Immunological Implications and Molecular Diagnostics of Genitourinary Cancer

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Immunological Implications and Molecular Diagnostics of Genitourinary Cancer
Copyright Page
Contents
List of contributors
About the editor
Preface
Acknowledgments
Editorial advisory board
Editorial management committee
1 Introduction to the molecular aspects and viral therapy of genitourinary tumors
1.1 Background
References
2 Liquid biopsy of exosome markers for molecular diagnosis of genitourinary cancer
2.1 Introduction
2.2 Tissue biopsy versus liquid biopsy
2.3 Renal cell cancer
2.4 Bladder cancer
2.5 Prostate cancer
2.6 Conclusion
References
3 The molecular mechanism of novel oncogenes dysregulating signaling pathways associated with cervical carcinoma
3.1 Introduction
3.2 Cervical cancer overview
3.2.1 Epidemiology of cervical cancer
3.2.2 Anatomopathology of the cervix
3.2.3 The different cancers of the cervix
3.2.4 Risk factors of cervical cancer
3.3 The leading oncogenes related to cervical cancer development
3.3.1 Calponin 3
3.3.2 Antisilencing function 1B
3.3.3 Long noncoding RNA colorectal neoplasia differentially expressed
3.3.4 Proline-rich Protein 11
3.4 Conclusion
Acknowledgment
References
4 Role of epigenetic factors in cancer progression induced by inactivation of tumor suppressors genes
4.1 Introduction
4.2 Methylation of DNA
4.3 Histone code
4.4 The microRNAs
4.5 Conclusion
Acknowledgment
References
5 Exosomes as diagnostic and prognostic tools in prostate cancer
5.1 Introduction
5.2 Structure, biogenesis, and function of exosomes
5.2.1 Structure and biogenesis of exosomes
5.2.2 Functions of exosomes
5.3 The functional roles and tumor-derived exosomes in prostate cancer progression
5.3.1 The diagnosis potential of exosomes in prostate cancer
5.3.2 Future directions and applications of exosomes in prostate cancer
Acknowledgments
References
6 Adenovirus vectors for vaccination and cancer gene therapy
6.1 Introduction
6.2 Several approaches to overcome problems associated with the targeting of adenoviruses
6.3 General properties of adenovirus and adenovirus vector
6.4 Adenovirus tumor-selective replication
6.5 Genetic modification to alter transfection range of adenoviruses
6.5.1 1-Insertion of foreign ligand into fiber protein
6.5.2 2-Fiber mutation for generating targeted adenoviruses
6.5.3 3-Fiber exchange
6.5.4 4-Modification of other capsid proteins
6.6 Conclusion
Acknowledgment
References
7 Molecular diagnosis of human oncogenic viruses associated with prostate cancer: Human Papillomavirus and Epstein–Barr virus
7.1 Introduction
7.2 Molecular epidemiology of human papillomavirus and Epstein–Barr virus associated with prostate cancer worldwide
7.2.1 Prostate cancer
7.2.2 Human papillomavirus and prostate cancer
7.2.3 Epstein–Barr virus
7.2.4 Human papillomavirus and Epstein–Barr virus coinfection
7.3 Molecular diagnosis and prognostic biomarkers of prostate cancer
7.3.1 Blood biomarkers
7.3.1.1 Prostate-specific antigen
7.3.1.2 Prostate health index
7.3.1.3 4Kscore
7.3.1.4 Serum protein panel
7.3.2 Urinary biomarker
7.3.2.1 PCa antigen
7.3.2.2 Fusion TMPRSS2-ERG
7.3.3 Tissue biomarker
7.3.3.1 PTEN gene
7.3.3.2 ConfirmMDx
7.3.3.3 Oncotype DX Genomic Prostate Score
7.3.3.4 ProMark
7.3.4 Exosomes as a diagnostic and prognostic tool for prostate
7.3.4.1 Exosomal biomarkers
7.3.4.2 Cellular factors promoting the emergence and development of tumors via exosomes in cells infected with Epstein–Barr...
