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O Delattre

Publications and source records attributed to O Delattre.

At least 145 records · Page 8Linked to original sources
PubMed1991

Mapping of human chromosome 22 with a panel of somatic cell hybrids.

The adenylosuccinate lyase (ADSL) which is essential for generating adenylate, maps to the long arm of chromosome 22. By using a Chinese hamster ovary cell line deficient in ADSL activity, we have constructed a set of 17 somatic cell hybrids containing defined regions of human chromosome 22. This panel was extended with six additional hybrids, obtained in other laboratories using various methods of selection. Southern analysis of the hybrids with 38 chromosome 22 probes defined 14 different subregions which could be linearly organized on the long arm of chromosome 22. The order of the probes thus deduced is fully compatible with their previous localization and with the genetic map. The ADSL gene was further sublocalized between the MB and D22S22. This panel, which enables the rapid assignment of chromosome 22 single copy probes to small subregions, will be an important tool in the construction of a detailed physical map of this part of the genome.

Adenylosuccinate Lyase↗
PubMed1991

Parental origin of chromosome 22 loss in sporadic and NF2 neuromas.

It has recently been proposed that the maternally derived chromosome might be preferentially lost in nonfamilial cases of embryonal or early onset malignant tumors. This observation pointed to a potential role of the parental imprinting of the genome during gametogenesis which would be at least partly maintained in the somatic cells. Neuromas are benign tumors that develop from Schwann cells. They occur either sporadically or in individuals that have a genetic predisposition due to neurofibromatosis type 2 (NF2) and usually are multiple. Regardless of the context of occurrence, in approximately 40% of the investigated cases a loss of a chromosome 22 has been documented either by karyotype analysis or by monitoring somatic loss of heterozygosity. We have now examined the parental origin of the chromosome 22 lost in 19 cases of neuromas of patients with unaffected parents among which 11 were non-NF2 patients (sporadic and unique neuroma) and 8 were NF2 patients (bilateral acoustic or multiple neuromas). In both sets of tumors, the lost chromosome 22 can be of either parental origin. A close to threefold preference for the loss of the maternally derived chromosome was observed and should be either confirmed or disproved by studying a larger number of patients.

Adult↗
PubMed1990

Assessment of chromosome 22 anomalies in neurinomas by combined karyotype and RFLP analyses.

We report the cytogenetic study of 28 neurinomas; sixteen of them were also analysed using 11 polymorphic DNA markers for the loss of alleles of chromosome 22. Partial or total loss of chromosome 22 was found in nine cases. The results of the two approaches appear homogeneous, however, three tumors that yielded only cells with normal karyotypes demonstrated loss of constitutional heterozygosities. One of the tumors, which displayed an isodicentric or isopseudodicentric 22, was obtained in a patient with von Recklinghausen neurofibromatosis. It appears that loss of chromosome 22 is a characteristic of neurinomas whatever their context of occurrence.

Alleles↗
PubMed1990

Cytogenetic and molecular approaches of polyploidization in colorectal adenocarcinomas.

We present the cytogenetic analysis of 23 cases of polyploid colorectal adenocarcinomas. We took advantage of the high intratumoral heterogeneity of the karyotypes to identify clones, subclones, and cell-to-cell variations. This allowed us to reconstruct the chromosomal evolution of each tumor and to propose a schema of the chromosomal changes in relation to the endoreduplication process. All but one case were characterized by a relative deficiency of chromosomes 17p and 18. Other deficiencies affecting the late-replicating X, and to a lesser degree, 1p, 5q, 14, 15, 8p, 10, 21, and 4, and excesses affecting the early-replicating X, 8q, 13, 16, 17q, and 11 were frequently associated. This pattern of imbalances is very similar to that of the monosomic type previously described in near-diploid tumors. The pattern of the 23rd tumor corresponded to those of the trisomic type tumors. These data largely confirm the existence of two distinct processes of chromosomal evolution in colorectal adenocarcinomas, with a strong tendency to undergo endoreduplication for the monosomic type near-diploid tumors. To correlate cytogenetic and molecular data, allelic losses analyses were investigated for probes of chromosomes 17p and 18. In all 12 informative tumors, a loss of heterozygosity for probes of the short arm of chromosome 17 indicated the occurrence of a rearrangement of chromosome 17 before the endoreduplication. The same was true for allelic losses for probes of chromosome 18 found in 11 of 12 informative tumors. The correlation between cytogenetic and molecular data is thus excellent and indicates that losses of 17p and 18 are early events in the tumor process.

Adenocarcinoma↗
PubMed1990

Mapping of human chromosome 22 by in situ hybridization.

The second smallest chromosome of the human karyotype, i.e., chromosome 22, is involved in many congenital or acquired structural aberrations. This variety can be taken advantage of to determine the exact linear order, from centromere to telomere, of cloned probes and chromosomal breakpoints. Eleven probes were localized with respect to breakpoints of 11 der(22) of independent cell lines using in situ hybridization on metaphasic spreads. The deduced order of the tested probes and that of the breakpoints are in complete agreement with the published genetic map and the karyotypic analysis, respectively. This approach enables a correlation of the genetic map with the chromosomal banding.

Cell Line↗
PubMed1990

The neuroepithelioma breakpoint on chromosome 22 is proximal to the meningioma locus.

The recurrent translocation breakpoint on chromosome 22 of neuroepithelioma has been localized between two probes, D22S1 and D22S15, by both in situ hybridization and somatic cell hybrids. These two probes have further been shown to be genetically linked at theta = 0.0 and a lod score of 5.3. The two probes were unaffected by a partial deletion of the chromosome 22 long arm of a meningioma, showing that the meningioma locus is distal to that of the neuroepithelioma.

