Polymorphisms within autophagy-related genes as susceptibility biomarkers for pancreatic cancer: A meta-analysis of three large European cohorts and functional characterization.

Pancreatic ductal adenocarcinoma (PDAC) is one of the most lethal cancers with patients having unresectable or metastatic disease at diagnosis, with poor prognosis and very short survival. Given that genetic variation within autophagy-related genes influences autophagic flux and susceptibility to solid cancers, we decided to investigate whether 55,583 single nucleotide polymorphisms (SNPs) within 234 autophagy-related genes could influence the risk of developing PDAC in three large independent cohorts of European ancestry including 12,754 PDAC cases and 324,926 controls. The meta-analysis of these populations identified, for the first time, the association of the BID variant with an increased risk of developing the disease (OR = 1.

No Correlation between PD-L1 and NIS Expression in Lymph Node Metastatic Papillary Thyroid Carcinoma.

Approximately 90% of thyroid cancers are differentiated thyroid cancers (DTCs), originating from follicular epithelial cells. Out of these, 90% are papillary thyroid cancer (PTC), and 10% are follicular thyroid cancer (FTC). The standard care procedure for PTC includes surgery, followed by radioiodine (RAI) ablation and thyroid-stimulating hormone (TSH) suppressive therapy.

Novel biomarkers reveal mismatch between tissue and serum thyroid hormone status in amiodarone-induced hyperthyroidism.

Context: Serum TSH and thyroid hormone (TH) levels are routine markers of thyroid function. However, their diagnostic performance is limited under special conditions, e.g.

Hormonal changes in the first 24 postoperative hours after cardiac surgical procedures.

Background: Hormone level changes after heart surgeries are a widely observed phenomenon due to neurohormonal feedback mechanisms that may affect postoperative morbidity and mortality. The current study aimed to analyze the changes in thyroid and sex hormones in the first 24 postoperative hours after heart surgery.

Methods: This prospective, observational study (registered on ClinicalTrials.

The master role of polarized NIS expression in regulating iodine metabolism in the human body.

Objective: The aim of this study was to investigate how polarized sodium iodide symporter (NIS) expression may regulate iodide metabolism .

Materials And Methods: Polarized NIS expression was analyzed in tissues that accumulate iodide by the use of immunohistochemistry and polyclonal antibody against the C-terminal end of human NIS (hNIS).

Results: Iodide absorption in the human intestine occurs via NIS expressed in the apical membrane.

The Impact of l-Thyroxine Treatment of Donors and Recipients on Postoperative Outcomes After Heart Transplantation.

Objective: The effect of thyroid dysfunction on adverse outcomes has been studied in many different patient populations. The objective of this study was to investigate the effect of thyroid hormone supplementation of donors and recipients on postoperative outcomes after orthotopic heart transplantation.

Design: Retrospective.

Mechanism of anion selectivity and stoichiometry of the Na+/I- symporter (NIS).

I(-) uptake in the thyroid, the first step in thyroid hormone biosynthesis, is mediated by the Na(+)/I(-) symporter (NIS) with an electrogenic 2Na(+):1I(-) stoichiometry. We have obtained mechanistic information on NIS by characterizing the congenital I(-) transport defect-causing NIS mutant G93R. This mutant is targeted to the plasma membrane but is inactive.

The Na+/I symporter (NIS) mediates electroneutral active transport of the environmental pollutant perchlorate.

The Na(+)/I(-) symporter (NIS) is a key plasma membrane protein that mediates active I(-) uptake in the thyroid, lactating breast, and other tissues with an electrogenic stoichiometry of 2 Na(+) per I(-). In the thyroid, NIS-mediated I(-) uptake is the first step in the biosynthesis of the iodine-containing thyroid hormones, which are essential early in life for proper CNS development. In the lactating breast, NIS mediates the translocation of I(-) to the milk, thus supplying this essential anion to the nursing newborn.

Expression of the Na+/I- symporter (NIS) is markedly decreased or absent in gastric cancer and intestinal metaplastic mucosa of Barrett esophagus.

Background: The sodium/iodide symporter (NIS) is a plasma membrane glycoprotein that mediates iodide (I-) transport in the thyroid, lactating breast, salivary glands, and stomach. Whereas NIS expression and regulation have been extensively investigated in healthy and neoplastic thyroid and breast tissues, little is known about NIS expression and function along the healthy and diseased gastrointestinal tract.

