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Marc Ingenwerth, Tim Brandenburg, Dagmar Führer-Sakel, Moritz Goetz, Frank Weber, Henning Dralle, Hans-Ulrich Schildhaus, Kurt Werner Schmid, and Sarah Theurer

Medullary thyroid carcinomas (MTC) are rare and aggressive neuroendocrine tumors of the thyroid. About 70% of MTC are sporadic; approximately 50% of those harbour somatic RET mutation. DLL3 is widely expressed in many neuroendocrine tumors and has been evaluated as a potential therapeutic target. Since stromal desmoplasia in sporadic MTC has been identified as a reliable predictor of aggressive behaviour and development of lymph node metastases, a possible correlation of DLL3 expression with the presence of stromal desmoplasia was of particular interest. 59 paraffin-embedded samples of sporadic MTC with (44 cases) and without (15 cases) stromal desmoplasia and known lymph node status were included. DLL3 expression was determined by immunohistochemistry; no expression (0%), low expression (1-49%) and high expression (≥ 50 %) were correlated with clinicopathological data. The proportion of DLL3 positivity was significantly correlated with both stromal desmoplasia (p < 0.0001) and lymph node metastases (p < 0.0001). MTC without stromal desmoplasia consistently lack DLL3 expression. This is the first study to focus on MTC regarding DLL3 expression and the relationship to various factors. Our results demonstrate that expression of DLL3 in MTC represents a reliable surrogate marker for stromal desmoplasia and lymph node metastases and might be an indicator for aggressive clinical behaviour. DLL3 expression in >50% of tumor cells virtually excludes MTC without stromal desmoplasia.DLL3 was discussed as a potential therapeutic target in malignant tumors of other locations with positive immunohistochemical reaction and might therefore be a new therapeutic option in MTC, as well.

Open access

Rosalie Cabry, Philippe Merviel, Aicha Madkour, Elodie Lefranc, Florence Scheffler, Rachel Desailloud, Véronique Bach, and Moncef Benkhalifa

gavaging the pregnant dams) was associated with changes in puberty onset, spermatogenesis, and the development of ovarian follicles up to the F3 generation. The direct, toxic endocrine-disrupting effect (i.e. a dose-response relationship) has rarely been

Open access

I Savchuk, M L Morvan, J P Antignac, K Gemzell-Danielsson, B Le Bizec, O Söder, and K Svechnikov

development of and hormonal production by the HFA are critical for normal fetal maturation and survival. The HFA develop from the intermediate mesoderm and by GW7 have acquired two distinct zones, the inner fetal (FZ) and outer definitive zone (DZ) ( 2 ). In

Open access

Anna-Pauliina Iivonen, Johanna Känsäkoski, Kirsi Vaaralahti, and Taneli Raivio

Introduction Congenital hypogonadotropic hypogonadism (cHH) is a rare genetic disease that prevents pubertal development and causes infertility due to deficient secretion or action of gonadotropin-releasing hormone (GnRH) ( 1 ). Congenital

Open access

Fan Zhang, Jian Chen, Xinyue Lin, Shiqiao Peng, Xiaohui Yu, Zhongyan Shan, and Weiping Teng

levels of 62 children aged 7–9 years who were born to mothers with thyroid dysfunction during early pregnancy. They found that even mild and asymptomatic hypothyroidism in pregnant women, including SCH, could affect the development of intelligence in

Open access

Mette H Viuff and Claus H Gravholt

drug for a certain period of time. When the child with TS has finished treatment in the pediatric department, usually consisting of growth hormone treatment for promoting linear growth and induction of puberty to ensure appropriate development of

Open access

Monia Cito, Silvia Pellegrini, Lorenzo Piemonti, and Valeria Sordi

expressed in combination with NKX6.1 and PTF1α, key transcription factors in pancreas development, and it was demonstrated that hPSC-derived GP2 + cells, differentiated in pancreatic progenitors expressing high levels of NKX6.1, generate β-like cells more

Open access

Andrew R Dismukes, Vanessa J Meyer, Elizabeth A Shirtcliff, Katherine P Theall, Kyle C Esteves, and Stacy S Drury

aging spectrum, DHEA is positively associated with pubertal development. A steady increase in DHEA production is observed with adrenarche, the maturation of the adrenal gland ( 1 ) and the hallmark of pubertal initiation. The adrenal glands continue to

Open access

Monica F Stecchini, Zilda Braid, Candy B More, Davi C Aragon, Margaret Castro, Ayrton C Moreira, and Sonir R Antonini

, but that may be related to the skeletal maturation induced by androgen excess ( 2 ). The development of secondary CPP has been extensively reported in patients with lately diagnosed or poorly controlled congenital adrenal hyperplasia (CAH), and other

Open access

Marilena Nakaguma, Fernanda A Correa, Lucas S Santana, Anna F F Benedetti, Ricardo V Perez, Martha K P Huayllas, Mirta B Miras, Mariana F A Funari, Antonio M Lerario, Berenice B Mendonca, Luciani R S Carvalho, Alexander A L Jorge, and Ivo J P Arnhold

defects in pituitary development (such as HESX1 , GLI2 , OTX2 ) ( 2 ). The most common genes implicated are those encoding GH1 and GHRHR in IGHD and PROP1 in CPHD, especially in certain geographical regions. Until now, most studies used the