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C Jeanpierre

Publications and source records attributed to C Jeanpierre.

25 records · Page 2Linked to original sources
PubMed1991

[Antioncogenes: models for tumors in children].

The chromosomal assignment of genes responsible for malformation syndromes associated with increased susceptibility to malignancy could be determined owing to specific constitutional chromosomal abnormalities or to family studies. For certain types of tumors, somatic chromosomal rearrangements (loss of alleles) occur at the same locus indicating the presence of a recessive suppressor gene or an antioncogène. For other types of tumors chromosomal rearrangements involving regions different from the locus for predisposition suggest genetic heterogeneity and/or implication of genes for tumor progression. These genes which are also involved in development and regulation of differentiation and cell growth, may undergo a differential genomic imprinting.

Alleles↗
PubMed1990

Constitutional and somatic deletions of two different regions of maternal chromosome 11 in Wilms tumor.

Loss of heterozygosity for 11p markers and preferential loss of maternal alleles have been described in Wilms tumor. In this report we describe the molecular characterization of the constitutional and somatic 11p rearrangements in a del(11p13) WAGR patient with Wilms tumor. Both rearrangements led to loss of maternal alleles for two different regions of 11p, namely, 11p13 and 11p14----p15. This result clearly suggests that Knudson's hypothesis of two hits at the same locus does not necessarily apply to Wilms tumor. Moreover, the loss of 11p15 maternal alleles in the tumor is not incompatible with maternal inheritance of predisposition at 11p13. The putative roles of these two loci are discussed.

Alleles↗
PubMed1989

Characterization of a panel of somatic cell hybrids for subregional mapping along 11p and within band 11p13. Subdivision of the WAGR complex region.

The short arm of chromosome 11 carries genes involved in malformation syndromes, including the aniridia/genitourinary abnormalities/mental retardation (WAGR) syndrome and the Beckwith-Wiedemann syndrome, both of which are associated with an increased risk of childhood malignancy. Evidence comes from constitutional chromosomal aberrations and from losses of heterozygosity, limited to tumor cells, involving regions 11p13 and 11p15. In order to map the genes involved more precisely, we have fused a mouse cell line with cell lines from patients with constitutional deletions or translocations. Characterization of somatic cell hybrids with 11p-specific DNA markers has allowed us to subdivide the short arm into 11 subregions, 7 of which belong to band 11p13. We have thus defined the smallest region of overlap for the Wilms' tumor locus bracketed by the closest proximal and distal breakpoints in two of these hybrids. The region associated with the Beckwith-Wiedemann syndrome spans the region flanked by two 11p15.5 markers, HRAS1 and HBB. These hybrids also represent useful tools for mapping new markers to this region of the human genome.

Antibodies, Monoclonal↗
PubMed1988

Mapping of a human fibrillar collagen gene, pro alpha 1 (XI) (COL11A1), to the p21 region of chromosome 1.

Type XI collagen is a minor and poorly characterized structural component of cartilage. Recently, cDNA and genomic clones coding for the pro alpha 1 chain of human Type XI collagen, formerly 1 alpha collagen, have been isolated and fully characterized. Here we have used one such probe to establish the chromosomal localization of the pro alpha 1 (XI) collagen gene (COL11A1) by hybridization to filter-bound DNA isolated from flow-sorted chromosomes and by in situ hybridization on metaphase chromosomes. This combination of approaches has enabled us to locate COL1A11 in the p21 region of chromosome 1. This represents the first mapping of a Type XI collagen gene and the first assignment of a collagen locus to chromosome 1. These studies also provide additional evidence for the nearly uniform dispersion of the human fibrillar collagen genes in the human genome.

Chromosome Banding↗
PubMed1981

[The infusion of packed red cells. Usual difficulties (author's transl)].

This infusion used instead of whole blood has become increasingly common. However in our, as in other french institutions, the volume and the hematocrit of blood contained in each unit varies often notably. In addition, because of their high viscosity packed erythrocytes cannot be transfused rapidly enough. For transfusion in emergency situations and transfusion in operating room, following suggestions could be made to blood banks: --each unit should provide information on its content (volume and hematocrit or hemoglobin content); --units with low blood content should be transfused outside the operating room, whereas units containing high volumes should be reserved for peroperative transfusion in order to reduce charge of manipulation; --packed erythrocytes units should be prepared in order to allow same transfusion rates as whole blood (i.e. an average of 100 ml per minute for one transfusion line); --packed erythrocytes units should contain about 80 ml of plasma for an average total concentrate volume of 260 ml in order to provide enough antibacterial defense components; --units of fresh whole blood should be provided when approximately 150 p. cent of recipient's blood volume has been replaced in order to maintain the critical platelet level.

Blood Sedimentation↗