Cellular and Molecular Mechanisms of Hormonal Carcinogenesis Environmental Influences

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ContributionsJames Huff (Editor), Jeffrey Allen Boyd (Editor), J. Carl Barrett (Editor)
The Physical Object
Number of Pages504
ID Numbers
Open LibraryOL7598662M
ISBN 100471022020
ISBN 109780471022022

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Cellular and Molecular Mechanisms of Hormonal Carcinogenesis: Environmental Influences (Progress in Clinical and Biological Research) Skip to main content Try Prime. ISBN: OCLC Number: Description: xix, pages: illustrations ; 24 cm. Contents: 1. Hormonal Carcinogenesis and Environmental Influences: Background and Overview / James Huff, Jeff Boyd and J.

Carl Barrett Time Trends in Hormone-Dependent Cancer / C.S. Muir and R.J. Black Influence of Diet on Tumors of Hormonal Tissues / Ghanta N. Rao Mechanisms of Molecular Carcinogenesis – Volume 2 1st ed. Edition Together with Volume 1, this book provides an inclusive overview of the molecular and cellular mechanisms of carcinogenesis and offers comprehensive insights into related clinical and therapeutic : Hardcover.

Progress in our understanding of hormonal carcinogenic processes has been a direct result of the advances made in cell biology, endocrinology, and carcinogenesis at the molecular level. The newer fields of molecular genetics and cytogenetics already have and are expected to continue to playa major role in furthering our understanding of the cellular and molecular events in hormonal carcinogenesis.

Since our previous symposium inthe pace of research in hormones and cancer has accelerated. Progress in our understanding of hormonal carcinogenic processes has been a direct result of the advances made in cell biology, endocrinology, and carcinogenesis at the molecular level.

Cellular and Molecular Mechanisms of Hormonal Carcinogenesis: Environmental Influences Edited by James Huff (National Institute of Environmental Health Sciences), Jeff Boyd (University of Pennsylvania Medical Center), and J.

Carl Barrett (National Institute of Enviromental Health Sciences). Together with Volume 1, this book provides an inclusive overview of the molecular and cellular mechanisms of carcinogenesis and offers comprehensive insights into related clinical and.

• Steroid hormones bind to nuclear receptors, which serve as on-off switches Æ development and differentiation of reproductive tissues, brain, bone and skin • Protein/amino acid hormones bind to receptor sites on cell membrane and use second messengers that activate or deactivate enzymes which modify protein pathways within the Size: 1MB.

Prog Clin Biol Res. ;xiii-xix, Cellular and molecular mechanisms of hormonal carcinogenesis. Environmental influences. [No authors listed]. Little is known about the mechanisms involved in estrogen stimulation of carcinogenesis and less is known about how to prevent or treat cancer through estrogenic pathways.

To better understand how estrogens mediate their carcinogenic effects, the respective roles of estrogen receptor alpha (ER-α) and estrogen receptor beta (ER-β) must be Author: William A. Ricke, Karin Williams, Jalissa Wynder, Ganesh Palapattu, Yuzhuo Wang, Gerald R. Cunha. [Show full abstract] Toxicity and Carcinogenesis in September focused on the latest research in molecular mechanisms of metal-induced toxicity and carcinogenesis.

The conference promoted a. A direct physical interaction of TRbPV with cellular proteins, namely the regulatory subunit of the phosphatidylinositol 3-kinase (p85alpha), the pituitary tumor transforming gene (PTTG) and beta-catenin, that are critically involved in cell proliferation, motility, migration, angiogenesis and metastasis suggest a novel mode of non-genomic action, whereby mutant TR isoform acts as an oncogene in Cited by: In this section, the molecular mechanisms that contribute to HPV-induced carcinogenesis are described.

Numerous studies have ascribed many biochemical activities, e.g. the ability of the viral proteins E6 or E7 to bind cellular factors, and biological properties, e.g. the immortalization of cells, to other HPV proteins. Liver Regeneration and Carcinogenesis Molecular and Cellular Mechanisms.

