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Leukemia, Myeloid, Acute clinical trials

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NCT ID: NCT03787498 Completed - Clinical trials for High-risk Myelodysplastic Syndrome (MDS)

A Study of PLX2853 in Relapsed or Refractory Acute Myeloid Leukemia or High Risk Myelodysplastic Syndrome

Start date: March 19, 2019
Phase: Phase 1
Study type: Interventional

The purpose of this research study is to evaluate safety, pharmacokinetics, pharmacodynamics and preliminary efficacy of the investigational drug PLX2853 in subjects with Relapsed or Refractory Acute Myeloid Leukemia or High-risk Myelodysplastic Syndrome

NCT ID: NCT03760237 Completed - Clinical trials for Leukemia, Myeloid, Acute

Cardiovascular Function in Acute Leukemia

Start date: December 10, 2018
Phase:
Study type: Observational [Patient Registry]

An observational, prospective study to describe the rates and predictors of cardiovascular events in patients with acute leukemia.

NCT ID: NCT03755154 Completed - Clinical trials for Relapsed or Refractory Multiple Myeloma

Study of a New Intravenous Drug, Called S65487, in Patients With Acute Myeloid Leukemia, Non Hodgkin Lymphoma, Multiple Myeloma or Chronic Lymphocytic Leukemia

Start date: July 17, 2019
Phase: Phase 1
Study type: Interventional

The purpose of this first in human study is to assess safety, tolerability, Pharmacokinetic (PK) and preliminary clinical activity and to estimate the Maximum Tolerated Doses (MTD(s))/ Recommended Phase 2 Doses (RP2D(s)) of S65487 as single agent administered intravenously (i.v.) in adult patients with refractory or relapsed Acute Myeloid Leukemia (AML), Non-Hodgkin Lymphoma (NHL), Multiple Myeloma (MM) or Chronic Lymphocytic Leukemia (CLL).

NCT ID: NCT03735875 Completed - Clinical trials for Recurrent Acute Myeloid Leukemia

Venetoclax and Quizartinib in Treating Patients With FLT3-mutated Recurrent or Refractory Acute Myeloid Leukemia

Start date: January 25, 2019
Phase: Phase 1/Phase 2
Study type: Interventional

This phase Ib/II trial studies the side effects and best dose of venetoclax in combination with quizartinib and how well they work in treating patients with acute myeloid leukemia that has come back or does not respond to treatment, and who are FLT3-mutation positive. Venetoclax and quizartinib may stop the growth of cancer cells by blocking some of the enzymes needed for cell growth.

NCT ID: NCT03730012 Completed - Clinical trials for Acute Myeloid Leukemia (AML)

A Study of ASP2215 (Gilteritinib) Combined With Atezolizumab in Patients With Relapsed or Treatment Refractory FMS-like Tyrosine Kinase (FLT3) Mutated Acute Myeloid Leukemia (AML)

Start date: June 19, 2019
Phase: Phase 1/Phase 2
Study type: Interventional

The purpose of this study was to determine the safety and tolerability of gilteritinib given in combination with atezolizumab in participants with relapsed or treatment refractory FMS-like tyrosine kinase 3 (FLT3) mutated AML and to determine the composite complete remission (CRc) rate for participants who either discontinued the study or completed 2 cycles of gilteritinib given in combination with atezolizumab. This study also evaluated pharmacokinetics (PK), response to treatment, remission and survival. Adverse events (AEs), clinical laboratory results, vital signs, electrocardiograms (ECGs), and Eastern Cooperative Oncology Group (ECOG) performance status scores were also assessed.

NCT ID: NCT03728699 Completed - Clinical trials for Acute Myeloid Leukemia

Microbiota Changes in Acute Myeloid Leukemia Patients Undergoing Intensive Chemotherapy

Start date: January 2, 2018
Phase:
Study type: Observational

This is a prospective, observational study to collect stool and blood from acute myeloid leukemia patients undergoing intensive chemotherapy.

