Acute Leukemia

DNMT3A R882 mutations were associated with older age, higher white blood cell count, and FAB M4 and M5 subtypes compared to wildtype DNMT3A in a cohort of cytogenetically normal AML patients.

PMID 24512939 · El Ghannam et al., 2014 · Open in CIViC

In a large cohort of AML patients (mean = 48 years), DNMT3A mutation (64.5% of which were R882) had no prognostic value on overall, relapse free and event free survival.

PMID 23632886 · Gaidzik et al., 2013 · Open in CIViC

In a large cohort (n=1770) of AML patients (18-60 years old), DNMT3A mutation status (65.4% of which were R882) had no prognostic value for overall, relapse free and event free survival. This was true… (full text at CIViC)

PMID 23632886 · Gaidzik et al., 2013 · Open in CIViC

In a large cohort of young AML patients (18-60 years old), DNMT3A R882 mutations were associated with reduced relapse free survival in the entire cohort as well as the subset of patients with cytogene… (full text at CIViC)

PMID 23632886 · Gaidzik et al., 2013 · Open in CIViC

DNMT3A R882 mutation was associated with reduced relapse free and overall survival in ELN-unfavorable, cytogenetically normal AMLs.

PMID 23632886 · Gaidzik et al., 2013 · Open in CIViC

Therapy-related AML was less common in patients with DNMT3A mutations (64.5% of which were R882) than patients wildtype for DNMT3A in a large cohort of younger (18-60) AML patients.

PMID 23632886 · Gaidzik et al., 2013 · Open in CIViC

DNMT3A mutations (64.5% R882) were associated with older age, higher white blood cell count and cytogenetically normal AML in a large cohort of younger (18-60) AML patients.

PMID 23632886 · Gaidzik et al., 2013 · Open in CIViC

DNMT3A R882 mutations were associated with cytogenetically normal AML in a large cohort of younger (18-60) AML patients.

PMID 23632886 · Gaidzik et al., 2013 · Open in CIViC

DNMT3A mutations were associated with achievement of complete remission in a large cohort of younger (18-60) AML patients.

PMID 23632886 · Gaidzik et al., 2013 · Open in CIViC

Complete remission rate was not different between young AML patients (<60 years old) with or without DNMT3A mutations (60% of which were R882).

PMID 22490330 · Ribeiro et al., 2012 · Open in CIViC

Young AML patients (415 patients; <60 years old) with DNMT3A R882 mutations (n=58) have shorter overall and relapse-free survival than patients with wildtype DNMT3A.

PMID 22490330 · Ribeiro et al., 2012 · Open in CIViC

DNMT3A R882 mutations occur most often in de novo AML patients with intermediate risk cytogenetics (39/194 intermediate risk patients vs 0/89 low and high risk).

PMID 22081665 · LaRochelle et al., 2011 · Open in CIViC

DNMT3A mutations (59% of which were R882) were associated with intermediate risk cytogenetics (including normal karyotype) and not favorable risk cytogenetic abnormalities (PML::RARA, RUNX1::RUNX1T1, … (full text at CIViC)

PMID 21067377 · Ley et al., 2010 · Open in CIViC

Daunorubicin treatment resulted in similar overall survival and disease free survival in de novo AML patients with DNMT3A R882 mutation compared to those who do not harbor this mutation.

PMID 22081665 · LaRochelle et al., 2011 · Open in CIViC

Idarubicin increases the overall survival and disease free survival in de novo AML patients with DNMT3A R882 mutation compared to those who do not harbor this mutation.

PMID 22081665 · LaRochelle et al., 2011 · Open in CIViC

The DNMT3A mutational hotspot at Arg882 (DNMT3A(R882H)) cooperates with NRAS mutation to transform hematopoietic stem/progenitor cells and induce acute leukemia development. Mechanistically, DNMT3A(R8… (full text at CIViC)

PMID 27344947 · Lu et al., 2016 · Open in CIViC

DNMT3A R882P somatic mutation, together with R882H, R882C and R882S were identified from Acute Myeloid Leukemia (AML) patients. And R882P, R882H and R882C were revealed as significant hotspot mutation… (full text at CIViC)

PMID 21067377 · Ley et al., 2010 · Open in CIViC

Ph- ALL (Philadelphia chromosome negative acute lymphoblastic leukemia) gene expression profiles cluster into two main groups, Ph like and non-Ph like ALL. Non-Ph like ALL have favorable outcomes whe… (full text at CIViC)

PMID 27019113 · Yasuda et al., 2016 · Open in CIViC

A screen for fusion genes in Ph- AYA-ALL (Philadelphia chromosome negative acute lymphoblastic leukemia in adolescents and young adults) was performed using RNA-seq from multiple cohorts of ALL patien… (full text at CIViC)

PMID 27019113 · Yasuda et al., 2016 · Open in CIViC

Integrated genomic analysis of was performed for 1,988 childhood and adult B-ALL cases. 106 cases (5.3%) showed DUX4 rearrangements, commonly with the IGH region. These cases were characterized by a u… (full text at CIViC)

PMID 30643249 · Gu et al., 2019 · Open in CIViC

The HT93A cell line was established from a patient with acute myelogenous leukemia (AML-M3). The patient was a 66 yr old man and was successfully induced to first and second remission with combined ch… (full text at CIViC)

PMID 10706884 · Iijima et al., 2000 · Open in CIViC

In a study of 176 ALL patients, consisting of 136 B- and 40 T-lineage, multiplex nested RT-PCR was used to look for ETV6 fusions. One patient had ETV6::ABL2 fusion. Patient was a 17 year old with kary… (full text at CIViC)

