Download or read book Mammary Tumorigenesis and Malignant Progression written by Robert B. Dickson and published by Springer. This book was released on 1994-07-31 with total page 384 pages. Available in PDF, EPUB and Kindle. Book excerpt: The current volume represents the fourth over a period of five years in our series on Advances in the Cellular and Molecular Biology of Breast Cancer. The first three volumes were entitled Breast Cancer: Cellular and Molecular Biology, Regulatory Mechanisms in Breast Cancer, and Genes, Oncogenes, and Hormones, respectively. Throughout this series, we have tried to take a broad look at cutting-edge topics in basic science research into breast cancer. This attempt has resulted in a wide range of subject material, including rodent and human model systems, oncogenes, suppressor genes, growth factors, hormones, tumor-host interactions, and determinants of metastases. Since our last volume, research in breast cancer has continued to proceed at an explosive rate. We hope the current volume will provide the reader with some of the excitement felt by the editors and authors as we begin to understand this all-too-common disease. The first section of this book is devoted to the basic processes of proli feration, differentiation, and malignant progression of breast cancer. T.l. Anderson and W.R. Miller lead off with a detailed description of controls on proliferation in the normal human breast and in breast cancer. This chapter strongly emphasizes pathological aspects. The second chapter, by M.R. Stampfer and P. Yaswen, presents a corresponding viewpoint through a presentation of experiments with human mammary epithelial cells in culture. The second section of the book emphasizes the genetic basis for breast cancer onset and malignant progression. Chapter 3, by M.-C. King and S.
Download or read book Mammary Tumorigenesis and Malignant Progression written by Robert B Dickson and published by . This book was released on 1994-07-01 with total page 380 pages. Available in PDF, EPUB and Kindle. Book excerpt:
Download or read book Mammary Tumor Cell Cycle Differentiation and Metastasis written by Robert B. Dickson and published by Springer Science & Business Media. This book was released on 2012-12-06 with total page 432 pages. Available in PDF, EPUB and Kindle. Book excerpt: Mammary Tumor Cell Cycle, Differentiation and Metastasis is the fifth volume since 1988 in a series designed to broadly examine current advances in the cellular and molecular biology of breast cancer. As in previous volumes, the editors have invited recognized experts in cutting-edge topics to provide a chapter focused on their area of research. The editors have turned to the researchers who study rodent models of the disease and to those who study the cellular and molecular basis of human breast cancer. The first section of the book is devoted to new mouse models of mammary development and tumorigenesis. The second section moves to studies of human breast cancer and focuses on receptors, signalling, and the cell cycle. The final section deals with defective tissue interactions in human breast cancer. We are now in a period of extremely rapid accumulation of data on the molecular and cellular biology of breast cancer. These findings are highlighted in chapters from Mammary Tumor Cell Cycle, Differentiation and Metastasis: Advances in Cellular and Molecular Biology of Breast Cancer.
Download or read book Holland Frei Cancer Medicine written by Robert C. Bast, Jr. and published by John Wiley & Sons. This book was released on 2017-03-10 with total page 2004 pages. Available in PDF, EPUB and Kindle. Book excerpt: Holland-Frei Cancer Medicine, Ninth Edition, offers a balanced view of the most current knowledge of cancer science and clinical oncology practice. This all-new edition is the consummate reference source for medical oncologists, radiation oncologists, internists, surgical oncologists, and others who treat cancer patients. A translational perspective throughout, integrating cancer biology with cancer management providing an in depth understanding of the disease An emphasis on multidisciplinary, research-driven patient care to improve outcomes and optimal use of all appropriate therapies Cutting-edge coverage of personalized cancer care, including molecular diagnostics and therapeutics Concise, readable, clinically relevant text with algorithms, guidelines and insight into the use of both conventional and novel drugs Includes free access to the Wiley Digital Edition providing search across the book, the full reference list with web links, illustrations and photographs, and post-publication updates
