Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
2005-11-22
pubmed:abstractText
EphA2 is a receptor tyrosine kinase that is overexpressed by many human cancers, and is often associated with poor prognostic features. It is involved in many processes crucial to malignant progression, such as migration, invasion, metastasis, proliferation, survival and angiogenesis. Inducing EphA2 downregulation by any one of several mechanisms (antibody-mediated inhibition of signalling, antibody-mediated downregulation of total EphA2 expression and siRNA-mediated inhibition of expression) has been shown to decrease tumour growth, prolong survival and inhibit angiogenesis in multiple preclinical models of ovarian, breast and pancreatic cancer. Targeting EphA2 is especially attractive in ovarian cancer, in which overexpression is present in > 75% of cases. This disease is highly responsive to chemotherapy, and EphA2 inhibition is especially effective in combination with taxanes. This demonstrated efficacy, along with the low expression of EphA2 by normal adult tissues and lack of demonstrable toxicities in preclinical models, suggest that long-term treatment with EphA2-targeting agents is an attractive approach for ovarian cancer therapy.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
1744-7631
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
9
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1179-87
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed:year
2005
pubmed:articleTitle
EphA2 as a target for ovarian cancer therapy.
pubmed:affiliation
Department of Gynecologic Oncology, U.T.M.D. Anderson Cancer Center, Houston, TX 77030, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, Non-P.H.S., Review, Research Support, Non-U.S. Gov't, Research Support, N.I.H., Extramural