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J M de Campos

Publications and source records attributed to J M de Campos.

At least 19 recordsLinked to original sources
PubMed2005

[Esthesioneuroblastoma treatment].

INTRODUCTION: Esthesioneuroblastoma is an uncommon malignancy of the olfactory neuroepithelium. The best treatment has yet to be defined. The purpose of this study is to analyze the tumors's behaviour to choose the ideal treatment, the therapeutic strategy and the patterns of failure. MATERIALS AND METHODS: We carry out a revision of the series published between 1994 to 2004. In these series, we found 39 papers with 713 patients. DISCUSSION CONCLUSIONS: In this review the 5-years survival rate is 51.2%. Through the analysis of 583 partients found in 34 publications, surgery (alone or combined) is the treatment most used (78%). The commonly management is surgical in combination with radiotherapy (47%).

Esthesioneuroblastoma, Olfactory↗
PubMed2003

CpG island methylation status and mutation analysis of the RB1 gene essential promoter region and protein-binding pocket domain in nervous system tumours.

A series of 136 nervous system tumours were studied to determine the methylation status of the CpG island contained within the promoter region of the RB1 gene, as well as mutation analysis of the essential promoter region and exons 20-24 (and surrounding intronic regions) coding for the protein-binding pocket domain. Methylation of the RB1 CpG island was detected in 26 samples corresponding to nine glioblastomas, three anaplastic astrocytomas, one mixed oligo-astrocytoma, one ependymoma, two medulloblastomas, two primary central nervous system lymphomas, two neurofibrosarcomas, and six brain metastasis from solid tumours. No inactivating mutations were found within the RB1 promoter region, whereas one glioblastoma and one oligodendroglioma displayed similar sequence variations consisting of 12 and 8 base pair deletions at intron 21. These results suggest that RB1 CpG island hypermethylation is a common epigenetic event that is associated with the development of malignant nervous system tumours.

CpG Islands↗
PubMed2001

Mutation analysis of the p73 gene in nonastrocytic brain tumours.

Loss of heterozygosity (LOH) involving the distal chromosome 1 p36 region occurs frequently in nonastrocytic brain tumours, but the tumour suppressor gene targeted by this deletion is unknown. p73 is a novel gene that has high sequence homology and similar gene structure to the p53 gene; it has been mapped to 1 p36, and may thus represent a candidate for this tumour suppressor gene. To determine whether p73 is involved in nonastrocytic brain tumour development, we analysed 65 tumour samples including 26 oligodendrogliomas, 4 ependymomas, 5 medulloblastomas, 10 meningiomas, 2 meningeal haemangiopericytomas, 2 neurofibrosarcomas, 3 primary lymphomas, 8 schwannomas and 5 metastatic tumours to the brain, for p73 alterations. Characterization of allelic loss at 1 p36-p35 showed LOH in about 50% of cases, primarily involving oligodendroglial tumours (22 of 26 cases analysed; 85%) and meningiomas (4 of 10; 40%). PCR-SSCP and direct DNA sequencing of exons 2 to 14 of p73 revealed a missense mutation in one primary lymphoma: a G-to-A transition, with Glu291Lys change. 8 additional cases displayed no tumour-specific alterations, as 3 distinct polymorphic changes were identified: a double polymorphic change of exon 5 was found in one ependymoma and both samples derived from an oligodendroglioma, as follows: a G-to-A transition with no change in Pro 146, and a C-to-T variation with no change in Asn 204: a delG at exon 3/+12 position was identified in 4 samples corresponding to 2 oligodendrogliomas, 1 ependymoma and 1 meningioma, and a C-to-T change at exon 2/+10 position was present in a metastatic tumour. Although both LOH at 1 p36 and p73 sequence changes were evidenced in 4 cases, it is difficult to establish a causal role of the p73 variations and nonastrocytic brain tumours development.

Brain Neoplasms↗
PubMed2001

Chromosomal abnormalities in pituitary adenomas.

Cytogenetic studies were conducted on 30 pituitary adenomas, using both direct and/or short-term in vitro culture methods. An apparently normal chromosome complement was found in 14 tumors; 5 adenomas were characterized by hyperdiploid or near-triploid modal chromosome numbers. Recurrent numerical deviations were identified in 12 samples, which primarily involved gains of chromosomes 4, 7, 8, 9, 12, and 20 by gains, and losses of chromosomes 10, 14, 19, and 22. Four adenomas were shown to have structural chromosome rearrangements with no apparent recurrent pattern of involvement.

Adenoma↗
PubMed2001

Analysis of p73 gene in meningiomas with deletion at 1p.

