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Thyroid : Official Journal of the American Thyroid Association|June 14, 2003
Thyrotropin receptor mutations and thyroid hyperfunctioning adenomas ten years after their first discovery: unresolved questionsF Arturi, D Scarpelli, A Coco, et al.
Cancer Research|July 15, 1992
Insulin receptor expression and function in human breast cancer cell linesG Milazzo, F Giorgino, G Damante, et al.
The Journal of Clinical Endocrinology and Metabolism|December 1, 1996
Cold thyroid nodule reduction with L-thyroxine can be predicted by initial nodule volume and cytological characteristicsG L La Rosa, A M Ippolito, L Lupo, et al.
Thyroid : Official Journal of the American Thyroid Association|March 29, 2001
Absence of sodium/iodide symporter gene mutations in differentiated human thyroid carcinomasD Russo, D Manole, F Arturi, et al.
The Journal of Clinical Endocrinology and Metabolism|June 8, 2000
Expression of pendrin and the Pendred syndrome (PDS) gene in human thyroid tissuesJ M Bidart, C Mian, V Lazar, et al.
Oncogene|November 2, 1995
Activating mutations of the TSH receptor in differentiated thyroid carcinomasD Russo, F Arturi, M Schlumberger, et al.
Molecular Endocrinology (Baltimore, Md.)|November 1, 1996
Overexpression of membrane glycoprotein PC-1 in MDA-MB231 breast cancer cells is associated with inhibition of insulin receptor tyrosine kinase activityA Belfiore, A Costantino, F Frasca, et al.
Molecular and Cellular Biology|April 17, 1999
Insulin receptor isoform A, a newly recognized, high-affinity insulin-like growth factor II receptor in fetal and cancer cellsF Frasca, G Pandini, P Scalia, et al.
Clinical Cancer Research : an Official Journal of the American Association for Cancer Research|August 3, 1999
Insulin and insulin-like growth factor-I (IGF-I) receptor overexpression in breast cancers leads to insulin/IGF-I hybrid receptor overexpression: evidence for a second mechanism of IGF-I signalingG Pandini, R Vigneri, A Costantino, et al.
Thyroid : Official Journal of the American Thyroid Association|December 29, 2000
A Phe 486 thyrotropin receptor mutation in an autonomously functioning follicular carcinoma that was causing hyperthyroidismP Camacho, D Gordon, E Chiefari, et al.
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