Relevant bibliographies by topics / Breast – Cancer – Pathophysiology

Contents

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

Academic literature on the topic 'Breast – Cancer – Pathophysiology'

Author: Grafiati
Published: 4 June 2021
Last updated: 30 January 2023

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Journal articles on the topic "Breast – Cancer – Pathophysiology"

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Voutsadakis, Ioannis A. "The TSH/Thyroid Hormones Axis and Breast Cancer." Journal of Clinical Medicine 11, no. 3 (2022): 687. http://dx.doi.org/10.3390/jcm11030687.

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Breast cancer, the most prevalent female carcinoma, is characterized by the expression of steroid nuclear receptors in a subset of cases. The most important nuclear receptor with prognostic and therapeutic implications is the Estrogen Receptor (ER), which is expressed in about three out of four breast cancers. The Progesterone Receptor (PR) and the Androgen Receptor (AR) are also commonly expressed. Moreover, non-steroid nuclear receptors, including the vitamin D receptor (VDR) and the thyroid receptors (TRs), are also present in breast cancers and have pathophysiologic implications. Circulating thyroid hormones may influence breast cancer risk and breast cancer cell survival, through ligating their canonical receptors TRα and TRβ but also through additional membrane receptors that are expressed in breast cancer. The expression of TR subtypes and their respective isotypes have diverse effects in breast cancers through co-operation with ER and influence on other cancer-associated pathways. Other components of the TSH/thyroid hormone axis, such as TSH and selenoiodinase enzymes, have putative effects in breast cancer pathophysiology. This paper reviews the pathophysiologic and prognostic implications of the thyroid axis in breast cancer and provides a brief therapeutic perspective.
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Nelson, Erik R., Ching-yi Chang, and Donald P. McDonnell. "Cholesterol and breast cancer pathophysiology." Trends in Endocrinology & Metabolism 25, no. 12 (2014): 649–55. http://dx.doi.org/10.1016/j.tem.2014.10.001.

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Kuroi, Katsumasa, Kojiro Shimozuma, Tetsuya Taguchi, et al. "Pathophysiology of seroma in breast cancer." Breast Cancer 12, no. 4 (2005): 288–93. http://dx.doi.org/10.2325/jbcs.12.288.

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Piller, Neil B. "Pathophysiology of Breast Cancer-Related Lymphoedema." Current Breast Cancer Reports 12, no. 4 (2020): 225–29. http://dx.doi.org/10.1007/s12609-020-00377-w.

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Pandrangi, Santhi Latha, Prasanthi Chittineedi, Rajasekhar Chikati, et al. "Role of Lipoproteins in the Pathophysiology of Breast Cancer." Membranes 12, no. 5 (2022): 532. http://dx.doi.org/10.3390/membranes12050532.

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Breast cancer is one of the most common malignancies in women and the leading cause of cancer mortality. Hypercholesterolemia and obesity are potential risk factors for the incidence of breast cancer, and their detection can enhance cancer prevention. In this paper, we discuss the current state of investigations on the importance of lipoproteins, such as low denisity lipoproteins (LDL) and high density lipoproteins (HDL), and cholesterol transporters in the progression of breast cancer, and the therapeutic strategies to reduce breast cancer mortality. Although some research has been unsuccessful at uncovering links between the roles of lipoproteins and breast cancer risk, major scientific trials have found a straight link between LDL levels and incidence of breast cancer, and an inverse link was found between HDL and breast cancer development. Cholesterol and its transporters were shown to have significant importance in the development of breast cancer in studies on breast cancer cell lines and experimental mice models. Instead of cholesterol, 27-hydroxycholesterol, which is a cholesterol metabolite, is thought to promote propagation and metastasis of estrogen receptor-positive breast cancer cell lines. Alteration of lipoproteins via oxidation and HDL glycation are thought to activate many pathways associated with inflammation, thereby promoting cellular proliferation and migration, leading to metastasis while suppressing apoptosis. Medications that lower cholesterol levels and apolipoprotein A-I mimics have appeared to be possible therapeutic agents for preventing excessive cholesterol’s role in promoting the development of breast cancer.
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Nazih, Hassan, and Jean Marie Bard. "Cholesterol, Oxysterols and LXRs in Breast Cancer Pathophysiology." International Journal of Molecular Sciences 21, no. 4 (2020): 1356. http://dx.doi.org/10.3390/ijms21041356.

