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Alterations In Estrogen Receptor Signaling Pathways In Breast Cancer Cells With Acquired Antiestrogen Resistance
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Book Synopsis Alterations in Estrogen Receptor Signaling Pathways in Breast Cancer Cells with Acquired Antiestrogen Resistance by : Lei Chen
Download or read book Alterations in Estrogen Receptor Signaling Pathways in Breast Cancer Cells with Acquired Antiestrogen Resistance written by Lei Chen and published by . This book was released on 2005 with total page 138 pages. Available in PDF, EPUB and Kindle. Book excerpt:
Book Synopsis Endocrine Therapy in Breast Cancer by : William R. Miller
Download or read book Endocrine Therapy in Breast Cancer written by William R. Miller and published by CRC Press. This book was released on 2002-03-08 with total page 395 pages. Available in PDF, EPUB and Kindle. Book excerpt: This reference evaluates and describes the latest strategies for hormone suppression and blockade in the management of early and advanced stage breast cancer and explores the effects of tamoxifen, selective estrogen receptor modulators (SERMs), aromatase inhibitors, and their combination on both breast cancers and normal tissues. Endocrine T
Book Synopsis Molecular Mechanisms of Drug Resistance And Strategies of Sensitization in Breast Cancer, 2nd edition by : Yan Cheng
Download or read book Molecular Mechanisms of Drug Resistance And Strategies of Sensitization in Breast Cancer, 2nd edition written by Yan Cheng and published by Frontiers Media SA. This book was released on 2024-01-11 with total page 198 pages. Available in PDF, EPUB and Kindle. Book excerpt: Basic scientific background Breast cancer is one of the most common cancer and the most frequent cause of cancer death among women worldwide. Currently, subtyping breast cancers into hormone receptor (HR) positive, human epidermal growth factor receptor-2 overexpressing (HER2+), and triple negative breast cancer (TNBC) is the basis of diagnosing and treating this disease. The main treatment strategies for breast cancer include surgery, endocrine therapy, molecular targeted therapy, chemotherapy, radiotherapy, immunotherapy and gene therapy. However, resistance of breast cancer cells to chemotherapeutic agents, molecular targeted therapies and immunotherapy may occur either intrinsically or de nova, and is often ultimately responsible for treatment failure. Therefore, drug resistance poses a major challenge to breast cancer treatment. Current developments: Drug resistance in breast cancer is a complex clinical condition originating from a wide range of molecular alterations. The development of endocrine therapy resistance is believed to be associated with many cellular changes, such as ESR1 gene mutations, bypassing estrogen signaling pathway and altered tamoxifen metabolism. Meanwhile, changes in immune response, alternation of drug-binding property and downstream pathways are involved in the mechanisms of drug resistance in HER2+ breast cancer. In addition, resistance to chemotherapeutic agents predominantly arises from increased drug efflux and cross resistance. Current studies suggest that treatment strategies and therapeutics have to be designed specifically to each patient in different clinical situations. The use of modern genomic, proteomic and functional analytical techniques has contributed to identify novel genes and signaling networks involved in breast cancer drug resistance. Moreover, the use of high-throughput techniques in combination with bioinformatics and systems biology approaches has aided the interrogation of clinical samples and allowed the identification of molecular signatures and genotypes that predict responses to certain drugs. Despite much progress has been made in the field of breast cancer drug resistance, such as combination therapy and drug-loaded nanoparticles, the complexity and variability of drug resistance mechanism still inevitably lead to the continuous occurrence of drug resistance. Therefore, with the increasing amounts of anti-breast cancer agents, there are now unprecedented opportunities to understand and overcome drug resistance through further research into mechanisms and corresponding strategies, which will help achieve lasting disease control and bring survival benefits to patients with advanced cancer. Papers of interest: The current Research Topic of Frontiers in Pharmacology focuses on publishing Original Research, Review articles and Case Reports focusing on (a) elucidating mechanisms of drug resistance in breast cancer, target mutations, tumor microenvironment, undiscovered genes and signaling pathways; (b) promising drug delivery systems that can enhance the sensitivity of anti- breast cancer agents to various tumors; (c) strategies that can improve patient care during bio-chemotherapeutic treatments; (d) small molecule compounds that are effective against drug-resistant breast tumors (e) biomarkers of chemotherapy resistance in breast cancer patients and (f) in vitro and in vivo models. Guidelines for article of submission: - Authors must stick to the set guidelines for ethical practices by the Frontiers journals. - The main content of the article must have certain innovation and research significance. - The authors should describe the construction method of drug-resistant cell lines when using them for experiments in the article.
