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Dear Editor:
We read the “Letter to Editor” by Borkar et al. regarding our article [1]. We found this letter interesting and informative. It provides useful data about the authors’ experience regarding management of pediatric glioblastoma multiforme (GBM) with a considerable sample size of 70 patients at their medical center.
The strength of this report is performing genetic analyses in a group of pediatric patients and notable finding of uncommon epidermal growth factor receptor amplification and phosphate and tensin homolog gene deletion as opposed to p53 expression in 63% of cases and loss of p16 (68%) and p27 (54%) immunoexpression which are significant alterations in pediatric GBM compared to their adult counterpart [2].
Unfortunately we do not currently have access to detailed genetic or molecular study techniques at our center. Therefore, we are not able to perform more studies about molecular genetics of described patients. All we know are those mentioned in the article: the first patient’s tumor was negative for p53 and had a Ki-67 index of 30%. The second patient’s left hemisphere tumor showed a Ki-67 index of 24%, and the tumor nuclei were negative for p53. The right hemisphere tumor had a Ki-67 index of 11%, and 10% of the nuclei were positive for p53. Hence, we cannot accept or refuse available literature about relationship between genetic factors and long-term survival in pediatric GBM.
Mahmoud Reza Khalatbari
Mehrdokht Hamidi
Yashar Moharamzad
References
Khalatbari MR, Hamidi M, Moharamzad Y (2011) Glioblastoma multiforme with very rapid growth and long-term survival in children: report of two cases and review of the literature. Childs Nerv Syst 27:1347–1352
Suri V, Das P, Pathak P, Jain A, Sharma MC, Borkar SA et al (2009) Pediatric glioblastomas: a histopathological and molecular genetic study. Neuro Oncol 11:274–280
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Khalatbari, M.R., Hamidi, M. & Moharamzad, Y. Glioblastoma multiforme with very rapid growth and long-term survival in children: report of two cases and review of the literature. Childs Nerv Syst 28, 9 (2012). https://doi.org/10.1007/s00381-011-1628-1
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DOI: https://doi.org/10.1007/s00381-011-1628-1