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experience. Radiol Oncol 2010; 44: 113-20. Chakrabarti I, Cockburn M, Cozen W, Wang YP, Preston-Martin S. A population-based description of glioblastoma multiforme in Los Angeles County, 1974-1999. Cancer 2005; 104: 2798-806. Kachanov DY, Dobrenkov KV, Shamanskaya TV, Abdullaev RT, Inushkina EV, Savkova RF, et al. Solid tumors in young children in Moscow Region of Russian Federation. Radiol Oncol 2008; 42: 39-44. Stupp R, Tonn JC, Brada M, Pentheroudakis G; ESMO Guidelines Working Group. High-grade malignant glioma: ESMO Clinical Practice Guidelines for

, Zhang X et al. An integrated genomic analysis of human glioblastoma multiforme. Science 2008; 321:1807-12. PMid:18772396 PMCid:PMC2820389 10.1126/science.1164382PMid:18772396PMCid:PMC2820389 7. Verhaak RG, Hoadley KA, Purdom E et al. Integrated genomic analysis identifies clinically relevant subtypes of glioblastoma characterized by abnormalities in PD GFRA, IDH1, EGFR, and NF1. Cancer Cell 2010; 17: 98-110. PMid:20129251 PMCid:PMC2818769 8. Van Meir EG, Hadjipanayis CG, Norden AD et

Introduction Glioblastoma multiforme (GBM), a grade IV astrocytoma as defined by the World Health Organization (WHO), is the most common brain tumors in adults, accounting for 54% of all gliomas and 16% of primary brain tumors.[ 1 , 2 ] The standard of care for GBM, as defined by the Stupp protocol, is maximal safe surgical resection followed by oral consumption of temozolomide (TMZ), which is normally administered concurrently with radiation. Even with such aggressive treatments, the median survival of an GBM is only 15 months after its initial diagnosis.[ 3 , 4

-PK expression on survival in patients with glioblastoma multiforme. Radiother Oncol 2011; 101: 127-31. 7. Mannino M, Chalmers AJ. Radioresistance of glioma stem cells: intrinsic characteristic or property of the ‘microenvironment-stem cell unit’? Mol Oncol 2011; 5: 374-86. 8. Bao S, Wu Q, McLendon RE, Hao Y, Shi Q, Hjelmeland AB, et al. Glioma stem cells promote radioresistance by preferential activation of the DNA damage response. Nature 2006; 444: 756-60. 9. Singh SK, Hawkins C, Clarke ID, Squire JA, Bayani J, Hide T, et al. Identification of human brain tumor

classification of brain tumors. Neurosurg Focus 2005;18(4):1-6. 5. Altaner C. Glioblastoma and stem cells - minireview. Neoplasma 2008;55(5):369-74. 6. De Angelis LM, Mellinghoff IK. Virchow 2011 or how to ID(H) human glioblastoma. J Clin Oncol 2011;29(34):4473-4. 7. Moller HG, Rasmussen AP, Andersen HH, et al. A systematic review of MicroRNA in glioblastoma multiforme: micro-modulators in the mesenchymal mode of migration and invasion. Mol Neurobiol 2013;47(1):131-44. 8. Olar A, Aldape KD. Using the molecular classification of glioblastoma to inform personalized treatment. J

of human glioblastoma with immunosuppression by orogastric cyclosporin. Arq Neuropsiquiatr 2011, 69, 112-117. 6. Dagg C.P., Karnofsky D.A., Roddy J.: Growth of transplantable human tumors in the chick embryo and hatched chick. Cancer Res 1956, 16, 589-597. 7. De Magalhães N., Liaw L.-H.L., Berns M.: An instruction on the in vivo shell-less chorioallantoic membrane 3- demensional tumor spheroid model. Cytotechnology 2010, 62, 279-283. 8. Deb P., Sharma M.C., Mahapatra A.M., Agarwal D., Sarkar C.: Glioblastoma multiforme with long term survival. Neurol India 2005

. Coulon A, Lafitte F, Hoang-Xuan K, Martin-Duverneuil N, Mokhtari K, Blustajn J, et al. Radiographic findings in 37 cases of primary CNS lymphoma in immunocompetent patients. Eur Radiol 2002; 12: 329-40. 11. Haldorsen IS, Espeland A, Larsson E-M. Central nervous system lymphoma: characteristic findings on traditional and advanced imaging. AJNR Am J Neuroradiol 2011; 32: 984-92. 12. Yamashita K, Yoshiura T, Hiwatashi A, Togao O, Yoshimoto K, Suzuki SO, et al. Differentiating primary CNS lymphoma from glioblastoma multiforme: assessment using arterial spin labeling

analysis of the EORTC-NCIC trial. Lancet Oncol 2009; 10: 459-66. Martinez R, Schackert G, Esteller M. Hypermethylation of the proapoptotic gene TMS1/ASC: prognostic importance in glioblastoma multiforme. J Neurooncol 2007; 82: 133-9. Burton EC, Lamborn KR, Forsyth P, Scott J, O'Campo J, Uyehara-Lock J, et al. Aberrant p53, mdm2, and proliferation differ in glioblastomas from long-term compared with typical survivors. Clin Cancer Res 2002; 8: 180-7. Steinbach JP, Blaicher HP, Herrlinger U, Wick W, Nägele T, Meyermann R, et al. Surviving glioblastoma for more than 5

2009, 106, 399-404. 9. Grodzik M., Sawosz E., Wierzbicki M., Orlowski P., Hotowy A., Niemiec T., Szmidt M., Mitura K., Chwalibog, A.: Nanoparticles of carbon allotropes inhibit glioblastoma multiforme angiogenesis in ovo . Int J Nanomed 2011, 6, 3041-3048. 10. Hagedorn M., Javerzat S., Gilges D., Meyre A., de Lafarge B., Eichmann A., Bikfalvi A.: Accessing key steps of human tumour progression in vivo by using an avian embryo model. Proc Natl Acad Sci USA 2005, 101, 1643-1648. 11. Laurin T., Smitz U., Riediger D., Frank H.G., Stoll C.: Chorioallantoic membrane of


INTRODUCTION: Recently, researchers have been considering as adverse prognostic factors in primary glioblastomas not only clinical indicators but also various cellular, genetic and immunological markers. The aim of the present article was to report a case of primary glioblastoma multiforme with poor survival in a patient after surgical intervention, and to determine the unfavorable prognostic markers. CASE REPORT: We present a 71-year-old man with histologically verified glioblastoma multiforme and a postoperative survival of 48 days. The patient did not receive any radiotherapy and adjuvant therapy with temozolomide because of the short survival. Serum and transcription levels of TNF-α, CD44, YKL-40 and IL-6 were determined by molecular-biological and immunological analyses. We found very high transcription levels of the genes CD44, YKL-40 and IL-6, increased gene expression of TNF-α, and elevated serum concentrations of TNF-α, YKL-40 and IL-6 and reduced serum concentration of CD44. CONCLUSION: Molecular-biological and immunological analyses support the hypothesis that glioblastoma multiforme is presented by a heterogeneous group of glial tumors with different clinical course and prognosis. The high expression levels of TNF-α, CD44, YKL-40, and IL-6 indicate that the tumor can be categorized as mesenchymal subtype of glioblastoma multiforme, which accounts for the rapid clinical course and lethal outcome of the condition.