Book Synopsis Estrogen Receptor Gene Alterations in Human Breast Cancer by : Qiu-Xia Zhang
Download or read book Estrogen Receptor Gene Alterations in Human Breast Cancer written by Qiu-Xia Zhang and published by . This book was released on 1997 with total page 144 pages. Available in PDF, EPUB and Kindle. Book excerpt:
Book Synopsis Altered Estrogen Receptor and Transforming Growth Factor Pathways in Models of Estrogen-autonomous and of Antiestrogen-resistant MCF-7 Human Breast Cancer Cells by : Mary E. Herman
Download or read book Altered Estrogen Receptor and Transforming Growth Factor Pathways in Models of Estrogen-autonomous and of Antiestrogen-resistant MCF-7 Human Breast Cancer Cells written by Mary E. Herman and published by . This book was released on 1995 with total page 316 pages. Available in PDF, EPUB and Kindle. Book excerpt: The progression of breast tumors to steroid-autonomous and antiestrogen-resistant phenotypes confounds our ability to treat breast cancer with antiestrogens, the most efficacious hormone treatment used clinically. We developed two models in the MCF-7 cell line, an estrogen receptor-positive human breast cancer cell line, to assess the relative importance of the estrogen receptor pathway and the transforming growth factor (TGF) pathways during this progression. MCF-7 cells maintained long-term in steroid-deprived conditions exhibited a decreased growth reliance on estrogen despite elevated levels of estrogen receptor. Antiestrogen sensitivity was maintained and estrogen receptor function appeared normal. Expression of TGF$alpha$ and the TGF-$beta$s was transiently altered in response to steroid-deprivation; basal expression was partially reestablished in the long-term steroid-deprived sublines. We observed decreased growth responsiveness to TGF$alpha$ and the TGF-$beta$s, suggesting that these autocrine factors were not primary growth regulators of the steroid-autonomous MCF-7 sublines. Our second model involved long-term exposure of MCF-7 cells to the antiestrogen, trans-OH-tamoxifen (TOT). The resulting phenotype showed a growth-stimulation, rather than growth-inhibition in response to TOT and deregulation of progesterone receptor expression. Several other parameters of estrogen receptor structure and function, including responsiveness to pure antiestrogens, were analyzed and appeared normal, despite a 40% reduction in estrogen receptor content. This subline exhibited decreased growth-inhibition in response to retinoic acid and a complete loss of growth suppression by TGF-$beta$1. Insensitivity to TGF-$beta$1 could not be accounted for by loss of TGF-$beta$ receptor or cell signalling. Growth-stimulation by TOT was partly, and insensitivity to TGF-$beta$ fully, reversible upon maintenance in TOT-deprived culture conditions. Interestingly, this subline expressed elevated levels of TGF-$beta$ mRNAs and secreted, bioactive protein. The altered growth responsiveness of this model should prove useful in understanding antiestrogen resistance. Furthermore, it may provide insight into the potential role(s) of the TGF-$beta$s in tumor progression.
