Literature DB >> 2200539

N-ras mutations in adult de novo acute myelogenous leukemia: prevalence and clinical significance.

J P Radich1, K J Kopecky, C L Willman, J Weick, D Head, F Appelbaum, S J Collins.   

Abstract

Point mutations of the N-ras proto-oncogenes have been previously detected in 20% to 60% of samples of acute myelogenous leukemia (AML), but the clinical significance of these mutations is presently unclear. We directly sequenced polymerase chain reaction (PCR) amplified N-ras fragments to determine the frequency of N-ras point mutations in 55 adult patients with de novo AML. Mutations were present in 8 of 55 (15%) patients. These mutations were usually in codon 12, 13, or 61, but one patient had mutations in both codons 13 and 61, and another had an unusual point mutation in N-ras codon 60. A comparison of patients with and without N-ras mutations showed no statistically significant differences in pretreatment clinical variables, response to induction therapy, or survival, except for a possibly higher percentage of FAB M4 subtypes in patients with the N-ras mutation. These data together with previous reports suggest that the presence of N-ras point mutations do not clearly define a unique clinical or biologic subset of AML patients.

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Year:  1990        PMID: 2200539

Source DB:  PubMed          Journal:  Blood        ISSN: 0006-4971            Impact factor:   22.113


  25 in total

1.  RAS mutations are frequent in FAB type M4 and M5 of acute myeloid leukemia, and related to late relapse: a study of the Japanese Childhood AML Cooperative Study Group.

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2.  Down-regulation of microRNAs 222/221 in acute myelogenous leukemia with deranged core-binding factor subunits.

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Journal:  Neoplasia       Date:  2010-11       Impact factor: 5.715

3.  Design of Hydrazide-Bearing HDACIs Based on Panobinostat and Their p53 and FLT3-ITD Dependency in Antileukemia Activity.

Authors:  Xiaoyang Li; Yuqi Jiang; Yuri K Peterson; Tongqiang Xu; Richard A Himes; Xin Luo; Guilin Yin; Elizabeth S Inks; Nathan Dolloff; Stephanie Halene; Sherine S L Chan; C James Chou
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4.  Activated Ca2+/calmodulin-dependent protein kinase IIgamma is a critical regulator of myeloid leukemia cell proliferation.

Authors:  Jutong Si; Steven J Collins
Journal:  Cancer Res       Date:  2008-05-15       Impact factor: 12.701

Review 5.  Small molecule inhibitors in acute myeloid leukemia: from the bench to the clinic.

Authors:  Muneera Al-Hussaini; John F DiPersio
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6.  Trisomy 11 as an isolated abnormality in acute myeloid leukemia is associated with unfavorable prognosis but not with an NPM1 or KIT mutation.

Authors:  Faisal M Alseraye; Zhuang Zuo; Carlos Bueso-Ramos; Sa Wang; L Jeffrey Medeiros; Gary Lu
Journal:  Int J Clin Exp Pathol       Date:  2011-04-25

7.  Apoptosis repressor with caspase recruitment domain is regulated by MAPK/PI3K and confers drug resistance and survival advantage to AML.

Authors:  P Y Mak; D H Mak; H Mu; Y Shi; P Ruvolo; V Ruvolo; R Jacamo; J K Burks; W Wei; X Huang; S M Kornblau; M Andreeff; B Z Carter
Journal:  Apoptosis       Date:  2014-04       Impact factor: 4.677

Review 8.  Molecular pathogenesis of acute myeloid leukemia: a diverse disease with new perspectives.

Authors:  Felicitas Thol; Arnold Ganser
Journal:  Front Med China       Date:  2010-12-01

Review 9.  Gene mutations of acute myeloid leukemia in the genome era.

Authors:  Tomoki Naoe; Hitoshi Kiyoi
Journal:  Int J Hematol       Date:  2013-01-29       Impact factor: 2.490

10.  Cause and consequences of genetic and epigenetic alterations in human cancer.

Authors:  B Sadikovic; K Al-Romaih; J A Squire; M Zielenska
Journal:  Curr Genomics       Date:  2008-09       Impact factor: 2.236

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