Relevant bibliographies by topics / Endocrine and local signalling pathways

Academic literature on the topic 'Endocrine and local signalling pathways'

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Published: 10 December 2022
Last updated: 28 January 2023

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Journal articles on the topic "Endocrine and local signalling pathways"

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Colella, Marco, Danila Cuomo, Antonia Giacco, Massimo Mallardo, Mario De Felice, and Concetta Ambrosino. "Thyroid Hormones and Functional Ovarian Reserve: Systemic vs. Peripheral Dysfunctions." Journal of Clinical Medicine 9, no. 6 (June 1, 2020): 1679. http://dx.doi.org/10.3390/jcm9061679.

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Thyroid hormones (THs) exert pleiotropic effects in different mammalian organs, including gonads. Genetic and non-genetic factors, such as ageing and environmental stressors (e.g., low-iodine intake, exposure to endocrine disruptors, etc.), can alter T4/T3 synthesis by the thyroid. In any case, peripheral T3, controlled by tissue-specific enzymes (deiodinases), receptors and transporters, ensures organ homeostasis. Conflicting reports suggest that both hypothyroidism and hyperthyroidism, assessed by mean of circulating T4, T3 and Thyroid-Stimulating Hormone (TSH), could affect the functionality of the ovarian reserve determining infertility. The relationship between ovarian T3 level and functional ovarian reserve (FOR) is poorly understood despite that the modifications of local T3 metabolism and signalling have been associated with dysfunctions of several organs. Here, we will summarize the current knowledge on the role of TH signalling and its crosstalk with other pathways in controlling the physiological and premature ovarian ageing and, finally, in preserving FOR. We will consider separately the reports describing the effects of circulating and local THs on the ovarian health to elucidate their role in ovarian dysfunctions.
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Matarazzo, Ilaria, Elena Toniato, and Iole Robuffo. "Psychobiome Feeding Mind: Polyphenolics in Depression and Anxiety." Current Topics in Medicinal Chemistry 18, no. 24 (January 16, 2019): 2108–15. http://dx.doi.org/10.2174/1568026619666181210151348.

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Recently gut bacterial populations seem to be involved in many functions and in the pathogenesis of several medical conditions. Traditionally the intestinal microbiome has been recognized to play an important role in metabolizing food compounds in simpler chemical structures for the absorption of different nutrients, and in maintenance control of gastrointestinal pathogens species. Bacterial populations are implicated in a complicated network of interactions within the immune system, epithelial cells local endocrine system, that affects the peripheral and the central nervous system, via blood circulation. Microbiome influencing the mind via immune, endocrine and metabolic signalling, is able to exert some clinical effects in different mental diseases. It releases endocrine substances through several pathways involved in the modulation of neuroinflammation and production of several neurotrasmitter precursors. It has recently been named psychobiome. It is known that phenolic compounds are able to influence microbiome proliferation and to exert several roles, especially regarding neuroinflammation in depressive and anxious behaviour. The clinical effects are reported in the literature. The aim of this study is to highlight the interaction between polyphenols and microbiota- gut-brain axis.
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Brandt, Claus, and Bente K. Pedersen. "The Role of Exercise-Induced Myokines in Muscle Homeostasis and the Defense against Chronic Diseases." Journal of Biomedicine and Biotechnology 2010 (2010): 1–6. http://dx.doi.org/10.1155/2010/520258.

