The biology of cancer:
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New York
W.W. Norton & Company
[2023]
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| Ausgabe: | Third edition, International student edition |
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| Links: | http://bvbr.bib-bvb.de:8991/F?func=service&doc_library=BVB01&local_base=BVB01&doc_number=034225820&sequence=000001&line_number=0001&func_code=DB_RECORDS&service_type=MEDIA http://bvbr.bib-bvb.de:8991/F?func=service&doc_library=BVB01&local_base=BVB01&doc_number=034225820&sequence=000003&line_number=0002&func_code=DB_RECORDS&service_type=MEDIA |
| Umfang: | xxi, 865, A8, G48, I40 Seiten Illustrationen, Diagramme |
| ISBN: | 9780393887655 9780393887662 9780393690217 |
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| 245 | 1 | 0 | |a The biology of cancer |c Robert A. Weinberg, Massachusetts Institute of Technology ; with chapters by Richard Goldsby, Amherst College, Michael Hemann, Massachusetts Institute of Technology, Tyler Jacks, Massachusetts Institute of Technology |
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Datensatz im Suchindex
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xvii Detailed Contents Chapter 1: The Biology and Genetics of Cells and Organisms Mendel establishes the basic rules of genetics Mendelian genetics helps to explain Darwinian evolution Mendelian genetics governs how both genes and chromosomes behave Chromosomes are altered in most types of cancer cells 1.4 Mutations causing cancer occur in both the germ 1.5 line and the soma Genotype embodied in DNA sequences creates 1.6 phenotype through proteins Gene expression patterns also control phenotype 1.7 Modification of chromatin proteins and DNÀ 1.8 controls gene expression Unconventional RNA molecules also affect 1.9 the expression of genes Metazoa are formed from components conserved 1.10 over vast evolutionary time periods Gene cloning techniques revolutionized the study 1.11 of normal and malignant cells Additional reading 1.1 1.2 1.3 26 Tumor virus genomes persist in virus-transformed cells by becoming part of host-cell DNA Retroviral genomes become integrated into the 3.7 chromosomes of infected cells A version of the src gene carried by RSV is also 3.8 present in uninfected cells RSV exploits a kidnapped cellular gene to 3.9 transform cells 3.10 The vertebrate genome carries a large group of proto-oncogenes Slowly transforming retroviruses activate 3.11 proto-oncogenes by inserting their genomes adjacent to these cellular genes Some retroviruses naturally carry oncogenes 3.12 3.13 Bacterial cancers 3.14 Synopsis and prospects Key concepts Thought questions Additional reading 27 29 Chapt er 4: Cellular Oncogenes 3.6 1 2 4 6 9 9 12 17 20 24 Transfection of DNA provides a
strategy for detecting nonviral oncogenes Oncogenes discovered in human tumor cell lines 4.2 are related to those carried by transforming retroviruses Proto-oncogenes can be activated by genetic 4.3 changes affecting either protein expression level or structure 4.4 Variations on a theme: the myc oncogene can arise via at least three additional distinct mechanisms A diverse array of structural changes in proteins 4.5 can also lead to oncogene activation 4.6 Synopsis and prospects Key concepts Thought questions Additional reading 79 82 84 86 88 89 92 94 95 97 98 99 101 4.1 Chapter 2: The Nature of Cancer 31 Tumors arise from normal tissues Tumors arise from many specialized cell types throughout the body 2.3 Some types of tumors do not fit into the major classifications 2.4 Cancers seem to develop progressively 2.5 Tumors are monoclonal growths 2.6 Cancers occur with vastly different frequencies in different human populations 2.7 The risks of cancers often seem to be increased by assignable influences, including lifestyle 2.8 Specific chemical agents can induce cancer 2.9 Both physical and chemical carcinogens act as mutagens 2.10 Mutagens may be responsible for some human cancers 2.11 Synopsis and prospects Key concepts Thought questions Additional reading 32 2.1 2.2 34 42 44 49 51 54 56 57 60 61 63 64 65 Chapt er 3: Cancer as an Infectious Disease 67 3.1 3.2 68 3.3 3.4 3.5 Peyton Rous discovers a chicken sarcoma virus Rous sarcoma virus is discovered to transform infected cells in culture The continued presence of RS V is needed to maintain transformation Viruses containing