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Breast cancer is the most frequent cancer among women. In 2018, it is estimated that 627,000 women died from breast cancer. This is approximately 15% of all cancer deaths among women (WHO 2018). Breast cancer is a multifactorial chronic disease. While important progress has been made to treat patients, many questions regarding aspects of this disease relating to carcinogenesis are still open. During carcinogenesis, cells exhibit cholesterol homeostasis deregulation. This results in an accumulation of intracellular cholesterol, which is required to sustain their high growth rate. Cholesterol efflux and influx are two metabolic pathways that are necessary to prevent cholesterol accumulation in the cells. Liver X receptors (LXRs) are nuclear receptors that, upon activation, induce the expression of ABC transporters, responsible for promoting cholesterol efflux, and the expression of IDOL (inducible degrader of low-density lipoprotein receptor), in charge of reducing cholesterol influx. Oxysterols, oxygenated derivatives of cholesterol formed through different pathways, have been discovered as LXR-specific ligands. Some oxysterols are involved in tumor formation while others are considered anti-tumor agents. In the present review, we discuss the involvement of cholesterol, oxysterols and LXRs in breast cancer pathophysiology, with an emphasis on the biological effects of LXR ligands.
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Holtkamp, W., W. Wuttke, G. A. Nagel, U. Michel, and G. Holzapfel. "Pathophysiology of hyperprolactinemia in human breast cancer." Journal of Steroid Biochemistry 28 (January 1987): 5. http://dx.doi.org/10.1016/0022-4731(87)91114-9.

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Lucke-Wold, Brandon, Elizabeth Klaas, Shahd Mohamed, Jordan Poe, Ramya Reddy, and Abeer Dagra. "Innovative Approaches for Breast Cancer Metastasis to the Brain." Archives of Medical Case Reports and Case Study 6, no. 4 (2022): 01–09. http://dx.doi.org/10.31579/2692-9392/147.

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Breast cancer metastasis is a continued concern for patients with recent development in our understanding of disease progression. In this paper, we highlight the pathophysiology behind breast cancer metastasis. Blood brain barrier disruption plays a critical component in progression. We then investigate the current treatment strategies and recommended guidelines. This focuses on radiation and medical management. Finally, we address the role of surgical intervention. The data is organized into tables and figures to highlight key components. Finally, we address emerging treatments and pre-clinical data. The paper will serve as a user-friendly guide for clinicians and researchers to help formulate a strategy to manage breast cancer metastasis patients sufficiently.
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Umamaheswari, Amineni, SudheerKumar Katari, Chiranjeevi Pasala, et al. "Pathophysiology of matrix metalloproteinases in breast cancer progression." Journal of Clinical and Scientific Research 8, no. 3 (2019): 145. http://dx.doi.org/10.4103/jcsr.jcsr_67_19.

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Nelson, E. R., S. E. Wardell, J. S. Jasper, et al. "27-Hydroxycholesterol Links Hypercholesterolemia and Breast Cancer Pathophysiology." Science 342, no. 6162 (2013): 1094–98. http://dx.doi.org/10.1126/science.1241908.

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Dissertations / Theses on the topic "Breast – Cancer – Pathophysiology"

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O'Mahony, Susan. "An investigation into the pathophysiology of breast cancer-related lymphoedema." Thesis, University of Cambridge, 2012. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.610025.

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Bennett, Britton Thomas Mark. "Investigations into the pathophysiology of breast cancer-related lymphoedema (BCRL)." Thesis, University of Cambridge, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.612001.

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Bains, Salena Raminder Ramanjeet Kaur. "An investigation into the pathophysiology of breast cancer-related lymphoedema." Thesis, King's College London (University of London), 2015. http://kclpure.kcl.ac.uk/portal/en/theses/an-investigation-into-the-pathophysiology-of-breast-cancerrelated-lymphoedema(925c62ae-02ef-47bc-8589-fd248a9aad47).html.

