CD98 expression is decreased in papillary carcinoma of the thyroid and Hashimoto’s thyroiditis

Abstract

CD98 expression is down-regulated in thyroid papillary carcinoma; this may relate to the better prognosis associated with many of these tumours.

Surgery in the setting of Hashimoto's thyroiditis

“…This is certainly consistent with studies demonstrating an association between HT and PTC 24 . The two pathological processes may display similar genetic alterations, including human 8‐oxoguanine deoxyribonucleic acid glycosylase loss of heterozygosity, 25 down‐regulation of CD98 expression 26 and RET/PTC gene rearrangements 27 . Smaller numbers of minimally invasive follicular carcinoma and Hürthle cell carcinoma also occurred, but none of our patients who underwent thyroidectomy were found to have lymphoma.…”

Potential relationship between Hashimoto's thyroiditis and BRAFV600E mutation status in papillary thyroid cancer

“…Several biomolecular profiles, such as P63 gene expression, phosphatidylinositol 3-kinase/Akt pathway, and CD98 expression, affect Hashimoto's thyroiditis and PTC. 30,33,34 Among the biomolecular profiles, BRAF V600E mutation is one of the strongest predictor markers for extrathyroidal invasion, lymph node metastasis, and advanced tumor stages, among others in PTC. 5,7,35,36 Xing et al 37 studied patients with an overall median follow-up time of 33 months after initial treatment.…”

The Thyroid Gland: A Crossroad in Inflammation-Induced Carcinoma? An Ongoing Debate with New Therapeutic Potential.

“…Interestingly, Matsumoto et al have shown that Niban, a recently identified molecular marker of renal carcinogenesis, was overexpressed in thyroid tumors, particularly in those with an oxyphilic cytoplasm, and in HT, mainly in scattered cells with oxyphilic cell metaplasia [91]. Similarly, Anderson et al demonstrated that the expression of CD98, a component of a cell surface amino acid transporter, was decreased in inflamed areas of both HT and PTC compared to normal follicular cells, follicular adenoma or carcinoma, multinodular goiter and Grave's disease [92]. Since CD98 binds and activates 1-integrin, thus promoting anchorage-independent growth, they conclude that this down-regulation of CD98 could explain, in part, the good prognosis of PTC, particularly in the context of HT.…”