Relevant bibliographies by topics / Endocrine resistance

Academic literature on the topic 'Endocrine resistance'

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Published: 4 June 2021
Last updated: 1 February 2022

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Journal articles on the topic "Endocrine resistance"

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Pinto, Ana Catarina, and Martine J. Piccart-Gebhart. "IN5 ADVANCES IN ENDOCRINE THERAPY AND ENDOCRINE RESISTANCE." Breast 22 (November 2013): S19—S20. http://dx.doi.org/10.1016/s0960-9776(13)70020-1.

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Zheng, L. H., Y. H. Zhao, H. L. Feng, and Y. J. Liu. "Endocrine resistance in breast cancer." Climacteric 17, no. 5 (December 19, 2013): 522–28. http://dx.doi.org/10.3109/13697137.2013.864268.

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Lei, Jonathan T., Meenakshi Anurag, Svasti Haricharan, Xuxu Gou, and Matthew J. Ellis. "Endocrine therapy resistance: new insights." Breast 48 (November 2019): S26—S30. http://dx.doi.org/10.1016/s0960-9776(19)31118-x.

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KRAEMER, WILLIAM J. "Endocrine responses to resistance exercise." Medicine & Science in Sports & Exercise 20, Sup 1 (October 1988): S152—S157. http://dx.doi.org/10.1249/00005768-198810001-00011.

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Johnston, Stephen R. D. "Molecular insights into endocrine resistance." European Journal of Cancer Supplements 3, no. 3 (October 2005): 225–36. http://dx.doi.org/10.1016/s1359-6349(05)80279-4.

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Dixon, J. M. "Endocrine Resistance in Breast Cancer." New Journal of Science 2014 (September 17, 2014): 1–27. http://dx.doi.org/10.1155/2014/390618.

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Around 70% of all breast cancers are estrogen receptor alpha positive and hence their development is highly dependent on estradiol. While the invention of endocrine therapies has revolusioned the treatment of the disease, resistance to therapy eventually occurs in a large number of patients. This paper seeks to illustrate and discuss the complexity and heterogeneity of the mechanisms which underlie resistance and the approaches proposed to combat them. It will also focus on the use and development of methods for predicting which patients are likely to develop resistance.
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Nicholson, Robert I., Iain R. Hutcheson, Janice M. Knowlden, Helen E. Jones, Maureen E. Harper, Nicola Jordan, Steve E. Hiscox, Denise Barrow, and Julia M. W. Gee. "Nonendocrine Pathways and Endocrine Resistance." Clinical Cancer Research 10, no. 1 (January 1, 2004): 346s—354s. http://dx.doi.org/10.1158/1078-0432.ccr-031206.

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Miller, Todd W. "Endocrine Resistance: What Do We Know?" American Society of Clinical Oncology Educational Book, no. 33 (May 2013): e37-e42. http://dx.doi.org/10.14694/edbook_am.2013.33.e37.

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Adjuvant therapy with antiestrogens targeting estrogen receptor α (ER) signaling prevents disease recurrence in many patients with early-stage ER+ breast cancer. However, a significant number of cases exhibit de novo or acquired endocrine resistance. While other clinical subtypes of breast cancer (HER2+, triple-negative) have disproportionately higher rates of mortality, ER+ breast cancer is responsible for at least as many deaths because it is the most common subtype. Therefore, identifying mechanisms that drive endocrine resistance is a high clinical priority. A large body of experimental evidence indicates that oncogenic signaling pathways underlie endocrine resistance, including growth factor receptor tyrosine kinases (HER2, epidermal growth factor receptor [EGFR], fibroblast growth factor receptor 1/2 [FGFR], insulin-like growth factor-1 receptor [IGF-1R]/ insulin receptor [InsR]), PI3K/AKT/ mTOR, MAPK/ERK, Src, CDK4/CDK6, and ER itself. Combined targeting of ER and such pathways may be the most effective means to combat antiestrogen resistance, and clinical trials testing such strategies show promising results. Herein, we discuss pathways associated with endocrine resistance, biomarkers that may be useful to predict response to targeted agents, and avenues for further exploration to identify strategies for the treatment of patients with endocrine-resistant disease.
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Dzhelyalova, M. A. Dzhelyalova, and V. F. Semiglazov Semiglazov. "Endocrine resistance in breast cancer treatment." Pharmateca 11_2020 (October 23, 2020): 21–29. http://dx.doi.org/10.18565/pharmateca.2020.11.21-29.

