTS:
Normal thyroid tissues rarely expressed Id-1 or Id-2. Moreover, whilst Id-1 expression was more elevated in malignant thyroid tissue than in hyperplastic thyroid tissue, Id-2 expression was more variable. No significant differences were observed between histologic subtypes of thyroid carcinomas with respect to Id-1 or Id-2 expression. Follicular adenomas showed higher expressions of Id-1 and Id-2 than thyroid carcinomas. No significant association was found between clinicopathological parameters and Id-1 expression, though Id-2 expression was significantly reduced in metastatic, stage IV tumors.CONCLUSION:
The expressions of Id-1 and Id-2 were elevated in hyperplastic and neoplastic thyroid tissues. However, neither appears suitable as a marker of malignancy or an aggressive phenotype, although Id-2 expression in advanced thyroid carcinomas may reflect a favorable prognosis.
Full text:
Available
Index:
WPRIM (Western Pacific)
Main subject:
Phenotype
/
Prognosis
/
Thyroid Gland
/
Thyroid Neoplasms
/
Carcinoma, Papillary
/
Adenoma
/
Cell Differentiation
/
Adenocarcinoma, Follicular
/
Inhibitor of Differentiation Protein 1
/
Inhibitor of Differentiation Protein 2
Type of study:
Prognostic study
Limits:
Humans
Language:
English
Journal:
Korean Journal of Pathology
Year:
2006
Type:
Article
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