Biomedical subjects

M Poisson

Publications and source records attributed to M Poisson.

At least 37 records · Page 2Linked to original sources

PubMed1996

[Supratentorial gliomas: neuropsychological study of long-term survivors].

A battery of psychologic tests was administered to 32 patients, aged from 26 to 61 years, who had survived 2 years or more after treatment with surgery and radiotherapy for supratentorial gliomas (18 low grade and 14 high grade) without evidence of recurrent tumor on MRI. Two groups were identified. A first group of 17 patients had neuropsychologic scores similar to estimated premorbid level (group I). A second group of 15 patients had abnormal neuropsychologic scores, lower that their estimated premorbid level (group II). In comparison with "normal" patients, those with abnormal neuropsychologic scores were older at the time of treatment, had a lower post-operative Karnofski Performance Status, a longer delay between surgery and the date of the tests and more often had left sided lesions. Comparison of Karnofski Performance Status between the post-operative time point and the date of neuropsychological evaluation did not show a significant change over time in groups I and II except in 3 patients who experienced progressive deterioration. Vigorous treatment of gliomas with surgery, radiotherapy and sometimes chemotherapy does not induce a substantial cognitive dysfunction in about half of the long term survivors (53%). Cognitive dysfunction is identified in the other half that could be related to post-operative sequelae (due to the tumor itself or to surgery) and/or to radiotherapy- and chemotherapy-induced delayed toxicity.

Adult↗

PubMed1996

[Iridium 192 brachytherapy of supra-tentorial high grade glioma recurring in irradiated areas: technique and preliminary results of the Pitié-Salpêtrière hospital group].

UNLABELLED: Our aim was to analyse feasibility and preliminary results obtained with iridium 192 re-irradiation of recurrent high grade gliomas. MATERIAL AND METHODS: a technique for implanting rigid plastic tubes afterloaded with iridium 192 wires was developed that utilised a stereotactic Leksell frame. Nineteen glioblastomas and one anaplastic glioma (12 males and 8 females: age: 20-69 years, median: 50) were implanted between January 1993 and December 1994. Previous treatments included surgery (18/20). 55-60 Gy external beam radiotherapy (20/20), and chemotherapy (16/20); interval between initial treatment and retreatment with iridium 192 was 6 to 39 months (median: 10). Maximum diameter of the tumour at the moment of implantation was 2.1-10.1 cm (median: 6.4 cm) and tumour volume 2.122 cm3 (median: 22 cm3). All tumours were supra-tentorial (right hemisphere: 9; left hemisphere: 11). Karnofsky index was 60-100 (median: 80). Implantation was carried out under local anaesthesia; tumour contours were visualised using either a CT-scan (16/20) or a MRI (4/20). Dosimetry was carried out using two orthogonal films and CT-scan images. Total dose on the reference isodose was 40-60 Gy (60 Gy: 9; 50 Gy: 7; 40 Gy: 4); dose-rate was 0.24-0.73 Gy/h (median: 0.38). RESULTS: probability of overall survival is 90% at 6 months, 55% at one year, and 26% at two years. Median survival is 56 weeks. Eleven patients died from local failure, and three from leptomeningeal metastasis. Six patients are alive, 15-30 months after the implantation. Two were reoperated for brain necrosis. Three patients showed evidence of bacterial meningitis, and three others of skin necrosis. CONCLUSION: according to this preliminary analysis, results obtained after reirradiation of high grade gliomas with iridium 192 are encouraging. More patients and longer follow-up are needed to draw definitive conclusions.

Adult↗

PubMed1996

[Central nervous system infections in patients with malignant diseases].

