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B Dutrillaux

Publications and source records attributed to B Dutrillaux.

At least 199 records · Page 11Linked to original sources
PubMed1992

New gene assignments to rabbit chromosomes; implications for chromosome evolution.

The genes for SOD1 and SOD2 (superoxide dismutases 1 and 2), RB1 (retinoblastoma), TYMS (thymidylate synthase), and TK1 (thymidine kinase) were mapped by in situ hybridization using biotinylated probes to rabbit chromosomes 6, 12, 8, 9, and 19, respectively. This confirms their proposed homoeologies with human chromosomes 21, 6, 13, 18, and 17, respectively, and provides additional information on the modification of these chromosomes during evolution.

Animals↗
PubMed1992

Chromosomal localization of the ovine beta-casein gene by non-isotopic in situ hybridization and R-banding.

The ovine beta-casein gene (CNS2) has been mapped to a specific chromosome band using nonradioactive in situ hybridization and simultaneous fluorescent R-banding. The probe pTZ-E4 was a fragment of the ovine beta-casein gene inserted in the plasmid pTZ18R and labeled with biotin-11-dUTP. It hybridized to band q32 of ovine chromosome 4. The discrepancy between this result and the previous localization of this gene on cattle chromosome 6 may be explained by the very great similarity of the banding patterns of ovine and bovine chromosomes 4 and 6.

Animals↗
PubMed1992

Chromosomal rearrangements and speciation of sportive lemurs (Lepilemur species).

Theoretical configurations of meiotic chromosomes of potential hybrids between the different Lepilemur species were examined, and the classification of this genus was reviewed in the light of this information. Among the chromosomal rearrangements that occurred during the chromosomal evolution of the sportive lemurs, only those which would generate a pronounced reproductive barrier were considered in relation to the geographic distribution of this genus. The analysis showed that the pattern of geographic distribution is compatible with the inferred chronological occurrence of these chromosomal rearrangements in the phylogenetic tree of the genus Lepilemur.

Animals↗
PubMed1992

Co-amplification of transcriptionally active epidermal growth factor receptor and ribosomal genes in the human hepatoma cell line Li7A.

A high level of expression of the functional product of the epidermal growth factor receptor (EGFR) gene was detected in the human hepatocarcinoma cell line Li7A and it was found to correlate with gene amplification. The karyotype was paratriploid, with 15 rearranged chromosomes, several of which contained abnormally banded regions (ABRs). The search for DNA sequences co-amplified with the EGFR gene, using the in-gel renaturation technique, allowed us to detect an amplified DNA band (La1) of about 30 kb. This DNA was used as a probe for in situ hybridization on chromosomes, to locate the amplified segment. In normal lymphocytes, the DNA of band La1 hybridized to chromosome regions in which repetitive DNAs are located, i.e. on juxtacentromeric regions, the site of alphoid and CCATT satellite DNA, and on the short arms of acrocentrics, the site of ribosomal RNA (RNR) genes. In Li7A cells, it hybridized to the same regions and, in addition, to several chromosome arms corresponding to ABRs. The same ABRs hybridized to EGFR and RNR probes, but neither Alu sequences nor various probes for other repetitive sequences were recognized. They also exhibited nucleolus organizer region staining characterizing functionally active (RNR) genes. It was concluded that transcriptionally active genes were co-amplified in the same ABRs, although they originated from different chromosomes, i.e. chromosome 7 for EGFR and acrocentrics for RNR genes.

Blotting, Northern↗
PubMed1992

Physical mapping of human loci homologous to the chicken nov proto-oncogene.

The human locus (novH) corresponding to the nov protooncogene overexpressed in avian nephroblastoma has been identified and mapped on chromosome 8q24.1. Another locus sharing homology with novH and corresponding to the connective tissue growth factor (CTGF) gene has also been mapped on chromosome 6q23.1. The chromosomal assignment of nov and CTGF proximal to c-myc and c-myb respectively is of interest because chromosomal abnormalities involving these regions have been associated with different human tumors including Wilms'.

Animals↗
PubMed1992

[Chromosome abnormalities and adenine metabolism in human glial tumors].

