View clinical trials related to Chronic Myeloid Leukemia.
Filter by:Multi-center, open-label, non-randomized trial to evaluate long-term safety and efficacy of nilotinib. Approximately 20 patients will be enrolled in this trial at 3 centers in Mexico, which means all ongoing patients participating on [CAMN107A2109] excluding discontinued patients. During this study, patients will receive nilotinib orally, at a dose of 400 mg b.i.d. Patients will normally receive nilotinib on an outpatient basis. This trial will have a maximum of 24 months of follow-up time.
Rationale: At present, virtually no evidence exists regarding mid to long-term patient-reported health outcomes (e.g., health related quality of life-HRQOL) of CML patients treated with Imatinib. Purpose: the results of this research will provide preliminary evidence-based data on an number of issues from the patients' perspective, including adherence to therapy issues.
This is a phase II efficacy (indicates the capacity for beneficial change or therapeutic effect) and safety study of Dasatinib in patients with relapsed Chronic Myeloid Leukemia (CML) following a Stem Cell Transplant (SCT) and who are not benefiting from other treatment, such as imatinib therapy. A relapse is when an illness that has seemed to be getting better, or to have been cured, comes back or gets worse again. A total of 50 patients ≥18 years of age will be registered on the trial.
The purpose of this study is to evaluate the efficacy and the safety of dasatinib in subject with chronic phase chronic myeloid leukemia(CML) who are either resistant to or intolerant of imatinib mesylate.
Standard therapy with Imatinib (IM) significantly prolongs the survival of Ph+CML patients who obtain a complete cytogenetic response (CCgR). Elderly patients (i.e., at least 65 years) have similar cytogenetic responses and survival, but they usually show a low compliance. The aim of the study is to evaluate the percentage of elderly patients who maintain a CCgR with intermittent imatinib therapy with respect to standard daily administration.
Research Hypothesis: Treatment with dasatinib 100 mg QD is superior to imatinib 600 mg QD in terms of complete cytogenetic response (CCyR) in chronic phase (CP) Philadelphia chromosome-positive (Ph+) Chronic Myeloid Leukemia (CML) subjects who are imatinib failures or who have achieved only a suboptimal response after 3-18 months (12-77 weeks) of therapy with imatinib 400 mg. Primary Objective: The primary objective of this study is to compare the rate of CCyR of dasatinib (100mg QD) to high-dose imatinib (600 mg QD) therapy at 6 months after randomization in CP Ph+ CML subjects who are imatinib failures or who have achieved only a suboptimal response after 3 - 18 months of imatinib monotherapy at 400 mg/day.
A randomized multi-center study comparing the effect of dasatinib and imatinib on malignant stem cells in newly diagnosed chronic phase chronic myeloid leukemia (CML) patients. The research hypothesis is that treatment with dasatinib 100 mg daily (QD) results in greater and more rapid depletion of the Philadelphia (Ph) -positive stem cell pool within 6 months of therapy than imatinib 400 mg QD in newly diagnosed CML patients. The study duration is 18 months and approximately 40 patients will be recruited to the study.
It is a phase 4 study, not randomised and multicentric. Within 2 months after the diagnosis, the patients daily receive imatinib by oral way during at least 1 year (260mg/m² once a day), i.e. until the cytogenetic analysis. Beyond 1 year of treatment, if a haematological relapse or a loss of the cytogenetic response is observed, the nature of the treatment suggested to the patient is left with the appreciation of the investigator. Later on, discontinuation of imatinib is discussed if a molecular remission (negative RT-PCR) is obtained and maintained for at least 2 years.
Rationale: DCC-2036 is a potent broad spectrum inhibitor of BCR-ABL kinase. Inhibition of BCR-ABL has been validated for effective treatment of chronic myeloid leukemia (CML). The emergence of mutant forms of BCR-ABL which resist inhibition by imatinib, dasatinib, and nilotinib is associated with loss of efficacy in treatment of the disease. DCC-2036 is a potent inhibitor of resistant mutants of BCR-ABL including the T315I mutation, and would therefore be expected to effectively treat patients who fail to respond to other BCR-ABL inhibitors. DCC-2036 also inhibits FLT3-ITD, TIE2, KDR, LYN and TRKA kinases. Purpose: to assess the safety and tolerability in patients after continuous administration of DCC-2036 and to determine recommended doses for the conduct of a Phase 2 efficacy trial.
This is an extension of our ongoing clinical trial using ex vivo expanded autologous Cytokine-induced killer (CIK) cells as an adoptive cellular immunotherapy for haematological malignancies. The pre-existing clinical trial targets patient with acute myeloid leukemia or MDS, and relapsed disease post allogeneic transplant. Chronic myeloid leukemia (CML) is a disease with good response to kinase inhibitors. There are however patients in transformed phase of the disease who do not respond to these treatment. A small proportion of patients with response to Imatinib may develop mutations resulting in drug resistance. In addition, the vast majority of patients with a good response to the kinase inhibitors still have persistent CML cells detectable at a molecular level. It is known that the CML progenitors are not sensitive to the kinase inhibitors. On the other hand, immune mediated mechanism is known to be able to eradicate CML as shown by efficacy of donor lymphocyte infusion in the allogeneic transplant setting. Early clinical trials have shown clearance of bcr-abl using peptide vaccination. There is also convincing mouse data showing eradication of CML at molecular level by autologous CIK cells, but no clinical trial has been done using CIK cells for CML. We therefore plan to expand our current CIK trial to include CML as a disease, for CML patients with various degree of response to the kinase inhibitors which have already offered its maximal effect. We aim to study whether autologous CIK cells may further improve disease response, either in the eradiation of minimal residual disease, or in conjunction with chemotherapy for control of high tumour load disease.