Bibliographies thématiques / Chronic hypoxia, dormancy, breast cancer

Littérature scientifique sur le sujet « Chronic hypoxia, dormancy, breast cancer »

Auteur : Grafiati

Publié le 11 mars 2023

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Articles de revues sur le sujet "Chronic hypoxia, dormancy, breast cancer"

Carcereri de Prati, Alessandra, Elena Butturini, Antonella Rigo, Elisa Oppici, Michele Rossin, Diana Boriero et Sofia Mariotto. « Metastatic Breast Cancer Cells Enter Into Dormant State and Express Cancer Stem Cells Phenotype Under Chronic Hypoxia ». Journal of Cellular Biochemistry 118, n^o 10 (3 mai 2017) : 3237–48. http://dx.doi.org/10.1002/jcb.25972.

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Ferrer, Alejandra, Christopher T. Roser, Markos H. El-Far, Vibha Harindra Savanur, Adam Eljarrah, Marina Gergues, Joshua A. Kra, Jean-Pierre Etchegaray et Pranela Rameshwar. « Hypoxia-mediated changes in bone marrow microenvironment in breast cancer dormancy ». Cancer Letters 488 (septembre 2020) : 9–17. http://dx.doi.org/10.1016/j.canlet.2020.05.026.

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Endo, Hiroko, Hiroaki Okuyama, Masayuki Ohue et Masahiro Inoue. « Dormancy of Cancer Cells with Suppression of AKT Activity Contributes to Survival in Chronic Hypoxia ». PLoS ONE 9, n^o 6 (6 juin 2014) : e98858. http://dx.doi.org/10.1371/journal.pone.0098858.

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YILDIRIM ŞİMŞİR, Ilgın, Utku Erdem SOYALTIN et Candeğer YILMAZ. « Obesity and Breast Cancer : Adipose Tissue, Adipocytokines, Chronic Inflammation, and Hypoxia ». Turkish Journal of Endocrinology and Metabolism 22, n^o 4 (2018) : 244–53. http://dx.doi.org/10.25179/tjem.2017-57808.

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Li, Li-Ting, Fang-Fang Zhao, Zhi-Mei Jia, Li-Qing Qi, Xi-Zhu Zhang, Lu Zhang, Ying-Ying Li et al. « Cannabinoid receptors promote chronic intermittent hypoxia-induced breast cancer metastasis via IGF-1R/AKT/GSK-3β ». Molecular Therapy - Oncolytics 23 (décembre 2021) : 220–30. http://dx.doi.org/10.1016/j.omto.2021.09.007.

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Jain, Nityanand, Ingrida Mitre, Dina Nitisa, Valdis Pirsko et Inese Cakstina-Dzerve. « Identification of Novel Endogenous Controls for qPCR Normalization in SK-BR-3 Breast Cancer Cell Line ». Genes 12, n^o 10 (17 octobre 2021) : 1631. http://dx.doi.org/10.3390/genes12101631.

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Normalization of gene expression using internal controls or reference genes (RGs) has been the method of choice for standardizing the technical variations in reverse transcription quantitative polymerase chain reactions (RT-qPCR). Conventionally, ACTB and GAPDH have been used as reference genes despite evidence from literature discouraging their use. Hence, in the present study we identified and investigated novel reference genes in SK-BR-3, an HER2-enriched breast cancer cell line. Transcriptomic data of 82 HER2-E breast cancer samples from TCGA database were analyzed to identify twelve novel genes with stable expression. Additionally, thirteen RGs from the literature were analyzed. The expression variations of the candidate genes were studied over five successive passages (p) in two parallel cultures S1 and S2 and in acute and chronic hypoxia using various algorithms. Finally, the most stable RGs were selected and validated for normalization of the expression of three genes of interest (GOIs) in normoxia and hypoxia. Our results indicate that HSP90AB1, DAD1, PFN1 and PUM1 can be used in any combination of three (triplets) for optimizing intra- and inter-assay gene expression differences in the SK-BR-3 cell line. Additionally, we discourage the use of conventional RGs (ACTB, GAPDH, RPL13A, RNA18S and RNA28S) as internal controls for RT-qPCR in SK-BR-3 cell line.

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Scherbakov, Alexander M., Yulia S. Lobanova, Valentina A. Shatskaya et Mikhail A. Krasil’nikov. « The breast cancer cells response to chronic hypoxia involves the opposite regulation of NF-kB and estrogen receptor signaling ». Steroids 74, n^o 6 (juin 2009) : 535–42. http://dx.doi.org/10.1016/j.steroids.2009.02.003.

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Zihlif, M., et F. Hamadan. « 173 Hepatocyte nuclear factor 4, alpha (HNF4A) : A potential biomarker in MCF7 breast cancer cell line response to chronic hypoxia ». European Journal of Cancer 51 (septembre 2015) : S21. http://dx.doi.org/10.1016/s0959-8049(16)30070-3.

