<?xml version="1.0"?>
<Articles JournalTitle="Basic &amp; Clinical Cancer Research">
  <Article>
    <Journal>
      <PublisherName>Tehran University of Medical Sciences</PublisherName>
      <JournalTitle>Basic &amp; Clinical Cancer Research</JournalTitle>
      <Issn>2228-6527</Issn>
      <Volume>14</Volume>
      <Issue>4</Issue>
      <PubDate PubStatus="epublish">
        <Year>2023</Year>
        <Month>10</Month>
        <Day>29</Day>
      </PubDate>
    </Journal>
    <title locale="en_US">Mutations in IDH1/2 Genes Predict Better Disease Outcome of Glioma Patients-A Study From Western India</title>
    <FirstPage>202</FirstPage>
    <LastPage>212</LastPage>
    <AuthorList>
      <Author>
        <FirstName>Nikul</FirstName>
        <LastName>Gohil</LastName>
        <affiliation locale="en_US">The Gujarat cancer &amp; Research Institute</affiliation>
      </Author>
      <Author>
        <FirstName>Neha</FirstName>
        <LastName>Bhalala</LastName>
        <affiliation locale="en_US">Ex-staff-The Gujarat cancer &amp; Research Institute</affiliation>
      </Author>
      <Author>
        <FirstName>Mittal</FirstName>
        <LastName>Mistry</LastName>
        <affiliation locale="en_US">The Gujarat cancer &amp; Research Institute</affiliation>
      </Author>
      <Author>
        <FirstName>Trupti</FirstName>
        <LastName>Trivedi</LastName>
        <affiliation locale="en_US">The Gujarat cancer &amp; Research Institute</affiliation>
      </Author>
    </AuthorList>
    <History>
      <PubDate PubStatus="received">
        <Year>2023</Year>
        <Month>05</Month>
        <Day>16</Day>
      </PubDate>
      <PubDate PubStatus="accepted">
        <Year>2023</Year>
        <Month>08</Month>
        <Day>23</Day>
      </PubDate>
    </History>
    <abstract locale="en_US">Introduction: Isocitrate Dehydrogenase (IDH) plays an important role in cellular metabolism. In gliomas, the mutational status of IDH1/2 genes have paramount significance, however, study from Western India is limited. Therefore, in the current study, we sought to explore the clinical impact of IDH1/2 mutations on glioma patients from Western India.
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Materials and Method: A total of 50 pre-therapeutic, histopathologically confirmed patients with astrocytoma tumors were included and IDH1/2 mutations were detected using real-time PCR. IDH1/2 mutations were correlated with clinicopathological parameters and disease outcomes. Data were evaluated by SPSS software.
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Results: &#xA0;The overall incidence of IDH1/2 mutations was noted in 24% (12/50) of glioma patients. Out of 12 patients whose tumors showed IDH mutations, 83% of patients have IDH1 mutations, whereas 17% showed IDH2 mutation. &#xA0;Further, in IDH1 mutations, IDH1 R132H &amp; IDH1 R132C mutations were noted in, 80% and 20% of patients, respectively. &#xA0;When correlated with clinicopathological parameters, a significant inverse correlation was found with patients' age (&#x3C7;2= 9.75, r = -0.476, p=0.001) and grade of tumors (&#x3C7;2=17.51, r =-0.636, p=0.0001). In Kaplan-Meier survival analysis, apart from age (Log rank=5.443, p=0.020), IDH mutation status (Log rank=3.855, p=0.050), and both, IDH mutation and low-grade glioma tumors (Log rank=6.492, p=0.039) remained significant parameters for predicting better 24 months PFS and OS of glioma patients. However, in multivariate survival analysis using the Cox Proportional Hazard Forward Stepwise Model, only a combination of low-grade glioma with the presence of IDH mutation emerged at step one as a positive significant independent prognostic factor that predict better PFS (HR=2.92, 95% CI=1.12-7.61, p=0.028) &#xA0;and OS &#xA0;(HR=3.0, 95% CI=1.45-6.19, p=0.003).
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Conclusion: Based on this data, we concluded that for glioma patients, apart from patients' age, low-grade tumors with the presence of IDH mutations remained significant independent positive prognosticators and would be helpful to clinicians for better management of glioma patients.</abstract>
    <web_url>https://bccr.tums.ac.ir/index.php/bccrj/article/view/482</web_url>
  </Article>
</Articles>