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Chronic inflammation is involved in the pathogenesis of insulin resistance, atherosclerosis, neurodegeneration, and tumour growth. Regular exercise offers protection against type 2 diabetes, cardiovascular diseases, colon cancer, breast cancer, and dementia. Evidence suggests that the protective effect of exercise may to some extent be ascribed to the antiinflammatory effect of regular exercise. Here we suggest that exercise may exert its anti-inflammatory effect via a reduction in visceral fat mass and/or by induction of an anti-inflammatory environment with each bout of exercise. According to our theory, such effects may in part be mediated via muscle-derived peptides, so-called “myokines”. Contracting skeletal muscles release myokines with endocrine effects, mediating direct anti-inflammatory effects, and/or specific effects on visceral fat. Other myokines work locally within the muscle and exert their effects on signalling pathways involved in fat oxidation and glucose uptake. By mediating anti-inflammatory effects in the muscle itself, myokines may also counteract TNF-driven insulin resistance. In conclusion, exercise-induced myokines appear to be involved in mediating both systemic as well as local anti-inflammatory effects.
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Ziliotto, Silvia, Julia M. W. Gee, Ian O. Ellis, Andrew R. Green, Pauline Finlay, Anna Gobbato, and Kathryn M. Taylor. "Activated zinc transporter ZIP7 as an indicator of anti-hormone resistance in breast cancer." Metallomics 11, no. 9 (2019): 1579–92. http://dx.doi.org/10.1039/c9mt00136k.

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Drew, Janice E. "Signalling Pathways Implicated in Obesity Associated Cancers." Open Obesity Journal 6, no. 1 (September 3, 2014): 44–49. http://dx.doi.org/10.2174/1876823701406010044.

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Intensive research over recent years has provided irrefutable evidence of links between obesity and the risk of an increasing number of human cancers. The predicted economic burden is causing significant concern. This has prompted investigation of the underlying mechanisms with a focus on deregulated metabolic pathways. A number of metabolic processes and associated signalling pathways are associated with the development of obesity. These include a number of interlinking pathways regulating endocrine, redox, inflammation, immunity and lipogenic processes. The identification of deregulated metabolic pathways in obesity with promotion of carcinogenesis has targeted research on the signalling molecules involved. Consequently this mini review is focused on aberrant signalling of deregulated pathways provoked by diets that lead to obesity and their role in carcinogenesis. Knowledge of the signalling molecules involved will assist in directing and establishing dietary manipulation strategies to restore metabolic health in obese individuals. Importantly the identified diversity of signalling pathways linked to obesity related cancers will permit design of more effective combinatorial and multi-targeted cancer therapies in the future.
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Almstedt, Katrin, and Marcus Schmidt. "Targeted Therapies Overcoming Endocrine Resistance in Hormone Receptor-Positive Breast Cancer." Breast Care 10, no. 3 (2015): 168–72. http://dx.doi.org/10.1159/000405017.

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Breast cancer is a heterogeneous disease with different molecular subtypes. Most tumours are hormone receptor positive (luminal subtype) with potential endocrine responsiveness. Endocrine therapy is commonly used in these patients. Disease progression caused by endocrine resistance represents a significant challenge in the treatment of breast cancer. To understand the mechanisms of resistance of long-term oestrogen-deprived breast cancer cells, it is important to focus on cross-talk between steroid receptor signalling and other growth factor receptors and intracellular pathways. (Pre-)clinical trials showed that co-targeting these pathways can restore endocrine sensitivity. The focus of the current review is on the intracellular PI3K/AKT/mTOR signalling pathway and cyclin-dependant kinases (CDKs) in oestrogen receptor (ER)-positive breast cancer. Study results clearly show that both inhibition of the PI3K/AKT/mTOR pathway and CDK4/6 are promising ways to improve the efficacy of endocrine treatment in ER-positive breast cancer patients with comparably few side effects. Further clinical trials are needed to identify the patient population who would benefit most from a dual inhibition.
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AlFakeeh, A., and C. Brezden-Masley. "Overcoming endocrine resistance in hormone receptor–positive breast cancer." Current Oncology 25 (June 14, 2018): 18. http://dx.doi.org/10.3747/co.25.3752.