DNA molecules are also able to induce cancer Tumor viruses induce multiple changes in cell phenotype including acquisition of tumorigenicity 104 107 111 117 120 122 123 123 Chapt er 5: Growth Factors, Receptors, and Cancer 125 Normal metazoan cells control each other’s lives The Src protein functions as a tyrosine kinase The EGF receptor functions as a tyrosine kinase An altered growth factor receptor can function as an oncoprotein A growth factor gene can become an oncogene: the case of sis Transphosphorylation underlies the operations of many receptor tyrosine kinases Yet other types of receptors enable mammalian cells to communicate with their environment Nuclear receptors sense the presence of lowmolecular-weight lipophilic ligands Integrin receptors sense association between the cell and the extracellular matrix 126 129 132 5.1 5.2 5.3 5.4 5.5 5.6 69 5.7 72 5.8 74 5.9 77 102 135 138 141 147 153 154
xviii Detailed contents The Ras protein, an apparent component of the downstream signaling cascade, functions as a G-protein 5.11 Synopsis and prospects Key concepts Thought questions Additional reading Chapter 6: Cytoplasmic Signaling Circuitry Programs Many of the Traits of Cancer A signaling pathway reaches from the cell surface into the nucleus The Ras protein stands in the middle of a 6.2 complex signaling cascade Tyrosine phosphorylation controls the location 6.3 and thereby the actions of many cytoplasmic signaling proteins 6.4 SH2 and SH3 groups explain how growth factor receptors activate Ras and acquire signaling specificity 6.5 Ras-regulated signaling pathways: A cascade of kinases forms one of three important signaling pathways downstream of Ras 6.6 Ras-regulated signaling pathways: a second downstream pathway controls inositol lipids and the Akt/PKB kinase 6.7 Ras-regulated signaling pathways: a third downstream pathway acts through Rai, a distant cousin of Ras 6.8 The JAK-STAT pathway allows signals to be transmitted from the plasma membrane directly to the nucleus 6.9 Cell adhesion receptors emit signals that converge with those released by growth factor receptors 6.10 The canonical and non-canonical Wnt pathways control diverse cellular phenotypes 6.11 G-protein-coupled receptors can also drive normal and neoplastic proliferation 6.12 Four additional “dual-address” signaling pathways contribute in various ways to normal and neoplastic proliferation 6.13 The Hippo signaling circuit integrates diverse inputs to govern diverse cell phenotypes 6.14 Well-designed
signaling circuits require both negative and positive feedback controls 6.15 Synopsis and prospects Key concepts Thought questions Additional reading 159 162 167 169 169 171 6.1 Chap iter 7: Tumor Suppressor Genes 7.1 7.2 7.3 7.4 7.5 7.6 Cell fusion experiments indicate that the cancer phenotype is recessive The recessive nature of the cancer cell phenotype requires a genetic explanation The retinoblastoma tumor provides a solution to the genetic puzzle ofTSGs Incipient cancer cells eliminate wild-type copies ofTSGs by a variety of mechanisms The Rb gene often undergoes loss of heterozygosity in tumors Loss-of-heterozygosity events can be used to find TSGs 7.7 Promoter methylation represents an important mechanism for inactivating TSGs TSGs and their encoded proteins function in diverse ways The NF1 protein acts as a negative regulator 7.9 of Ras signaling 7.10 APC facilitates egress of cells from colonic crypts 7.11 KEAP1 regulates cellular response to oxidative stress Not all familial cancers can be explained by 7.12 inheritance of mutant TSGs Synopsis and prospects 7.13 Key concepts Thought questions Additional reading 7.8 5.10 172 176 Chapt:er 8: pRb and Control of the Cell Cycle Clock Cell growth and division is coordinated by a complex array of regulators Cells make decisions about growth and 8.2 quiescence during a specific period in the Gj phase Cyclins and cyclin-dependent kinases constitute 8.3 the core components of the cell cycle clock Cyclin-CDK complexes are also regulated by 8.4 CDK inhibitors Viral oncoproteins reveal how pRb blocks 8.5 advance through the
