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EGFR Mutations in Lung Cancer: Correlation with Clinical Response to Gefitinib Therapy
Results suggest that EGFR mutations may predict sensitivity to gefitinib, and treatment with the EGFR kinase inhibitor gefitsinib causes tumor regression in some patients with NSCLC, more frequently in Japan. Expand
An integrated view of copy number and allelic alterations in the cancer genome using single nucleotide polymorphism arrays.
The simultaneous measurement of DNA copy number changes and loss of heterozygosity events by SNP arrays should strengthen the ability to discover cancer-causing genes and to refine cancer diagnosis. Expand
The Nf2 tumor suppressor, merlin, functions in Rac-dependent signaling.
Insight is provided into the normal cellular function of merlin and how Nf2 mutation contributes to tumor initiation and progression by placing merlin in a signaling pathway downstream of the small GTPase Rac. Expand
Genome coverage and sequence fidelity of phi29 polymerase-based multiple strand displacement whole genome amplification.
Major efforts are underway to systematically define the somatic and germline genetic variations causally associated with disease. Genome-wide genetic analysis of actual clinical samples is, however,… Expand
Epidermal Growth Factor Receptor Activation in Glioblastoma through Novel Missense Mutations in the Extracellular Domain
The results suggest extracellular missense mutations as a novel mechanism for oncogenic EGFR activation and may help identify patients who can benefit from EGFR kinase inhibitors for treatment of glioblastoma. Expand
PI3K/PTEN/AKT pathway. A critical mediator of oncogenic signaling.
A number of the components of the PI3K/PTEN/Akt pathway have been found mutated or deregulated in a wide variety of human cancers highlighting the key role of this pathway in cellular transformation. Expand
Activating Mutations of the Noonan Syndrome-Associated SHP2/PTPN11 Gene in Human Solid Tumors and Adult Acute Myelogenous Leukemia
It is demonstrated that mutations in PTPN11 occur at low frequency in several human cancers, especially neuroblastoma and AML, and suggest that Shp2 may be a novel target for antineoplastic therapy. Expand
In conclusion, direct genetic alterations leading to deregulated PI3K/Akt signalling are common in a significant fraction of human malignancies. The forthcoming decade should witness the development… Expand
Identifying and characterizing a novel activating mutation of the FLT3 tyrosine kinase in AML.
Results suggest that mutations at N841 represent a significant new activating mutation in patients with AML and that patients with such mutations may respond to small-molecule FLT3 inhibitors such as PKC412. Expand
Identity between the PCPH proto-oncogene and the CD39L4 (ENTPD5) ectonucleoside triphosphate diphosphohydrolase gene.
- J. Paez, J. Recio, A. Rouzaut, V. Notario
- Biology, Medicine
- International journal of oncology
- 1 December 2001
It is reported that PCPH is structurally and functionally identical to the mammalian ectonucleoside triphosphate diphosphatase CD39L4 (ENTPD5), recently described as a member of the lymphoid activation antigen () CD39 protein family. Expand