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Relevancia Evaluación Nuevo primero Antiguo primero

Eligibility Leukemia, Myeloid NCT00512083

- 10/01/2018 - 1 formulario, 2 itemgroups, 9 items, 1 idioma
Itemgroups: Inclusion Criteria, Exclusion Criteria
Phase II Study of AS1411 Combined With Cytarabine to Treat Acute Myeloid Leukemia; ODM derived from: https://clinicaltrials.gov/show/NCT00512083

Eligibility Leukemia, Myeloid NCT00611247

- 07/03/2017 - 1 formulario, 2 itemgroups, 20 items, 1 idioma
Itemgroups: Inclusion Criteria, Exclusion Criteria
Phase 2 Study of Temozolomide to Treat Poor Risk / Refractory Acute Myeloid Leukemia; ODM derived from: https://clinicaltrials.gov/show/NCT00611247

dbGaP phs001027 Epigenomics Studies in Acute Myeloid Leukemia (AML) - pht005214.v3.p1

- 27/02/2024 - 6 formularios, 1 itemgroup, 5 items, 1 idioma
Itemgroup: pht005214
Principal Investigator: Francine Garrett-Bakelman, MD, PhD, University of Virginia, Charlottesville, VA, USA; Weill Cornell Medical College, New York, NY, USA MeSH: Acute Myeloid Leukemia https://www.ncbi.nlm.nih.gov/projects/gap/cgi-bin/study.cgi?study_id=phs001027 Acute Myeloid Leukemia (AML) remains a clinical challenge since most patients diagnosed with AML will die from the disease. Some patients harbor treatment-refractory disease and many others relapse with disease that in many cases is resistant to treatments. Our study was designed to understand the molecular basis of disease progression in AML through assessing genomics signatures in patient specimens collected through an international collaboration which assembled samples from 138 AML patients which experienced disease relapse and normal hematopoietic cells (n=15). It is hoped that this resource will help researchers understand mechanisms of disease relapse in AML and contribute to the general pool of data available for analyses for this disease and general research use.

pht005215.v3.p1

1 itemgroup 2 items

pht005216.v3.p1

1 itemgroup 9 items

pht005217.v3.p1

1 itemgroup 11 items

Eligibility

1 itemgroup 3 items

pht005652.v1.p1

1 itemgroup 2 items

dbGaP phs001219 Detection of Genes Predisposing to Hematologic Malignancies - pht007857.v1.p1

- 26/04/2023 - 6 formularios, 1 itemgroup, 2 items, 1 idioma
Itemgroup: pht007857
Principal Investigator: Neil E. Caporaso, MD, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA MeSH: Leukemia, Lymphocytic, Chronic, B-Cell,Hodgkin Disease,Lymphoma, Non-Hodgkin,Waldenstrom Macroglobulinemia,Leukemia, Hairy Cell,Leukemia, Myeloid, Acute,Leukemia, Myelomonocytic, Juvenile https://www.ncbi.nlm.nih.gov/projects/gap/cgi-bin/study.cgi?study_id=phs001219 We have been conducting genetic studies on families at high risk of different hematologic malignancies, in order to define the related tumors in the families, define precursor and other related conditions, and map and identify susceptibility genes. We have focused mainly on four types of lymphoid malignancies: chronic lymphocytic leukemia (CLL), Hodgkin lymphoma (HL), non-Hodgkin lymphoma (NHL), and Waldenström macroglobulinemia (WM). A few families with a rare lymphoma subtype, hairy cell leukemia (HCL) are included. In addition, single large pedigrees with acute myeloid leukemia (AML), and juvenile myelomocytic leukemia (JMML) are included. Families are ascertained for having at least two patients with the same hematologic malignancy and are classified by the type of malignancy that predominates in the family. Multiple types of lymphoid malignancies are often found in the same family. Other data has shown that these conditions aggregate together in families. Verification of cancer diagnoses is obtained through medical records, pathology reports, and flow cytometry. Family members with precursor traits are also included, monoclonal B-cell lymphocytosis (MBL) in CLL families and IgM monoclonal gammopathy of undetermined significance (MGUS) in WM families.