Most chromosome aberrations in gliomas are numerical, resulting in either gains or deficiencies of whole chromosomes. In tumors of low malignancy, the karyotype is frequently normal or exhibits a loss of sex chromosome and a gain of chromosome 7. These two anomalies may not be directly related to malignancy. In the highly malignant cases, the two most frequent aberrations are the gain of chromosome 7 and the loss of chromosome 10, other anomalies such as losses or deletions of chromosomes, 9, 22, 6, 13 and 14 being detected at various frequencies. Several of these chromosomes carry important genes of adenine metabolism: AK1 and AK3 (adenylate kinase) and MTAP (methylthioadenosine phosphorylase) for chromosome 9; ADK (adenosine kinase) and mitochondrial ATPase for chromosome 10; ADSL (adenylosuccinate lyase) for chromosome 22, NP (nucleoside phosphorylase) for chromosome 14. We performed the corresponding assays of enzyme activity on both fresh tumors and tumors grafted on nude mice, which showed that these enzymes had a relatively low activity although the tumors were proliferating. However, chromosome losses do not seem to directly cause the metabolic alterations by gene dosage effect. Interestingly, chromosome 10, frequently deficient, also carries genes of importance for glycolysis (hexokinase) and glutamate metabolism (glutamate dehydrogenase and glutamate oxaloacetate transaminase). The deficiency for these genes could be taken into account for a better type of chemotherapy by antimetabolics.

Adenine↗
PubMed1992

Chromosomal assignment of two human B-raf(Rmil) proto-oncogene loci: B-raf-1 encoding the p94Braf/Rmil and B-raf-2, a processed pseudogene.

The B-raf gene is the human homolog of the avian c-Rmil proto-oncogene encoding a 94-kDa serine/threonine kinase detected in avian cells. We have previously shown that this protein contains amino-terminal sequences not found in other proteins of the mil/raf gene family. These sequences are encoded by three exons in the avian genome. We report that these three exons are conserved in the human B-raf gene and that they encode an amino acid sequence similar to that of the avian c-Rmil gene, indicating that in both avian and mammalian species the product of the B-raf/c-Rmil gene is a 94-kDa protein. We also identified two human B-raf loci: B-raf-1, located on chromosome 7q34, which encodes the functional B-raf/Rmil gene product, and B-raf-2, an inactive processed pseudogene located on chromosome Xq13.

Amino Acid Sequence↗
PubMed1991

Adaptation to 5-fluorouracil of the heterogeneous human colon tumor cell line HT-29 results in the selection of cells committed to differentiation.

The HT-29 cell line contains a small proportion of differentiated polarized, enterocytic and mucus-secreting cell types (less than 95%) which can be selected under various pressure conditions, e.g., glucose deprivation or methotrexate. The purpose of the present work was to investigate whether this also applies to 5-fluorouracil (FUra). Stepwise adaptation of exponentially growing cells to 1, 5, 10 and 20 microM FUra results, after a phase of high mortality, in the emergence of adapted sub-populations with stable growth rates and curves, and IC50 6, 18, 37, and 110 times higher than in untreated cells respectively. FUra-adapted cells are all differentiated, according to 2 phenotypes: (I) polarized dome-forming cells which express carcinoembryonic antigen at their apical surface and (2) goblet cells which secrete a mucus of colonic immunoreactivity. These phenotypes are present in the parental population and are different from those selected e.g., by glucose deprivation or methotrexate. This differentiation pattern is maintained when the cells are subcultured in drug-free medium. Resistance to FUra is acquired through gene amplification as substantiated by a 4- to 6-fold increase of thymidylate synthase gene copies in cells stably adapted to the drug. Whether the same mechanism or others are responsible for the first steps of resistance to FUra remains to be elucidated. Altogether, these results support the hypothesis that some of the cells which are present in the parental line and are committed to differentiation possess advantages which allow them to immediately resist and secondarily adapt to FUra. Comparison of the differentiation characteristics of FUra-adapted cells with those from cells selected under other pressure conditions suggests that resistance and adaptation to either type of pressure may depend on the differentiated phenotype to which the cells are committed.

Blotting, Northern↗
PubMed1991

Detection of translocations of 10p by non-radioactive in situ hybridization of VIM gene in SV40-transformed human cell lines.

