Relevant bibliographies by topics / ER-positive

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'ER-positive'

Author: Grafiati
Published: 14 March 2023

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Journal articles on the topic "ER-positive"

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Susman, Ed. "ER-Positive Breast Cancer." Oncology Times 27, no. 4 (February 2005): 58. http://dx.doi.org/10.1097/01.cot.0000287844.29669.86.

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Solberg, Erik. "Idrettsutøvere er positive til screening." Tidsskrift for Den norske legeforening 131, no. 17 (2011): 1632. http://dx.doi.org/10.4045/tidsskr.11.0807.

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Mamounas, Terry. "Personalizing Treatment for Node-Positive, ER-Positive Breast Cancer." Oncology Times 39, no. 6 (March 2017): 36. http://dx.doi.org/10.1097/01.cot.0000515196.45322.1e.

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Deng, Hao, Li Yin, Xin-Tian Zhang, Li-Jiang Liu, Mo-Lin Wang, and Zhao-Yi Wang. "ER-α variant ER-α36 mediates antiestrogen resistance in ER-positive breast cancer stem/progenitor cells." Journal of Steroid Biochemistry and Molecular Biology 144 (October 2014): 417–26. http://dx.doi.org/10.1016/j.jsbmb.2014.08.017.

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Ruijtenbeek, R., A. Umar, L. van Houten, R. Hilhorst, J. A. Foekens, R. de Wijn, and J. W. Martens. "Differential protein kinase activity in ER-positive and ER-negative breast cancer." Journal of Clinical Oncology 27, no. 15_suppl (May 20, 2009): e22142-e22142. http://dx.doi.org/10.1200/jco.2009.27.15_suppl.e22142.

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e22142 Background: Specific protein tyrosine kinases (PTKs) promote cancer progression and are potential drug targets. The presence of the estrogen receptor (ER) is an important criterion in deciding on treatment of patients with breast cancer. Since PTKs can affect the tumors' receptor function, we investigated in our first proof-of-principle study whether it is possible to discriminate ER-positive (ER+) from ER-negative (ER-) tumors based on PTK activity using microarrays containing many PTK peptide substrates. Methods: Cryosections of 12 ER+ and 12 ER- breast tumors were lysed in the presence of appropriate protease and phosphatase inhibitors. The protein kinase activity in the lysates was monitored in vitro using PamChip peptide microarrays, which comprise of 253 PTK peptide substrates derived from known human phosphorylation sites. Peptide phosphorylation through active kinases can be monitored in samples in real time, using a fluorescently labeled phospho-tyrosine specific antibody. Results: Phosphorylation activity profiles were determined in quadruplicate using multiple independent sample preparations. Using ANOVA analysis, out of 253 peptides, several peptides with a different phosphorylation signal in ER+ and ER- samples were found: 22 with p < 0.02 including VEGFR1, 2 and 3 and ADAM9. Multivariate unsupervised analysis using Principle Component Analysis showed a clustering of ER+ samples vs. ER- samples. Predictive analysis was performed using Partial-Least Squares Discriminant Analysis without explicit feature selection. The prediction error obtained from within experiment cross validation was typically in the range 10–20%. The error rate for between experiment prediction was 20%. An average predictive profile was constructed in which peptides with a relatively large weight were included, e.g. ADAM9 and BCAR1. Conclusions: Using PamChip peptide microarrays we have shown that differences in protein kinase activity exist between ER+ and ER- breast tumors. Our in vitro assay is a promising tool to investigate the interplay between kinase and nuclear receptor mediated signaling, with potential relevance to patient selection for targeted therapies. No significant financial relationships to disclose.
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Aasland, Aadne, Arne Backer Grønningsæter, and Peter Meylakhs. "Flere positive – men er alt negativt?" Nordisk Østforum 24, no. 04 (January 10, 2011): 375–95. http://dx.doi.org/10.18261/issn1891-1773-2010-04-03.

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Perron, Michelle. "Investigating Metformin for ER-Positive Breast Cancer." Oncology Times 42, no. 13 (July 5, 2020): 1,12–12. http://dx.doi.org/10.1097/01.cot.0000688420.18453.c6.

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Colleoni, M., and E. Montagna. "Neoadjuvant therapy for ER-positive breast cancers." Annals of Oncology 23 (September 2012): x243—x248. http://dx.doi.org/10.1093/annonc/mds305.

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Wang, Weiqi, Bing Xu, Zhaoxu Zhang, Kehua Fang, and Xiaotian Chang. "RCC2 Expression Stimulates ER-Positive Breast Tumorigenesis." Journal of Oncology 2020 (May 23, 2020): 1–13. http://dx.doi.org/10.1155/2020/5619462.

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Objective. Regulator of chromosome condensation 2 (RCC2) has been reported to be involved in the regulation of cell cleavage. This study investigated the effect of RCC2 expression on breast tumorigenesis. Methods. MCF-7 cells originating from estrogen receptor-positive (ER+) breast cancer were transfected with anti-RCC2 siRNA or RCC2-expressing plasmids. Cell proliferation, apoptosis, migration, and cytokine production in the transfected cells were examined using the CCK-8 assay, wound healing assay, and flow cytometry, respectively. PCR array was used to investigate the tumorigenic pathway of RCC2 in MCF-7 cells transfected with the anti-RCC2 siRNA. MCF-7 cells were also transfected with lentivirus-containing anti-RCC2 short hairpin RNA and were injected into BALB/c nude mice to generate tumor-bearing mice. Tumor growth in the mouse model was examined using magnetic resonance imaging by diffusion-weighted imaging analysis. Results. Western blotting and immunohistochemistry detected significantly increased expression of RCC2 in ER + breast tumor tissues compared with breast fibroadenoma samples. Inhibiting RCC2 expression decreased cell migration and stimulated apoptosis in MCF-7 cells, while overexpressing RCC2 stimulated cell migration and inhibited apoptosis. The inhibition of RCC2 expression significantly decreased breast tumor growth and IL-6 levels in the tumor-bearing mice. PCR array demonstrated that inhibiting RCC2 expression significantly decreased the expression of IGF1 and TWIST1, two well-known tumor-enhancing genes, in MCF-7 cells; conversely, overexpressing RCC2 increased the expression levels of these two genes in the transfected cells. This result was verified in the mouse model following inhibition of RCC2 expression in MCF-7 cells. Additionally, estradiol-17β suppressed MCF-7 cell apoptosis, stimulated cell proliferation and cell migration, and increased RCC2, IGF1, and TWIST1 expression. The siRNA-mediated inhibition of RCC2 expression alleviated the inhibitory effects of estrogen on apoptosis in MCF-7 cells, while overexpressing RCC2 enhanced the estrogen-driven inhibition of apoptosis. Modifying RCC2 expression had no impact on MCF-7 cell proliferation in the presence or absence of estradiol-17β. Conclusions. Our results suggest that estrogen-induced RCC2 expression prompts IGF1, TWIST1, and IL-6 expression, stimulates cell migration, and inhibits apoptosis to contribute to ER + breast tumorigenesis.
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McAndrew, Nicholas P., and Richard S. Finn. "Management of ER positive metastatic breast cancer." Seminars in Oncology 47, no. 5 (October 2020): 270–77. http://dx.doi.org/10.1053/j.seminoncol.2020.07.005.

