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Systems Biology of Cancer

Tác giả: Thiagalingam, Sam

Chủ đề:

Chủ đề: Medicine; Cancer

Nhà xuất bản: Cambridge University Press

Năm xuất bản: 2015

Loại tài liệu: Book

Mô tả vật lý: 595 p.

Định danh: 978-0-521-49339-0

Ngôn ngữ: en

Đọc trực tuyến

With over 200 types of cancer diagnosed to date, researchers the world over have been forced to rapidly update their understanding of the biology of cancer. In fact, only the study of the basic cellular processes, and how these are altered in cancer cells, can ultimately provide a background for rational therapies. Bringing together the state-of-the-art contributions of international experts, Systems Biology of Cancer proposes an ultimate research goal for the whole scientific community: exploiting systems biology to generate in-depth knowledge based on blueprints that are unique to each type of cancer.

Cover
Half-title
Title page
Copyright information
Dedication
Table of contents
List of contributors
Preface
Part 1 Introduction to modular organization of the networks of gene functions and cancer
- Chapter 1 Systems biology of cancer progression
  - Background
  - Introduction
  - Multi-modular molecular networks of cancer progression depict heterogeneity in genetic and epigenetic alterations
  - Driver versus passenger alterations
  - Emerging MMMN models
  - Role of the microenvironment in cancer progression
  - Future perspectives
  - References
- Chapter 2 Lessons from cancer genome sequencing
  - Background
  - Introduction
  - Next-generation sequencing technologies
    - Sequencing template preparation
    - Sequencing by synthesis
      - Fluorescent methods
      - Non-fluorescent methods
    - Sequencing by ligation
    - Sequencing through DNA observation
  - Analysis of sequencing information
    - Single nucleotide variations
    - Somatic mutations and inheritance
    - Structural variations
    - Drivers and passengers
  - Cancer genome sequencing strategies
    - Paired-end mapping
    - Single nucleotide polymorphism profiling
    - Targeted resequencing
    - Whole genome sequencing
  - Conclusion
  - References
- Chapter 3 Application of bioinformatics to analyze the expression of tissue-specific and housekeeping genes in cancer
  - Genomic technology for identifying tissue of origin for metastatic cancer
  - Introduction
  - Expression of tissue-specific genes in tumors
    - Hepatocyte-specific expression signature and dedifferentiation of liver cancer
    - Identification of tissue-specific genes
    - Expression of neuron and glia-specific genes in brain tumors
    - Breast tumors with two distinct types of differentiation
    - The remarkable heterogeneity of lung cancers
  - Expression of maintenance genes in tumors
    - Maintenance genes frequently under-expressed in cancers: tumor suppressors?
    - Genes always expressed in tumors define a minimum set of survival genes
  - Acknowledgment
  - Concluding remarks
  - References
Part 2 Alterations in the regulatory networks of cellular and molecular events
- Chapter 4 Events at DNA replication origins and genome stability
  - Introduction
    - Origin licensing
    - The cell cycle and genome stability
    - Origin firing
    - Positive regulation of origin licensing factors
      - CDC6 stabilization
      - Transcription
    - Negative regulation of origin licensing factors
      - CDK-mediated phosphorylation
      - CDT1 degradation
      - Geminin
  - Inappropriate origin licensing
    - Consequences of CDT1 over-expression
    - Cell cycle-dependent degradation of CDT1 and geminin prevents re-replication
      - CDT1 degradation
        
        Geminin degradation
    - Consequences of geminin depletion
    - Consequences of re-replication
      - Acute consequences of re-replication: DNA damage and checkpoint activation
      - Long-term consequences of re-replication: induction of genome instability and cancer
    - Future questions
  - Insufficient origin licensing
    - Origin licensing checkpoint
    - Origin licensing defects in higher eukaryotes
      - G1 arrest in normal cells
      - Apoptosis in cancer cells
    - Origin licensing defects in yeast
    - Future questions
  - Acknowledgments
  - References
- Chapter 5 Systems biology approaches bring new insights in the understanding of global gene regulatory mechanisms and their deregulation in cancer
  - Introduction
  - The high-throughput revolution
    - Monitoring global gene expression levels: from cDNA arrays to RNA deep sequencing
    - Genome-wide mapping of binding sites: from PCR microarrays to high-throughput sequencing
    - Bioinformatics approaches: in silico deciphering of transcriptional networks
  - Transcription as a complex gene expression regulatory system
    - Systematic annotation of the genome, or find the common marks for regulation
      - Annotation of functional elements
      - Pol II promoter characterization
    - Structural and mechanistic insights from genome-wide studies
      - Genome-wide chromatin architecture
      - Histone marks and histone variants: transcription in the context of chromatin
      - Mechanistic insight of transcription regulation processes
        