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Madaio, R. A., G. Spalletta, L. Cravello, M. Ceci, L. Repetto, and G. Naso. "Overcoming Endocrine Resistance in Breast Cancer." Current Cancer Drug Targets 10, no. 5 (August 1, 2010): 519–28. http://dx.doi.org/10.2174/156800910791517226.

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Dissertations / Theses on the topic "Endocrine resistance"

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Tewari, Nilanjana. "Mechanisms underlying obesity-related insulin resistance." Thesis, University of Nottingham, 2016. http://eprints.nottingham.ac.uk/34081/.

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This thesis investigates the effect of body composition on insulin resistance and the impact of supplementation with nutritional support or carbohydrate treatment. Insulin resistance occurs as a response to a number of stressors, including surgery. However, the mechanism underlying the development of insulin resistance is as yet unclear. Adipose tissue distribution appears to play a role in the development of insulin resistance and obesity-related complications. In obese and non-obese patients undergoing open abdominal surgery who received preoperative carbohydrate or placebo, there was a significant fall in perioperative insulin sensitivity and changes in the expression of genes relating to carbohydrate and fat oxidation. There was no influence of perioperative carbohydrate or obesity on change in insulin sensitivity. Patients undergoing neoadjuvant chemotherapy for oesophageal cancer underwent pre and post chemotherapy assessment of insulin sensitivity and body composition. There was a significant reduction in insulin sensitivity despite minimal change in body composition and adequate nutritional intake. These studies have provided further information about the optimal methods for assessment of insulin sensitivity and body composition as well as an insight into mechanisms underlying the association between body composition and insulin sensitivity.
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Ertefai, Benyamin. "Resistance mechanisms during endocrine treatment in breast cancer." Thesis, Cardiff University, 2016. http://orca.cf.ac.uk/95393/.

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Prolonged endocrine therapy is the mainstay of treatment for ER+ breast cancer patients. However, resistance develops in many patients which leads to more aggressive disease. Understanding the mechanisms of acquired resistance that emerge as a consequence of prolonged endocrine treatment remains critical. This study aimed to use gene expression profiling to discover induced mechanisms shared by a panel of MCF7-derived acquired resistant cells that underpin endocrine resistant growth. The in vitro panel represents resistance to oestrogen deprivation, tamoxifen or fulvestrant and includes long-term (3year) models to better-mimic clinical endocrine exposure. Affymetrix 1.0ST microarrays detected 572 genes induced in all resistant models versus MCF7. Over-represented ontologies, pathways and functional classification for these genes revealed induction of oxidative phosphorylation (OxPhos) and TCA cycle enzymes in the resistant models, a finding further confirmed by mass spectrometry. Increased oxygen consumption, NADH dehydrogenase and/or cytochrome C oxidase activity was detected in resistant cells, and targeting with OxPhos inhibitors Metformin or Antimycin A confirmed growth-dependency on OxPhos. Western blotting for AMPK (energy sensor) activity and its downstream anabolic targets (ACC, mTOR/P70S6K) showed Metformin reduced fatty acid and protein synthesis in growth-sensitive endocrine resistant cells. In silico analysis inferred clinical relevance since many TCA/OxPhos genes associated with earlier relapse in ER+ and/or tamoxifen treated patients. Monitoring basal glycolysis (extracellular lactate) and growth impact of 2DG or glutamine restriction demonstrated glycolysis and glutaminolysis also contribute to endocrine resistance. The microarrays furthermore revealed that metabolic kinases PCK2, ALDH18A1 and PFKFB2, and components of cell response to Zn were commonly-induced which may additionally help endocrine resistant growth. This study has revealed increased OxPhos arises as a consequence of prolonged endocrine treatment and is a key bioenergetic pathway sustaining resistance. Since resistant growth is Metformin-sensitive, such targeting of this energy pathway (alongside further antihormones or glycolysis/glutaminolysis inhibitors) could help treat resistance.
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McNeil, Catriona Mairi Garvan Institute of Medical Research Faculty of Medicine UNSW. "Downstream targets of the oestrogen receptor and endocrine resistance." Publisher:University of New South Wales. Garvan Institute of Medical Research, 2008. http://handle.unsw.edu.au/1959.4/41025.