Infections of the nervous system remain a significant source of morbidity and mortality in patients with cancer. This paper reviews the main pathogens and emphasizes some of the principles of diagnosis and management of nervous system infections in cancer patients. Due to immunosuppression, diagnosis is more difficult in this group, secondary to the multitude of potential pathogens, and often by their atypical presentations. Fever or headache are often the only symptoms. Clinical history and general examination should guide appropriate studies such as neuroimaging. CSF analysis, cultures, and brain biopsy. Diagnostic evaluation should be pursued rapidly and aggressively since specific treatments can often reduce morbidity and mortality. Bacterial infections are generally due to break-down of the natural barriers and neutropenia. In neutropenia, Pseudomonas aeruginosa, and Enterobacteriae are the most frequent etiology. If all causes of immunodepression are included, Listeria monocytogenes meningitis is the main bacterial infection encountered. Fungal infections have emerged as a major cause of death among cancer patients. The prognosis of cryptococcosis and histoplasmosis meningitis are markedly improved with new antifungal therapy. Aspergillosis and Mucormycosis, which may cause cerebral abcesses and secondary vascular complications, are almost always fatal. The incidence of meningo-cerebral Candidiasis is often underestimated. Similar to Histoplasmosis, it is frequently disseminated. Viral infections are mainly seen in patients with T-lymphocyte defects. Herpes-simplex virus and Varicella-Zoster virus encephalitis should quicky lead to intravenous treatment with Acyclovir. As in AIDS patients, cerebral toxoplasmosis is the most frequent parasitic infection and appropriate therapy greatly reduces morbidity. It should be emphasized that multitude pathogens are often seen in cancer patients. Despite development of new therapeutic agents, central nervous system infections should still be considered life-threatening. Therefore, antibacterial, antifungal, and antiviral prophylaxis should be the rule for all cancer patients.

Central Nervous System Diseases↗

PubMed1995

Incidence of germ-line p53 mutations in patients with gliomas.

Epidemiological studies on intracranial tumors have suggested that the observed familial aggregation of a proportion of gliomas may be due to inherited predisposition to their development. In the Li-Fraumeni syndrome (LFS) associated with germ-line mutations of the p53 gene, nervous-system tumors are observed with increased frequency. However, the contribution of germ-line p53 mutation to the incidence of brain tumors has not been investigated. In order to address this point, we have performed 2 independent investigations. First, we have examined an unselected series of brain tumors. Whenever the presence of a p53 mutation in the tumor was observed, the possible germ-line origin of the mutation was investigated. Germ-line p53 mutations were also analyzed in constitutional DNA of patients with gliomas that had been selected for an unusual personal or familial history of cancer. Germ-line p53 mutations were detected in 1 out of 80 unselected cases and in 3 out of 15 selected cases (20%). We conclude that germ-line p53 mutation may contribute to a small fraction of gliomas that develop in the general population. The presence of a personal or familial history of cancer in a patient with glioma should prompt the search for a germ-line p53 mutation. However, the low frequency of p53 germ-line mutation suggests that alterations of this gene may not account for most familial cases of gliomas.

Amino Acid Sequence↗

PubMed1995

Frequent loss of heterozygosity on chromosome 9, and low incidence of mutations of cyclin-dependent kinase inhibitors p15 (MTS2) and p16 (MTS1) genes in gliomas.

Four cyclin-dependent kinase inhibitors called p15, p16, p21 and p27 have been identified in mammals. Because these proteins participate in the control of cell cycle, they are potential targets for somatic mutations during carcinogenesis. In order to document the prevalence of p15 and p16 alterations in gliomas, we looked for loss of heterozygosity of chromosome 9p where these genes are localized. Allelic losses were observed in 31 of 44 investigated cases. In all cases they involved the p15/p16 locus. We then looked for mutations in the p16 and p15 genes in 46 gliomas. A total of three DNA variants were observed which were all present in the matched constitutional DNA. They may be unrelated to tumor development. A single somatic mutation was detected. It involved a C to G substitution in codon 93 of p16 and is predicted to change a threonine into an arginine. Taken together, these data indicate that inactivation by point mutation of these two cyclin-dependent kinase inhibitors is uncommon in glial tumor carcinogenesis, but that there may be a tumor suppressor gene on 9p in the vicinity of p16 and p15 genes.

Base Sequence↗

PubMed1995

Mitochondria-bound hexokinase as target for therapy of malignant gliomas.

Hexokinase plays an important role in glucose-utilizing tissues like normal brain and cancers. In these tissues, hexokinase (HK) is mainly bound to mitochondria (mHK). Our objectives were to evaluate total HK (tHK) activity and mHK fraction in gliomas and to determine whether mHK binding could be targeted for therapy. Tumors were obtained from 26 patients and 13 were xenografted. HK, lactate and ATP were measured in cytosol and mitochondria extracts. The tHK expressed in mU/mg protein were 147 +/- 19 and 78 +/- 12, in fresh gliomas and xenografts, respectively, and of 489 in the normal brain. The mHK fraction was 76% in normal brain, 74 +/- 4% in fresh tumors and 53 +/- 6% in xenografts. Lactate/mHK ratios were higher in gliomas than in normal brain. The ATP was 10, 52 +/- 31 and 19 +/- 8 nmol/mg protein in normal brain, xenografts and fresh gliomas respectively. Loss of one copy of chromosome 10 which carries the HK1 gene, was evidenced in 11 of the 13 xenografted gliomas. The anti-tumor effect of lonidamine (LND), which affects glycolysis in interfering with mHK activity, was tested in nude mice bearing 4 gliomas. LND (125 mg/kg, given i.p., twice daily for 5 days) led to a growth inhibition of TG-7-RO of 72%, with 2-fold growth retardation, and had no effect for TG-8-OZ. Intermediate LND-sensitivities for TG-11-DU and TG-10-PY were noted. The LND-sensitivity was correlated with the mHK activity (R2 = 0.73) and mHK fraction (R2 = 0.88). HK binding to mitochondria is a key of glycolysis in malignant gliomas, and targetting this binding with appropriate agents could be an effective therapeutic approach.

