ISBN: 9789048175055

Molecular Mechanisms of Cancer by Georg F. Weber Estimated delivery … Meer...

Molecular Mechanisms of Cancer by Georg F. Weber Estimated delivery 3-12 business days Format Paperback Condition Brand New Description of growth-controlling genes (oncogenes and tumor- Telomerase, the enzyme that prevents cell sen- suppressor genes) has advanced our mechanistic cence, is expressed in these precursor cells and may understanding of oncology (Chapter 3). Publisher Description Cancer may constitute the most extensively studied functions constitute a second line of defense that disease entity of our time. Nevertheless, our com- protects against transforming defects in oncogenes prehension of the cellular and molecular pathology or tumor-suppressor genes and are here considered of malignant transformation is incomplete. In view as metasuppressor genes. Advances in the molecular of the diverse clinical presentations of various explanations of growth dysregulation, metastasis malignancies, doubts may be raised as to whether it formation, extension of life span, and loss of ma- is appropriate to refer to cancer as one group of dis- tenance of genomic and epigenetic integrity in ease states. The notion of malignant tumors as a cancer suggest models for their causal connection. pathologic and pathophysiologic class of conditions The mechanisms of growth control, senescence, and begs the question for defining criteria that charac- anchorage dependence are linked on the molecular terize all malignant growths, regardless of their tis- level (Chapter 8). In cells that are not fully differ- sue of origin. Toward this goal, the recognition that tiated, the overactivation of oncogene pathways tumor development is caused by the dysregulation also induces the expression of metastasis genes. of growth-controlling genes (oncogenes and tumor- Telomerase, the enzyme that prevents cell sen- suppressor genes) has advanced our mechanistic cence, is expressed in these precursor cells and may understanding of oncology (Chapter 3). However, be further activated by growth factor signaling. Details ISBN 9048175054 ISBN-13 9789048175055 Title Molecular Mechanisms of Cancer Author Georg F. Weber Format Paperback Year 2010 Pages 645 Edition 1st Publisher Springer GE_Item_ID:137802617; About Us Grand Eagle Retail is the ideal place for all your shopping needs! With fast shipping, low prices, friendly service and over 1,000,000 in stock items - you're bound to find what you want, at a price you'll love! Shipping & Delivery Times Shipping is FREE to any address in USA. Please view eBay estimated delivery times at the top of the listing. Deliveries are made by either USPS or Courier. We are unable to deliver faster than stated. International deliveries will take 1-6 weeks. NOTE: We are unable to offer combined shipping for multiple items purchased. This is because our items are shipped from different locations. Returns If you wish to return an item, please consult our Returns Policy as below: Please contact Customer Services and request "Return Authorisation" before you send your item back to us. Unauthorised returns will not be accepted. Returns must be postmarked within 4 business days of authorisation and must be in resellable condition. Returns are shipped at the customer's risk. We cannot take responsibility for items which are lost or damaged in transit. For purchases where a shipping charge was paid, there will be no refund of the original shipping charge. Additional Questions If you have any questions please feel free to Contact Us. Categories Baby Books Electronics Fashion Games Health & Beauty Home, Garden & Pets Movies Music Sports & Outdoors Toys , Nieuw, Festpreisangebot, [LT: FixedPrice], ISBN-13: 9789048175055, Book Title: Molecular Mechanisms of Cancer, Subject Area: Science, Medical, Publication Name: Molecular Mechanisms of Cancer, Item Length: 10.2 in, Subject: Life Sciences / Molecular Biology, Life Sciences / Cell Biology, Oncology, Research, Publication Year: 2010, Type: Textbook, Format: Trade Paperback, Language: English, Item Width: 7.6 in, Item Weight: 56.5 Oz, Number of Pages: Xiv, 645 Pages, Springer Netherlands<

2010, ISBN: 9789048175055

Kartoniert, 660 Seiten, 280mm x 210mm x 36mm, Sprache(n): eng Molecular Mechanisms of Cancer describes molecular processes whose deregulation is important in the formation of tumors. The … Meer...

Kartoniert, 660 Seiten, 280mm x 210mm x 36mm, Sprache(n): eng Molecular Mechanisms of Cancer describes molecular processes whose deregulation is important in the formation of tumors. The material is developed from basic cell signaling pathways to their roles in the clinical manifestation of specific cancers. Topics covered include molecular events intrinsic to tumor cells (leading to growth deregulation, extended lifespan, and the ability to invade surrounding tissue), protective mechanisms that prevent transformation (including DNA repair and epigenetic regulation), tumor-host interactions (with the endocrine system, the immune system, and blood vessel formation), and the underlying molecular defects of individual cancers. This book is an essential resource for researchers, graduate students and oncologists. It will also aid in drug discovery by identifying molecular targets.Cancer may constitute the most extensively studied functions constitute a second line of defense that disease entity of our time. Nevertheless, our com- protects against transforming defects in oncogenes prehension of the cellular and molecular pathology or tumor-suppressor genes and are here considered of malignant transformation is incomplete. In view as metasuppressor genes. Advances in the molecular of the diverse clinical presentations of various explanations of growth dysregulation, metastasis malignancies, doubts may be raised as to whether it formation, extension of life span, and loss of ma- is appropriate to refer to cancer as one group of dis- tenance of genomic and epigenetic integrity in ease states. The notion of malignant tumors as a cancer suggest models for their causal connection. pathologic and pathophysiologic class of conditions The mechanisms of growth control, senescence, and begs the question for defining criteria that charac- anchorage dependence are linked on the molecular terize all malignant growths, regardless of their tis- level (Chapter 8). In cells that are not fully differ- sue of origin. Toward this goal, the recognition that tiated, the overactivation of oncogene pathways tumor development is caused by the dysregulation also induces the expression of metastasis genes. of growth-controlling genes (oncogenes and tumor- Telomerase, the enzyme that prevents cell sen- suppressor genes) has advanced our mechanistic cence, is expressed in these precursor cells and may understanding of oncology (Chapter 3). However, be further activated by growth factor signaling. Versandkostenfreie Lieferung DNA, immunesystem, Angiogenesis, celldivision, genes, molecularmechanisms, Regulation, senescence, tissue<

