Genome-wide association analysis identifies SNPs predictive of leukemic cell sensitivity to cytarabine in pediatric AML

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Genome-wide association analysis identifies SNPs predictive of leukemic cell sensitivity to cytarabine in pediatric AML

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im Oktober 2018 veröffentlichter wissenschaftlicher Artikel

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wetenschappelijk artikel

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наукова стаття, опублікована в жовтні 2018

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Genome-wide association analys ...... to cytarabine in pediatric AML

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Genome-wide association analys ...... to cytarabine in pediatric AML

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Genome-wide association analys ...... to cytarabine in pediatric AML

@en

Genome-wide association analys ...... to cytarabine in pediatric AML

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Genome-wide association analys ...... to cytarabine in pediatric AML

@en

Genome-wide association analys ...... to cytarabine in pediatric AML

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P1476

Genome-wide association analys ...... to cytarabine in pediatric AML

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P2093

Huiyun Wu

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James R Downing

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Jatinder K Lamba

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Jeffrey E Rubnitz

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Kristine R Crews

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Raul C Ribeiro

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Roya Rafiee

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Salma A Bargal

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Stanley B Pounds

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Xueyuan Cao

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P2860

Gemcitabine and arabinosylcytosin pharmacogenomics: genome-wide association and drug response biomarkers

Human insulin receptor and its relationship to the tyrosine kinase family of oncogenes

Estimation of the multiple testing burden for genomewide association studies of nearly all common variants

GPR56 identifies primary human acute myeloid leukemia cells with high repopulating potential in vivo.

Autocrine IGF-1/IGF-1R signaling is responsible for constitutive PI3K/Akt activation in acute myeloid leukemia: therapeutic value of neutralizing anti-IGF-1R antibody

Data quality control in genetic case-control association studies.

Potential mechanisms of resistance to cytarabine in AML patients.

Gemtuzumab ozogamicin in children and adolescents with de novo acute myeloid leukemia improves event-free survival by reducing relapse risk: results from the randomized phase III Children’s Oncology Group trial AAML0531.

Maintenance of the hematopoietic stem cell pool in bone marrow niches by EVI1-regulated GPR56.

MN1 overexpression is an important step in the development of inv(16) AML.

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34859-34875

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P31

scholarly article

P356

10.18632/ONCOTARGET.26163

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P407

English

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P478

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P577

2018-10-09T00:00:00Z

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P698

30405880

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P921

genome-wide association study

leukemia

P932

6201857

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