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
42 - Head and neck 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
Over the last decade two highly specific, robust molecular targets have proven practical and relevant for therapy and prognosis in squamous cell cancers of the head and neck (HNC): the epidermal growth factor receptor (EGFR) and human papillomavirus (HPV). EGFR and its signaling pathways are key regulators of cell growth. The first experimental studies with anti-EGFR antibodies in human tumor models took place 25 years ago, culminating in the approval of an EGFR targeting agent in 2006 as the first new treatment for HNC in over 45 years. Recent studies have also identified HPV as a causative factor in oropharyngeal HNC. If current trends continue, there will soon be over 20 000 cases of HPV-caused oropharynx cancer in the United States. To date, EGFR and HPV are the most clinically relevant molecular targets in HNC.
EGFR expression in HNC
The epidermal growth factor receptor (EGFR) is a member of the ERBB family of tyrosine kinase receptors. EGFR regulates a variety of cellular functions by activating downstream effectors in cellular growth, differentiation, and survival pathways. Other ERBB family members include ERBB2 (HER2, Neu), ERBB3 (HER3), and ERBB4 (HER4). The family members all contain a unique extra-cellular domain along with a transmembrane domain and a tyrosine kinase domain that is structurally conserved across family members, although HER3 is kinase dead (Figure 42.1).
- Type
- Chapter
- Information
- Molecular OncologyCauses of Cancer and Targets for Treatment, pp. 497 - 505Publisher: Cambridge University PressPrint publication year: 2013