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Biomedical subjects

J Vaquero

Publications and source records attributed to J Vaquero.

At least 19 recordsLinked to original sources
PubMed1998

Immune-cell system provides the development of extraneural tumors in the ethyl-nitrosourea model of neurocarcinogenesis.

Immunological suppression of the immune-cell system by means of cyclosporin-A was performed at a stage corresponding to microtumor development in the ethyl-nitrosourea (ENU) model of neurocarcinogenesis. The results that we have obtained suggest that this immunological manipulation is related to the appearance of extraneural undifferentiated tumors, suggesting that the immune-cell system is effective in immunocompetent rodents for providing extraneural ENU carcinogenesis.

Animals↗
PubMed1998

Primary intraparenchymatous spinal cord melanoma.

A case of primary melanoma arising from the spinal cord parenchyma at the Th 10-11 level, in a 50-year old female, is presented. In this patient, Magnetic Resonance Imaging (MRI) showed an intraparenchymatous lesion, with rounded borders, and an associated intramedullary cyst. On the basis of these findings and the long duration of symptoms, an erroneous preoperative diagnosis of intramedullary ependymoma was made.

Diagnostic Errors↗
PubMed1998

Allelic status of 1p, 14q, and 22q and NF2 gene mutations in sporadic schwannomas.

Schwannomas are common benign tumours of schwann cell origin, frequently found in patients with neurofibromatosis type 2 (NF2). Inactivation of the NF2 tumour suppressor gene appears to be a molecular event responsible for the development of up to 60% of cases, but no data are available on other superimposed secondary or alternative molecular abnormalities in those schwannomas lacking NF2 gene inactivation. We analysed 23 sporadic schwannomas for mutations in the NF2 gene and for the allelic status at 1p, 14q and 22q, as alterations of these genomic regions appear to be related to tumour progression in meningiomas, another NF2-associated neoplasm. Nine samples displayed allelic losses for markers on chromosome 22, and deletions at 1p were detected in two. No case showed losses for 14q. Three tumours displayed NF2 gene mutations, at exons 2, 7 and 12. Our results confirm that inactivation of the NF2 gene is a primary event in schwannoma development, and provide data suggesting that allelic loss at 1p may contribute to the pathogenesis of a small subgroup of this histological tumour type.

Alleles↗
PubMed1998

Six novel mutations in the NF2 tumor suppressor gene.

Six novel mutations were identified in the NF2 tumor suppressor gene in a panel of meningiomas and neurinomas. Screening was performed using a combination of single-strand conformation polymorphism and heteroduplex analyses on polymerase chain reaction-amplified DNA from tumors and matched peripheral blood lymphocytes. Mutations involved exons 2, 7, 11 and 12, and corresponded to three frameshift, one nonsense, one missense and one polymorphism.

Chromosome Aberrations↗
PubMed1997

Radiographic visualization of patellar tendon grafts for the reconstruction of the anterior cruciate ligament.

The new biodegradable interference screws offer very many advantages for anterior cruciate ligament replacement with patellar tendon. However, their radiolucency makes it impossible to identify the anchorage sites. We describe an imaging technique of the plasty and its anchorage sites by means of a radiopaque contrast that is commonly used in radiology (Iopamidol; Bracco, Milan, Italy). It is an easy technique that does not extend the time of surgery, it is harmless, and allows us to identify malpositioning or impingement of the plasty.

Anterior Cruciate Ligament↗
PubMed1996

Gangliosides modulate the growth rate and cell phenotype of a murine primitive neuro-ectodermal tumour.

Intratumoural administration of gangliosides (GSD) into a murine primitive neuro-ectodermal tumour, growing in the epicranial subcutaneous tissue of syngenic rats, results in a decrease in the tumour growth rate and causes a more differentiated phenotype of tumour cell, with immunohistochemical expression of neuronal markers. These findings suggest that the potential usefulness of intralesional administration of GSD for the control of tumours of primitive neuro-epithelial character could be considered.

Animals↗
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

Growth-inhibiting effect of intratumoral recombinant human tumor necrosis factor on an experimental model of primitive neuroectodermal tumor.

The effect of intratumoral administration of recombinant human tumor necrosis factor on an experimental model of primitive neuroectodermal neoplasia was studied. A clear inhibition of tumor growth was achieved by immunotherapy that consisted in intralesion injections of 100 micrograms of tumor necrosis factor daily, the first three days of each week, for a period of four weeks. At this time, tumor size was 2.21 +/- 0.66 cm2 (mean +/- standard deviation) in the treated group, versus 7.62 +/- 0.43 cm2 in the control group. These data support previous studies on the influence of tumor necrosis factor on the development of ethyl-nitrosourea-induced tumors, and suggest the potential usefulness of this cytokine in human primitive neuroectodermal neoplasms.