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Endocrine therapy, a major modality in the treatment of hormone receptor (hr)–positive breast cancer (bca), has improved outcomes in metastatic and nonmetastatic disease. However, a limiting factor to the use of endocrine therapy in bca is resistance resulting from the development of escape pathways that promote the survival of cancer cells despite estrogen receptor (er)–targeted therapy. The resistance pathways involve extensive cross-talk between er and receptor tyrosine kinase growth factors [epidermal growth factor receptor, human epidermal growth factor receptor 2 (her2), and insulin-like growth factor 1 receptor] and their downstream signalling pathways—most notably pi3k/akt/mtor and mapk. In some cases, resistance develops as a result of genetic or epigenetic alterations in various components of the signalling pathways, such as overexpression of her2 and erα co-activators, aberrant expression of cell-cycle regulators, and PIK3CA mutations. By combining endocrine therapy with various molecularly targeted agents and signal transduction inhibitors, some success has been achieved in overcoming and modulating endocrine resistance in hr-positive bca. Established strategies include selective er downregulators, anti-her2 agents, mtor (mechanistic target of rapamycin) inhibitors, and inhibitors of cyclin-dependent kinases 4 and 6. Inhibitors of pi3ka are not currently a treatment option for women with hr-positive bca outside the context of clinical trial. Ongoing clinical trials are exploring more agents that could be combined with endocrine therapy, and biomarkers that would help to guide decision-making and maximize clinical efficacy. In this review article, we address current treatment strategies for endocrine resistance, and we highlight future therapeutic targets in the endocrine pathway of bca.
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Bao, Haibo, Hui Zhu, Peihan Yu, Guanghua Luo, Ru Zhang, Qian Yue, and Jichao Fang. "Time-Series Transcriptomic Analysis Reveals the Molecular Profiles of Diapause Termination Induced by Long Photoperiods and High Temperature in Chilo suppressalis." International Journal of Molecular Sciences 23, no. 20 (October 14, 2022): 12322. http://dx.doi.org/10.3390/ijms232012322.

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Survival and adaptation to seasonal changes are challenging for insects. Many temperate insects such as the rice stem borer (Chilo suppressalis) overcome the adverse situation by entering diapause, wherein development changes dynamically occur and metabolic activity is suppressed. The photoperiod and temperature act as major environmental stimuli of diapause. However, the physiological and molecular mechanisms that interpret the ecologically relevant environmental cues in ontogenetic development during diapause termination are poorly understood. Here, we used genome-wide high-throughput RNA-sequencing to examine the patterns of gene expression during diapause termination in C. suppressalis. Major shifts in biological processes and pathways including metabolism, environmental information transmission, and endocrine signalling were observed across diapause termination based on over-representation analysis, short time-series expression miner, and gene set enrichment analysis. Many new pathways were identified in diapause termination including circadian rhythm, MAPK signalling, Wnt signalling, and Ras signalling, together with previously reported pathways including ecdysteroid, juvenile hormone, and insulin/insulin-like signalling. Our results show that convergent biological processes and molecular pathways of diapause termination were shared across different insect species and provided a comprehensive roadmap to better understand diapause termination in C. suppressalis.
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SKOUDY, Anouchka, Meritxell ROVIRA, Pierre SAVATIER, Franz MARTIN, Trinidad LEÓN-QUINTO, Bernat SORIA, and Francisco X. REAL. "Transforming growth factor (TGF)beta, fibroblast growth factor (FGF) and retinoid signalling pathways promote pancreatic exocrine gene expression in mouse embryonic stem cells." Biochemical Journal 379, no. 3 (May 1, 2004): 749–56. http://dx.doi.org/10.1042/bj20031784.

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Extracellular signalling cues play a major role in the activation of differentiation programmes. Mouse embryonic stem (ES) cells are pluripotent and can differentiate into a wide variety of specialized cells. Recently, protocols designed to induce endocrine pancreatic differentiation in vitro have been designed but little information is currently available concerning the potential of ES cells to differentiate into acinar pancreatic cells. By using conditioned media of cultured foetal pancreatic rudiments, we demonstrate that ES cells can respond in vitro to signalling pathways involved in exocrine development and differentiation. In particular, modulation of the hedgehog, transforming growth factor β, retinoid, and fibroblast growth factor pathways in ES cell-derived embryoid bodies (EB) resulted in increased levels of transcripts encoding pancreatic transcription factors and cytodifferentiation markers, as demonstrated by RT-PCR. In EB undergoing spontaneous differentiation, expression of the majority of the acinar genes (i.e. amylase, carboxypeptidase A and elastase) was induced after the expression of endocrine genes, as occurs in vivo during development. These data indicate that ES cells can undergo exocrine pancreatic differentiation with a kinetic pattern of expression reminiscent of pancreas development in vivo and that ES cells can be coaxed to express an acinar phenotype by activation of signalling pathways known to play a role in pancreatic development and differentiation.
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Edwin Thanarajah, Sharmili, and Marc Tittgemeyer. "Food reward and gut-brain signalling." Neuroforum 26, no. 1 (February 25, 2020): 1–9. http://dx.doi.org/10.1515/nf-2019-0020.