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The transcription factor c-Myc is an early downstream target of oestrogen action in breast cancer cells in culture and it has been speculated that aberrant c-Myc expression may mediate antioestrogen resistance. However, studies of c-Myc protein expression as either a prognostic or predictive marker in human breast cancer have been limited and contradictory, as have been studies of c-Myc expression during breast cancer evolution. In order to assess the relationship between c-Myc protein expression and outcome from breast cancer, a representative cohort of 292 women with invasive ductal carcinoma (IDC) and linked clinicopathological data was assembled and tissue microarrays (TMA) generated from the archived breast cancer specimens. Detailed assessments of the expression of cyclin D1, cyclin E, p21WAF1/Cip1 and p27Kip1 were also conducted and analysed in relation to c-Myc expression using immunohistochemistry. Changes in c-Myc protein expression in a TMA model of breast cancer evolution were also conducted. Finally the cell-cycle effects of low-level constitutive c-Myc expression and high-level inducible c-Myc expression were evaluated in MCF-7 cells in vitro. Key novel results obtained were that c-Myc protein expression changed from preferentially nuclear to preferentially cytoplasmic during the evolution of breast cancer. In women with early invasive breast carcinoma, a "high-risk" cytoplasmic predominant c-Myc expression pattern was defined (~13% of cases) that independently predicted for poor outcome generally, among ER positive cases and in ER postive cases treated with endocrine therapy. In vitro studies confirmed that c-Myc overexpression was associated with resistance to the anti-proliferative effects of anti-oestrogens with persistence of both cyclin D1-cdk4 and cyclin E-cdk2 activities in the face of anti-oestrogen treatment. Further novel findings were that high cyclin D1 expression (upper 10% of expressors) was an independent predictor of poor outcome among ER positive breast cancer cases. Amongst ER + PR positive cases, both "high-risk" c-Myc expression and high level cyclin D1 expression were independent predictors of poor outcome. In summary, these data indicate that aberrant expression of the cell cycle proteins c-Myc and cyclin D1 may result in poor breast cancer outcomes in hormone receptor positive breast cancer and reinforces the importance of the cell cycle as a potential site of therapeutic manipulation in endocrine-resistant breast cancer.
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Moore, Kate. "Collateral resistance to oestrogen and erbB receptor activated growth in endocrine resistant breast cancer." Thesis, University of Edinburgh, 2007. http://hdl.handle.net/1842/24993.

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A panel of breast cancer cell lines (MIII, LCC1, LCC2, LCC9, LY2) derived from the MCF-7 breast cancer cell line with varying oestrogen and anti-oestrogen insensitivity (termed ‘resistant’) was used as a model to determine signalling pathways which may contribute to the development of this insensitivity. 17β-oestradiol (E2) only significantly stimulated growth in MCF-7, MIII and LCC1 cell lines. Resistant cells were insensitive to growth factors, while MCF-7 cells remained responsive. MIII and LCC1 cells retained some tamoxifen sensitivity, while the remaining cell lines were unaffected. ERα expression was determined and ‘cross-talk’ was investigated by monitoring ERα activation via phosphorylation of serine residues 118 and 167 (P-S118/167) using western blotting. MIII, LCC1 and LCC2 cell lines expressed more ERα than MCF-7 cells, which may account for elevated basal growth in these lines. The remaining cell lines expressed similar ERα levels to MCF-y cells, hence another mechanism must account for elevated basal growth in these cells. ERα was subject to E2 ‘turnover’ in all cells, indicating all cells contain functional ERα. ERα activation was then elucidated by observing P-S-118 and P-S167. Of interest, E2 significantly enhanced P-S118 in LCC1 cells to a greater extent than MCF-7cells. Little or no P-S117 was observed in LCC9 cells irrespective of treatment. LCC1 and LCC9 cell lines were further investigate in comparison to MCF-7 cells as they displayed a progressive loss of E2 and anti-E2­ ­sensitivity. No differences in P-S167 expression were observed between cell lines subject to control or E2 treatment; HRGβ enhanced P-S167 to an equal extent in all cells. To investigate which upstream molecules may account for the changes in P-S118, the expression and activation of Akt, MEK and ERK were determined. Total levels of all three proteins were equivalent in all cells. Akt was significantly constitutively phosphorylated in the resistant cell lines compared to MCF-7 cells, suggesting this pathway is important in the development of resistance. TGFα and HRGβ significantly enhanced P-Akt in al three cell lines to a similar extent. HRGβ enhanced P-MEK in MCF-7, LCC1 and LCC9 cell lines, but this diminished as resistance progressed, suggesting a reduction in the involvement of this pathway. However, expression of P-ERK, which is downstream of MEK, was equivalent across all three cell lines, indicating that P-ERK was not responsible for endocrine resistance in this model. The novel recombinant humanised anti-erbB2 monoclonal antibody 2C4 (2C4) inhibited growth factor enhanced proliferation in MCF-7 cells via diminished P-Akt and PERKI/II activation. 2C4 significantly reduced HRGβ-enhanced P-Akt and P-ERKI/II in the resistant cell lines indicating these pathways may be partially responsible for some growth of these cells.
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Burmi, Rajpal Singh. "Identification of genes associated with endocrine resistance in breast cancer." Thesis, Cardiff University, 2006. http://orca.cf.ac.uk/55621/.

