Identification of Molecular Markers Altered During Transformation of Differentiated Into Anaplastic Thyroid Carcinoma

Wiseman, Sam M.; Griffith, Obi L.; Deen, Shaun; Rajput, Ashish; Masoudi, Hamid; Gilks, Blake; Goldstein, Lynn C.; Gown, Allen M.; Jones, Steven J.M.

doi:10.1001/archsurg.142.8.717

Cited by 89 publications

(68 citation statements)

References 48 publications

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“…Increasing evidence suggests that DTC can progress, or undergo anaplastic transformation, into ATC. 119 In an IHC marker panel study of ATC and DTC, Gal-3 expression was found to be up-regulated in ATC compared with adjacent associated DTC foci, although the change was not statistically significant. 119 The variability in reported study results highlights the need for the development of a standardized protocol and criteria for evaluation of Gal-3 expression.…”

Section: Immunohistochemical Studies Evaluating Gal-3 Expression In Tmentioning

confidence: 93%

“…119 In an IHC marker panel study of ATC and DTC, Gal-3 expression was found to be up-regulated in ATC compared with adjacent associated DTC foci, although the change was not statistically significant. 119 The variability in reported study results highlights the need for the development of a standardized protocol and criteria for evaluation of Gal-3 expression. Several studies have shown encouraging results for ability of Gal-3 to discriminate thyroid cancer from benign thyroid nodules.…”

Section: Immunohistochemical Studies Evaluating Gal-3 Expression In Tmentioning

confidence: 93%

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Diagnostic Utility of Galectin-3 in Thyroid Cancer

Chiu

Strugnell

Griffith

et al. 2010

The American Journal of Pathology

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136

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Galectin-3 (Gal-3), which has received significant recent attention for its utility as a diagnostic marker for thyroid cancer, represents the most well-studied molecular candidate for thyroid cancer diagnosis. Gal-3 is a protein that binds to ␤-galactosidase residues on cell surface glycoproteins and has also been identified in the cytoplasmic and nuclear compartment. This marker has been implicated in regulation of normal cellular proliferation and apoptosis, as well as malignant transformation and the metastasis of cancer cells. We here present a mechanistic review of Gal-3 and its role in cancer development and progression. Gal-3 expression studies in thyroid tissue and cytologic tumor specimens and their methodological considerations are also discussed in this article. Despite great variance in their methodology, the majority of immunohistochemical studies found that Gal-3 was differentially expressed in thyroid carcinoma compared with benign and normal thyroid specimens, suggesting that Gal-3 is a good diagnostic marker for thyroid cancer. Recent studies have also demonstrated improved methodological reliability. On the other hand, Gal-3 genomic expression studies have shown inconsistent results for diagnostic utility and are not recommended. Overall, the development of Gal-3 as a diagnostic marker for thyroid cancer represents a promising avenue for future study, and its clinical application could significantly reduce the number of diagnostic thyroid operations performed for cases of indeterminant fine needle aspiration biopsy cytology, and thus positively impact the current management of thyroid nodular disease. (Am J

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Section: Immunohistochemical Studies Evaluating Gal-3 Expression In Tmentioning

confidence: 93%

Section: Immunohistochemical Studies Evaluating Gal-3 Expression In Tmentioning

confidence: 93%

Diagnostic Utility of Galectin-3 in Thyroid Cancer

Chiu

Strugnell

Griffith

et al. 2010

The American Journal of Pathology

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136

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“…Several genes involved in cell proliferation and cell cycle regulation have been shown to be dysregulated in these tumors (6). In addition, it has been recently reported that thyroidspecific transcription factors crucial for thyroid organogenesis and differentiation, such as Pax8, TTF-1, and TTF-2 (FOXE1), are expressed in thyroid neoplasms (7).…”

