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Frozen tumor specimens, along with matched normal tissue, were available from four patients, and paraffin-embedded material was used from the other patients.
Overexpression of Sphk2 is associated with gefitinib resistance in non-small cell lung cancer.
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Fixed focal neurologic deficits (eg, cranial-nerve palsies) generally do not improve, but encephalopathies can improve dramatically with treatment.
Surveillance testing with serum tumor markers or imaging has been shown to have clinical value for certain cancers (e.
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We also assessed MET amplification using quantitative PCR, and it did not differ significantly among the groups (Fig.
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This phenomenon has been well exemplified by the experience with dasatanib as a second-line treatment for cases of chronic myelogenous leukemia with acquired imatinib resistance ().
MET amplification leads to gefitinib resistance in lung cancers by activating ERBB3 signaling.
Because these tumors are by definition noninvasive and incapable of metastasizing, they should be curable with surgical resection; however, such lesions, when identified, are often centrally located and may require a lobectomy.
Synergistic effects of protein tyrosine kinase inhibitor genistein with camptothecins against three cell lines in vitro.
Minor wording problems - Clinical uses - "As at August 2012" should be "As of August 2012".
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Use of a microfluidic-based isolation device and sequence amplification technology allowed for detection of EGFR mutations in circulating tumor cells from 11 (92%) of 12 patients.
Because A549 xenografts were much larger than both LoVo and Calu-6 xenografts at the end of the study, the total amount of gefitinib in the A549 xenografts was actually quite similar to that in LoVo tumors.
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Novel cancer agents have brought about significant improvements in patient survival while reducing systemic toxicities, when compared with cytotoxic chemotherapy.
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ATF4 was induced and eIF2α was phosphorylated in A549 cells treated with EGFR inhibitors.
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Protein kinases are a group of enzymes that possess a catalytic subunit that transfers the gamma (terminal) phosphate from (often ATP) to one or more in a protein substrate side-chain, resulting in a conformational change affecting protein function.
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