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AbstractThe increasing availability of ultra-processed, energy dense food is contributing to the spread of the obesity pandemic, which is a serious health threat in today’s world. One possible cause for this association arises from the fact that the brain is wired to derive pleasure from eating. Specifically, food intake activates reward pathways involving dopamine receptor signalling. The reinforcing value of specific food items results from the interplay between taste and nutritional properties. Increasing evidence suggests that nutritional value is sensed in the gut by chemoreceptors in the intestinal tract and the hepatic portal vein, and conveyed to the brain through neuronal and endocrine pathways to guide food selection behaviour. Ultra-processed food is designed to potentiate the reward response through a combination of high fat and high sugar, therebye seeming highly appetizing. There is increasing evidence that overconsumption of processed food distorts normal reward signalling, leading to compulsive eating behaviour and obesity. Hence, it is essential to understand food reward and gut-brain signalling to find an effective strategy to combat the obesity pandemic.
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Dissertations / Theses on the topic "Endocrine and local signalling pathways"

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Chan, Chin-ho. "Signalling pathways of M918T RET mutant in multiple endocrine neoplasia type 2B." Click to view the E-thesis via HKUTO, 2005. http://sunzi.lib.hku.hk/hkuto/record/B34603244.

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陳展豪 and Chin-ho Chan. "Signalling pathways of M918T RET mutant in multiple endocrine neoplasia type 2B." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2005. http://hub.hku.hk/bib/B34603244.

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Cerqueira, Vera. "Role of intracellular signalling pathways in conferring resistance to endocrine therapies in breast cancer." Thesis, University of Edinburgh, 2010. http://hdl.handle.net/1842/4511.

