Active clinical trials for "Leukemia, Myeloid"

During the last fifteen years, the landscape of AML diagnosis and therapeutical options has markedly evolved. Refined genetic and prognostic characterizations, together with new drug approvals and new allogeneic hematopoietic stem cell transplantation (HSCT) procedures, have increased patient journey diversity.

This study is conducted in patients with newly diagnosed CP CML (Chronic Phase Chronic Myeloid Leukemia) who have achieved EMR (< 10% IS BCR-ABL) at 3 months after first line treatment with dasatinib. Subjects will be allocated to 80mg QD based on EMR (Early Molecular Response) achievement and early safety profile following a standard of care approach.

This is a registry study in adult patients with newly diagnosed or refractory/relapsed myeloid neoplasms Investigator's sites: 60-70 sites in Germany and Austria Estimated duration of observation of an individual patient: 10 years maximum Objectives To register all patients with acute myeloid leukemia and related precursor neoplasms, acute leukemia of unambiguous lineage, with higher risk myelodysplastic syndromes (MDS with excess blasts 2), and with myeloid neoplasms with germline predisposition, newly diagnosed or relapsed/refractory in all participating centers (completeness) To perform timely analyses of disease-related genetic markers (incidences, treatment recommendations) To assess patient and family history, clinical characteristics and outcome data (event-free survival [EFS], cumulative incidence of relapse [CIR], cumulative incidence of death [CID], overall survival [OS]) To assess biological disease features and correlate with clinical outcome data (prognostic and predictive markers) To store biosamples from all patients (e.g., bone marrow, blood, plasma, normal tissue, e.g., skin biopsy, buccal swap, finger nails, hairs, or sputum) To assess quality of life

The purpose of the study is to describe and characterize CML in a large pediatric cohort of patients.

Tyrosine kinase inhibitors (TKI) have revolutionized the management and prognosis of chronic myeloid leukemia (CML). Daily treatment with TKI, which is necessary due to lack of cure, is frequently associated with moderate, chronic and sometimes severe adverse effects. The ability to permanently stop treatment with TKI has thus become a major goal in CML to prevent the occurrence of adverse events, improve quality of life and reduce the general cost of the treatment; we talk about Treatment Free Remission (TFR). It now remains to be demonstrated in a comparative prospective study that a strategy of de-escalation of the TKI treatment dose before treatment discontinuation optimizes TFR results. At the same time, it is possible to reduce adverse reactions and improve the quality of life of patients. In this context, the investigator propose to conduct a randomized clinical trial including CML patients, allowing to compare the results of TFR at 24 months between a sudden stop of treatment after a maintenance phase of dosage for 12 months and a de-escalation arm of dose (dosage reduced by 50%) for 12 months before stopping. A secondary immunological translational objective of this project will be to compare the quantitative and qualitative evolution of innate CD8 T cells between the 2 arms (abrupt cessation of ITK treatment versus progressive withdrawal) and look for a predictive innate CD8 T cells blood signature at the time of stopping treatment of a successful TFR in both arms.

The purpose of this study is to determine the clinical benefit of XY0206 therapy in participants with FLT3-ITD mutated AML who are refractory to or have relapsed after prior AML therapy as shown with overall survival (OS) compared to salvage chemotherapy. In addition, this study is also to investigate the efficacy of XY0206 as assessed by CR/CRh rate in these subjects。

This phase Ib trial tests the safety, side effects, and best dose of SNDX-5613 when given in combination with the standard chemotherapy treatment (daunorubicin and cytarabine) in treating patients with newly diagnosed acute myeloid leukemia that has changes in the NPM1 gene or MLL/KMT2A gene. SNDX-5613 blocks signals passed from one molecule to another inside cancer cells that are needed for cancer cell survival. Drugs used in chemotherapy, such as daunorubicin and cytarabine, work in different ways to stop the growth of cancer cells, either by killing the cells, by stopping them from dividing, or by stopping them from spreading. Adding SNDX-5613 to the standard chemotherapy treatment may be able to shrink or stabilize the cancer for longer than the standard chemotherapy treatment alone.

The purpose of this study is to determine the safety, efficacy and pharmacokinetics of mitoxantrone hydrochloride liposome injection combined with chemotherapy in previously untreated de novo acute myeloid leukemia.

Genetic mutations have closely linked to the pathogenesis and prognostication of myeloid cancers. In addition, a number of molecularly targeted agents have been developed in recent years. With the advent of next generation sequencing (NGS), we now are able to detect a wide range of mutations more rapidly, accurately, and economically. In this study, the investigators will use NGS to screen and analyze myeloid-associated gene mutations in the participants, and aim to build up the mutational landscapes of the various myeloid cancers, and investigate how these mutations are linked to clinical outcome.

According to the French National Cancer Institute, 35 000 new hematologic cancers are observed in France representing 10% of the new cancers. Chronic Myeloid Leukemia (CML) is a cancer involving the bone marrow and blood cells, the median age at diagnosis is 53 years in the Western world. The prognosis is worse than many other cancers with net survival at 5 years of 26%. Since the approval of imatinib, additional tyrosine kinase inhibitors (TKIs) have been approved by the European Medicine Agency, including the second-generation TKIs nilotinib, dasatinib, and bosutinib and the third-generation TKI ponatinib. Despite their effect on the evolution of CML, there is increasing of cardiovascular toxicities which can impact patient morbidity and mortality. The majority of the cardiovascular toxicities are associated with the second- and third-generation TKIs. Nilotinib and ponatinib cardiovascular toxicity including arterial and venous thromboembolism has decrease the benefit/risk ratio, 10% of patients treated with nilotinib 300 mg twice daily and 15.9% treated with 400 mg twice daily experienced a vascular complication including myocardial infarction /ischemic heart disease, cerebrovascular accidents, or peripheral arterial disease. Regarding ponatinib, serious arterial occlusive adverse reactions occurred in 19% of patients. In an attempt to reduce major adverse cardiovascular events MACE due to nilotinib and ponatinib, currently, then approach is driven by usual clinical practice without any robust published evidence. The investigators aim to perform a national clinical trial, multicenter, prospective, randomized, with two parallel comparative arms: experimental group with cardiovascular active prevention vs non active cardiovascular active prevention based on usual clinical practice. Our hypothesis is that active prevention of cardiovascular toxicities with optimal medical treatment improves the benefit-risk ratio in CML patients. The primary objective is Event Free Survival (EFS) at month 24.