Sentences with word «gefitinib»

They also analysed the patients» cancers for mutations in two other molecules, one called EGFR which is the target of existing drugs gefitinib and erlotinib, and another called KRAS.
Researchers and physicians have shown success treating EGFR lung cancer, for example with EGFR inhibitors gefitinib and erlotinib.
International researchers prospectively analyzed and compared tumor and matched plasma DNA for EGFR mutations from 1060 patients that were screened as part of a phase IV, open - label, single - arm, first - line gefitinib in EGFR mutation positive Caucasian patients.
Post-hoc analysis of the efficacy of first - line gefitinib revealed there was similar progression - free survival (PFS) for those with EGFR mutation positive tissue (9.7 months [CI 8.5 - 11.0]-RRB- versus both mutation positive tissue and plasma (10.2 months [CI 8.5 - 12.5]-RRB-.
It's been an important question — many lung cancers depend on over-activation of the gene EGFR, but then when EGFR inhibitors like gefitinib or erlotinib are used, the cancers tend to activate other «kinases» that allow the cancer to by - pass around this dependence.
Combining gefitinib with the conventional treatment, which is called methotrexate, could reduce the need to remove the Fallopian tube in a significant number of cases.
The lung cancer drug — called gefitinib — helps by blocking a protein that is known to encourage cell growth, and which was found to be present in high levels at the site of ectopic pregnancies.
Tan and colleagues asked what are these kinases that allow lung cancer to evade gefitinib, and what other drug might turn them off.
Drugs such as gefitinib and erlotinib are supposed to block those growth signals in lung cancer cells, but not every cancer responds to them.
Similar to Tam, gefitinib blocked the hypoxic effect in ER - α — positive primary samples and cell lines but had no effect on ER - α — negative primary samples or cell lines (Fig. 2C).
There was the 2004 Science publication by Matt Meyerson's group showing a correlation between patient mutations in the EGFR genes and their response to gefitinib therapy in lung cancer.
In tests on EGFR - dependent lung cancer cell lines, Tan and colleagues show that the drugs gefitinib and bosutinib «showed additive and synergistic effects.»
Sure enough, when the team gave the drugs erlotinib and gefitinib to flies, they were more likely to be knocked out by alcohol.
For example, epidermal growth factor (EGFR) mutations may result in sensitivity to drugs that are EGFR tyrosine kinase inhibitors (TKIs), such as erlotinib or gefitinib, whereas individuals with the EGFR T790M mutation are more resistant to these drugs.
June - Koo Lee, M.D., of Seoul National University Hospital, Seoul, Republic of Korea, and colleagues performed a meta - analysis of randomized controlled trials that compared first - generation EGFR TKI (erlotinib and gefitinib) treatment with conventional chemotherapy in patients with advanced NSCLC without mutation of the EGFR gene.
Approximately 10 - 15 % of Caucasian and 30 - 35 % of Asian patients with NSCLC have a mutation in the epidermal growth factor receptor (EGFR), which can be successfully targeted with EGFR inhibitors called tyrosine kinase inhibitors (TKI), such as erlotinib, gefitinib and afatinib.
The VA - UAB team says, based on its lab studies, that honokiol binds more strongly with EGFR than does the drug gefitinib (sold as Iressa), which is commonly used to treat head and neck cancers.
Osimertinib showed preclinical evidence of concentrations in mouse brain tissue 5 - to 25-fold higher than in plasma, [16] and has shown greater penetration of the BBB in mouse models than gefitinib, rociletinib, or afatinib.
EGF receptor gene mutations are common in lung cancers from «never smokers» and are associated with sensitivity of tumors to gefitinib and erlotinib.
[21] In the recently presented FLAURA study, in which osimertinib was used in untreated patients with advanced EGFR - mutant NSCLC, the HR for systemic disease control and CNS control similarly favored osimertinib over erlotinib or gefitinib, supporting the preclinical data that showed osimertinib's penetration across the BBB and providing support for using this agent in first - line management of EGFR - mutant patients with brain metastases.
Not surprisingly, RIPK2 inhibitor 1 was more efficacious at 100 nM at inhibiting NFκB activity when compared with RIPK2 inhibitor 2, gefitinib, or regorafenib (P values comparing RIPK2 inhibitor 1 vs. RIPK2 inhibitor 2, gefitinib, and regorafenib inhibition of MDP - driven NFκB activation were 0.0015, 0.0006, and 0.004, respectively).
Since both gefitinib and our RIPK2 inhibitors can inhibit RIPK2, either our drug has more affinity for RIPK2 or the off - target effects of RIPK2 inhibitor 1 are beneficial to aid in recovery from inflammation injury using the DSS model.
Interestingly, a newly characterized RIPK2 inhibitor, gefitinib, can also inhibit intestinal inflammation injury but only promote a 41 % survival versus 73 % survival with RIPK2 inhibitor 1 (Fig. 6B; Table 2).
Furthermore, our identified RIPK2 inhibitors appear to have more affinity for the active site of RIPK2 than others, are more efficacious at inhibition of proliferation, and can effectively resolve lung inflammation and intestinal inflammation more robustly than gefitinib (Fig. 6B; Table 2).
N = 10 — 25 and P value of Rassf1a − / − (DSS) vs. wild type (DSS) was < 0.0001; Rassf1a − / − (DSS) vs. 1a − / − (DSS + inhibitor 1 or 2 or gefitinib) was < 0.0001.
P values for RIPK inhibitor treated vs. MDP (no drug) were < 0.0001 (inhibitor 1), 0.06 (inhibitor 2), < 0.006 (gefitinib), 0.0002 (regorafenib), and 0.0008 (ponatinib).
On Monday, FDA has greenlighted Iressa (gefitinib) as treatment for patients with metastatic NSCLC characterized by certain EGFR gene mutations.
These include imatinib, sold under the brand name Gleevec for chronic myeloid leukemia; gefitinib, sold as Iressa for metastatic non-small cell lung cancer; and sunitinib, marketed as Sutent, for renal cell cancer and gastrointestinal stromal tumors.
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