Track topics on Twitter Track topics that are important to you
It's an observational study based on 98 patients included in the STIM trial to extend the monitoring of patients and to have molecular and clinical data, with long follow up. Are there late relapses? What has become patients who relapsed during STIM trial and restarted TKI (inhibitor tyrosine kinase) treatment?
Chronic myeloid leukemia (CML) is an hematopoietic stem cell disorder in which a t (9;22) (q34;q11) reciprocal chromosomal translocation gives rise to Philadelphia chromosome (Ph) and generates the BCR-ABL1 fusion gene encoding a constitutively activated protein tyrosine kinases (PTK). Tyrosine kinase Inibitors (TKIs) such as imatinib, by blocking BCR-ABL1 kinase activity, selectively eradicate CML cells and induce durable responses and prolong survival.
CML patients treated with TKI are monitored by BCR-ABL1 RT-qPCR (Reverse Transcription real-time quantitative Polymerase Chain Reaction) performed from peripheral blood samples.
A first multicenter study entitled STIM trial demonstrated that imatinib could be safely discontinued in patients with complete molecular remission (CMR) for at least 2 years (undetectable BCR-ABL1 transcript by RT-qPCR).
Around 40% of these patients remain in a prolonged treatment-free remission (TFR) after treatment cessation. All molecular relapsing patients were sensitive when imatinib was re-challenged.
The purpose of this STIM-FU study is to follow all the patients included in the STIM trial in order to evaluate their molecular status, vital status and ongoing treatment in patient with a first molecular relapse.
This long term follow up will allow us to predict if a constant long term control of the disease is possible and to better define the clinical and biological CML-related factors predictive for a molecular relapse after TKI discontinuation.
Time Perspective: Prospective
Chronic Myeloid Leukemia
Interruption of the treatment by Imatinib
Active, not recruiting
University Hospital, Bordeaux
Published on BioPortfolio: 2016-09-12T18:38:21-0400
The primary purpose of this study is to estimate the major cytogenetic response rates of BMS-354825 and imatinib (800 mg/d) in subjects with chronic phase, Philadelphia chromosome positive...
This study assessed the efficacy and safety of generic imatinib in patients with chronic myeloid leukemia (CML) in Jordan. It was a multicenter, non-interventional, open-label, prospective...
In order to distinguish between clonal instability driven by imatinib in CML and actual changes with secondary clones induced by imatinib we would like to investigate the karyotype of non-...
The purpose of this study is to see what effect an investigational drug dasatinib (BMS-354825) has on subjects who are in chronic phase Philadelphia chromosome chronic myeloid leukemia (Ph...
This study will evaluate the proportion of subjects with chronic myeloid leukemia chronic phase that sustain major molecular response after imatinib discontinuation. To be eligible for thi...
ZNF224 is a KRAB-zinc finger transcription factor that exerts a key tumor suppressive role in chronic myelogenous leukemia. In this study, we identify the receptor tyrosine kinase Axl as a novel targe...
Tyrosine kinase inhibitors have achieved unprecedented efficacy in the treatment of chronic myeloid leukemia (CML); however, imatinib resistance has emerged as a major problem in the clinic. Because t...
Does switching to a second-generation tyrosine kinase inhibitor or increasing imatinib dose have long-term benefits in chronic myeloid leukemia patients with suboptimal responses under upfront standard-dose of imatinib?
The use of generic drugs after patent expiration of their originators is a relative novelty in the treatment of chronic cancer patients in Western countries. In this observational study we analyzed a ...
BCR-ABL kinase mutations, accounting for clinical resistance to tyrosine kinase inhibitor (TKI) such as imatinib, frequently occur in acquired resistance or in advanced phases of chronic myeloid leuke...
A pyrimidine and thiazole derived ANTINEOPLASTIC AGENT and PROTEIN KINASE INHIBITOR of BCR-ABL KINASE. It is used in the treatment of patients with CHRONIC MYELOID LEUKEMIA who are resistant or intolerant to IMATINIB.
The phase of chronic myeloid leukemia following the chronic phase (LEUKEMIA, MYELOID, CHRONIC-PHASE), where there are increased systemic symptoms, worsening cytopenias, and refractory LEUKOCYTOSIS.
A tyrosine kinase inhibitor and ANTINEOPLASTIC AGENT that inhibits the BCR-ABL kinase created by chromosome rearrangements in CHRONIC MYELOID LEUKEMIA and ACUTE LYMPHOBLASTIC LEUKEMIA, as well as PDG-derived tyrosine kinases that are overexpressed in gastrointestinal stromal tumors.
An alkylating agent having a selective immunosuppressive effect on BONE MARROW. It has been used in the palliative treatment of chronic myeloid leukemia (MYELOID LEUKEMIA, CHRONIC), but although symptomatic relief is provided, no permanent remission is brought about. According to the Fourth Annual Report on Carcinogens (NTP 85-002, 1985), busulfan is listed as a known carcinogen.
Clonal hematopoetic disorder caused by an acquired genetic defect in PLURIPOTENT STEM CELLS. It starts in MYELOID CELLS of the bone marrow, invades the blood and then other organs. The condition progresses from a stable, more indolent, chronic phase (LEUKEMIA, MYELOID, CHRONIC PHASE) lasting up to 7 years, to an advanced phase composed of an accelerated phase (LEUKEMIA, MYELOID, ACCELERATED PHASE) and BLAST CRISIS.