pht007858.v1.p1

1 itemgroup 6 items

Eligibility

1 itemgroup 1 item

pht007859.v1.p1

1 itemgroup 3 items

pht007860.v1.p1

1 itemgroup 10 items

pht007861.v1.p1

1 itemgroup 5 items

dbGaP phs000759 Spectrum of Mutations in Myeloid Neoplasms - pht003911.v1.p1

- 07/12/2022 - 4 formularios, 1 itemgroup, 5 items, 1 idioma
Itemgroup: pht003911
Principal Investigator: Kevin White, PhD, University of Chicago, Chicago, IL, USA MeSH: Leukemia, Myeloid, Acute,Neoplasm, therapy related,Monosomy 7 https://www.ncbi.nlm.nih.gov/projects/gap/cgi-bin/study.cgi?study_id=phs000759 Patients with myeloid malignancies bearing high-risk cytogenetic abnormalities lack effective therapies and have a poor overall survival. -7/del(7q) is identified in half of high-risk myeloid neoplasms. We recently identified *CUX1* to be a haploinsufficient myeloid tumor suppressor gene located within the commonly deleted segment of 7q22. Here we identify the spectrum of somatic mutations that co-occur with loss of *CUX1* and chromosome 7 in patients with *de novo* acute myeloid leukemia (AML) or a therapy-related myeloid neoplasm. -7/del(7q) leukemias have a distinct mutational profile characterized by low frequencies of alterations in major leukemogenic pathways, including genes encoding transcription factors, cohesin, and DNA-methylation-related proteins. In contrast, RAS pathway activating mutations occurred in 40% of -7/del(7q) samples, a significantly higher frequency than other AMLs and higher than previously reported. As targeted therapeutics advance, our data provide guidance for which pathways are most relevant in the treatment of adverse-risk myeloid leukemia.

pht003912.v1.p1

1 itemgroup 5 items

pht003913.v1.p1

1 itemgroup 6 items

pht003914.v1.p1

1 itemgroup 5 items

dbGaP phs000549 Clonal Evolution of Pre-Leukemic HSC Precedes Human AML - pht002990.v1.p1

- 28/11/2022 - 5 formularios, 1 itemgroup, 2 items, 1 idioma
Itemgroup: pht002990
Principal Investigator: Ravindra Majeti, MD, PhD, Stanford University, Stanford, CA, USA MeSH: Leukemia, Myeloid, Acute https://www.ncbi.nlm.nih.gov/projects/gap/cgi-bin/study.cgi?study_id=phs000549 Acute myeloid leukemia is an aggressive clonal malignancy of the bone marrow that is the direct result of sequential acquisition of mutations in a single lineage of cells. In this study, we investigate a model in which this mutational acquisition occurs serially in long-lived self-renewing hematopoietic stem cells eventually resulting in frank acute myeloid leukemia. Coding mutations in multiple AML patients were identified using exome sequencing followed by sanger sequencing validation. The level of these mutations was then assessed in residual hematopoietic stem cells from each patient using targeted deep sequencing. These population-level estimates of mutant allele burden were then validated in single cell assays targeted to the identified mutations. This allowed for determination of the order of acquisition of the mutations that preceded the development of the leukemia. The results of this study identify pre-leukemic hematopoietic stem cell clones that could contribute to patient relapse and outcome.

pht002992.v1.p1

1 itemgroup 5 items

pht002993.v1.p1

1 itemgroup 6 items

pht002991.v1.p1

1 itemgroup 3 items

Eligibility

1 itemgroup 1 item

dbGaP phs000414 Whole Genome Sequencing of CBF-Leukemia - Eligibility

- 12/10/2022 - 4 formularios, 1 itemgroup, 1 item, 1 idioma
Itemgroup: IG.elig
Principal Investigator: James R. Downing, MD, Dept. of Pathology, St. Jude Children's Research Hospital, Memphis, TN, USA MeSH: Acute Myeloid Leukemia https://www.ncbi.nlm.nih.gov/projects/gap/cgi-bin/study.cgi?study_id=phs000414 Pediatric *de novo* acute myeloid leukemia (AML) is a heterogeneous disease that can be divided into clinically distinct subtypes based on the presence of specific chromosomal abnormalities or gene alterations. One of the best characterized subtypes of AML involves leukemias with alterations of the core-binding factor (CBF)-complex, which comprises the FAB subtypes M2 and M4Eo and associates with a favorable outcome. Patients with the AML M2 subtype harbor a translocation between chromosomes 8 and 21 [t(8;21)] that yields the chimeric fusion gene *RUNX1(AML1)-RUNX1T1(ETO)*, while patients with AML M4Eo express the chimeric fusion gene *CBFβ-SMMHC(MYH11)* as a result of an inversion/translocation event of chromosome 16 [inv(16)/t(16;16)]. In an effort to define the total complement of genetic changes in CBF-leukemia, we performed paired-end whole genome sequencing (WGS) on diagnostic leukemia blasts and matched germ line samples from 17 pediatric CBF-leukemia patients using the Illumina platform. Somatic alterations, including single nucleotide variations (SNVs) and structural variations (SVs), including insertions, deletions, inversions, and inter- and intra-chromosomal rearrangements, were detected using complementary analysis pipelines (Bambino, CREST and CONSERTING). Recurrent screening of identified mutations will be performed in a cohort of approximately 94 cases of CBF-leukemias.