Blotting, Southern↗
PubMed1990

Simultaneous localization of cosmids and chromosome R-banding by fluorescence microscopy: application to regional mapping of human chromosome 11.

A technique for nonradioactive in situ hybridization on human metaphase chromosomes has been developed to localize human cosmid clones. The simple procedure using two fluorescent dyes (fluorescein and propidium iodide) allows the simultaneous identification of chromosomal R-bands and hybridization signal in a single screening of the slides. This technique has been used for rapid correlation of the genetic and physical map of chromosome 11q13-qter in the region of genes responsible for ataxia-telangiectasia and tuberous sclerosis.

Cell Line↗
PubMed1990

[A joint study of mutation of the Ki-ras oncogene and overexpression of the Tp53 oncogene in colorectal cancer].

Twenty-five colorectal tumors (rectum 6, left colon 13, right colon 6) were studied with respect to the overexpression of p53 and the activation by point mutation of the Ki-ras oncogene. Single point mutations on codon 12 and codon 13 were analyzed after PCR amplivication, dotblotting and sequential hybridization with 12 different oligonucleotides. The intranuclear concentration of p53 protein was measured by flow cytometry after immunofluorescence staining with monoclonal antibody Pab 421. Twelve tumors were found to significantly overexpress p53 and 6 of them had an activated Ki-ras (5 on codon 12, 1 on codon 13). Of 13 tumors which failed to demonstrate over expression of p53, 8 had an activated Ki-ras (5 on codon 12, 3 on codon 13). In our series, p53 overexpression and ki-ras activation appeared to be independent.

Adenocarcinoma↗
PubMed1989

Preservation of chromosome and DNA characteristics of human colorectal adenocarcinomas after passage in nude mice.

Twenty-seven human colorectal adenocarcinomas were implanted s.c. into nude mice. A comparative study of chromosomes and DNA between fresh tumor (FT) and xenografted tumor cells (XT) could be performed in 9 cases. Losses or deletions were consistently found in FTs as well as in XTs, particularly on chromosomes 17 and/or 18. This was correlated with loss of heterozygosity for these chromosomes. Comparison between corresponding FT and XT karyotypes showed great similarities. However, the tendency toward polyploidization, which exists in FTs, appeared to be more pronounced in XTs. Passage in nude mice makes it possible to repeat cytogenetic analyses in order to obtained interpretable metaphases. Xenografting not only increases the number of tumorigenic cells, but also eliminates human normal stromal or blood cells and gives unambiguous data on allelic loss.

Adenocarcinoma↗
PubMed1989

Multiple genetic alterations in distal and proximal colorectal cancer.

Multiple genetic alterations were investigated in colorectal cancer, including changes in DNA content, mutations in ras oncogenes, and deletions involving chromosomes 5, 17, and 18. A non-random association of deletions and mitotic abnormalities by site was seen, with both types of alterations occurring significantly more frequently in distal tumours. In contrast, the frequency of c-Ki-ras mutations did not differ between proximal and distal cancers. In addition, deletions were significantly associated with each other and with change in DNA content. The data provide strong support for the hypothesis that proximal and distal colon carcinoma might differ in the genetic mechanisms in their initiation and/or progression.

Adenocarcinoma↗
PubMed1988

Loss of alleles on chromosome 18 and on the short arm of chromosome 17 in polyploid colorectal carcinomas.

The zygosity of 19 colorectal carcinomas (either near-diploid or polyploid) from patients known to be heterozygous for RFLPs located on chromosome 18 or on the short arm of chromosome 17 has been examined. In most cases, at least one allele was significantly under-represented. The reason for the absence of complete loss of heterozygosity was investigated for 5 polyploid tumors. It was shown that the diploid component which, in these tumors, is essentially composed of non-neoplastic cells, remains heterozygous as the polyploid component invariably loses heterozygosity. The results strongly suggest that many colorectal carcinomas originate from a single cell which had lost at least part of either chromosome 18 or of one short arm of chromosome 17, or both.

Adult↗
PubMed1988

Recurrent t(11;22) breakpoint mapping by chromosome flow sorting and spot-blot hybridization.

The breakpoint of the recurrent t(11;22) translocation, one of the most frequent chromosome anomalies encountered in human population, always involves bands 11q23.2 and 22q11.2. The involvement of the C lambda locus of the immunoglobulin lambda gene cluster on chromosome 22 has been suggested: however, in situ hybridization experiments have yielded conflicting results. In order to solve these discrepancies by another approach, we have used bivariate flow sorting to separate the chromosomes of interest and to map the specific breakpoints by direct spot-blot hybridization with the gene-specific radiolabelled DNA probes, Alu, V lambda, ets. The results showed unambiguously that in the t(11;22) patient analysed, a set of C lambda and V lambda genes was translocated to the der(11) chromosome. Since V lambda genes are situated proximally to C lambda genes, we demonstrate that, in the case studied here, the chromosome 22 breakpoint is not located within or even immediately close to the C lambda region.

Cell Line↗
PubMed1988

Studies on the human chromosome 3 centromere with a newly cloned alphoid DNA probe.

Starting from a chromosome-specific DNA library, we have isolated a human chromosome-specific satellite DNA sequence. This sequence of 635 base pairs (bp) consists of 3.7 alpha DNA monomers of 170-171 bp. Under high stringency it hybridizes to the centromere of chromosome 3 in a region composed of 2,750 bp tandem repeats characterized by the regular spacing of Hind III and TaqI restriction enzyme recognition sites. It has diverged and undergone amplification after the human speciation. The amplification allows an easy monitoring of the chromosome 3 centromere by in situ hybridization with a nonradioactive probe.

Animals↗