cell cycle pRb is deployed by the cell cycle clock to serve 8.6 as a guardian of the restriction-point gate E2F transcription factors enable pRb to implement 8.7 growth-versus-quiescence decisions A variety of mitogenic signaling pathways control 8.8 the phosphorylation state of pRb The Мус protein governs decisions to proliferate or 8.9 differentiate 8.10 TGF-ß prevents phosphorylation of pRb and thereby blocks cell cycle progression pRb function and the controls of differentiation 8.11 are closely linked 8.12 Control of pRb function is perturbed in most if not all human cancers Synopsis and prospects 8.13 Key concepts Thought questions Additional reading 253 254 259 265 268 268 272 273 273 275 8.1 177 182 184 189 198 200 202 204 208 211 217 218 221 229 230 231 233 234 Chapter 9: p53: Master Guardian and Executioner 9.1 9.2 9.3 9.4 9.5 9.6 9.7 235 9.8 236 9.9 240 9.10 242 9.11 244 9.12 247 DNA tumor viruses lead to the discovery of p53 p53 is discovered to be a tumor suppressor gene Inherited mutations affecting p53 predispose individuals to a variety of tumors Mutant versions of p53 interfere with normal p53 function p53 protein molecules usually have short lifetimes Various signals cause p53 induction DNA damage and deregulated growth signals cause p53 stabilization Mdm2 destroys its own creator ARF and p53-mediated apoptosis protect against cancer by monitoring intracellular signaling p53 functions as a transcription factor that halts cell cycle advance in response to DNA damage and attempts to aid in the repair process Prolonged DNA damage and oncogene activation can
induce p53-dependent senescence The apoptosis program participates in normal tissue development and maintenance 276 280 282 287 292 295 297 301 302 307 309 311 315 318 320 320 323 324 324 327 327 330 332 333 335 340 341 345 348
Detailed contents Apoptosis is a complex biochemical program that often depends on mitochondria 9.14 Both intrinsic and extrinsic apoptotic programs can lead to cell death 9.15 Cancer cells deploy numerous ways to inactivate their apoptotic machinery 9.16 p53 inactivation provides an advantage to incipient cancer cells at a number of steps in tumor progression 9.17 Additional forms of cell death may limit the survival of cancer cells 9.18 Synopsis and prospects Key concepts Thought questions Additional reading 11.9 9.13 Chapter 10: Eternal Life: Cell Immortalization and Tumorigenesis Normal cell populations appear to register the number of cell generations separating them from their ancestors in the early embryo 10.2 Cells need to become immortalized in order to form a cell line 10.3 Cancer cells need to become immortal in order to form tumors 10.4 The proliferation of cultured cells is also limited by the telomeres of their chromosomes 10.5 Telomeres are complex molecular structures that are not easily replicated 10.6 Incipient cancer cells can escape crisis by expressing telomerase 10.7 Telomerase plays a key role in the proliferation of human cancer cells 10.8 Some immortalized cells can maintain telomeres without telomerase 10.9 Telomeres play different roles in the cells of laboratory mice and in human cells 10.10 Telomerase-negative mice show both decreased and increased cancer susceptibility 10.11 The mechanisms underlying cancer pathogenesis in telomerase-negative mice may also operate during the development of human tumors 10.12 Synopsis and prospects Key concepts