Adenosine Triphosphate↗

PubMed1995

Analysis of the NF2 tumor-suppressor gene and of chromosome 22 deletions in gliomas.

Recurrent deletions of chromosome fragments observed in neoplasms are thought to participate in tumor development through the inactivation of tumor-suppressor genes. In gliomas, the most frequent deletions involve chromosome arms 9p, 10q, 17p, 19q and 22q. We have analysed deletions of chromosome 22 in gliomas by studying loss of heterozygosity (LOH) at 8 microsatellite loci. LOH for this chromosome fragment was observed in 17/70 (24%) cases, most of them encompassing the region which encodes the gene altered in neurofibromatosis 2 (NF2), an inherited disease which predisposes to tumors of the nervous system. To investigate the possible involvement of the NF2 tumor-suppressor gene in the tumorigenesis of gliomas, we searched for alterations in its genomic structure and in its mature transcript. Northern-blot and reverse transcriptase-PCR experiments showed that the NF2 transcript is expressed and does not demonstrate obvious structural alterations. Moreover, analysis, at the genomic level, of the 16 coding exons of the NF2 gene by denaturing gradient gel electrophoresis failed to detect any somatically acquired point mutations. Altogether, these data strongly suggest that, although gliomas demonstrate recurrent chromosome 22 deletions most frequently encompassing the NF2 region, the NF2 gene is not altered in these tumors.

Base Sequence↗

PubMed1995

Radiation-induced cognitive dysfunction: an experimental model in the old rat.

PURPOSE: To develop a model of radiation-induced behavioral dysfunction. METHODS AND MATERIALS: A course of whole brain radiation therapy (30 Gy/10 fractions/12 days) was administered to 26 Wistar rats ages 16-27 months, while 26 control rats received sham irradiation. Sequential behavioral studies including one-way avoidance, two-way avoidance, and a standard operant conditioning method (press-lever avoidance) were undertaken. In addition, rats were studied in a water maze 7 months postradiation therapy. RESULTS: Prior to radiation therapy, both groups were similar. No difference was found 1 and 3 months postradiation therapy. At 6-7 months postradiation therapy, irradiated rats had a much lower percentage of avoidance than controls for one-way avoidance (23% vs. 55%, p < or = 0.001) and two-way avoidance (18% vs. 40%, p < or = 0.01). Seven months postradiation therapy the reaction time was increased (press-lever avoidance, 11.20 s vs. 8.43 s, p < or = 0.05) and the percentage of correct response was lower (water maze, 53% vs. 82%) in irradiated rats compared with controls. Pathological examination did not demonstrate abnormalities of the irradiated brains at the light microscopic level. CONCLUSION: Behavioral dysfunction affecting mainly memory can be demonstrated following conventional radiation therapy in old rats. This model can be used to study the pathogenesis of radiation-induced cognitive changes.

Aging↗

PubMed1995

Primary central nervous system lymphoma: treatment with chemotherapy and radiotherapy.

Between 1989 and 1993, 22 HIV negative patients with primary central nervous system lymphoma (PCNLS) were treated with three different regimens. In group A, 13 patients received preradiotherapy systemic and intrathecal methotrexate (MTX), radiotherapy (RT) and three courses of post-RT chemotherapy (CT) with thiotepa and procarbazine. In group B, 4 patients received a similar CT only after RT and without intrathecal MTX in 3/4 cases. In group C, 5 elderly patients received CT alone. In group A, 9/13 patients achieved response after pre-RT CT and 12/13 were in complete response (CR) after RT. After a median follow-up of 27 months, 8/13 (62%) patients are alive but 4 have leucoencephalopathy and cognitive dysfunction. In group B, all 4 patients were in CR after RT but the 3 patients who did not receive intrathecal MTX died within 10 months with meningeal recurrence. In group C, 4/5 patients had a response to CT. 2 patients died of recurrent tumour at 5 and 10 months, and 2 are living in CR 11+ and 21+ months after diagnosis, 1 after salvage CT. Combined treatment with RT and CT is useful in PCNSL but adequate treatment of the meninges is required. CT alone is sometimes of value in elderly patients in whom RT is not indicated.