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Resistance to tamoxifen, Faslodex and oestrogen-deprivation represents a major hurdle in breast cancer management, and determining the underlying factors driving resistant growth may improve treatment and prognosis. Expression microarrays (Atlas Plastic Human 12K Microarrays GeneSifter software) were used to identify genes altered in breast cancer models with acquired resistance to tamoxifen (TamR) or Faslodex (FasR) versus their parental MCF-7 cell line through cluster analysis, t-testing and ontological examination. Selected genes were verified by PCR, Western blotting and immunocytochemistry. Alongside known breast cancer-related genes (PEA3, vitronectin), two novel genes increased in resistance were the securin/cell-cycle regulator Pituitary Tumour-Transforming Gene-1 (PTTG1) (p=0.013 and p=0.013 in TamR and FasR cells respectively), and GDNF receptor-a3 (GFRa3) (p=0.014 in TamR cells) that promotes cell survival signalling via its coreceptor RET. Increased levels of PTTG1, GFRa3, or their family members were observed in further endocrine resistant states, including an additional faslodex-resistant model that has progressed to a highly-aggressive state (FasR-Lt) and cells resistant to oestrogen-deprivation (X-MCF-7). PTTG1 and GFRa3 induction in response to an anti-EGFR agent in the resistant models implicated these genes in limiting its growth inhibitory effect, and GFR<x3 ligand (arternin) was shown to overcome anti-EGFR response (78% growth recovery). mRNA studies in clinical disease revealed a significant association of PTTG1 with lymph node spread (p=0.001), high tumour grade (p=0.001) and proliferation (p<0.001), while GFRa3 was enriched in ER-negative tumours (p=0.01), showing loss of tubular differentiation (p=0.04) and expressing EGFR (p=0.013), profiles implying roles in clinical resistance and aggressive tumour behaviour. Promisingly, PTTG1 or GFRo3 siRNA significantly reduced cell growth (by 72% p=0.003 and 81% p=0.004 respectively), proliferative capacity (by 23% p<0.001 and 32% p<0.001 respectively) and induced apoptosis (by 43% p=0.05 and 103% p=0.05 respectively) in resistant models. Cumulatively, these data indicate PTTG1 and GFRa3 may provide useful biomarkers and perhaps new therapeutic targets for multiple resistant states.
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Atefi, Mohammad Sadegh. "Estrogen receptor signaling and mechanism of resistance to endocrine therapy." Diss., Restricted to subscribing institutions, 2008. http://proquest.umi.com/pqdweb?did=1581647181&sid=19&Fmt=2&clientId=1564&RQT=309&VName=PQD.

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Wallace, I. R. "The influence of dietary and endocrine factors on insulin resistance." Thesis, Queen's University Belfast, 2014. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.677846.

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Insulin resistance is a characteristic feature of type 2 diabetes mellitus (DM ) and is associated with increased cardiovascular disease. This thesis presents one randomised controlled trial and two cross-sectional analyses, examining the influence of fruit and vegetable consumption and endocrine factors (se~ hormone binding globulin and vitamin D) on insulin resistance. After a 4 week diet of 1-2 portions fruit and vegetables per day, 105 overweight (8MI 27 - 35kg/m2), nondiabetic subjects at elevated cardiovascular disease risk (>20% 1 O-year CVD risk), were randomised to follow a diet of 1-2,4 or 7 or more portions fruit and vegetables per day for the 12-week intervention. Insulin resistance was assessed pre and post intervention using a two-step euglycaemic hyperinsulinaemic clamp. In the cross-sectional analyses, baseline clamp assessments were correlated with sex hormone binding globulin concentration and with vitamin D concentration respectively. Increasing fruit and vegetable consumption was not associated with a change in insulin resistance. Sex hormone binding globulin concentration was inversely correlated with insulin resistance, independent of androgen concentrations and adiposity in the subgroup of 28 postmenopausal women. No association was demonstrated in men. Vitamin D was not associated with insulin resistance. In overweight people at high risk of cardiovascular disease, increased fruit and vegetable intake has no effect on insulin resistance. Weight was maintained in our study and it is possible that alterations in weight have a greater impact on insulin resistance than dietary composition. We suggest that beneficial effects of fruit and vegetable consumption are not mediated by change in insulin resistance. We demonstrate an inverse association between sex hormone binding globulin concentration and insulin resistance, primarily peripheral insulin resistance. We demonstrate no association between vitamin D and insulin resistance and suggest that an association between vitamin D and type 2 DM may be mediated via effects on insulin secretion.
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Chen, Chun. "Systems Biology Study of Breast Cancer Endocrine Response and Resistance." Diss., Virginia Tech, 2013. http://hdl.handle.net/10919/51965.