Thought questions Additional reading 349 359 363 366 367 370 372 373 373 11.1 11.2 11.3 11.4 11.5 11.6 11.7 11.8 Most human cancers develop over many decades of time Histopathology provides evidence of multi-step tumor formation Cells accumulate genetic and epigenetic alterations as tumor progression proceeds Cancer development seems to follow the rules of Darwinian evolution Multi-step tumor progression helps to explain familial polyposis and field cancerization Intra-tumor diversification can outrun Darwinian selection Tumor stem cells further complicate the Darwinian model of clonal succession and tumor progression Multiple lines of evidence reveal that normal cells are resistant to transformation by a single mutated gene 448 451 453 458 460 462 465 470 475 476 476 375 10.1 Chapter 11: Multi-Step Tumorigenesis Human cells are constructed to be highly resistant to immortalization and transformation 11.10 Mammalian evolution contributed to the complexity of human cell transformation 11.11 Nonmutagenic agents, including those favoring cell proliferation, make important contributions to tumorigenesis 11.12 Mitogenic agents, key governors of human cancer incidence, can act as human tumor promoters 11.13 Chronic inflammation often serves to promote tumor progression in mice and humans 11.14 Inflammation-dependent tumor promotion operates through defined signaling pathways 11.15 Metabolism is the elusive heart of the cancer process 11.16 Synopsis and prospects Key concepts Thought questions Additional reading xix 376 Chapter 12: Shaping and Characterizing the Cancer Genome
Tissues are organized to minimize the progressive accumulation of mutations 12.2 The properties of stem cells make them good candidates to be cells-of-origin of cancer 12.3 Apoptosis, drug pumps, and DNA replication quality control mechanisms offer tissues a way to minimize the accumulation of mutant preneoplastic cells 12.4 Cell genomes are under constant attack from endogenous biochemical processes 12.5 Cell genomes are under occasional attack from exogenous mutagens and their metabolites 12.6 Cells deploy a variety of defenses to protect DNA molecules from attack by mutagens 12.7 Repair enzymes fix DNA that has been altered by mutagens 12.8 Inherited defects in nucleotide-excision repair, base-excision repair, and mismatch repair lead to specific cancer susceptibility syndromes 12.9 A variety of other DNA repair defects confer increased cancer susceptibility 12.10 The karyotype of cancer cells is often changed through alterations in chromosome structure 12.11 The karyotype of cancer cells is often changed through alterations in chromosome number 12.12 Advances in genome sequencing technologies have fueled a revolution in cancer genomics 12.13 Genomic analysis reveals that human cancers differ with respect to mutational burden, patterns of mutations, and copy number gains and losses 12.14 Cancer genomes contain driver and passenger gene mutations 12.15 Cancer genomic studies reveal both inter-tumoral and intra-tumoral heterogeneity 12.16 Synopsis and prospects Key concepts Thought questions Additional reading 479 12.1 378 380 384 389 391 396 399 401 403 406 409 412 413
413 415 416 419 424 429 480 483 485 491 494 501 502 508 514 520 524 528 529 534 535 539 546 547 547 431 432 437 443 Chapter 13: Dialogue Replaces Monologue: Heterotypic Interactions and the Biology of Angiogenesis 549 13.1 13.2 Normal and neoplastic epithelial tissues are formed from interdependent cell types The extracellular matrix represents a critical component of the tumor microenvironment 551 561
XX Detailed contents Tumors resemble wounded tissues that do not heal Experiments directly demonstrate that stromal cells are active contributors to tumorigenesis 13.5 Macrophages and myeloid cells play important roles in activating the tumor-associated stroma 13.6 Endothelial cells and the vessels that they form ensure tumors adequate access to the circulation 13.7 Tripping the angiogenic switch is essential for tumor expansion 13.8 The angiogenic switch initiates a highly complex process 13.9 Anti-angiogenesis therapies have been employed to treat cancer 13.10 Nervous tissue contributes to tumor growth 13.11 Synopsis and prospects Key concepts Thought questions Additional reading 563 Chapter 14: Moving Out: Invasion and Metastasis 609 13.3 13.4 The invasion-metastasis cascade begins with local invasiveness Epithelial-mesenchymal