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Breast cancer-related lymphoedema (BCRL) is a chronic condition with associated physical and psychological sequelae. BCRL affects up to 25% of breast cancer patients, yet the aetiology is incompletely understood. The work described within this thesis will help further advance the understanding of the pathophysiology of BCRL, with a focus on whether patients are predisposed to developing BCRL. Studies were conducted using qualitative and quantitative lymphoscintigraphy to assess the lymphatic system in breast cancer patients. The first study investigated muscle lymph flow in the upper limb. Lymphatic clearance rates were measured to investigate whether there was an abnormality in lymph flow prior to axillary lymph node surgery in patients who subsequently developed BCRL. Secondly, patients were assessed for the presence of upper limb lymphovenous communications to determine if these acted as a protective mechanism against the development of BCRL. Finally, in order to determine if there was a global dysfunction of the lymphatic system in patients previously treated for breast cancer, lower limb lymphatic function was assessed. The first study demonstrated that those who went on to develop BCRL had a higher pre-operative muscle lymph flow compared with those who did not, indicating an underlying constitutional difference. The second study showed evidence of the presence of lymphovenous communications in several breast cancer patients studied, however the numbers were too small to show any correlation with the development of BCRL. The final study showed that patients with BCRL had significantly impaired lower limb lymph flow compared with non-BCRL patients. Intriguingly, several non-BCRL patients were also found to have impaired lower lymph flow, raising the question of whether systemic treatment with chemotherapy was a significant contributory factor to this phenomenon. In conclusion, these studies add evidence in support of the hypothesis that constitutional factors contribute to the development of BCRL.
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Suwiwat, Supaporn. "Versican : regulation, purification, and biological properties of a candidate prognostic indicator for breast cancer /." Title page, table of contents and summary only, 2003. http://web4.library.adelaide.edu.au/theses/09PH/09phs9679.pdf.

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Hinzey, Adam H. "Social Influences on Breast Cancer Pathophysiology and Allodynia Following Nerve Injury: Mechanisms and Mediators." The Ohio State University, 2017. http://rave.ohiolink.edu/etdc/view?acc_num=osu1462842633.

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Thiebaut, Charlène. "Modalités de régulation d’ERα36 et leurs conséquences sur la physiopathologie de la glande mammaire". Thesis, Université de Lorraine, 2019. http://www.theses.fr/2019LORR0090/document.