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Dissertations / Theses on the topic "ER-positive"

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Xu, Yuanming, Fang Zhao, Quan Qiu, Kun Chen, Juncheng Wei, Qingfei Kong, Beixue Gao, et al. "The ER membrane-anchored ubiquitin ligase Hrd1 is a positive regulator of T-cell immunity." NATURE PUBLISHING GROUP, 2016. http://hdl.handle.net/10150/621464.

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Identification of positive regulators of T-cell immunity induced during autoimmune diseases is critical for developing novel therapies. The endoplasmic reticulum resident ubiquitin ligase Hrd1 has recently emerged as a critical regulator of dendritic cell antigen presentation, but its role in T-cell immunity is unknown. Here we show that genetic deletion of Hrd1 in mice inhibits T-cell proliferation, production of IL-2, and differentiation of Th1 and Th17 cells, and consequently protects mice from experimental autoimmune encephalomyelitis. Hrd1 facilitates T-cell proliferation by the destruction of cyclin-dependent kinase inhibitor p27(kip1), and deletion of p27(kip1) in Hrd1-null T-cells rescues proliferative capacity but not the production of cytokines, including IL-2, IFN-γ and IL-17. T-cell expression of Hrd1 is higher in patients with multiple sclerosis than in healthy individuals, and knockdown of Hrd1 in human CD4(+) T cells inhibits activation and differentiation to Th1 and Th17 cells. Our study identifies Hrd1 as a previously unappreciated positive regulator of T cells and implies that Hrd1 is a potential therapeutic target for autoimmune diseases.
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Henryka, Gawrzak Sylwia. "Identification and functional analysis of molecular mechanisms involved in the latency of ER positive breast cancer." Doctoral thesis, Universitat de Barcelona, 2016. http://hdl.handle.net/10803/402624.

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Breast cancer is the most frequently diagnosed cancer and remains the second leading cause of death among women in Europe and United States. In this malignancy, metastasis remains to be an incurable condition, and therefore the major cause of death. Metastatic lesions can appear within a wide time ranging from months to years or decades after primary tumor resection. In particular, in the estrogen receptor (ER) positive breast cancer subgroup metastatic latency continues to be a major challenge for the researchers, clinicians and patients. This thesis reports the identification and functional analysis of molecular mechanisms involved in the latency of ER positive breast cancer. For that purpose we based our research on a comprehensive approach that relies on genetically engineered human breast cancer cells, experimental mouse models, unbiased whole- genome screen and clinical data. The first part of the thesis describes a novel mouse model of breast cancer dormancy. We showed that metastatic cells home the bone and enter the latency phase as micrometastatic lesions where tumor growth is restricted mainly due to the equilibrated ratios of cell proliferation and cell death. This experimental mouse model was used to identify genes relevant for long- latent relapse. To this end, we performed in vivo loss-of- function shRNA screening. In the screening we challenged a whole-genome library of shRNA to uncover genes whose depletion negatively regulates dormancy. Among the candidate genes revealed by the screen we focused on MSK1 as a long-latent metastasis regulator. The in vivo and in vitro validation results indicate that MSK1 plays a role in homing and differentiation of metastatic cells. We showed that MSK1 promotes the expression luminal transcription factors - FOXA1 and GATA-3. Therefore, MSK1 depletion is beneficial for metastatic cells leading to a partial phenotype shift towards a more aggressive and poorly differentiated basal population. Furthermore, our data suggest that MSK1 may be involved in metastatic cell plasticity by remodeling the chromatin. Importantly, low MSK1 gene expression levels associate with early metastasis in ER positive breast cancer.
El cáncer de mama es el tipo de cáncer más frecuentemente diagnosticado, siendo la segunda causa de muerte entre las mujeres de Europa y Estados Unidos. En esta enfermedad, la metástasis sigue siendo incurable, y por ello es la principal causa de muerte. Las lesiones metastásicas pueden aparecer dentro de un amplio periodo de tiempo que va desde meses hasta años o incluso décadas después de la extirpación del tumor primario. Concretamente, en el subgrupo de cáncer de mama RE positivo, este largo periodo de latencia es el principal desafío para investigadores, médicos y pacientes. En esta tesis se muestra la identificación y el análisis funcional de mecanismos moleculares implicados en la latencia del cáncer de mama RE positivo. Para este propósito, nuestros estudios se han llevado a cabo mediante una estrategia experimental basada en líneas celulares de cáncer de mama genéticamente modificadas, modelos experimentales de ratón, análisis global del genoma y datos clínicos. La primera parte de la tesis describe un novedoso modelo de ratón de dormancia de cáncer de mama. Observamos que, en nuestro modelo, las células metastásicas llegan al hueso y entran en una fase de latencia en forma de lesiones micrometastásicas en la que el crecimiento del tumor se ve impedido, principalmente debido a que la tasa de proliferación celular se iguala a la tasa de muerte celular. Este modelo experimental de ratón se usó para identificar genes relevantes en el proceso de latencia y por tanto en la recurrencia a largo plazo. Para ello, llevamos a cabo un análisis in vivo de pérdida de función con shRNA. En este análisis utilizamos una amplia librería de shRNA para descubrir genes cuya eliminación regula la dormancia de manera negativa. Entre los genes candidatos identificados en este análisis nos focalizamos en MSK1 como un regulador de la metástasis latente. La validación in vitro e in vivo indica que MSK1 juega un papel en el anidamiento y la diferenciación de las células metastásicas.
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VITALE, STEFANIA. "Role of endocrine therapy in combination with anti-HER2 therapy and CDK4/6 inhibitors in hormone receptor positive/HER2 positive breast cancer." Doctoral thesis, Università di Siena, 2019. http://hdl.handle.net/11365/1073185.