7.4 Conclusion
References
8 Molecular characterization of oncogenic biomarkers associated with genitourinary cancers: the case of prostate cancer
8.1 Introduction
8.2 General information about prostate cancer
8.2.1 Definition
8.2.2 Carcinogenesis
8.2.3 Tumor development
8.2.4 Epidemiology of prostate cancer
8.2.4.1 Epidemiology of prostate cancer on a global scale
8.2.4.2 Epidemiology of prostate cancer in Africa
8.2.4.3 Epidemiology of prostate cancer in Morocco
8.3 Tumor development
8.3.1 Risk factors for prostate cancer
8.3.1.1 Family history
8.3.1.2 Hormonal and other growth factors
8.3.1.2.1 Androgens
8.3.1.2.2 Vitamin D and its receptor
8.3.1.2.3 Insulin growth factor 1
8.3.1.3 Environmental factors: diet and other factors
8.3.1.3.1 Foods at risk
8.3.1.3.2 Protective foods
8.3.1.4 Other factors
8.3.2 Genetic mutations responsible for prostate cancer
8.3.2.1 HOXB13 variants
8.3.2.2 Mutations in the BRAF gene
8.4 Methods for studying genetic polymorphisms
8.4.1 Classical genotyping methods
8.4.1.1 High-throughput genotyping
8.4.1.1.1 Spoligotyping
8.4.1.2 VNTR typing
8.4.1.3 Double-repetitive-element-polymerase chain reaction
8.4.1.4 Biochips, multiparametric biosensors
8.4.1.4.1 Biosensors
8.4.1.5 DNA chips and oligonucleotide chips
8.4.1.6 Protein chips
8.5 Conclusion
Acknowledgments
References
9 Diagnostic screening of the microdeleation mutations in the azoospermia factor-gene cluster of the Y chromosome and; pros...
9.1 Background for our hypothesis on the azoospermia factor gene cluster among Arabs for future gene therapy of infertility
9.2 Landscape of the azoospermia factor gene cluster and chromosome Y chromosome structure
9.3 Global heterogeneity and ethnicity of familial infertility clustering of azoospermia factor microdeletion variants amon...
9.4 Familial infertility clustering and consanguinity among Arabian populations
9.5 Diagnostic criteria and medical conditions as set by WHO criteria for infertility diagnosis
9.6 Types of microdeletions in the azoospermia factor gene cluster of Y chromosome
9.7 Genetic diagnosis of azoospermia factor microdeletion by multiplex polymerase chain reaction technology
9.7.1 Clinical conditions
9.7.2 Multiplex polymerase chain reaction protocol to be used in diagnosis of the azoospermia factor microdeletions of Y ch...
9.7.3 Ethical criteria and consideration adopted for blood samples and YDNA
9.7.4 Clinical criteria and the practical cut-off value for azoospermia factor testing
9.7.5 Practical recommendations for inclusion criteria and stratification of Azoospermia
9.7.6 Commercial kits available in the market to be used
9.7.6.1 Promega kit for DNA extraction from blood samples
9.7.6.2 Devyser azoospermia factor 2 for azoospermia factor microdeletion detection
9.8 Influence of the use of in vitro fertilization technology
9.9 Gene therapy application of azoospermia factor gene in different genealogical lineages of the Y-chromosome
References
10 Recent advances in high-risk human papillomavirus genotype relationship with bladder cancer tumor genesis
10.1 Introduction
10.2 Human papillomaviruses
10.3 Epidemiology of bladder cancer
10.4 Global prevalence of human papillomavirus in bladder cancer
10.4.1 Prevalence of high-risk human papillomavirus by histological type
10.4.1.1 Transitional cell carcinoma or urothelial carcinoma
10.4.1.2 Squamous cell carcinomas
10.4.1.3 Other histological types of bladder cancer
10.5 Recent evidence for high-risk human papillomavirus involvement in bladder cancer
10.5.1 Integration of human papillomavirus DNA
10.5.2 Human papillomavirus and p16 overexpression status in bladder cancer