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Les récepteurs nucléaires aux œstrogènes, ERα66 et ERβ1, sont les principaux médiateurs des effets des œstrogènes. Ces hormones régulent le développement physiologique de la glande mammaire mais participent aussi à la progression du cancer sein. L’expression d’ERα66 est d’ailleurs utilisée dans la classification moléculaire des tumeurs mammaires afin d’orienter la stratégie thérapeutique. Depuis son clonage, le variant des récepteurs alpha aux œstrogènes, ERα36, a été principalement décrit dans la littérature pour son rôle dans la progression des tumeurs mammaires et dans l’acquisition de résistances aux anti-œstrogènes comme le Tamoxifène. Si une forte expression d’ERα36 dans les cellules cancéreuses mammaires apparaît nettement comme un facteur de mauvais pronostic, peu de données sont disponibles concernant son rôle dans le développement de la glande mammaire saine. C’est pourquoi le premier objectif de ce travail était de déterminer le rôle d’ERα36 dans le développement physiologique de cette glande. Grâce à une approche pluridisciplinaire, incluant des études in vivo sur un modèle de souris transgéniques MMTV-ERα36 et des études in vitro et in silico sur des cellules épithéliales mammaires immortalisées, nous avons montré que l’expression d’ERα36 perturbe le phénotype des cellules épithéliales mammaires et conduit à l’apparition d’altérations structurales des canaux mammaires à l’âge adulte. De plus, nous avons mis en évidence que les alkylphénols, qui sont des perturbateurs endocriniens œstrogèno-mimétiques, stimulent l’expression endogène de ce variant dans les cellules MCF-10A et augmentent leurs capacités migratoires sans pour autant amplifier les effets d’ERα36 sur l’histologie des canaux mammaires. En parallèle, afin de mieux comprendre l’implication d’ERα36 au moment de l’initiation et de la progression tumorale, nous avons étudié les modalités de régulation de l’expression de ce variant dans les cellules cancéreuses mammaires. Les résultats obtenus indiquent que l’expression d’ERα36 est positivement corrélée au statut de méthylation de sa région promotrice et que l’ARNm codant ce variant est la cible d’hsa-miR136-5p. Enfin, le dernier objectif de ce travail était de développer une approche visant à identifier in silico de nouveaux partenaires d’ERα36. L’ensemble de ce travail s’inscrit dans une démarche de raffinement de la classification moléculaire actuelle des tumeurs mammaires en y ajoutant une composante associée à l’expression d’ERα36<br>The estrogen nuclear receptors, represented by the canonical forms ERα66 and ERβ1, are the main mediators of the estrogenic effects in mammals. These hormones, which regulate the physiological development of the mammary gland, participate in the initiation and progression of breast cancer. In fact, ERα66 expression is a key molecular classifier of breast tumors used in order to guide the therapeutic strategies toward hormonotherapy. However, in 30% of cases, therapeutic failures are observed, which highlights the importance of identifying new biomarkers. The estrogen receptor variant, ERα36, has been cloned in 2005 and mainly described in the literature to be involved in the progression of mammary tumors and in the acquired resistance to anti-estrogen drugs, such as Tamoxifen. Even if a high expression of ERα36 in breast cancer cells appears to be associated with a poor prognosis, few data are available concerning its role in the normal development of the mammary gland. Therefore, the aim of this work was to determine the role of ERα36 in the physiological development of the mammary gland. Thanks to a multidisciplinary approach, that combines in vivo studies on MMTV-ERα36 transgenic mice, and in vitro and in silico studies on immortalized normal epithelial mammary cells (MCF-10A), we showed that ERα36 expression is sufficient to disturb the mammary epithelial cells phenotype, leading to the emergence of structural alterations of mammary ducts at adulthood. Moreover, we showed that exposure to the estrogen mimicking compounds alkylphenols stimulates the endogenous expression of this variant in MCF-10A cells, and increases their migratory ability. Then, in order to get a better understanding of ERα36 contribution to tumor initiation and/or progression, we studied classical and epigenetic regulation of this variant expression in breast cancer cells. Our results show that ERα36 expression is positively correlated with the methylation status of its promoter region, and that the ERα36 mRNA is the target of the microRNA, has-miR-136-5p. Finally, the last aim of this work was to develop a bioinformatic approach in order to study the ERα36 partners. To summarize, all of this work falls within a need of the current breast tumor molecular classification refinement by adding a component related with ERα36 expression
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Suwiwat, Supaporn. "Versican : regulation, purification, and biological properties of a candidate prognostic indicator for breast cancer / Supaporn Suwiwat." Thesis, 2003. http://hdl.handle.net/2440/22057.

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"December 2003"<br>Includes bibliographical references (leaves 106-128)<br>xii, 128 leaves : ill., plates ; 30 cm.<br>Thesis (Ph.D.) -- University of Adelaide, Dept. of Medicine and The Hanson Institute, 2004
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Tonsing-Carter, Eva Y. "Modulation of the Mdm2 signaling axis sensitizes triple-negative breast cancer cells to carboplatin." Thesis, 2014. http://hdl.handle.net/1805/6306.

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Triple-negative breast cancers (TNBCs) are highly refractive to current treatment strategies, and new multi-targeted treatments need to be elucidated. Combination therapy that includes targeting the murine double minute 2 (Mdm2) signaling axis offers a promising approach. Protein-protein interaction inhibitors such as Nutlin-3a block the binding of key signaling molecules such as p53, p73α, and E2F1 to the hydrophobic pocket of Mdm2 and can lead to activation of cell-death signaling pathways. Since clinical trials for TNBC are evaluating the DNA damaging agent carboplatin, the objective of this thesis was to evaluate the therapeutic potential and mechanism of action of combination carboplatin and Nutlin-3a to treat TNBC. In TNBC cell lines with a mutant p53 background, we determined if modulation of Mdm2 function in the context of carboplatin-mediated DNA damage resulted in a synergistic inhibition of cell growth. Several ratios of carboplatin:Nutlin-3a were strongly synergistic in increasing cell death, with combination indices of 0.5 and lower. Mechanistic studies indicated that drug sensitivity and Mdm2 expression were dependent on p73. Mdm2 localized to a larger degree in the chromatin fraction isolated from cells treated with the combination treatment consistent with observations by others that Mdm2 binds to the Mre11/Rad50/Nbs1 complex, inhibits the DNA damage response, and increases drug sensitivity. In vivo efficacy experiments were conducted in the TMD231 orthotopic mammary fat pad model in NOD.Cg-PrkdcscidIl2rgtm1Wjl/SzJ (NSG) mice. For assessment of baseline tumor burden and randomization, fluorescent imaging of E2-Crimson expressing TMD231 cells was performed. Following Nutlin-3a and carboplatin combination treatment, there was a statistically significant reduction in primary tumor volume as well as lung metastases with significantly increased probability of survival compared to Vehicle and single drug treatments (p<0.001). While there was a decrease in bone-marrow cellularity, this did not lead to bone-marrow aplasia, and body weights recovered to normal levels within 7 days post-treatment. The present studies demonstrate the promise of Mdm2 as a therapeutic target in combination with conventional therapy, increase our understanding of how to potentiate DNA damage in cancers, and may lead to new clinical therapies for triple-negative primary and metastatic breast cancer.
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Mojahed, Diana. "Rapid breast pathology tissue evaluation using optical coherence tomography (OCT)." Thesis, 2021. https://doi.org/10.7916/d8-6k52-4906.

