R V Lloyd

University of Wisconsin–Madison, Madison, Wisconsin, United States

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Publications (485)1722.27 Total impact

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    ABSTRACT: Follicular variant of papillary thyroid cancer (FVPTC) is the most common and fastest growing subtype of papillary thyroid cancer (PTC) with features of both PTC and follicular thyroid cancer (FTC). The purpose of this study was to determine the patient and tumor features associated with lymph node metastases (LNM) in FVPTC.
    Annals of Surgical Oncology 08/2014; · 4.12 Impact Factor
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    ABSTRACT: Thyroid carcinoma is the most common endocrine malignancy, and papillary thyroid carcinoma represents the most common thyroid cancer. Papillary thyroid carcinomas that invade locally or metastasize are associated with a poor prognosis. We found that, during epithelial-mesenchymal transition (EMT) induced by transforming growth factor-β1 (TGF-β1), papillary thyroid carcinoma cells acquired increased cancer stem cell-like features and the transcription factor paired-related homeobox protein 1 (PRX-1; alias PRRX1), a newly identified EMT inducer, was markedly up-regulated. miR-146b-5p was also transiently up-regulated during EMT, and in siRNA experiments miR-146b-5p had an inhibitory role on cell proliferation and invasion during TGF-β1-induced EMT. We conclude that papillary thyroid carcinoma tumor cells exhibit increased cancer stem cell-like features during TGF-β1-induced EMT, that miR-146b-5p has a role in cell proliferation and invasion, and that PRRX1 plays an important role in papillary thyroid carcinoma EMT and disease progression.
    The American journal of pathology. 06/2014;
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    Ricardo Lloyd, Zhenying Guo, Heather Hardin
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    ABSTRACT: Thyroid cancer is one of the most rapidly increasing malignancies. The reasons for this increase is not completely known, but increases in the diagnosis of papillary thyroid microcarcinomas and follicular variant of papillary thyroid carcinomas along with the enhanced detection of well differentiated thyroid carcinomas are probably all contributing factors. Although most cases of well differentiated thyroid carcinomas are associated with an excellent prognosis, a small percentage of patients with well differentiated thyroid carcinomas as well as most patients with poorly differentiated and anaplastic thyroid carcinomas have recurrent and/or metastatic disease that is often fatal. The cancer stem cell model suggests that a small number of cells within a cancer, known as cancer stem-like cells, are responsible for resistance to chemotherapy and radiation therapy, as well as for recurrent and metastatic disease.. In this review we will focus on current studies about thyroid cancer stem-like cells, the processes of epithelial to mesenchymal transition, and mesenchymal to epithelial transition that provide plasticity to cancer stem-like cell growth in addition to the role of microRNAs in cancer stem cell development and regulation. Understanding the biology of cancer stem cells, epithelial to mesenchymal transition and the metastatic cascade should lead to the design of more rational targeted therapies for highly aggressive and fatal thyroid cancers.
    Endocrine Related Cancer 04/2014; · 5.26 Impact Factor
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    ABSTRACT: Pituitary lactotrophs secrete prolactin. This process is enhanced by estrogen and inhibited by dopamine. Prolactinomas are benign neoplasms that rarely increase in size and are classified according to size as microadenomas (10 mm diameter). The clinical features of prolactinomas most commonly result from prolactin’s effect on the gonads and breast in women and from mass effect in men. This review details the clinical features and management of patients with prolactinomas.
    Expert Review of Endocrinology &amp Metabolism 01/2014; 7(2).
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    ABSTRACT: Histological and cytological criteria in predicting clinical outcomes in patients with oncocytic poorly differentiated carcinoma (PDC) of the thyroid were investigated. In a set of 102 PDC patients, we performed a computer-assisted evaluation of cell size based on two different methods. Univariate analysis showed that cell size was a discriminant prognostic parameter in oncocytic PDC (30 cases) but not in the non-oncocytic carcinomas cases (72 cases). Patients with oncocytic PDC with small medium cell size had a significantly increased risk of death (p=0.029) and a decrease of disease-free survival (p=0.014). This correlation was absented in cases of non-oncocytic PTC, where age and extensive vascular invasion were significant indicators of progression. The proposed morphological signature shows a robust discriminatory ability when tested on the oncocytic PDC group and cell size assessment could thus be proposed as an inexpensive and readily evaluable parameter for predicting prognosis and planning therapy in this tumor type.