10.5.3 Pathological clinical course
10.5.3.1 Passage of a guard and upper stage
10.5.3.2 Human papillomavirus status and bladder cancer recurrence
10.6 Detection of human papillomavirus infection in bladder cancer
10.7 Human papillomavirus treatment and prevention
10.8 Conclusion
References
11 Tumor-associated macrophages in prostate cancer: role in progression and therapy
11.1 Introduction
11.2 Prostate cancer initiation, progression, and immunity
11.3 Cancer and macrophage
11.4 Tumor-associated macrophages and prostate cancer
11.4.1 Prostate cancer progression and tumor-associated macrophage
11.4.2 Tumor-associated macrophages as mediators of immunosuppression in prostate cancer
11.4.3 Prostate cancer stem cells and tumor-associated macrophage
11.4.4 Tumor-associated macrophages and angiogenesis in prostate cancer
11.4.5 Role of tumor-associated macrophages in Extracellular matrix (ECM) remodeling, invasion, and metastasis
11.4.6 Chemo- and radio-resistance in prostate cancer and tumor-associated macrophage
11.4.7 Therapeutic implication of macrophages in prostate cancer
11.4.8 Macrophage-mediated prostate cancer cytotoxicity
11.4.8.1 Regulation of macrophage polarization
11.4.8.2 Strategies modulating macrophage recruitment
11.4.8.3 Inhibitory strategies against tumor-associated macrophage
11.4.8.4 Gene modification in macrophage
11.5 Conclusion
Acknowledgment
References
12 Emerging therapeutic targets of genitourinary tumors
12.1 Introduction
12.2 PD-1
12.3 Von Hippel–Lindau tumor suppressor/HIF2-vascular endothelial growth factor
12.4 Vascular endothelial growth factor receptor
12.5 Indoleamine-2,3-dioxygenase
12.6 Androgen receptor
12.7 Conclusion
References
13 Cell–cell differentiation induction: model for cervical cancer
13.1 Introduction
13.2 Cervical cancer
13.2.1 Epidemiology of cervical cancer
13.2.2 Anatomopathology of the cervix
13.2.3 Risk factors of cervical cancer
13.3 Overview of cellular differentiation
13.3.1 Principle of cell differentiation
13.3.1.1 Universal cell differentiation markers
13.3.1.2 Specific cell differentiation markers
13.3.2 Correlation between cell growth and cell differentiation
13.3.3 Cellular models for the study of proliferation and differentiation
13.3.3.1 Myoblasts
13.3.3.2 Differentiation of myoblasts
13.3.4 Virus interaction and cell proliferation/differentiation
13.4 Cell differentiation study methods
13.5 Tumor differentiation: case of cervical cancer
13.5.1 Generality of tumor differentiation
13.5.2 Cell differentiation of cervical carcinoma
13.6 Conclusion
Acknowledgment
References
14 The clinical significance of long noncoding RNAs expression in cervical cancers
14.1 Introduction
14.2 Long noncoding RNAs as potential biomarker candidates
14.2.1 Long noncoding RNAs s as biomarkers for screening of cervical cancer
14.3 Long noncoding RNAs as biomarkers for diagnosis and early detection of cervical cancers
14.4 Long noncoding RNAs as biomarkers of prognosis and survival
14.5 Long noncoding RNAs in cervical cancer treatment and therapy
14.5.1 Long noncoding RNAs in resistance to treatment of cervical cancer
14.5.2 Long noncoding RNAs in cervical cancer therapy
14.6 Conclusions
Acknowledgment
References
15 Triple-negative breast cancer and its correlation with viral agents
15.1 Introduction
15.2 Breast cancer presentation
15.2.1 Histological types of breast cancer
15.2.1.1 Ductal carcinoma in situ
15.2.1.2 Lobular carcinoma in situ
15.2.1.3 Invasive ductal carcinoma
15.2.1.4 Invasive lobular carcinoma
15.2.1.5 Metaplastic carcinoma
15.2.1.6 Inflammatory breast cancer
