Journal of Clinical Endocrinology & Metabolism, doi:10.1210/jc.2005-0952
The Journal of Clinical Endocrinology & Metabolism Vol. 90, No. 10 5906
Copyright © 2005 by The Endocrine Society
Letter re: Id1 Gene Expression in Hyperplastic and Neoplastic Thyroid Tissues
Annavarapu Srinivas Rao,
Peter E. Goretzki,
Josef Köhrle and
Georg Brabant
Department of Gastroenterology, Hepatology and Endocrinology (A.S.R., G.B.), Medical School Hannover, D-30625, Hannover, Germany; Lukas Krankenhaus (P.E.G.), 41464 Neuss, Germany; and Institut fur Experimentelle Endokrinologie (J.K.), Charite, Universtatsmedizin Berlin, 10117 Berlin, Germany
Address correspondence to: Georg Brabant, Department of Gastroenterology, Hepatology and Endocrinology, Medical School Hannover, Carl-Neuberg Strasse 1, D-30625, Hannover, Germany. E-mail: brabant.georg{at}mh-hannover.de.
To the editor:
The molecular signatures of cancer cells have recently been delineated in more detail. There exist distinct differences in the molecular characteristics of cells derived from a metastasis compared with primary tumor lines (1). Consequently, the tissue of origin of a given cell line has become more important. In a recent publication, Kebebew et al. (2) delineated significant differences in expression of Id1, a member of the inhibitor of DNA binding helix-loop-helix protein family, when comparing a thyroid carcinoma cell line FTC-133, assumed to be of primary origin, to cell lines derived from metastases (FTC-236, FTC-238). They interpreted these findings as enhanced proliferation and decreased differentiation of the cell lines. We agree that tumor progression may play an important role in the metastatic process, but we would like to point out that the frequently used FTC-133 cell line is not derived from the primary site of the tumor, as stated by the authors and a number of others (4, 5, 6, 7, 8, 9, 10, 11, 12), but has its own origin from a lymph node metastasis (3). FTC-133 [European Collection of Cell Cultures (ECACC) 94060901] and FTC-238 (ECACC 94060902) cell lines have been deposited at ECACC with their description. Both the FTC-236 and FTC-238 cell lines were established from subsequent metastases and originate from the same patient as does FTC-133.
Accurate designation of the original tissue source of the cell lines is relevant not only for studies on the mechanisms of metastasis, but also for analyses of signal transduction and tumor progression.
Footnotes
A response to this letter was invited, but the authors of the original article chose not to provide one.
Received April 29, 2005.
References
- Minn AJ, Kang Y, Serganova I, Gupta GP, Giri DD, Doubrovin M, Ponomarev V, Gerald WL, Blasberg R, Massague J 2005 Distinct organ-specific metastatic potential of individual breast cancer cells and primary tumors. J Clin Invest 115:4455[CrossRef][Medline]
- Kebebew E, Peng M, Treseler PA, Clark OH, Duh QY, Ginzinger D, Miner R 2004 Id1 gene expression is up-regulated in hyperplastic and neoplastic thyroid tissue and regulates growth and differentiation in thyroid cancer cells. J Clin Endocrinol Metab 89:61056111[Abstract/Free Full Text]
- Goretzki PE, Frilling A, Simon D, Roeher HD 1990 Growth regulation of normal thyroids and thyroid tumours in man. Recent Results Cancer Res 118:4863[Medline]
- Kesmodel S, Prabakaran I, Canter R, Menon C, Molnar-Kimber K, Fraker D 2005 Virus-mediated oncolysis of thyroid cancer by a replication-selective adenovirus driven by a thyroglobulin promoter-enhancer region. J Clin Endocrinol Metab 90:34403448[Abstract/Free Full Text]
- Elisei R, Vivaldi A, Agate L, Ciampi R, Molinaro E, Piampiani P, Romei C, Faviana P, Basolo F, Miccoli P, Capodanno A, Collecchi P, Pacini F, Pinchera A 2005 All-trans-retinoic acid treatment inhibits the growth of retinoic acid receptor ß messenger ribonucleic acid expressing thyroid cancer cell lines but does not reinduce the expression of thyroid-specific genes. J Clin Endocrinol Metab 90:24032411[Abstract/Free Full Text]
- Xu J, Moatamed F, Caldwell JS, Walker JR, Kraiem Z, Taki K, Brent GA, Hershman JM 2003 Enhanced expression of nicotinamide N-methyltransferase in human papillary thyroid carcinoma cells. J Clin Endocrinol Metab 88:49904996[Abstract/Free Full Text]
- Takeda T, Inaba H, Yamazaki M, Kyo S, Miyamoto T, Suzuki S, Ehara T, Kakizawa T, Hara M, DeGroot LJ, Hashizume K 2003 Tumor-specific gene therapy for undifferentiated thyroid carcinoma utilizing the telomerase reverse transcriptase promoter. J Clin Endocrinol Metab 88:35313538[Abstract/Free Full Text]
- Park JW, Yeh MW, Wong MG, Lobo M, Hyun WC, Duh QY, Clark OH 2003 The heat shock protein 90-binding geldanamycin inhibits cancer cell proliferation, down-regulates oncoproteins, and inhibits epidermal growth factor-induced invasion in thyroid cancer cell lines. J Clin Endocrinol Metab 88:33463353[Abstract/Free Full Text]
- Kitazono M, Robey R, Zhan Z, Sarlis NJ, Skarulis MC, Aikou T, Bates S, Fojo T 2001 Low concentrations of the histone deacetylase inhibitor, depsipeptide (FR901228), increase expression of the Na+/I symporter and iodine accumulation in poorly differentiated thyroid carcinoma cells. J Clin Endocrinol Metab 86:34303435[Abstract/Free Full Text]
- Hoelting T, Duh QY, Clark OH, Herfarth C 1996 Somatostatin analog octreotide inhibits the growth of differentiated thyroid cancer cells in vitro, but not in vivo. J Clin Endocrinol Metab 81:26382641[Abstract]
- Soula-Rothhut M, Coissard C, Sartelet H, Boudot C, Bellon G, Martiny L, Rothhut B 2005 The tumor suppressor PTEN inhibits EGF-induced TSP-1 and TIMP-1 expression in FTC-133 thyroid carcinoma cells. Exp Cell Res 304:187201[CrossRef][Medline]
- Havekes B, Schroder van der Elst JP, van der Pluijm G, Goslings BM, Romijn JA, Smit JW 2000 Beneficial effects of retinoic acid on extracellular matrix degradation and attachment behaviour in follicular thyroid carcinoma cell lines. J Endocrinol 167:229238[Abstract]