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Leukemia, Myeloid clinical trials

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NCT ID: NCT03381781 Not yet recruiting - Clinical trials for Acute Myeloid Leukemia

Decitabine,Cytarabine and Arsenic Trioxide for Acute Myeloid Leukemia With p53 Mutations

Start date: March 2018
Phase: Phase 2
Study type: Interventional

This is a prospective,uncontrolled and multi-institution trial.The aim is to identify if using decitabine,cytarabine and ATO as the therapy of acute myeloid leukemia(AML) with p53 mutations has better relapse free survival and complete response than using decitabine and cytarabine. TP53 mutation is commonly associated with poor cancer patient prognosis yet no mutant p53 (mp53)-targeting regimen was clinically established. Particularly, p53 mutation is associated with extremely poor prognosis in myelodysplastic syndromes (MDS) and acute myeloid leukemia (AML) patients. Decitabine (DAC) is a FDA approved drug for MDS treatment. In two independent clinical trials reported recently, DNA demethylating drug DAC treatment yielded a surprisingly high rate of complete remission (CR) in mp53-harboring AML/MDS patients (Welch, NEJM, 2016; Chang, BJH, 2017). Notably, all of the mp53-expressing patients in the two clinical studies relapsed quickly. Arsenic trioxide (ATO) is a FDA approved drug for M3-AML treatment. Despite of the observed efficacy in treating non-APL patients, ATO is not yet approved for non-APL cancer treatment. ATO plays key role in regulating both wild-type p53 (wtp53) and mp53. Our published and unpublished data suggest ATO potentially hijacks nuclear iASPP-mediated STRaND pathway via exposing iASPP's RaDAR nuclear import code (Lu, Cancer Cell, 2013; Lu, Cell, 2014; Lu, Nat Rev Mol Cell Biol, 2016; Lu, unpublished). Our unpublished data also suggests a key role of ATO in regulating mp53 (Lu, The 17th International p53 Workshop, 2017). ATO is widely reported to be able to degrade and thus inhibit mp53's oncogenic function (Hamadeh, BBRC, 1999)(Liu, Blood, 2003). ATO suppressed cancer cell growth by targeting mp53 for degradation by Pirh2 degradation pathway (Yang, JBC, 2011; Yan, PLOS one, 2014); Here we explore the potential of combination of DAC and ATO in improving the mp53-harboring AML/MDS patients' relapse free survival (RFS) and the ability to thoroughly eliminate mp53 subclone. Basic researches aiming to explore the mechanisms how mp53 cells responds to DAC and/or ATO treatment and how mp53 cells develop resistance to DAC and/or ATO will be coupled. We designate trials aiming for a better treatment regimen for mp53 patients as 'PANDA-Trials'.

NCT ID: NCT03283228 Not yet recruiting - Clinical trials for Adult Acute Myeloid Leukemia

Cd11b and Cd56 as Prognostic Markers in Acute Myeloid Leukemia

Start date: December 1, 2017
Phase: N/A
Study type: Observational

1. Detect the expression of marker CD56 and CD11b in newly diagnosed cases of adult AML. 2. Study correlation between CD56 and CD11b expression with haematological parameters in cases of adult AML.

NCT ID: NCT03228303 Not yet recruiting - Clinical trials for Chronic Myeloid Leukemia

Nilotinib Versus Imatinib in Treatment of Patients With Newly Diagnosed Chronic Myeloid Leukemia

Start date: December 1, 2017
Phase: Early Phase 1
Study type: Interventional

Nilotinib vs imatinib in patients with newly diagnosed CML-CP

NCT ID: NCT03214718 Not yet recruiting - Clinical trials for Chronic Myeloid Leukemia Patients

Myeloid Derived Suppressor Cells and Chronic Myeloid Leukemia

Start date: August 5, 2017
Phase: N/A
Study type: Interventional

The suppression of the immune system creates a permissive environment for development and progression of cancer. One population of immunosuppressive cells that have become the focus of intense study is myeloid derived suppressor cells , immature myeloid cells able to induce immune-escape, angiogenesis, and tumor progression. Two different subpopulations have been identified and studied: granulocytic and monocytic myeloid derived suppressor cells with a different immunophenotype and immunosuppressive properties

NCT ID: NCT03116477 Not yet recruiting - Clinical trials for Acute Myeloid Leukemia, in Relapse

Study Investigating the Efficacy of the Addition of Crenolanib to Chemotherapy vs Chemotherapy Alone in Patients With R/R FLT3 Mutated AML

Start date: August 2017
Phase: Phase 3
Study type: Interventional

This is a multi-center, randomized, trial to evaluate the efficacy of adding crenolanib to salvage chemotherapy versus salvage chemotherapy alone in subjects with relapsed/refractory FLT3-mutant AML. Approximately 320 subjects will be randomized 1:1 to receive either salvage chemotherapy (HAM or FLAG-Ida) with crenolanib (treatment arm 1) or salvage chemotherapy (HAM or FLAG-Ida) alone (treatment arm 2).

NCT ID: NCT03053206 Not yet recruiting - Clinical trials for Acute Myeloid Leukemia, in Relapse

A Prospective, Interventional Study Assessing Response to Cytarabine, Daunorubicin and Etoposide (ADE) for First Relapse of Paediatric Acute Myeloid Leukemia

Start date: February 15, 2017
Phase: Phase 2
Study type: Interventional

One-third to one-half of patients with AML relapse and in general relapsed AML patients have a poor prognosis. The treatment of relapsed AML consists of induction chemotherapy followed by Allogenic Stem Cell Transplant (ASCT). However, at present there is no standard salvage chemotherapy regimen for relapsed AML, as no study has shown any one regimen to be significantly superior. Anthracyclines, Fludarabine, Etoposide and cytarabineare active agents in AMLand have been used as monotherapy and in combination in refractory and relapsed AML patients. According to previous studies the present CR rate of different regimens ranges from 50-70%. A retrospective analysis (unpublished) conducted at IRCH, AIIMS on relapsed AML patients treated with ADE (Cytarabine, Daunorubicin and Etoposide) chemotherapy showed the CR rates of approximately 70%. Therefore, we have planned this study to test the efficacy and toxicity of ADE induction chemotherapy in relapsed AML patients in a prospective manner.

