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F Apiou

Publications and source records attributed to F Apiou.

49 records · Page 3Linked to original sources
PubMed1993

Chromosome anomalies in mammary carcinoma from transgenic WAPRAS mice: compression with human data.

Transgenic WAPRAS mice, obtained by infection of the construct WAP promoter murine gene and the HRAS human protooncogene, develop mammary adenocarcinoma within 1-3 months after pregnancy. A cytogenetic analysis was performed on 17 tumors from 10 mice. Almost all detected anomalies were chromosome gains. The resulting trisomies affected recurrently chromosomes 1, 15, 19, 17, 7, and 12, in decreasing order of involvement. Although in situ hybridization showed that the transgene was integrated in chromosome 1, the duplication of this chromosome did not depend on the presence or absence of the transgene. Comparison with human data indicates that the 3 most frequently duplicated chromosomes in WAPRAS mice correspond to the human chromosome segments most frequently duplicated or amplified in breast cancer, i.e., 1q, 8q, and 11q13. None of the chromosome segments often deleted in human tumors were found to be duplicated in the mouse tumors.

Adenocarcinoma↗
PubMed1993

Identification of a human guanine nucleotide-releasing factor (H-GRF55) specific for Ras proteins.

A critical step in the activation of cellular Ras is the release of bound GDP. Oligonucleotide primers derived from a mouse cDNA sequence homologous to the Saccharomyces cerevisiae CDC25 gene product were used to screen a human brain cDNA library. The cloning led to the isolation of a 2.8-kb cDNA predicted to encode a protein of 488 amino acids. This protein was produced in Escherichia coli as a glutathione S-transferase fusion protein and functioned in vitro as a specific guanine nucleotide-releasing factor. Polyclonal antibodies raised against the last 281 amino acids of the protein allowed a protein in the molecular weight range of 55 kDa to be identified in human cortex homogenates. Analysis by Northern blotting led to the identification of a 5.5-kb mRNA in brain poly(A)+ RNA. The functionality of the encoded protein was evaluated after expression in different cells: (i) in Saccharomyces cerevisiae the effects of the cdc25.5 and RAS2 Ala-22 mutations were reversed; (ii) in chinese hamster ovary cells, a RAS-responsive element was transactivated as demonstrated by the expression of a CAT reporter gene under the control of the polyomavirus enhancer. Finally, in situ hybridization on of human chromosomes revealed a localization on band 15q2.4.

Amino Acid Sequence↗
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

Cytogenetic and molecular analysis of a de novo tandem duplication of chromosome 21.

We have characterised by cytogenetic and molecular analysis a de novo tandem duplication of chromosome 21. High resolution chromosome examination of lymphocytes revealed the following karyotype in 90% of the cells: 46,XY,dir dup (21)(pter----q22.300::q11.205----qter). Of these cells, 10% showed a normal karyotype. Gene dosage of chromosome 21 sequences by a slot blot method indicated that the duplication extends from D21S16 to D21S55. In situ hybridization with probes close to the borders of the duplicated segment confirmed the gene dosage data and gave results consistent with a true tandem duplication of chromosome 21. Pulsed field gel electrophoresis of the patient's DNA showed an abnormal restriction band common to D21S55 and D21S16, confirming that the junction point between the two homologous parts of the tandem chromosome brings these two sequences into proximity. Restriction fragment length polymorphism analysis indicated that the abnormal chromosome was maternal in origin and that the rearrangement of chromosome 21 could not have occurred at a post-zygotic stage of development but resulted from a recombination event during maternal gametogenesis. The possible mechanisms of formation of the abnormal chromosome are discussed, as is the presence of cells with normal chromosomes 21, in the patient.

Alleles↗
PubMed1991

The use of synthetic tandem repeats to isolate new VNTR loci: cloning of a human hypermutable sequence.

Synthetic tandem repeats (STRs) of oligonucleotides have previously been shown to detect polymorphic loci in the human genome. Here, we report results from the use of three such probes to screen a human cosmid library. Nine of the 45 positive clones that were analyzed appear to contain highly polymorphic minisatellite or VNTR loci. The degree of enrichment for minisatellite sequences varied with the choice of STR: one provided a 15- to 20-fold enrichment (4 polymorphic loci among 10 clones), whereas 2 others gave a 3- to 5-fold enrichment (5 polymorphic probes in a total of 35 clones) compared to random screening. The 9 VNTR markers have been localized by linkage analysis in the CEPH panel and/or by in situ hybridization. Eight probes identify new loci, one of which maps to an interstitial region. One of the VNTR loci (identified by probe CEB1) was found to be hypermutable, with 52 mutation events identified among 310 children characterized in 40 CEPH families. The parental origin of the mutation could be identified in all instances, and only one mutation was found to be of maternal origin. The mutation rate in males was estimated to be approximately 15%. Segregation analysis of flanking markers suggests that mutations are not associated with crossing over. As the only previously described hypermutable minisatellite loci in humans have equal rates of male and female mutations, these observations establish that a second type of hypermutable minisatellite exists in the human genome. In neither case does the generation of new alleles appear to be associated with unequal crossing over.

Base Sequence↗
PubMed1990

Chromosomal reallocation of the chicken c-myb locus and organization of 3'-proximal coding exons.

In the course of our studies concerning the tissue-specific expression of the c-myb proto-oncogene, we have established the nucleotide sequence of the chicken c-myb 3'-proximal coding exons. In situ hybridization performed with different genomic DNA probes corresponding to nearly all the c-myb gene allowed us to localize the corresponding locus on the large acrocentric chromosome 3 in chicken. Our sequencing data also indicate that the 3'-proximal noncoding sequences represented in c-myb mRNA species are derived from non-contiguous exons.

Animals↗
PubMed1978

Dose-effect studies on estrogen induced mammary cancers in mice.

Castrated male (C3H X RIII) F1 mice were treated with graded doses of estradiol-17-beta and estrone in a life-span experiment. Estradiol-17-beta incorporated into paraffin pellets was implanted under the skin for continuous resorption. These pellets contained 1 microgram, 2.5 microgram, 5 microgram, 10 microgram or 100 microgram of hormone. Estron was given orally, mixed with the food at 3 daily dosages: 0.06 microgram, 0.6 microgram and 6 microgram. Although the smallest dosages of both hormones induced vaginal estrus in castrated females, they did not produce mammary tumors. The mammary tumor incidence reached progressively almost 100% in response to the increase of the hormonal dosages. The absence of effect of low doses of estrogen in mice is compared with the absence of an excess of breast cancers among women using oral contraceptives.

Animals↗
PubMed1976

[The cancerogenic activity of gamma-butyrolactone in mice].

Gamma-butyrolactone has been tested for its carcinogenic activity in pure strain XVII/G and C3H Mice. No tumours were observed in mice which received the compound in injections at birth, after skin painting, gavage, or mixed with their food.

4-Butyrolactone↗