    Human pathology 01/2014; · 3.03 Impact Factor
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    ABSTRACT: Understanding the molecular mechanisms involved in thyroid cancer progression may provide targets for more effective treatment of aggressive thyroid cancers. Epithelial mesenchymal transition (EMT) is a major pathologic mechanism in tumor progression and is linked to the acquisition of stem-like properties of cancer cells. We examined expression of ZEB1 which activates EMT by binding to the E-box elements in the E-cadherin promoter, and expression of E-cadherin in normal and neoplastic thyroid tissues in a tissue microarray which included 127 neoplasms and 10 normal thyroid specimens. Thyroid follicular adenomas (n = 32), follicular thyroid carcinomas (n = 28), and papillary thyroid carcinomas (n = 57) all expressed E-cadherin and were mostly negative for ZEB1 while most anaplastic thyroid carcinomas (ATC, n = 10) were negative for E-cadherin, but positive for ZEB1. A validation set of 10 whole sections of ATCs showed 90 % of cases positive for ZEB1 and all cases were negative for E-cadherin. Analysis of three cell lines (normal thyroid, NTHY-OR13-1; PTC, TPC-1, and ATC, THJ-21T) showed that the ATC cell line expressed the highest levels of ZEB1 while the normal thyroid cell line expressed the highest levels of E-Cadherin. Quantitative RT-PCR analyses showed that Smad7 mRNA was significantly higher in ATC than in any other group (p < 0.05). These results indicate that ATCs show evidence of EMT including decreased expression of E-cadherin and increased expression of ZEB1 compared to well-differentiated thyroid carcinomas and that increased expression of Smad7 may be associated with thyroid tumor progression.
    Endocrine Pathology 10/2013; · 1.60 Impact Factor
  • Ricardo V Lloyd
    Human pathology 08/2013; 44(8):1455-6. · 3.03 Impact Factor
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    ABSTRACT: Recent reports indicate that hobnail papillary thyroid carcinoma (HPTC) is a rare, but very aggressive variant of papillary thyroid carcinoma. The authors describe the cytological features of five HPTC on fine-needle aspiration biopsies (FNAB). Moreover, their immunophenotype and the presence of B-RAF mutation by pyrosequencing were investigated. The patients' (three females and two males) age ranged from 27 to 86 (mean 65) years. Tumor size ranged from 2 to 9 cm (mean 4.2 cm). FNAB were highly cellular with a bloody background and scant colloid. The cells were arranged in papillary-like clusters or in micropapillary groups. The cell population consisted of medium-sized cells with "tear-drop" cytoplasm, apically placed nuclei that produced a surface bulge leading to a hobnail appearance. At higher magnification, nuclei showed variable degrees of atypia, occasional pink intranuclear pseudoinclusions, and grooves. Nuclear stratification and atypical mitotic figures were usually present. Immunocytochemistry revealed positive staining for thyroglobulin, thyroid transcriptor factor-1, Hector Battifora Mesothelial Antigen-1, partial loss of E-cadherin expression, and nuclear expression of p53 protein. B-RAF mutation was present in three out of five cytological cases. Immunohistochemical and molecular results were confirmed on histological sections. Recognizing the unique cytological features of HPTC should help to avoid misdiagnosis of this rare variant. Diagn. Cytopathol. 2013. © 2013 Wiley Periodicals, Inc.
    Diagnostic Cytopathology 08/2013; · 1.49 Impact Factor
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    ABSTRACT: Extra-appendiceal colonic carcinoids are uncommon neuroendocrine tumors with a poor prognosis compared with carcinoids of other gastrointestinal origins. Few studies have examined the clinicopathologic profile and behavior of this rare tumor. A retrospective analysis was performed on patients with colonic carcinoid tumors evaluated at a single tertiary care center between 1996 and 2012. Collected data included patient and tumor characteristics, presentation, treatment, recurrence, and survival. Results were integrated into a comprehensive review of the colonic carcinoid literature. In total, 114 patients with colorectal carcinoid tumors were identified, and 15 patients with extra-appendiceal tumors were analyzed. The mean age was 58.6 ± 3.0 y, and subjects were predominantly male (73.3%). The most common presenting problem was abdominal pain (33.3%), although 26.7% of patients were asymptomatic. Cecal tumors were the most prevalent (73.3%), and most patients underwent right hemicolectomy. Three patients with lesions < 1 cm were treated endoscopically. The mean tumor diameter was 2.9 ± 0.5 cm, with lymph node or distant metastasis present in 53.3% and 26.7%, respectively. All but two patients underwent a presumed curative resection. During a mean follow-up of 4.2 ± 1.0 y, there was only one death (non-carcinoid specific). Eleven patients were alive without evidence of disease at last follow-up and three patients were alive with disease, one of whom initially had a presumed curative resection that recurred. This case series further elucidates the clinicopathologic characteristics of colonic carcinoid tumors, which aids physicians in guiding the diagnosis and management of these rare tumors.