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Breast cancer is the most prevalent form of cancer in women and accounts for 519,000 annual deaths (WHO Statistics). It has long been established that oestrogen (E2) stimulates tumour growth of oestrogen receptor (ER) positive breast cancer and is involved in the pathogenesis of the disease. Consequently, therapeutic approaches targeting the ER were developed. The use of endocrine therapy is an integral component in treating breast cancer however resistance to such drugs is a major limitation. Unfortunately, even initially responding tumours eventually develop resistance - acquired resistance. The aim of this study was to determine which intracellular pathways may be important in conferring acquired endocrine resistance. In order to do so, a three-stage MCF-7 cell model emulating the clinical development of acquired endocrine was used. MCF-7/LCC1 (LCC1) and MCF-7/LCC9 (LCC9) cells lines were derived from the oestrogen dependent and antioestrogen sensitive MCF-7 cell line. LCC1 cells remain responsive to endocrine therapies but their growth is not dependent on oestrogenic stimulus. LCC9 cells, on the other hand are fully resistant to endocrine therapies and completely oestrogen independent. A number of different cell membrane receptors and intracellular pathways have been implicated in endocrine resistance including HER receptor family, PI3K/Akt & MEK/ERK pathways. These pathways are of particular interest since they are able to activate ER in the absence of oestrogenic stimulus. It is likely that several pathways may be important in conferring resistance to endocrine therapies therefore the experiments in this study focussed on the transcriptional regulation of HER receptors, the activation of the Akt pathway and its implication to basic cellular processes. Following E2 treatment (48h), HER2/3/4 mRNA and protein levels were reduced in MCF- 7 and LCC1 but not in the endocrine-resistant LCC9 cell line as measured by QRT-PCR and Western blotting. The anti-estrogen fulvestrant (ICI 182,780) reversed the E2 modulation. A previous study has shown that ER and the HER2 promoter compete for limiting amounts of SRC-1 in oestrogen-responsive ZR-75-1 cells, causing HER2 repression after E2 stimulation (Newman et al.,Oncogene, 19, 490-7, 2000). ER RNAi abolished E2 repression of HER2 in MCF-7 and LCC1 cells. Furthermore, LCC9 cells have reduced SRC-1 recruitment to ER (assessed by ChIP) allowing SRC-1 to bind to the HER2 promoter. SRC-1 RNAi reduced HER2 transcription in MCF7 cells in a manner similar to E2 whilst it did not restore E2 repression in LCC9 suggesting that the latter cells have alternative mechanisms regulating HER2 transcription. RNAis against the other two p160 co-activators TIF2 and AIB1 did not restore E2 mediated HER2 repression in LCC9 cells. The importance of redundancy between p160 co-activators was also determined by performing double knockouts. SRC-1/TIF2 and TIF2/AIB1 double siRNAs had little effect on HER2 mRNA levels however SRC-1/AIB1 siRNA restored oestrogen mediated downregulation of HER2 transcription in LCC9 cells. This data indicates that SRC-1 and AIB1 co-activators play a role in the transcriptional regulation of HER receptor particularly in MCF-7 and LCC1 cells. The regulation of this transcriptional mechanism is altered in resistant LCC9 cells but, as evidenced by the double knockouts, p160 coactivators are still able to affect HER expression in these cells. This mechanism was further studied in primary breast cancer tumour material. The importance of the Akt pathway in this cell line model was also investigated as phospho-Akt levels are elevated in LCC1 and LCC9 cells. This in turn was shown to activate mTOR and ER (Ser167 residue phosphorylation) thereby contributing to increased growth and ligand independent activation of the oestrogen receptor respectively. Activation of PI3K and PTEN is unchanged in LCC1 and LCC9 cells suggesting that these proteins are not responsible for elevated Akt phosphorylation. In contrast, these cells do express higher levels of phospho-IGFR due to the high availability of receptor ligands (IGFI & IGFII). This is likely to be, at least partially, responsible for the elevated Akt activation. Moreover, the role of Akt isoforms was also determined as they are known to have different functions. The levels of Akt 2 phosphorylation are higher in endocrine resistant cell lines in comparison to parental MCF-7 cells. Interestingly, the Akt 3 phosphorylation is present in all cell lines whilst Akt 1 phosphorylation is minimal. Nevertheless, Akt RNAi studies reveal that Akt 1 and 2 siRNA dramatically reduce growth in MCF-7, LCC1 and LCC9 cells. These results suggest that Akt 2 phosphorylation may play a part in conferring endocrine resistance but the other isoforms are also important for normal cellular growth. The cell cycle profiles of LCC1 and LCC9 are very similar to MCF-7. Similarly, migration levels are unchanged in endocrine resistant cell lines. However, in the presence of antioestrogenic drugs, apoptosis in LCC1 and LCC9 cells in reduced in comparison to the parental MCF-7 cell line. Furthermore, LCC1 and LCC9 cells have higher invasion rates. The deregulation of HER receptor expression and elevated Akt activation may together confer survival advantage in LCC1 and LCC9 cells whilst also increasing their invading potential.
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Jiang, Zhirui. "Mechanism of growth failure in mucopolysaccharidosis VII mice." Thesis, 2018. http://hdl.handle.net/2440/115373.