        Mechanisms of action of the transcriptional machinery
        
        Non-productive PIC formation
        
        Transient and permanent regulation of expression
        
        TFIIB new function: gene looping
  - New insights brought by systems biology in the understanding of transcription deregulation in cancer
    - Decipher the oncogenic TF network
      - p53 network
      - The network of the Myc family proteins
    - Expected application of the high-throughput technology in cancer research
  - Acknowledgments
  - References
- Chapter 6 Regulation and dysregulation of protein synthesis in cancer cells
  - Introduction
  - Mechanisms of regulation of protein synthesis
  - Update on protein synthesis factors and cancer
  - Initiation factor eIF4E and the 4E binding proteins
  - Other protein synthesis factors and cancer
    - eIF2
    - eIF2B
    - eIF3
    - eIF4A, 4B and 4G
    - eIF6
  - Signal transduction pathways for control of protein synthesis
  - Significance of mRNA structure
  - Clinical implications
  - Acknowledgments
  - Concluding remarks
  - References
Part 3 Events responsible for aberrant genetic and epigenetic codes in cancer
- Chapter 7 Genomic instability and carcinogenesis
  - Genetic alterations in cancer
    - Historical perspective
    - The scales of instability
      - Mutation, insertion, and deletion
      - Chromosomal rearrangements and aneuploidy
      - Intermediate-scale rearrangements
  - Introduction
  - Causes of genetic instability
    - Aneuploidy, CIN, and MIN
    - The mutator hypothesis
    - Oncogenes and tumor suppressors
    - Genomic integrity during the cell division cycle
      - Ploidy
      - Translocations, chromosome loss, and mutation
  - Effects of genetic instability
    - Multi-hit hypothesis and clonal selection
  - Outlook
  - References
- Chapter 8 Epigenomic code
  - Introduction
  - Techniques to study the epigenome
  - The epigenetic machinery
  - Epigenetic marks in normal cells
  - DNA hypomethylation in cancer
  - Gene silencing in cancer by DNA hypermethylation
  - MiRNAs and cancer
  - Mechanisms leading to DNA hypermethylation in cancer
  - Cancer as a genetic and epigenetic disease
  - Future directions
  - Histone modifications in cancer cells
  - References
- Chapter 9 MicroRNA epigenetic systems and cancer
  - Introduction
  - MicroRNAs and cancer
    - MiRNA biogenesis and mRNA targeting
    - Impaired miRNA biogenesis and cancer
    - MiRNAs as tumor suppressor genes
      - The let-7 family
      - The miR-15a/miR-16 cluster
    - MiRNAs play a direct role in cancer progression
    - MiRNAs as oncogenes
      - miR-17-92 cluster
      - miR-21
    - MiRNAs and metastasis
      - MiRNAs as metastatic inducers
      - MiRNAs as metastatic suppressors
  - MiRNAs and epigenetic machinery
    - MiRNAs as effectors of the epigenetic machinery
    - MiRNAs as targets of the epigenetic machinery
  - MiRNAs and systems biology
    - Gene regulatory networks
    - Cell signaling networks
    - Protein networks
    - Metabolic networks
  - Conclusions
  - References
- Chapter 10 Dietary and environmental influences on the genomic and epigenomic codes in cancer
  - Background
  - Introduction
  - Nutritional genomics and cancer
  - Nutritional epigenomics and cancer
    - Nutrition and epigenetic modifications
    - Epigenetic impacts of dietary bioactive components on cancer
    - Epigenetic impacts of food contaminants and environmental factors on cancer
    - Critical periods for stable epigenetic aberrations
  - Summary and future directions
  - References
Part 4 Functional networks of events that modulate phenotypic manifestation of cancer
- Chapter 11 Regulatory signaling networks in cell transformation and cancer
  - Introduction
  - Signaling pathways involved in cancer
    - Transformation models
      - p53
      - Telomerase
      - PP2A
      - RB
      - RAS
  - Technical tools for the discovery of oncogenes and tumor suppressors
    - Genetic tools
      - Loss-of-function tools
      - Gain-of-function tools
        