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In clinical practice, patients with advanced ER+/HER2+ BC are treated with a combination of anti-HER2 and chemotherapy as first choice but it is clear that a proportion of these derive prolonged benefit from the combination of hormonal therapy (HT) and anti-HER2 therapy (AH2T). Preclinical evidence from cellular models of BC indicates that ER and HER2 pathways are strictly interdependent and that targeting both pathways in ER+/HER2+ BC might be an effective therapeutic strategy; few trials investigated this combination showing a significant, albeit modest, clinical improvement. CDK4/6 pathway acts downstream of both the ER and HER2 pathways. CDK4/6 inhibitors (PD)have shown synergistic activity with HT or AH2T but data on the combination of PD with both HT and AH2T in ER+/HER2+ BC are lacking. PD activity is dependent on an intact RB pathway; therefore we analyzed whether Cyclin D/Rb/E2F pathway might help discriminating the subgroup of ER+/HER2+ BC resistant to PD therapy. We developed a gene expression signature of Rb-loss-of-function, the RBsig, that included a final set of 87 genes that is predictive of resistance to PD in BC cell lines. An in-silico analisys on a meta-dataset of neoadjuvant trials has also shown a good performance of RBsig in prediction of a better response to neoadjuvant chemotherapy. These data suggest RBsig as a potential marker for identifying patients with differential benefit from chemotherapy or HT+PD, both in combination with AH2T.
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Ali, Remah. "Histone Deacetylation as a Mechanism of YPEL3 Down-regulation in ER-a Positive Breast Cancer Cell Lines." Wright State University / OhioLINK, 2013. http://rave.ohiolink.edu/etdc/view?acc_num=wright1376431934.

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Campbell, Esther Jennifer. "Targeting within ER positive early breast cancer : patient selection for current therapies and novel therapeutic approaches in a heterogeneous group." Thesis, University of Glasgow, 2013. http://theses.gla.ac.uk/4272/.

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Over 1 million women a year are diagnosed with Breast Cancer. The majority, approximately 70% express the oestrogen receptor (ER). ER positive breast cancer has historically been perceived as a ‘good cancer’, although many woman with ER+ breast cancer still succumb to their disease and globally breast cancer is the leading cause of female cancer deaths. The advent of gene expression profiling and the definition of the molecular instrinsic subtypes has defined at least two subtypes of ER positive breast cancers (luminal A and luminal B) that differ markedly in terms of biological behaviour, response to adjuvant therapies and most importantly patient outcome. The focus of this research is ER+ breast cancer and targeting patient therapy in this heterogeneous group. This work attempts to translate our understanding of the biology of the ER and cell signalling interactions to aid the correct identification of patients for both current therapy and more novel therapeutic approaches. Following a hypothesis generating pilot study examining whether the level of ER influences response to endocrine therapy, 557 formalin fixed paraffin embedded (FFPE) breast cancer specimens retrieved at time of definitive surgery from early breast cancer patients with available accurate 15 years follow up data were analysed to measure ER, Progesterone receptor (PgR), HER2 and Ki67 expression using immunohistochemistry. Tumour expression of ER, PgR and the combined endocrine receptor (CER), which considers the expression level of both hormone receptors and hypothesised to more accurately quantify endocrine responsiveness by acting as a surrogate marker of a functioning ER signalling pathway, were analysed. The results suggest that in this cohort of ER+ endocrine treated patients CER is a better predictor of endocrine response than either the ER of PgR independently. The CER was thereafter utilised as a surrogate marker of oestrogen receptor signalling pathway to develop a scoring system which included HER2 IHC expression and tumour histological grade, as surrogate markers of the 3 key pathways (ER signalling, HER2 signalling and proliferation). These were chosen as previous studies comparing various gene prognostic profiles indicate commonality in sampling groups of the genes representing their activation. The scoring system, named the Clinical Outcome Score (COS) was developed to represent a pragmatic equivalent of gene prognostic profiles utilising currently routinely measured tumour markers. We hypothesised that COS as an indicator of tumour biology may aid identification of risk in the very challenging group, ER+/HER2 negative patients with intermediate grade and low disease burden, and may help guide adjuvant therapy decisions particularly the indication for chemotherapy . In this exploratory analysis, the distribution of COS scores (2-10) followed a linear response with a notable separation between low scores (2-4) and high scores (5-10). Importantly, when analysed in combination with tumour burden, low COS may help identify patients with nearly 100% long term survival, however in all analysis high COS was associated with a highly significant poorer outcome in terms of early recurrence, late recurrence and 15 year breast cancer specific survival. This group of high risk ER+ breast cancer patients represent a real challenge (and concern) in the treatment of early breast cancer, as there is increasing evidence that ER+ tumours are relatively chemo-in senstive and the response to chemotherapy agents is limited. As a secondary analysis, within our cohort of ER+/ HER2- endocrine treated patients we retrospectively analysed the benefit of chemotherapy in patients with low and high COS scores and the results indicate lack of benefit in the cohort of patients diagnosed 1995-1998. Investigating novel therapeutic targets focusing on the subtypes of breast cancer, and tumour biology involved in endocrine resistance is now beginning to take precedence in breast cancer research. Two potential new therapeutic targets in ER+ breast cancer were studied. The first is the sodium iodide symporter, NIS, a transmembrane glycoprotein which has been exploited for the safe delivery of radio-iodide in the treatment of thyroid cancers for many years. NIS is expressed in many breast cancers, however most breast cancers expressing NIS lack functional uptake as demonstrated by scintography studies and in vivo animal work. In vitro results suggest that the ER is important in NIS regulation and function. In addition MAPK and PI3K-Akt signalling pathways may have a role in NIS regulation- both these pathways are often activated in ER+ breast cancer and known to have extensive crosstalk with the ER. Utilising ER+ and ER negative breast cancer cell lines we examined NIS function following gene delivery with a human NIS (hNIS) transfected plasmid and assessed function and expression of NIS following ER knockdown by siRNA. Our results suggest that the ER phenotype is important but not necessarily the ER per say. We examined NIS expression in a mixed ER+ and ER- cohort (n=50) of patient tumour samples using real time RT-PCR, and report high levels of NIS mRNA expression was limited to ER+ breast tumours. Prompting analysis of NIS expression, cellular location and correlations with cell signalling proteins in 300 ER+ breast cancers using IHC . Significant correlations were identified with key members of the PI3K-Akt and MAPK supporting their role in NIS regulation in vivo. Importantly, in both patient cohorts NIS was found to be significantly associated with poor outcome, and we hypothesis that this is an effect of enhanced growth factor signalling and activation of pathways in biologically more aggressive ER+ cancer (ER+/PgR-) may also regulate NIS and suggest future directions of research. Lastly, as a pilot study expression of Src kinase, a non receptor tyrosine kinase implicated in tamoxifen resistance and breast cancer virulence, was analysed by IHC in the ER+ breast cancer patient cohort. Interestingly nuclear Src kinase was found to be associated with improved outcome and hypothesise that Src Kinase expression in breast cancer may have varying roles in the different subtypes of breast cancer, an important consideration as Src Kinase inhibitors are currently in clinical trials. This pilot study formed a hypothesis that was subsequently examined in another student’s PhD thesis.
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Li, Jianhui. "Cornichon Proteins: Unexpected Roles in Plant Pathogen Infection, ER Morphology Maintenance and Pollen Development." Diss., Virginia Tech, 2017. http://hdl.handle.net/10919/77687.

