Principles of Cancer Genetics

Gebonden Engels 2016 2e druk 9789401774826
Verwachte levertijd ongeveer 9 werkdagen

Samenvatting

This is the second edition of a widely used textbook that consolidates the basic concepts of the cancer gene theory and provides a framework for understanding the genetic basis of cancer. Particular attention is devoted to the origins of the mutations that cause cancer, and the application of evolutionary theory to explain how the cell clones that harbor cancer genes tend to expand. Focused on the altered genes and pathways that cause the growth of the most common tumors, Principles of Cancer Genetics is aimed at advanced undergraduates who have completed introductory coursework in genetics, biology and biochemistry, medical students and medical house staff. For students with a general interest in cancer, this book provides a highly accessible and readable overview. For more advanced students contemplating future study in the field of oncology and cancer research, this concise book will be useful as a primer.

Specificaties

ISBN13:9789401774826
Taal:Engels
Bindwijze:gebonden
Uitgever:Springer Netherlands
Druk:2

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Inhoudsopgave

<p> </p> <p>Preface</p> <p>Chapter 1: The Genetic Basis of Cancer</p><p>The cancer gene theory</p><p>Cancers are invasive tumors</p><p>Cancer is a unique type of genetic disease</p><p>What are cancer genes and how are they acquired?</p><p>Mutations alter the human genome</p><p>Genes and mutations</p><p></p>Single nucleotide substitutions<p></p><p>Gene silencing is marked by cytosine methylation: epigenetics</p><p>Environmental mutagens, mutations and cancer</p><p>Inflammation promotes the propagation of cancer genes</p><p>Stem cells, Darwinian selection and the clonal evolution of cancers</p><p>Selective pressure and adaptation:  hypoxia and altered metabolism</p><p>Multiple somatic mutations punctuate clonal evolution</p>Tumor growth leads to cellular heterogeneity<p></p><p>Tumors are distinguished by their spectrum of driver gene mutations and passenger gene mutations</p><p>Colorectal cancer: a model for understanding the process of tumorigenesis</p><p>Do cancer cells divide more rapidly than normal cells?</p><p>Germline cancer genes allow neoplasia to bypass steps in clonal evolution</p><p>Cancer syndromes reveal rate-limiting steps in tumorigenesis</p><p>The etiolog</p>ic triad: heredity, the environment, and stem cell division<p></p><p>Understanding cancer genetics</p><p> </p><p>Chapter 2:  Oncogenes</p><p>What is an oncogene?</p><p>The discovery of transmissible cancer genes</p><p>Viral oncogenes are derived from the host genome</p><p>The search for activated oncogene</p><p></p><p></p><p></p><p></p><p></p>s:  the RAS gene family<p></p>Complex genomic rearrangements: the MYC gene family<p></p><p>Proto-oncogene activation by gene amplification</p><p>Proto-oncogenes can be activated by chromosomal translocation</p><p> </p><p>Chromosomal translocations in liquid tumors</p><p>Chronic myeloid leukemia and the Philadelphia chromosome</p><p>Oncogenic activation of transcription factors in Prostate cancer and Ewing’s sarcoma </p>Oncogene discovery in the genomic era: mutations in PIK3CA <p></p><p>Selection of tumor-associated mutations</p><p>Multiple modes of proto-oncogene activation</p><p>Oncogenes are dominant cancer genes</p><p>Germline mutations in RET and MET confer cancer predisposition</p><p>Proto-oncogene activation and tumorigenesis</p><p> </p><p></p>Chapter 3:  Tumor Suppressor Genes<p></p><p>What is a tumor suppressor gene?