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As a robust system, cells can wisely choose and switch between different signaling programs according to their differentiation stages and external environments. Cancer cells can hijack this plasticity to develop drug resistance. For example, breast cancers that are initially responsive to endocrine therapy often develop resistance robustly. This process is dynamically controlled by interactions of genes, proteins, RNAs and environmental factors at multiple scales. The complexity of this network cannot be understood by studying individual components in the cell. Systems biology focuses on the interactions of basic components, so as to uncover the molecular mechanism of cell physiology with a systemic and dynamical view. Mathematical modeling as a tool in systems biology provides a unique opportunity to understand the underlying mechanisms of endocrine response and resistance in breast cancer. In Chapter 2, I focused on the experimental observations that breast cancer cells can switch between estrogen receptor α (ERα) regulated and growth factor receptor (GFR) regulated signaling pathways for survival and proliferation. A mathematical model based on the signaling crosstalk between ERα and GFR was constructed. The model successfully explains several intriguing experimental findings related to bimodal distributions of GFR proteins in breast cancer cells, which had been lacking reasonable justifications for almost two decades. The model also explains how transient overexpression of ERα promotes resistance of breast cancer cells to estrogen withdrawal. Understanding the non-genetic heterogeneity associated with this survival-signaling switch can shed light on the design of more efficient breast cancer therapies. In Chapter 3, I utilized a novel strategy to model the transitions between the endocrine response and resistance states in breast cancer cells. Using the experimentally observed estrogen sensitivity phenotypes in breast cancer (sensitive, hypersensitive, and supersensitive) as example, I proposed a useful framework of modeling cell state transitions on the energy landscape of breast cancer as a dynamical system. Grounded on the most possible routes of transitions on the breast cancer landscape, a state transition model was developed. By analyzing this model, I investigated the optimum settings of two intuitive strategies, sequential and intermittent treatments, to overcome endocrine resistance in breast cancer. The method used in this study can be generalized to study treatment strategies and improve treatment efficiencies in breast cancer as well as other types of cancer.
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Bokhari, Ali, Sathvika Gaddam, and Deepika 7471363 Nallala. "A Case of Compensated Thyroid Hormone Resistance." Digital Commons @ East Tennessee State University, 2019. https://dc.etsu.edu/asrf/2019/schedule/50.

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INTRODUCTION Impaired sensitivity to thyroid hormone is described as any process that interferes with the effectiveness of thyroid hormone and includes defects in thyroid hormone action, transport, or metabolism. Here we present a case of a 60-year-old man with resistance to thyroid hormone (RTH), the most common form of impaired sensitivity. CASE A 60-year-old male presented to the endocrinology clinic with complaints of fatigue, decreased concentration, and impaired memory. He denied neck swelling, neck pain, peripheral edema, or any significant changes in weight, temperature sensitivity, bowel habits, and mood. His family history was significant for difficult to control thyroid disease in his brother and son. Thyroid exam was normal. Seven years ago, he was diagnosed with hypothyroidism of undetermined etiology with an elevated Thyroid Stimulating Hormone (TSH) and started on Levothyroxine. TSH was within normal limits in the first 3 years of therapy but TSH and free T4 remained high since then. MRI of the brain could not be done to rule out TSH secreting adenoma as he had pieces of metal in his face. In the absence of overt signs or symptoms of hyperthyroidism except atrial fibrillation, and a normal alpha subunit, IGF1, and prolactin, a TSH secreting adenoma is considered less likely. Levothyroxine was stopped and thyroid hormone levels were rechecked in 1 month that revealed elevated TSH with normal T3 and T4, representing compensated RTH. Genetic counseling was provided to the patient but he refused genetic testing. DISCUSSION The incidence of RTH is approximately 1 in 50,000 live births. In approximately 85 percent of cases it is due to mutations in the gene encoding the thyroid hormone receptor beta (TR-beta), while the other 15% are yet to be determined. It is characterized by reduced responsiveness of target tissue to thyroid hormones. The hallmark of RTH is the paucity of signs and symptoms of thyroid dysfunction despite the presence of high serum T4 and T3 concentrations. Clinical features include goiters, hyperactivity, and tachycardia. It can be diagnosed after other causes of hyperthyroxinemia are ruled out and confirmed with genetic testing.
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Sadler, Amanda J. "Identification of novel genes associated with endocrine resistance in breast cancer." Thesis, University of Reading, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.485503.