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Cornichon (CNI) proteins are a conserved family of proteins among eukaryotes, from Erv14 in the yeast Saccharomyces cerevisiae to CNI homologs (CNIHs) in mammals and plants. Erv14 functions as a cargo receptor of coat protein complex II (COPII) for protein trafficking from the endoplasmic reticulum (ER) to the Golgi apparatus, en route to their final destinations. By interacting with specific cargo proteins, CNI proteins regulate key steps of embryo polarity in Drosophila, budding in yeast, and synaptic transmission in the mammalian brain. However, we have very limited understanding of plant CNIHs. Positive-strand RNA viruses assemble their viral replication complexes (VRCs) at specific host organelle membranes. With a better understanding of host factors involved in targeting viral replication proteins to the preferred organelles, we expect to block trafficking of viral replication proteins and thus, viral infection, by manipulating the required host proteins. Brome mosaic virus (BMV) is a model of positive-strand RNA viruses and its replication can be recapitulated in yeast. Importantly, BMV replication protein 1a is the only required viral protein to form VRCs at the perinuclear ER membrane in yeast. I demonstrate that Erv14 and COPII coat proteins are required for targeting BMV 1a to the perinuclear ER in yeast, suggesting a novel function of COPII vesicles in protein trafficking to the perinuclear ER membrane and in the BMV VRC formation. As for cellular functions, I show that plant CNIHs complement the defective distribution of BMV 1a in yeast mutant lacking Erv14. Taking advantage of Arabidopsis thaliana knockout mutants and knockdown of gene expression in Nicotiana benthamina, I also discover that CNIHs unexpectedly play crucial roles in pollen development, infection of a bacterial pathogen, and maintenance of ER tubules. I further confirm that CNI proteins are also required for maintaining ER tubules in yeast, suggesting a novel and conserved role in shaping ER morphology. Therefore, these findings indicate the functional diversity and redundancy of CNI proteins in key cellular processes and suggest a novel strategy to control plant pathogenic viruses and bacteria by manipulating plant CNIHs.
Ph. D.
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Li, Jianhui, Shai Fuchs, Jiantao Zhang, Sebastian Wellford, Maya Schuldiner, and Xiaofeng Wang. "An unrecognized function for COPII components in recruiting the viral replication protein BMV 1a to the perinuclear ER." COMPANY OF BIOLOGISTS LTD, 2016. http://hdl.handle.net/10150/622581.

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Positive-strand RNAviruses invariably assemble their viral replication complexes (VRCs) by remodeling host intracellular membranes. How viral replication proteins are targeted to specific organelle membranes to initiate VRC assembly remains elusive. Brome mosaic virus (BMV), whose replication can be recapitulated in Saccharomyces cerevisiae, assembles its VRCs by invaginating the outer perinuclear endoplasmic reticulum (ER) membrane. Remarkably, BMV replication protein 1a (BMV 1a) is the only viral protein required for such membrane remodeling. We show that ER-vesicle protein of 14 kD (Erv14), a cargo receptor of coat protein complex II (COPII), interacts with BMV 1a. Moreover, the perinuclear ER localization of BMV 1a is disrupted in cells lacking ERV14 or expressing dysfunctional COPII coat components (Sec13, Sec24 or Sec31). The requirement of Erv14 for the localization of BMV 1a is bypassed by addition of a Sec24-recognizable sorting signal to BMV 1a or by overexpressing Sec24, suggesting a coordinated effort by both Erv14 and Sec24 for the proper localization of BMV 1a. The COPII pathway is well known for being involved in protein secretion; our data suggest that a subset of COPII coat proteins have an unrecognized role in targeting proteins to the perinuclear ER membrane.
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Warasiha, Benjamart. "Cytochrome P450 mRNA profile in human breast cancer cell lines." Thesis, Robert Gordon University, 2008. http://hdl.handle.net/10059/364.

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Cytochrome P450 enzymes (P450s) are involved in cancer development and treatment due to their roles in the oxidative metabolism of various endogenous (e.g. oestrogen) and exogenous (e.g. tamoxifen) compounds. It is well-known that intermediate P450 metabolites derived from oestrogen metabolism are associated with breast carcinogenesis. The main aim of this project was to profile the cytochrome P450 and P450-regulatory nuclear receptor mRNAs in a series of breast cancer cell lines (BCCs) and compare this profile with normal breast cells. This study used the qualitative reverse transcriptasepolymerase chain reaction (RT-PCR) to detect mRNA expression of target genes. Results showed CYP1B1, CYP2D6, CYP2J2, CYP2R1, CYP2U1 and CYP4X1 mRNA to be present in all cell lines. CYP2A6, CYP2C8, CYP2C18, CYP2F1 and CYP4Z1 mRNA were expressed in oestrogen receptor (ER)-positiveCaucasian and ER-negative Afro- Caribbean BCCs. Although no differences in P450 mRNA were observed between the different ethnic groups, these preliminary findings suggest potential similarities in the ERpositive Caucasian and ER-negative Afro-Caribbean BCCs which warrant further investigation The CYP4Z1 PCR product was identified as two distinct bands. Specific primer sets were used to demonstrate potential intron retention in CYP4Z1. Using established in vitro models for the study of regulatory mechanisms of CYP4Z1, T47D and ZR-75-1 breast cancer cell lines were used to determine the appropriate nuclear receptors (i.e. progesterone receptor, glucocorticoid receptor or peroxisome proliferator-activated receptor alpha ). These findings suggest that there may be an alternative receptor mechanism involved in CYP4Z1 mRNA induction in these cells. In conjunction, pre-treatment of these two cell lines with the RNA synthesis inhibitor actinomycin D followed by the agonists showed a significant reduction (p < 0.05) of CYP4Z1 mRNA levels and inhibited CYP4Z1 induction by either progesterone, dexamethasone or pirinixic acid, indicating that these agonists have effects on CYP4Z1 mRNA transcription or stability. In contrast, cycloheximide differentially affected the level of CYP4Z1 mRNA induction by these agonists. Taken together, these results suggest that CYP4Z1 mRNA induction in T47D and ZR-75-1 is mediated through differential cell type specific regulatory mechanisms and there is evidence for differential regulation of the splice variants.
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Ji, Hye Kang. "The positive emotion elicitation process of Chinese consumers toward a U.S. apparel brand a cognitive appraisal perspective /." online access from Digital Dissertation Consortium access full-text, 2007. http://libweb.cityu.edu.hk/cgi-bin/er/db/ddcdiss.pl?3291278.