    Journal of Surgical Research 06/2013; · 2.02 Impact Factor
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    ABSTRACT: Cancer stem-like cells are a subpopulation of self-renewing stem cells in cancers that are more resistant to chemotherapy and radiation therapy. Evidence supporting the existence of cancer stem-like cells in thyroid and in many other solid tissue cancers is rapidly accumulating. These cells have been studied using specific biomarkers such as CD133, CD44, and aldehyde dehydrogenase enzymes. Putative cancer stem-like cells can be studied in vitro using serum-free media supplemented with basic fibroblast growth factor and epidermal growth factor grown in nonadherent culture (ultra-low attachment plates) or in extracellular matrix leading to cell spheres formation in vitro. Cancer stem-like cells can also be separated by fluorescent cell sorting and used for in vitro or in vivo studies. Injection of enriched populations of cancer stem-like cells (also referred to as tumor initiating cells) into immunodeficient mice often results in rapid growth of xenografts, which express cancer stem-like cell biomarkers. Human cancer stem-like cells have been identified in thyroid cancer cell lines including papillary, follicular, medullary, and anaplastic carcinoma cell lines. They have also been identified in primary thyroid cancers and have been shown to have similar properties as the cancer stem-like cells in thyroid cancer cell lines. Immunohistochemical staining with CD133 and other biomarkers has been used to characterize thyroid cancer stem-like cells in paraffin sections of thyroid cancers. Recent studies of epithelial-mesenchymal transition in which cells lose their epithelial features and acquire mesenchymal phenotypes have shown that these changes are present in thyroid cancers. Biomarkers used to characterize epithelial-mesenchymal transition have also been studied in primary thyroid cancers. A close relationship between epithelial-mesenchymal transition and stem cell features of cancers has been identified in recent studies. New discoveries in this field may lead to more effective therapies for highly aggressive and lethal thyroid cancers.
    Human pathology 03/2013; · 3.03 Impact Factor
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    ABSTRACT: Cancer stem-like cells are a subpopulation of self-renewing cells that are more resistant to chemotherapy and radiation therapy than the other surrounding cancer cells. The cancer stem cell model predicts that only a subset of cancer cells possess the ability to self-renew and produce progenitor cells that can reconstitute and sustain tumor growth. Evidence supporting the existence of cancer stem-like cells in the thyroid, pituitary, and in other endocrine tissues is rapidly accumulating. These cells have been studied using specific biomarkers including: CD133, CD44, Nestin, Nanog, and aldehyde dehydrogenase enzyme. Putative cancer stem-like cells can be studied in vitro using serum-free media supplemented with basic fibroblast growth factor and epidermal growth factor grown in low attachment plates or in extracellular matrix leading to sphere formation in vitro. Cancer stem-like cells can also be separated by fluorescent cell sorting and used for in vitro or in vivo studies. Injection of enriched populations of cancer stem-like cells (also referred to as tumor initiating cells) into immunodeficient mice results in growth of xenografts which express cancer stem-like biomarkers. Human cancer stem-like cells have been identified in thyroid cancer cell lines, in primary thyroid cancers, in normal pituitary, and in pituitary tumors. Other recent studies suggest the existence of stem cells and cancer stem-like cells in endocrine tumors of the gastrointestinal tract, pancreas, lungs, adrenal, parathyroid, and skin. New discoveries in this field may lead to more effective therapies for highly aggressive and lethal endocrine cancers.