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The purpose of this work was to develop novel optical imaging technology and algorithms as a nondestructive method for detection and diagnosis of cancer in breast specimens. There are many ways in which the diagnosis of disease can benefit from fast and intelligent optical imaging technology. Our existing ability to provide this diagnosis depends on time-consuming pathology analysis. Optical coherence tomography (OCT) is a non-invasive optical imaging modality that provides depth-resolved, high-resolution images of tissue microstructure in real-time. OCT could provide a rapid evaluation of specimens while patients are still in the office, and has strong potential to improve the efficiency in evaluation of breast pathology specimens (biopsy or surgical). In this work, we demonstrate an imaging system to address this unmet clinical need, artificial intelligence algorithms to interpret the images, and early work towards miniaturizing the technology. We present an OCT system that achieves a line scan rate of 250kHz, meaning we can image a pathology cassette in 41 seconds, which is more than double the fastest scan rate in the field. By utilizing a multiplexed superluminescent diode (SLD) light source, which has strong noise performance over imaging speed, we achieve high resolution imaging under 5 um in tissue (axially and laterally). The system features a 1.1 mm 6-dB sensitivity fall-off range when imaging at 250 kHz. The scanner features large-area scanning with the implementation of a 2-axis motorized stage, enabling visualization of areas up to 10 cm x 10 cm (prior work visualizes 3 mm x 3mm). We showcase the results of demonstrating the performance of this system on a 100-patient clinical imaging study of breast biopsies, as well as imaging of clinical pathology specimens from the breast, prostate, lung, and pancreas in an IRB-approved study. Further, we show our work towards developing artificial intelligence (AI) for cancer detection within OCT images. Using retrospective data, we developed a type of AI algorithm known as a convolutional neural network (CNN) to classify OCT images of breast tissue from 49 patients. The binary cancer classification achieved 94% accuracy, 96% sensitivity, and 92% specificity. This framework had higher accuracy than the 88% accuracy of 7 clinician readers combined in our lab’s earlier multi-reader study. Lastly, we demonstrate a supercontinuum light source based on a 1 mm2 Si3N4 photonic chip for OCT imaging that has better performance than the state-of-the-art laser. Existing broadband laser sources for OCT are large, bulky, and have high excess noise. Our Si3N4 chip fundamentally eliminates the excess noise common to lasers and achieves 105 dB sensitivity and 1.81 mm 6-dB sensitivity roll-off with only 300 µW power on the sample.
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Zafar, Anjum. "Novel chromatin-associated role of Protein Kinase C family members in regulating inducible genes and microRNAs during epithelial to mesenchymal transition." Phd thesis, 2012. http://hdl.handle.net/1885/149888.

