Book contents
- Frontmatter
- Dedication
- Contents
- List of Contributors
- Preface
- Part 1.1 Analytical techniques: analysis of DNA
- Part 1.2 Analytical techniques: analysis of RNA
- Part 2.1 Molecular pathways underlying carcinogenesis: signal transduction
- Part 2.2 Molecular pathways underlying carcinogenesis: apoptosis
- Part 2.3 Molecular pathways underlying carcinogenesis: nuclear receptors
- Part 2.4 Molecular pathways underlying carcinogenesis: DNA repair
- Part 2.5 Molecular pathways underlying carcinogenesis: cell cycle
- Part 2.6 Molecular pathways underlying carcinogenesis: other pathways
- Part 3.1 Molecular pathology: carcinomas
- 42 Head and neck cancer
- 43 Lung cancer
- 44 Esophageal cancer
- 45 Gastric cancer
- 46 Small-bowel tumors: molecular mechanisms and targeted therapy
- 47 Colon and rectal cancer
- 48 Pancreatic cancer
- 49 Hepatocellular carcinoma
- 50 Renal-cell carcinomas
- 51 Bladder cancer
- 52 Prostate cancer
- 53 Targeted therapies in breast cancer
- 54 Molecular targets for epithelial ovarian cancer
- 55 Testicular cancer: germ-cell tumors (GCTs)
- 56 Cervical cancer
- Part 3.2 Molecular pathology: cancers of the nervous system
- Part 3.3 Molecular pathology: cancers of the skin
- Part 3.4 Molecular pathology: endocrine cancers
- Part 3.5 Molecular pathology: adult sarcomas
- Part 3.6 Molecular pathology: lymphoma and leukemia
- Part 3.7 Molecular pathology: pediatric solid tumors
- Part 4 Pharmacologic targeting of oncogenic pathways
- Index
- References
52 - Prostate cancer
from Part 3.1 - Molecular pathology: carcinomas
Published online by Cambridge University Press: 05 February 2015
- Frontmatter
- Dedication
- Contents
- List of Contributors
- Preface
- Part 1.1 Analytical techniques: analysis of DNA
- Part 1.2 Analytical techniques: analysis of RNA
- Part 2.1 Molecular pathways underlying carcinogenesis: signal transduction
- Part 2.2 Molecular pathways underlying carcinogenesis: apoptosis
- Part 2.3 Molecular pathways underlying carcinogenesis: nuclear receptors
- Part 2.4 Molecular pathways underlying carcinogenesis: DNA repair
- Part 2.5 Molecular pathways underlying carcinogenesis: cell cycle
- Part 2.6 Molecular pathways underlying carcinogenesis: other pathways
- Part 3.1 Molecular pathology: carcinomas
- 42 Head and neck cancer
- 43 Lung cancer
- 44 Esophageal cancer
- 45 Gastric cancer
- 46 Small-bowel tumors: molecular mechanisms and targeted therapy
- 47 Colon and rectal cancer
- 48 Pancreatic cancer
- 49 Hepatocellular carcinoma
- 50 Renal-cell carcinomas
- 51 Bladder cancer
- 52 Prostate cancer
- 53 Targeted therapies in breast cancer
- 54 Molecular targets for epithelial ovarian cancer
- 55 Testicular cancer: germ-cell tumors (GCTs)
- 56 Cervical cancer
- Part 3.2 Molecular pathology: cancers of the nervous system
- Part 3.3 Molecular pathology: cancers of the skin
- Part 3.4 Molecular pathology: endocrine cancers
- Part 3.5 Molecular pathology: adult sarcomas
- Part 3.6 Molecular pathology: lymphoma and leukemia
- Part 3.7 Molecular pathology: pediatric solid tumors
- Part 4 Pharmacologic targeting of oncogenic pathways
- Index
- References
Summary
Introduction
Prostate cancer (PCa) is the most frequently diagnosed, and the second leading cause of death from cancer in North American and European men (1). It has the highest incidence rate among all epithelial tumors in the United States. Approximately 1 in 6 men over the age of 65 is diagnosed with PCa (2). Age, racial background, dietary factors, life-style related factors, and androgens are known contributors to the risk of PCa.
Heterogeneity in PCa
There is a high variability in the natural history of PCa ranging from indolent and asymptomatic to aggressive and metastatic disease. It is also multi-focal and heterogeneous in clinical, histological, and biological dispositions. Healthy glands, precursor, and neoplastic lesions with varying degrees of differentiation often exist in juxtaposition and evolve independently in the same PCa tissue (3,4).
Prostate intra-epithelial neoplasia (PIN) is thought to be a precursor lesion for PCa. High-grade PIN with increased nuclear enlargement, prominent nucleoli, chromatin alterations, and luminal complexity in acinar epithelium is often detected together with PCa in biopsy samples (4,5). PIN shares many common genetic, molecular, and phenotypic characteristics of prostate adenocarcinoma (3,5).
Gleason grade has been used to indicate the severity of the disease.AhigherGleason grade suggests a poorly diferentiated, advanced carcinoma and is used as a prognostic indicator (4).
- Type
- Chapter
- Information
- Molecular OncologyCauses of Cancer and Targets for Treatment, pp. 591 - 597Publisher: Cambridge University PressPrint publication year: 2013
References
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