Objective To characterize co-deletion of chromosome 1p/19q and IDH1/2 mutation in Chinese brain tumor patients and to assess their associations with clinical features. Methods In a series of 528 patients with gliomas, pathological and radiological materials were reviewed. Pathological constituents of tumor subsets, incidences of 1p/19q co-deletion and IDH1/2 mutation in gliomas by regions and sides in the brain were analyzed. Results Overall, 1p and 19q was detected in 339 patients by FISH method while the sequence of IDH1/2 was determined in 280 patients. Gliomas of frontal, temporal and insular origin had significantly different pathological constituents of tumor subsets (P<0.001). Gliomas of frontal origin had significantly higher incidence of 1p/19q co-deletion (50.4%) and IDH1/2 mutation (73.5%) than those of non-frontal origin (27.0% and 48.5%, respectively) (P<0.001), while gliomas of temporal origin had significantly lower incidence of 1p/19q co-deletion (23.9%) and IDH1/2 mutation (41.7%) than those of non-temporal origin (39.9% and 63.2%, respectively) (P = 0.013 and P = 0.003, respectively). Subgroup analysis confirmed these findings in oligoastrocytic and oligodendroglial tumors, respectively. Although the difference of 1p/19q co-deletion was not statistically significant in temporal oligodendroglial tumors, the trend was marginally significant (P = 0.082). However, gliomas from different sides of the brain did not show significant different pathological constituents, incidences of 1p/19q co-deletion or IDH1/2 mutation. Conclusion Preferential distribution of pathological subsets, 1p/19q co-deletion and IDH1/2 mutation were confirmed in some brain regions in Chinese glioma patients, implying their distinctive tumor genesis and predictive value for prognosis.
References
[1]
Ohgaki H, Kleihues P (2005) Epidemiology and etiology of gliomas. Acta Neuropathol 109: 93–108.
[2]
Louis DN, Ohgaki H, Wiestler OD, Cavenee WK, Burger PC, et al. (2007) The 2007 WHO classification of tumours of the central nervous system. Acta Neuropathol 114: 97–109.
[3]
Schwartzbaum JA, Fisher JL, Aldape KD, Wrensch M (2006) Epidemiology and molecular pathology of glioma. Nat Clin Pract Neurol 2: 494–503, 1–516.
[4]
Kraus JA, Koopmann J, Kaskel P, Maintz D, Brandner S, et al. (1995) Shared allelic losses on chromosomes 1p and 19q suggest a common origin of oligodendroglioma and oligoastrocytoma. J Neuropathol Exp Neurol 54: 91–95.
[5]
van den Bent MJ, Carpentier AF, Brandes AA, Sanson M, Taphoorn MJ, et al. (2006) Adjuvant procarbazine, lomustine, and vincristine improves progression-free survival but not overall survival in newly diagnosed anaplastic oligodendrogliomas and oligoastrocytomas: a randomized European Organisation for Research and Treatment of Cancer phase III trial. J Clin Oncol 24: 2715–2722.
[6]
Cairncross G, Berkey B, Shaw E, Jenkins R, Scheithauer B, et al. (2006) Phase III trial of chemotherapy plus radiotherapy compared with radiotherapy alone for pure and mixed anaplastic oligodendroglioma: Intergroup Radiation Therapy Oncology Group Trial 9402. J Clin Oncol 24: 2707–2714.
[7]
Kros JM, Gorlia T, Kouwenhoven MC, Zheng PP, Collins VP, et al. (2007) Panel review of anaplastic oligodendroglioma from European Organization For Research and Treatment of Cancer Trial 26951: assessment of consensus in diagnosis, influence of 1p/19q loss, and correlations with outcome. J Neuropathol Exp Neurol 66: 545–551.
[8]
Cairncross JG, Ueki K, Zlatescu MC, Lisle DK, Finkelstein DM, et al. (1998) Specific genetic predictors of chemotherapeutic response and survival in patients with anaplastic oligodendrogliomas. J Natl Cancer Inst 90: 1473–1479.
[9]
Kaloshi G, Benouaich-Amiel A, Diakite F, Taillibert S, Lejeune J, et al. (2007) Temozolomide for low-grade gliomas: predictive impact of 1p/19q loss on response and outcome. Neurology 68: 1831–1836.
[10]
Kujas M, Lejeune J, Benouaich-Amiel A, Criniere E, Laigle-Donadey F, et al. (2005) Chromosome 1p loss: a favorable prognostic factor in low-grade gliomas. Ann Neurol 58: 322–326.