15.2.1.7 Metastatic breast cancer
15.2.2 Stages of breast cancer
15.2.3 Molecular types of breast cancer
15.3 A focus on triple-negative breast cancer
15.4 Risk factors associated with triple-negative breast cancer
15.5 Implications of viral agents in triple-negative breast cancer
15.6 The special case of triple-negative breast cancer
15.7 Treatment modalities of triple-negative breast cancer
15.7.1 Current treatment strategies and limitations
15.8 Natural anticancer agents in triple-negative breast cancer
15.9 Conclusion
Acknowledgments
References
16 Role of exosomes in bladder cancer diagnosis and therapy
16.1 Introduction
16.2 Exosomes: nanovesicles of endosomal origin
16.2.1 Exosome heterogeneity
16.2.2 Functions of exosomes
16.2.3 Roles of exosomes in bladder cancer
16.3 Urinary biomarkers for bladder cancer diagnosis
16.3.1 Exosomes therapy applications for bladder cancers
16.4 Conclusions
Acknowledgments
References
17 Upper urinary tract urothelial cell carcinoma
17.1 Introduction
17.2 Epidemiology
17.2.1 Frequency
17.2.2 Age
17.2.3 Sex
17.2.4 Risk factors—ethiopathogenesis
17.2.4.1 Tobacco
17.2.4.2 Occupational origin
17.2.4.2.1 Aromatic amines
17.2.4.2.2 Chlorinated solvents
17.2.4.3 Drug origin
17.2.4.3.1 Abuse of analgesics (phenacetin)
17.2.4.3.2 Cyclophosphamide and ifosfamide
17.2.4.4 Heredity
17.2.4.5 Other factors
17.2.4.5.1 Lithiasis
17.2.4.5.2 Urinary tract infections
17.2.4.5.3 Aristolochic acid nephropathy (Balkan endemic nephropathy and Chinese herbal nephropathy)
17.2.4.5.4 Blackfoot disease
17.2.4.6 History of bladder tumor: in 20%–30% of patients with upper tract urothelial carcinomas
17.2.4.6.1 Anatomopathology
17.2.4.7 Clinical
17.2.4.7.1 Circumstances of discovery
17.2.4.8 Paraclinical
17.2.4.8.1 Imaging
17.2.4.8.2 Endoscopy
17.2.4.9 Preoperative prognostic factors
17.2.4.10 Treatment
17.2.4.10.1 Localized upper tract urothelial carcinomas
High-risk upper tract urothelial carcinomas
17.2.4.10.2 Metastatic disease
17.3 Surveillance
References
18 Testicular cancer
18.1 Introduction
18.2 Clinical presentation
18.3 Investigations
18.3.1 Serum tumor markers
18.3.2 Imagery
18.3.2.1 Scrotal doppler
18.4 Abdomino-pelvic and thoracic imaging
18.5 Surgical management
18.6 Retroperitoneal lymphadenectomy for staging
18.7 Treatment after RPLND or residual mass resection
References
19 A comprehensive survey on spectrum of BRCA1 and BRCA2 pathogenic variants in breast and ovarian cancer
19.1 Introduction
19.2 BRCA1
19.3 BRCA2
19.4 BRCA-associated breast and ovarian cancer
19.5 BRCA1 and BRCA2 genes mutations in breast and/or ovarian cancer
19.6 BRCA1 and BRCA2 recurrent/founder variants in North Africa
19.7 BRCA1 and BRCA2 recurrent/founder variants worldwide
19.8 BRCA1- and BRCA2-specific variants in North Africa and Worldwide
References
20 Molecular and epidemiological characterization of bladder tumors
20.1 Introduction
20.2 Anatomy of the urinary system
20.2.1 Kidneys
20.2.2 Urinary tract
20.2.3 Bladder
20.3 Bladder cancer
20.3.1 Epidemiology
20.3.2 Risk factors for bladder cancer
20.3.3 The diagnosis
20.4 Six-molecular characterization of bladder tumors
20.4.1 Point mutations
20.4.1.1 RAS family genes
20.4.1.2 The FGFR3 gene
20.4.1.3 The p53 gene
20.5 Chromosomal aberrations
20.5.1 Epigenetic aberrations
20.6 Conclusion
Acknowledgments
References
21 Impact of signaling in the development pathway of genitourinary cancers
21.1 Introduction
21.2 General principles of cell signaling
21.3 Impact of androgen receptor alterations on signaling pathways related to cell differentiation and prostate cancer prog...