transitions profoundly 14.2 reshape the phenotypes of carcinoma cells Epithelial-mesenchymal transitions are often 14.3 induced by contextual signals 14.4 EMTs are programmed by transcription factors that orchestrate key steps of embryogenesis 14.5 Signals released by an array of stromal cell types contribute to the induction of invasiveness and intravasation 14.6 EMT-inducing transcription factors may enable entrance into the stem cell state 14.7 EMT-inducing transcription factors help drive malignant progression including metastatic dissemination 14.8 The invasiveness of carcinoma cells depends on clearance of obstructing ECM 14.9 Motility enables cancer cells to move into space excavated by MMPs 14.10 Intravasation and the formation of
circulating tumor cells: first steps in perilous journeys 14.11 Colonization represents the most complex and challenging step of the invasion-metastasis cascade 14.12 Successful metastatic colonization often involves complex adaptations 14.13 An example of extreme metastatic specialization: metastasis to bone requires the subversion of osteoblasts and osteoclasts 14.14 Occult micrometastases threaten the long-term survival of many cancer patients 14.15 Synopsis and prospects Key concepts Thought questions Additional reading 575 576 582 588 592 594 599 601 606 607 607 MHC molecules play key roles in antigen recognition byT cells 15.6 T cells that recognize MHCT have different roles from those that recognize MHC-II 15.7 Dendritic cell activation of naive T cells is a key step in the generation of functional helper and cytotoxic T cells 15.8 Tumor antigens are targets of the immune response to cancer Natural killer cells contribute to anti-cancer 15.9 immunity 15.10 Macrophages make multiple contributions to tumor development 15.11 Regulatory T cells are indispensable negative regulators of the immune response that are co-opted by tumors to counteract immune attack 15.12 Immune checkpoints act to limit immune responses 15.13 Synopsis and prospects Key concepts Thought questions Additional reading 15.5 710 714 714 717 721 722 725 727 730 734 736 736 14.1 612 Chapt:er 16: Cancer Immunotherapy 615 16.1 622 633 637 643 646 651 656 657 667 677 679 685 686 692 693 694 Vaccination can prevent cancer caused by infectious agents Vaccination against human papillomaviruses 16.2 prevents
cervical cancer Therapeutic vaccination is a potential treatment 16.3 for cancer 16.4 Passive immunization with antibodies can be used to treat cancer Lymphoma and breast cancer can be treated wi th 16.5 monoclonal antibodies 16.6 Antibody-drug conjugates deliver toxic drugs to cells displaying tumor antigens Cancer can be treated by adoptive cell transfer 16.7 CART cells have predetermined specificity and 16.8 bypass МНС-dependent antigen presentation Checkpoint inhibition is a distinct type of 16.9 immunotherapy that modifies the behavior of immune cells 16.10 Checkpoint immunotherapies based on mouse studies have been applied in the oncology clinic 16.11 Resistance to immune checkpoint inhibitors commonly arises 16.12 Lethal encounters between T cells and cancer cells can be encouraged by constructing bi-specific antibodies 16.13 T-cell-dependent immunotherapies can be hampered by T-cell exhaustion 16.14 Synopsis and Prospects Key Concepts Thought questions Additional reading Chanter 17: The Rational Treatment of Cancer Chapter 15: Crowd Control: Tumor Immunology 15.1 15.2 15.3 15.4 Ihe immune system continuously conducts surveillance of tissues The human immune system plays a critical role in warding off various types of human cancer The immune system functions to destroy foreign invaders and abnormal cells in the body’s tissues The diversity of В cell andT cell receptors arises from the stochastic diversification of the genes that encode them 697 698 17.1 17.2 700 17.3 704 17.4 708 The development and clinical use of effective therapies will depend on accurate