NCT ID: NCT02903277 Not yet recruiting - Clinical trials for Leukemia, Myelogenous, Chronic, BCR-ABL Positive

National Observatory of Chronic Myeloid Leukemia Adolescent and Young Adults Treated With Tyrosine Kinase Inhibitors in First Intent

Start date: November 2016
Phase: N/A
Study type: Observational

The median age of onset of chronic myeloid leukemia (CML) in chronic phase PC is about 60 years. However CML affects all age groups including 18-25 year olds, called adult-young adolescents (AJA). In France, there is no record of CML and especially not for this particular population, only a European Register of CML in children up to 18 years has been set up under the coordination of Professor "Frederic Millot", pediatrics, CHU Poitiers. Malignancies diagnosed in this population usually have characteristics, evolution, therapeutic strategies with tyrosine kinase inhibitors (TKIs) are a real therapeutic revolution with an overall survival very significantly augmented but at present only a minority of patients may one day consider a final judgment of treatment. AJA are the most exposed patients to the complications, the socio-economic repercussions, professional and personal of a very long-term treatment. But there is little data in the literature concerning this population. Two studies show that diagnosis of CML presents with poor prognostic factors (high skoal), the observed responses are poorer compared to older patients but it is accompanied difference in survival in all cases with a decline of about 70 mois. However, these studies have focused solely on the patients included in the study receiving optimized treatment is not the standard treatment at the time. It is clearly demonstrated that the inclusion in a study brings a benefit to the patient. However, the majority of AJA are not included in a study. The investigators therefore want to describe the AYA population of CML in France and compare the evolution of patients included or not in a protocol. The investigators also want to investigate specific issues of the age of these patients as the reproductive desire. Indeed, while it does not seem to be any risk of teratogenicity for men treated with ITK, this risk is clearly established for women and requires specific supported. Another important point is that of the quality of life. The state of physical and mental health and his feelings, physical activity and its limitations and well-being was assessed by the SF-3612 questionnaire. The results of this analysis were compared with those already obtained for the general population (not representative of Italian adults with cancer sample) and adjusted for sex, age, geographic region, marital status and education level . There seems to be young people and women who express a feeling more pejorative. This does not only covers the frequency of side effects but also on physical activity and well-being. the affected population will be noted that that is particularly involved in the social, professional and in the development of his personal life. The impact of treatment on quality of life must be considered under penalty of seeing the difficulties of compliance. But several studies have demonstrated the negative impact of poor adherence in response to treatments .

NCT ID: NCT02883036 Not yet recruiting - Clinical trials for Chronic Myeloid Leukemia

Vitro Study of Tigecycline to Treat Chronic Myeloid Leukemia

Start date: September 2016
Phase: N/A
Study type: Observational

Chronic myeloid leukemia (CML) is a myeloproliferative neoplasm companies with the BCR-ABL fusion gene encoded by the Philadelphia (Ph) chromosome. The BCR-ABL fusion protein(the formation of the chimeric gene BCR/ABL on chromosome 22 and a reciprocal ABL/BCR on chromosome 9,it has no expanded name) plays key role on CML leukemogenesis by activating its downstream signaling pathway of survival and proliferation. Imatinib, a targeted competitive inhibitor of a BCR-ABL tyrosine kinase, changed the clinical treatment and prognosis of CML. As its optimized generation, other tyrosine kinase inhibitors (TKIs), dasatinib and nilotinib have more potent anti-leukemic activity and less side-effect. However, acquired resistance to TKIs is one of the main obstacles to effective CML treatment and is involved in gene amplication of ABL tyrosine kinase point mutations. The outcomes of patients with these ABL tyrosine kinase point mutations have linked to worse prognosis and higher mortality generally. Metabolic adaptations are common in cancer cells, and cancer cells become more dependent on mitochondrial biogenesis. Tigecycline, as a broad-spectrum antibiotics, inhibits mitochondrial biogenesis as its an interesting "side-effect".In recent study,researchers indicated that tigecycline can eradicate cancer stem cells by targeting mitochondrial.Here, the investigators test tigecycline's anti-leukemic activity to chronic myeloid leukemia in vitro.

NCT ID: NCT02698124 Not yet recruiting - Clinical trials for Acute Myeloid Leukemia

Decitabine for Chemotherapy Unfit Korean AML Patients in Real Practice

PURPLE-D
Start date: March 2016
Phase: N/A
Study type: Observational

Prospective multicenter, open-lab el, observational, single arm study of decitabine. Subjects will be elderly patients with newly diagnosed, treatment-naïve AML who are unfit to receive and not candidate for intensive induction chemotherapy (iIC)

NCT ID: NCT02687425 Not yet recruiting - Clinical trials for Leukemia, Myelogenous, Chronic, BCR-ABL Positive

Safety and Efficiency Study of Pioglitazone in Combination With Imatinib Mesylate to Treat Chronic Myelogenous Leukemia

SESPI
Start date: February 2016
Phase: Phase 2
Study type: Interventional

The purpose of this study is to assess the safety and efficiency of adding pioglitazone to chronic phase chronic myelogenous leukemia patients having received imatinib mesylate who have acquired a stable molecular response but not complete molecular response.