SV40-transformed human fibroblasts exhibit characteristic chromosome imbalances, fairly well correlated with the activity of enzymes encoded by genes located on chromosome segments either in deficiency or in excess. However, a major discrepancy existed for the expression of vimentin gene (VIM), which was high, even though the map location of the gene (10p) was missing in many cell lines. An in situ hybridization technique using a biotinylated probe for the human VIM was applied to detect eventual cryptic translocations, as chromosome 10p is difficult to identify. In two cell lines (WI 98 and HEL1 HBLT) in which a loss of copy number of 10p was assumed after karyotyping, a signal for VIM was detected in unidentified short arms of derivative chromosomes. This exemplifies that in situ hybridization is a powerful complement to classical cytogenetics to detect rearrangements in highly rearranged karyotypes from transformed or cancerous cells. These results also strengthen the interpretation of the correlation between karyotypic and metabolic imbalances in transformed cells.

Cell Line, Transformed↗
PubMed1991

Relationships between UMPK and PGD activities and deletions of chromosome 1p in colorectal cancers.

A deletion involving a large segment of the short arm of chromosome 1(1p-) occurs in about 50% of colorectal cancers. It was previously noticed that, in these tumors, many deletions affect genes encoding for enzymes of the de novo pathway of nucleotide synthesis. The gene for uridine monophosphate kinase (UMPK), mapped on 1p32, is generally involved in del(1p). The activity of the corresponding enzyme was measured and compared to that of 6-phosphogluconate dehydrogenase (PGD), encoded by a gene also mapped on chromosome 1p and frequently deleted, but involved in another metabolism. It was found that a clear relationship exists between activity and the number of chromosome 1p for PGD but not for UMPK, both on primary tumors (PTs) and on tumors grafted into nude mice (GTs). By comparison to corresponding normal mucosae, the activity of PGD was high in PTs and GTs, but this increase was reduced in case of del(1p). The activity of UMPK being increased in PTs but not in GTs, it is assumed that the increase in PTs is due to non-cancerous cells, which are missing in GTs. The fact that no gene dosage effect exists, although the tendency for del(1p) coexists with the relative decrease of UMPK activity in cancerous by comparison to non-cancerous cells, suggests that either mutation or disregulation of UMPK gene occurred early.

Adult↗
PubMed1991

Activity of thymidylate synthetase, thymidine kinase and galactokinase in primary and xenografted human colorectal cancers in relation to their chromosomal patterns.

The relationship between chromosome anomalies and metabolic modifications in human colorectal cancers grafted into nude mice was studied. Two distinct chromosomal patterns have been demonstrated i.e., monosomic type (MT) characterized by multiple chromosome losses or deletions always involving chromosome 18, and trisomic type (TT) characterized by progressive gains of chromosomes. Grafted tumors conserve original karyotypes observed on corresponding primary tumors. Most changes involve the loss of chromosomes carrying genes encoding for enzymes of the de novo pathways and the gain of chromosomes carrying genes encoding for enzymes of the salvage pathways of nucleotide synthesis. In MT tumors the long arm (q) of chromosome 17 is frequently duplicated in association with a deletion of the short arm, forming an isochromosome 17q. The activities of 3 enzymes, thymidylate synthetase (TS) mapped on chromosome 18, thymidine kinase (TK) and galactokinase (GalK), both mapped on chromosome 17q, were studied. TS is a de novo enzyme and TK and GalK are salvage enzymes. A clear correlation could be demonstrated between tumor types and enzyme activities: MT tumors had lower TS and higher TK and GalK activities than TT tumors. These differences were too large to result from a gene dosage effect only. These data suggest that serial studies on grafted colorectal cancers give a better representation of metabolic disturbances than studies on fresh tumor samples, usually contaminated by non-cancerous cells.

Adult↗
PubMed1991

Genes occupy a fixed and symmetrical position on sister chromatids.

A high-resolution fluorescence methodology for nonisotopic in situ hybridization was applied to determine the positions occupied by several single-copy genes, DNA sequences, and integrated viral genomes on sister chromatids. The lateral and longitudinal mapping of the probes was performed on prometaphase and metaphase chromosomes. A fixed lateral position, exterior or median in relation to the longitudinal axis of the chromatids, was observed for a given probe, with a symmetrical position of the double fluorescent spots. This position appears to be independent of chromosome condensation stage from prometaphase to metaphase. These observations suggest an opposite helical-handedness conformation of DNA on both chromatids with a mirror symmetry. They support the model of chromosome packaging recently proposed by Boy de la Tour and Laemmli. Moreover, our results indicate that the last stages of chromosome condensation occur by packing down the coils without further coiling.