diagnosis of disease Surgery, radiotherapy, and chemotherapy are the major pillars on which current cancer therapies rest The present and future use of chemotherapy requires improved understanding of how anti-cancer drugs work Differentiation, synthetic lethality, and cell cycle checkpoints can be exploited to kill cancer cells 737 738 740 742 745 748 750 754 757 761 767 768 769 771 773 777 778 778 781 784 792 796 801
Detailed contents 17.5 17.6 17.7 17.8 17.9 17.10 17.11 17.12 17.13 Functional and biochemical considerations dictate that only a subset of the defective proteins in cancer cells are attractive targets for drug development Pharmaceutical chemists can generate and explore the biochemical properties of a wide array of potential drugs Drug candidates and their targets must be examined in cell models as an initial measurement of their utility in whole organisms Studies of a drug’s action in laboratory animals are an essential part of pre-clinical testing Promising candidate drugs are subjected to rigorous clinical tests in Phase I trials in humans Phase II and III trials provide credible indications of clinical efficacy Tumors often develop resistance to initially effective therapy Targeting Bcl-2 to induce cell death Gleevec paved the way for the development of many other highly targeted compounds 803 811 815 819 821 17.14 EGF receptor antagonists may be useful for treating a wide variety of tumor types 17.15 Proteasome inhibitors yield unexpected therapeutic benefit 17.16 B-Raf discoveries have led to inroads into the melanoma problem 17.17 Synopsis and prospects: challenges and opportunities on the road ahead Key concepts Thought questions Additional reading 855 863 864 864 Abbreviations A:1 824 826 827 830 xxi 841 847 852 G:1 Index 1:1
INTERNATIONAL STUDENT EDITION NOT FOR SALE IN THE UNITED STATES DR CANADA leading edge lamellipodium (Μ) focal adhesions (Μ) peripheral „actin belt (Μ) actin stress fibers (Μ) cell-cell adherens junctions (E) X Щ Table of contents Chapter 7: Tumor Suppressor В The Biology of Cancer, Third Edition The gold standard text in cancer biology, thoroughly updated with the latest research. Incorporating the most important advances in the rapidly-evolving field of cancer biology, this book remains the defining course text on its subject. Students, instructors, researchers, and clinicians the world over admire its authoritative content, clear explanations, extensive full-color art program, and pedagogical features that promote a deep conceptual understanding of the science through the lens of fascinating tales of scientific discovery. Demo User 0 Such additional mutations might include, for example, genes that push the progeny toward a neoplastic growth INTESTINAL CRYPTS Villus puzzle of TSGs 7.4 Incipient cancer cells eliminate ED Transi! Amplifying Compartment variety of mechanisms 7.5 The Rb gene often undergoes ES Îÿ/Stoo^âhi) Transcript 7.7 Promoter methylation represents an important 7.8 TSGs and their encoded proteins function in diverse ways The protein called p-catenin governs much of this out migration behavior. As described in Section 6.10, levels of soluble ß-catenin in the cytoplasm are controlled by ф Chapter 7: Tumor Suppressor Genes I Available for the first time this edition, the Norton Ebook provides an active reading experience, enabling students to highlight,
take notes, search, and read offline. Narrated animations are embedded throughout and cover selected topics. Instructors can add their own content and notes that students can see as they are reading the text. Norton Ebooks can be viewed on all devices and are born accessible, with content and features designed from the start for all learners. Access to the Norton Ebook is included automatically with all new print texts. It can be accessed separately at digital.wwnort.com/cancer3 |
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| genre | (DE-588)4123623-3 Lehrbuch gnd-content |
| genre_facet | Lehrbuch |
| id | DE-604.BV048962076 |
| illustrated | Illustrated |
| indexdate | 2025-01-29T15:01:09Z |
| institution | BVB |
| isbn | 9780393887655 9780393887662 9780393690217 |
| language | English |
| oai_aleph_id | oai:aleph.bib-bvb.de:BVB01-034225820 |