        MicroRNAs
        
        ORFs and cDNAs
    - Integration of genomic approaches
  - Concluding remarks
  - References
- Chapter 12 RAS signaling networks
  - Introduction
  - RAS proteins
    - RAS isoforms and their homologies
    - Post-translational modifications for membrane trafficking
  - Regulation of RAS protein activation and inactivation
    - RAS activity regulatory mechanisms
    - RAS-guanine nucleotide exchange factors
    - Signaling networks initiating RAS activation
    - RAS-GTPase-activating proteins
  - Downstream signaling by activated RAS
    - Signaling through PI3Kinase, influencing cell survival and protein translation
    - Signaling through RAF, influencing cell cycle progression and transcription
    - Signaling through PLCepsi, influencing calcium signaling
    - Signaling through RAL GDS, influencing vesicle transport, and cell cycle
  - Mechanisms of aberrant RAS signaling in cancer
    - GAP deletion
    - Mutation or amplification of RAS effectors
      - B-RAF
      - PI3K/AKT
    - RAS-activating mutations
    - Growth factor receptor activation
  - Current anti-cancer therapeutics targeting RAS signaling networks
    - Antisense oligonucleotides
    - Farnesyl transferase inhibitors
    - Kinase inhibitors of RAS effectors
    - Interference with survival pathways (AKT, PKC δ)
    - Inhibitors of upstream activators of RAS (receptor tyrosine kinase inhibitors)
  - References
- Chapter 13 PI3K pathway in cancer
  - Introduction
  - The pathway
  - RAS
  - AKT "master" kinase
  - AKT-independent pathways
  - PI3K pathway in tumors
  - Acknowledgments
  - References
- Chapter 14 TGFβ and BMP signaling in cancer
  - Introduction
  - Smads mediate TGFβ signaling
  - TGFβ synthesis and activation
  - TGFβ signal transduction pathway
  - The bone morphogenetic protein (BMP) signaling pathway
  - TGFβ in cell proliferation and apoptosis
  - TGFβ in development - mouse models
  - TGFβ in immunosuppression
  - TGFβ signaling in cancer progression and metastasis
  - Context and tissue-specific Smad signaling alterations and defective cytostatic responses
  - TGFβ in epithelial to mesenchymal transition (EMT) and cancer stem-like cells (CSCs)
  - The TGFβ signaling pathway as a therapeutic target in cancer
  - Inhibitors
    - Antibodies
    - Antisense oligonucleotides
    - Small-molecule inhibitors
  - Acknowledgments
  - References
- Chapter 15 The Wnt signaling network in cancer
  - Introduction
  - Wnt signaling components and pathways
    - Canonical or Wnt/β-catenin pathway
    - Extracellular and membrane-bound modulators of Wnt signaling
    - Non-canonical or β-catenin-independent Wnt pathways
    - Wnt pathway specificity and Wnt pathway network
  - Wnt signaling in cancer
    - Tumorigenic potential of Wnts in animal models
    - Upregulated Wnt/β-catenin signaling in human tumors
    - Upregulated β-catenin-independent Wnt signaling in human tumors
    - Wnt signaling activation and Wnt network in cancer
  - Delineating the Wnt signaling network through large-scale genetic screens
    - RNAi techniques
    - Wnt/β-catenin assays and readouts
    - Applications to Wnt/β-catenin signaling
  - Defining the Wnt signaling network through interaction proteomics
    - Affinity-purification mass-spectrometry (AP-MS)
    - Protein-protein interactions and complexes
    - Proteomics: fundamentals
    - Yeast two-hybrid (Y2H)
  - The targetome of the Wnt/β-catenin pathway
    - Introduction
    - Methods: how to identify Wnt/β-catenin target genes
      - Differential display PCR (DDRT-PCR)
      - DNA microarray
      - Next-generation sequencing
    - Results of exemplified Wnt/β-catenin targetome studies
      - The transcriptomic side of Wnt
      - The Wnt/β-catenin pathway has a multi-level targetome
      - Target genes differ in time point after activation
      - The regulational side of Wnt
      - The biological side of Wnt
      - Wnt signaling results in a waterfall modification of the transcriptome
      - Wnt targetomes are specific for cell type
    - Conclusions
  - Wnt signaling as target for small interfering molecules
    - Introduction
    - Exemplified molecules interfering with the Wnt pathway
