KRAS and CREBBP mutations: a relapse-linked malicious liaison in childhood high hyperdiploid acute lymphoblastic leukemia.

PubWeight™: 0.96‹?› | Rank: Top 15%

🔗 View Article (PMC 4530204)

Published in Leukemia on April 28, 2015

Authors

K Malinowska-Ozdowy1, C Frech1, A Schönegger2, C Eckert3, G Cazzaniga4, M Stanulla5, U zur Stadt6, A Mecklenbräuker1, M Schuster2, D Kneidinger1, A von Stackelberg3, F Locatelli7, M Schrappe8, M A Horstmann6, A Attarbaschi9, Christoph Bock10, G Mann9, O A Haas11, R Panzer-Grümayer1

Author Affiliations

1: Children's Cancer Research Institute (CCRI), Leukemia Biology Group, Vienna, Austria.
2: Research Center for Molecular Medicine (CeMM), Vienna, Austria.
3: Department of Pediatric Oncology/Hematology, Charité Universitätsmedizin Berlin, Berlin, Germany.
4: Centro Ricerca Tettamanti, University of Milano-Bicocca, Ospedale San Gerardo, Monza, Italy.
5: Department of Pediatric Hematology and Oncology, Hannover Medical School, Hannover, Germany.
6: Clinic of Pediatric Hematology and Oncology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
7: Department of Pediatric Hematology-Oncology, IRCCS Bambino Gesù Hospital, Rome, Italy.
8: Department of Pediatrics, Medical University of Schleswig Holstein, Kiel, Germany.
9: St. Anna Kinderspital, Medical University Vienna, Vienna, Austria.
10: 1] Max Planck Institute for Informatics, Saarbrücken, Germany. [2] CeMM Research Center for Molecular Medicine of the Austrian Academy of Sciences, Vienna, Austria. [3] Department of Laboratory Medicine, Medical University of Vienna, Vienna, Austria.
11: 1] Children's Cancer Research Institute (CCRI), Leukemia Biology Group, Vienna, Austria [2] St. Anna Kinderspital, Medical University Vienna, Vienna, Austria.

Articles citing this

Mutational landscape, clonal evolution patterns, and role of RAS mutations in relapsed acute lymphoblastic leukemia. Proc Natl Acad Sci U S A (2016) 0.82

The role of the RAS pathway in iAMP21-ALL. Leukemia (2016) 0.79

Integration of genetic and clinical risk factors improves prognostication in relapsed childhood B-cell precursor acute lymphoblastic leukemia. Blood (2016) 0.78

Childhood acute lymphoblastic leukemia: Integrating genomics into therapy. Cancer (2015) 0.78

ZNF384-related fusion genes define a subgroup of childhood B-cell precursor acute lymphoblastic leukemia with a characteristic immunotype. Haematologica (2016) 0.78

Control of CREB expression in tumors: from molecular mechanisms and signal transduction pathways to therapeutic target. Oncotarget (2016) 0.76

Clonal and microclonal mutational heterogeneity in high hyperdiploid acute lymphoblastic leukemia. Oncotarget (2016) 0.75

The Role of Histone Protein Modifications and Mutations in Histone Modifiers in Pediatric B-Cell Progenitor Acute Lymphoblastic Leukemia. Cancers (Basel) (2017) 0.75

Genomic characterization of paediatric acute lymphoblastic leukaemia: an opportunity for precision medicine therapeutics. Br J Haematol (2016) 0.75

Genetic drivers of vulnerability and resistance in relapsed acute lymphoblastic leukemia. Proc Natl Acad Sci U S A (2016) 0.75

High hyperdiploid childhood acute lymphoblastic leukemia: Chromosomal gains as the main driver event. Mol Cell Oncol (2015) 0.75

A novel independence test for somatic alterations in cancer shows that biology drives mutual exclusivity but chance explains most co-occurrence. Genome Biol (2016) 0.75

Genomic and transcriptional landscape of P2RY8-CRLF2-positive childhood acute lymphoblastic leukemia. Leukemia (2016) 0.75

Articles cited by this

Fast and accurate short read alignment with Burrows-Wheeler transform. Bioinformatics (2009) 190.94

A framework for variation discovery and genotyping using next-generation DNA sequencing data. Nat Genet (2011) 59.36

Genome-wide analysis of genetic alterations in acute lymphoblastic leukaemia. Nature (2007) 17.68

Sensitive detection of somatic point mutations in impure and heterogeneous cancer samples. Nat Biotechnol (2013) 16.13

VarScan 2: somatic mutation and copy number alteration discovery in cancer by exome sequencing. Genome Res (2012) 15.90

Mutational processes molding the genomes of 21 breast cancers. Cell (2012) 11.22

Clonal evolution in cancer. Nature (2012) 11.07

Hyperactive Ras in developmental disorders and cancer. Nat Rev Cancer (2007) 10.27

Genomic analysis of the clonal origins of relapsed acute lymphoblastic leukemia. Science (2008) 9.25

Acute lymphoblastic leukemia. N Engl J Med (2004) 7.83

Rubinstein-Taybi syndrome caused by mutations in the transcriptional co-activator CBP. Nature (1995) 7.11

RAS oncogenes: weaving a tumorigenic web. Nat Rev Cancer (2011) 6.45

Inactivating mutations of acetyltransferase genes in B-cell lymphoma. Nature (2011) 5.20