    Endocrine Pathology 02/2013; · 1.60 Impact Factor
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    ABSTRACT: The pituitary is the master endocrine gland of the body. It undergoes many changes after birth, and these changes may be mediated by the differentiation of pituitary stem cells. Stem cells in any tissue source must display (1) pluripotent capacity, (2) capacity for indefinite self-renewal, and (3) a lack of specialization. Unlike neural stem cells identified in the hippocampus and subventricular zone, pituitary stem cells are not associated with one specific cell type. There are many major candidates that are thought to be potential pituitary stem cell sources. This article reviews the evidence for each of the major cell types and discuss the implications of identifying a definitive pituitary stem cell type.
    Pituitary 02/2013; · 2.67 Impact Factor
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    ABSTRACT: Islet-1 (Isl1) is a transcription factor involved in the embryogenesis of islets of Langerhans. Immunohistochemically, Isl1 is a sensitive lineage-specific marker for pancreatic neuroendocrine neoplasms (NENs) and their metastases. Its specificity has not been documented, nor have large numbers of NENs from other parts of the gut or other organs been studied. We examined Isl1 expression in 203 primary NENs (gastroenteropancreatic, lung, breast, and ovarian neoplasms) and 40 hepatic NEN metastases (enteropancreatic and lung neoplasms) from known primaries. The correlation between Isl1 and CDX2 expression was studied using a tissue microarray containing 46 pancreatic NENs. Immunostaining for Isl1 and CDX2 was also performed in selected NENs from other sites. Isl1 was positive in 90% of pancreatic, 89% of duodenal, 100% of rectal, 38% of colonic, 14% of appendiceal, and 6% of ileal primaries. Isl1 was negative in all other NENs. Among metastatic neoplasms, 76% of pancreatic and 2 of 2 rectal NEN metastases were Isl1 positive, whereas all other tested metastases were negative. The overall sensitivity and specificity of Isl1 in identifying primary pancreatic NENs was 88% and 80%, respectively. Thirty-six of 46 pancreatic NENs in the tissue microarray were Isl1 positive; 4 were Isl1 negative but CDX2 positive. Our findings confirm that Isl1 is a sensitive marker of pancreatic origin in cases of metastatic NEN. However, Isl1 does not distinguish pancreatic NEN from duodenal and colorectal NEN, even when used in association with CDX2.
    The American journal of surgical pathology 01/2013; · 4.06 Impact Factor
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    ABSTRACT: Well-differentiated small intestinal neuroendocrine tumors are rare malignancies. They arise from enterochromaffin cells and very little is known about differential microRNA (miRNA) expression. The aim of this study was to identify the miRNA profile of well-differentiated small intestinal neuroendocrine tumors, which may have a critical role in tumor development, progression and potentially develop miRNAs as novel clinical biomarkers. Specimens from two test groups, 24 small intestinal neuroendocrine tumor specimens at different stages of malignancy, are included in this study. Total RNA from the first test group, five primary tumors, five mesentery metastases and five liver metastases was hybridized onto the Affymetrix Genechip miRNA arrays to perform a genome-wide profile. The results were validated by using quantitative real-time PCR (QRT-PCR) and northern blot analyses. We then expanded the investigation to laser capture microdissected small intestinal neuroendocrine tumor cells and immuno-laser capture microdissected normal enterochromaffin cells of the first test group. Furthermore, a second test group, three primary tumors, three mesentery metastases and three liver metastases, was included in the study. Thus, two independent test groups validated the data by QRT-PCR. Moreover, we characterized nine miRNAs, five (miR-96, -182, -183, -196a and -200a), which are upregulated during tumor progression, whereas four (miR-31, -129-5p, -133a and -215) are downregulated. Several online software programs were used to predict potential miRNA target genes to map a number of putative target genes for the aberrantly regulated miRNAs, through an advanced and novel bioinformatics analysis. Our findings provide information about pivotal miRNAs, which may lead to further insights into tumorigenesis, progression mechanisms and novel therapeutic targets recognition.Modern Pathology advance online publication, 18 January 2013; doi:10.1038/modpathol.2012.216.
