Regulatory Mechanisms in Breast Cancer

Regulatory Mechanisms in Breast Cancer

Author: Marc E. Lippman

Publisher: Springer Science & Business Media

Published: 2012-12-06

Total Pages: 455

ISBN-13: 1461539404

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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.


Metastasis

Metastasis

Author: Lalage Wakefield

Publisher: IOS Press

Published: 2007

Total Pages: 172

ISBN-13: 9781586037536

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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


Attempts to Understand Metastasis Formation II

Attempts to Understand Metastasis Formation II

Author: Ursula Günthert

Publisher: Springer Science & Business Media

Published: 2012-12-06

Total Pages: 297

ISBN-13: 3642611095

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Within the last decade the molecular biology of tumor models has revealed the identification of several metastasis- related molecules. These volumes attempt to review the most recent approaches of their mechanisms, regulation and way to treat their malignant alterations. The first volume covers the presentation of proteases and inhibitors and their role in invasion of tumor cells, also cell adhesion molecules and their interaction with the extracellular matrix. In the second volume the regulation of tumor progression and angiogenesis by cytokines, growth factors and motility factors is outlined. The third volume deals with detection of micrometastases and therapeutic approaches, such as immunotherapy, gene therapy, chemotherapy and surgical strategies to combat metastatic spread.


Holland-Frei Cancer Medicine

Holland-Frei Cancer Medicine

Author: Robert C. Bast, Jr.

Publisher: John Wiley & Sons

Published: 2017-03-10

Total Pages: 2004

ISBN-13: 111900084X

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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


Possible Mechanisms for Regulation of Breast Tumor Micrometastasis by NME Genes

Possible Mechanisms for Regulation of Breast Tumor Micrometastasis by NME Genes

Author:

Publisher:

Published: 1997

Total Pages: 24

ISBN-13:

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Metastatic dissemination of primary breast tumors is controlled by positive and negative regulators. We found that expression of a catalytically inactive nucleoside diphosphate kinase B (NDPK B/T) in MDA-MB-435 human breast carcinoma cells significantly decreases their metastatic dissemination in a nude mouse assay. Inhibition of metastatic dissemination of primary tumors formed by these cells occurs prior to formation of detectable micrometastasis. Our structural studies suggests that wild type NDPK B and highly homologous NDPK A form different oligomers that may occupy specific binding sites We hypothesize that NDPK B/T displaces wild type NDPK B from specific binding sites, acting in effect as a dominant negative mutant. These results suggest that NDPK B acts as a positive regulator of metastatic potential of human tumor cells and that specific inhibition of NDPK B may be a target for potential anti-metastasis therapeutics.


Cancer Metastasis — Related Genes

Cancer Metastasis — Related Genes

Author: D.R. Welch

Publisher: Springer Science & Business Media

Published: 2006-04-11

Total Pages: 275

ISBN-13: 0306478218

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Being diagnosed with cancer is devastating. But when the cancer cells have to spread to form secondary colonies, the prognosis for the patient is worse. If meaningful improvements in survival are to occur, then control of metastasis will be a foundation. Relatively little is known about the control of the metastatic process at the molecular level. This volume begins to explore our current knowledge regarding the underlying molecular and biochemical mechanisms controlling the metastatic phenotype. While all of the authors attempted to put their findings into a context for translation to the clinical situation, the state-of-the-art does not fully allow this. Nonetheless, we write these summaries of our work as an early effort toward that end. I am grateful to all of the authors who have contributed generously of their time and energies to make this volume a reality. To metastasize, neoplastic cells dissociate from the primary tumor, enter a circulatory compartment (typically lymphatics or blood vasculature), survive transport, arrest, exit the circulation and finally proliferate at a discontinuous site in response to local growth factors. Unless cells accomplish every step of the metastatic cascade, metastases cannot develop. The process is highly inefficient, i. e. ,


Epigenetic Regulation of a Gene, MS-1, in Cells of Different Metastatic Potential

Epigenetic Regulation of a Gene, MS-1, in Cells of Different Metastatic Potential

Author:

Publisher:

Published: 2005

Total Pages:

ISBN-13:

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Breast cancer is the most common malignancy and a major cause of cancer-related death among Canadian women. Although treatment of primary breast tumours is highly successful through surgery, metastatic breast cancer is difficult to treat. Cancer progression and metastasis require the accumulation of numerous genetic and epigenetic alterations. Normal cells that acquire such alterations can transform into cancer cells, resulting in primary tumour formation. Primary tumours are a heterogeneous population, containing cells of various metastatic potentials. Cells that acquire a high potential for metastasis can spread to secondary locations. Our model system consists of two subpopulations, with different metastatic potential, derived from the same rat mammary adenocarcinoma. Using this model, a differentially expressed novel gene, termed MS-1, was discovered. Due to significant expression of this gene in the poorly metastatic subpopulation and lack of expression in the highly metastatic subpopulation, MS-1 may have involvement in metastasis suppression. Several breast cancer metastasis suppressor genes have been identified on the basis that they are down-regulated during the progression of metastasis. Epigenetic mechanisms, such as DNA methylation, account for loss of expression in several of these genes. Hypermethylation of CpG islands within gene promoters results in deacetylation of histone proteins and produces a compact chromatin structure that is unfavourable for transcription. A CpG island spans the 5 untranslated region, exon 1 and part of intron 1 of the MS-1 gene. Our data reveals aberrant methylation patterns of this CpG island in our model. Also, MS-1 expression appears to be partially induced by both DNA methylation and histone deacetylation inhibitors. Following a screen of several cancer cell lines of various metastatic potential, it appears that the presence of DNA methylation in the CpG island of MS-1 correlates with the lack of MS-1 expression. Therefo.


Gene Regulation and Therapeutics for Cancer

Gene Regulation and Therapeutics for Cancer

Author: Surinder K. Batra

Publisher: CRC Press

Published: 2021-03-22

Total Pages: 322

ISBN-13: 1351778331

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Differential gene regulation and targeted therapy are the critical aspects of several cancers. This book covers specific gene regulation and targeted therapies in different malignancies. It offers a comprehensive assessment of the transcriptional dysregulation in cancer, and considers some examples of transcriptional regulators as definitive oncogenic drivers in solid tumors, followed by a brief discussion of transcriptional effectors of the programs they drive, and discusses its specific targets. Most targeted therapeutics developed to date have been directed against a limited set of oncogenic drivers, exemplified by those encoding cell surface or cytoplasmic kinases that function in intracellular signaling cascades.