    - Strategies to find new modulators of the Wnt/β-catenin pathway
    - The Wnt pathway and clinical trials
    - Conclusions
  - Omics data analysis and integration
    - Clustering multidimensional data
    - Enrichment analyses
    - Processing omics data
    - Networks
    - Conclusion
    - In silico prediction of Wnt targets
  - Computer simulation of Wnt circuits
    - Introduction
    - Simulation of the Drosophila segment polarity network
    - Simulation of the Wnt/β-catenin pathway
    - Conclusions
      - Outlook
    - Simulation of Wnt pathway oscillatory dynamics and pattern formation
  - Acknowledgments
  - References
- Chapter 16 Apoptotic pathways and cancer
  - Apoptosis proteins
    - Bcl-2 family of proteins
    - Overview
    - Caspase proteases
    - Death domain (DD) superfamily
    - Endonucleases
    - IAPs and their antagonists
  - Introduction
  - Apoptotic pathways
    - The intrinsic pathway
    - Regulation of the intrinsic pathway
    - Crosstalk between the intrinsic and extrinsic pathways
    - Regulation of the extrinsic pathway
    - The extrinsic pathway
  - Integration of proximal apoptotic signals
    - NF-κB and cytokine-induced apoptosis
    - p53 and genotoxic stress-induced apoptosis
    - FoxO and growth factor deprivation-induced apoptosis
  - Deregulation of apoptosis in cancer
    - Alterations in the proximal regulators
    - Deregulation of the intrinsic pathway in cancer
    - Deregulation of the extrinsic pathway in cancer
  - Apoptosis modulation for cancer therapy
    - Exploiting the intrinsic pathway for cancer therapy
    - Exploring the extrinsic pathway for cancer therapy
    - Other proapoptotic cancer therapies
  - Acknowledgments
  - Conclusion
  - References
- Chapter 17 Molecular links between inflammation and cancer
  - Introduction
  - Orchestrating cancer-related inflammation: transcription factors
  - Orchestrating cancer-related inflammation: cytokines and chemokines
  - An intrinsic and an extrinsic pathway link inflammation and cancer
  - Acknowledgments
  - Overview
  - References
- Chapter 18 Cancer metastasis
  - Introduction
  - Metastasis as a complex, multistep event
  - Intravasation
  - Extravasation
  - Colonization
  - Organ-specific metastasis
  - Cancer therapies directed at metastasis
  - Conclusion
  - References
- Chapter 19 Cancer metabolism
  - Introduction
  - Enhanced glucose metabolism is a central feature of cancer cell metabolism
  - Metabolic reprogramming mediates flux of glucose carbons to anabolic pathways for proliferation and survival
  - The fate of glycolytic metabolites
  - The pentose phosphate pathway
  - The impact of mitochondrial metabolism changes in cancer
  - Glutamine requirements for cancer cell proliferation
  - Analytical and computational frameworks for studying cancer metabolism
  - General considerations
  - Conclusion
  - References
- Chapter 20 Tumor microenvironment: blood vascular system in cancer metastasis
  - Blood vascular system in the pathogenesis of cancer metastasis
    - Blood vascular system in the spread of cancer cells
    - Blood vascular system in organ-specific metastasis
  - Introduction
  - Blood vascular system associated factors/events that play a role in cancer metastasis
    - Vascular pathways
    - Cellular and non-cellular components of blood
      - Cellular components
      - Leukocytes
      - Platelets
      - Non-cellular components of blood
    - Blood vessels
      - Neovascularization/angiogenesis
      - Endothelial cells
      - Pericytes
      - Endothelial basement membrane
  - Therapeutic prospects
  - Acknowledgments
  - Epilogue
  - References
Part 5 Current state of the evolving MMMN cancer progression models of cancer
- Chapter 21 Genetic alterations in glioblastoma multiforme
  - Introduction
  - Large-scale genetic changes
  - Mutations in genetic pathways
    - Receptor tyrosine kinase pathways
      - EGFR pathway
      - VEGFR pathway
      - Growth factor networks
      - PDGFR pathway
      - TòRI pathway
    - PI3K/AKT pathway
      - PI3K
      - PTEN
      - AKT
      - Ras
      - STAT
    - p53 pathway
      - TP53
  - p14ARF/MDM2/MDM4