Book Synopsis Bidirectional Signaling Between Breast Cancer and the Tumor Microenvironment by :
Download or read book Bidirectional Signaling Between Breast Cancer and the Tumor Microenvironment written by and published by . This book was released on 2014 with total page 0 pages. Available in PDF, EPUB and Kindle. Book excerpt: Estrogen Receptor-alpha (ER-alpha) expression in breast cancer is a standard biomarker predicting positive response to endocrine therapies targeting the ER-alpha signaling pathway. Despite ER-alpha's predictive potential, resistance to therapies remains a significant problem. Particularly in advanced disease, response rate to endocrine therapy agent tamoxifen is as low as 30%. The microenvironment in which metastatic breast cancers reside represent an unnatural context of signaling that might contribute to therapy efficacy at these sites. Indeed, ER-alpha expression is lost in one-fifth of recurrences and metastases, and the mechanism by which this occurs is unknown. This thesis work investigates the interactions of breast cancer cells with the tumor microenvironment and associated endocrine therapy resistance. Using a microfluidic co-culture model of the tumor microenvironment, I demonstrated that ER-alpha expression is reduced in response to soluble, non-estrogenic signaling from the tumor microenvironment. Multiple factors both within and between microenvironments were found to contribute to breast cancer cell growth. The complexity of the tumor microenvironment requires the identification of targets that more broadly target extracellular signaling factors. This led me to identify alterations in stromal nuclear receptors, which as targetable regulators of gene expression represent good targets for therapy. Breast cancer cells induce down-regulation of PPAR-gamma expression in stromal fibroblasts. Activation of PPAR-gamma by agonist rosiglitazone blocks stroma-induced breast cancer cell growth, implicating the inhibition of this pathway as an essential step for breast cancer cells in setting up a permissive growth environment. This bidirectional signaling model also has two major implications. For the stroma, interaction with the breast cancer cells alters the expression of a key regulator of adipogenesis, suggesting shifts in the differentiation state of the stromal fibroblasts. For the tumor cells, stroma-induced breast cancer cell growth induces endocrine therapy resistance. The loss of ER-alpha serves as a functional biomarker of this resistance, in which the ER-alpha-positive breast cancer cell line MCF-7 serves as a "biosensor" for the activity of the microenvironment. These results add to our understanding of the role of the tumor microenvironment in endocrine therapy resistance, and further implicate a number of novel targets for therapy in endocrine therapy-resistant breast cancer.
Book Synopsis Regulation of Estrogen Receptor Alpha Expression by Translation Or Degradation and the Relevance to Tamoxifen Resistance in Breast Cancer by : Chun Gong
Download or read book Regulation of Estrogen Receptor Alpha Expression by Translation Or Degradation and the Relevance to Tamoxifen Resistance in Breast Cancer written by Chun Gong and published by . This book was released on 2017-01-26 with total page pages. Available in PDF, EPUB and Kindle. Book excerpt: This dissertation, "Regulation of Estrogen Receptor Alpha Expression by Translation or Degradation and the Relevance to Tamoxifen Resistance in Breast Cancer" by Chun, Gong, 龚纯, was obtained from The University of Hong Kong (Pokfulam, Hong Kong) and is being sold pursuant to Creative Commons: Attribution 3.0 Hong Kong License. The content of this dissertation has not been altered in any way. We have altered the formatting in order to facilitate the ease of printing and reading of the dissertation. All rights not granted by the above license are retained by the author. Abstract: Breast cancer is one of the most prevalent cancers affecting women worldwide. In the breast, estrogen receptor alpha (ERα), upon binding with ligands, activates gene transcription and promotes cell growth and proliferation. Tamoxifen, a selective antagonist of ERα in breast, has been proved to be effective therapeutically. In spite of this, resistance remains a prominent issue and underlying mechanisms are not yet fully understood. Aberrant regulation of ER expression at genetic and transcriptional levels has been implicated as the mechanisms accounting for tamoxifen resistance. However, regulation of ERα expression at translational level including protein synthesis and degradation has not yet been characterized and its relevance to tamoxifen resistance has not been described. At level of protein synthesis, eukaryotic translation initiation factor 4E (eIF4E) selectively enhances the translation of 4E-sensitive mRNAs which contain long and complex 5''-untraslated regions (5''-UTR). eIF4E is often over-expressed in cancers. In silico analysis revealed that ERα contained a highly structured 5''-UTR similar to reported eIF4E-sensitive mRNAs, suggesting that ERα mRNA might be eIF4Esensitive. We showed by polysome fractionation and subsequent Q-PCR quantification that the ERα mRNAs were more actively translated in the cell line expressing higher levels of eIF4E. Consistently, transient transfection of eIF4E into an ERα-positive cell line resulted in enhanced protein expression of