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Short stature due to progressive growth failure in mucopolysaccharidosis (MPS) does not respond to current treatment. The mechanism behind impaired bone growth in MPS is poorly understood but is crucial to the development of improved strategies to alter bone growth. Bone length was measured in 5 mouse models of MPS to determine the best model for further analysis. The severe MPS VII mouse model (Gus mps/mps strain) [mps/mps superscript] displayed the greatest reduction in bone length and was chosen as the model for studying bone shortening in MPS. Bone formation was delayed in both the primary and secondary ossification centres in MPS VII mice. The growth plate was thickened with enlarged chondrocytes in the resting (RZ) and hypertrophic zones (HZ) but there was a reduced number of chondrocytes in the proliferative zone (PZ) and HZ. Chondrocytes progress through the cell cycle to proliferate and withdraw from the cell cycle to differentiate. Immunohistochemical analysis of cell cycle regulators in the MPS VII growth plate revealed that fewer chondrocytes progressed to mitotic division for proliferation. Fewer HZ chondrocytes progressed to cell cycle withdrawal for terminal differentiation in MPS VII growth plate. Thus, MPS VII chondrocytes while committed to the cell cycle were unable to progress normally through the different stages. Circulating GH, T3 and IHH levels in MPS VII mice were not significantly different from normal. However, IGF1 production in MPS VII mice was reduced both in the circulation and in primary hepatocytes culture, suggesting an impaired GH/IGF1 signaling pathway in MPS VII mice, which may limit the proliferation of chondrocytes in the growth plate. This dysfunction of GH/IGF1 signaling was not caused by a deficiency of the hepatic growth hormone receptor but was associated with a reduction in tyrosine phosphorylation of STAT5 in MPS VII liver. Responsiveness of MPS VII chondrocytes to GH was decreased and local growth plate expression of GHR was reduced, indicating that GHR deficiency may cause the reduced proliferation in MPS VII growth plate. Proliferation and differentiation of chondrocytes are also regulated by locally expressed factors such as IHH, PTHrP and IGF1. Reduced IHH protein level was observed in MPS VII growth plate and in chondrocyte culture, suggesting a potential relationship between IHH and the reduced number of chondrocytes in the PZ of MPS VII growth plate. Persistent expression of Pthrpr and Sox9 and elevated IGF1 secretion by chondrocytes indicated relationships between altered PTHrP and IGF1 signalling pathways and the delayed hypertrophic transition of chondrocytes in the MPS VII growth plate. This thesis highlights that the bone phenotype of MPS is established before birth and suggests that the decreased numbers of chondrocytes in the PZ and HZ of MPS VII growth plate are the results of disruptions in the pace of cell cycle progression. Decreased GHR level would also contribute to reduction of chondrocyte proliferation. Although a decrease in circulating IGF1 level and a decrease in IHH expression in the growth plate was observed, a direct relationship between these observations and short stature cannot be established.
Thesis (Ph.D.) -- University of Adelaide, School of Biological Sciences, 2018
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Books on the topic "Endocrine and local signalling pathways"

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Newell-Price, John, Alia Munir, and Miguel Debono. Normal function of the endocrine system. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0182.

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Endocrinology is the study of hormones (and their glands of origin), their receptors, the intracellular signalling pathways they invoke, and their associated diseases. The clinical specialty of endocrinology focuses specifically on the endocrine organs, that is, the organs whose primary function is hormone secretion, including the hypothalamus, the pituitary, the thyroid, the parathyroid, the adrenal glands, the pancreas, and the reproductive organs.
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Book chapters on the topic "Endocrine and local signalling pathways"

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Aiderus, Abdul Aziz Bin, and Anita K. Dunbier. "Aromatase Inhibitor Resistance via Non-endocrine Signalling Pathways." In Resistance to Targeted Anti-Cancer Therapeutics, 169–90. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-17972-8_9.

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Proud, Christopher G., Harinder S. Hundal, and Peter M. Taylor. "2 Nutrient sensing in animal cells and integration of nutrient and endocrine signalling pathways." In Topics in Current Genetics, 25–64. Berlin, Heidelberg: Springer Berlin Heidelberg, 2004. http://dx.doi.org/10.1007/978-3-540-39898-1_3.