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Zarzynska, Joanna Magdalena. « The Importance of Autophagy Regulation in Breast Cancer Development and Treatment ». BioMed Research International 2014 (2014) : 1–9. http://dx.doi.org/10.1155/2014/710345.

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Breast cancer (BC) is a potentially life-threatening malignant tumor that still causes high mortality among women. One of the mechanisms through which cancer development could be controlled is autophagy. This process exerts different effects during the stages of cancer initiation and progression due to the occurring superimposition of signaling pathways of autophagy and carcinogenesis. Chronic inhibition of autophagy or autophagy deficiency promotes cancer, due to instability of the genome and defective cell growth and as a result of cell stress. However, increased induction of autophagy can become a mechanism which allows tumor cells to survive the conditions of hypoxia, acidosis, or chemotherapy. Therefore, in the development of cancer, autophagy is regarded as a double-edged sword. Determination of the molecular mechanisms underlying autophagy regulation and its role in tumorigenesis is an essential component of modern anticancer strategies. Results of scientific studies show that inhibition of autophagy may enhance the effectiveness of currently used anticancer drugs and other therapies (like radiotherapy). However, in some cases, the promotion of autophagy can induce death and, hence, elimination of the cancer cells and reduction of tumor size. This review summarizes the current knowledge on autophagy regulation in BC and up-to-date anticancer strategies correlated with autophagy.

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Mirabelli, Caitlynn N., Rachel La Selva, John Heath, Steven Hébert, Jutta Steinberger, Jialin Jiang, Claudia Kleinman, Sidong Huang et Josie Ursini-Siegel. « Abstract 126 : Defining how oxidative stress drives the evolution of aggressive breast cancers ». Cancer Research 82, n^o 12_Supplement (15 juin 2022) : 126. http://dx.doi.org/10.1158/1538-7445.am2022-126.

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Abstract Breast cancer is the most commonly diagnosed malignancy in women worldwide. It is a molecularly heterogeneous disease, which poses difficulties in the treatment of more advanced cancers. Despite this fact, the mechanisms contributing to the emergence of aggressive breast cancers remains poorly understood. We focus on reactive oxygen species (ROS), which are induced by a variety of stimuli in breast cancer cells. Moderately elevated ROS levels are tumor-promoting and facilitate the emergence of more aggressive tumours. Our laboratory has developed a unique model of HER2+ breast cancer that evolved to acquire more aggressive properties under conditions of chronic oxidative stress. We identified 20 transcription factors/co-regulators that were specifically overexpressed in these aggressive breast cancers, compared to their parental counterparts. We hypothesize that these transcription factors are central to the ability of breast tumors to adapt to chronic oxidative stress and acquire more aggressive properties. To test this, I have performed an in vivo functional shRNA screen to identify those transcriptional regulators that drive an aggressive phenotype. This will be followed by functional validation studies to interrogate whether and how these unique transcription factors overexpressed in aggressive breast cancers impact tumour growth, metastasis, and drug resistance. Mechanistically, we will explore whether and how these transcriptional responses mediate adaptive responses to tumor microenvironmental stressors, including altered metabolism, hypoxia, and tumor immune responses. This research will broaden our understanding of how breast cancers adapt to oxidative stress responses and represents a necessary first step in the development of novel therapeutics against these invulnerable malignancies. Citation Format: Caitlynn N. Mirabelli, Rachel La Selva, John Heath, Steven Hébert, Jutta Steinberger, Jialin Jiang, Claudia Kleinman, Sidong Huang, Josie Ursini-Siegel. Defining how oxidative stress drives the evolution of aggressive breast cancers [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2022; 2022 Apr 8-13. Philadelphia (PA): AACR; Cancer Res 2022;82(12_Suppl):Abstract nr 126.

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Thèses sur le sujet "Chronic hypoxia, dormancy, breast cancer"

Minovés-Kotski, Mélanie. « Effets délétères de l’hypoxie intermittente associée au syndrome d’apnées obstructives du sommeil sur la croissance et la dissémination métastatique du cancer du sein : implication de la voie HIF1/VEGF/Endothéline ». Thesis, Université Grenoble Alpes, 2021. https://thares.univ-grenoble-alpes.fr/2021GRALV001.pdf.

