[Ischemic complications following surgical treatment of moyamoya disease: risk factors and prevention]. / Ishemicheskie oslozhneniya khirurgicheskogo lecheniya patsientov s bolezn'yu moiya-moiya: faktory riska i metody profilaktiki.

BACKGROUND: One of the most difficult problems in surgical treatment of moyamoya disease is prevention of ischemic perioperative complications. The risk of these events is significantly higher compared to other cerebrovascular diseases (up to 30%). OBJECTIVE: To identify unfavorable prognostic factors of perioperative cerebral ischemic complications, to determine the group of high-risk patients and to develop the guidelines for perioperative management of these patients. MATERIAL AND METHODS: We analyzed clinical and diagnostic data and postoperative outcomes in 80 patients with various forms of moyamoya disease. These patients underwent 134 different interventions. Staged revascularization of both hemispheres was performed in 40 patients (80 surgeries). Most patients (n = 55) underwent combined brain revascularization (79 surgeries). RESULTS: Persistent postoperative complications (ischemic stroke) developed in 7 cases (5.3%). Transient neurological impairment was observed in 36 cases (27%). Statistical analysis revealed the following risk factors of perioperative complications: critical stenosis/occlusion of posterior cerebral artery (OR 9.704), severe perfusion deficit (OR 5.393) and previous TIA or ischemic stroke within 3 months prior to surgery (OR 6.433). If at least two of these signs are present, sensitivity of prognosis for postoperative complications is 80.7% and 88.6%, respectively. CONCLUSION: Patients with moyamoya disease are at high risk of perioperative complications due to complex rearrangement of collateral cerebral circulation and high sensitivity of brain to local and systemic hemodynamic changes. Patients with risk factors require careful perioperative management to exclude pathogenetic factors provoking ischemia. Early surgical treatment is advisable to reduce the risk of ischemic and hemorrhagic lesions following natural course of disease and severe perioperative complications.

[The research of the connective tissue dysplasia effect on dental eruption and hard tissues mineralization]. / Vliyanie displazii soedinitel'noi tkani na sroki prorezyvaniya i stepen' mineralizatsii zubov cheloveka.

OBJECTIVE: The purpose of this investigation was to explore the quality of 38, 48 teeth's hard tissues at different eruption stages and mandibular bone in different postpartum ontogenesis periods. MATERIAL AND METHODS: The research involved 102 male patients divided into groups according to their age: 15-20, 21-30 years old, they were extracted one tooth 38, 48 without inflammatory process signs and a fragment of the mandibular bone alveolar part in the projection of the teeth 38, 48 for orthodontic indications. In the comparison group (49 observations without signs of connective tissue dysplasia), in the study group (53 observations with signs of connective tissue dysplasia) we extracted teeth 38, 48 which were in the bone tissue. We analyzed condition of crown and root systems of extracted 38, 48 teeth, densitometric density of mineral component, size of enamel prisms, size of prismatic shells of organic matrix, spatial organization of collagen fibers in bone tissue, size characteristics of bone plates and mineralization centers of bone tissue. Processing of the obtained data was performed by methods of variation statistics using standard packages Microsoft Excel 2008, Statistica 12.0. RESULTS: The paper reveals one of the surgical dentistry pressing issues related to the tething mechanism of lower human wisdom teeth, considered by the authors from the position of tissue disorders in collagen type 1 observed in connective tissue dysplasia. At age of 15-20 years in connective tissue dysplasia, the enamel prisms hypomineralized areas are generalized; at age of 21-30 years the hypomineralized areas are characterized by local changes. At the age of 15-20 years in connective tissue dysplasia the bone plates splitting is observed at the level of most fibrils, collagen fibers have insufficiently oriented direction in contrast to the age group of 21-30 years where bone plates splitting is characteristic for single fibrils and collagen fibrils are clearly oriented. CONCLUSION: Morphological and histological changes in teeth 38, 48 and in bone tissue prevent correct and timely teething at 15-20 years and create more favorable conditions for teething at 21-30 years with a slower rate in connective tissue dysplasia, but in both groups teeth eruption occurs under unfavorable anatomic conditions.

[Research of the structure of the mineral component of tooth enamel in connective tissue dysplasia by densitometry and atomic force microscopy in the early postpartum ontogenesis period]. / Issledovanie struktury mineral'nogo komponenta emali zubov pri displazii soedinitel'noi tkani metodami densitometrii i atomno-silovoi mikroskopii v rannem postnatal'nom periode ontogeneza.