PMID 22373549 · Zhou et al., 2012 · Open in CIViC

The patient derived MT-ALL cell line was established from a mature T-ALL in first relapse. Uncultured blasts had an immunophenotype of mature CD3+ TCRa/b+ T lymphocytes with a functional T-cell rece… (full text at CIViC)

PMID 12406085 · Griesinger et al., 2002 · Open in CIViC

Rearrangements involving the neurotrophic receptor kinase genes (NTRK1, NTRK2, and NTRK3; hereafter referred to as TRK) produce oncogenic fusions in a wide variety of cancers in adults and children. I… (full text at CIViC)

PMID 29920189 · Taylor et al., 2018 · Open in CIViC

Two AML cell lines, IMS-M2 and M0-91, with the ETV6-NTRK3 fusion were treated with entrectinib. Sequencing of these cell lines found no other driver mutations in 265 other cancer genes suggesting the… (full text at CIViC)

PMID 29237803 · Smith et al., 2018 · Open in CIViC

Two family pedigrees (one family with three generations and a small 4 member family spanning two generations) are presented. Exome sequencing was performed with 8 individuals from the first family, an… (full text at CIViC)

PMID 25807284 · Noetzli et al., 2015 · Open in CIViC

The A687V EZH2-mutant SUP-B8 B-ALL cell line exhibited the greatest sensitivity to EZH2 inhibitor (GSK126) compared to 7 other EZH2 wild-type B-ALL cell lines by cell proliferation assay. The increase… (full text at CIViC)

PMID 25253781 · Ott et al., 2014 · Open in CIViC

In mouse models, constitutive NOTCH signaling contributes to the genesis of breast cancer, medulloblastoma, and T cell leukemia, whereas in human cancer its role is best exemplified by T cell acute ly… (full text at CIViC)

PMID 17646409 · O'Neil et al., 2007 · Open in CIViC

AML MOLM14 cells were cocultured with FLT3 inhibitor AC220 (10 nM) and selected proteins expressed in the bone marrow microenvironment. FL and FGF2 were the only proteins that increased viability >2 s… (full text at CIViC)

PMID 27671675 · Traer et al., 2016 · Open in CIViC

In this preclinial trial, the AML cell line KG1 with FGFR1OP2-FGFR1 mutation was treated with Ponatinib. This drug effectively inhibits both FGFR phosphorylation and viability for KG1 cells at IC50 va… (full text at CIViC)

PMID 21482694 · Gozgit et al., 2011 · Open in CIViC

In this preclinial trial, the AML cell line EOL1 with FIP1L1-PDGFR alpha mutation was treated with Ponatinib. This drug effectively inhibits both PDGFR phosphorylation and viability for EOL1 cells at … (full text at CIViC)

PMID 21482694 · Gozgit et al., 2011 · Open in CIViC

In a preclinical trial, EOL1 AML cell lines with the FIP1L1-PDGFRa fusion mutation were treated with the tyrosine kinase inhibitors (TKI) ponatinib, sorafenib, and sunitinib. Ponatinib was similarly e… (full text at CIViC)

PMID 21482694 · Gozgit et al., 2011 · Open in CIViC

A panel of 13 FLT3 tyrosine kinase inhibitors was tested against Ba/F3 cells transfected with FLT3 D593del using MTT growth/survival assay, and results were compared to Ba/F3 cells transfected with FL… (full text at CIViC)

PMID 28077790 · Nguyen et al., 2017 · Open in CIViC

A panel of 13 FLT3 tyrosine kinase inhibitors was tested against Ba/F3 cells transfected with FLT3 D593del using MTT growth/survival assay, and results were compared to Ba/F3 cells transfected with FL…

In a Phase 1-2 trial of patients with relapsed / refractory AML, patients were enrolled in 7 dose-escalation or dose-expansion cohorts. Gilteritinib monotherapy was well tolerated, generated high resp… (full text at CIViC)

PMID 28645776 · Perl et al., 2017 · Open in CIViC

An in-vitro saturation mutagenesis screen of 50 independently derived FLT3-ITD clones was performed to identify mutations that confer resistance to ponatinib. Mutations at 3 AL residues (D835 [n = 31]… (full text at CIViC)

PMID 23430109 · Smith et al., 2013 · Open in CIViC

In a retrospective study of 15 acute myeloid leukemia patients, the patients with FLT3 D835 mutation (n=2) were associated with improved response to sunitinib treatment (2/2 vs. 2/7) compared to FLT3 … (full text at CIViC)

PMID 15459012 · Fiedler et al., 2005 · Open in CIViC

D835G was originally identified from an AML patient. Transfection of D835G into Ba/F3 cells led to IL3 independent growth, indicating an oncogenic driver effect for the variant in these cells. This ev… (full text at CIViC)

PMID 28077790 · Nguyen et al., 2017 · Open in CIViC

Ba/F3 cells were transfected to express FLT3-ITD or FLT3 tyrosine kinase domain mutations. Immunoblots revealed gilteritinib IC50s of 2nM, 1.6nM, and 5nM for D835H, FLT3-ITD, and wildtype (cell line: … (full text at CIViC)

PMID 27908881 · Lee et al., 2017 · Open in CIViC

Three children with relapsed or refractory FLT3-ITD-positive AML were treated with sorafenib. FLT3 mutations were assessed before treatment and at the time of resistance. During the initiation of the … (full text at CIViC)

PMID 23969938 · Baker et al., 2013 · Open in CIViC

Mouse Ba/F3 cells with FLT3 mutations were evaluated for sorafenib resistance. Cells with single FLT3 (D835H/Y) mutants were resistant to sorafenib (IC50 81 nm/210 nM) whereas cells with FLT3 (ITD) m… (full text at CIViC)

PMID 23969938 · Baker et al., 2013 · Open in CIViC