Animals↗
PubMed1991

Cytogenetic study of Hapalemur aureus.

The karyotype of Hapalemur aureus was compared with those of other Hapalemur species, allowing us to determine the phylogenetic position of this species on the evolutionary tree of the Lemuridae.

Animals↗
PubMed1991

High recurrence of rearrangements involving chromosome 14 in an ataxia telangiectasia lymphoblastoid cell line and in its mutagen-treated derivatives.

The cytogenetic characterization of CH cell line obtained by Epstein-Barr-virus transformation of the lymphocytes of a patient affected by ataxia telangiectasia is reported. Control CH cells and 2 subcultures treated with the mutagens R7000 or NQO were developed in parallel and studied. A common chromosome anomaly, a der(14) t(11;14) (q13.2;q32), was found in all the studied karyotypes, indicating that it occurred either in vivo or early in vitro. In non-treated cultures, additional anomalies were present in 6 derived subclones. All R-7000 treated cells had the same karyotype corresponding to one of the subclones observed without prior treatment. All NQO-treated cells acquired 2 common anomalies, and could be differentiated into 2 subclones because of the addition of a t(7;14) or a t(11;14). Chromosome 14 was involved in various rearrangements after breakage in band q11.2 or q12 in 6/8 subclones. This was not correlated with tumorigenicity, which was clearly increased in mutagen-treated cells as tested by in vitro growth in semi-solid medium and in vivo by grafts into nude mice or growth on the chorio-allantoic membrane of chick embryos. The CH cell line and its derivatives appear to be a promising in vitro system, showing various stages progressing towards malignancy, and reproducing a number of chromosome anomalies spontaneously occurring in AT patients.

4-Nitroquinoline-1-oxide↗
PubMed1991

Identification of a break-prone structure in the 9q1 heterochromatic region.

The unusual behaviour of the 9q1 human chromosome region is studied in various conditions. In controls with normal chromosomes 9, del(9q1) is the most frequent spontaneously occurring deletion. This deletion is highly inducible by melphalan, an S phase-dependent alkylating agent. This may correspond to the uncovering of pre-existing DNA breaks in this region. In a 46,XX,9qh+ control, melphalan does not induce deletions any more efficiently than in donors with normal chromosomes 9. In a 46,XY,inv(9) (p11q1205) donor, all deletions of inv(9) affect the short, but not the long, arm. This indicates that the sensitive segment is not the whole heterochromatic region, but rather a limited structure. The high rate of rearrangements affecting this structure may be responsible for somatic crossing over, leading to loss of heterozygosity for 9q, and to the frequent occurrence of inv(9) in human populations.

Cells, Cultured↗
PubMed1991

Breast cancer genetic evolution: I. Data from cytogenetics and DNA content.

A general scheme of chromosome alterations occurring during tumor progression is proposed from the cytogenetic study of 113 breast carcinomas. For 76 of these tumors, chromosome numbers and rate of chromosome rearrangements were correlated with DNA content studied by flow cytometry. A series of 536 cases was used as control for flow cytometry. The following evolution can be proposed: 1. occurrence of unbalanced rearrangements decreasing chromosome number and DNA content; 2. correlatively to the rate of chromosome rearrangements, formation of endoreduplications leading to hyperploid sidelines; 3. persistence of the near diploid cells and decrease of chromosome number to about 35 and of DNA index to .85; 4. more frequently, elimination of the near diploid cells and complete passage to hyperploidy; 5. further losses of chromosomes in the hyperploid tumors, whose karyotypes can decrease to about 55 chromosomes and a DNA index of 1.35; 6. eventually, occurrence of a second endoreduplication, leading to an apparent near tetraploidy. The rate of rearranged chromosomes may reach 80% in both near diploid tumors with 35-40 and hyperploid tumors with 55-65 chromosomes which can be regarded as those with the highest degree of tumor progression. It is shown that the increase of chromosome number and DNA index above diploidy is very limited, and that all tumors with more than 50 chromosomes and 1.35 DNA content passed through endoreduplication. This results in many possible losses of heterozygosity in these cases.

Adenocarcinoma↗