OBJECTIVE: To give a quantitative and qualitative characteristic of the structure of the enamel's mineral component structure of impacted teeth with or without connective tissue dysplasia in different periods of early postnatal human ontogenesis using densitometry and atomic force microscopy. MATERIALS AND METHODS: The study involved 120 males with and without connective tissue dysplasia (CTD), which were divided into 3 equal subgroups (60 people with CTD and 60 people without CTD), 20 people in each, according to age: 15-20, 21-30, 31-40 years old. Each of the examined was removed either 3.8 or 4.8 tooth. To study the inorganic component of tooth enamel, a densitometric assessment of enamel's optical density was carried out using computed tomography in the Kodak Dental Systems software (Trophy 2000) and preparation of thin sections of tooth samples 3.8 or 4.8 for atomic force microscopy (AFM) according to the methods of Omsk State Medical University. RESULTS: The structure of tooth enamel in connective tissue dysplasia in the early postpartum period of ontogenesis is characterized by pronounced polymorphisms and an insufficient level of maturity. The ordering and orientation of the enamel prisms are disturbed due to insufficient packing density and a large distance between the enamel prisms at the age of 15-20, 21-30. The established changes indicate the incomplete nature of amelogenesis with connective tissue dysplasia at the indicated ages. CONCLUSIONS: In case of connective tissue dysplasia in the early postnatal period of ontogenesis, an incomplete amelogenesis is observed. This process is manifested by lower values of the mineral component's optical density, low packing of enamel prisms, a large distance between enamel prisms and their irregular shape.

[Modern trends in diagnosis and surgical treatment of moyamoya disease]. / Sovremennye tendentsii diagnostiki i khirurgicheskogo lecheniya bolezni moiyamoiya.

This review is devoted to moyamoya disease. It is a rare chronic steno-occlusive cerebrovascular disease. However, moyamoya disease is increasingly diagnosed by neurosurgeons in our country. Unlike atherosclerotic lesions of cerebral arteries, pathogenesis and course of this disease are much more complex and variable. Therefore, specialists often have certain difficulties in diagnosis, management and treatment of these patients. To date, a large number of surgical interventions have been proposed for the treatment of moyamoya disease. Revascularization approaches include direct procedures (extra-intracranial microanastomoses), indirect methods (synangioses) and combined revascularization. The purpose of the review is to systematize current literature data on the pathogenesis, diagnosis, clinical patterns and surgical treatment of patients with moyamoya disease. results Outcomes of surgical revascularization and the role of its various components in combined approach are under particular attention.

[Combination of double and indirect two-sided revascularization of the brain in the treatment of moyamoya disease]. / Sochetanie kombinirovannoi dvustvol'noi pryamoi i nepryamoi revaskulyarizatsii golovnogo mozga s dvukh storon v lechenii bolezni moyamoya.

An adult patient with progressive chronic cerebral ischemia associated with moyamoya disease who underwent combined revascularization of both cerebral hemispheres in step-by-step fashion is reported in the article. The feature of this case is a large volume of revascularization procedures with double-barrel extra-intracranial anastomoses combined with indirect synangioses. This surgical approach ensured early postoperative development of extensive collateral network and complete compensation of impaired cerebral circulation. Particular attention is paid to description and discussion of preoperative diagnosis, the choice of surgical treatment, as well as the features of surgical technique. The advantages and disadvantages of this approach are discussed in comparison with literature data.

Diffuse glioneuronal tumour with oligodendroglioma-like features and nuclear clusters (DGONC) - a molecularly defined glioneuronal CNS tumour class displaying recurrent monosomy 14.