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Hamy, Anne-Sophie. "Identification of Factors Predicting Sensitivity or Resistance to Neoadjuvant Chemotherapy in Breast Cancer Neoadjuvant treatment : the future of patients with breast cancer Neoadjuvant treatment for intermediate/high-risk HER2-positive and triple-negative breast cancers: no longer an “option” but an ethical obligation Long-term outcome of the REMAGUS 02 trial, a multicenter randomised phase II trial in locally advanced breast cancer patients treated with neoadjuvant chemotherapy with or without celecoxib or trastuzumab according to HER2 status BIRC5 (survivin) : a pejorative prognostic marker in stage II/III breast cancer with no response to neoadjuvant chemotherapy Beyond Axillary Lymph Node Metastasis, BMI and Menopausal Status Are Prognostic Determinants for Triple-Negative Breast Cancer Treated by Neoadjuvant Chemotherapy Pathological complete response and prognosis after neoadjuvant chemotherapy for HER2-positive breast cancers before and after trastuzumab era: results from a real-life cohort The presence of an in situ component on pre-treatment biopsy is not associated with response to neoadjuvant chemotherapy for breast cancer Chemosensitivity, tumor infiltrating lymphocytes (TILs), and survival of postpartum PABC patients treated by neoadjuvant chemotherapy Lymphovascular invasion after neoadjuvant chemotherapy is strongly associated with poor prognosis in breast carcinoma New insight for pharmacogenomics studies from the transcriptional analysis of two large-scale cancer cell line panels Biological network-driven gene selection identifies a stromal immune module as a key determinant of triple-negative breast carcinoma prognosis A Stromal Immune Module Correlated with the Response to Neoadjuvant Chemotherapy, Prognosis and Lymphocyte Infiltration in HER2-Positive Breast Carcinoma Is Inversely Correlated with Hormonal Pathways Stromal lymphocyte infiltration after neoadjuvant chemotherapy is associated with aggressive residual disease and lower disease-free survival in HER2-positive breast cancer Interaction between molecular subtypes, stromal immune infiltration before and after treatment in breast cancer patients treated with neoadjuvant chemotherapy COX2/PTGS2 Expression Is Predictive of Response to Neoadjuvant Celecoxib in HER2-negative Breast Cancer Patients Celecoxib With Neoadjuvant Chemotherapy for Breast Cancer Might Worsen Outcomes Differentially by COX-2 Expression and ER Status: Exploratory Analysis of the REMAGUS02 Trial Comedications influence immune infiltration and pathological response to neoadjuvant chemotherapy in breast cancer." Thesis, Université Paris-Saclay (ComUE), 2019. http://www.theses.fr/2019SACLS129.

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La chimiothérapie néoadjuvante (CNA) est utilisée dans les cancers du sein agressifs ou localement avancés (CS). Au delà des bénéfices cliniques, elle représente une opportunité pour monitorer in vivo la sensibilité d’une tumeur à un traitement.A partir de l’analyse de sets de données de patients traités par CNA, nous souhaitons identifier des mécanismes associes à la résistance ou sensibilité au traitement. Dans la première partie, nous avons évalué des paramètres, cliniques, anatomopathologiques et transcriptomiques. Nous avons démontré que des éléments non explorés comme la présence d’embols après CNA revêtaient une information pronostique importante. Dans une 2ème partie, nous avons analysé l’impact de l’infiltrat immunitaire dans le cancer du sein, et avons décrit les changements observés entre des échantillons avant et après CNA. Nous avons montré que l’impact pronostique des TILs était différent avant et après CNA, et était opposé dans les CS triple négatif ou HER2-positif. Finalement, nous avons analysé l’impact des comédications pendant la CNA. Nous avons trouvé des effets positifs – via l’augmentation de l’infiltrat immunitaire et la réponse au traitement – et des effets négatifs avec des effets délétères dans certains sous groupes de patients. En conclusion, la situation néoadjuvante représente une plateforme pour générer et potentiellement valider des hypothèses de recherche. La mise à disposition de jeux de données de patients traités par chimiothérapie néoadjuvante constituerait une ressource majeure pour accélérer la recherche contre le cancer du sein
Neoadjuvant chemotherapy (NAC i.e. chemotherapy before surgery) is increasingly being used for aggressive or locally advanced breast cancer (BCs). Beyond clinical benefits, it represents an opportunity to monitor in vivo sensitivity to treatment. Based on the analysis of datasets of BCs patients treated with NAC, we aimed at identifying mechanisms associated with resistance or sensitivity to treatment.In the first part, we evaluated biological, clinical, pathological and transcriptomic patterns. We demonstrated that unexplored pathological features such as post-NAC lymphovascular invasion may carried an important prognostic information.In a second part, we analyzed impact of imune infiltration in BC and we described extensively the changes of tumor infiltrating lymphocytes (TILs) between pre and post-NAC samples. We showed that the prognostic impact of TILs was different before and after NAC, and was opposite in TNBC and HER2-positive BCs. Finally, we investigated the impact of comedications use during NAC. We found both positive effects - while enhancing immune infiltration and response to treatment - and negative effects with deleterisous oncologic outcomes in specific patients subgroups. In conclusion, the neoadjuvant setting represents a platform to both generate and potentially validate research hypotheses aiming at increasing the efficacy of treatment. The public release of real-life datasets of BC patients treated with NAC would represent a major resource to accelerate BC research
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Books on the topic "ER-positive"

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Yu, Yibing. Nong cun liu shou er tong ji ji xin li yan jiu: A study on positive psychology of left-behind children in China. Beijing Shi: She hui ke xue wen xian chu ban she, 2018.

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Ouwen and Dafei, eds. 0-3 Sui hai zi de zheng mian guan jiao: Ying xiang hai zi yi sheng de tou san nian = Positive discipling : the first three years. Beijing: Beijing lian he chu ban gong si, 2015.