pht002729.v1.p1

1 itemgroup 5 items

pht002730.v1.p1

1 itemgroup 5 items

pht002731.v1.p1

1 itemgroup 6 items

dbGaP phs000413 Transcriptome Sequencing of Pediatric AML FAB-M7 - Eligibility

- 12/10/2022 - 6 formularios, 1 itemgroup, 1 item, 1 idioma
Itemgroup: IG.elig
Principal Investigator: James R. Downing, MD, Dept. of Pathology, St. Jude Children' Research Hospital, Memphis, TN, USA MeSH: Acute Megakaryoblastic Leukemia,Acute Myeloid Leukemia https://www.ncbi.nlm.nih.gov/projects/gap/cgi-bin/study.cgi?study_id=phs000413 High resolution analysis of DNA copy number abnormalities and loss-of-heterozygosity on acute myeloblastic leukemia samples utilizing SNP arrays has demonstrated that in contrast to pediatric ALL, de novo AML is characterized by a very low burden of genomic alterations (Radtke, et al., PNAS, 2009). Samples for this study represented a cross-section of the different subtypes of pediatric AML. The only AML subtype that was an outlier from the above observations was acute megakaryocytic leukemia (AML FAB-M7), with the majority of these cases being characterized by complex chromosomal rearrangements and a high number of copy number alterations. To more fully define the genomic landscape of this subtype, we performed transcriptome sequence analysis on 14 pediatric FAB-M7 cases and mutation recurrence screening in a panel of 62 adult and pediatric AML FAB-M7 samples using the Illumina platform. Our results identified chromosomal rearrangements resulting in the expression of novel fusion transcripts in 11/14 cases. Remarkably, in 7/14 cases we detected an inversion on chromosome 16 that results in the juxtaposition of the CBFA2T3 gene next to the GLIS2 gene resulting in a CBFA2T3-GLIS2 chimeric gene that encoded an in frame fusion protein. This fusion led to the acquisition or preservation of self-renewal in colony forming assays, providing functional evidence for a role in leukemogenesis. In addition to novel chimeric transcripts, we found mutations in genes previously identified to play a role in megakaryoblastic leukemia that carry a proliferative advantage to the cell, such as JAK2 and MPL. These data demonstrate that AML FAB-M7 is characterized by cooperating Class I and Class II mutations leading to leukemogenesis.

pht002733.v2.p1

1 itemgroup 5 items

pht002734.v2.p1

1 itemgroup 6 items

pht003037.v1.p1

1 itemgroup 14 items

pht003038.v1.p1

1 itemgroup 2 items

pht002732.v2.p1

1 itemgroup 5 items

On-Study - Acute Myeloid Leukemia (AML) - On-Study Form - Previously Untreated Patients - 2019404v4.0 - Acute Myeloid Leukemia (AML) - On-Study Form - Previously Untreated Patients

- 27/09/2021 - 1 formulario, 4 itemgroups, 32 items, 1 idioma
Itemgroups: CRF Header, AML: Form Administration, AML: Disease Description, Comments
Acute Myeloid Leukemia (AML) - On-Study Form - Previously Untreated Patients Source Form: NCI FormBuilder: https://formbuilder.nci.nih.gov/FormBuilder/formDetailsAction.do?method=getFormDetails&formIdSeq=8D071CA6-C045-F391-E040-BB89AD4376C0

Daunorubicin Acute Myeloid Leukemia NCT02140242 - Adverse events and Death sheet

- 20/09/2021 - 12 formularios, 4 itemgroups, 35 items, 1 idioma
Itemgroups: Adverse Events, Adverse Events specification, Death Sheet, Comments
Randomized Comparison Between Two Dose Levels of Daunorubicin and Between One Versus Two Cycles of Induction Therapy for Adult Patients With Acute Myeloid Leukemia <=60 Years. See further details on: https://www.clinicaltrials.gov/ct2/show/NCT02140242 Principal Investigator: PD Dr. med. Christoph Röllig, MSc Source:PD Dr. med. Christoph Röllig, MSc Universitätsklinikum Dresden

Visit 1 - Medical History

6 itemgroups 47 items

Visit Registration/Randomization I

5 itemgroups 20 items

Visit 13 (End of Study)

20 itemgroups 182 items

Drop out Sheet and visit

15 itemgroups 90 items

Visit 7 (Day 15 Induction I)

10 itemgroups 87 items

Visit 8 (before Day 1 Induction II)

9 itemgroups 123 items

Leukemia Daunorubicin Cytarabine Oblimersen NCT00085124 CALGB - Cytogenetics

- 20/09/2021 - 1 formulario, 1 itemgroup, 25 items, 1 idioma
Itemgroup: Cytogenetics
CALGB: CYTOGENETICS REFERRAL FORM NCT00085124 Daunorubicin and Cytarabine With or Without Oblimersen in Treating Older Patients With Previously Untreated Acute Myeloid Leukemia Source Form: NCI FormBuilder: https://formbuilder.nci.nih.gov/FormBuilder/formDetailsAction.do?method=getFormDetails&formIdSeq=B229EF62-6ADF-5120-E034-0003BA12F5E7

Eligibility Acute Myeloid Leukemia NCT01382147

- 20/09/2021 - 1 formulario, 2 itemgroups, 19 items, 1 idioma
Itemgroups: Inclusion Criteria, Exclusion Criteria
Evaluation of "Dose-dense Therapy" by S-HAM in Comparison to Conventionally Timed Double Induction in Patients With Acute Myeloid Leukemia (AML); ODM derived from: https://clinicaltrials.gov/show/NCT01382147

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