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Effets délétères de l’hypoxie intermittente associée au syndrome d’apnées obstructives du sommeil sur la croissance et la dissémination métastatique du cancer du sein : implication de la voie HIF-1/VEGF/EndothélineLe syndrome d’apnées obstructives du sommeil (SAOS) est une pathologie fréquente caractérisée par la survenue d’épisodes nocturnes d’apnées répétées à l’origine de cycles récurrents d’hypoxie-réoxygénation appelés hypoxie intermittente (HI). L’hypoxie intermittente, stimulus chronique et systémique, est à présent reconnue comme le principal facteur responsable d’effets délétères du SAOS au niveaucardiovasculaire et métabolique. De récentes études cliniques ont identifié le SAOS comme étant associé à une surmortalité par cancer tandis que des études précliniques ont confirmé qu’il pouvait promouvoir le développement tumoral. Chez l’animal il a été démontré que l’exposition à l’hypoxie intermittente favorise la croissance tumorale primaire et métastatique notamment sur modèles murins de mélanome. A ce jour aucune étude n’a évalué l’impact de l’hypoxie intermitente sur le développement et la dissémination métastatique du cancer du sein.L'objectif principal de ce travail de thèse est d’explorer l’impact de l’hypoxie intermittente sur le SAOS développement du cancer du sein et de comprendre comment le déséquilibre induit par l’hypoxie intermittente à l’échelle du macro-environnement contribue au développement tumoral. L’évaluation de l’implication de la voie de l’endothéline sur les effets observés a été mené par l’utilisation d’un antagoniste des récepteurs à l’ET-1.Le protocole expérimental a été mené sur un protocole expérimental associant un modèle murin de tumeur mammaire orthotopique et deux modèles de culture cellulaire. Cette approche mixte a été rendue possible grâce à la mise au point, au cours de cette thèse, d’un dispositif in vitro d’exposition cellulaire à l’hypoxie intermittente.Ce travail transversal a permis de montrer que l’hypoxie intermittente induite par le SAOS conduit à une accélération de la croissance tumorale et favorise la dissémination tumorale chez les animaux exposés et que ce phénomène engage la voie de l’endothéline 1.Mots-clés : SAOS, hypoxie intermittente, cancer du sein, endothéline 1, macitentan
Obstructive Sleep Apnea Syndrome (OSA) is a prevalent disease characterised by the occurrence of repeated nocturnal episodes of apnea leading to recurrent cycles of hypoxia-reoxygenation called intermittent hypoxia (IH). Intermittent hypoxia is a chronic and systemic stimulus which is considered as the main factor responsible for the deleterious cardiovascular and metabolic effects induced by OSA. Recent clinicalstudies have showed OSA is associated with excess mortality due to cancer and preclinical studies have confirmed that OSA promote tumour development. In animals, exposure to intermittent hypoxia has been shown to promote primary and metastatic tumour growth, particularly in murin models of melanoma. To date, no study has evaluated the impact of intermittent hypoxia on growth and metastatic power of breast cancer in apreclinical study.The main objective of this thesis was to explore the impact of intermittent hypoxia on the development of breast cancer and to understand how the imbalance induced by intermittent hypoxia at the macro-environmental scale contributes to tumour development. Involvement of the endothelin pathway was evaluated by an ET-1 receptor antagonist.The experimental protocol was carried out on preclinical models combining a mouse model of orthotopic mammary tumour and two additional cell culture models. This mixed approach has been carried out thanks to the development of an in vitro device for cellular exposure to intermittent hypoxia.This cross-sectional work has shown that intermittent hypoxia induced by OSA leads to accelerated tumour growth and favours tumour dissemination in exposed animals and that this phenomenon involved the endothelin 1 pathway.Keywords: OSA, intermittent hypoxia, breast cancer, endothelin 1, macitentan, macroenvironment, preclinical studies

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Rossin, Michele. « Chronic hypoxia induces dormancy in breast cancer cell line MDA-MB-231 ». Doctoral thesis, 2018. http://hdl.handle.net/11562/979184.

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The tumor microenvironment (TME) is recognized as a key factor in multiple stages of disease progression, local resistance, immune-escaping and metastasis. TME is the product of developing crosstalk between different cells types and components, which provide an essential communication network through the secretion of growth factors and chemokines, and induce oncogenic signals enhancing cancer-cell proliferation and invasion. The rapid proliferation of tumor cells and the aberrant structure of the blood vessels within tumors result in a marked heterogeneity in the perfusion of the tumor tissue with regions of low oxygen or hypoxia. Although most of the tumor cells die in these hypoxic conditions, a part of them can adapt and survive for many days or months in a dormant state. Dormant tumor cells are characterized by cell cycle arrest in G0/G1 phase as well as low metabolism and, are refractive to common chemotherapy giving rise to metastasis. Despite these features, the cells retain their ability to proliferate when conditions improve. Exposing human breast cancer cell line exposure MDA-MB-231 to at least three cycles of 1% O2 hypoxia and reoxygenation, we select a subpopulation of hypoxia resistant cells. These cells, designed as chMDA-MB-231, stably survive under 1% O2 hypoxia condition by entering in dormant state. The reprogramming of cells into tumor dormancy results from the low p-ERK/p-p38 ratio that is described as the molecular switch of tumor dormancy in restrictive environment. This dormant state is reversible since once replaced in normoxia the cells recover the proliferation rate in 2 weeks. Moreover, the data in this thesis demonstrate that cycling hypoxic/reoxygenation stress selects dormant MDA-MB-231 cells that present the cancer stem-like phenotype characterized by CD24-/CD44+/ESA+ expression and spheroid forming capacity. Different reports recognize autophagy as a mechanism activated by microenvironment stresses that may contribute to survival of cells in tumor dormancy. Interestingly, we found that chMDA-MB-231 cells have a high level of autophagy, as measured by the detection of autophagolysome and LC3-II expression, suggesting that autophagy may be the survival mechanism of dormant chMDA-MB-231 cells. We believe that the proposed experimental approach to select dormant breast cancer cells could provide a rationale for the development of novel agents to target dormant tumor cells population.

