Differential oncogenic expression in thyroid follicular and Hürthle cell carcinomas

Masood, Shahla; Auguste, Louis‐Joseph; Westerband, Alex; Belluco, Claudio; Valderama, Elsa; Attie, Joseph N.

doi:10.1016/s0002-9610(05)80334-4

Cited by 55 publications

(26 citation statements)

References 8 publications

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“…There is experimental evidence that exogenous IGF-I may increase the proliferation rates of thyroid carcinoma cell lines [128]. Furthermore, IGF-I protein and mRNA were found to be expressed in subsets of thyroid carcinomas [129]. Immunoreactive IGF-I and IGFBPs were also found in extracts of normal and nodular thyroid tissue obtained from patients with non toxic goiter at surgery [130].…”

Section: Igf-i R Pathway In Thyroid Cancermentioning

confidence: 99%

The IGF-I/IGF-I Receptor Pathway: Implications in the Pathophysiology of Thyroid Cancer

Ciampolillo¹,

Tullio²,

Giorgino

2005

CMC

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The biological actions of the insulin-like growth factor(IGF)-I are mediated by its activation of the IGF-I receptor (IGF-I R), a transmembrane tyrosine kinase linked to the Akt and ras-raf-MAPK cascades. A functional IGF-I R is required for the cell to progress through the cell cycle. Most importantly, cells lacking this receptor cannot be transformed by any of a number of dominant oncogenes, a finding that proves that the presence of the IGF-I R is important for the development of a malignant phenotype. Consistent with this role, it has been well established that IGF-I can protect cells from apoptosis under a variety of circumstances. For example, IGF-I prevents apoptosis induced by overexpression of c-myc in fibroblasts, by interleukin-3 withdrawal in interleukin-3-dependent hemopoietic cells, etoposide, a topoisomerase I inhibitor, anti-cancer drugs, UV-B irradiations, and serum deprivation. While the anti-apoptotic effect of IGF-I has been clearly demonstrated, the molecular mechanisms by which IGF-I inhibits apoptosis induced by these various stimuli remain unknown. We have previously documented increased IGF-I and IGF-I receptor immunoreactivity in human thyroid carcinomas with a corresponding up-regulation of IGF-I mRNA. Immunoreactivity for IGF-I and IGF-I receptor positively correlated with tumor diameter, but not with the occurrence of lymph node metastases. Several recent studies have identified new signaling pathways emanating from the IGF-I receptor that affect cancer cell proliferation, adhesion, migration and apoptosis, which represent critical functions for cancer cell survival and metastasizing capacity. In this review, various aspects of the IGF-I/IGF-I R pathway and its relationship to thyroid cancer are discussed.

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Section: Igf-i R Pathway In Thyroid Cancermentioning

confidence: 99%

The IGF-I/IGF-I Receptor Pathway: Implications in the Pathophysiology of Thyroid Cancer

Ciampolillo¹,

Tullio²,

Giorgino

2005

CMC

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“…The follicular-derived neoplasms (adenoma, carcinoma, and the follicular variant of papillary carcinoma) manifest overlapping cytomorphologic features and not infrequently pose diagnostic and treatment difficulties (1)(2)(3)(4). Previous molecular studies of thyroid tumors have been limited to individual or multiple targeted markers and have failed to define any diagnostic or prognostic markers (5)(6)(7)(8)(9)(10)(11)(12)(13)(14). Novel approaches are needed to identify reliable markers for pathological classification and to predict disease progression.…”

Section: Introductionmentioning

confidence: 99%

Gene Expression Profiling of Differentiated Thyroid Neoplasms

Chevillard¹,

Ugolin²,

Vielh

et al. 2004

Clinical Cancer Research

120

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Purpose: The purpose of this research was to identify novel genes that can be targeted as diagnostic and clinical markers of differentiated thyroid tumors.Experimental Design: Gene expression analysis using microarray platform was performed on 6 pathologically normal thyroid samples and 12 primary follicular and papillary thyroid neoplasms. Microarrays containing probes for 5,760 human full-length cDNAs were used for hybridization with total RNA from normal and tumor thyroid samples labeled with Cy3-dUTP and Cy5-dUTP, respectively. Scanned array images were recorded, and data analysis was performed. Selected sets of differentially expressed genes were analyzed using quantitative real-time reverse transcription-PCR for verification.Results: We identified 155 genes that differentiate histologically normal thyroid tissues from benign and malignant thyroid neoplasms. Of these 75 genes were differentiated between follicular neoplasms (adenoma and carcinoma) and the follicular variant of papillary carcinoma. Purely follicular neoplasms (adenomas and carcinomas) shared many genetic profiles, and only 43 genes were distinctly different between these tumors. Hierarchical cluster analysis also differentiated conventional papillary carcinoma from its follicular variant and follicular tumors. The differentially expressed genes were composed of members of cell differentiation, adhesion, immune response, and proliferation associated pathways. Quantitative real-time reverse transcription-PCR analysis of selected genes corroborated the microarray expression results.Conclusions: Our study show the following: (1) differences in gene expression between tumor and nontumor bearing normal thyroid tissue can be identified, (2) a set of genes differentiate follicular neoplasm from follicular variant of papillary carcinoma, (3) follicular adenoma and carcinoma share many of the differentiated genes, and (4) gene expression differences identify conventional papillary carcinoma from the follicular variant.

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“…World Health Organization classification considered them as an oxyphilic variant of follicular thyroid tumors, but they were recognized as a distinct clinicopathologic entity later. 3 Considering the radionuclide imaging, Hurthle cell tumors rarely trap radioactive iodine or Tc-99m sodium pertechnetate. Only approximately 5% of Hurthle cell neoplasms (including benign Hurthle cell adenomas) show hot nodular lesions on the Tc-99m thyroid scan, 4 and less than 10% of Hurthle cell carcinoma take up radioiodine.…”

Section: Discussionmentioning

confidence: 99%

Thyrotoxicosis

Wong

Au-Yong

Tong

2003

Clinical Nuclear Medicine

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Hurthle cell carcinoma of the thyroid is a rare type of thyroid neoplasm. The most common clinical presentation is a single palpable thyroid nodule. The neoplasm typically presents as a nonfunctioning or cold nodule on a Tc-99m sodium pertechnetate or radioiodine thyroid scan. We report a case of Hurthle cell carcinoma of the thyroid in a woman presenting with thyrotoxicosis. The Tc-99m thyroid scan was also interesting in that the nodule was a hot or hyperfunctioning area, resulting in a rare scintigraphic finding in a rare tumor. Clinicopathologic aspects and related issues are further discussed.

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Differential oncogenic expression in thyroid follicular and Hürthle cell carcinomas

Cited by 55 publications

References 8 publications

The IGF-I/IGF-I Receptor Pathway: Implications in the Pathophysiology of Thyroid Cancer

The IGF-I/IGF-I Receptor Pathway: Implications in the Pathophysiology of Thyroid Cancer

Gene Expression Profiling of Differentiated Thyroid Neoplasms

Thyrotoxicosis

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