Adult↗

PubMed1995

Incorporation, release and in-vitro antibacterial activity of liposomal aminoglycosides against Pseudomonas aeruginosa.

Amikacin, netilmicin and tobramycin were incorporated into either anionic or cationic liposomes prepared by sonication. The influence of lipid constituents (charges) on encapsulation efficiency was determined after lysis of vesicles by 0.2% (v/v) Triton X-100. The in-vitro activities of the liposomal aminoglycosides were evaluated against Pseudomonas aeruginosa by agar dilution and compared with free antibiotics. Normal human pooled sera, incubated at 37 degrees C, were supplemented with anionic or cationic liposomes containing known fixed concentrations of amikacin, netilmicin or tobramycin. At various time intervals (0-48 h), samples were taken and antibiotic concentrations determined by the enzyme multiplied immunoassay technique (EMIT). The encapsulation efficiency of cationic liposomes (amikacin 17.1 +/- 1.55%, netilmicin: 5.63 +/- 1.13%, tobramycin 6.7 +/- 0.5%) was approximately 30% higher than that of anionic liposomes (amikacin 12.3 +/- 0.95%, netilmicin 4.0 +/- 0.06%, tobramycin 5.13 +/- 0.18%). Anionic and cationic liposomes in human serum still retained 79.13 +/- 4.04% and 82.71 +/- 2.6% of amikacin, 50.67 +/- 1.8% and 38.6 +/- 0.8% of netilmicin, and 89.09 +/- 1.0% and 88.93 +/- 0.4% of tobramycin, respectively, after 48 h of incubation at 37 degrees C under 5% CO2. The MICs of amikacin (2, 16 and 2 mg/L), netilmicin (2, 1 and 4 mg/L) and tobramycin (1, 2 and 4 mg/L) in free, anionic or cationic liposomal formulations, respectively, were relatively comparable except for anionic liposomal amikacin for which the MIC was increased eight-fold. Empty cationic or anionic liposomes had no effect on bacterial growth. Cationic liposomes containing aminoglycosides should be evaluated further for the treatment of pseudomonal infection.

Amikacin↗

PubMed1995

[Gliomatous meningitis of hemispheric tumors. Study of 22 cases in adults].

Twenty-two patients suffering from diffuse leptomeningeal gliomatosis (LG) were identified at the Salpêtrière Hospital between January 1989 and January 1994: 20 patients had a known primary supratentorial glioma when LG was diagnosed (8 glioblastomas, 5 anaplastic astrocytomas, 3 anaplasic oligodendrogliomas, 2 astrocytomas and 2 oligodendrogliomas); 2 patients had primary LG. The delay between the discovery of the primary tumour and the development of LG was 5 +/- 4 months in glioblastomas and 22 +/- 16 months for others gliomas. In 1/2 primary LG, autopsy demonstrated an hippocampic astrocytoma which was undetected pre-mortem even on MRI; in the second patient with primary LG no autopsy was obtained and the diagnosis was based on meningeal biopsy. An epidemiological study was made by comparing 13 LG with 275 supratentorial gliomas without LG who were seen during the same period. The incidence of symptomatic LG was 4.7% and was more frequent in anaplasic astrocytomas (6.5%) and anaplasic olidendrogliomas (11.4%) than in glioblastomas (3%) but the difference was not statistically significant. The age at diagnosis of LG was 56 +/- 11 years in glioblastomas and 41 +/- 7 in others gliomas, related to tumour histology. Among the 22 studied cases, only 27% had a meningeal syndrome; multifocal neurological involvement was present in 74% of patients combining at various degree signs of cerebral, cranial nerves and roots or spinal cord dysfunction. Contrast enhancing lesions in the meninges or ventricules on CT/MRI were found in 82% of cases and 45% had an hydrocephalus. In the CSF 94% of patients had a protein level over 1 milligram and 47% of them had a low glucose level < 2.7 mmol/l; malignant cells were found in 47% of cases. Among 11 patients who received radiotherapy and/or chemotherapy, 3 improved and 2 were stable and their survival ranged from 6 to 34+ months. Criteria allowing diagnosis of LG are defined and the therapeutic option are reviewed.

