Active clinical trials for "Leukemia, Myelogenous, Chronic, BCR-ABL Positive"

The aim of the study is to assesse the levels of various biomarkers, specifically interleukin (IL)-6, platelet-derived microparticles (PDMPs), 11, 12 soluble vascular cell adhesion molecule 1 (sVCAM-1), transforming growth factor (TGF) β1, and sCTLA-4, in TKI-treated patients with CML. To measure the fluctuations in the levels of sCTLA-4, TGFβ1, and PDMPs, and to clarify the clinical significance of these biomarkers during TKI therapy in patients with CML..

To expresse TIGIT in NK Cells in Patients with Chronic Myeloid Leukemia

Research on the mechanism of dasatinib down-regulates the expression of PD-1 in CMV-activated NKG2C+NK cells and enhances killing pH + leukemia stem cells.

Objectives: The objective of this study is to measure and delineate the symptom burden experienced by patients with chronic myeloid leukemia (CML). The Primary Aim is to develop and validate an M. D. Anderson Symptom Inventory (MDASI) module (the MDASI-CML), compliant with FDA standards for patient-reported outcomes (PROs), to measure the severity of multiple symptoms and the impact of these symptoms on daily functioning in patients with CML. The Secondary Aims are: to develop a detailed description of the severity and interference with daily activities of symptoms experienced by patients with CML; to assess the impact of symptom severity in CML on standard functioning and quality of life (QOL) measures including Eastern Cooperative Oncology Group (ECOG) Performance Status and single-item QOL scale; to evaluate the MDASI-CML as an estimate of functional status and QOL in patients with CML; to identify common clusters of symptoms and symptom patterns occurring over multiple measurement time points in patients with CML; 5, to define the qualitative symptom burden of patients with CML; 6. to explore the feasibility of the Interactive Voice Response (IVR) system in measuring symptom severity and interference with daily activities over time in patients with CML.

Patients who suffer from chronic myeloid leukemia are treated by tyrosin kinase inhibitors (TKI) saying imatinib, nilotinib, dasatinib, bosutinib and ponatinib. These drugs are highly efficient with excellent response allowing some patients to definitely stop their cancer treatment. However, in 30% of cases, when the treatment is stopped, pains could arise in shoulders, hips, joints… These symptoms occurring after the withdrawal of a drug are odd and biologically unexplained so far. This study seeks to discover the biological factors behind these symptoms called 'TKI withdrawal syndrome' by the scientific community.

Primary objective : To identify epigenetic dysregulations of in vivo TKI-resisting CML cells Hypothesis : An epigenetic dysregulation is involved in the in vivo survival of a CML cell subclone despite the use of TKIs

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.

The investigators will evaluate the outcomes of allogeneic stem cell transplantation which is the only curative treatment modality in the patients with chronic myeloid leukemia after failing tyrosine kinase inhibitor therapy. However, any update was not reported on the transplant outcomes in the patients failed TKI therapy, thus necessitating update of this data. Also, the European Group for Blood and Marrow Transplantation (EBMT) risk score is still of value, but insufficient numbers of patients have been transplanted in recent years and after TKI therapy to allow a robust reanalysis. Our study hypothesis is that allogeneic SCT treatment modality can rescue CML patients who failed TKI therapy due to resistance or to intolerance with improved survival and long-term outcomes. Also, another hypothesis will be examined if the EBMT risk score proposed pre-imatinib era can reproduce similar prognostic risk stratification of long-term outcomes in the patients treated with TKI.

The purposes of this study are to investigate expression and frequency of ABL point mutations, a major cause of resistance in imatinib failed CML Asian patients and to find causes of Asian-specific resistance to cancer-targeting therapies through a prospective investigation of dynamics of point mutations and expression of new point mutations during nilotinib treatment.

Multi-Center, national, non-drug, prospective cohort study Target patient number is 100 The amount of CD45+/CD34+/CD38-/CD26+ levels of chronic myeloid leukemia (CML) stem cells in CML patients with and without BCR-ABL hematopoiesis will be compared. There will be 2 arms; Patients with BCR-ABL-positive hematopoiesis CML patients with BCR-ABL activity inhibition under tyrosine kinase inhibitor (TKI) therapy