mentioning

confidence: 99%

FOXA1 Is a Potential Oncogene in Anaplastic Thyroid Carcinoma

Nucera

Eeckhoute

Finn

et al. 2009

Clinical Cancer Research

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Purpose: FOXA1 is a mammalian endodermal transcription factor belonging to the human forkhead box gene family that plays a role in certain tumor types. Here, we investigated the potential role of FOXA1 in human thyroid carcinomas. Experimental Design: We examined the level of FOXA1 expression and gene copy number by immunohistochemistry and fluorescence in situ hybridization, respectively, in a cohort of benign and malignant thyroid tumors. In addition, we examined the role of FOXA1 in the proliferation of an undifferentiated thyroid carcinoma cell line by short hairpin RNA-mediated silencing. Results: We show that FOXA1 is overexpressed in human anaplastic thyroid carcinomas (ATC). In addition, we identify FOXA1 DNA copy number gain within the 14q21.1 locus in both an ATC cell line and human ATC cases. Silencing of FOXA1 in an ATC cell line causes G 1 growth arrest and reduction of cell proliferation. Moreover, we observe a potential link between FOXA1 and the cell cycle machinery by identifying p27 kip1 upregulation on FOXA1 silencing. Conclusions: FOXA1 is overexpressed in aggressive thyroid cancers and involved in cell cycle progression in an ATC cell line. Therefore, FOXA1 may be an important oncogene in thyroid tumorigenesis and a potential new therapeutic target for the treatment of anaplastic thyroid cancers.

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“…10,11 ATCs are often found in association with histologically well differentiated thyroid cancer elements, 12 while showing persistent genetic changes of differentiated carcinoma, coupled with additional abnormalities in several canonical pathways, including the PTEN-AKT, retinoblastoma, and p53 pathways. 9,13 During the transformation from PTC or FTC to ATC, thyroid tumors lose their differentiated characteristics, 14 such as the ability to produce thyroglobulin and their avidity for radioactive iodine, and develop more aggressive cancer characteristics.…”

Section: Figurementioning

confidence: 99%

Anaplastic thyroid cancer – an overview of genetic variations and treatment modalities

Reddi¹,

Kumar²,

Kulstad³

2015

AGG

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Anaplastic thyroid carcinoma (ATC) is a rare but highly aggressive malignancy that accounts for about 1%-2% of all thyroid cancer diagnoses but is responsible for up to 30%-40% of thyroid cancer deaths. ATCs are poorly differentiated tumors that develop on the background of preexisting, often undiagnosed, papillary thyroid carcinoma or follicular thyroid carcinoma, through progressive accumulation of changes in several oncogenic and tumor suppressor pathways, including p53, RAS, RAF, Wnt-β-catenin and the PTEN-AKT pathways. Consequently, the 1-year survival rate after diagnosis ranges from 5% to 15%. Current therapeutic approaches are aimed at common late oncogenic changes and involve inhibition of MAPK and PI3K cell proliferation pathways or restoration of p53 and PTEN tumor suppressor pathways. Since singlemodality therapy has limited effect on anaplastic thyroid cancer, aggressive multimodal treatments are now the treatment of choice, in spite of which, the mean survival time from diagnosis to death continues to remain at about 6 months. The current review attempts to summarize the genetics involved in the development and progression of ATC and provides some insight into the therapeutic options being evaluated for this aggressive cancer.

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Identification of Molecular Markers Altered During Transformation of Differentiated Into Anaplastic Thyroid Carcinoma

Abstract: Hypothesis: A change in tumor expression profile will be observed during the transformation of differentiated into anaplastic thyroid carcinoma.

Cited by 89 publications

References 48 publications

Diagnostic Utility of Galectin-3 in Thyroid Cancer

Diagnostic Utility of Galectin-3 in Thyroid Cancer

FOXA1 Is a Potential Oncogene in Anaplastic Thyroid Carcinoma

Anaplastic thyroid cancer – an overview of genetic variations and treatment modalities

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Identification of Molecular Markers Altered During Transformation of Differentiated Into Anaplastic Thyroid Carcinoma

Abstract: Hypothesis: A change in tumor expression profile will be observed during the transformation of differentiated into anaplastic thyroid carcinoma.

Cited by 89 publications

References 48 publications

Diagnostic Utility of Galectin-3 in Thyroid Cancer

Diagnostic Utility of Galectin-3 in Thyroid Cancer

FOXA1 Is a Potential Oncogene in Anaplastic Thyroid Carcinoma

Anaplastic thyroid cancer &ndash; an overview of genetic variations and treatment modalities

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Anaplastic thyroid cancer – an overview of genetic variations and treatment modalities