AIMS: DNA methylation-based central nervous system (CNS) tumour classification has identified numerous molecularly distinct tumour types, and clinically relevant subgroups among known CNS tumour entities that were previously thought to represent homogeneous diseases. Our study aimed at characterizing a novel, molecularly defined variant of glioneuronal CNS tumour. PATIENTS AND METHODS: DNA methylation profiling was performed using the Infinium MethylationEPIC or 450 k BeadChip arrays (Illumina) and analysed using the 'conumee' package in R computing environment. Additional gene panel sequencing was also performed. Tumour samples were collected at the German Cancer Research Centre (DKFZ) and provided by multinational collaborators. Histological sections were also collected and independently reviewed. RESULTS: Genome-wide DNA methylation data from >25 000 CNS tumours were screened for clusters separated from established DNA methylation classes, revealing a novel group comprising 31 tumours, mainly found in paediatric patients. This DNA methylation-defined variant of low-grade CNS tumours with glioneuronal differentiation displays recurrent monosomy 14, nuclear clusters within a morphology that is otherwise reminiscent of oligodendroglioma and other established entities with clear cell histology, and a lack of genetic alterations commonly observed in other (paediatric) glioneuronal entities. CONCLUSIONS: DNA methylation-based tumour classification is an objective method of assessing tumour origins, which may aid in diagnosis, especially for atypical cases. With increasing sample size, methylation analysis allows for the identification of rare, putative new tumour entities, which are currently not recognized by the WHO classification. Our study revealed the existence of a DNA methylation-defined class of low-grade glioneuronal tumours with recurrent monosomy 14, oligodendroglioma-like features and nuclear clusters.

Integrated molecular characterization of IDH-mutant glioblastomas.

AIMS: Mutations of isocitrate dehydrogenase (IDH)1/2 affect almost all astrocytomas of WHO grade II and III. A subset of IDH-mutant astrocytic tumours progresses to IDH-mutant glioblastoma or presents with the histology of a glioblastoma at first presentation. We set out here to assess the molecular spectrum of IDH-mutant glioblastomas. METHODS: We performed an integrated molecular analysis of a mono-centric cohort (n = 97); assessed through genome-wide DNA methylation analysis, copy-number profiling and targeted next generation sequencing using a neurooncology-tailored gene panel. RESULTS: Of these 97 IDH-mutant glioblastomas, 68 had a glioblastoma at first presentation ('de novo' IDH-mutant glioblastoma) and 29 emerged from a prior low-grade lesion ('evolved' IDH-mutant glioblastoma). Unsupervised hierarchical clustering of DNA methylation data disclosed that IDH-mutant glioblastoma ('de novo' and 'evolved') formed a distinct group separate from other diffuse glioma subtypes. Homozygous deletions of CDKN2A/B were found to be associated with shorter survival. CONCLUSIONS: This study demonstrates DNA methylation patterns in IDH-mutant glioblastoma to be distinct from lower-grade astrocytic counterparts but homogeneous within de novo and evolved IDH-mutant glioblastomas, and identifies CDKN2A as a marker for possible genetic sub-stratification.

Novel MYC-driven medulloblastoma models from multiple embryonic cerebellar cells.

Group3 medulloblastoma (MBG3) that predominantly occur in young children are usually associated with MYC amplification and/or overexpression, frequent metastasis and a dismal prognosis. Physiologically relevant MBG3 models are currently lacking, making inferences related to their cellular origin thus far limited. Using in utero electroporation, we here report that MBG3 mouse models can be developed in situ from different multipotent embryonic cerebellar progenitor cells via conditional expression of Myc and loss of Trp53 function in several Cre driver mouse lines. The Blbp-Cre driver that targets embryonic neural progenitors induced tumors exhibiting a large-cell/anaplastic histopathology adjacent to the fourth ventricle, recapitulating human MBG3. Enforced co-expression of luciferase together with Myc and a dominant-negative form of Trp53 revealed that GABAergic neuronal progenitors as well as cerebellar granule cells give rise to MBG3 with their distinct growth kinetics. Cross-species gene expression analysis revealed that these novel MBG3 models shared molecular characteristics with human MBG3, irrespective of their cellular origin. We here developed MBG3 mouse models in their physiological environment and we show that oncogenic insults drive this MB subgroup in different cerebellar lineages rather than in a specific cell of origin.

Genomic profiling of Acute lymphoblastic leukemia in ataxia telangiectasia patients reveals tight link between ATM mutations and chromothripsis.

Recent developments in sequencing technologies led to the discovery of a novel form of genomic instability, termed chromothripsis. This catastrophic genomic event, involved in tumorigenesis, is characterized by tens to hundreds of simultaneously acquired locally clustered rearrangements on one chromosome. We hypothesized that leukemias developing in individuals with Ataxia Telangiectasia, who are born with two mutated copies of the ATM gene, an essential guardian of genome stability, would show a higher prevalence of chromothripsis due to the associated defect in DNA double-strand break repair. Using whole-genome sequencing, fluorescence in situ hybridization and RNA sequencing, we characterized the genomic landscape of Acute Lymphoblastic Leukemia (ALL) arising in patients with Ataxia Telangiectasia. We detected a high frequency of chromothriptic events in these tumors, specifically on acrocentric chromosomes, as compared with tumors from individuals with other types of DNA repair syndromes (27 cases total, 10 with Ataxia Telangiectasia). Our data suggest that the genomic landscape of Ataxia Telangiectasia ALL is clearly distinct from that of sporadic ALL. Mechanistically, short telomeres and compromised DNA damage response in cells of Ataxia Telangiectasia patients may be linked with frequent chromothripsis. Furthermore, we show that ATM loss is associated with increased chromothripsis prevalence in additional tumor entities.