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Gei hai zi yi ke jian kang de xin: Collected edition of positive and hopeful stories for youngsters. Beijing Shi: Xin shi jie chu ban she, 2008.

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Harvey, Joshua. Mindful Triage--Positive Psychology and Life in the Er. Lulu Press, Inc., 2011.

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Lindner, Friedrich W. Mac-Benac, Er Lebet Im Sohne, Oder, das Positive der Freymaurerey. Creative Media Partners, LLC, 2015.

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Lindner, Friedrich W. Mac-Benac, Er Lebet Im Sohne, Oder, das Positive der Freymaurerey. Creative Media Partners, LLC, 2018.

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Cassidy, Jim, Donald Bissett, Roy A. J. Spence OBE, Miranda Payne, Gareth Morris-Stiff, and Amen Sibtain. Colorectal cancer. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199689842.003.0015_update_001.

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Breast cancer reviews the epidemiology and aetiology of this malignancy, with particular attention to the genetics underlying familial breast cancer, its pathology along with its receptors, oestrogen receptor (ER), the growth factor receptor HER2, and epidermal growth factor receptor (EGFR), and the bearing these have on treatment and prognosis. The benefits of breast cancer screening in the population and families at higher risk are discussed. Presenting symptoms and signs are followed by investigation including examination, bilateral mammography, and core biopsy of suspicious lesions. Management of non-invasive in situ disease is considered. Invasive breast cancer is staged according to TNM guidelines. Early breast cancer is defined, managed frequently by breast conserving surgery and sentinel node biopsy from the axilla. A positive sentinel node biopsy requires clearance of the axilla. Larger lesions may require mastectomy. Breast radiotherapy is indicated after breast conserving surgery. Following surgery, the risk of systemic micrometastatic disease is estimated from the primary size, lymph node spread, and tumour grade. Adjuvant chemotherapy improves treatment outcome in all but very good prognosis premenopausal breast cancer, and intermediate or poor prognosis postmenopausal breast cancer. This is combined with trastuzumab in HER2 positive disease. Adjuvant endocrine therapy is recommended for all ER positive breast cancer, tamoxifen in premenopausal, aromatase inhibitors in postmenopausal women. Neoadjuvant chemotherapy may be used in large operable breast cancers to facilitate breast conserving surgery. Locally advanced breast cancer is defined, its high risk of metastatic disease requiring full staging before treatment. Systemic therapy is often best first treatment, according to receptor profile. Metastatic breast cancer although incurable can be controlled for years using endocrine therapy, chemotherapy, trastuzumab, palliative radiotherapy, and bisphosphonates as appropriate. Male breast cancer is uncommon, but management similar.
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Book chapters on the topic "ER-positive"

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Ritzenthaler, Christophe, and Rabab Elamawi. "The ER in Replication of Positive-Strand RNA Viruses." In Plant Cell Monographs, 309–30. Berlin, Heidelberg: Springer Berlin Heidelberg, 2006. http://dx.doi.org/10.1007/7089_061.

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Rilling, Jürgen. "Begeht der Bauunternehmer, der eine Bauwesenversicherung abschließt, eine positive Vertragsverletzung, wenn er diese ohne Feuerversicherung abschließt?" In Baurechtsberater Bauherren, 256–57. Wiesbaden: Vieweg+Teubner Verlag, 1998. http://dx.doi.org/10.1007/978-3-322-87217-3_128.

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Schuler, Larissa, Thomas Metzger, and Christian Sinn. "Die literarische Inszenierung von ›68‹." In Historisches Erzählen in der Gegenwartsliteratur, 255–68. Bielefeld, Germany: transcript Verlag, 2022. http://dx.doi.org/10.14361/9783839463796-016.

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Metzger, Schuler und Sinn widmen sich in diesem Beitrag der Frage, wie sich an Uwe Timms die 68-er-Bewegung reflektierenden Trilogie Heißer Sommer (1974), Kerbels Flucht (1980) und Rot (2001), das Verhältnis zwischen einem wissenschaftlich zu differenzierenden, komplexen Phänomen und seiner narrativ-fiktionalen Konstruktion einerseits analytisch klären lässt und wie sich andererseits die gewonnenen Erkenntnisse didaktisch perspektivieren lassen. Damit wird im besten Sinne interdisziplinär gearbeitet: Indem literarische Texte durch Anschaulichkeit und emotionale Beteiligung ein vertieftes historisches Verständnis erlauben und der historische Kontext wiederum hilft, die literarischen Texte zu verstehen, entsteht »im besten Fall eine positive Wechselwirkung von Geschichte und Literatur» (von Brand)
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"Selberg’s sieve—Kvadrater er positive." In Opera de Cribro, 89–138. Providence, Rhode Island: American Mathematical Society, 2010. http://dx.doi.org/10.1090/coll/057/07.

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"The positive, negative, photo-ER, and electromagnetorheological (EMR) effects." In Studies in Interface Science, 83–113. Elsevier, 2005. http://dx.doi.org/10.1016/s1383-7303(05)80018-3.

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Nordeide, Britt Iren. "Tekstar på nynorsk i klasserom der bokmål er hovudmål – ei undersøking av lærarar sin bruk av og haldning til tekstar på nynorsk." In Form og formidling knytt til nynorsken, 101–27. Cappelen Damm Akademisk/NOASP, 2022. http://dx.doi.org/10.23865/noasp.175.ch4.

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Forsking på kva tekstar ein les i skulen i Noreg har helst handla om lesing av skjønnlitteratur og sakprosa, og mindre om kva målform tekstane som vert lesne i klasseromma, har. Fleirtalet av norske born møter nynorsk for første gong i skulen, og skulen har såleis eit viktig formidlingsoppdrag. Dette skjer i klasserommet, og undervisinga som vert gitt, er avhengig av læraren sin kunnskap og haldningar, kva læremiddel som er tilgjengelege, og korleis desse læremidla vert nytta. I artikkelen kjem det fram at lærarane som var med i denne studien, stort sett er positive til å lese tekstar på nynorsk. Tekstane som desse lærarane brukar, er i stor grad skjønnlitterære tekstar, henta frå læreverk i norskfaget og knytte opp til estetiske arbeidsmåtar der elevane sine opplevingar av tekst spelar ei sentral rolle. Lærarane brukar læreverka i stor grad, men er kritiske til det dei meiner er eit snevert tekstutval, spesielt når det gjeld sakprosatekstar på nynorsk.
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Caiazza, F., W. Thomas, and BJ Harvey. "Rapid Activation of cPLA2α Induced by Estrogen in ER-Positive and ER-Negative Breast Cancer Cell Lines." In The Endocrine Society's 92nd Annual Meeting, June 19–22, 2010 - San Diego, P1–60—P1–60. Endocrine Society, 2010. http://dx.doi.org/10.1210/endo-meetings.2010.part1.p2.p1-60.