The p73 gene has been mapped to 1p36.33, a chromosome region that is frequently deleted in a wide variety of neoplasms including meningiomas. The protein encoded by p73 shows structural and functional similarities to p53 and may thus represent a candidate tumor suppressor gene. To determine whether p73 is involved in the development of meningiomas, we examined 30 meningioma samples with proven 1p deletion for mutations of p73. Sequence analysis of the entire coding region of the p73 gene revealed previously reported polymorphisms in eight cases. A tumor-specific missense mutation as a result of an A-to-G transition with an Asn204Ser change was found in one meningioma that nevertheless retained the normal allele. These results suggest that if p73 plays a role in meningioma carcinogenesis, it must be in a manner different from the Knudson two-hit model.

Chromosome Deletion↗
PubMed2001

Arachnoid cysts: entrapped collections of cerebrospinal fluid variably communicating with the subarachnoid space.

Despite decades of investigation and discussion of the mechanisms involved in the pathophysiology of arachnoid cysts, fundamental issues concerning these entities remain poorly defined and controversial. Cine-mode magnetic resonance imaging (MRI) has shown two patterns of cerebrospinal fluid (CSF) flow within the cavity in patients harbouring arachnoid cysts. Some cysts present a harmonic flow with a patent flow entry zone. All these patients had intermittent, non-progressive and non-localizing symptoms requiring no surgery according to our criteria. The second pattern of CSF flow is more chaotic and is characterized by the presence of swirls throughout the entire cardiac cycle. This pattern is associated with a more disabling clinical picture. Some of these patients required surgical treatment. During surgery, an endoscope was used for inspection purposes revealing, above all, that arachnoid cysts always and variably communicate with the subarachnoid space. The CSF enters the cyst either through a patent flow entry zone or through minute perforations in areas more loosely packed of the arachnoid network that behave as a flexible mesh able to modify the area of flowing CSF. The slipstreams of CSF within arachnoid cysts may not be channelled properly leading to possible damage of the surrounding brain parenchyma.

Adolescent↗
PubMed2000

High-resolution analysis of chromosome arm 1p alterations in meningioma.

Loss of heterozygosity (LOH) for loci on chromosome arm 1p is a relatively common event in human meningioma, and this anomaly has been proposed to be associated with the development of grade II or grade III forms (atypical and anaplastic meningiomas). Nevertheless, the limited data available do not allow the establishment of the frequency and the extent of the affected 1p regions. To determine the status of chromosome 1p in meningiomas, we have performed a comprehensive analysis of LOH on 1p in 100 meningiomas using a high density of 1p-marker loci. Allelic loss was found in 35% of tumors, most corresponding to nontypical meningiomas that also displayed losses for loci on chromosome 22. Although some tumors displayed complex rearrangements leading to distinct 1p deletions, the patterns of loss indicated two main target regions: 1p36 and 1p34-p32, which represent the most frequently involved regions, whereas 1p22 and 1p21.1-1p13 regions appeared deleted in some tumors. These results suggest that there may be several putative tumor suppressor genes on 1p, the inactivation of which may be important in the pathogenesis of meningiomas, as well as in other tumor types.

Brain Neoplasms↗
PubMed2000

hRAD54 gene and 1p high-resolution deletion-mapping analyses in oligodendrogliomas.

The hRAD54 protein belongs to a superfamily of DNA helicases, and mutations in genes with DNA helicase function have been found to be responsible for cancer-prone syndromes (xeroderma pigmentosum, Bloom syndrome, Werner syndrome). hRAD54 thus could be a candidate modifier gene in tumors characterized by allelic imbalance at 1p32, the chromosome region in which this gene is located. Using a panel of 38 1p and five 1q markers, we therefore performed deletion-mapping analysis on a series of 35 oligodendrogliomas, which were also studied for mutations in the hRAD54 gene. Deletions of the short arm of chromosome 1 were evidenced in 26 tumors, mostly involving 1p36-1p13; all thus displayed loss of the 1p32 region. We used PCR/SSCP to examine all 18 exons of the hRAD54 gene for mutations in 25 tumors, but the mobility shifts detected corresponded to previously identified polymorphic changes: T-to-C transition at nucleotide 2865 (with no amino acid change) and at nucleotide 3008, at the 3' untranslated region. We conclude that hRAD54 gene alterations are not required for malignant transformation of oligodendrogliomas.

Chromosome Deletion↗
PubMed2000

Camino intracranial pressure monitor: prospective study of accuracy and complications.