ERα. Moreover, subcelluar fractionation showed that eIF4E was bound with ERα mRNAs in the nucleus thus participating in transportation of mRNAs from the nucleus into the cytoplasm. Therefore, eIF4E could positively modulate protein synthesis of ERα by enhancing mRNA export in the nucleus as well as translation in the cytoplasm. Their positive correlation was validated in vivo using 106 Chinese breast cancer samples (Chi-square test, p=0.004). It was also found that elevated expression of eIF4E could mediate resistance to tamoxifen treatment and enhance cell survival. This could be due to enhanced expression of ERα or activation of PI3K/Akt pathway upon eIF4E over-expression. At the level of degradation, ERα is conjugated to poly-ubiquitin chains catalyzed by multiple enzymes and degraded by 26S polysomes. Carboxyl-terminus of Hsc70- interacting protein (CHIP) is an E3 enzyme specific for ERα degradation through interaction with ERα''s ligand-binding domain (LBD). Various splicing variants of ERα have been reported and implicated in tamoxifen resistance by interfering with functions of ERα wild type. Variants ERαΔ4, ERαΔ5, ERαΔ6/7 and ERαΔ7 with different degrees of truncation in their LBDs and differential expression were detected or reported in human breast cancers. Their interactions with CHIP may be different, resulting in variations in degradation. We found that the degradation of ERαΔ6/7 through ubiquitin-proteasome pathway was impaired whilst the degradation of other variants were less affected. This finding suggests that the binding site of CHIP to ERαmight be located within the peptide sequences encoded by exon6. Furthermore, as ERαΔ6/7 plays a dominant negative role in regulating functions of ERα wild type, aborted degradation of this variant may result in accumulation of this variant in the cell, inhibiting and in
Book Synopsis The Heterogeneity of Cancer Metabolism by : Anne Le
Download or read book The Heterogeneity of Cancer Metabolism written by Anne Le and published by Springer. This book was released on 2018-06-26 with total page 186 pages. Available in PDF, EPUB and Kindle. Book excerpt: Genetic alterations in cancer, in addition to being the fundamental drivers of tumorigenesis, can give rise to a variety of metabolic adaptations that allow cancer cells to survive and proliferate in diverse tumor microenvironments. This metabolic flexibility is different from normal cellular metabolic processes and leads to heterogeneity in cancer metabolism within the same cancer type or even within the same tumor. In this book, we delve into the complexity and diversity of cancer metabolism, and highlight how understanding the heterogeneity of cancer metabolism is fundamental to the development of effective metabolism-based therapeutic strategies. Deciphering how cancer cells utilize various nutrient resources will enable clinicians and researchers to pair specific chemotherapeutic agents with patients who are most likely to respond with positive outcomes, allowing for more cost-effective and personalized cancer therapeutic strategies.
Book Synopsis Dissecting the Role of Estrogen Receptor Palmitoylation in Breast Cancer Cells by :
Download or read book Dissecting the Role of Estrogen Receptor Palmitoylation in Breast Cancer Cells written by and published by . This book was released on 2013 with total page 0 pages. Available in PDF, EPUB and Kindle. Book excerpt: Estrogen signaling is primarily mediated by two estrogen receptors (ERs), ER[alpha] and ER[beta]. ER[alpha] is expressed in ~70% of breast cancers and is an important diagnostic and therapeutic target. Developing better treatment options and overcoming limitations of endocrine therapy depend on a detailed understanding of ER[alpha]-signaling pathways. ER[alpha], a member of the class I nuclear receptor superfamily of transcription factors, localizes mainly to the nucleus and interacts with DNA regulatory sequences either directly or through interaction with other transcription factors to regulate gene transcription. ER[alpha] is also rapidly activates signaling cascades. S-palmitoylation, a reversible lipid modification is catalyzed by palmitoyl acyl-transferases (PAT), which increase affinity of proteins to the membrane. Based on the results of previous studies, it is hypothesized that palmitoylation of ER[alpha] regulates extranuclear and nuclear signaling of ER[alpha]. We utilized palmitoylation-defective mutant ER[alpha]C447A-expressing MDA-MB-468 breast cancer cells to dissect the role of palmitoylation in a breast cancer cell line model. The substitution of ER[alpha] palmitoylation site abrogated ER[alpha] palmitoylation, membrane localization and estrogen-dependent phosphorylation of ERK1/2 in MDA-MB-468 cell line. Besides loss of E2-dependent extranuclear signaling, the substitution of palmitoylation sites led to the loss of other ER[alpha]-dependent events in ER[alpha]C447A-expressing MDA-MB-468 cells, such as decreased E2-dependent S118 phosphorylation, impaired regulation of certain target genes, and loss of estrogen-dependent cell cycle inhibition. This study thus highlights the importance of ER[alpha] palmitoylation in both nuclear and extranuclear ER signaling pathways in breast cancer cells. A better understanding of the mechanisms of estrogen action will help us to design more effective drugs affecting signal pathways depending on both membrane and nuclear receptors.