Download or read book The Role of E2f5 in Mammary Gland Development and Breast Cancer Progression written by Briana To and published by . This book was released on 2020 with total page 129 pages. Available in PDF, EPUB and Kindle. Book excerpt: Dysregulation of mammary developmental processes have resulted in breast cancer development and progression. Thus, understanding normal mammary gland development is critical to understanding how cancer cells are initiated and maintained. Transcriptomic profiling of various mammary gland developmental phases, including virgin, pregnancy, lactation and involution, revealed distinct gene expression patterns associated at each stage. Pathway analysis predicted a role for transcription factors E2F1-4 during different stages of development. The importance of E2Fs in mammary development was confirmed by the defects observed in the mammary glands of mice deficient for various E2Fs. To examine if compensation occurs among activator E2Fs in the mammary gland, we analyzed mammary gland development in double E2F knockout mice. Our analysis revealed that compensation does occur among activator E2Fs in the mammary gland. However, this compensation appears to be very specific, as E2F2 can compensate for E2F1 but not E2F3 loss. Although the role of E2F1-4 has been characterized in mammary gland development, little is known about E2F5, an E2F demonstrating repressor activity. Using bioinformatic analysis, we predicted a role for E2F5 in terminal end bud differentiation and developmental stages. To further examine the role of E2F5 in normal mammary gland development, we generated a mammary-specific E2F5 knockout mouse model (E2F5CKO). Analysis of mammary gland development in E2F5CKO mice reveal only modest mammary gland defects. However, we found that E2F5CKO animals develop mammary tumors after a prolonged latency. Using transcriptomic profiling, we identified oncogenes that are dysregulated in E2F5CKO tumors, potentially contributing to tumorigenesis. Through these studies, we have identified a novel role of E2F5 as a tumor suppressor in breast cancer and further elucidated roles of E2Fs in mammary gland development.
Download or read book Adhesion Signaling in Mammary Gland Development Tumorigenesis and Cancer Progression written by Martine Hester Adriana Maria Miltenburg and published by . This book was released on 2010 with total page 154 pages. Available in PDF, EPUB and Kindle. Book excerpt:
Download or read book Comparative Oncology written by Alecsandru Ioan Baba and published by . This book was released on 2007 with total page 787 pages. Available in PDF, EPUB and Kindle. Book excerpt:
Download or read book Selected Aspects of Cancer Progression Metastasis Apoptosis and Immune Response written by Hans E. Kaiser and published by Springer Science & Business Media. This book was released on 2008-05-20 with total page 251 pages. Available in PDF, EPUB and Kindle. Book excerpt: The processes of tumor metastasis, apoptosis and anti-tumor immune response are among the most complex yet rapidly advancing fields in the area of cancer research. This monograph, with its leading authorship, presents a comprehensive coverage of the recent advances in the various key concepts in these fundamental aspects of human cancer. It contains state-of-the-science reviews on invasion, metastasis, angiogenesis, apoptosis and immunologic aspects related to cancer.
Download or read book Circulating Tumor Cells in Breast Cancer Metastatic Disease written by Roberto Piñeiro and published by Springer Nature. This book was released on 2020-04-17 with total page 177 pages. Available in PDF, EPUB and Kindle. Book excerpt: This book is aimed to summarise the key aspects of the role of circulating tumour cells (CTCs) in breast cancer, with special attention to their contribution to tumour progression and establishment of metastatic disease. We aim to give a clear overview of the knowledge about CTCs, framed in the context of breast cancer, by analysing basic and clinical research carried out so far. In a broader sense, we will address what are the main clinical needs of this disease based on its molecular heterogeneity (subtypes) and lay out the knowledge and understanding that CTCs are giving about it and how they are contributing and can still improve the better monitoring and management of breast cancer patients. We will discuss the evidences of the use of CTCs as a tool to monitor cancer progression and therapy response, based on the prognostic and predictive value they have, as well as a tool to unravel mechanisms of resistance to therapy and to identify new biomarkers allowing to predict therapy success. Moreover, we will analyse the main aspects of ongoing clinical trials and how they can contribute to determine the clinical utility of CTCs as a breast cancer biomarker. We will also touch upon general knowledge or basic notions of the biology of the metastatic process in epithelial cancers, in order to understand the origin and biology of CTCs. In this sense, we will pay special attention to EMT (epithelial to mesenchymal transition), dormancy and minimal residual disease, three key aspects that determine the outcome of the disease. We will also cover general aspects on the isolation and characterization techniques applies to the study of CTCs, and also the possibilities that the study of CTCs, as a biomarker with biological function, is opening in terms of understanding the biology of metastatic cells and the identification of therapeutic targets based on the functional and molecular characterization of CTCs. Lastly, we will try to foresee the future of CTCs in terms of clinical application and implementation in the clinical routine.
