We are analyzing https://link.springer.com/article/10.1186/s13045-017-0410-6.

Title:
Genetic alterations of m6A regulators predict poorer survival in acute myeloid leukemia | Journal of Hematology & Oncology
Description:
Methylation of N6 adenosine (m6A) is known to be important for diverse biological processes including gene expression control, translation of protein, and messenger RNA (mRNA) splicing. However, its role in the development of human cancers is poorly understood. By analyzing datasets from the Cancer Genome Atlas Research Network (TCGA) acute myeloid leukemia (AML) study, we discover that mutations and/or copy number variations of m6A regulatory genes are strongly associated with the presence of TP53 mutations in AML patients. Further, our analyses reveal that alterations in m6A regulatory genes confer a worse survival in AML. Our work indicates that genetic alterations of m6A regulatory genes may cooperate with TP53 and/or its regulator/downstream targets in the pathogenesis and/or maintenance of AML.
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Keywords {🔍}

genes, regulatory, patients, aml, additional, file, mutations, genetic, alterations, number, leukemia, figure, copy, data, mutation, article, acute, survival, cancer, table, myeloid, andor, deletion, efs, gene, tcga, pubmed, research, alkbh, cell, mettl, determine, molecular, google, scholar, expression, rna, gain, group, flt, eventfree, pdf, loss, risk, npm, significance, including, poorer, fto, clinicopathological,

Topics {✒️}

acute myeloid leukaemia longitudinal follow-ups show n6-methyladenosine rna demethylase anti-leukemic therapies remains n6-methyladenosine-encoded epitranscriptomics acute myeloid leukemia regulator/downstream targets contribute article download pdf chronic lymphocytic leukemia performed kaplan-meier analysis acute lymphoblastic leukemia m6a regulatory gene white blood cell rna m6a modification m6a rna modification m6a regulatory enzymes privacy choices/manage cookies deletion/copy number loss gene copy number medical research council alkbh5 gene encoding tp53 wild-type patients creative commons license m6a regulatory genes tp53 signaling pathway decreased cell proliferation spur future research regulator/downstream targets poorer cytogenetic risk unfavorable cytogenetic risk copy number variations gene encoding m6a perturbation mediated copy number gain full access kaplan-meier curves copy number variation encode splicing regulators event-free survival cytogenetic risk status poor risk genotypes european economic area play crucial roles broad physiological functions reference population represented including point mutations log-rank test mol clin oncol wild-type tp53 copy number loss

Questions {❓}

FLT3 mutations in acute myeloid leukemia: what is the best approach in 2013?

Schema {🗺️}

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         headline:Genetic alterations of m6A regulators predict poorer survival in acute myeloid leukemia
         description:Methylation of N6 adenosine (m6A) is known to be important for diverse biological processes including gene expression control, translation of protein, and messenger RNA (mRNA) splicing. However, its role in the development of human cancers is poorly understood. By analyzing datasets from the Cancer Genome Atlas Research Network (TCGA) acute myeloid leukemia (AML) study, we discover that mutations and/or copy number variations of m6A regulatory genes are strongly associated with the presence of TP53 mutations in AML patients. Further, our analyses reveal that alterations in m6A regulatory genes confer a worse survival in AML. Our work indicates that genetic alterations of m6A regulatory genes may cooperate with TP53 and/or its regulator/downstream targets in the pathogenesis and/or maintenance of AML.
         datePublished:2017-02-02T00:00:00Z
         dateModified:2017-02-02T00:00:00Z
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         license:http://creativecommons.org/publicdomain/zero/1.0/
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            RNA modification
            m6A
            Leukemia
            Acute myeloid leukemia
            TP53 mutation
            Oncology
            Hematology
            Cancer Research
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ScholarlyArticle:
      headline:Genetic alterations of m6A regulators predict poorer survival in acute myeloid leukemia
      description:Methylation of N6 adenosine (m6A) is known to be important for diverse biological processes including gene expression control, translation of protein, and messenger RNA (mRNA) splicing. However, its role in the development of human cancers is poorly understood. By analyzing datasets from the Cancer Genome Atlas Research Network (TCGA) acute myeloid leukemia (AML) study, we discover that mutations and/or copy number variations of m6A regulatory genes are strongly associated with the presence of TP53 mutations in AML patients. Further, our analyses reveal that alterations in m6A regulatory genes confer a worse survival in AML. Our work indicates that genetic alterations of m6A regulatory genes may cooperate with TP53 and/or its regulator/downstream targets in the pathogenesis and/or maintenance of AML.
      datePublished:2017-02-02T00:00:00Z
      dateModified:2017-02-02T00:00:00Z
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         RNA modification
         m6A
         Leukemia
         Acute myeloid leukemia
         TP53 mutation
         Oncology
         Hematology
         Cancer Research
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         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1186%2Fs13045-017-0410-6/MediaObjects/13045_2017_410_Fig1_HTML.gif
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