</p><p>The discovery of recessive cancer phenotypes</p><p>Retinoblastoma and Knudson’s two-hit hypothesis</p><p>Chromosomal localization of the retinoblastoma gene</p><p>The mapping and cloning of the retinoblastoma gene </p><p>Tumor suppressor gene inactivation: the second ‘hit’ and loss of heterozygosity</p>Recessive genes, dominant traits<p></p><p>APC inactivation in inherited and sporadic colorectal cancers</p><p>TP53 inactivation: a frequent event in tumorigenesis </p><p>Functional inactivation of p53: tumor suppressor genes and oncogenes interact</p><p>Mutant TP53 in the germl</p>ine:  L<p></p>i Fraum<p></p>eni syn<p></p>drome<p></p><p>Ga</p>ins-of-function caused by cancer-associated mutations in TP53<p></p><p>Cancer predisposition: allelic penetrance, relative risk and the odds ratio</p><p>Breast cancer susceptibility:  BRCA1 and BRCA2</p><p>Genetic losses on chromosome 9:  CDKN2A</p><p>Complexity at CDKN2A:  neighboring and overlapping genes</p><p>Genetic losses on chromosome 10:  PTEN</p><p>SMAD4 and the maintenance of stromal architecture</p>Two distinct genes cause neurofibromatosis<p></p><p>From flies to humans, Patched proteins regulate developmental morphogenesis</p><p>von Hippel-Lindau disease</p><p>NOTCH1: tumor suppressor gene or oncogene?</p><p>Multiple endocrine neoplasia type 1</p><p>Most tumor suppressor genes are tissue-specific </p><p>Modeling cancer syndromes in mice</p><p></p>Genetic variation and germline cancer genes<p></p><p>Tumor suppressor gene inactivation during colorectal tumorigenesis</p><p>Inherited tumor suppressor gene mutations: gatekeepers and landscapers</p><p>Maintaining the genome: caretakers </p><p> </p><p>Chapter 4:  Genetic Instability and Cancer</p><p>What is genetic instability?</p><p></p>The majority of cancer cells are aneuploid<p></p><p>Aneuploid cancer cells exhibit chromosome instability</p><p>Chromosome instability arises early in colorectal tumorigenesis</p><p>Chromosomal instability accelerates clonal evolution</p><p>Aneuploidy can result from mutations th</p>at directly im<p></p>pact mitosis<p></p><p>STAG2</p> and<p></p> the cohesion <p></p>of sister chromatids<p></p><p>Other genetic and epigenetic causes of aneuploidy</p>Transition from tetraploidy to aneuploidy during tumorigenesis  <p></p><p>Multiple forms of genetic instability in cancer</p><p>Defects in mismatch repair cause hereditary nonpolyposis colorectal cancer</p><p>Mismatch repair-deficient cancers have a distinct spectrum of mutations</p><p>Defects in nucleotide excision repair cause xeroderma pigmentosum</p><p>NER syndromes: clinical heterogeneity and pleiotropy</p><p></p>DNA repair defects and mutagens define two steps towards genetic instability<p></p><p>Defects in DNA crosslink repair cause Fanconi anemia</p><p>A defect in DNA double strand break responses causes ataxia-telangiectasia</p><p>A unique form of genetic instability underlies Bloom syndrome </p><p>Aging and cancer:  insights from the progeroid syndromes</p><p>Instability at the end: telomeres and telomerase</p><p>Overview: genes and genetic stability</p><p></p> <p></p><p>Chapter 5:  Cancer Genomes</p><p>Discovering the genetic basis of cancer: from genes to genomes</p><p>What types of genetic alterations are found in tumor cells?</p><p>How many genes are mutated in the various types of cancer?</p><p>What is the significance of the mutations that are found in cancers?</p><p>When do cancer-associated mutations occur?</p><p></p>How many different cancer genes are there? <p></p>How many cancer gene</p>s are required for th<p></p>e development <p></p>of cancer?<p></p><p>Cance</p>r genetics sha<p></p>pes our understanding<p></p> of metastasis<p></p><p>Tumors are genetically heterogenous</p><p>Beyond the exome: the ‘dark matter’ of the cancer genome</p><p>A summary:  the genome of a cancer cell</p><p> </p><p></p>Chapter 6:  Cancer Gene Pathways<p></p><p>What are cancer gene pathways?