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 ORIGINAL ARTICLE
Year : 2014  |  Volume : 62  |  Issue : 1  |  Page : 32--36

Fluorescence in situ hybridization for 1p, 19q status in a cohort of glial neoplasms


1 Section of Neuropathology, Departments of Neurological Sciences and Pathology, Section of Neurosurgery, Christian Medical College, Vellore, Tamil Nadu, India
2 Department of Neurological Sciences, Section of Neurosurgery, Christian Medical College, Vellore, Tamil Nadu, India

Correspondence Address:
Geeta Chacko
Departments of Neurological Sciences and Pathology, Section of Neuropathology, Christian Medical College, Vellore - 632 004, Tamil Nadu
India
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Source of Support: None, Conflict of Interest: None


Read associated Erratum: Erratum with this article

DOI: 10.4103/0028-3886.128275

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Objective: The objective of the following study is to determine 1p, 19q status in a cohort of glial neoplasms. Materials and Methods: Fluorescence in situ hybridization for determination of 1p, 19q deletions in 100 glial neoplasms diagnosed between January 2007 and March 2011, was performed using Vysis dual color probes localizing to 1p36/1q25; 19q13/19p13. Results: Out of the 100 tumors, 78 tumors were either pure oligodendroglial (OD) neoplasms or had an OD component. 1p and 19q codeletions were seen in 72.7% of oligodendrogliomas (World Health Organization [WHO] Grade II), 90.9% of anaplastic oligodendrogliomas (WHO Grade III), 22.2% of mixed oligoastrocytomas (WHO Grade II) and 42.9% of the anaplastic oligoastrocytomas (WHO Grade III). Of the 29 tumors that were diagnosed as glioblastoma multiforme (GBM), 11 had an OD component of which four showed codeletions of 1p and 19q (36.4%) and two tumors showed epidermal growth factor receptor (EGFR) amplification (20%) without 1p19q codeletions. Amongst the remaining 18 GBMs without an OD component, three cases showed EGFR amplification (16.7%), one case showed isolated deletion of 1p and none showed 1p19q codeletions. Polysomies involving 1p and/or 19q with or without deletions were seen in 76.9% of mixed oligoastrocytic tumors, 7.7% of pure OD tumors and one glioblastoma. Conclusions: 1p19q codeletion is an early molecular change in the genesis of OD tumors, which is retained at the time of progression. Mixed tumors more frequently show polysomies of 1p and 19q. The presence of codeletion in a third of the GBMs with an OD component with its absence in GBMs without an OD component, justifies categorization of these tumors as a separate entity.






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