NCT ID: NCT03723681 Completed - Clinical trials for Acute Myeloid Leukemia (AML)

Study of Quizartinib in Combination With Standard Therapies in Chinese Participants With Newly Diagnosed Acute Myeloid Leukemia (AML)

Start date: November 5, 2018
Phase: Phase 1
Study type: Interventional

20 mg or 40 mg of quizartinib will be given to Chinese patients who were just diagnosed with AML. The study drug will be given to them along with standard therapies. The purpose is to find out the highest dose they can stand.

NCT ID: NCT03720366 Completed - Clinical trials for Leukemia, Myeloid, Acute

A Study of Perpetrator Drug Interactions of Enasidenib in AML Patients

Start date: October 4, 2018
Phase: Phase 1
Study type: Interventional

This is a 2-part, open-label, interventional study conducted in approximately 42 subjects with AML harboring an IDH2 mutation. The overall study is a 3-arm investigation of the PK effects of enasidenib at steady state on the probe compounds. (Part 1), followed by treatment continuation up to 28 months (Part 2). Each arm utilizes different probe compounds; enrolls a separate cohort of approximately 14 subjects; and consists of 2 parts - investigation of the PK effects of enasidenib on the respective probe compound(s) (Part 1), followed by an enasidenib treatment extension (Part 2).

NCT ID: NCT03719534 Completed - Clinical trials for Acute Myeloid Leukemia

Haplo HCT vs Haplo-cord HCT for Patients With AML

Start date: June 1, 2017
Phase: Phase 3
Study type: Interventional

Patients who have acute myeloid leukemia and will undergo haplo-identical donor hematopoeitic cell transplantation (haplo HCT) are potential candidates of this trial. Participants will randomized into two arms: Arm A will undergo a typical haplo HCT, while Arm B will receive an coinfusion of an unrelated cord blood unit (haplo-cord HCT) in addition to Arm A. Progression-free survival, overall survival, cumulative incidence of relapse and nonrelapse mortality will be recorded as endpoints.

NCT ID: NCT03719183 Completed - Clinical trials for Acute Myeloid Leukemia

Comparison of Diagnostic Yield Among M-FISH, FISH Probe Panel and Conventional Cytogenetic Analysis in AML

Start date: January 1, 2019
Phase:
Study type: Observational

Conventional cytogenetic studies have been the gold standard for more than five decades for detecting genetic alterations that are greater than 10 Mb (mega base pairs) in size. Conventional cytogenetic studies have paved the way in identifying specific chromosomal aberrations associated with clinically and morphologically definitive subsets of hematological neoplasms. Fluorescence in situ hybridization (FISH) has become a reliable and rapid complementary test in targeting critical genetic events associated with diagnostics and prognosis in hematological neoplasms. In the current health care environment, which increasingly focuses on value and efficiency, it is critical for pathologists and clinicians to effectively navigate this environment and judiciously incorporate these high-complexity and expensive techniques into routine patient care. While conventional karyotyping provides a comprehensive view of the genome, FISH can detect cryptic or submicroscopic genetic abnormalities and identify recurrent genetic abnormalities in nondividing cells. As a consequence, it is commonly extrapolated that FISH will improve the sensitivity of detecting all genetic abnormalities compared with conventional karyotyping analysis. This assumption has then been translated in clinical practice to having clinicians and pathologists routinely ordering both conventional karyotyping and FISH studies in patients with hematological neoplasms. Depending on how comprehensive the FISH panel is, the cost for this testing may be quite expensive, and its additive value remains questionable. It is common practice for laboratories to use FISH panels in conjunction with karyotyping both in diagnostic specimens and during follow-up to monitor response to therapy. Multiplex FISH (M-FISH) represents one of the most significant developments in molecular cytogenetics of the past decade. In tumor and leukemia cytogenetics, two groups have been targeted by M-FISH to identify cryptic chromosome rearrangements not detectable by conventional cytogenetic studies: those with an apparently normal karyotype (suspected of harboring small rearrangements not detectable by conventional cytogenetics) and those with a complex aberrant karyotype (which are difficult to karyotype accurately due to the sheer number of aberrations).