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Society for Endocrinology BES 2017

Harrogate, UK
06 Nov 2017 - 08 Nov 2017

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SfE BES 2017 will be on the 6-8 November 2016 in Harrogate, UK.

Oral Communications

Bone, Calcium and Neoplasia

ea0050oc6.1 | Bone, Calcium and Neoplasia | SFEBES2017

Photoperiod-induced central actions of thyroid hormone are essential for medullary bone formation

Butterfield Natalie , Miszkiewicz Justyna , Logan John , Leitch Victoria , Yoshimura Takashi , Bassett Duncan , Williams Graham

Seasonal reproduction enables animals outside tropical regions to rear offspring in a favourable environment. Increasing day length triggers a hypothalamic relay involving thyrotropin, the type 2 deiodinase enzyme and thyroid hormone, which activates the hypothalamic-pituitary-gonadal axis to induce reproductive competence. Photoperiod regulates calcium metabolism and the egg-laying cycle in the Japanese quail (Coturnix japonica), and we hypothesised that activity of ...

ea0050oc6.2 | Bone, Calcium and Neoplasia | SFEBES2017

Glucocorticoids activation by 11beta-hydroxysteroid dehydrogenase type 1 protects against inflammatory bone loss in a murine model of chronic inflammation

Hardy Rowan , Fenton Chloe , Begum Rumina , Naylor Amy , Saghir Atif , Lavery Gareth , Cooper Mark , Raza Karim

Local and systemic bone loss is a common complication in patients with chronic inflammatory disease. Previously, we have identified that glucocorticoid (GC) activation by the enzyme 11beta-hydroxysteroid dehydrogenase type 1 (11β-HSD1) is increased within tissues such as bone during systemic inflammation. However, whilst effective at suppressing inflammation, in excess, GCs drive osteoporosis. To determine the contribution of 11β-HSD1 activated glucocorticoids to inf...

ea0050oc6.3 | Bone, Calcium and Neoplasia | SFEBES2017

Generation of multiple endocrine neoplasia type 1 and death-domain-associated protein pluripotent stem cell lines to investigate mechanisms of pancreatic neuroendocrine tumourigenesis

Dissanayake Kumara , Davidson Lindsay , Poland Conor , Newey Paul

Background: Despite a wealth of gene-discovery studies identifying recurrently mutated genes in hereditary and sporadic endocrine tumours, the molecular mechanisms underpinning tumourigenesis frequently remain ill-defined, in part reflecting a lack of physiologically relevant model systems to investigate gene function. Here, using pancreatic neuroendocrine tumours as an example, we explored the utility of human induced pluripotent stem cell (iPSCs) and CRISPR/Cas9 gene-editing...

ea0050oc6.4 | Bone, Calcium and Neoplasia | SFEBES2017

G-protein coupled oestrogen receptor mediates Hippo pathway signalling and survival outcomes in colorectal cancer patients

Basker Karthik , Arvaniti Anastasia , Rahman Habibur , Gondal Ali , Gilligan Lorna , Foster Paul

Oestrogenic effects on colorectal cancer (CRC) incidence, proliferation, and patient survival remains controversial. We have previously shown enzymic pathways favouring oestradiol (E2) synthesis are upregulated in CRC, and stimulation of the G-protein coupled oestrogen receptor (GPER) by E2 increases CRC proliferation. Here we interrogated The Cancer Genome Atlas (TCGA) Colon Adenocarcinoma (COAD) database to determine all oestrogen metabolism enzymes and...

ea0050oc6.5 | Bone, Calcium and Neoplasia | SFEBES2017

Tumor immunosuppressive environment and tamoxifen resistance in rats exposed to EE2 in utero can be prevented with HDAC and DNMT inhibitors

Bouker Kerrie , Andrade Fabia De Oliveira , Hil Leena

Maternal exposures during pregnancy to endocrine disrupting chemicals increase daughter’s breast cancer risk in humans and animal models. We have previously found that these exposures also pre-program offspring’s mammary tumors to exhibit increased resistance to antiestrogen therapy, and that treatment with valproic acid (HDAC inhibitor) and hydralazine (DNMT inhibitor) prevented antiestrogen resistance. Here we investigated if maternal exposure to ethinyl estradiol ...

ea0050oc6.6 | Bone, Calcium and Neoplasia | SFEBES2017

Calcium-sensing receptor (CaSR) mutations in hypercalcaemic and hypocalcaemic patients cluster at the extracellular dimer interface

Olesen Mie K , Gorvin Caroline M , Thakker Rajesh V , Hannan Fadil M

Loss- and gain-of-function mutations of the calcium-sensing receptor (CaSR) cause familial hypocalciuric hypercalcaemia (FHH) and autosomal dominant hypocalcaemia (ADH), respectively. The CaSR is a homodimeric receptor that has a 612 amino acid extracellular domain (ECD), which binds extracellular calcium (Ca2+e) and mediates dimer interactions upon ligand binding. The ECD consists of lobes 1 and 2, and a cysteine-rich domain (CRD). To elucidate the struc...