MuSiC: identifying mutational significance in cancer genomes. Genome Res (2012) 4.73

Origins of chromosome translocations in childhood leukaemia. Nat Rev Cancer (2003) 4.58

Molecular response to treatment redefines all prognostic factors in children and adolescents with B-cell precursor acute lymphoblastic leukemia: results in 3184 patients of the AIEOP-BFM ALL 2000 study. Blood (2010) 4.17

CREBBP mutations in relapsed acute lymphoblastic leukaemia. Nature (2011) 3.72

The genomic landscape of hypodiploid acute lymphoblastic leukemia. Nat Genet (2013) 3.43

Key pathways are frequently mutated in high-risk childhood acute lymphoblastic leukemia: a report from the Children's Oncology Group. Blood (2011) 3.40

Prognostic effect of chromosomal abnormalities in childhood B-cell precursor acute lymphoblastic leukaemia: results from the UK Medical Research Council ALL97/99 randomised trial. Lancet Oncol (2010) 3.02

Risk-adjusted therapy of acute lymphoblastic leukemia can decrease treatment burden and improve survival: treatment results of 2169 unselected pediatric and adolescent patients enrolled in the trial ALL-BFM 95. Blood (2008) 2.68

Long-term outcome in children with relapsed acute lymphoblastic leukemia after time-point and site-of-relapse stratification and intensified short-course multidrug chemotherapy: results of trial ALL-REZ BFM 90. J Clin Oncol (2010) 2.53

Molecular allelokaryotyping of pediatric acute lymphoblastic leukemias by high-resolution single nucleotide polymorphism oligonucleotide genomic microarray. Blood (2007) 2.31

Using Drosophila melanogaster as a Model for Genotoxic Chemical Mutational Studies with a New Program, SnpSift. Front Genet (2012) 2.21

Ras pathway mutations are prevalent in relapsed childhood acute lymphoblastic leukemia and confer sensitivity to MEK inhibition. Blood (2014) 2.00

Targeting oncogenic Ras signaling in hematologic malignancies. Blood (2012) 1.67

High hyperdiploid childhood acute lymphoblastic leukemia. Genes Chromosomes Cancer (2009) 1.49

PathScan: a tool for discerning mutational significance in groups of putative cancer genes. Bioinformatics (2011) 1.46

Mutations of FLT3, NRAS, KRAS, and PTPN11 are frequent and possibly mutually exclusive in high hyperdiploid childhood acute lymphoblastic leukemia. Genes Chromosomes Cancer (2008) 1.39

Genetic landscape of high hyperdiploid childhood acute lymphoblastic leukemia. Proc Natl Acad Sci U S A (2010) 1.37

Ras proteins: paradigms for compartmentalised and isoform-specific signalling. Cell Mol Life Sci (2007) 1.30

The origin and nature of tightly clustered BTG1 deletions in precursor B-cell acute lymphoblastic leukemia support a model of multiclonal evolution. PLoS Genet (2012) 1.23

ETV6/RUNX1-positive relapses evolve from an ancestral clone and frequently acquire deletions of genes implicated in glucocorticoid signaling. Blood (2011) 1.21

Relapsed childhood high hyperdiploid acute lymphoblastic leukemia: presence of preleukemic ancestral clones and the secondary nature of microdeletions and RTK-RAS mutations. Leukemia (2010) 1.19

CREBBP HAT domain mutations prevail in relapse cases of high hyperdiploid childhood acute lymphoblastic leukemia. Leukemia (2012) 1.18

RAS mutation is associated with hyperdiploidy and parental characteristics in pediatric acute lymphoblastic leukemia. Leukemia (2005) 1.17

Histone-modifying enzymes: regulators of developmental decisions and drivers of human disease. Epigenomics (2012) 1.10

Nondisjunction of chromosomes leading to hyperdiploid childhood B-cell precursor acute lymphoblastic leukemia is an early event during leukemogenesis. Blood (2002) 1.08

Whole exome sequencing identifies novel recurrently mutated genes in patients with splenic marginal zone lymphoma. PLoS One (2013) 1.05

Prenatal origin of hyperdiploid acute lymphoblastic leukemia in identical twins. Leukemia (2003) 1.03

Ras signaling requires dynamic properties of Ets1 for phosphorylation-enhanced binding to coactivator CBP. Proc Natl Acad Sci U S A (2010) 1.01

Use of allogeneic hematopoietic stem-cell transplantation based on minimal residual disease response improves outcomes for children with relapsed acute lymphoblastic leukemia in the intermediate-risk group. J Clin Oncol (2013) 1.00

Is histone acetylation the most important physiological function for CBP and p300? Aging (Albany NY) (2012) 0.95

Minimal residual disease after induction is the strongest predictor of prognosis in intermediate risk relapsed acute lymphoblastic leukaemia - long-term results of trial ALL-REZ BFM P95/96. Eur J Cancer (2012) 0.93

Small sizes and indolent evolutionary dynamics challenge the potential role of P2RY8-CRLF2-harboring clones as main relapse-driving force in childhood ALL. Blood (2012) 0.91

Doxorubicin or daunorubicin given upfront in a therapeutic window are equally effective in children with newly diagnosed acute lymphoblastic leukemia. A randomized comparison in trial CoALL 07-03. Pediatr Blood Cancer (2012) 0.86