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Actes de conférences sur le sujet "Chronic hypoxia, dormancy, breast cancer"

Pirsko, V., I. Cakstina, M. Priedīte, D. Berzina, D. Nitisa, M. Nakazawa-Miklasevica, Z. Daneberga et E. Miklasevics. « PO-227 The effect of chronic mild hypoxia on genomic instability in HER2-overexpression breast cancer cell line SK-BR-3 ». Dans Abstracts of the 25th Biennial Congress of the European Association for Cancer Research, Amsterdam, The Netherlands, 30 June – 3 July 2018. BMJ Publishing Group Ltd, 2018. http://dx.doi.org/10.1136/esmoopen-2018-eacr25.744.

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Quintela-Fandino, M., L. Manso, S. Mouron, JF Lopez-Acosta, JA García-Saenz, E. Holgado, T. Pascual-Martinez et al. « Abstract OT3-01-02 : CNIO-BR-008 trial : Reversion of T-cell exhaustion caused by chronic treatment with hypoxia-inducing antiangiogenic treatment by durvalumab in HER2-negative breast cancer : A pilot proof-of-concept trial ». Dans Abstracts : 2016 San Antonio Breast Cancer Symposium ; December 6-10, 2016 ; San Antonio, Texas. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.sabcs16-ot3-01-02.

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Lima, Juliana Ferreira de, Rebecca Correia de Oliveira, Antônio Carlos Toshihiro Nisida, Ricardo Faure et Luis Henrique Gebrim. « RELATIONSHIP BETWEEN BODY MASS INDEX (BMI) AND SURGICAL COMPLICATIONS AFTER BREAST ONCOLOGICAL SURGERY ». Dans Scientifc papers of XXIII Brazilian Breast Congress - 2021. Mastology, 2021. http://dx.doi.org/10.29289/259453942021v31s1068.

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Introduction: Obesity is a multifactorial chronic disease that can predispose to several comorbidities, including breast cancer. The Department of Health estimates the number of overweight people in Brazil is 65%. The relationship between weight and height (BMI, Body Mass Index) has been used by WHO to assess the degree of obesity in the population. Breast cancer is responsible for more than 8,000 deaths each year in Brazil. Despite advances in systemic treatment, surgery is one of the main treatments used, and obesity is a relevant factor that worsens the oncological prognosis and is predictive of perioperative complications. Objectives: The aim of this study is to assess the relationship between obesity and surgical complications in 5,657 breast cancer patients undergoing surgical treatment (conservative or radical) at Pérola Byington Hospital. Methods: A retrospective, cross-sectional study was carried out with 5,657 patients undergoing surgical treatment (conservative or radical) by the Braziliann Unified Health System (SUS) at the Women’s Health Reference Center at Hospital Pérola Byington from January 2011 to December 2019. Data were collected from the medical records of the institution. The patients were divided into six groups according to BMI=W/H2 (25), followed by hematoma, diagnosed in 72 patients, 59.7% overweight women. The third most common complication was infection of the surgical site in only 19 patients (0.3%), with 78.9% in overweight women. This fact can be explained by inadequate perfusion, deficiency of macro and micronutrients and hypoxia that impairs collagen synthesis, resulting in poor healing, causing dehiscence. From these data presented, it is possible to infer thatcomplications such as seroma, hematoma, infection of the surgical wound, dehiscence, and even loss of the surgical flap are strongly associated with increased body weight. Conclusions: We came to the conclusion that the increase in body weight, especially in patients with a BMI> 25, is an unfavorable factor for the occurrence of surgical complications in patients with breast cancer, and it is essential to provide guidance on the risks of complications in the preoperative evaluation for adjusting the best surgical procedure and mainly for considering late reconstruction.

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