OBJECTIVES: The fibreoptic device is a type of intracranial pressure monitor which seems to offer certain advantages over conventional monitoring systems. This study was undertaken to analyse the accuracy, drift characteristics, and complications of the Camino fibreoptic device. METHODS: One hundred and eight Camino intracranial pressure (ICP) devices, in their three modalities, were implanted during 1997. The most frequent indication for monitoring was severe head injury due to road traffic accidents. RESULTS: Sixty eight probe tips were cultured; 13.2% of the cases had a positive culture without clinical signs of infection, and 2.9% had a positive culture with clinical signs of ventriculitis. The most common isolated pathogen was Staphylococcus epidermidis. All patients were under cephalosporin prophylaxis during monitoring. Haemorrhage rate in patients without coagulation disorders was 2.1% and 15.3% in patients with coagulation abnormalities. Drift characteristics were studied in 56 cases; there was no drifting from the values expected according to the manufacturer's specifications in 34 probes. There was no relation between direction of the drift and duration of placement, nor between drift and time. CONCLUSIONS: Although the complication and drift rates were similar to those reported elsewhere, there was no correlation between the direction of the drift and long term monitoring despite the fact that some published papers refer to overestimation of values with time with this type of device.

Adolescent↗
PubMed1999

NF2 gene mutations and allelic status of 1p, 14q and 22q in sporadic meningiomas.

Formation of meningiomas and their progression to malignancy may be a multi-step process, implying accumulation of genetic mutations at specific loci. To determine the relationship between early NF2 gene inactivation and the molecular mechanisms that may contribute to meningioma tumor progression, we have performed deletion mapping analysis at chromosomes 1, 14 and 22 in a series of 81 sporadic meningiomas (54 grade I (typical), 25 grade II (atypical) and two grade III (anaplastic)), which were also studied for NF2 gene mutations. Single-strand conformational polymorphism analysis was used to identify 11 mutations in five of the eight exons of the NF2 gene studied. All 11 tumors displayed loss of heterozygosity (LOH) for chromosome 22 markers; this anomaly was also detected in 33 additional tumors. Twenty-nine and 23 cases were characterized by LOH at 1p and 14q, respectively, mostly corresponding to aggressive tumors that also generally displayed LOH 22. All three alterations were detected in association in seven grade II and two grade III meningiomas, corroborating the hypothesis that the formation of aggressive meningiomas follows a multi-step tumor progression model.

Adolescent↗
PubMed1997

A dedicated prosthesis for open thoracostomy.

Due to our dissatisfaction with the mutilation caused by the skin-lined open thoracostomy, we have developed a dedicated prosthesis that is expected to avoid or to substitute for the classic operation. The prosthesis is a corrugated silicone tube with an oval flange at one end (to fix it internally) and a mobile ring on the other (to fix it externally). It is inserted at the bottom of the empyematic cavity after 3 cm of a rib is removed. We have used it in 20 patients whose empyema was secondary to pneumonia (12) or complications of pneumonectomy (4), lobectomy (2), decortication (1), or pleuroscopy (1). Six of those patients have already been cured and their prosthesis removed after 54 to 305 days. In 1 with a persistent postpneumonectomy bronchopleural fistula the device was removed after 299 days and the patient was submitted to a limited thoracoplasty. Six other patients still have unresolved cavities and have been using the prosthesis for 63 to 302 days. Seven patients died of their underlying disease (bilateral pneumonia, 2; acquired immunodeficiency syndrome, 2; mesothelioma, 1; heart failure and pulmonary embolism, 1; unknown, 1) after using the prosthesis for 11 to 160 days. In those patients from whom the prosthesis already has been removed, the scar looks like those commonly seen after removal of an ordinary chest tube. Based on these early favorable results we feel most encouraged to persist in this research. Nevertheless, we are aware that a larger number of patients and a longer follow-up will be necessary before we may make definitive recommendations.

Empyema, Pleural↗
PubMed1995

Allelic loss at 1p and 19q frequently occurs in association and may represent early oncogenic events in oligodendroglial tumors.

The molecular mechanisms underlying the genesis and progression of oligodendroglial tumors are poorly understood, since only restricted information on loss of heterozygosity from isolated cases is available. The commonest alterations appear to involve deletion of 1p and 19q, while loss of heterozygosity for 9p, chromosome 10 or epidermal growth factor receptor gene amplification have been described in single tumors. We have applied restriction fragment length polymorphism analysis to 14 loci covering chromosome 1 and 7 loci on chromosome 19 in a series of 25 tumors with an oligodendroglial component to determine precisely the participation of these suppressor genes in the genesis of tumors. Twenty-two and 19 of the 25 samples displayed LOH at 1p and 19q, respectively, and both anomalies were detected in association in 17 samples, including low- and high-grade oligodendrogliomas as well as mixed oligo-astrocytomas. Our findings suggest that inactivation of tumor suppressor genes located on 1p and 19q represent cooperative alterations occurring at early stages of oncogenic transformation of oligodendroglial neoplasms.

Chromosome Deletion↗
PubMed1995

Allelic status of chromosome 1 in neoplasms of the nervous system.