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The epithelial to mesenchymal transition (EMT) is a key step in cancer progression and metastasis. A small subpopulation of tumor cells formed thereby, referred to as Cancer Stem Cell (CSC) cells, potentially have a significant role for metastatic tumor initiation and recurrence. The epigenetic regulation underpinning control of gene expression programs in EMT and CSC formation processes are not well understood, largely because an appropriate inducible in vitro human model is lacking. This thesis describes the establishment of a novel human in vitro rapidly inducible breast cancer EMT model amenable to detailed analysis of epigenetic processes. The human breast cancer epithelial cell line, MCF-7 was stimulated with the PKC pathway inducer, PMA. This results in the emergence of a significant cancer stem cell-like subpopulation amidst almost complete mesenchymal conversion. The epithelial cells, CSC-like and non-CSC (NCSC) mesenchymal subpopulations were shown to be distinct in their transcriptional programs and microRNA profiles. The novel role of PKC isoforms as chromatin-associated enzymes in EMT and CSC formation processes has been indentified for the first time in this thesis. Chromatin immuno-precipitation (ChIP) assays revealed that non-phosphorylated PKC-theta predominated in the epithelial state across the promoter of uPAR, whilst phosphorylated PKC-thata predominated in the mesenchymal state of MCF-7 cells. In contrast, PKC-beta recruitment on the uPAR promoter predominated in mesenchymal state with little enrichment detected in the epithelial state. Similarly, phosphorylated H3T6, which is a surrogate for active PKC-beta was highly recruited in the mesenchymal state in comparison to epithelial state. Interestingly, inactive forms of PKC-theta and PKC-beta form complexes with LSD1 and Zeb1 on the chromatin template in epithelial cells. However, in mesenchymal cells, active PKC-theta switches its association to the active mark Pol II instead of LSD1 and Zeb1. Importantly, the data suggest that although phosphorylated PKC-theta is required for PKC-beta recruitment in the mesenchymal state, the two PKC isozymes, PKC-theta and PKC-beta play opposing roles in regulating transcription of inducible EMT genes. For the first time it has been shown that PKC-theta and PKC-beta tether to chromatin on the promoters of microRNA 200 family members during the process of the epithelial to mesenchymal transition. Not only does Pol II co-exist with PKC-theta in the mesenchymal state on the miR 200c promoter but, also, epigenetic tags such as LSD1 and Zeb-1 co-exist with Pol II in mesenchymal state, suggesting that ""Pol II capturing"" occurs in a PKC-theta containing repressive complex. Additionally, it was shown that PKC activity is important in controlling EMT and CSC formation by regulating EMT associated inducible genes and microRNAs. Collectively, the data presented in this thesis suggest that PKC isozymes might have ""dual role"" consisting of signal transduction role and chromatin associated role in controlling EMT and CSC formation processes. Furthermore, a previously undescribed layer of chromatin-tethered enzymes with interconnected function regulates transcription of EMT-associated inducible genes and microRNAs, include PKC isozymes, histone demethylases and DNA methyltransferases. -- provided by Candidate.
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Books on the topic "Breast – Cancer – Pathophysiology"

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J, Thomas Jeremy St, and Dixon, J. M. (J. Michael), eds. Breast cancer. Clinical Pub., 2012.

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Rosen's breast pathology. Lippincott-Raven, 1997.

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Rosen's breast pathology. 3rd ed. Lippincott Williams & Wilkins, 2008.

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Miller, W. R. Estrogen and breast cancer. Springer, 1996.

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Estrogen and breast cancer. R.G. Landes Co., 1996.

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1945-, Lippman Marc E., and Dickson Robert B. 1952-, eds. Breast cancer: Cellular and molecular biology. Kluwer Academic Publishers, 1988.

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1952-, Body Jean-Jacques, ed. Tumor bone diseases and osteoporosis in cancer patients: Pathophysiology, diagnosis, and therapy. Marcel Dekker, 2000.

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Carole, Lester Susan, ed. Diagnostic pathology: Breast. Amirsys, 2012.

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Daniel, Medina, and Organ Systems Coordinating Center (National Cancer Institute), eds. Cellular and molecular biology of mammary cancer. Plenum Press, 1987.

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Rosen's Breast Pathology. 2nd ed. Lippincott Williams & Wilkins, 2001.

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Book chapters on the topic "Breast – Cancer – Pathophysiology"

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Sahni, Sachin, and James Khan. "Persistent Breast Cancer Pain." In Breast Cancer [Working Title]. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.96546.