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Pearce, Simon H. S., and Catherine J. Owen. "Endocrine Autoimmunity." In Oxford Textbook of Endocrinology and Diabetes 3e, edited by John A. H. Wass, Wiebke Arlt, and Robert K. Semple, 50–58. Oxford University Press, 2021. http://dx.doi.org/10.1093/med/9780198870197.003.0007.

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The elucidation of the molecular basis for the rare monogenic polyendocrinopathy syndromes including autoimmune polyendocrinopathy type 1, has also allowed novel insights into key points of normal immune homeostasis such as thymic T-lymphocyte antigen receptor selection and the role of peripheral regulatory T cells. These fundamental advances have had far-reaching implications beyond those for endocrine patients. In contrast, the common, complex autoimmune endocrinopathies have been shown to be determined by numerous genetic variants within immune system receptors and signalling pathways along with a small number of variants in the target tissue antigens. A variety of environmental risk factors have been identified for several of these conditions, but it remains to be clarified how these impact pathogenesis at a molecular level. Moreover, the mainstay of therapies for these conditions is hormone replacement and there remains a ‘translational gap’ whereby information about disease pathogenesis has yet to be converted to useful patient advances.
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Haugan Moi, Line L., Marianne Hauglid, Ingvild S., Jennifer Gjerde, Ernst A., and Gunnar Mellgre. "Steroid Receptor Coactivators and Their Expression, Regulation and Functional Role in Endocrine Responsive and Resistant Breast Cancer." In Breast Cancer - Carcinogenesis, Cell Growth and Signalling Pathways. InTech, 2011. http://dx.doi.org/10.5772/22192.

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Hughes, CE, and CTL Huang. "Signalling Pathways Involved in Regulation of β-Cell Proliferation in Pregnancy." In The Endocrine Society's 92nd Annual Meeting, June 19–22, 2010 - San Diego, OR32–4—OR32–4. Endocrine Society, 2010. http://dx.doi.org/10.1210/endo-meetings.2010.part3.or2.or32-4.

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Wells, Cameron I., and Greg O’Grady. "Physiology of the small bowel." In Duodenum and Small Bowel, edited by John A. Windsor, Sanjay Pandanaboyana, Anil K. Agarwal, Samiran Nundy, and Dirk J. Gouma, 18–36. Oxford University PressOxford, 2022. http://dx.doi.org/10.1093/med/9780192862440.003.0002.

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Abstract The small intestine has multiple physiological roles, including digestion, absorption, motility, secretion, sensation, intestinal barrier, and immunological functions. Small bowel activity takes place almost entirely unnoticed by healthy individuals; however, these functions are often affected in pathological and postoperative states. A complex interplay of tightly controlled luminal, neural, and hormonal processes regulate small intestinal function, with bidirectional signalling in neural, endocrine, and immunological pathways. An understanding of normal and altered small bowel physiology is critical for the care of patients undergoing gastrointestinal surgery.
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Siddle, Kenneth, and Gemma V. Brierley. "Molecular Aspects of Hormone Regulation." In Oxford Textbook of Endocrinology and Diabetes 3e, edited by John A. H. Wass, Wiebke Arlt, and Robert K. Semple, 12–21. Oxford University Press, 2021. http://dx.doi.org/10.1093/med/9780198870197.003.0003.

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Hormones travel in the bloodstream to exert effects on target tissues, which are often anatomically remote from the site of hormone secretion. They achieve this by binding and activating receptors, which usually are highly selective or specific. Receptors are grouped into several families according to their molecular structure and mechanism of action. Common classes of receptors important in endocrinology include cell surface G-protein-coupled receptors, receptor tyrosine kinases, and cytokine-like receptors, and intracellular nuclear hormone receptors. In this chapter the basic anatomy of the signalling pathways emanating from these receptors is described, and the principles and mechanisms of information coding and transmission, and how these may go awry in endocrine disease, are discussed.
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Hwang, K., L. Mitchell, C. Rapelje, R. Sitruk-Ware, and PL Morris. "Selective Progesterone Receptor Modulator Ulipristal Differentially Regulates Expression and Activation of Multiple Signalling Pathways in Human Breast Cancer and Normal Human Mammary Epithelial Cells." In The Endocrine Society's 92nd Annual Meeting, June 19–22, 2010 - San Diego, P2–52—P2–52. Endocrine Society, 2010. http://dx.doi.org/10.1210/endo-meetings.2010.part2.p2.p2-52.