Download or read book Breast Cancer Scientific and Clinical Progress written by Marvin A. Rich and published by Springer Science & Business Media. This book was released on 2012-12-06 with total page 407 pages. Available in PDF, EPUB and Kindle. Book excerpt: Effective control of breast cancer depends on three types of research accomplishment -- understanding the disease's origins and progression: successfully applying this knowledge to methods of detection, diagnosis and treatment: and finding ways to make these advances truly available to the public as effectively as possible. The significant progress that is occurring across this entire spectrum of pioneering investigation is reflected in these proceedings of the 1987 biennial conference of the International Association for Breast Cancer Research. The first section of the book focuses on oncogenes and chemical effectors that may play key roles in early cell transformation leading to breast cancer. Research discussed includes identification of specific oncogenes which appear to be involved in the disease, study of their activation and expression, examination of the biological effects of various growth factors isolated from breast cancer cell lines, and investigation of the molecular mechanisms by which estrogens promote and stimulate growth of breast cancers. The second group of chapters deals with several other complex factors and phenomena which may influence tumor formation in the breast, for example, expression of abnormalities by fibroblasts, disruption of epithelial-mesenchymal interactions, and loss of ability nili to synthesize normal basal lamina resulting in alterations in the extracellular matrix. Clarification of the processes of normal mammary gland development and differentiation is central to much of this work.
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.
Download or read book Regulatory Mechanisms in Breast Cancer written by Marc E. Lippman and published by Springer Science & Business Media. This book was released on 2012-12-06 with total page 455 pages. Available in PDF, EPUB and Kindle. Book excerpt: In Breast Cancer: Cellular and Molecular Biology [Kluwer Academic Pub lishers, 1988], we tried to present an introduction to the emerging basic studies on steroid receptors, oncogenes, and growth factors in the regulation of normal and malignant mammary epithelium. The response to this volume was superb, indicating a tremendous interest in basic growth regulatory mechanisms governing breast cancer and controlling its malignant progres sion. In the two years since its publication, much new and exciting in formation has been published and the full interplay of regulatory mechanisms is now beginning to emerge. We have divided this book into four sections that we hope will unify important concepts and help to crystallize areas of consensus and/or disagreement among a diverse group of basic and clinical scientists working on the disease. The first section is devoted to studies on oncogenes, antioncogenes, proliferation, and tumor prognosis. The first chapter, by Sunderland and McGuire, introduces the characteristics of breast cancer as studied by patho logists to establish prognostic outcome. Of particular interest is a new proto oncogene called HER-2 (or neu), which is rapidly becoming accepted as a valuable new tumor marker of poor prognosis. The second chapter, by Lee Bookstein and Lee, introduces the best known antioncogene, the retinoblas toma antioncogene, whose expression is sometimes lost in breast cancer. Malignant progression appears to be influenced by the balance of proto oncogene and antioncogene expression.
Download or read book Essentials of Glycobiology written by Ajit Varki and published by CSHL Press. This book was released on 1999 with total page 694 pages. Available in PDF, EPUB and Kindle. Book excerpt: Sugar chains (glycans) are often attached to proteins and lipids and have multiple roles in the organization and function of all organisms. "Essentials of Glycobiology" describes their biogenesis and function and offers a useful gateway to the understanding of glycans.