Book Synopsis Role of Mevalonate Pathway Inhibition on Estrogen Receptor Expression and Its Role in Mitochondrial Cholesterol Transport in Breast Cancer by : Melanie A Neagley
Download or read book Role of Mevalonate Pathway Inhibition on Estrogen Receptor Expression and Its Role in Mitochondrial Cholesterol Transport in Breast Cancer written by Melanie A Neagley and published by . This book was released on 2018 with total page pages. Available in PDF, EPUB and Kindle. Book excerpt: While use of hydroxmethylglutaryl (HMG)-coenzyme A (CoA) reductase inhibitors (statins) has been linked to beneficial pleiotropic effects including a lowered incidence of certain types of cancer and increased response to some forms of chemotherapy, clinical results have failed to be consistent and significant. Research has begun to focus on characterizing the pathways by which statins impact cancer cell biology, in the hopes of finding better pharmacological targets to produce more potent and efficacious results. Data presented in this paper show inhibition of the mevalonate pathway using lovastatin, digeranyl bisphosphonate (DGBP) and zoledronic acid can reduce the expression levels of both ER and ER in T47D and MCF7 breast cancer cell lines. This effect is reversed with the addition of mevalonate and is dependent on both farnesyl transferase and geranylgeranyl protein transferase-1 activity. This reduction attenuates the response of both cell lines to the proliferative effects of estradiol and the anti-proliferative effects of ER-dependent fulvestrant. Lastly, we show that the reduction of ER and ER levels is a result of decreased transcriptional activity.While estrogen receptor (ER) positive breast cancers are often treated with endocrine manipulation in the form of either ligand synthesis inhibition or receptor activation inhibition, some breast cancers are naturally resistant to such therapies and many more develop resistance over the course of treatment. One cause of such resistance is mutations which lead to constitutively active estrogen receptors which do not require ligand binding for activation. Research is beginning to explore compounds known as selective estrogen receptor degraders (SERDs), which can reduce the concentration of these activated receptors. The reduction of ER levels through mevalonate inhibition could also lead to possible therapies in cases of endocrine therapy resistant breast cancer.The hypothesis of this research is that inhibition of the mevalonate pathway reduces ER levels in breast cancer cell lines through combined inhibition of receptor prenylation together with alterations in mitochondrial cholesterol transport. Changes in mitochondrial cholesterol levels may promote inhibition of estrogen signaling through changes in the concentration of mitochondrial cholesterol metabolites.
Book Synopsis Resistance to Tamoxifen: A Consequence of Altered P27Kipl Regulation During Breast Cancer by :
Download or read book Resistance to Tamoxifen: A Consequence of Altered P27Kipl Regulation During Breast Cancer written by and published by . This book was released on 2002 with total page 0 pages. Available in PDF, EPUB and Kindle. Book excerpt: While approximately 70% of breast cancers express the estrogen receptor (ER) at diagnosis, only two thirds of these will respond to antiestrogens such as Tamoxifen (TAM). Unfortunately, ER positive tumors that are initially responsive, invariably acquire resistance to hormonal therapies (reviewed in (1)).: TAM-resistant tumors usually show continued expression of the ER (2, 3). Estradiol regulates cell proliferation and development in the mammary gland. The elucidation of mechanisms whereby estradiol:ER influences cell cycle regulators and how these are blocked by Tamoxifen is highly relevant to the development of new treatments for steroid resistant breast cancer. Both estrogens and antiestrogens influence the cell cycle during the early Ol phase (4). The cell cycle is governed by a family of cyclin dependent kinases (cdks), whose activity is regulated by positive effectors, the cyclins, by phosphorylation and by negative regulators, the cdk inhibitors (reviewed in (5-7)). p27 or kinase inhibitor protein 1 (KIP 1) is strongly expressed in normal mammary epfthelial cells (8). That p27 protein levels are frequently reduced in primary breast cancers and this correlates with poor prognosis, suggests that p27 is an important negative regulator of the normal breast cell cycle (8-10) . The cellular abundance of p27 is importantly regulated by ubiquitin-mediated proteolysis (11). p27 protein decreases when quiescent MCF-7 breast cancer cells are stimulated to reenter the cell cycle with estradiol treatment and p27 increases when antiestrogens induce Gi arrest ((12, 13) and PNAS manuscript appended).