    Modern Pathology 01/2013; · 5.25 Impact Factor
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    ABSTRACT: Background The necessity and frequency of post-operative surveillance for appendiceal carcinoid tumors ≤1 cm is undetermined. Methods A retrospective review of all patients with appendiceal carcinoid tumors ≤1 cm managed at an academic, tertiary referral center. Clinicopathologic characteristics, treatment, surveillance, recurrence, and survival were assessed and analyzed. Results Over a 16-year period, 31 patients met inclusion criteria. Appendicitis (n=17) and pelvic mass (n=5) were the most common presentations. Median tumor diameter was 5 mm (range=1-10 mm). Two patients had mesoappendiceal involvement. No patients had regional lymph node involvement or distant metastasis. Post-operatively, 14 patients (45%) received follow-up recommendations, including one or more of the following: imaging (n=9), medical oncology referral (n=7), colonoscopy (n=5), or laboratory studies (n=5). There were no recurrences or disease-specific deaths during a median follow-up period of 5 years (range=0-15 years). Conclusions Appendiceal carcinoids ≤1 cm are unlikely to recur. Therefore, post-operative surveillance may be unnecessary.
    American journal of surgery 01/2013; · 2.36 Impact Factor
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    ABSTRACT: Pituitary tumor-transforming gene (PTTG1) has been implicated in several oncogenic processes. The aim of this study was to determine PTTG expression in brain tumors. We investigated 88 benign and malignant brain tumors. PTTG immunoexpression was evaluated using a scale of 0 to 3. PTTG immunoexpression was nuclear and cytoplasmic in most tumors, except for medulloblastomas and hemangiopericytomas. Expression was highest in medulloblastomas. Higher grade gliomas including glioblastoma multiforme (GBM) IV and astrocytoma III had the highest level of PTTG expression, whereas low-grade gliomas had the lowest levels of PTTG expression. Hemangiopericytomas had the lowest levels of PTTG immunoreactivity, with meningiomas and schwannomas exhibiting similarly low PTTG levels. Nuclear PTTG immunoreactivity was higher than cytoplasmic in higher-grade tumors. Our results indicate that PTTG immunoexpression is higher in aggressive brain tumors including medulloblastomas, GBM IV, and astrocytoma III, whereas in more benign tumors, PTTG immunoexpression is lower.
    Anticancer research 01/2013; 33(1):119-22. · 1.71 Impact Factor
  • Ryan Gertz, Rakesh Sarda, Ricardo Lloyd
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    ABSTRACT: The initial presentation of follicular thyroid carcinoma is rarely related to metastatic lesions. Presented here is the case of a 70-year-old woman with the initial presentation of a 13-cm chest wall mass identified as a metastatic follicular thyroid carcinoma. The chest wall lesion had features of a poorly differentiated carcinoma with areas of necrosis, an insular growth pattern focally and increased mitotic activity. A small follicular carcinoma was subsequently identified. The primary tumor was a 1-cm well-differentiated follicular carcinoma with capsular and vascular invasion. This represents a rare presentation of a follicular thyroid carcinoma with initial recognition of a large, dedifferentiated metastatic lesion from a small primary carcinoma. Dedifferentiation and metastasis in the context of microcarcinoma is an exceptionally rare event and suggests other mechanisms may be involved in disease spread other than simply increased cell proliferation.
    Endocrine Pathology 12/2012; · 1.60 Impact Factor
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    ABSTRACT: OBJECTIVES: Pancreatic endocrine tumors (PETs) share numerous features with gastrointestinal neuroendocrine (carcinoid) tumors. Targets of novel therapeutic strategies previously assessed in carcinoid tumors were analyzed in PETs (44 cases). METHODS: Activating mutations in EGFR, KIT, and PDGFRA and nonresponse mutations in KRAS were evaluated. Copy number of EGFR and HER-2/neu was quantified by fluorescence in situ hybridization. Expression of EGFR, PDGFRA, VEGFR1, TGFBR1, Hsp90, SSTR2A, SSTR5, IGF1R, mTOR, and MGMT was measured immunohistochemically. RESULTS: Elevated EGFR copy number was found in 38% of cases but no KRAS nonresponse mutations. VEGFR1, TGFBR1, PDGFRA, SSTR5, SSTR2A, and IGF1R exhibited the highest levels of expression in the largest percentages of PETs.Anticancer drugs BMS-754807 (selective for IGF1R/IR), 17-(allylamino)-17-demethoxygeldanamycin (17-AAG, targeting Hsp90), and axitinib (directed toward VEGFR1-3/PDGFRA-B/KIT) induced growth inhibition of human QGP-1 PET cells with IC50 values (nM) of 273, 723, and 743, respectively. At growth-inhibiting concentrations, BMS-754807 inhibited IGF1R phosphorylation; 17-AAG induced loss of EGFR, IGF1R, and VEGFR2; and axitinib increased p21(CDKN1A) expression without inhibiting VEGFR2 phosphorylation. CONCLUSIONS: Results encourage further research into multidrug strategies incorporating inhibitors targeting IGF1R or Hsp90 and into studies of axitinib combined with conventional chemotherapeutics toxic to tumor cells in persistent growth arrest.