Adult↗

PubMed1994

Evaluation of single-photon emission tomography imaging of supratentorial brain gliomas with technetium-99m sestamibi.

Single-photon emission tomography (SPET) with technetium-99m sestamibi (MIBI) was carried out in 61 adult patients with supratentorial expanding brain lesions. Thirty-one patients had pathologically proven malignant glioma. Ten patients had pathologically proven low-grade glioma, while another 12 patients had a clinical diagnosis of low-grade glioma. The other eight patients had a variety of lesions including radiation necrosis (3), abscess (2), ischaemic stroke (2) and primary brain lymphoma (1). SPET was performed 15 min after administration of 740-930 MBq MIBI and transverse, sagittal and coronal views were reconstructed. Using computed tomography or magnetic resonance imaging guidance, a MIBI uptake index was computed as the ratio of counts in the lesion to counts in the contralateral homologous region. In high-grade gliomas, the MIBI index ranged from 1.9 to 6.6 (mean 3.6 +/- 1.4) whereas it ranged from 0.8 to 1.7 (1.1 +/- 0.2) in the pathologically proven low-grade group (P < 0.01). No significant difference was found between the two low-grade groups (1.1 +/- 0.2 vs 1.1 +/- 0.2). No overlap was found between high-grade and low-grade glioma index values. Patients with suspected radiation necrosis, cerebral abscess or ischaemic stroke did not demonstrate high MIBI uptake (0.9-2.2), whereas one patient with brain lymphoma did (3.9). This study suggests that MIBI SPET imaging is of value in distinguishing low-from high-grade supratentorial gliomas in adults.

Adult↗

PubMed1994

Osteosarcoma following radiation treatment for meningioma: report of a case and effective treatment with chemotherapy.

A case of effective chemotherapy in postirradiation sarcoma is reported. A 30-year-old woman underwent a subtotal resection of a benign mixed meningioma followed by a course of radiotherapy. Five years later she developed a skull tumor which was resected. Histological study showed sarcomatous change corresponding most likely to a postirradiation osteosarcoma. Adjuvant chemotherapy (methotrexate, carboplatin, and VP16) was given. A progression occurred 8 months later and the patient was treated unsuccessfully with tamoxifen, LHRH, and later with high dose methotrexate and carboplatin. Six months later a lung metastasis was discovered and she received four cycles of IVP (ifosfamide, vepeside, cisplatin) alternating with IVA (ifosfamide, vepeside, adriamycin). Within 4 months the primary and lung tumours had decreased substantially without evidence of progression at follow-up 5 months later. We conclude that IVP/IVA regimen is a potentially useful therapy when an osteosarcoma of the skull is in progression.

Adult↗

PubMed1994

Analysis of oncogene expression in primary human gliomas: evidence for increased expression of the ros oncogene.

Expression of a panel of oncogenes and potential oncogenes was studied in normal human brain and in 17 human gliomas, including three low- and 14 high-malignancy-grade tumors. PolyA RNA was isolated from glioma biopsies and used as template for reverse transcriptase-catalyzed synthesis of radioactively labeled cDNA. Labeled cDNA was then hybridized to filters to which probes for various oncogenes had been attached. Increased signal intensity, as compared with that of normal brain, was observed for the ros oncogene in six of 17 gliomas, including gliomas of both low and high malignancy grades. Increased ros expression was verified by Northern blot analysis in one tumor. These results suggest that increased ros expression may play a role in tumorigenesis in a significant proportion of gliomas. Increased expression of other genes, including the erbA2, mel, and ets oncogenes was observed in a smaller proportion of the gliomas tested, suggesting a possible role for these oncogenes in individual tumors but no generalized role in development or progression of human gliomas.

Adult↗

PubMed1994

A cytogenetic study of 19 recurrent gliomas.

A cytogenetic analysis was performed on 19 recurrent gliomas all of which had been treated by radiotherapy. All cases exhibited clonal chromosomal anomalies, the tumors were classified into four categories in relation to their mono- or polyclonality and to the presence or absence of a clonal evolution. Polyclonal tumors without clonal evolution had a delay of recurrence significantly longer than monoclonal or polyclonal tumors with clonal evolution. This difference could be related to the presence of clones with different malignant potential, which could be differentiated by their pattern of chromosomal aberrations. The malignant potential of "highly malignant" clones resulted from the juxtaposition of imbalances, such as monosomy 10, as in high-grade primary gliomas, and presumably radiation-induced structural rearrangements. That of clones of low malignancy was almost limited to the presence of multiple balanced structural rearrangements, probably induced by radiation.