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Fortunately, with advances in screening and management, the prognosis of breast cancer has substantially improved. However, as patients with breast cancer are living much longer, consequences of management are becoming increasingly apparent, particularly persistent pain after breast cancer surgery. This pain disorder, referred to as Post-Mastectomy Pain Syndrome (PMPS) is common and typically presents as pain with neuropathic features around the surgical incision. This pain disorder is associated with negative effects on the patient’s social and psychological well-being as well as increased healthcare expenditures. Despite the common occurrence of this disorder, it is vastly under-recognized with a lack of preventative and treatment options. This chapter aims to outline the management of persistent breast surgery pain. The pathophysiology and etiology will be reviewed, followed by tools that clinicians can implement in order to appropriately diagnose neuropathic pain. Pertinent risk factors that are commonly seen in practice will be outlined, followed by non-pharmacological, pharmacological, and interventional therapeutic options that can be offered.
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Rezacova, Monika. "Natural Products and Their Bioactive Compounds as Breast Cancer Therapeutics." In Handbook of Research on Natural Products and Their Bioactive Compounds as Cancer Therapeutics. IGI Global, 2022. http://dx.doi.org/10.4018/978-1-7998-9258-8.ch002.

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Breast cancer is one of the most common types of cancer in the Western world. It is cancer that is curable and has great life expectancy afterwards, but the treatment often combines surgery with chemotherapy and/or hormone therapy. This creates a need for more effective and less toxic therapeutic and preventive strategies for breast cancers as well as strategies to overcome increasing resistance to hormonal and targeted therapy. This chapter focuses on chemopreventative and anti-cancer activities of different bioactive compounds obtained from dietary sources, herbal approach, and use of natural compounds such as diindolylmethane, biochanin A, curcumin, Epigallocatechin Gallate, genistein, lycopene, shikonin, sulforaphane, and resveratol. Understanding the pathophysiology of action of these compounds and their potential preventive and therapeutic effects on cancer may provide a rationale for further studies.
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"Breast surgery." In Oxford Handbook for Medical School, edited by Kapil Sugand, Miriam Berry, Imran Yusuf, et al. Oxford University Press, 2019. http://dx.doi.org/10.1093/med/9780199681907.003.0032.

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Chapter 32 provides an overview of breast surgery including common presenting symptoms, an approach to clinical assessment, and the investigation and management of breast lumps. An approach to the clinical assessment of breast lumps is described, including helpful mnemonics to assist in the recall of the key questions to ask in a focused history (including appropriate identification of risk factors). A systematic approach to breast examination is presented, followed by the key imaging modalities used to identify a breast lump, including mammography, ultrasound, fine needle aspiration cytology, and sometimes magnetic resonance imaging. The pathophysiology and genetic contributions of the BRCA1 and BRCA2 genes are described. The role of screening for breast cancer is described in detail, including commonly used descriptions of grading and staging of disease. The management of options including chemotherapy, radiotherapy, and adjuvant treatment (such as tamoxifen, anastrozole, and trastuzumab) are provided. Common benign breast lumps include fibroadenomas, breast cysts, duct ectasia, breast abscesses, and fat necrosis and the presentation and management of each are described. Breast surgery may form part of the management of breast cancer and include mastectomy, wide local excision, sentinel lymph node biopsy, axillary dissection, and breast reconstruction at a later date. Essential clinical skills including focused history taking, a systematic approach to breast examination is provided.
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Cosentino, Giulia, Ilaria Plantamura, and Marilena V. Iorio. "Pathophysiology rolesr and translational opportunities of miRNAs in breast cancer." In MicroRNA in Human Malignancies. Elsevier, 2022. http://dx.doi.org/10.1016/b978-0-12-822287-4.00026-8.

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Segovia-Mendoza, Mariana, Blanca Estela Fernández-López, Cristina Lemini, Angeles Carlos-Reyes, and Heriberto Prado-Garcia. "Role of Membrane Estrogen Receptor (GPER1) on the Function of Immune Cells and Its Consequences on Breast Cancer Pathophysiology." In Interdisciplinary Cancer Research. Springer International Publishing, 2022. http://dx.doi.org/10.1007/16833_2022_48.

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Hadji, Peyman. "Impact of breast cancer and its treatment on bone loss and fracture risk—pathophysiology and management." In Marcus and Feldman's Osteoporosis. Elsevier, 2021. http://dx.doi.org/10.1016/b978-0-12-813073-5.00056-3.

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Gooren, Louis J. G. "Male reproductive health." In Oxford Textbook of Endocrinology and Diabetes. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780199235292.003.9146.

