Sentences with phrase «imatinib in»

However, the General Court upheld the EMA's decision refusing Teva's generic application for imatinib in view of nilotinib's orphan drug exclusivity pertaining to CML.

These mutant kinases are attractive therapeutic targets, as demonstrated by the efficacy of imatinib in BCR - ABL — positive chronic myelogenous leukemia (CML), 5 as well as in MPD associated with activating alleles involving PDGFRA or PDGFRB.2, 6,7 In addition, activating mutations in the FLT3 receptor tyrosine kinase are the most common genetic event in acute myeloid leukemia (AML), and specific inhibitors of the FMS - like tyrosine kinase 3 (FLT3) have entered late - stage clinical trials.8 Although mutations in tyrosine kinases and in other genes have been identified in a subset of MPD and AML, in many cases the genetic events that contribute to the molecular pathogenesis of these diseases remain unknown.

[44] Two other phase II clinical trials evaluated the efficacy of imatinib in patients with melanoma — including mucosal melanomas — harboring KIT mutations and / or amplifications, with a subset of cases involving mucosal primaries, and both found a disease control rate of approximately 50 %.

The team tested a combination of PGE1 and the TKI drug called imatinib in a mouse model of CML.

Not exact matches

Ghalaut VS, Sangwan L, Dahiya K, Ghalaut PS, Dhankhar R, Saharan R. Effect of imatinib therapy with and without turmeric powder on nitric oxide levels in chronic myeloid leukemia.

Effect of imatinib therapy with and without turmeric powder on nitric oxide levels in chronic myeloid leukemia

The analysis suggests that patients with complex indels in KIT would benefit from drugs such as imatinib, sunitnib and sorafenib, which target mutations in this gene.

In future, it may be possible to measure BCR - ABL levels in individual cells in the clinic — this will help us identify the resistant high BCR - ABL cells and better understand how patients develop resistance to imatinib treatment with the aim of combatting this resistance to make response more durable and the treatment more effective.&raquIn future, it may be possible to measure BCR - ABL levels in individual cells in the clinic — this will help us identify the resistant high BCR - ABL cells and better understand how patients develop resistance to imatinib treatment with the aim of combatting this resistance to make response more durable and the treatment more effective.&raquin individual cells in the clinic — this will help us identify the resistant high BCR - ABL cells and better understand how patients develop resistance to imatinib treatment with the aim of combatting this resistance to make response more durable and the treatment more effective.&raquin the clinic — this will help us identify the resistant high BCR - ABL cells and better understand how patients develop resistance to imatinib treatment with the aim of combatting this resistance to make response more durable and the treatment more effective.»

• A patient's undifferentiated small bowel sarcoma was found to contain a KIT gene deletion, resulting in a revised diagnosis of GIST (gastrointestinal stromal tumor) that was successfully treated with imatinib.

[12] It was marketed in 2001 by Novartis as imatinib mesylate (Gleevec in the US, Glivec in Europe).

In the late 1990s, STI - 571 (imatinib, Gleevec / Glivec) was identified by the pharmaceutical company Novartis (then known as Ciba Geigy) in high - throughput screens for tyrosine kinase inhibitorIn the late 1990s, STI - 571 (imatinib, Gleevec / Glivec) was identified by the pharmaceutical company Novartis (then known as Ciba Geigy) in high - throughput screens for tyrosine kinase inhibitorin high - throughput screens for tyrosine kinase inhibitors.

After a median follow - up period of 36 months, three patients randomized to continue treatment (17 %) and 10 patients in the discontinuation arm (67 %) had a molecular relapse; all three of the former patients had stopped imatinib treatment after randomization.

In 2001 imatinib was approved for the treatment of chronic myeloid leukemia, a disease that is almost universally caused by a single genetic mutation, known as the Philadelphia chromosome, and its resulting mutant protein.

Over time, imatinib has also proven effective in treating multiple forms of cancer.

After completing a series of preclinical studies, Dr. Druker spearheaded the highly successful clinical trials of imatinib for CML, which led to FDA approval of the drug in record time.

In one report, a patient with an L576P KIT mutation in whom imatinib therapy had previously failed experienced marked reduction in tumor burden in response to dasatinib treatmenIn one report, a patient with an L576P KIT mutation in whom imatinib therapy had previously failed experienced marked reduction in tumor burden in response to dasatinib treatmenin whom imatinib therapy had previously failed experienced marked reduction in tumor burden in response to dasatinib treatmenin tumor burden in response to dasatinib treatmenin response to dasatinib treatment.

Phase II, open - label, single - arm trial of imatinib mesylate in patients with metastatic melanoma harboring c - Kit mutation or amplification.

The use of alternative KIT inhibitors following progression on imatinib has achieved clinical benefit in patients with advanced GIST.

Efficacy and safety of sunitinib in patients with advanced gastrointestinal stromal tumour after failure of imatinib: a randomised controlled trial.

Future studies will test and compare the efficacy of imatinib and allosteric compounds in mouse models of breast cancer.

The adenosine triphosphate (ATP)-- competitive kinase inhibitors imatinib (STI571; trade name: Gleevec), dasatinib, and nilotinib inhibit multiple tyrosine kinases in addition to ABL1 and ABL2 (5).

This gatekeeper Thr residue is not conserved in the JAK kinase family, but the Phe958 residue of JAK1 is the homologous residue of Phe317 in ABL kinase, which is close to the gatekeeper residue and was also found to be mutated in imatinib - resistant BCR - ABL positive patients13, 29,30 (Online Supplementary Figure S6A and S6B).

It has been shown in imatinib - resistant CML that drug resistance conferred by mutations does not necessarily correlate with proliferative advantage and increased kinase activity.34 Other, non-activating mutations or drug - resistance mechanisms, might be acquired by tumor cells.

The 10 - year survival rate in subjects receiving first - line treatment with imatinib ranged from 64.4 % to 84.4 %.

Here patients treated with imatinib become resistant because of the acquisition of mutations in the ABL kinase domain.13

Final Results of Landmark Imatinib Study in CML Show Long - Term Benefit: Results of the IRIS study revealed that imatinib shows persistent efficacy over time without unacceptable late toxic or cumulative effects.

He has played a key role in the discovery and development of multiple approved drugs, including imatinib (Gleevec), dasatinib (Sprycel), and enzalutamide (Xtandi).

In a significant, yet unusual judgment the Court of Justice of the European Union (CJEU) upheld the General Court's decision (T - 140 / 12; Teva Pharma v. EMA) that had affirmed the European Medicines Agency's (EMA) rejection of Teva's generic drug application for Glivec ® (active substance - imatinib), not due to the reference product's own orphan drug exclusivity but in view of orphan drug exclusivity of a similar medicinal product — Tasigna ® (active substance - nilotinibIn a significant, yet unusual judgment the Court of Justice of the European Union (CJEU) upheld the General Court's decision (T - 140 / 12; Teva Pharma v. EMA) that had affirmed the European Medicines Agency's (EMA) rejection of Teva's generic drug application for Glivec ® (active substance - imatinib), not due to the reference product's own orphan drug exclusivity but in view of orphan drug exclusivity of a similar medicinal product — Tasigna ® (active substance - nilotinibin view of orphan drug exclusivity of a similar medicinal product — Tasigna ® (active substance - nilotinib).