[Posterior decompression of the craniovertebral junction in children with Chiari malformation: a surgery extent issue]. / Zadnyaya dekompressiya kraniovertebral'nogo perekhoda pri anomalii Kiari-1 u detei: vybor ob''ema operatsii.

AIM: The study objective was to develop a rational approach for defining the extent of posterior decompression in children with Chiari 1 malformation. MATERIAL AND METHODS: Posterior decompression was performed in 76 children with Chiari 1 malformation, under 18 years of age, in the period between 2001 and 2015. Fifty two (68%) children had syringomyelia. Extradural decompression (EDD) was performed in 14 (18%) cases, extra-arachnoid duraplasty (EAD) in 21 (28%) cases, intra-arachnoid dissection and duraplasty in 21 (28%) cases, and foramen of Magendie stenting and duraplasty in 20 (26%) cases. RESULTS: Complications occurred in 15 (20%) patients, with one of them being fatal (case fatality rate, 1.3%). The complication rate was higher after (1) intra-arachnoid dissection (p=0.0009) and stenting (p=0.02). Re-operation was required in 8 (11%) patients. The overall rate of complications and re-operations was lowest after EAD (10%). CONCLUSION: EAD is the method of choice for Chiari 1 malformation in children. EDD can be adopted as a primary option, but it requires selection of relevant patients. Intra-arachnoid dissection, with/without stenting, is not advisable as a primary intervention, but may be inevitable in the re-operation case.

[Surgical treatment of cerebral vascular diseases].

Theoretical and practical aspects of the complex treatment of brain and spinal vascular diseases using microsurgical, endovascular and radiosurgical methods are considered. Authors present the data demonstrating that, due to the implementation of the program of development of vascular centers in the Russian Federation, considerable progress was made in the treatment of cerebral aneurisms and hemorrhagic stroke. In author's opinion, wide introduction of surgical methods in the treatment of occlusive lesions of the blood vessels supplying the brain is needed.

[Comparative characteristics of genetic aberrations in glioblastomas in children and adults].

Glioblastomas in children and adults are a heterogeneous group of tumors that can be divided into at least three different subgroups: pediatric glioblastomas, IDH1-mutant glioblastomas in adults (the most favorable prognostic subtype), and IDH1-wild type glioblastomas in adults. According to the frequency of detected cytogenetic aberrations (amplification of the MYC/MYCN, EGFR and PDGRFA oncogenes, homozygous deletion of the CDKN2A gene, and deletion of the PTEN gene), pediatric glioblastomas bear analogy to the subgroup of IDH1-mutant glioblastomas in adults.

Outcome analysis of childhood pilocytic astrocytomas: a retrospective study of 148 cases at a single institution.

BACKGROUND: Pilocytic astrocytomas (PAs) are characterized by an excellent prognosis although several factors of adverse outcome have been reported. The mitogen-activated protein kinase pathway plays a major role in their tumorigenesis. AIM: To report a series of 148 PAs in children to define clinicopathological and biological prognostic factors. METHODS: Clinical data were collected from patient files and mail inquiry. Pathological specimens were centrally reviewed. The three major KIAA1549:BRAF fusion subtypes were analysed by reverse transcription - polymerase chain reaction (RT-PCR) in a subset of 47 frozen cases and by fluorescence in situ hybridization on formalin-fixed paraffin-embedded tissue in 23 cases. Tumour location, age at surgery, extent of surgical removal, histological subtype and KIAA1549:BRAF fusion by RT-PCR were searched for prognostic significance. RESULTS: Pilomyxoid astrocytoma (PMA) and the hypothalamo-chiasmatic (H/C) location were associated with a worse prognosis [P < 0.001 for overall survival (OS) and P = 0.001 for progression-free survival (PFS)]. Patients who underwent complete surgical excision had a better OS (P = 0.004) and a longer PFS (P < 0.001) than the others. Age was also a strong prognostic factor for OS but not for PFS. Infants (<1 year) and young children (<3 years) had a much worse outcome than the others (P < 0.001 and P = 0.004 respectively). KIAA1549:BRAF fusion status was not predictive of outcome. CONCLUSION: This study highlights the good prognostic factors of PAs but H/C PA remains a subgroup with dismal prognosis associated with young age, PMA variant and incomplete surgery. Search for KIAA1549:BRAF fusion in tumours with PA pattern is recommended even though the prognostic impact is still unclear.