By using five highly polymorphic markers, the allelic status of chromosome 1 was established in a series of 236 tumors of the nervous system, including all major histologic subtypes: gliomas, meningiomas, neurinomas, neuroblastomas, medulloblastomas, etc. Loss of alleles at 1p was observed at significant frequencies in neuroblastomas (26% of cases), meningiomas (32%), and malignant gliomas (37%) (primarily oligodendrogliomas [94%]). This anomaly was also detected in two of 23 neurinomas, two of three neurofibrosarcomas, one primary lymphoma, and two metastatic tumors of the brain. The analysis of tumors displaying partial 1p deletions suggests the existence of two distinct regions, 1p36 and 1p35-p32, in which loci nonrandomly involved in the development of neurogenic neoplasms might be located.

Alleles↗
PubMed1994

Molecular analysis of chromosome 1 abnormalities in human gliomas reveals frequent loss of 1p in oligodendroglial tumors.

Alterations of the short arm of chromosome 1 are recurrently found in cytogenetic analysis of malignant gliomas, and deletions of 1p36-p32 region characterize at least the higher-grade tumors, glioblastoma multiforme. Molecular analysis of tumor-derived and normal genomic DNA from 57 cases of gliomas, using a panel of chromosome 1-specific DNA probes showed LOH in 16 tumors. Allelic losses on 1p were primarily restricted to glioblastoma multiforme (2/11) and to tumors with a major oligodendroglial component: grade II oligodendrogliomas (6/6), grade III anaplastic oligodendrogliomas (5/6) and grade II-III mixed oligo-astrocytomas (2/3). Losses for 1q markers were detected in only 1 tumor (glioblastoma multiforme). Our data suggest that anomalies of 1p primarily characterize oligodendrogliomas, whereas they are rare events in astrocytic tumors and indicate that a tumor-suppressor gene on 1p36-p32 is involved in the development of brain tumors with oligodendroglial differentiation.

Alleles↗
PubMed1994

Molecular and cytogenetic analysis of chromosome 9 deletions in 75 malignant gliomas.

A deletion mapping analysis of chromosome 9 has been performed on a series of 75 samples derived from malignant gliomas. A total of 27 tumors displayed different deletions for the loci studied (D9S1, NRASLI, D9S18, IFNA, and IFNBI). In most instances, losses involving the markers located on the short arm of chromosome 9 were observed, and only two samples were characterized by losses of the short and long arms. Either partial or complete homozygous deletions of IFN genes were observed in 15 cases, and 12 other samples showed hemizygous deletions for these genes. The results show that the 9p abnormalities are not exclusive to high-grade astrocytic tumors, as some low-grade samples (two astrocytoma grade II and six oligodendrogliomas) displayed this anomaly which, in a few instances, was the sole abnormality detected.

Chromosome Deletion↗
PubMed1994

Allelic loss at 1p is associated with tumor progression of meningiomas.

Next to chromosome 22 anomalies, deletions of the short arm of chromosome 1 have previously been described as the most frequent alteration detected by cytogenetic analysis of meningiomas. To determine the incidence of these deletions, we have analyzed a series of 50 meningiomas for the loss of alleles at four chromosome 1 loci. Thirteen samples displayed LOH for the markers studied; in one instance, the results were compatible with loss of the entire chromosome 1, whereas in the other 12 samples deletions of the short arm were observed. Eleven of the meningiomas had previously been shown to have loss of alleles on chromosome 22, and 12 of them were characterized by increased tumor aggressiveness. These findings suggest that deletion of Ip (or the alteration of a locus located there) might represent a secondary, but nonrandom alteration in meningiomas, perhaps contributing to meningioma tumor progression.

Alleles↗
PubMed1994

Ascertainment of chromosome 7 gains in malignant gliomas by cytogenetic and RFLP analyses.

The incidence of gains involving chromosome 7 was determined independently using cytogenetic and molecular genetic analyses in a series of 57 malignant gliomas. Coincidental results were observed in the group of tumors in which trisomy 7 was identified on the same cells that also displayed other clonal abnormalities (i.e., losses of chromosome 10, and structural rearrangements of 1p, 9p, etc., and the presence of dmin). On the other hand, molecular detection of gain of material from this chromosome was obtained in only one of nine cases in which trisomy 7 had been identified as a solitary anomaly at the cytogenetic level. Thus, although trisomy 7 has been identified as a clonal abnormality in about 60% of gliomas analyzed cytogenetically so far, our findings suggest that the anomaly may be representative of tumor parenchyma in half of them, while in the remaining cases (mainly those in which trisomy 7 is observed at the cytogenetic level as the sole chromosomal deviation) our data agree with those suggesting that the anomaly is the result of an in vitro non-disjunction, or represent in vivo mosaicism of the non-tumoral cells.

Blotting, Southern↗