    Pancreas 12/2012; · 2.95 Impact Factor
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    ABSTRACT: Recent reports indicate that papillary thyroid carcinoma with hobnail features, also designated as micropapillary variant of papillary thyroid carcinoma, is a rare but very aggressive variant of papillary thyroid carcinoma. We examined the histopathologic and immunohistochemical features of 24 cases of papillary thyroid carcinoma with hobnail/micropapillary component to determine the prognostic significance of the amount of hobnail/micropapillary features in these tumors. The patients included 18 women and 6 men. Ages ranged from 28 to 78 years (mean, 57 years). Tumor size ranged from 1 to 5.8 cm (mean, 3 cm). The average follow-up time was 106 months (range, 4-274 months). Twelve cases (50%) of papillary thyroid carcinoma showed more than 30% hobnail/micropapillary features, and all but 3 cases were associated with an aggressive behavior. During the follow-up, 6 of these patients died of disease after a mean of 44.8 months, and 3 patients remained alive with extensive disease after a mean follow-up of 32.3 months. Metastases to lymph nodes or distant organs showed a hobnail pattern of growth similar to the primary tumor. The remaining 3 patients with prominent hobnail/micropapillary features were alive with no evidence of disease after a mean follow-up of 125.3 months. The other 12 papillary thyroid carcinoma cases (50%) showed less than 30% hobnail/micropapillary features. Nine of these patients were alive without disease after a mean of 162 months, and 1 patient died of sepsis, which was not related to thyroid tumor after 155 months. Two patients in this group died of disease after 21 and 163 months, respectively. These findings confirm earlier observations that papillary thyroid carcinoma with hobnail/micropapillary features is an aggressive variant of papillary thyroid carcinoma. Tumors with more than 30% hobnail/micropapillary features were often very aggressive, although 2 patients with tumors with 10% hobnail/micropapillary features also had poor outcomes.
    Human pathology 10/2012; · 3.03 Impact Factor
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    ABSTRACT: Epithelial-mesenchymal transition is an important mechanism of epithelial tumor progression, local invasion and metastasis. The E-cadherin (CDH1) repressor SLUG (SNAI2) and the basic helix-loop-helix transcription factor TWIST1 inhibit CDH1 expression in poorly differentiated malignancies as inducers of epithelial-mesenchymal transition. Epithelial-mesenchymal transition has been implicated in progression from well to poorly differentiated/anaplastic thyroid carcinoma but the expression of SNAI2 and TWIST1 proteins and their phenotypic association in human thyroid cancers has not been extensively studied. We examined the expression of SNAI2, TWIST1 and CDH1 by immunohistochemistry in a panel of well-differentiated and anaplastic thyroid cancers and by qRT-PCR in thyroid cell lines. Ten normal thyroids, 33 follicular adenomas, 56 papillary thyroid carcinomas including 28 follicular variants, 27 follicular carcinomas and 10 anaplastic thyroid carcinomas were assembled on a tissue microarray and immunostained for SNAI2, TWIST1 and CDH1. Most (8/10) anaplastic thyroid carcinomas demonstrated strong nuclear immunoreactivity for SNAI2 with associated absence of CDH1 in 6/8 cases (75%). TWIST1 was expressed in 5/10 anaplastic thyroid carcinomas with absence of CDH1 in 3/5 (60%) cases. These findings were confirmed in whole sections of all anaplastic thyroid carcinomas and in a separate validation set of 10 additional anaplastic thyroid carcinomas. All normal thyroids, follicular adenomas, papillary and follicular thyroid carcinomas were negative for SNAI2 and TWIST1 (P<0.0001) and all showed strong diffuse immunoreactivity for CDH1 (P=0.026). Expression of SNAI2, TWIST1 and CDH1 mRNA varied in a normal thyroid, papillary carcinoma and two anaplastic thyroid carcinoma cell lines tested, but the highest levels of CDH1 mRNA were detected in the normal thyroid cell line while the anaplastic thyroid carcinoma cell line demonstrated the highest levels of SNAI2 and TWIST1 mRNA. Our findings support the role of epithelial-mesenchymal transition in the development of anaplastic thyroid carcinoma.Modern Pathology advance online publication, 17 August 2012; doi:10.1038/modpathol.2012.137.
