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B Carritt

Publications and source records attributed to B Carritt.

At least 37 records · Page 2Linked to original sources
PubMed1992

A gene from human chromosome region 3p21 with reduced expression in small cell lung cancer.

A combination of cytogenetic and molecular studies has implicated the p21 region of human chromosome 3 as the probable site of a gene the loss of which contributes to the development of small cell lung cancer. We report here the isolation of a gene from this region which is expressed in normal lung tissue and in cell lines derived from a number of different types of tumor, but the expression of which in small cell lung cancer cell lines is undetectable by RNA blot analysis. Although the more sensitive polymerase chain reaction did detect transcripts, a novel quantitative polymerase chain reaction assay showed that their concentration in small cell lung cancer cell lines is less than 3% of that in normal lung.

Carcinoma, Small Cell↗
PubMed1991

The human homolog of the mouse brown gene maps to the short arm of chromosome 9 and extends the known region of homology with mouse chromosome 4.

The mouse brown locus encodes a tyrosinase-related protein, TRP-1. The human homolog of TRP-1 was recently cloned from a melanoma cDNA library and sequenced. We have made oligonucleotide primers corresponding to the human TRP1 3' untranslated region and used them to map the human TRP1 gene by species-specific PCR in human/rodent somatic cell hybrids. By this means, the human TRP1 gene has been mapped to the short arm of chromosome 9.

Animals↗
PubMed1991

An unusually proximal deletion on the short arm of chromosome 3 in a patient with small cell lung cancer.

The tumors of patients with small cell lung carcinoma (SCLC) frequently exhibit the loss of alleles at polymorphic loci on the short arm of chromosome 3. We report the genotype analysis of six SCLC patients obtained using 15 chromosome 3 probes that identified 19 restriction fragment length polymorphisms (RFLPs). Five of the six patients were reduced to homozygosity in the tumor DNA at every informative 3p locus, and thus did not serve to delineate the deletion. However, the RFLP analysis of the tumor DNA of the sixth patient demonstrated both heterozygous and hemizygous loci on 3p and allowed the definition of an interstitial deletion that extends proximal to the D3S2 locus at 3p14.2-p21 to include at least 3p13-p14. The exclusion of the D3F15S2 locus from the deleted region, observed in this patient, is an uncharacteristic feature of SCLC deletions. This deletion includes the location of D3S30 and D3S4, and thus serves to map these loci within the proximal half of chromosome 3.

Alleles↗
PubMed1991

Assignment of the fucosidase pseudogene FUCA1P to chromosome region 2q31----q32.

FUCA1P is a pseudogene of the structural fucosidase gene FUCA1. The former has been mapped to human chromosome 2, whereas the latter has been localized to chromosome 1p34----p36. We have further localized FUCA1P to chromosomal band 2q31----q32 by fluorescent in situ hybridization and digital imaging microscopy. This localization was confirmed by linkage analysis between FUCA1P and the COL3A1 gene in 2q24----q32 which gave maximal lod scores of 4.03 at 3% recombination.

Cells, Cultured↗
PubMed1990

Restriction fragment length polymorphism (RFLP) at the DNF15S2 locus in three ethnic groups of Singapore.

Three different ethnic groups from Singapore comprising 79 Chinese, 34 Malays and 23 Indians of Dravidian origin, were investigated for the HindIII RFLP at the DNF15S2 locus. The three populations had very similar allele frequencies and the frequency of rarer(S) allele was significantly (p less than 0.01) lower (0.21) in these ethnic groups compared to that in Caucasians (0.41). The phenotypic distributions were at Hardy-Weinberg equilibrium.

China↗
PubMed1989

Transposition, amplification, and divergence in the origin of the DNF15 loci, a polymorphic repetitive sequence family on chromosomes 1 and 3.