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Saini, Karan Singh, Shankar Suman, and Rituraj Konwar. "Immune-Endocrine Perspectives of Breast Cancer." In Breast Cancer: Current Trends in Molecular Research, 22–61. BENTHAM SCIENCE PUBLISHERS, 2022. http://dx.doi.org/10.2174/9781681089522112010005.

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Cancer is the consequence of the recalcitrant multiplication of the transformed cells. Cancer cells grow and proliferate at a fast pace and do not follow normal regulation of cell division. Breast cancer is a heterogeneous group of diseases, which is the second leading cause of death among women. Although androgen is primarily considered a male steroid hormone, it also has an important role in the female reproductive system. The literature evidence suggests the role of androgen receptors (AR) in the normal development of the breast. At puberty, the expression of AR is even more than ER, suggesting its importance during the process of sexual development; its activity maintains the ER-induced cell proliferation and normal development of the breast. Epidemiological studies have suggested a positive correlation between high endogenous androgens and the risk of breast cancer in both pre- and postmenopausal women. In both ER and PR-positive breast cancers, AR is expressed in 60-70% of the cases. AR is also reported to be co-expressed with ER in around 80-90% of breast cancer cases and is considered an independent prognostic factor of ER-positive breast cancers. Tumor-microenvironment has a complex role in tumor initiation, progression, and metastasis. Tumor-infiltrating and resident cells secretes a variety of inflammatory and anti-inflammatory cytokines, which in turn either inhibit or promote tumor growth. Immunosuppressive and immuno-inductive effects of androgen have been reported in various studies. Androgens have been reported to influence the adaptive immune system more than the innate immune system in many ways. Crosstalk of androgen and cytokine signaling has many effects in breast cancer epidemiology. So, in this chapter, we will discuss the various immune-endocrine perspectives of breast cancers.
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Wang, Xiaojing, and Jun Liang. "Estrogen Receptor Degraders for the Treatment of ER-Positive Breast Cancer." In Medicinal Chemistry Reviews, 151–64. Medicinal Chemistry Division of the American Chemical Society, 2016. http://dx.doi.org/10.29200/acsmedchemrev-v51.ch10.

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Kyriazopoulos, Ioannis, George Koutromanos, Aggeliki Voudouri, and Apostolia Galani. "Educational Robotics in Primary Education." In Research Anthology on Computational Thinking, Programming, and Robotics in the Classroom, 782–806. IGI Global, 2022. http://dx.doi.org/10.4018/978-1-6684-2411-7.ch034.

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The purpose of this chapter is to review the literature referring to the utilization of educational robotics (ER) in primary education. Keyword-based search in particular bibliographic databases returned 21 journal papers for the eight-year period of 2012-2019. The factors that were studied in each of them are as follows: learning environment, area of knowledge/course subjects, pedagogical framework, learning activities, robotic equipment, research methodology, and main findings. The outcomes, among other things, showed that the majority of ER activities took place in a formal learning environment and that ER is appropriate for teaching subjects of STEM education. Though many researches took into account various learning theories that support collaboration, problem-solving, discovery, and construction of knowledge, there were some researches that lacked any pedagogical framework. In spite of the positive cognitive and affective outcomes of ER in learning, there are aspects that require further investigation.
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Conference papers on the topic "ER-positive"

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Farhat, G., S. Cummings, N. Parimi, A. Huang, J. Cauley, T. Rohan, F. Hubbell, et al. "Sex Hormones and Risk of Estrogen Receptor (ER)-Positive and ER-Negative Breast Cancer." 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-09-907.

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Gokmen-Polar, Y., RA Toroni, S. Badve, E. Bruckheimer, MS Kinch, and KD Miller. "Dual targeting of EphA2 and ER restores tamoxifen sensitivity in ER/EphA2-positive breast cancer." 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-3020.

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Halpern, N., A. Sonnenblick, L. Kaduori, B. Uziely, Y. Goldberg, D. Katz, T. Allweis, et al. "Abstract P4-05-08: Oncotype Dx assay in BRCA positive ER positive breast cancer patients." In Abstracts: Thirty-Sixth Annual CTRC-AACR San Antonio Breast Cancer Symposium - Dec 10-14, 2013; San Antonio, TX. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/0008-5472.sabcs13-p4-05-08.

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Gralow, J. "Abstract ES5-3: Late recurrence in ER-positive breast cancer." In Abstracts: 2018 San Antonio Breast Cancer Symposium; December 4-8, 2018; San Antonio, Texas. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-es5-3.

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Lee, Nathan V., Jing Yuan, Koleen Eisele, Joan Q. Cao, Cory L. Painter, John Chionis, Chaoting Liu, et al. "Abstract LB-136: Mechanistic exploration of combined CDK4/6 and ER inhibition in ER-positive 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-lb-136.

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Bianchini, G., G. Bianchini, R. Alvarez, Y. Qi, C. Hatzis, T. Iwamoto, C. Shiang, et al. "The Molecular Anatomy of Breast Cancer Stroma; Independent Prognostic Role in ER-Positive and ER-Negative Cancers." 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-09-105.

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Berg, PE, S. Awate, and SP Kirolikar. "P5-04-01: BP1, a Homeotic Transcription Factor, Indirectly Upregulates ER-alpha in ER Positive Cell Lines." 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-p5-04-01.

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Iwamoto, T., D. Booser, V. Valero, JL Murray, K. Koenig, FJ Esteva, NT Ueno, et al. "P1-07-09: Estrogen Receptor (ER) mRNA and ER-Related Gene Expression in Breast Cancers That Are 1%-10% ER-Positive by Immunohistochemistry." 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-p1-07-09.

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Sedletcaia, Anna, Helen A. Unger, Naamah Plotzker, and Marina K. Holz. "Abstract 2253: New targets of mTORC1 pathway in ER-positive cells." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-2253.

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Metzger, Otto, and Robert van den Heuvel. "SET2,3 to inform on chemotherapy decisions in ER-positive breast cancer." In ASCO Annual Meeting 2022, edited by Otto Metzger and Stefan Rauh. Baarn, the Netherlands: Medicom Medical Publishers, 2022. http://dx.doi.org/10.55788/2c7c62f7.