    - RB1 pathway
  - Other mutations
    - MGMT
    - NF1
  - Newly identified pathways
    - Isocitrate dehydrogenases
    - Stem cells
    - Future paths
  - References
- Chapter 22 Breast cancer
  - Epidemiology
  - Introduction
  - Pathological classification of breast cancer
  - Molecular classification of breast cancer
  - Mutational landscape of breast cancer genomes
  - The cell of origin
  - Breast cancer stem cells
  - Metastasis
  - Summary and outlook
  - Treatment
  - References
- Chapter 23 The role of growth factor-induced changes in cell fate in prostate cancer progression
  - Introduction
  - Prostate gland development and prostate cancer
  - Epithelial-mesenchymal transition (EMT)
  - Models to study EMT and invasion of prostate cancer
  - Aberrant expression of epithelial and mesenchymal markers in prostate cancer
  - Deregulation of EMT-inducing transcription factors in prostate cancer
    - SNAIL genes
    - TWIST
    - ZEB genes
  - Influence of growth factor-induced signaling on cell fates and prostate cancer progression
    - Hedgehog (Hh)
    - Wnt ligands
    - Transforming growth factor-ò family
    - Fibroblast growth factors
  - Epidermal growth factor
    - Insulin-like growth factors
  - Conclusion
  - References
- Chapter 24 Colon cancer
  - Etiology, staging, screening, and therapy
    - Etiology
    - Familial vs. sporadic colorectal cancer
    - Screening
    - Staging
    - Therapy
  - Introduction
  - Molecular basis of colorectal cancer
    - APC/β-catenin pathway
    - PIK3CA/PTEN pathway
    - Ras/Raf pathway
    - Genomic instability
    - TGF-βRII/SMAD pathway
    - TP53/BAX pathway
    - Epigenetic abnormality
      - Systems biology approach
    - Genomics of colorectal cancer
    - Metabolomics of colorectal cancer
    - Proteomics of colorectal cancer
    - Transcriptomics of colorectal cancer
  - Conclusion and perspective
  - References
- Chapter 25 Biology of human stomach cancer
  - Epidemiology
    - Associated host genotypes
    - Pathology classification
  - Introduction
  - Inherited susceptibility
    - Familial clustering
    - Hereditary diffuse gastric cancer (HDGC)
    - Hereditary non-polyposis colorectal cancer (HNPCC)
    - Li-Fraumeni and Peutz-Jeghers syndromes
    - Adenomatous polyposis syndromes
    - Other syndromes
  - Molecular alterations
    - Chromosomal instability
    - Microsatellite instability
  - Acquired somatic alterations
    - E-cadherin alteration
    - TFF1 loss
    - c-MET overexpression
    - FHIT alterations
    - Kinases/phosphatases
    - p53 mutations
    - Apoptosis signaling alterations
    - Growth factor alterations
    - Methylation silencing alterations
    - Angiogenesis signaling alterations
    - Other alterations
  - Molecular profiling: prognostic and diagnostic markers
    - Chemosensitization markers
    - Serum markers
  - Potential targets for treatment and intervention
  - References
- Chapter 26 Pancreatic cancer
  - Introduction
  - The proposed progression model of pancreatic cancer
  - Molecular genetics of pancreatic cancer
  - The multimodal molecular network (MMMN) and pancreatic cancer
  - Impact of high-throughput genomic approaches on systems biology of PDA
  - Informatics support for systems biology of PDA
  - Future directions in PDA systems biology research
  - References
- Chapter 27 Deregulated signaling networks in lung cancer
  - Introduction
  - Lung morphogenesis and histopathology
    - Lung histology
    - Regulation of lung development
    - Lung cancer pathophysiology
  - Lung cancer genomics
    - Genetic driver mutations and alterations
    - The lung cancer genome
    - Epigenetic alterations
    - Non-coding RNAs
    - Molecular subtype classification of lung cancer
  - Deregulated signaling networks in lung cancer
    - Oncogenic RAS signaling
    - RTK signaling
    - PI3K/mTOR signaling
    - Developmental gene regulatory networks
  - Therapeutic strategies in lung cancer treatment
    - Exploiting oncogene "addiction"
    - Cancer genomics and personalized medicine
    - Drug resistance
  - Conclusions
  - References
- Chapter 28 Modular signaling in hematopoietic malignancies
