Time filter

Source Type

Hayashi T.,A+ Network | Hayashi T.,University of Sfax | Mete O.,A+ Network | Mete O.,Endocrine Oncology Site Group
Diagnostic Histopathology | Year: 2014

Paragangliomas can occur in a variety of anatomic locations in the head and neck region and can create diagnostic challenges for practicing pathologists. The most recent data suggest that at least 30-40% of paragangliomas are associated with inherited disease. Occasional VHL-, TMEM127-, and SDHA-related head and neck paragangliomas have been described; however, the bulk of hereditary disease in the head and neck paraganglioma is associated with SDHD, SDHC, SDHB, and SDHAF2 mutations. While the distinction of paragangliomas from other head and neck neoplasms is very important, the clinical responsibility of surgical pathologists has evolved and also includes the integration of SDHB immunohistochemistry into the routine pathology practice. In this article, we highlight an approach to clinicopathological diagnosis of head and neck paragangliomas along with a comprehensive discussion on genotype-biochemical profile correlation and synoptic report approach in paragangliomas. © 2014 Elsevier Ltd.

Gucer H.,Recep Tayyip Erdogan University | Bagci P.,Marmara University | Bedir R.,Recep Tayyip Erdogan University | Sehitoglu I.,Recep Tayyip Erdogan University | And 3 more authors.
Endocrine Pathology | Year: 2016

This study compared the expression profile of HBME-1 and claudin-1 in 90 papillary thyroid carcinomas (PTCs) with respect to the tumor architecture and invasive growth as reflected in 46 BRAF-like, 31 non-invasive RAS, and 13 invasive RAS-like phenotypes. Individual tumors were given an expression score (max 300) by multiplying the percent positive tumor cells by the intensity score (range 0–3). The higher expression of HBME-1 and claudin-1 distinguished BRAF-like phenotype from RAS-like phenotype. The same correlation was also retained for both markers when comparing BRAF-like phenotype with non-invasive and invasive RAS-like phenotypes. The expression scores and positivity rates for both markers did not yield any statistical difference among BRAF-like PTCs. Except the higher positivity rate of HBME-1, invasive RAS-like tumors were not statistically different than their non-invasive counterparts with respect to the positivity rate of claudin-1 and the expression scores of both markers. A central lymph node dissection or selective lymph node sampling was available in 20 specimens. The absence of claudin-1 expression has not been a feature of lymph node metastasis in this series. Despite the limited number of nodal sampling, BRAF-like phenotype and claudin-1 positivity status have been considered the best determinants of positive predictive value and negative predictive value in the prediction of lymph node metastasis among variables, respectively. Adoption of the simplified architectural classification approach to PTCs showed distinct biomarker expression profile in this series; however, immunohistochemistry for HBME-1 and claudin-1 does not seem to be useful in the distinction of invasive RAS-like PTCs from their non-invasive counterparts. Given the overlapping molecular signatures within the RAS-like phenotype, further studies with additional biomarkers are still needed to identify distinct protein expression signatures of non-invasive RAS-like phenotype as this diagnostic category still remains a surgical diagnosis at this time. © 2016 Springer Science+Business Media New York

Duan K.,A+ Network | Mete O.,A+ Network | Mete O.,Endocrine Oncology Site Group
Diagnostic Histopathology | Year: 2016

Primary hyperparathyroidism is a common endocrine disorder and the most prevalent cause of hypercalcemia worldwide. While most cases are sporadic, 5-10% of cases are inherited as part of a familial syndrome: multiple endocrine neoplasia (MEN-1, MEN-2A, MEN-4), hyperparathyroidism jaw-tumor syndrome (HPT-JT), familial hypocalciuric hypercalcemia (FHH), neonatal severe hyperparathyroidism (NSHPT), autosomal dominant moderate hyperparathyroidism (ADMH), or familial isolated hyperparathyroidism (FIHPT). Recent developments in molecular pathology identified specific germline mutations (MEN1, RET, CDKIs, CDC73/HRPT2, CaSR, GNA11, AP2S1) implicated in their pathogenesis. In contrast to sporadic primary hyperparathyroidism which is usually caused by a solitary parathyroid adenoma, hereditary hyperparathyroidism tend to present with multiglandular parathyroid disease, with variable penetrance according to the genetic syndrome. As a result, the clinical severity of each familial condition varies tremendously, resulting in distinct prognosis and treatment strategies. With the advent of molecular testing, genetic subtyping has become an integral part of treatment decision making, requiring correlation with clinical and pathologic findings. This review provides an update on the current knowledge of hereditary hyperparathyroidism and its associated genetic syndromes. © 2016 Elsevier Ltd.

Monsalves E.,University of Toronto | Juraschka K.,Toronto Western Hospital | Tateno T.,Ontario Cancer Institute | Agnihotri S.,University of Toronto | And 5 more authors.
Endocrine-Related Cancer | Year: 2014

Pituitary adenomas are common intracranial neoplasms. Patients with these tumors exhibit a wide range of clinically challenging problems, stemming either from results of sellar mass effect in pituitary macroadenoma or the diverse effects of aberrant hormone production by adenoma cells. While some patients are cured/controlled by surgical resection and/or medical therapy, a proportion of patients exhibit tumors that are refractory to current modalities. New therapeutic approaches are needed for these patients. Activation of the AKT/phophotidylinositide-3-kinase pathway, including mTOR activation, is common in human neoplasia, and a number of therapeutic approaches are being employed to neutralize activation of this pathway in human cancer. This review examines the role of this pathway in pituitary tumors with respect to tumor biology and its potential role as a therapeutic target. © 2014 Society for Endocrinology. Published by Bioscientifica Ltd.

Laws Jr. E.R.,Harvard University | Laws Jr. E.R.,Brigham and Womens Hospital | Ezzat S.,Endocrine Oncology Site Group | Ezzat S.,Ontario Cancer Institute | And 7 more authors.
Pituitary Disorders: Diagnosis and Management | Year: 2013

Do you want to be up to date on the latest concepts of diagnosis and treatment of patients suffering from disorders of the pituitary gland? Are you looking for an expert guide to the best clinical management? If so, this is the book for you, providing a full analysis of pituitary disorder management from acromegaly to Addison's Disease; from Cushing's Disease to hypopituitarism; from hormone disorders to hormone replacement Well-illustrated throughout and with contributions from leading specialists in pituitary disease, inside you'll find comprehensive and expert coverage, including: • Diagnosing pituitary disease • Management options for each disorder • Complications that can occur • Psychological and psychosocial effects of pituitary disease • What outcomes you and your patients can expect over the long term • Current research and clinical trials related to pituitary disease Pituitary Disorders: Diagnosis and Management is the perfect clinical tool for physicians and health care providers from many related disciplines, and an essential companion for the best quality management of pituitary patients. © 2013 John Wiley & Sons, Ltd.

Discover hidden collaborations