Methods: Thus, we investigated NIS expression by immunohistochemical analysis in 155 gastrointestinal tissue samples and by immunoblot analysis in 17 gastric tumors from 83 patients.

Hydrocortisone and purinergic signaling stimulate sodium/iodide symporter (NIS)-mediated iodide transport in breast cancer cells.

The sodium/iodide symporter (NIS) mediates a remarkably effective targeted radioiodide therapy in thyroid cancer; this approach is an emerging candidate for treating other cancers that express NIS, whether endogenously or by exogenous gene transfer. Thus far, the only extrathyroidal malignancy known to express functional NIS endogenously is breast cancer. Therapeutic efficacy in thyroid cancer requires that radioiodide uptake be maximized in tumor cells by manipulating well-known regulatory factors of NIS expression in thyroid cells, such as TSH, which stimulates NIS expression via cAMP.

The Na+/I- symporter mediates iodide uptake in breast cancer metastases and can be selectively down-regulated in the thyroid.

Purpose: The Na(+)/I(-) symporter (NIS) is a key plasma membrane protein that mediates active iodide (I(-)) transport in the thyroid, lactating breast, and other tissues. Functional NIS expression in thyroid cancer accounts for the longstanding success of radioactive iodide ((131)I) ablation of metastases after thyroidectomy. Breast cancer is the only other cancer demonstrating endogenous functional NIS expression.

Advances in Na(+)/I(-) symporter (NIS) research in the thyroid and beyond.

The Na(+)/I(-) symporter (NIS) is a plasma membrane glycoprotein that mediates active iodide uptake in the thyroid-the essential first step in thyroid hormone biosynthesis-and in other tissues, such as salivary and lactating mammary glands. Thyroidal radioiodide uptake has been used for over 60 years in the diagnosis and effective treatment of thyroid cancer and other diseases. However, the NIS cDNA was only isolated in 1996 by expression cloning in Xenopus laevis oocytes, marking the beginning of the molecular characterization of NIS and the study of its regulation, both in the thyroid and other tissues.

Kinetics of perrhenate uptake and comparative biodistribution of perrhenate, pertechnetate, and iodide by NaI symporter-expressing tissues in vivo.

Unlabelled: Pertechnetate (as (99m)TcO(4)(-)), (123)I(-), and (131)I(-) have a long and successful history of use in the diagnosis and therapy of thyroid cancer, with uptake into thyroid tissue mediated by the sodium-iodide symporter (NIS). NIS has also emerged as a potential target for radiotherapy of nonthyroid malignancies that express the endogenous or transfected symporter. Perrhenates (as (188)ReO(4)(-) and (186)ReO(4)(-)) are promising therapeutic substrates of NIS, although less is known about their behavior in vivo.

Immunohistochemical profile of the sodium/iodide symporter in thyroid, breast, and other carcinomas using high density tissue microarrays and conventional sections.

Extrathyroidal cancers could potentially be targeted with (131)I, if the Na(+)/I(-) symporter (NIS) were functional. Using immunohistochemical methods we probed 1278 human samples with anti-NIS antibody, including 253 thyroid and 169 breast conventional whole tissue sections (CWTS). Four high density tissue microarrays containing a wide variety of breast lesions, normal tissues, and carcinoma cores were tested.

The sodium/iodide Symporter (NIS): characterization, regulation, and medical significance.

The Na(+)/I(-) symporter (NIS) is an integral plasma membrane glycoprotein that mediates active I(-) transport into the thyroid follicular cells, the first step in thyroid hormone biosynthesis. NIS-mediated thyroidal I(-) transport from the bloodstream to the colloid is a vectorial process made possible by the selective targeting of NIS to the basolateral membrane. NIS also mediates active I(-) transport in other tissues, including salivary glands, gastric mucosa, and lactating mammary gland, in which it translocates I(-) into the milk for thyroid hormone biosynthesis by the nursing newborn.

Na(+)/I(-) symporter activity requires a small and uncharged amino acid residue at position 395.

Active iodide uptake in the thyroid is mediated by the Na(+)/I(-) symporter (NIS), a key plasma membrane glycoprotein. Several NIS mutations have been shown to cause I(-) transport defect, a condition that, if untreated, can lead to congenital hypothyroidism and, ultimately, cretinism. The study of I(-) transport defect-causing NIS mutations provides valuable insights into the structure-function and mechanistic properties of NIS.