[Stereotactic radiotherapy and radiosurgery in treatment of patients with deep-seated pilocytic astrocytomas].

Pilocytic astrocytoma (PA) is a low-grade glial tumor (WHO grade I) with predominant occurrence in pediatric patients. According to many authors, stereotactic radiosurgery (SRS) and radiotherapy (SRT) promote long-term remission or retardation of tumor progression in patients with in inoperable lesions after incomplete resection or recurrence. Therefore it is essential to determine the role of SRS and SRT in complex management of patients with deep-seated PA. Since April 2005 till May 2010 101 patient with intracranial PA was treated in department for radiation therapy of Burdenko Neurosurgical Institute. The series consisted of 70 pediatric patients (below 17 years inclusively) and 31 adults, of them--51 male and 50 female patients. Mean age was 15.1 years (9.8 years in children and 28.7 in adults). In 90 patients (89.2%) tumors were previously histologically verified (tumor resection in 83 cases and biopsy in 7). In 11 (10.8%) patients diagnosis of PA was based on clinical and neurovisualization data. In most cases SRT (66 (66.3%) patients) was preformed, the rest 35 (34.7%) patients were treated by SRS. Median follow-up from the onset of disease reached 52 months (2-228 months). Catamnestic data were available in 88 (87%) patients. By the end of catamnestic follow-up (December 2010) 87 (98.8%) patients treated by SRS and SRT were alive. Median follow-up from the start of radiation treatment was 22.7 months (6-60 months). Progression of tumor was observed in 20 patients (22.7%), in 18 of them due to cyst growth. 18 patients were reoperated. In 12 operated patients histological examination and its comparative analysis were performed. We found that alterations in the tumor tissue, accompanied by regression of solid component and progression of cystic portion, represent reactive-degenerative changes in the tumor as a consequence of radiation-induced pathomorphism. SRS and STR are effective techniques for treatment of patients with primary and recurrent PA despite regardless of localization of the tumor. There procedures should be performed shortly after non-radical resection. Control of tumor growth by the present time (median follow-up is 22.7 months) reaches 98%. "Progression" of the tumor due to enlargement of cystic portion shortly after SRT and SRS represents reactive-degenerative alterations in the tumor tissue and should not be evaluated as true recurrence; without neurological deterioration these cases do not require special treatment.

RNAi screening in glioma stem-like cells identifies PFKFB4 as a key molecule important for cancer cell survival.

The concept of cancer stem-like cells (CSCs) has gained considerable attention in various solid tumors including glioblastoma, the most common primary brain tumor. This sub-population of tumor cells has been intensively investigated and their role in therapy resistance as well as tumor recurrence has been demonstrated. In that respect, development of therapeutic strategies that target CSCs (and possibly also the tumor bulk) appears a promising approach in patients suffering from primary brain tumors. In the present study, we utilized RNA interference (RNAi) to screen the complete human kinome and phosphatome (682 and 180 targets, respectively) in order to identify genes and pathways relevant for the survival of brain CSCs and thereby potential therapeutical targets for glioblastoma. We report of 46 putative candidates including known survival-related kinases and phosphatases. Interestingly, a number of genes identified are involved in metabolism, especially glycolysis, such as PDK1 and PKM2 and, most prominently PFKFB4. In vitro studies confirmed an essential role of PFKFB4 in the maintenance of brain CSCs. Furthermore, high PFKFB4 expression was associated with shorter survival of primary glioblastoma patients. Our findings support the importance of the glycolytic pathway in the maintenance of malignant glioma cells and brain CSCs and imply tumor metabolism as a promising therapeutic target in glioblastoma.

[A new entity in WHO classification of tumors of the central nervous system--embryonic tumor with abundant neuropil and true rosettes: case report and review of literature].