Download or read book Evolution in Mammary Cancer written by Maryknoll Linscott and published by . This book was released on 2024 with total page 0 pages. Available in PDF, EPUB and Kindle. Book excerpt: Breast cancer, a highly heterogeneous disease, is a product of dynamic variation and selection of mutant clones. The continuous evolution of breast tumor cells has important implications for patient outcomes due to its impacts on treatment response, resistance, and relapse. While a wealth of studies has been conducted on the genetic and epigenetic aberrations that confer a fitness advantage to tumor cells, the sources of selective pressure remain to be understood. Using various clinically relevant mouse models of breast cancer, this dissertation investigates whether and how three factors, which are not mutually exclusive, drive the selection of genetically distinct breast tumor clones: the source of oncogenic signaling (namely, the specific oncogene sustaining an activating mutation); the context of oncogenic signaling (namely, the reproductive history of the mammary cell undergoing transformation); and the strength of oncogenic signaling (as determined by oncogene expression levels). In the first set of experiments directed at modeling breast cancer as a multistage disease, we evaluated how clinically relevant oncogenes Myc and PIK3CA shape the progression of premalignant clones to mammary tumors. By using a well-studied carcinogen, DMBA (7,12-Dimethylbenz[a]anthracene), stereotypical Hras, Kras, and Nras mutations (exons 12, 13, and 61) were randomly introduced in our mouse models. Mice were engineered for mammary-specific, doxycycline (Dox)-inducible expression of either Myc (iMyc mice) or PIK3CAH1047R (iPIK mice). However, despite the introduction of possibly innumerable mutations in the entire organism, only mammary tumors were observed in our studies. These tumors only arose when Myc and PIK3CAH1047R were individually expressed in the mammary glands of our mouse models, which signifies that the tumors occurred in a stepwise fashion. Notably, a different set of Ras-initiated cells comprised the dominant population in Myc- versus PIK3CAH1047R-driven tumors, which suggests that each oncogene prefers to cooperate with specific mutant Ras family member(s). We discovered that while Myc selects for the outgrowth of Nrasmut and Krasmut tumors, PIK3CAH1047R only selects for the outgrowth of Krasmut tumors. Based on our findings, we propose that cooperating oncogenes provide selective pressure for genetically distinct Ras-initiated premalignant clones. In a second set of experiments, we evaluated how parity impacts the progression of premalignant clones. We first tested whether parity blocks tumorigenesis by modifying our first set of experiments to include one or two rounds of parity after DMBA initiation and before inducing the expression of an oncogenic transgene. Despite the known protective effects of pregnancy against breast cancer, our parity protocols did not block tumorigenesis, regardless of cooperating oncogene (Myc vs. PIK3CAH1047R) and the number (one vs. two) and timing (peri-pubertal vs. adulthood) of pregnancies. However, parity did impact which clones progressed to malignancy. In both Myc- and PIK3CAH1047R-expressing models, the prevalence of Krasmut tumors was decreased in the context of parity, which implies that parity exerted selective pressure against the progression of Krasmut clones. Moreover, this selective pressure appears stronger as the number of pregnancies increases regardless of the cooperating oncogene and timing of pregnancy, as demonstrated by the decreased prevalence of Krasmut tumors. Lastly, pubertal parity revealed a slightly stronger selection against the Krasmut premalignant clone in PIK3CAH1047R-expressing models compared to adult parity. Thus, parity can exert contextual selection against specific Ras-initiated premalignant clones. In a third and final set of experiments aimed at targeting "undruggable" Myc-driven tumorigenesis, we discovered that Myc selects for a threshold level of PI3K signaling activation. While previous studies show that Myc cooperates with oncogenic Ras, targeted therapies against Ras remain limited to G12C Kras mutants, which is rare in human breast cancer. Hypothesizing that Myc/Ras cooperation involves the activation of a specific downstream Ras effector pathway, namely the phosphoinositide 3-kinase (PI3K) pathway, we generated a mouse model that expresses both iPIK transgene and constitutive, mammary-specific Myc transgene (cMyc). By inducing various levels of PIK3CAH1047R expression, we demonstrated that Myc requires a minimum level of PI3K pathway activation to generate mammary tumors reliably with decreased latency and increased multiplicity. These tumors also lack stereotypical Ras mutations, which implies that PI3K pathway activation relieved the selective pressure to select for Rasmut Myc-driven tumors. In addition, PIK3CAH1047R expression was reactivated by gene-switch mutations in Myc-expressing relapse tumors, further reinforcing a strong selective pressure for PI3K pathway activation.
