View clinical trials related to Leukemia.
Filter by: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) .
The purpose of this study is to determine the recommended Phase 2 dose(s) (RP2Ds) of JNJ-75276617 in combination with a conventional chemotherapy backbone in pediatric and young adult participants with relapsed/refractory acute leukemia harboring histone-lysine N-methyltransferase 2A1 ([KMT2A1], nucleophosmin 1 gene (NPM1), or nucleoporin alterations in Part 1 (Dose Escalation) and to further evaluate safety at the RP2D(s) of JNJ-75276617 in combination with chemotherapy in pediatric and young adult participants with relapsed/refractory acute leukemia harboring KMT2A1, NPM1, or nucleoporin alterations and safety at the RP2D(s) of JNJ-75276617 as monotherapy in a select low burden of disease cohort in Part 2 (Dose Expansion).
estimation of the clinical characters and out come of adult acute myeloid leukemia patients • correlation of the estimated clinical characters and outcome to the expression of CD200
MiRNAs are noncoding RNAs (ncRNAs) that drive post-transcriptional negative regulation of gene expression by promoting the degradation or translational blockade of their target mRNAs. MiRNAs are 21-24-nucleotide-long RNA molecules that are processed from longer RNA precursors (pri-miRNAs) , and either the 5' or the 3' strand of the mature miRNA duplex is loaded into the Argonaute (AGO) family of proteins to form a miRNA-induced silencing complex (miRISC) When bound to AGO proteins, mature miRNAs destabilize or inhibit the translation of partially complementary target mRNAsMiRNA-124 has been shown to be a tumor suppressor, and a decrease in its expression level is typical of tumors of various localization, but there is no evidence of the role of miRNA-124 in the development of NHL . There are a number of studies reflecting the involvement of miRNA-124 in hematopoiesis. Liu et al. showed that miRNA-124 regulates Tip110 that is involved in the differentiation of hematopoietic stem cellsThe let-7 family has been shown to influence the pathogenesis of a variety of hematological malignancies through the changing expression of a number of oncogenic pathways, particularly those related with MYC and that might affect hematopoietic carcinogenesis through the modulation of inflammatory pathways
This is a phase I, interventional, single arm, open label, treatment study to evaluate the safety and tolerability of anti-CD33 CAR-T cells in patients with relapsed and/or refractory, high risk hematologic malignancies.
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.
Acute lymphoblastic leukemia (ALL) is the most common childhood malignancy in the world. It is a malignant clonal proliferation of lymphoid progenitor cells, but most commonly of the B cell lineage (B ALL). . Acute Lymphoblastic Leukemia (ALL) is a heterogeneous disease that causes malignant hematological disorders at any age. It mainly affects children aged 2 to 5; in fact, 60% of pediatric leukemia cases are ALL, with an incidence of 3-4 cases per 100,000 per year. It is divided into two subtypes B-ALL and T-ALL depending on whether transformation occurs in B- or T-cell precursors, respectively . Leukemic cells apply multiple immune evasion mechanisms resulting in tumor progression. One of the most important immune escape mechanisms is over expression of immune checkpoint receptors and their ligands such as PD-1 and PD-L1 . The PD-1 receptor plays a crucial role in a broad spectrum of immune regulatory mechanisms . It is a negative co-receptor that down regulates T-cell activity . PDL 1, which is known as B7 H1 , is a cell surface protein of B7 family member . PD L1 is expressed on all types of lympho hematopoietic cells at variable levels and is constitutively expressed on T cells, B cells, macrophages, and dendritic cells . Tumors exploit the PD-1/PD-L1 pathway to evade host immune surveillance . PD-1/PD-L1 pathway controls the induction and maintenance of immune tolerance within the tumor microenvironment. The activity of PD-1 and its ligands PD-L1 or PD-L2 are responsible for T cell activation, proliferation, and cytotoxic secretion in cancer to produce anti-tumor immune responses .
1. To evaluate expression levels of CD135 2. To assess the frequency of FLT3 gene mutations (ITD) 3. association between FLT3-ITD mutation and CD135 expression and their correlation with hematological, immunophenotypic,and biochemical features.
Chronic lymphocytic leukemia (CLL) is a clonal lymphoproliferative disorder that is characterized by heterogeneous presentation at the clinical and molecular levels. ITGA4 protein has been found to be deregulated in CLL with adverse clinical outcome. ITGA4 gene (CD49d) encodes a member of the integrin alpha chain family of proteins and is considered a negative prognosticator in CLL with aggressive course and short time to treatment. The aim of the study: is to investigate ITGA4 gene expression pattern in CLL.
Flumatinib is an orally available TKI with high selectivity and potency against BCR-ABL1 kinase. It's a multi-center, open-label, real world study to explore the efficacy and safety of Flumatinib versus Imatinib as the first line therapy in patients with chronic myleiod leukemia(CML) in chronic phase(CP).