  - Introduction
  - Acute myeloid leukemia: a malignancy that requires the combined effect of at least two classes of mutations
  - AML fusion proteins: more than just arrest of differentiation
  - Role for HOXA homeobox proteins in MLL-translocation leukemias
  - Assessing response of AML blasts to cytokines by phosphoflow cytometry predicts response to therapy
  - Dyregulated NF-κB signaling in multiple myeloma
  - Dysregulated NF-κB signaling in DLBCL
  - Bcl6-mediated ATR and BLIMP repression critical for BCR-type DLBCL
  - Dysregulated NF-κB signaling in MALT lymphomas
  - Burkitt's lymphoma: escape from Myc-driven apoptosis
  - CLL tumor suppressors: the del13q14 controversy
  - CLL: poised for death, rescued by BCR signaling?
  - Conclusion
  - References
Part 6 Applications of comprehensive cancer progression models in the fight against cancer
- Chapter 29 Role of network biology and network medicine in early detection of cancer
  - Introduction
    - New era of molecular markers of early detection
    - Types of biomarkers for cancer research
      - Clinical validation of biomarkers
      - Predictive (stratification) biomarkers
      - Prognostic biomarkers
      - Screening biomarkers (diagnostic)
      - Surrogate end point biomarkers
    - Importance of early detection
    - Overdiagnosis and risk stratification
    - Network biology, network medicine, and biomarker discovery
    - Cancer: a systems biology disease paradigm
    - Mode of action network identification
    - Role of modularity in biologic network connectevity
    - Sub-network approach to gene expression profiles
  - Summary
  - References
- Chapter 30 Systems biology in cancer biomarkers for early detection, diagnosis, and prognosis
  - Definition of systems approach
  - Introduction
  - What is systems biology now?
  - Systems approach to biomarker research?
  - Systematic approach to the development of diagnostic biomarkers
    - Wet lab discovery
    - In silico discovery from data mining
  - Future roles of systems biology in cancer biomarker discovery and validation
  - System screening
  - References
- Chapter 31 Prognosis of cancer
  - Historical perspectives
  - Introduction
  - General prognostic factors
  - General prognostic histological biomarkers
    - Tumor grade
    - Intra-tumoral lymphocytic infiltration
    - Tumor stage
    - Epithelial-mesenchymal transition tumor phenotype (EMT)
  - Oncogenes
    - KRAS (KI-RAS2 Kirsten rat sarcoma viral oncogene homolog)
    - BRAF (v-raf-1 murine leukemia viral oncogene homolog B1)
    - MYC (myelocytomatosis viral oncogene homolog)
    - p53
    - PI3KCA/PTEN
    - Ataxia-Telangiectasia-Mutated (ATM)
    - Breast cancer susceptibility gene (BRCA) mutation
    - Excision repair cross-complementing rodent repair deficiency, complementation group 1 (ERCC1)
  - Altered cellular metabolism
    - Thymidylate synthase (TS)
    - Des-γ-carboxy prothrombin (DCP)
  - Cell surface receptor expression
    - CXCR4
    - Epidermal growth factor receptor (EGFR)
    - HER2 (Human epidermal growth factor receptor type 2)
  - Oncofetal serum biomarkers
    - Cancer antigen 125 (CA-125)
    - Carcinoembryonic antigen (CEA)
    - Cancer antigen (CA 15-3)
    - Cancer antigen 19-9 (CA 19-9)
    - Alpha-feto-protein (AFP)
    - Human chorionic gonadotropin (hCG)
  - Role of imaging in cancer prognosis
    - CT (computed tomography)
    - Functional tumor imaging with PET (positron emission tomography)
    - Role of adjunct imaging with MRI
  - Future directions
  - References
- Chapter 32 Cancer pharmacogenomics: challenges, promises, and its application to cancer drug discovery
  - Introduction
  - Recent advances in cancer genomics and pharmacogenomics
    - Advances in genomics data generation
    - Advances in data mining and exploitation
    - Cancer genomics' impact on disease understanding
    - Impact of cancer pharmacogenomics in drug discovery and developments
      - Personalized medicine
      - Cancer cell line panels as important discovery platform for personalized medicine strategy development
  - Discussion
  - Acknowledgment
  - References
Index
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