    Modern Pathology 08/2012; · 5.25 Impact Factor

Publication Stats

11k Citations
1,722.27 Total Impact Points

Institutions

  • 2011–2014
    • University of Wisconsin–Madison
      • • Department of Pathology and Laboratory Medicine
      • • Department of Surgery
      Madison, Wisconsin, United States
    • University of California, San Francisco
      • Department of Pathology
      San Francisco, CA, United States
    • Duke University Medical Center
      • Division of Endocrinology, Metabolism, and Nutrition
      Durham, NC, United States
  • 1989–2013
    • University of Toronto
      • • Division of Neurosurgery
      • • Laboratory Medicine Program
      • • Saint Michael's Hospital
      • • Department of Laboratory Medicine and Pathobiology
      Toronto, Ontario, Canada
  • 2010–2012
    • Università degli Studi di Torino
      • Dipartimento di Biotecnologie Molecolari e Scienze per la Salute
      Torino, Piedmont, Italy
  • 1993–2012
    • Mayo Clinic - Rochester
      • Department of Laboratory Medicine & Pathology
      Rochester, MN, United States
  • 1995–2011
    • Mayo Foundation for Medical Education and Research
      • • Department of Pathology
      • • Department of Laboratory Medicine
      Rochester, Michigan, United States
  • 2009
    • Imperial College London
      Londinium, England, United Kingdom
    • Queen's University
      • Department of Pathology and Molecular Medicine
      Kingston, Ontario, Canada
  • 2000–2009
    • University of Santiago de Compostela
      • • Departamento de Anatomía y Produción Animal
      • • Department of Physiology
      Santiago de Compostela, Galicia, Spain
    • Kitasato University
      Edo, Tōkyō, Japan
  • 2008
    • Brigham and Women's Hospital
      • Department of Pathology
      Boston, MA, United States
    • St. Michael's Hospital
      Toronto, Ontario, Canada
  • 2005
    • State University of New York Downstate Medical Center
      • Department of Radiology
      Brooklyn, NY, United States
    • ΓΕΝΙΚΟ ΝΟΣΟΚΟΜΕΙΟ ΑΘΗΝΩΝ "Γ. ΓΕΝΝΗΜΑΤΑΣ"
      Athínai, Attica, Greece
  • 2004
    • Gulhane Military Medical Academy
      • Department of Pathology
      Ankara, Ankara, Turkey
  • 2002–2003
    • St. Jude Children's Research Hospital
      • Department of Pathology
      Memphis, Tennessee, United States
    • Ospedale di Circolo e Fondazione Macchi Varese
      Varese, Lombardy, Italy
    • Wakayama Medical University
      Wakayama, Wakayama, Japan
  • 1997–2003
    • Nippon Medical School
      • Department of Neurosurgery
      Tokyo, Tokyo-to, Japan
  • 1984–2002
    • University of Michigan
      • • Department of Human Genetics
      • • Department of Pathology
      Ann Arbor, MI, United States
  • 2001
    • University of Cincinnati
      • Department of Pathology and Laboratory Medicine
      Cincinnati, OH, United States
    • Complejo Hospitalario Universitario de Santiago
      Santiago, Galicia, Spain
  • 1983–1999
    • Concordia University–Ann Arbor
      Ann Arbor, Michigan, United States
  • 1998
    • Mayo Clinic - Scottsdale
      Scottsdale, Arizona, United States
  • 1994
    • Tokyo Medical University
      • Department of Neurosurgery
      Tokyo, Tokyo-to, Japan
  • 1991
    • The Princess Margaret Hospital
      Toronto, Ontario, Canada
  • 1987
    • Henry Ford Hospital
      • Department of Internal Medicine
      Detroit, MI, United States
  • 1986
    • Vanderbilt University
      Nashville, Michigan, United States