</p><p>Cellular pathways are defined by protein-protein interactions</p><p>Individual biochemical reactions, multistep pathways, and networks</p><p>Protein phosphorylation is a common regulatory mechanism </p><p>Signals from the cell surface:  protein tyrosine kinases </p><p>Membrane-associated GTPases:  the RAS pathway</p><p></p>An intracellular kinase cascade: the MAPK pathway<p></p><p>Genetic alterations of the RAS pathway in cancer </p><p>Membrane-associated lipid phosphorylation: the PI3K/AKT pathway</p><p>Control of cell growth and energetics:  the mTOR pathway </p><p>Genetic alterations in the PI3K/AKT and mTOR pathways define roles in cell survival</p><p>The STAT pathway transmits cytokine signals to the cell nucleus</p><p>Morphogenesis and cancer:  the WNT/APC pathway</p>Dysregulation of the WNT/APC pathway in cancers<p></p><p>Notch signaling mediates cell-to-cell communication</p><p>Morphogenesis and cancer:  the Hedgehog pathway</p><p>TGF-/ SMAD signaling maintains adult tissue homeostasis</p><p>MYC is a downstream effector of multiple cancer gene pathways</p> activation is triggere</p>d by damaged or incompletely<p></p> replicated chromosom<p></p>es <p></p><p>p53 is controlled b</p>y protein kinases enc<p></p>oded by <p></p>tumor suppressor genes<p></p><p>p53 induces the transcription of genes that suppress cancer phenotypes</p><p>Feedback loops dynamically control p53 abundance </p><p>The DNA damage signaling network activates interconnected repair pathways</p><p>Inactivation of the pathways to apoptosis in cancer</p><p>RB1 and the regulation of the cell cycle</p><p>Several cancer gene pathways converge on cell cycle regulators</p><p></p>Many cancer cells are cell cycle checkpoint-deficient<p></p><p>Chromatin modification is recurrently altered in many types of cancer</p><p>Summary: putting together the puzzle  </p><p> </p><p>Chapter 7:  Genetic Alternations in Common Cancers</p><p>Cancer genes cause diverse diseases</p><p>Cancer incidence and prevalence</p><p>Lung cancer</p><p></p><p>Prostate cancer</p><p>Breast cancer</p><p>Colorectal cancer</p><p>Endometrial cancer</p><p>Melanoma of the skin</p><p>Bladder cancer</p><p>Lymphoma</p><p>Cancers in the kidney</p>Thyroid cancer<p></p><p>Leukemia</p><p>Cancer in the pancreas</p><p>Ovarian cancer</p><p>Cancers of the oral cavity and pharynx</p><p>Liver cancer</p><p>Cancer of the uterine cervix</p><p>Stomach cancer</p><p></p>Brain tumors<p></p><p> </p><p>Chapter 8: Cancer Genetics in the Clinic</p><p>The uses of genetic information</p><p>Elements of cancer risk:  carcinogens and genes </p><p>Identifying carriers o</p>f germline cancer genes<p></p><p>Cance</p>r genes as biomarkers of ear<p></p>ly stage malignancies <p></p><p>Cancer </p>genes as biomarkers f<p></p>or diagnosis, prognosis and recurrence<p></p><p>Conventional anticancer therapies inhibit cell growth</p><p>Exploiting the loss of DNA repair pathways: synthetic lethality</p><p>On the horizon: achieving synthetic lethality in TP53-mutant cancers</p><p>Molecularly targeted therapy:  BCR-ABL and imatinib</p><p>Clonal evolution of therapeutic resistance</p><p>Targeting EGFR mutations</p><p></p>Antibody-mediated inhibition of receptor tyrosine kinases<p></p><p>Inhibiting Hedgehog signaling</p><p>A pipeline from genetically-defined targets to targeted therapies </p><p>Neoantigens are recognized by the immune system</p><p>The future of oncology </p><p>Index</p><p> </p><p></p> <p></p>

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        Principles of Cancer Genetics