2010, ISBN: 9048175054

[EAN: 9789048175055], Neubuch, [SC: 0.0], [PU: Springer Netherlands], DNA; IMMUNE SYSTEM; ANGIOGENESIS; CELL DIVISION; GENES; REGULATION; SENESCENCE; TISSUE, Druck auf Anfrage Neuware - P… Meer...

[EAN: 9789048175055], Neubuch, [SC: 0.0], [PU: Springer Netherlands], DNA; IMMUNE SYSTEM; ANGIOGENESIS; CELL DIVISION; GENES; REGULATION; SENESCENCE; TISSUE, Druck auf Anfrage Neuware - Printed after ordering - Cancer may constitute the most extensively studied functions constitute a second line of defense that disease entity of our time. Nevertheless, our com- protects against transforming defects in oncogenes prehension of the cellular and molecular pathology or tumor-suppressor genes and are here considered of malignant transformation is incomplete. In view as metasuppressor genes. Advances in the molecular of the diverse clinical presentations of various explanations of growth dysregulation, metastasis malignancies, doubts may be raised as to whether it formation, extension of life span, and loss of ma- is appropriate to refer to cancer as one group of dis- tenance of genomic and epigenetic integrity in ease states. The notion of malignant tumors as a cancer suggest models for their causal connection. pathologic and pathophysiologic class of conditions The mechanisms of growth control, senescence, and begs the question for defining criteria that charac- anchorage dependence are linked on the molecular terize all malignant growths, regardless of their tis- level (Chapter 8). In cells that are not fully differ- sue of origin. Toward this goal, the recognition that tiated, the overactivation of oncogene pathways tumor development is caused by the dysregulation also induces the expression of metastasis genes. of growth-controlling genes (oncogenes and tumor- Telomerase, the enzyme that prevents cell sen- suppressor genes) has advanced our mechanistic cence, is expressed in these precursor cells and may understanding of oncology (Chapter 3). However, be further activated by growth factor signaling., Books<

ISBN: 9789048175055

Cancer may constitute the most extensively studied functions constitute a second line of defense that disease entity of our time. Nevertheless, our com- protects against transforming defe… Meer...

Cancer may constitute the most extensively studied functions constitute a second line of defense that disease entity of our time. Nevertheless, our com- protects against transforming defects in oncogenes prehension of the cellular and molecular pathology or tumor-suppressor genes and are here considered of malignant transformation is incomplete. In view as metasuppressor genes. Advances in the molecular of the diverse clinical presentations of various explanations of growth dysregulation, metastasis malignancies, doubts may be raised as to whether it formation, extension of life span, and loss of ma- is appropriate to refer to cancer as one group of dis- tenance of genomic and epigenetic integrity in ease states. The notion of malignant tumors as a cancer suggest models for their causal connection. pathologic and pathophysiologic class of conditions The mechanisms of growth control, senescence, and begs the question for defining criteria that charac- anchorage dependence are linked on the molecular terize all malignant growths, regardless of their tis- level (Chapter 8). In cells that are not fully differ- sue of origin. Toward this goal, the recognition that tiated, the overactivation of oncogene pathways tumor development is caused by the dysregulation also induces the expression of metastasis genes. of growth-controlling genes (oncogenes and tumor- Telomerase, the enzyme that prevents cell sen- suppressor genes) has advanced our mechanistic cence, is expressed in these precursor cells and may understanding of oncology (Chapter 3). However, be further activated by growth factor signaling. New Textbooks>Trade Paperback>Medicine>Medical Ref>Spec Procedure, Springer Netherlands Core >1 >T<

ISBN: 9789048175055

Cancer may constitute the most extensively studied functions constitute a second line of defense that disease entity of our time. Nevertheless, our com- protects against transforming defe… Meer...

Cancer may constitute the most extensively studied functions constitute a second line of defense that disease entity of our time. Nevertheless, our com- protects against transforming defects in oncogenes prehension of the cellular and molecular pathology or tumor-suppressor genes and are here considered of malignant transformation is incomplete. In view as metasuppressor genes. Advances in the molecular of the diverse clinical presentations of various explanations of growth dysregulation, metastasis malignancies, doubts may be raised as to whether it formation, extension of life span, and loss of ma- is appropriate to refer to cancer as one group of dis- tenance of genomic and epigenetic integrity in ease states. The notion of malignant tumors as a cancer suggest models for their causal connection. pathologic and pathophysiologic class of conditions The mechanisms of growth control, senescence, and begs the question for defining criteria that charac- anchorage dependence are linked on the molecular terize all malignant growths, regardless of their tis- level (Chapter 8). In cells that are not fully differ- sue of origin. Toward this goal, the recognition that tiated, the overactivation of oncogene pathways tumor development is caused by the dysregulation also induces the expression of metastasis genes. of growth-controlling genes (oncogenes and tumor- Telomerase, the enzyme that prevents cell sen- suppressor genes) has advanced our mechanistic cence, is expressed in these precursor cells and may understanding of oncology (Chapter 3). However, be further activated by growth factor signaling., Springer Netherlands<