21.3.1 Androgen receptor
21.3.1.1 Genomic signaling pathway of the androgen receptor
21.4 Oncogenic alterations
21.4.1 Sphingosine kinase 1/sphingosine 1-phosphate
21.4.1.1 The sphingosine kinase 1/sphingosine 1-phosphate signaling pathway
21.5 Oncogenic alterations
21.5.1 Bone metastases of prostate cancer
21.6 Growth factor signaling pathway
21.7 Oncogenic alterations
21.7.1 Phosphatidylinositol-3-kinase
21.7.1.1 Phosphatidylinositol-3-kinase signaling pathway
21.8 Oncogenic alterations
21.9 Conclusion
21.10 Acknowledgments
References
22 Prostate cancer: genetic changes and viral-mediated immune regulation
22.1 Introduction
22.2 Epidemiology of prostate cancer
22.3 Viruses associated with prostate cancer
22.3.1 Human papillomavirus
22.3.2 Herperviruses
22.3.3 BK
22.3.4 XMRV
22.4 Carcinogenesis of the prostate: interaction between host genetics and viral infection
22.5 Viral-mediated immune deregulation
22.5.1 RNASEL (Ribonuclease L)
22.5.2 Toll-like receptors
22.5.2.1 Macrophage inhibitory cytokine 1
22.5.2.2 Interleukin-1 receptor antagonist
22.5.3 Other genes linked to inflammation
22.6 Conclusion
Acknowledgment
References
23 Dramatic impact of partial loss of PTEN function on tumorigenesis and progression of prostate cancer
23.1 Introduction
23.1.1 Gross Anatomical Features
23.1.1.1 The prostatic epithelium
23.1.1.2 Epithelial cells
23.1.1.3 Neuroendocrine cells
23.1.1.4 Basal cells
23.1.1.5 The prostatic stroma
23.2 Epidemiology
23.3 The PI3K/Akt signaling pathway
23.4 Changes in PTEN activity in health and disease
23.5 Posttranscriptional regulation of PTEN by noncoding RNAs
23.6 Posttranslational modification: phosphorylation
23.7 Posttranslational modification: ubiquitination
23.8 Other ubiquitin-like modifications: SUMOylation and ISGylation
23.8.1 Posttranslational modification: oxidation
23.8.2 Posttranslational modification: acetylation
23.9 PTEN loss in prostate cancer
23.9.1 Tumor PTEN affects immune infiltration
23.9.2 Various genetic aberrations in the PI3K-AKT-mTOR pathway in prostate cancer
23.10 Conclusion
Acknowledgment
References
24 Association between glucose consumption and cancer development: prostate cancer and bladder cancer
24.1 Introduction
24.2 Glycose metabolism
24.2.1 General scheme of dietary carbohydrate assimilation
24.2.2 Carbohydrate catabolism
24.2.3 Glycolysis (or Embden–Meyerhof pathway)
24.3 Regulation of glucose metabolism in cancer cells
24.3.1 Activation of hypoxia-inducible factor drives increased glycolysis
24.3.2 Glucose consumption in prostate cancer
24.3.3 Metabolic mechanisms in prostate cancer
24.3.3.1 PGC-1α and glucose metabolism
24.3.3.2 PGC-1α in prostate cancer
24.3.4 Androgens reprogram prostate cancer cell metabolism
24.3.5 Glucose consumption in bladder cancer
24.3.6 Metabolic mechanisms in bladder cancer
24.4 Conclusion
Acknowlegment
References
25 Oncogenic human viruses associated with prostate cancer: molecular epidemiology of Human Papillomavirus and Epstein–Barr...