[11]
Hoang-Xuan K, Capelle L, Kujas M, Taillibert S, Duffau H, et al. (2004) Temozolomide as initial treatment for adults with low-grade oligodendrogliomas or oligoastrocytomas and correlation with chromosome 1p deletions. J Clin Oncol 22: 3133–3138.
[12]
Jenkins RB, Blair H, Ballman KV, Giannini C, Arusell RM, et al. (2006) A t(1;19)(q10;p10) mediates the combined deletions of 1p and 19q and predicts a better prognosis of patients with oligodendroglioma. Cancer Res 66: 9852–9861.
[13]
Parsons DW, Jones S, Zhang X, Lin JC, Leary RJ, et al. (2008) An integrated genomic analysis of human glioblastoma multiforme. Science 321: 1807–1812.
[14]
Watanabe T, Nobusawa S, Kleihues P, Ohgaki H (2009) IDH1 mutations are early events in the development of astrocytomas and oligodendrogliomas. Am J Pathol 174: 1149–1153.
[15]
Sanson M, Marie Y, Paris S, Idbaih A, Laffaire J, et al. (2009) Isocitrate dehydrogenase 1 codon 132 mutation is an important prognostic biomarker in gliomas. J Clin Oncol 27: 4150–4154.
[16]
Yan H, Parsons DW, Jin G, McLendon R, Rasheed BA, et al. (2009) IDH1 and IDH2 mutations in gliomas. N Engl J Med 360: 765–773.
[17]
Bleeker FE, Atai NA, Lamba S, Jonker A, Rijkeboer D, et al. (2010) The prognostic IDH1(R132) mutation is associated with reduced NADP+-dependent IDH activity in glioblastoma. Acta Neuropathol 119: 487–494.
[18]
Larjavaara S, Mantyla R, Salminen T, Haapasalo H, Raitanen J, et al. (2007) Incidence of gliomas by anatomic location. Neuro Oncol 9: 319–325.
[19]
Duffau H, Capelle L (2004) Preferential brain locations of low-grade gliomas. Cancer 100: 2622–2626.
[20]
Zlatescu MC, TehraniYazdi A, Sasaki H, Megyesi JF, Betensky RA, et al. (2001) Tumor location and growth pattern correlate with genetic signature in oligodendroglial neoplasms. Cancer Res 61: 6713–6715.
[21]
Mueller W, Hartmann C, Hoffmann A, Lanksch W, Kiwit J, et al. (2002) Genetic signature of oligoastrocytomas correlates with tumor location and denotes distinct molecular subsets. Am J Pathol 161: 313–319.
[22]
Huang L, Jiang T, Yuan F, Li GL, Liu EZ, et al. (2008) Correlations between molecular profile and tumor location in Chinese patients with oligodendroglial tumors. Clin Neurol Neurosurg 110: 1020–1024.
[23]
Goze C, Rigau V, Gibert L, Maudelonde T, Duffau H (2009) Lack of complete 1p19q deletion in a consecutive series of 12 WHO grade II gliomas involving the insula: a marker of worse prognosis? J Neurooncol 91: 1–5.
[24]
Wu A, Aldape K, Lang FF (2010) High rate of deletion of chromosomes 1p and 19q in insular oligodendroglial tumors. J Neurooncol 99: 57–64.
[25]
Lai A, Kharbanda S, Pope WB, Tran A, Solis OE, et al. (2011) Evidence for sequenced molecular evolution of IDH1 mutant glioblastoma from a distinct cell of origin. J Clin Oncol 29: 4482–4490.
[26]
Ambros PF, Ambros IM (2001) Pathology and biology guidelines for resectable and unresectable neuroblastic tumors and bone marrow examination guidelines. Med Pediatr Oncol 37: 492–504.
[27]
Yasargil MG, Reeves JD (1992) Tumours of the limbic and paralimbic system. Acta Neurochir (Wien) 116: 147–149.
[28]
Sanai N, Polley MY, Berger MS (2010) Insular glioma resection: assessment of patient morbidity, survival, and tumor progression. J Neurosurg 112: 1–9.
[29]
Lang FF, Olansen NE, DeMonte F, Gokaslan ZL, Holland EC, et al. (2001) Surgical resection of intrinsic insular tumors: complication avoidance. J Neurosurg 95: 638–650.
[30]
Laigle-Donadey F, Martin-Duverneuil N, Lejeune J, Criniere E, Capelle L, et al. (2004) Correlations between molecular profile and radiologic pattern in oligodendroglial tumors. Neurology 63: 2360–2362.
