View clinical trials related to Chronic Myeloid Leukemia.
Filter by:Treatment of chronic myeloid leukemia (CML) has been revolutionized by tyrosine kinase inhibitor (TKI). Nevertheless, case of failure and suboptimal response are still observed even in children. Pediatric CML is a rare disease and differs from adult in terms of disease presentation and treatment response underlying a likely different CML biology. Molecular mechanisms that induce resistance to TKI are still poorly characterized except mutations in the tyrosine kinase domain of BCR::ABL1. We propose to search for a molecular signature to predict the response to TKI in the pediatric population.
Chronic myeloid leukemia (CML) is a stem cell (SC) neoplasm which originates from an incomplete process of differentiation of the hematopoietic stem cells (HSCs) to the adult cells which lead to accumulation of their immature form into the BM and the peripheral blood. It is characterized by the reciprocal translocation. The resulting oncoprotein, BCR/ABL1, is considered essential for the initiation and manifestation of the disease . In CML, leukemic stem cell (LSC) supposedly resides within the CD45+/ CD34+/CD38-/Lin- fraction of the leukemic clone (3). However, normal hematopoietic SC also exhibit this phenotype so that additional markers are required to discriminate CML LSC from normal SC. CD34+/CD38-/Lin- CML LSC specifically co-express dipeptidylpeptidase IV(DPPIV=CD26). This enzyme disrupts LSC-niche interactions by degrading stroma derived factor-1 (SDF-1). Moreover, CD26 is a robust biomarker for the quantification and isolation of CML LSC (4). It was reported that CD26+ LSCs were significantly correlated with BCR-ABL1 transcript level at diagnosis and after three months of treatment with tyrosine kinase inhibitor (TKI) .
Retrospective, non-interventional observational cohort study conducted among patients with CML.
Improving the quality of life and achieving Treatment-Free Remission(TFR) is a long-term goal of treatment in CML-CP patients, and deep molecular response (DMR) is necessary to achieve TFR. Cording to the historical literature, it is reported that patients with CML-CP take MMR as the therapeutic target, and the acquisition rate of DMR under long-term TKI treatment is 50%. The 2-year success rate of TFR patients was 50%. Therefore, maybe only 25% of patients with CML can successfully stop the drug for a long time. It cannot meet the withdrawal needs of patients with long-term drug survival. This study is to design a real-world observational registration study for optimal effect. On the premise of taking DMR as the target decision, through initial treatment intervention, improve the DMR rate, which will promote clinical practice, so as to improve the 2-year TFR rate of cml-cp patients. This study is a multicenter, observational, prospective registry to identify the optimal treatment for achieving TFR in CML patients. In this study, the investigators will assess the deep molecular response after 12 months of treatment and the 2-year treatment-free remission rate (TFR 2y) after drug discontinuation. Eligible participants with CML-CP can be enrolled. The observation period of all participants is at least 60 months, of which the first 36 months is the shortest treatment period, and the last 24 months is the TFR observation period after TKIs (Imatinib/Flumatinib/Nilotinb/ Dasatinib) withdrawal. During the treatment phase, participants can receive TKIs ± IFN (or other treatments) as first-line/second-line treatment, and the treatment plan will be adjusted according to the molecular response. Patients should accept TKI treatment for at least 3 years or more, and MR4/MR4.5 should achieve at least 2 years before discontinuation.
The purpose of this study is to evaluate the efficacy and safety of azacitidine，venetoclax，and flumatinib in newly diagnosed Philadelphia chromosome-positive acute leukemia and accelerated phase or blast phase chronic myeloid leukemia patients.
Uncontrolled, central registration system, all-case, multicenter, special drug use-results surveillance.
The aim of this study is to establish if consolidation of imatinib-treated patients in stable DMR through the addition of asciminib, can lead to superior rates of TFR1, compared to imatinib alone in Chronic Phase-Chronic Myelogenous Leukemia patients.
One of the ways that cancer grows and spreads is by avoiding the immune system.NK cells are immune cells that kill cancer cells, but are often malfunctioning in people with colorectal cancer and blood cancers. A safe way to give people with colorectal cancer and blood cancers fresh NK cells from a healthy donor has recently been discovered. The purpose of this study is to show that using two medicines (vactosertib and IL-2) with NK cells will be safe and will activate the donor NK cells. NK cells and vactosertib are experimental because they are not approved by the Food and Drug Administration (FDA). IL-2 (Proleukin®) has been approved by the FDA for treating other cancers, but the doses used in this study are lower than the approved doses and it is not approved to treat colorectal cancer or blood cancers.
This study aims to monitor the levels of soluble L-selectin (sCD62L) and secreted protein acidic rich in cysteine (SPARC) in chronic phase chronic myeloid leukemia (CP-CML) patients at baseline and after three and six months of imatinib therapy and evaluated the effect of imatinib on their levels and correlated their levels to clinical and laboratory parameters.
This will be a multicenter Phase II open-label study of asciminib in CML-CP patients who have been previously treated with one prior ATP- binding site TKI with discontinuation due to treatment failure, warning or intolerance. (2L patient cohort). In addition, newly diagnosed CML-CP patients who may have received up to 4 weeks of prior TKI are included in a separate 1L patient cohort.