| oclc_num | 1401183248 |
| open_access_boolean | |
| owner | DE-20 DE-19 DE-BY-UBM DE-384 DE-578 DE-29T DE-355 DE-BY-UBR DE-703 |
| owner_facet | DE-20 DE-19 DE-BY-UBM DE-384 DE-578 DE-29T DE-355 DE-BY-UBR DE-703 |
| physical | xxi, 865, A8, G48, I40 Seiten Illustrationen, Diagramme |
| publishDate | 2023 |
| publishDateSearch | 2023 |
| publishDateSort | 2023 |
| publisher | W.W. Norton & Company |
| record_format | marc |
| spelling | Weinberg, Robert A. 1942- Verfasser (DE-588)132123517 aut The biology of cancer Robert A. Weinberg, Massachusetts Institute of Technology ; with chapters by Richard Goldsby, Amherst College, Michael Hemann, Massachusetts Institute of Technology, Tyler Jacks, Massachusetts Institute of Technology Cancer Third edition, International student edition New York W.W. Norton & Company [2023] © 2023 xxi, 865, A8, G48, I40 Seiten Illustrationen, Diagramme txt rdacontent n rdamedia nc rdacarrier Genetik (DE-588)4071711-2 gnd rswk-swf Krebs Medizin (DE-588)4073781-0 gnd rswk-swf Biomedizin (DE-588)4647152-2 gnd rswk-swf Biologie (DE-588)4006851-1 gnd rswk-swf Carcinogenese (DE-588)4069853-1 gnd rswk-swf Molekularbiologie (DE-588)4039983-7 gnd rswk-swf (DE-588)4123623-3 Lehrbuch gnd-content Krebs Medizin (DE-588)4073781-0 s Genetik (DE-588)4071711-2 s Biologie (DE-588)4006851-1 s DE-604 Biomedizin (DE-588)4647152-2 s Carcinogenese (DE-588)4069853-1 s Molekularbiologie (DE-588)4039983-7 s Digitalisierung UB Augsburg - ADAM Catalogue Enrichment application/pdf http://bvbr.bib-bvb.de:8991/F?func=service&doc_library=BVB01&local_base=BVB01&doc_number=034225820&sequence=000001&line_number=0001&func_code=DB_RECORDS&service_type=MEDIA Inhaltsverzeichnis Digitalisierung UB Augsburg - ADAM Catalogue Enrichment application/pdf http://bvbr.bib-bvb.de:8991/F?func=service&doc_library=BVB01&local_base=BVB01&doc_number=034225820&sequence=000003&line_number=0002&func_code=DB_RECORDS&service_type=MEDIA Klappentext |
| spellingShingle | Weinberg, Robert A. 1942- The biology of cancer Genetik (DE-588)4071711-2 gnd Krebs Medizin (DE-588)4073781-0 gnd Biomedizin (DE-588)4647152-2 gnd Biologie (DE-588)4006851-1 gnd Carcinogenese (DE-588)4069853-1 gnd Molekularbiologie (DE-588)4039983-7 gnd |
| subject_GND | (DE-588)4071711-2 (DE-588)4073781-0 (DE-588)4647152-2 (DE-588)4006851-1 (DE-588)4069853-1 (DE-588)4039983-7 (DE-588)4123623-3 |
| title | The biology of cancer |
| title_alt | Cancer |
| title_auth | The biology of cancer |
| title_exact_search | The biology of cancer |
| title_full | The biology of cancer Robert A. Weinberg, Massachusetts Institute of Technology ; with chapters by Richard Goldsby, Amherst College, Michael Hemann, Massachusetts Institute of Technology, Tyler Jacks, Massachusetts Institute of Technology |
| title_fullStr | The biology of cancer Robert A. Weinberg, Massachusetts Institute of Technology ; with chapters by Richard Goldsby, Amherst College, Michael Hemann, Massachusetts Institute of Technology, Tyler Jacks, Massachusetts Institute of Technology |
| title_full_unstemmed | The biology of cancer Robert A. Weinberg, Massachusetts Institute of Technology ; with chapters by Richard Goldsby, Amherst College, Michael Hemann, Massachusetts Institute of Technology, Tyler Jacks, Massachusetts Institute of Technology |
| title_short | The biology of cancer |
| title_sort | the biology of cancer |
| topic | Genetik (DE-588)4071711-2 gnd Krebs Medizin (DE-588)4073781-0 gnd Biomedizin (DE-588)4647152-2 gnd Biologie (DE-588)4006851-1 gnd Carcinogenese (DE-588)4069853-1 gnd Molekularbiologie (DE-588)4039983-7 gnd |
| topic_facet | Genetik Krebs Medizin Biomedizin Biologie Carcinogenese Molekularbiologie Lehrbuch |
| url | http://bvbr.bib-bvb.de:8991/F?func=service&doc_library=BVB01&local_base=BVB01&doc_number=034225820&sequence=000001&line_number=0001&func_code=DB_RECORDS&service_type=MEDIA http://bvbr.bib-bvb.de:8991/F?func=service&doc_library=BVB01&local_base=BVB01&doc_number=034225820&sequence=000003&line_number=0002&func_code=DB_RECORDS&service_type=MEDIA |
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