Book • Edited by: Randy L. Jirtle. a tumor susceptibility gene) and is not milieu (e.g., hormone) dependent. the liver has been used extensively as a model for investigating the molecular mechanisms of cellular proliferation and carcinogenesis. Recently.

Mechanisms of Chemical Carcinogenesis provides information pertinent to the fundamental mechanisms of chemical carcinogenesis. This book surveys the interactions of chemical carcinogens with native DNA, the activation of normal cellular sequences, and the transforming role of the activated Edition: 1.

The mitochondrion as a primary site of action of steroid and thyroid hormones: presence and action of steroid and thyroid hormone receptors in mitochondria of animal cells. Mol Cell Cited by: It has been over a decade since the First International Symposium on Hormonal Carcinogenesis convened in 1.

Since then, the field has rapidly expanded with considerable progress in both breast and prostate cancers; while ovarian and endometrial cancer have been hampered, in part, due to the absence of suitable hormone-mediated animal models.

The pivotal role of cell proliferation in all phases (e.g., initiation, promotion, progression) of the multistep process of carcinogenesis is inextricably linked to positive and negative cell cycle control mechanisms as influenced by oncogenes, tumor suppressor genes, growth factors and their cognate receptors, hormones and their receptors, and Cited by: 4.

Molecular Mechanisms of Estrogen Carcinogenesis Article Literature Review (PDF Available) in Annual Review of Pharmacology 36(1) February with Reads How we measure 'reads'. Molecular and cellular mechanisms of cadmium carcinogenesis Article Literature Review in Toxicology () December with Reads How we measure 'reads'.

Endocrine and Hormonal Toxicology Edited by Philip W. Harvey, Kevin C. Rush and Andrew Cockburn AgrEvo UK Ltd, Saffron Walden, UK This is the first book to consider the integrated role of the classical endocrine system and hormones (including those from tissues outside the classical endocrine system) in toxicological : Hardcover.

One molecule with the potential to enhance these processes is insulin, a hormone known to maintain the growth and development of different cell types. It can affect the proliferation, migration, and ECM secretion by keratinocytes, endothelial cells, and fibroblasts.

Since our previous symposium inthe pace of research in hormones and cancer has accelerated. Progress in our understanding of hormonal carcinogenic processes has been a direct result of the advances made in cell biology, endocrinology, and carcinogenesis at the molecular level.

The newer. The pivotal role of cell proliferation in all phases (e.g., initiation, promotion, progression) of the multistep process of carcinogenesis is inextricably linked to positive and negative cell cycle control mechanisms as influenced by oncogenes, tumor suppressor genes, growth factors and their cognate receptors, hormones and their receptors, and Author: David E.

Malarkey, Mark J. Hoenerhoff, Robert R. Maronpot. Together with Volume 1, this book provides an inclusive overview of the molecular and cellular mechanisms of carcinogenesis and offers comprehensive insights into related clinical and therapeutic aspects. This second volume complements the first by presenting and concisely explaining the.

Dysregulation of gene expression is regarded as a major factor in a multi-stage model of chemical carcinogenesis. Especially the induction of cellular proto-oncogenes (Hanahan and Weinberg, ) and stimulation of proliferation of committed cells (Cohen, ) have been shown to play critical roles in the promotion stage after an initiating mutational by: Cellular & Molecular Medicine Consumer Health ovaries and the pancreas, and comparative endocrine carcinogenesis.

A third section of the book develops the whole body approach, in which chapters are devoted to hormonal mechanisms of toxicity to the immune, nervous, cardiovascular, gastrointestinal and reproductive systems, as well as to the.

At least three mechanisms are considered to be responsible for the carcinogenicity of estrogens; the most widely recognized is the receptor-mediated hormonal activity, which is generally related to stimulation of cellular proliferation, resulting in more opportunities for accumulation of genetic damage leading to carcinogenesis (16,17).Cited by: Hormonal Carcinogenesis IV [Li, Jonathan J., Li, Sara Antonia, Llombart-Bosch, Antonio] on *FREE* shipping on qualifying offers.