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Reports on the topic "ER-positive"

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Greene, Geoffrey. Multidomain Assembly of Nuclear Estrogen Receptors: Structural Insights into ER-Positive Breast Cancer Therapeutics. Fort Belvoir, VA: Defense Technical Information Center, April 2012. http://dx.doi.org/10.21236/ada562255.

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Greene, Geoffrey. Multi-Domain Assembly of Nuclear Estrogen Receptors: Structural Insights into ER-Positive Breast Cancer Therapeutics. Fort Belvoir, VA: Defense Technical Information Center, April 2013. http://dx.doi.org/10.21236/ada580416.

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Conrad, Susan E. A Role for MEK-Interacting Protein 1 in Hormone Responsiveness of ER Positive Breast Cancer Cells. Fort Belvoir, VA: Defense Technical Information Center, July 2010. http://dx.doi.org/10.21236/ada540806.

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Conrad, Susan E. A Role for MEK-Interacting Protein 1 in Hormone Responsiveness of ER Positive Breast Cancer Cells. Fort Belvoir, VA: Defense Technical Information Center, July 2009. http://dx.doi.org/10.21236/ada514031.

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Conrad, Susan E. A Role for MEK-Interacting Protein 1 In Hormone Responsiveness of ER Positive Breast Cancer Cells. Fort Belvoir, VA: Defense Technical Information Center, October 2011. http://dx.doi.org/10.21236/ada560599.

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Sagvaag, Hildegunn, Mikkel Magnus Thørrisen, Lisebet Skeie Skarpaas, and Randi Wågø Aas. Alkoholbruk og alkoholkultur blant ansatte i et forvaltningsorgan i Rogaland: En case-rapport fra forskningsprosjektet WIRUS. University of Stavanger, October 2021. http://dx.doi.org/10.31265/usps.111.

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Bakgrunn: WIRUS er et nasjonalt forskningsprosjekt om alkohol, arbeidsliv, sykefravær, sykenærvær og arbeidsplassbaserte intervensjoner. Prosjektet består av flere delstudier. Én av disse er en screeningstudie der ansatte i ulike virksomheter, på tvers av sektorer og bransjer, svarer på et spørreskjema som handler om bl.a. alkoholbruk, holdninger til arbeidsrelatert alkoholbruk og forventninger til virkninger av alkoholbruk. Én av virksomhetene som deltar i WIRUS er et forvaltningsorgan i Rogaland. I denne rapporten presenteres resultater fra spørreundersøkelsen blant ansatte i denne virksomheten. Målet med denne rapporten er å beskrive alkoholbruk, holdninger til arbeidsrelatert alkoholbruk og forventninger til virkninger av alkoholbruk blant ansatte i virksomheten. Alkoholbruk er kartlagt ved hjelp av Alcohol Use Disorders Identification Test (AUDIT), som er utviklet av Verdens helseorganisasjon (WHO). Virksomhetens resultater sammenliknes med de øvrige virksomhetene i WIRUS, og også resultater fra en tidligere utført befolkningsstudie i Norge. Rapporten kan brukes som et kunnskapsgrunnlag for arbeid med alkoholpolicy på arbeidsplassen, og for situasjoner i gråsonen mellom jobb og fritid. Resultatene for alkoholbruk viser at virksomhetens ansatte i gjennomsnitt rapporterte et noe høyere alkoholbruk enn ansatte i de øvrige virksomhetene i WIRUS (4,31 mot 4,00 av 40 mulige poeng på AUDIT-skalaen). Forskjellen var statistisk signifikant. Forekomsten av risikofylt alkoholbruk blant de ansatte var også noe høyere i virksomheten (12,5 %) enn hva som er funnet i de øvrige WIRUS-virksomhetene (11,4 %), men likevel lavere enn hva tidligere forskning har funnet i den generelle norske befolkningen (16,9 %). Forskjellen i andel risikodrikkere mellom virksomheten og de øvrige WIRUS-virksomhetene er imidlertid ikke statistisk signifikant. Virksomhetens ansatte rapporterte å ha noe mer positive (liberale) holdninger til arbeidsrelatert alkoholbruk enn ansatte i de øvrige WIRUS-virksomhetene (2,26 mot 2,14 av 4 poeng). Forskjellen var statistisk signifikant. Virksomhetens ansatte rapporterte også om marginalt mer positive forventninger til virkninger av alkoholbruk enn ansatte i de øvrige WIRUS-virksomhetene (1,80 mot 1,74 av 4 poeng), men denne forskjellen var ikke statistisk signifikant. Konklusjon og anbefalinger: Resultatene fra denne undersøkelsen tyder på at virksomhetens ansatte hadde noe høyere alkoholforbruk og noe mer positive (liberale) holdninger til jobbrelatert alkoholbruk enn alle ansatte i virksomhetene som deltar i WIRUS-prosjektet. Forekomsten av risikofylt alkoholbruk og forventninger til virkninger av alkoholbruk var imidlertid ikke signifikant forskjellig. Det var også svært få ansatte med høy risiko i virksomheten, og ingen som skåret ut med trolig avhengighet. Denne undersøkelsen gir i så måte ikke grunnlag for å anbefale særskilte tiltak for denne virksomheten, utover det som generelt kan betraktes som hensiktsmessig alkoholforebyggende arbeid i arbeidslivet.
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Abdulkadir, Sarki. SIRT3 Is a Mitochondrial Tumor Suppressor and Genetic Loss Results in a Murine Model for ER/PR-Positive Mammary Tumors Connecting Metabolism and Carcinogenesis. Fort Belvoir, VA: Defense Technical Information Center, September 2011. http://dx.doi.org/10.21236/ada569609.

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Abdulkadir, Sarki. SIRT3 Is a Mitochondrial Tumor Suppressor and Genetic Loss Results in a Murine Model for ER/PR-Positive Mammary Tumors Connecting Metabolism and Carcinogenesis. Fort Belvoir, VA: Defense Technical Information Center, September 2012. http://dx.doi.org/10.21236/ada577369.

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Abdulkadir, Sarki. SIRT3 Is a Mitochondrial Tumor Suppressor and Genetic Loss Results in a Murine Model for ER/PR-Positive Mammary Tumors Connecting Metabolism and Carcinogenesis. Fort Belvoir, VA: Defense Technical Information Center, September 2013. http://dx.doi.org/10.21236/ada594183.

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Gius, David, and Sarki Abdulkadir. SIRT3 is a Mitochondrial Tumor Suppressor and Genetic Loss Results in a Murine Model for ER/PR Positive Mammary Tumors Connecting Metabolism and Carcinogenesis. Fort Belvoir, VA: Defense Technical Information Center, September 2011. http://dx.doi.org/10.21236/ada554224.

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