Download or read book Metastasis written by Lalage Wakefield and published by IOS Press. This book was released on 2007 with total page 172 pages. Available in PDF, EPUB and Kindle. Book excerpt: Metastasis is the most dreaded aspect of the carcinogenic process. More than ninety percent of all cancer deaths are attributable to the consequences of the primary tumor successfully colonizing distant organs. Unlike the situation with colon cancer, a patient with breast cancer can never be considered 'cured', since as many as a third of breast cancer patients who have apparently curative surgery for their primary tumors ultimately relapse with metastatic disease, sometimes decades later. Much effort is now devoted to understanding this process of metastasis, and finding ways to predict and prevent its occurrence.This publication covers recent advances in the field, specifically as they relate to breast cancer. The availability of new tools and technological approaches has prompted a reconsideration of the very definition of a metastasis. Furthermore, a number of commonly held myths are being explored and a new definition of a metastasis, with important implications for clinical staging, is being proposed. Also, a novel conceptual framework for cancer progression based on the system-level dynamics of regulatory networks is presented and the role of chemokines in mediating some of
Download or read book Breast Cancer Metastasis and Drug Resistance written by Aamir Ahmad and published by Springer Nature. This book was released on 2019-08-27 with total page 427 pages. Available in PDF, EPUB and Kindle. Book excerpt: Resistance to therapies, both targeted and systemic, and metastases to distant organs are the underlying causes of breast cancer-associated mortality. The second edition of Breast Cancer Metastasis and Drug Resistance brings together some of the leading experts to comprehensively understand breast cancer: the factors that make it lethal, and current research and clinical progress. This volume covers the following core topics: basic understanding of breast cancer (statistics, epidemiology, racial disparity and heterogeneity), metastasis and drug resistance (bone metastasis, trastuzumab resistance, tamoxifen resistance and novel therapeutic targets, including non-coding RNAs, inflammatory cytokines, cancer stem cells, ubiquitin ligases, tumor microenvironment and signaling pathways such as TRAIL, JAK-STAT and mTOR) and recent developments in the field (epigenetic regulation, microRNAs-mediated regulation, novel therapies and the clinically relevant 3D models). Experts also discuss the advances in laboratory research along with their translational and clinical implications with an overarching goal to improve the diagnosis and prognosis, particularly that of breast cancer patients with advanced disease.
Download or read book New Methods to Study Human Mammary Development and Breast Cancer written by Ethan Samuel Sokol and published by . This book was released on 2017 with total page 153 pages. Available in PDF, EPUB and Kindle. Book excerpt: Breast cancer is fundamentally a disease of aberrant differentiation. Breast cancers arise from within the normal architecture of the mammary gland and resemble normal mammary epithelial cell types on a molecular and gene expression level. Many tumors become dependent on the signaling pathways that guide mammary differentiation and proliferation, and may be driven by transcription factors and signaling pathways that enforce cell state. It's no wonder then that many fundamental insights into breast cancer biology derive from study of the normal mammary gland. Mouse models of mammary gland development have helped identify many of the key genetic and hormonal drivers of mammary differentiation. However, these systems have some limitations. First, study of stem and progenitor cell differentiation decisions has been hampered by a lack of definitive markers of cell state. Second, validation of these pathways in human mammary tissue has been challenging due to a paucity of human model systems. This thesis describes work to overcome these limitations. Here I describe a computational method to identify regulators of cell state transitions without the need for definitive markers of cell state. Using this method, we identified RUNXI as a regulator of mammary stem cell differentiation, and demonstrated that RUNX1 is required for exit from the stem/progenitor state. RUNX1 inhibition expanded the pool of stem cells and blocked mammary morphogenesis. This thesis also describes the development of a 3D hydrogel culture system that supports the growth of primary human mammary epithelial tissues. The tissues exhibit all major cell types found in the mammary gland and are hormone responsive. We further adapted the culture system to study the early stages of breast cancer progression by injecting tumor cells into the tissues. Tumor cells interacted and intercalated with normal mammary epithelial cells before invading out of the tissues. We utilized this system to validate SMARCE1 as a regulator of human breast cancer progression. SMARCE1 expression is predictive of progression in early-stage epithelial tumors, and SMARCE1 is functionally required for basement membrane degradation. In our tissue model of tumor progression SMARCE1 was dispensable for cell growth and in situ spreading but was required for invasion.