Hormonal Carcinogenesis IV. BibTeX @ARTICLE{Li96estrogencarcinogenesis, author = {Jonathan J. Li and Alfonso Gonzalez and Snigdha Banerjee and Sushanta K. Banerjee and Sara Antonia Li}, title = {Estrogen carcinogenesis in the hamster kidney: a hormone-driven multi-step process.

In: Cellular Molecular Mechanisms of Hormonal Carcinogenesis}, journal = {Environmental Influences (Huff J, Boyd J, Barrett JC}, year =. Mechanisms of Molecular Carcinogenesis – Volume 1: Medicine & Health Science Books @   2. Epithelial-to-Mesenchymal Transition in Breast Cancer.

Breast carcinogenesis is a complex, multiple step process, involving several mechanisms that mediate cell proliferation, differentiation, apoptosis, epithelial-to-mesenchymal transition, and angiogenesis [].In breast cancers with a poorly differentiated phenotype, the tumor cell is characterized by stem cell-like features, which Cited by: 1.

Get this from a library. Molecular biology of cancer: mechanisms, targets, and therapeutics. [Lauren Pecorino] -- "The most engaging and accessible account of cancer biology that makes the link between our understanding of cancer and the development of new therapeutics crystal clear. -- Molecular.

Estrogens are considered to act as promoters in a multistep process of hormonal carcinogenesis, although the molecular mechanisms by which these hormones act in tumorigenesis are unclear at present. Estradiol is known to induce expression of certain proto‐oncogenes, and this led us to examine potential regulatory regions of the cellular c Cited by: 9.

Accordingly, his research focuses on the cellular and molecular mechanisms driving carcinogenesis. Together with his coworkers in Magdeburg and Graz, he is constantly engaged in the development of novel models mimicking the human situation in order to establish prognostic and predictive biomarkers and to generate novel therapies.

Abstract. The dawn of hormonal carcinogenesis began with Beatson’s (1) demonstration in that ovariectomy ameliorates the clinical course of breast cancer in women, carrying the implication that this cancer is due to/maintained by the continuous stimulus of ovarian hormone.

Get this from a library. Hormonal Carcinogenesis: Proceedings of the First International Symposium. [Jonathan J Li; Satyabrata Nandi; Sara Antonia Li] -- In the past decade there has been a growing public interest and resurgence in research in the field of hormonal carcinogenesis.

This is due to the widespread use of therapeutic hormonal agents. Genetic Mechanisms in Carcinogenesis and Tumor Progression: Proceedings of a Genentech-UCLA Symposium Held at Keystone, Colorado, January. Sridhar Mani, in Progress in Molecular Biology and Translational Science, Abstract.

Breast carcinogenesis and/or cancer growth and/or drug sensitivity has a multifactorial etiology—perhaps the least well-characterized aspect being that of the distant environmental influences, namely, the microbiota that inhabit humans. For the purposes of this chapter, and to keep the subject matter.

Weinstein IB, Carothers AM, Santella RM et al () Molecular mechanisms of mutagenesis and multistage carcinogenesis. In: Mendelsohn J, Howley PM, Israel MA, Liotta LA (eds) The molecular basis of cancer. Saunders WB, Philadelphia, pp 59–85 Google Scholar.

Carcinogenesis, also called oncogenesis or tumorigenesis, is the formation of a cancer, whereby normal cells are transformed into cancer cells. The process is characterized by changes at the cellular, genetic, and epigenetic levels and abnormal cell division is a physiological process that occurs in almost all tissues and under a variety of circumstances.Vol.

32(Suppl. 2), MECHANISMS OF OVARIAN CARCINOGENESIS 3 FIGURE 1.—(A) Multiple pathogenic mechanisms resulting in decreased negative feedback by gonadal steroids involved in ovarian tumorigenesis of mice. (B) Secondary (hormonally mediated) mechanism of ovarian tumorigenesis in mice associated with a compensatory overproduction of gonadotrophic hormones.Signal transduction is the process by which a chemical or physical signal is transmitted through a cell as a series of molecular events, most commonly protein phosphorylation catalyzed by protein kinases, which ultimately results in a cellular ns responsible for detecting stimuli are generally termed receptors, although in some cases the term sensor is used.

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