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Life expectancy is on average 7 years shorter for men than for women; from birth through senescence, death rates are higher for males than for females (1). Potentially contributing factors are male risk-taking behaviour (accidents, homicide, smoking, alcoholism, high professional and social achievement), less use of medical care, and possibly genetic and endocrine factors. This chapter will address the potential role of sex steroids in the sex disparity in morbidity and mortality. Male and female, and androgens and oestrogens, are usually considered as being antithetical, and sex differences are usually stressed while similarities receive much less attention. However, in both sexes the decline of sex steroid production in old age is associated with osteopenia. and also with an increase in cardiovascular disease. Moreover, the pathophysiology of breast and prostate cancer might show parallels. In reproductive medicine, advances in scientific knowledge and health care have been greater in women than in men. Strategies successful for women might be utilized to promote the health of (ageing) men. It is unfortunate that sex steroids, and particularly androgens, are often perceived as potentially harmful substances rather than being valued for their potentially beneficial actions. Concerning the difference in life expectancy between men and women, an historical comparison between castrati and intact singers in the 15th to 19th centuries demonstrated that both castrati and intact singers at that time had the same life expectancy of around 64 years; this indicates that testosterone deprivation shortly before puberty did not influence longevity. More recent studies show that sociological, lifestyle and professional factors may be of more importance (2).
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Conference papers on the topic "Breast – Cancer – Pathophysiology"

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Bockhorn, Jessica, Toby M. Ward, J. Chuck Harrell, Xiaofei Liu, Gaby Fuchs, and Mark D. Pegram. "Abstract 2018: Investigation of ITAF's role in the pathophysiology of breast cancer." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-2018.

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Nascimento, Renan Gomes do. "AN IN SÍLICO ANALYSIS DETECTED MEMBERS OF THE PLECKSTRIN HOMOLOGY-LIKE DOMAIN FAMILY B AS POTENTIAL PROGNOSTIC BIOMARKERS IN PATIENTS WITH BREAST CANCER." In Abstracts from the Brazilian Breast Cancer Symposium - BBCS 2021. Mastology, 2021. http://dx.doi.org/10.29289/259453942021v31s2034.

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Objectives: Despite advances in the molecular classification of breast cancer, our understanding of the pathophysiology of the disease is still limited mainly due to the considerable intratumoral heterogeneity. Thus, hundreds of other candidates for biomarkers are being investigated and studied for possible implications for diagnosis, prognosis, and personalized therapy. In this context, members of the Pleckstrin homology-like domain family B (PHLDB), which is composed of three genes located on different chromosomes: PHLDB1 (11q23.3), PHLDB2 (3q13.2), and PHLDB3 (19q13.3), are under investigation by different research groups as potential biomarkers in different types of cancer. It has been reported that the altered expression of these genes is involved in the tumorigenic process. In this study, we sought to understand the prognostic and predictive value of genes from the PHLDB family as potential biomarkers in breast oncology. Conclusions: Our findings provide new insights into the potential role of PHLDB family members as clinical predictors in breast cancer. Unlike what has already been described in the literature, it appears that members of the PHLDB family are potential tumor suppressor genes in breast cancer. Further clinical and experimental studies are needed to better understand the relationship between the expression of the members of the PHLDB family and the tumorigenic process of the breast and its prognostic and predictive values in breast cancer.
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Reports on the topic "Breast – Cancer – Pathophysiology"

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Nelson, Erik R., and Donald P. McDonnell. The Impact of 27-Hydroxycholesterol, a Macrophage-Synthesized Estrogen Receptor Agonist, on Breast Cancer Pathophysiology. Defense Technical Information Center, 2010. http://dx.doi.org/10.21236/ada539368.

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Brown, Deborah A. The Role of Spingolipid- and Cholesterol-Rich Membrane Domains in Pathophysiology of Cultured Human Breast Cancer. Defense Technical Information Center, 2001. http://dx.doi.org/10.21236/ada395838.

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Brown, Deborah A. The Role of Sphingolipid-and Cholesterol-Rich Membrane Domains in Pathophysiology and Cultured Human Breast Cancer. Defense Technical Information Center, 2004. http://dx.doi.org/10.21236/ada431301.

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McDonnell, Donald P. The Impact of 27-Hydroxycholesterol, a Macrophage-Produced Estrogen Receptor and Liver X Receptor Agonist, on Breast Cancer Pathophysiology. Defense Technical Information Center, 2011. http://dx.doi.org/10.21236/ada542371.

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