25.1 Introduction
25.1.1 History, taxonomy, and classification of human papillomavirus and Epstein–Barr virus
25.2 Molecular epidemiology of human papillomavirus and Epstein–Barr virus associated with prostate cancer worldwide
25.2.1 Epidemiology of prostate cancer worldwide
25.2.2 Human papillomavirus and prostate cancer
25.2.3 Epstein–Barr virus
25.2.4 Epidemiology of human papillomavirus and Epstein–Barr virus coinfection
25.3 Implications and associations of human papillomavirus and Epstein–Barr virus prostate cancer
25.3.1 Coinfection of human papillomavirus and Epstein–Barr virus
25.4 Conclusion
References
26 Genitourinary cancers immune biomarkers: a comprehensive overview
26.1 Introduction
26.2 Immune response in urogenital cancers
26.3 Immunotherapy of urogenital cancers
26.3.1 Checkpoint’s inhibitors
26.3.1.1 Anti-PD-1/ anti-PD-L1
26.3.1.2 Anti-cytotoxic T lymphocyte-associated protein 4 antibodies
26.3.2 Bacillus Calmette–Guerin
26.3.3 Monoclonal antibodies
26.3.4 Combined Therapies
26.3.5 Other therapies
26.3.6 Perspectives
26.3.7 Alternative therapies
26.4 Prostate and bladder cancers biomarkers
26.5 Renal cell carcinoma biomarkers
26.5.1 Pathologic and molecular subtypes of renal cell carcinoma
26.5.1.1 Kidney cancer biomarkers
26.5.1.1.1 Single-nucleotide polymorphisms
26.5.1.2 MicroRNA
26.5.1.3 The change in the DNA
26.5.1.4 DNA methylation
26.6 Recent trends in antitumor vaccines
References
27 The global genomic allelic heterogeneity of the HOXB 13 variants of prostate cancer and gene therapy application for dif...
27.1 Introduction
27.2 Background and hypothesis on the prostate cancer allelic heterogeneity associated with the genealogical lineages of po...
27.3 The landscape of the HOXB 13 gene cluster on chromosome 17
27.4 The landscape of the Short tandem repeat microsatellite on the nonrecombined region of the Y-chromosome
27.4.1 Characteristics of the short tandem repeat microsatellites of Y-chromosome and its application in human ancestry and...
27.4.2 Application of the Y-short tandem repeats in human ancestry and different genealogical lineages
27.4.3 Global studies on short tandem repeat of different genealogical lineages of ancestry
27.5 Global allelic heterogeneity of the HOXB 13 variants of prostate cancer among different genealogical lineages of popul...
27.6 Practices on the genetic diagnosis of the haplotypes of microsatellite short tandem repeats and the haplogroups of gen...
27.6.1 Human genomic DNA extraction and purification
27.6.2 Protocol optimization details for short tandem repeats analysis are as follows
27.6.3 Quality control and DNA purity
27.6.4 Protocol optimization for DNA amplification polymerase chain reaction
27.6.5 Genotyping of the short tandem repeat alleles on genetic analyzer and data analysis
27.6.5.1 World Health Organization online data on the global prevalence of prostate cancer
27.7 Practices on the genetic diagnosis of prostate cancer
27.7.1 Genotyping of the Y-chromosome short tandem repeats and haplogroup lineage prediction
27.7.2 Data deposition and availability in the international gene/banks
27.8 Gene therapy applications and future challenges against prostate cancer in different ethnicities of Y-chromosome
References
28 Impact of vitamin D status on breast cancer prognosis
28.1 Introduction
28.2 Vitamin D
28.2.1 Intakes of vitamin D
28.2.2 Vitamin D metabolism
28.2.3 Target cells
28.3 Vitamin D and breast cancer relationship
28.3.1 Vitamin D pathophysiology and link to cancer
28.3.2 Sun exposure and breast cancer relationship
28.3.3 Link between vitamin D-rich diet and breast cancer
28.3.4 Vitamin D supplementation and breast cancer relationship
28.3.5 Link between total vitamin D intake and breast cancer
28.3.6 Link between serum 25(OH)D and breast cancer
28.4 Vitamin D and breast cancer prognosis
28.4.1 Vitamin D and local breast cancer recurrence
28.4.2 Vitamin D and metastatic spread of breast cancer
28.4.3 Breast cancer survival and vitamin D
28.4.4 Prognosis of vitamin D and breast cancer by hormonal status (menopausal and nonmenopausal)
28.4.4.1 Postmenopausal women
28.4.4.2 Women in premenopause
28.4.5 Vitamin D and breast cancer prognosis by tumor hormone receptor status
28.5 Conclusion
References
Index
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