Book Synopsis Characterization of Epigenetic Plasticity and Chromatin Dynamics in Cancer Cell Models by : Diana Lea Gerrard
Download or read book Characterization of Epigenetic Plasticity and Chromatin Dynamics in Cancer Cell Models written by Diana Lea Gerrard and published by . This book was released on 2019 with total page 688 pages. Available in PDF, EPUB and Kindle. Book excerpt: Cancer progression is driven by cumulative changes that promote and maintain the malignant phenotype. Epigenetic alterations are central to malignant transformation and to the development of therapy resistance. Changes in DNA methylation, histone acetylation and methylation, noncoding RNA expression and higher-order chromatin structures are epigenetic features of cancer, which are independent of changes in the DNA sequence. Despite the knowledge that these epigenetic alterations disrupt essential pathways that protect cells from uncontrolled growth, how these modifications collectively coordinate cancer gene expression programs remains poorly understood. In this dissertation, I utilize molecular and informatic approaches to define and characterize the genome-wide epigenetic patterns of two important human cancer cell models. I further explore the dynamic alterations of chromatin structure and its interplay with gene regulation in response to therapeutic agents. In the first part of this dissertation, pancreatic ductal adenocarcinoma (PDAC) cell models were used to characterize genome-wide patterns of chromatin structure. The effects of histone acetyltransferase (HAT) inhibitors on chromatin structure patterns were investigated to understand how these potential therapeutics influence the epigenome and gene regulation. Accordingly, HAT inhibitors globally target histone modifications and also impacted specific gene pathways and regulatory domains such as super-enhancers. Overall, the results from this study uncover potential roles for specific epigenomic domains in PDAC cells and demonstrate epigenomic plasticity to HAT inhibitors. In the second part of this dissertation, I investigate the dynamic changes of chromatin structure in response to estrogen signaling over a time-course using Estrogen Receptor (ER) positive breast cancer cell models. Accordingly, I generated genome-wide chromatin contact maps, ER, CTCF and regulatory histone modification profiles and compared and integrated these profiles to determine the temporal patterns of regulatory chromatin compartments. The results reveal that the majority of alterations occur in regions that correspond to active chromatin states, and that dynamic chromatin is linked to genes associated with specific cancer growth and metabolic signaling pathways. To distinguish ER-regulated processes in tamoxifen-sensitive and in tamoxifen-resistant (TAMR) cell models, we determined the corresponding chromatin and gene expression profiles using ER-positive TAMR cancer cell derivatives. Comparison of the patterns revealed characteristic features of estrogen responsiveness and show a global reprogramming of chromatin structure in breast cancer cells with acquired tamoxifen resistance. Taken together, this dissertation reveals novel insight into dynamic epigenomic alterations that occur with extrinsic stimuli and provides insight into mechanisms underlying the therapeutic responses in cancer cells.