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The overall aims of this project were to identify rnRNAs overexpressed or underexpressed as MCF7 human breast cancer cells progress to growth pathways independent of oestrogen and resistant to the antioestrogen, fulvestrant. Growth of oestrogen maintained and long-term oestrogen deprived MCF7,cells with or without la-8M l7p-oestradiol for 7 days enabled the comparison of expression profiles to identify a number of oestrogen regulated genes, in addition to a number of genes differentially expressed in long-term oestrogen deprived cells compared to cells which had been deprived of oestrogen for just? days. Comparison of expression profiles for oestrogen maintained and oestrogen deprived cells following long-term exposure to fulvestrant revealed large alterations in a number of gene expression levels, particularly in the oestrogen maintained cells. Adrenomedullin may have a role in tumour survival and angiogenesis and consistent upregulation of adrenomedulin mRNA was observed during progression to oestrogen insensitivity in duplicate microarray experiments. Real-time RTPCR was able to confirm the increase in mRNA levels in long-term oestrogen deprived cells. Immunofluorescent staining using a monoclonal antibody specific for adrenomedullin showed an increase in the amount of protein in long-term oestrogen deprived cells. Following short and long-term treatment with tamoxifen and fulvestrant the abundance of adrenomedullin rnRNA was increased in oestrogen maintained cells but not in the long-term oestrogen deprived cells. Real time RT-PCR analysis of the GAiA family of transcription factors revealed a reciprocal relationship between GATA3 and GATA6 in ER positive cells and ER negative cells where GATA6 showed highest expression in the ER negative cells and GATA3 was highly expressed in the ER positive cells. Changes were observed in levels of all six of the GATA factors following long-term oestrogen deprivation indicating a functional role for these transcription factors in progression to endocrine resistance. Many potential targets have been identified by the use of microarrays but further validation of cell lines and tumour samples is required to examine the importance of these as possible markers of endocrine resistance in breast tumours.
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Books on the topic "Endocrine resistance"

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Cohen, Margo Panush, and Piero P. Foà, eds. Hormone Resistance and Other Endocrine Paradoxes. New York, NY: Springer New York, 1987. http://dx.doi.org/10.1007/978-1-4612-4758-6.

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Galland, Leo. The fat resistance diet: Reprogram your body to stay thin forever. Emmaus, Penna: Rodale, 2008.

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Hormone resistance and hypersensitivity: From genetics to clinical management. Basel: Karger, 2013.

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The Fat resistance diet: Unlock the secret of the hormone leptin to--eliminate cravings, supercharge your metabolism, lose weight, and reprogram your body to stay thin-forever. New York: Broadway Books, 2006.

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Audrey, Tea, ed. Can't lose weight?: Unlock the secrets that make you store fat! : this is the only book that investigates all the hidden causes of weight excess! Glendale, AZ: SCB International Inc., 2001.

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P, Cohen Margo, and Foà Piero P. 1911-, eds. Hormone resistance and other endocrine paradoxes. New York: Springer-Verlag, 1987.

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Wiffen, Philip, Marc Mitchell, Melanie Snelling, and Nicola Stoner. Therapy-related issues: endocrine system. Oxford University Press, 2012. http://dx.doi.org/10.1093/med/9780199603640.003.0021.

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Diabetes mellitus 444Monitoring and control 449Thyroid disorders 450Diabetes mellitus (DM) affects approximately 4% of the UK population. In 2009, Diabetes UK reported that 2.6 million people in the UK have diabetes.Type 2 diabetes accounts for 90% of all diabetes and is a result of insulin resistance and pancreatic β-cell dysfunction. Type 1 diabetes results from an absolute insulin deficiency secondary to autoimmune dysfunction....
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Beck-Peccoz, Paolo. Syndromes of Hormone Resistance on the Hypothalamic-Pituitary-Thyroid Axis (Endocrine Updates). Springer, 2004.

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Evanthia, Diamanti-Kandarkis, ed. Insulin resistance and polycystic ovarian syndrome: Pathogenesis, evaluation, and treatment. Totowa, N.J: Humana Press, 2007.

