| pubmed-article:17671639 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:17671639 | lifeskim:mentions | umls-concept:C0029016 | lld:lifeskim |
| pubmed-article:17671639 | lifeskim:mentions | umls-concept:C0597357 | lld:lifeskim |
| pubmed-article:17671639 | lifeskim:mentions | umls-concept:C0599894 | lld:lifeskim |
| pubmed-article:17671639 | lifeskim:mentions | umls-concept:C0920425 | lld:lifeskim |
| pubmed-article:17671639 | lifeskim:mentions | umls-concept:C1521840 | lld:lifeskim |
| pubmed-article:17671639 | pubmed:issue | 8 | lld:pubmed |
| pubmed-article:17671639 | pubmed:dateCreated | 2007-8-2 | lld:pubmed |
| pubmed-article:17671639 | pubmed:abstractText | Understanding the genetic origin of cancer at the molecular level has facilitated the development of novel targeted therapies. Aberrant activation of the ErbB family of receptors is implicated in many human cancers and is already the target of several anticancer therapeutics. The use of mAbs specific for the extracellular domain of ErbB receptors was the first implementation of rational targeted therapy. The cytoplasmic tyrosine kinase domain is also a preferred target for small compounds that inhibit the kinase activity of these receptors. However, current therapy has not yet been optimized, allowing for opportunities for optimization of the next generation of targeted therapy, particularly with regards to inhibiting heteromeric ErbB family receptor complexes. | lld:pubmed |
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