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<i style="mso-bidi-font-style:normal"><span style="font-size:11.0pt;font-family:"Times New Roman";mso-fareast-font-family: "Times New Roman";mso-bidi-font-family:Mangal;mso-ansi-language:EN-GB; mso-fareast-language:EN-US;mso-bidi-language:HI" lang="EN-GB">NRAS</span></i><span style="font-size:11.0pt;font-family:"Times New Roman";mso-fareast-font-family: "Times New Roman";mso-bidi-font-family:Mangal;mso-ansi-language:EN-GB; mso-fareast-language:EN-US;mso-bidi-language:HI" lang="EN-GB"> Mutations in <i style="mso-bidi-font-style:normal">de novo</i> acute leukemia: Prevalence and clinical significance</span>

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Title NRAS Mutations in de novo acute leukemia: Prevalence and clinical significance
 
Creator Dunna, Nageswara Rao
Vuree, Sugunakar
Anuradha, Cingeetham
Sailaja, Kagita
Surekha, Damineni
Digumarti, Raghunadha Rao
Rao, V R
Yadav, Satish Kumar
Reddy, Rajasekhar
Vishnupriya, Satti
 
Subject NRAS mutations
Acute lymphoblastic leukemia
Acute myeloid leukemia
GTPase
Hematopoietic malignancies
 
Description 207-210
The activating mutations of the Ras gene or
other abnormalities in Ras signaling pathway lead to uncontrolled growth
factor-independent proliferation of hematopoietic progenitors. Oncogenic
mutations in NRAS gene have been
observed with variable prevalence in hematopoietic malignancies. In the present
study, NRAS mutations were detected
using bidirectional sequencing in 264 acute leukemia cases — 129 acute
lymphocytic leukemia (ALL) and 135 acute myeloid leukemia (AML) and 245 age-
and gender-matched controls. Missense mutation was observed only in the 12th
codon of NRAS gene in 4.7% of
AML and 3.16% of ALL cases. The presence of NRAS
mutation did not significantly influence blast % and lactate dehydrogenase
(LDH) levels in AML patients. When the data were analyzed with respect to
clinical variables, the total leukocyte count was elevated for mutation
positive group, compared to negative group. In AML patients with NRAS mutations, 60% failed to achieve
complete remission (CR), as compared to 34.8% in mutation negative group. These
results indicated that NRAS mutations
might confer poor drug response. In AML, disease free survival (DFS) in NRAS mutation positive group was lesser,
compared to mutation negative group (9.5 months vs. 11.68 months). In ALL patients, DFS of NRAS mutation positive group was lesser than mutation negative
group (9.2 months vs. 27.5 months).
The CR rate was also lower for mutation-positive patients group, compared to
mutation-negative group. In conclusion, these results suggested that presence
of NRAS mutation at 12th
codon was associated with poor response and poorer DFS in both ALL and AML.
 
Date 2014-07-14T05:53:18Z
2014-07-14T05:53:18Z
2014-06
 
Type Article
 
Identifier 0975-0959 (Online); 0301-1208 (Print)
http://hdl.handle.net/123456789/29085
 
Language en_US
 
Rights CC Attribution-Noncommercial-No Derivative Works 2.5 India
 
Publisher NISCAIR-CSIR, India
 
Source IJBB Vol.51(3) [June 2014]