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Cabot, Sandra. Can't Lose Weight?: Unlock the Secrets That Keep You Fat! Ten Speed Press, 2002.

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Book chapters on the topic "Endocrine resistance"

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Shankar, Sudha S., and Helmut O. Steinberg. "Insulin Resistance and Hypertension." In Endocrine Hypertension, 239–50. Totowa, NJ: Humana Press, 2012. http://dx.doi.org/10.1007/978-1-60761-548-4_12.

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Saez, S. "Drug Resistance." In Endocrine Therapy of Breast Cancer III, 17–25. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-642-74504-1_3.

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Fu, Xiaoyong, Carmine De Angelis, Jamunarani Veeraraghavan, C. Kent Osborne, and Rachel Schiff. "Molecular Mechanisms of Endocrine Resistance." In Estrogen Receptor and Breast Cancer, 265–307. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-99350-8_11.

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Charmandari, Evangelia, Tomoshige Kino, and George P. Chrousos. "Primary Generalized Familial and Sporadic Glucocorticoid Resistance (Chrousos Syndrome) and Hypersensitivity." In Endocrine Hypertension, 69–87. Totowa, NJ: Humana Press, 2012. http://dx.doi.org/10.1007/978-1-60761-548-4_4.

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Hiscox, Stephen, Julia Gee, and Robert I. Nicholson. "Endocrine resistance and breast cancer invasion." In Metastasis of Breast Cancer, 137–50. Dordrecht: Springer Netherlands, 2007. http://dx.doi.org/10.1007/978-1-4020-5867-7_7.

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Jordan, V. Craig. "Drug Resistance to Antioestrogen Therapy." In Endocrine Therapy of Breast Cancer VI, 61–68. Berlin, Heidelberg: Springer Berlin Heidelberg, 1994. http://dx.doi.org/10.1007/978-3-642-78814-7_7.

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McLeod, James F., and John G. Haddad. "Syndromes of Vitamin D Resistance." In Hormone Resistance and Other Endocrine Paradoxes, 120–56. New York, NY: Springer New York, 1997. http://dx.doi.org/10.1007/978-1-4612-4758-6_5.

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Foà, Piero P. "Introduction: The Journey of the Endocrine Signal: A Paradigm of Murphy’s Law." In Hormone Resistance and Other Endocrine Paradoxes, 1–34. New York, NY: Springer New York, 1987. http://dx.doi.org/10.1007/978-1-4612-4758-6_1.

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Tager, Howard S. "Insulin Gene Mutations and Abnormal Products of the Human Insulin Gene." In Hormone Resistance and Other Endocrine Paradoxes, 35–61. New York, NY: Springer New York, 1987. http://dx.doi.org/10.1007/978-1-4612-4758-6_2.

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Safran, Marjorie, and Lewis E. Braverman. "Euthyroid Hyperthyroxinemia." In Hormone Resistance and Other Endocrine Paradoxes, 62–91. New York, NY: Springer New York, 1987. http://dx.doi.org/10.1007/978-1-4612-4758-6_3.

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Conference papers on the topic "Endocrine resistance"

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Chen, S., S. Masri, H. Chan, K. Petrossian, S. Phung, Y. Yuan, H. Li, and C. Kowolik. "Molecular Characterization of Endocrine Resistance." In Abstracts: Thirty-Second Annual CTRC‐AACR San Antonio Breast Cancer Symposium‐‐ Dec 10‐13, 2009; San Antonio, TX. American Association for Cancer Research, 2009. http://dx.doi.org/10.1158/0008-5472.sabcs-09-407.

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Rody, A., T. Karn, C. Solbach, E. Ruckhaeberle, L. Hanker, V. Mueller, M. Schmidt, R. Gaetje, U. Holtrich, and M. Kaufmann. "The Luminal B Marker NHERF1 Predicts Endocrine Resistance." In Abstracts: Thirty-Second Annual CTRC‐AACR San Antonio Breast Cancer Symposium‐‐ Dec 10‐13, 2009; San Antonio, TX. American Association for Cancer Research, 2009. http://dx.doi.org/10.1158/0008-5472.sabcs-09-3164.

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Yin, W., G. Liu, G. Di, Z. Shen, and Z. Shao. "Intermittent Hypoxia: Potential Factor of Resistance to Endocrine Therapy." In Abstracts: Thirty-Second Annual CTRC‐AACR San Antonio Breast Cancer Symposium‐‐ Dec 10‐13, 2009; San Antonio, TX. American Association for Cancer Research, 2009. http://dx.doi.org/10.1158/0008-5472.sabcs-09-5148.