Book Synopsis Extracellular Matrix: Pathobiology and Signaling by : Nikos Karamanos
Download or read book Extracellular Matrix: Pathobiology and Signaling written by Nikos Karamanos and published by Walter de Gruyter. This book was released on 2012-08-31 with total page 940 pages. Available in PDF, EPUB and Kindle. Book excerpt: Over the last decades cell biology and biological chemistry have increasingly turned their attention to the space between cells and revealed an elaborate network of macromolecules essential for structural support, cell adhesion and signaling. This comprehensive handbook of the extracellular matrix will give an overview of the current state of knowledge of matrix components (structure and function), their role in heath and disease (matrix pathobiology) and new aspects related to pharmacological targeting. It will provide an introduction to the extracellular matrix and detailed sections and chapters on: Importance of extracellular matrix in health and disease Matrix proteoglycans (aggrecan, versican, perlecan, SLRPs, syndecans, glypicans, serglycin) Matrix proteinases (remodeling, would healing, regulatory roles in health and disease, metalloproteinases, cystein proteases, plasmin and plasminogen activator system) Glycobiology (hyaluronan and sulfated glycosaminoglycans in cancer, inflammation and metabolic control) Collagens (supramolecular assembly, proteins binding collagen, scaffolds, bacterial and mutated collagens, procollagen proteinases) Cell surface receptors (integrins, syndecans, mechanical strain and TGFb, CD44 and DDR). Biotechnological and pharmacological outlook (matrix regulation by growth factors, hyaluronidases, pathobiology, disease targeting, delivery systems, EMT and proteomics). "The book Extracellular Matrix: Pathobiology and Signaling provides a comprehensive and up to date collection of very relevant topics for understanding the various facets of extracellular matrix and its interactions with cells in normal tissue as well as in disease. It represents the current front-line and will serve as a reference for extracellular matrix and posttranslational modifications." Dick Heinegård, Department of Clinical Sciences Lund, Section Rheumatology, Lund University, Sweden
Book Synopsis Hormone Action by : Bert W. O'Malley
Download or read book Hormone Action written by Bert W. O'Malley and published by . This book was released on 1974 with total page 488 pages. Available in PDF, EPUB and Kindle. Book excerpt: Hormone assays; Hormone receptors; Evaluation of biological effects of hormones; Purification and synthesis of hormones.
Book Synopsis Breast Cancer Biology by : Dil Afroze
Download or read book Breast Cancer Biology written by Dil Afroze and published by BoD – Books on Demand. This book was released on 2020-07-08 with total page 127 pages. Available in PDF, EPUB and Kindle. Book excerpt: This book offers a comprehensive overview of recent developments in the field of breast cancer biology. It is a complete and descriptive reference on motioning pathways and new treatment options for the future transnational scientists and clinicians working on cancer research and treatment. We greatly appreciate the work of all the contributors to this book. They have brought with them tremendous diversity of perspectives and fields, which is truly reflective of the complexity of the topic, and they have come together in this project to serve as the node of multidisciplinary collaboration in this field. Finally, we must acknowledge the thousands of cancer patients who have participated in the studies, and who have inspired us to gather information to significantly progress knowledge in the field in recent years.
Book Synopsis Targeted Therapies for Lung Cancer by : Ravi Salgia
Download or read book Targeted Therapies for Lung Cancer written by Ravi Salgia and published by Springer. This book was released on 2019-06-26 with total page 238 pages. Available in PDF, EPUB and Kindle. Book excerpt: This book contextualizes translational research and provides an up to date progress report on therapies that are currently being targeted in lung cancer. It is now well established that there is tremendous heterogeneity among cancer cells both at the inter- and intra-tumoral level. Further, a growing body of work highlights the importance of targeted therapies and personalized medicine in treating cancer patients. In contrast to conventional therapies that are typically administered to the average patient regardless of the patient’s genotype, targeted therapies are tailored to patients with specific traits. Nonetheless, such genetic changes can be disease-specific and/or target specific; thus, the book addresses these issues manifested in the somatically acquired genetic changes of the targeted gene. Each chapter is written by a leading medical oncologist who specializes in thoracic oncology and is devoted to a particular target in a specific indication. Contributors provide an in-depth review of the literature covering the mechanisms underlying signaling, potential cross talk between the target and downstream signaling, and potential emergence of drug resistance.
Book Synopsis Targeted Therapies in Breast Cancer by : Gw Sledge
Download or read book Targeted Therapies in Breast Cancer written by Gw Sledge and published by Clinical Pub. This book was released on 2012-06 with total page 0 pages. Available in PDF, EPUB and Kindle. Book excerpt: This new volume updates the reader on selected areas of targeted therapy in breast cancer, with special emphasis on chemoprevention strategies, drug resistance, biomarkers, combination chemotherapy, angiogenesis inhibition and pharmacogenomics in the context of clinical efficacy. This selected review of targeted therapies will guide the reader on effective treatment as part of an integrated programme of patient management.