Embryonic tumor with abundant neuropil and true rosettes (ETANTR) is a very aggressive rare tumor with unique histologic and molecular features occurring in very young children. At present approximately 80 cases of ETANTR have been documented in the literature since first description in 2000. We report seven patients with ETANTR below 4 years of age who underwent surgical resection in the Burdenko Neurosurgery Institute between 2005 and 2010. Four children have received different modality chemotherapy and radiotherapy and two patients were treated by chemotherapy alone. One child did not receive any adjuvant treatment. All children had local relapses, two of them were operated twice. A 2 year old girl underwent subtotal resection thrice. Histological examination showed that all tumors were composed of true multilayered rosettes admixed with large areas of paucicellular neuropil. By analysis of recurrences we have found that large areas of neuropil and number of true rosettes were lost and tumors acquired a resemblance to central nervous system primitive neuroectodermal tumors. In four cases frozen tumor material was available for array-based comparative genomic hybridization, which discovered trisomy of chromosome 2 and amplification at the 19q13.42 chromosome locus. Fluorescence in situ hybridization revealed amplification at the 19q13.42 chromosome locus in all cases.

[Influence of molecular-genetic factors on prognosis in patients with oligodendroglial tumors].

Previous studies demonstrated that patients with oligodendroglial tumors (OT) have longer overall and recurrence free survival than patients with other glial tumors of the same grade. Recent investigations showed high influence of genetic alterations on patients' outcome: overall and recurrence free survival increased in the case of presence 1p19q deletion and decreased in the presence of 9p or 10q deletion and/or EGFR amplification. In the series of 241 cases (107 male, 134 female patients, median age -- 38 years, (16-73)) we analyzed the impact of histology, tumor grade and genetic alterations on time to tumor progression (TTP). All patients underwent surgical resection of tumor or biopsy from 2000 to 2005. 70 patterns (oligodendroglioma (O) -- 13 cases, oligoastrocytoma (OA) -- 13, anaplastic oligodendroglioma (AO) -- 30, anaplastic oligoastrocytoma (AOA) -- 14) were assessed by fluorescent in situ hybridization. Median follow up was 24 months. The type of tumor (pure or mixed) didn't influence survival. TTP of patients with grade II and grade III tumors was 37.7 and 48.2 months, respectively (p = 0.035). Deletion 1p19q was noted in 34 (49%) cases. In pure O codeletion 1p19q was detected more frequently (in O -- 75%, in AO -- 56%) than in mixed tumors (in OA -- 31%, in AOA -- 35%). Deletions 9p, 10q and EGFR amplification were noted in 5, 6 and 4 cases, respectively. None of the tumors with 1pl9q deletion had other genetic alterations. Thus, we generated three prognostic groups: A -- deletion 1p19q; B -- balanced chromosomal profile; C -- deletion 9p. Median TTP in groups A, B and C was 46.6, 25.3 and 6.4 months, respectively (p < 0.001). The percentage of OT with 1p19q codeletion was lower than in previous studies. Pure O more frequently had 1p19q deletion than mixed tumors. Genetic alterations predict outcome stronger than histological criteria.

[Histobiological features of posterior cranial fossa meningiomas and their impact on follow-up].

Total removal of posterior cranial fossa meningiomas often leads to complications due to localization, direction and nature of tumor growth. Radical excision as well as histological grade are the principal factors determining recurrence of disease in follow-up period. The paper evaluates the role of ki67 in progression of posterior cranial fossa meningiomas. We performed 189 immunohistochemical studies and katamnestic analysis of patients operated in Burdenko Neurosurgical Institute (Moscow). We showed that level of expression of ki67 correlates with histological grade of posterior fossa meningiomas. We established that recurrence-free survival depends on ki67. This allows prediction of prognosis. Low expression of ki67 corresponds longer recurrence-free survival. If ki67 expression is over 4% recurrence within 2 years after surgery is observed significantly more frequently. Multifactor statistical analysis confirmed prognostic value of ki67 especially in females and patients below 50 because terms of recurrences in these populations are significantly smaller. Obtained data prove versatility of ki67 in neurooncology which should enable its wider application in neurosurgical clinics.

[Chromosome 17 abnormalities in medulloblastomas and their prognostic value].

The cytogenetic profile of chromosome 17 was studied in 180 medlloblastomas by the interphasic FISH technique, which revealed the high incidence of this aberration and its association with the poor clinical course of the disease. The interphasic cytogenetic analysis of chromosome 17 abnormalities in medulloblastoma biopsy specimens may be recommended for its inclusion into a complex of laboratory diagnostic methods used in the examination of these tumors.