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Anderson, H., H. Anderson, R. A'Hern, J. Salter, M. Hills, S. Detre, A. Larionov, et al. "Early Acquired Resistance to Endocrine Therapy: Extending the Neoadjuvant Model." In Abstracts: Thirty-Second Annual CTRC‐AACR San Antonio Breast Cancer Symposium‐‐ Dec 10‐13, 2009; San Antonio, TX. American Association for Cancer Research, 2009. http://dx.doi.org/10.1158/0008-5472.sabcs-09-2005.

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Chabot, Catherine, and Mark Basik. "Abstract 3564: ARID1A promotes endocrine resistance in ER+ breast cancer cells." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-3564.

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Liu, Zexuan, Junhao Liu, Weiwei Tang, Uday P. Pratap, Kristin A. Altwegg, Behnam Ebrahimi, Xiaonan Li, Gangadhara R. Sareddy, Suryavathi Viswanadhapalli, and Ratna K. Vadlamudi. "Abstract 733: Significance of PELP1/SETDB1 axis in endocrine therapy resistance." In Proceedings: AACR Annual Meeting 2021; April 10-15, 2021 and May 17-21, 2021; Philadelphia, PA. American Association for Cancer Research, 2021. http://dx.doi.org/10.1158/1538-7445.am2021-733.

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Johnston, SR. "Endocrine therapy combined with signal transduction inhibitors – a means to overcome resistance." In CTRC-AACR San Antonio Breast Cancer Symposium: 2008 Abstracts. American Association for Cancer Research, 2009. http://dx.doi.org/10.1158/0008-5472.sabcs-p1-1.

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Morrison, GD, X. Fu, S. Ithimakin, MF Rimawi, MS Wicha, CK Osborne, and R. Schiff. "P4-01-02: Endocrine Resistance: Mechanism, Tumorigenic Capacities, and New Therapeutic Strategies." In Abstracts: Thirty-Fourth Annual CTRC‐AACR San Antonio Breast Cancer Symposium‐‐ Dec 6‐10, 2011; San Antonio, TX. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/0008-5472.sabcs11-p4-01-02.

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Gokmen-Polar, Yesim, Yaseswini Nellamraju, Xiaoping Gu, Sarath C. Janga, and Sunil S. Badve. "Abstract 4187: Splicing factorsESRP1/ESRP2as regulators of endocrine resistance in breast cancer." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-4187.

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Li, Li, Jamunarani Veeraraghavan, Yiheng Hu, Xian Wang, Ying Tan, Rachel Schiff, and Xiaosong Wang. "Abstract 376: Therapeutic role ofESR1-CCDC170gene fusion in breast cancer endocrine resistance." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-376.

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Reports on the topic "Endocrine resistance"

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Bergamaschi, Anna. Targeted Approaches to Overcoming Endocrine Resistance in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, August 2010. http://dx.doi.org/10.21236/ada541957.

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Bergamaschi, Anna. Targeted Approaches to Overcoming Endocrine Resistance in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, August 2012. http://dx.doi.org/10.21236/ada567133.

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Bergamaschi, Anna. Targeted Approaches to Overcoming Endocrine Resistance in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, August 2011. http://dx.doi.org/10.21236/ada552549.

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Clarke, Robert, Milton Brown, Ayesha N. Shajahan, and Jacqueline Smith. Targeting the UPR to Circumvent Endocrine Resistance in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, October 2014. http://dx.doi.org/10.21236/ada613724.

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Lyerly, H. K. Developing a HER3 Vaccine to Prevent Resistance to Endocrine Therapy. Fort Belvoir, VA: Defense Technical Information Center, October 2014. http://dx.doi.org/10.21236/ada612924.

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Lyerly, H. K. Developing a HER3 Vaccine to Prevent Resistance to Endocrine Therapy. Fort Belvoir, VA: Defense Technical Information Center, October 2013. http://dx.doi.org/10.21236/ada597890.

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Lippman, Marc, and Liang Xu. Acquired Tamoxifen Resistance and Overexpression of Anti-Apoptotic Molecules: A Potential Strategy for Overcoming Endocrine Resistance. Fort Belvoir, VA: Defense Technical Information Center, February 2005. http://dx.doi.org/10.21236/ada434491.

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Klapperich, Catherine, and Jennifer Rosen. Barriers to Therapy: A Novel 3-D Model to Study the Effect of Tumor Interstitial Pressure on Endocrine-Resistant Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, July 2007. http://dx.doi.org/10.21236/ada475124.

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