Adolescent↗

PubMed1994

Purine and pyrimidine metabolism in human gliomas: relation to chromosomal aberrations.

Chromosomal aberrations in human gliomas are principally numerical. In tumours of low malignancy, karyotypes are frequently normal, but occasionally an excess of chromosome 7 and a loss of sex chromosome are observed. In highly malignant tumours, the most frequent aberrations are gain of chromosome 7, loss of chromosome 10 and less frequently losses or deletions of chromosomes 9, 22, 6, 13 and 14 or gains of chromosomes 19 and 20. To understand the meaning of these chromosome imbalances, the relationships between chromosome abnormalities and metabolic disturbances were studied. The losses or deletions observed affected principally chromosomes carrying genes encoding enzymes involved in purine metabolism. The activities of ten enzymes were measured: adenosine kinase, adenine phosphoribosyltransferase, adenylate kinase, methylthioadenosine phosphorylase, hypoxanthine phosphoribosyltransferase, adenylosuccinate lyase, inosine monophosphate dehydrogenase, adenosine deaminase, nucleoside phosphorylase and adenosine monophosphate deaminase. In parallel, two enzymes involved in pyrimidine metabolism, thymidine kinase and thymidylate synthase (TS), were studied. The activities of all these enzymes were measured on samples from 30 human primary glial tumours with low or high malignancy, six xenografted tumours at different passages, four portions of normal brain tissue and four non-glial brain neoplasms. As suggested by cytogenetic data, the enzymatic results showed a relatively low activity of purine metabolism in glial tumours when compared with normal brain and non-glial brain neoplasms. Considering the two enzymes involved in pyrimidine metabolism, only TS had higher activity in glial tumours of high malignancy than in normal brain. In comparison with normal brain, the balance between salvage and de novo pathways changes in gliomas, and even more in grafted tumours, in favour of de novo synthesis. The relation between chromosomes and metabolic imbalances does not correspond to a simple gene dosage effect in these tumours. These data suggest that the decrease of adenosine metabolism occurs before chromosomal aberrations appear, since it is observed in tumours of low malignancy when most karyotypes are still normal, and that the de novo pathway increases with tumour progression.

Adolescent↗

PubMed1994

Intrathecal synthesis of the anti-Hu antibody in patients with paraneoplastic encephalomyelitis or sensory neuronopathy: clinical-immunologic correlation.

We studied the intrathecal synthesis of the anti-Hu antibody (also called type 1 antineuronal nuclear autoantibody) in 14 patients with isolated paraneoplastic subacute sensory neuronopathy (SSN) and 16 with paraneoplastic encephalomyelitis (PEM). Patients with PEM had higher anti-Hu titers in the CSF (p = 0.003) but not in the serum than those with SSN. Only one patient (7%) with SSN had a positive intrathecal anti-Hu antibody synthesis whereas this was present in 14 (88%) of the 16 patients with PEM (p < 0.0001). The correlation between the intrathecal production of anti-Hu antibodies and PEM supports the role of autoimmune mechanisms in the pathogenesis of PEM. The absent intrathecal synthesis of anti-Hu antibodies in patients with SSN suggests easier accessibility of the systemic immune reaction to the sensory neurons probably due to the partial absence of blood-nerve barrier in the dorsal root ganglia.

Aged↗

PubMed1994

[Characterization of chromosomal rearrangements by in situ hybridization in glioblastoma].

In a case of glioblastoma, the following karyotype was determined: 47, X, - Y, + der(1) t(1;9)(p21;p23), t(1;9)(p21;p23), + 3, + 7, der(9) t(Y;9)(q11;p21), - 13, t(13;16)(p13,p11), del(14)(q11q22). Classical satellite DNAs are mainly located in chromosomes 1, 9, 15, 16 and Y. Because, most of these chromosomes were implicated in the rearrangements, a detailed cytogenetic study was undertaken. This study included in situ hybridization of the satellite and alphoid DNAs of chromosomes 1, 9, 16 and Y combined with various chromosome banding methods (DA-DAPI, quinacrine mustard and R-banding). The data obtained, demonstrated that the breakpoints were always located outside the areas containing the satellite and alphoid DNAs. The situation observed here differs from that reported in breast cancers for which a high proportion of the breakpoints occur within these areas. These findings suggest that in glioblastoma, chromosome rearrangements result from different mechanisms than those implicated in breast cancers. Thus, in cancers, chromosomal instabilities may result from several mechanisms.

Azacitidine↗