Sentences with phrase «with imatinib»

Patients with CML who have higher proportions of natural killer immune cells, and more mature natural killer cells, fare better when discontinuing therapy with imatinib.

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

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

CML patients treated with nilotinib had fewer treatment - emergent BCR - ABL mutations than those treated with imatinib, and among patients who did have a mutation, those treated with nilotinib had reduced rates of progression to accelerated phase and blast phase of the disease.

• 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.

When the mice received no treatment or were treated with imatinib alone, the human leukemia stem cells propagated and grew to relatively large numbers.

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

«Although TKIs such as the first - generation TKI imatinib mesylate (IM) and the second - generation TKIs dasatinib and nilotinib have markedly improved the prognosis of patients with chronic phase CML, a cure remains elusive.

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.»

• A patient with blood cancer who had received several diagnoses was found, through testing, to have an unusual form of acute myeloid leukemia (AML), which predicted responsiveness to imatinib.

The use of imatinib has dramatically improved treatment results for adults with c - KIT (CD117 positive) GIST.

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 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.

[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 %.

Our group treated 11 patients with advanced mucosal melanoma harboring KIT alterations as part of our completed phase II trial of imatinib.

Several phase 1 and 2 trials have been carried out using nonselective ATP - competitive inhibitors such as imatinib to treat patients with advanced breast cancer.

Several targeted drugs (e.g., imatinib [Gleevec ®], dasatinib [Sprycel ®]-RRB- are effective for treating CML because they attack cells with the Philadelphia chromosome, the genetic abnormality that is the hallmark of this type of leukemia.

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.

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.

Teva concluded that since the approval of nilotinib was based upon an exemption granted under Article 8 (3) with regard to the first orphan product (imatinib), it should not be entitled to same scope of orphan exclusivity as imatinib and thus should not be considered a hurdle towards the approval of generics referencing imatinib.