Abstract |
Cervical carcinoma is the second most common cause of cancer deaths in women worldwide. Treatments have not changed for decades and survival rates for advanced disease remain low. An exciting new molecular target for the treatment of cervical squamous cell carcinoma (SCC), and possibly for SCCs at other anatomical sites, is the oncostatin M receptor (OSMR). This cell surface cytokine receptor is commonly copy number gained and overexpressed in advanced cervical SCC, changes that are associated with significantly worse clinical outcomes. OSMR overexpression in cervical SCC cells results in enhanced responsiveness to the major ligand oncostatin M (OSM), which induces several pro-malignant effects, including a pro-angiogenic phenotype and increased cell migration and invasiveness. OSMR is a strong candidate for antibody-mediated inhibition, a strategy that has had a major impact on haematological malignancies and various solid tumours such as HER2-positive breast cancers.
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Authors | Maria M Caffarel, Nicholas Coleman |
Journal | The Journal of pathology
(J Pathol)
Vol. 232
Issue 4
Pg. 386-90
(Mar 2014)
ISSN: 1096-9896 [Electronic] England |
PMID | 24659184
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't, Review)
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Copyright | © 2013 The Authors. The Journal of Pathology published by John Wiley & Sons Ltd on behalf of Pathological Society of Great Britain and Ireland. |
Chemical References |
- Antineoplastic Agents
- OSMR protein, human
- Oncostatin M Receptor beta Subunit
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Topics |
- Animals
- Antineoplastic Agents
(therapeutic use)
- Carcinoma, Squamous Cell
(drug therapy, genetics, metabolism, pathology)
- Chromosomes, Human, Pair 5
- Drug Design
- Female
- Gene Amplification
- Gene Expression Regulation, Neoplastic
- Genetic Predisposition to Disease
- Humans
- Molecular Targeted Therapy
- Oncostatin M Receptor beta Subunit
(antagonists & inhibitors, genetics, metabolism)
- Phenotype
- Signal Transduction
(drug effects)
- Up-Regulation
- Uterine Cervical Neoplasms
(drug therapy, genetics, metabolism, pathology)
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