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Karavitaki, Niki. "Craniopharyngiomas." In Oxford Textbook of Endocrinology and Diabetes 3e, edited by John A. H. Wass, Wiebke Arlt, and Robert K. Semple, 288–95. Oxford University Press, 2021. http://dx.doi.org/10.1093/med/9780198870197.003.0033.

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Craniopharyngiomas are rare tumours with an incidence of around 0.13 cases per 100 000 person-years. There are two histological subtypes with distinct pathological features: adamantinomatous and papillary. Their pathogenesis remains to be elucidated and recent data suggest the implication of Wnt signalling pathway (for adamantinomatous) and activating mutations in BRAF (V600E) (for papillary). They may present with a variety of clinical manifestations attributed to pressure effects on vital structures of the brain (visual pathways, brain parenchyma, ventricular system, major blood vessels, and hypothalamo-pituitary system). Main management approach is surgery combined or not with adjuvant radiotherapy and, in cases of hypothalamic involvement, conservative surgery is advocated. Patients with craniopharyngioma suffer from significant long-term morbidities (mainly endocrine, visual, hypothalamic, neurobehavioural, and cognitive) attributed to the damage of critical neuronal structures by the primary or recurrent tumour and/or to the adverse effects of the therapeutic interventions and requiring lifelong care. The recent data on the pathogenesis of craniopharyngiomas are promising for the development of targeted therapies.
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Lietman, Steven A., and Michael A. Levine. "Molecular and clinical characteristics of the McCune–Albright syndrome." In Oxford Textbook of Endocrinology and Diabetes, 970–79. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780199235292.003.0704.

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Heterotrimeric guanine nucleotide-binding proteins (G proteins) couple extracellular receptor proteins to intracellular effector enzymes and ion channels. The observation that alterations in G protein-coupled signalling pathways can impact cellular function and proliferation, and cause human disease, has stimulated investigation into the molecular and pharmacological regulation of G protein expression and action. The most well characterized models for altered G protein expression defects have been based on naturally occurring mutations in GNAS, a complex gene at 20q13 which encodes the α‎ subunit of Gs, the G protein that stimulates adenylyl cyclase. Somatic mutations in GNAS (OMIM 139320) that activate Gα‎s are present in a subset of endocrine tumours and in patients with the McCune–Albright syndrome (OMIM 174800), a sporadic disorder characterized by increased hormone production and/or cellular proliferation of many tissues. By contrast, germline mutations of the GNAS gene that decrease expression or function of Gα‎s are present in subjects with Albright’s hereditary osteodystrophy (AHO), a heritable disorder associated with a constellation of developmental defects and, in many patients, reduced responsiveness to multiple hormones that signal through receptors that require Gα‎s to activate adenylyl cyclase EC 4.6.1.1 (i.e. pseudohypoparathyroidism type 1a (OMIM 103580)). McCune–Albright syndrome (MAS) and AHO represent contrasting gain of function and loss of function mutations in the GNAS gene, respectively. Clinical and biochemical analyses of subjects with these syndromes have extended our understanding of the developmental and functional consequences of dysfunctional G protein action, and have provided unexpected insights into the importance of cAMP as a regulator of the growth and/or function of many tissues. This chapter will focus on the clinical implications of activating mutations of GNAS as the basis for MAS.
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Conference papers on the topic "Endocrine and local signalling pathways"

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Ribas, Ricardo, Sunil Pancholi, Stephanie K. Guest, Aradhana Rani, Joanna Nikitorowicz-Buniak, Nikiana Simigdala, Allan Thornhill, et al. "Abstract 4157: Co-blockade of mTORC1, ERBB and estrogen receptor signalling pathways in endocrine resistance breast cancer: Combating tumor plasticity." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-4157.

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