Animals↗
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

Influence of the postnatal administration of tumor necrosis factor plus interferon-alpha 2b on the development of ethyl-nitrosourea-induced brain tumors in rats.

Using the experimental model of brain tumors induced by ethyl-nitrosourea (ENU), interferon-alpha 2b and human recombinant tumor necrosis factor-alpha (TNF) have been administered to Wistar rats between 100 and 130 days of life (one injection each week, by intraperitoneal route, of 100 micrograms of TNF and 10(4) IU of interferon-alpha 2b, in a total volume of 1 ml per injection). The results obtained suggest, that at this time, this association achieves a reduction in the number of so-called 'malignant schwannomas', but it does not influence the time of appearance nor the number of so-called 'malignant schwannomas', but it does not influence the time of appearance nor the number of so-called 'oligodendroglioma-like tumors'. On the basis of previous observations about cytokine modulation of these ENU-induced neoplasms, a different course of time for obtaining a postnatal biomodulation of both type of tumors is suggested.

Aging↗
PubMed1994

Gangliosides modulate the development of ethyl-nitrosourea induced brain tumors in rats.

The possible effect of gangliosides as biological modifiers of the ethyl-nitrosourea (ENU) model of neurocarcinogenesis in rats is studied. Wistar rats that were exposed to ENU during fetal life, were treated with gangliosides at a postnatal age corresponding to a stage of pretumor or microtumor development. The results obtained suggest that postnatal administration of gangliosides can influence the development of ENU-induced brain tumors, delaying the appearance of symptomatic neoplasms and improving survival with respect to controls. This finding suggests the potential usefulness of gangliosides in the control of neuroectodermal tumors.

Animals↗
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

Neurocytoma of spinal cord.

We report a case of spinal cord neurocytoma in a 67-year-old man who had experienced a progressive numbness of the left foot during the previous 4 years. Magnetic resonance imaging showed a well-defined intramedullary tumor located at the T10-T11 level. The pathological examination revealed histological characteristics described in neurocytomas. The tumor cells showed a uniform small nucleus and clear or slightly eosinophilic cytoplasm with frequent perinuclear halos, resembling the picture of oligodendroglioma. Some tumor cells exhibited mature ganglion cell appearance. Electron microscopy showed cells with microtubules and dense-core vesicles in their cytoplasm and cytoplasmic process. Immunohistochemically, the majority of tumor cells expressed synaptophysin and neuron-specific enolase. We conclude that this tumor is an exceptional case of neurocytoma located in the spinal cord, and consider that the term neurocytoma can be applied to tumors with neuronal differentiation intermediate between neuroblastoma and ganglioneuroma, even if arising in CNS outside of the intracranial ventricular system.

Aged↗
PubMed1994

Medulloblastoma in adulthood: prognostic factors influencing survival and recurrence.

Thirty adult patients presenting with medulloblastoma between 1974 and 1991 were studied and treated at Puerta de Hierro Clinic. After diagnosis, all patients were treated by surgery followed by radiotherapy and eight of them received adjuvant chemotherapy. We have studied the influence of some factors such as age, sex, location of tumour in the cerebellum, amount of surgical resection and histological variants on survival and recurrence of the disease. Only the histological type has a statistically significant influence on survival and recurrence: we have found that patients presenting classic medulloblastoma have a long survival and a long relapse-free interval.

Adolescent↗
PubMed1994

Brainstem haematomas: early and late prognosis.

The purpose of the present retrospective study is to analyse 14 patients harbouring brainstem haematomas and to discuss the early and late prognosis. The patients were divided into two groups: group A (survivors), 8 patients with follow-up duration ranging between 8 months and 12 years; and group B (nonsurvivors), 6 patients. At the time of onset or hospital admission, the former were under 50 years of age and had no important clinical history. Their degree of consciousness was altered only slightly or moderately and their brainstem haemorrhages were focal or only slightly diffuse. Three patients in this group underwent surgical treatment. The members of group B, who died within days of their admission to the hospital, were over 60 years of age, had a number of clinical antecedents and severe alterations of consciousness, while 83% of them presented diffuse brainstem haemorrhages. None of the patients of this group were treated surgically. It was concluded that: 1) the indications for surgery for these lesions were progressive hydrocephalus, increase in the mass effect with progressive symptomatology and suspected "cryptic vascular malformation" with risk of later rebleeding or brain tumour; 2) surgical treatment was necessary to improve the symptomatology in 3 patients in group A, although there were no significant differences between surgically treated and nonsurgically treated patients in the same group with respect to prognosis; 3) age, clinical history, degree of alteration of consciousness and type of haemorrhage are the major factors affecting the early and late prognosis of brainstem haemorrhages.

Adult↗