The loci DNF15S1 and DNF15S2 are members of a small repetitive sequence family at discrete chromosomal locations, namely, 1p36 and 3p21, respectively. Studies of the structure, arrangement, and interrelations of the family suggest that the single copy on chromosome 3 is the original member and that this gave rise to the several members on chromosome 1 by transposition, partial duplication, and amplification. Several restriction fragment length polymorphisms have been discovered at the DNF15S1 locus and these have been assigned to the different subfamilies of the repeat at this locus. The existence of these RFLPs, and the nonallelic restriction site variation also found in this sequence family, suggests that transposition and amplification occurred as discrete events. We sequenced across the ancient junction between chromosomes 1 and 3 and noted features which might explain the mechanics of the transposition and amplification events.

Base Sequence↗
PubMed1988

Direct molecular analysis of a deletion of 3p in tumors from patients with sporadic renal cell carcinoma.

Normal and tumorous nephrectomy specimens from seven renal cell carcinoma patients were subjected to a Southern analysis using chromosome #3-specific polymorphic probes. Three patients were not informative because of homozygosity at all loci studied. One patient showing heterozygosity at 3q in normal tissue had a tumor that remained heterozygous. In three patients the tumor showed loss of heterozygosity for a short arm market at 3p21. In one of them heterozygosity for a second short arm marker was also lost. Another of these three patients retained heterozygosity for this second short arm marker, as well as for a long arm marker, suggesting a chromosomal breakpoint between the loci for the two short arm markers. Our results demonstrate that the known involvement of a short arm region of chromosome #3 in the development of renal cell carcinoma can readily be further evaluated by direct molecular methods.

Alleles↗
PubMed1988

The assignment of the human gene coding for complement C5 to chromosome 9q22-9q33.

The presence or absence of the human gene for the fifth component of complement (C5) was analysed in 19 human-rodent hybrid cell lines by hybridization to a radiolabelled probe derived from a human C5 cDNA clone. The segregation of C5 in these hybrids suggested that the gene is localized on chromosome 9, in the region 9q21-9qter. In situ hybridization refined the assignment of C5 to chromosome 9q22-33.

Animals↗
PubMed1987

An alpha-fucosidase pseudogene on human chromosome 2.

In Chinese hamster-human hybrids with overlapping translocations, the major site of hybridization of a cDNA clone for the liver form of human alpha-L-fucosidase was 1p36.13----1p34, consistent with hybridization to the FUCAl locus. No hybridization to the FUCA2 locus on chromosome 6 was observed. Hybridization to a genomic sequence on chromosome 2 was, however, detected, thus defining a new FUCA-like locus. The restriction map of the alpha-fucosidase cDNA could be exactly superimposed upon its region of homology within a genomic clone containing this FUCA-like locus, suggesting that it is a processed pseudogene.

Animals↗
PubMed1987

Loss of heterozygosity for a chromosome 3 sequence presumably at 3p21 in small cell lung cancer.

A recombinant DNA fragment detecting a chromosome #3 restriction fragment length polymorphism presumably at p21 was hybridized to HindIII-digested DNA isolated from the leukocytes of 12 patients of small cell lung cancer. Four of them appeared to be heterozygous. Analysis of tumor material from these four patients revealed homozygosity for either one or the other restriction fragment in every case. Our findings suggest the presence on the short arm of chromosome #3 of a recessive mutant cancer gene contributing to the development of small cell lung cancer.

Carcinoma, Small Cell↗
PubMed1987

cDNA cloning, sequencing and chromosome mapping of a non-erythroid spectrin, human alpha-fodrin.

Several overlapping cDNA clones encompassing 2760 nucleotides of the alpha-subunit of a human non-erythroid spectrin (termed fodrin) were isolated from a human lung fibroblast cDNA library. DNA and RNA blot analyses indicated that a single copy alpha-fodrin gene encodes a 9-kb transcript. The cDNA clones were sequenced, and all were found to contain long open reading frames. The overlapping regions were identical except for a 60-nucleotide inframe insertion at position 1133 in the composite sequence. This result suggests that at least two distinct transcripts exist in fibroblast cells. The chromosomal location of human alpha-fodrin was assigned to 1p34-1p36.1 by hybridization to somatic cell hybrids, and it is thus distinct from that of human alpha-spectrin which has been mapped to 1q22-1q25. Alignment of the composite 919 amino acids of the predicted protein sequence of human alpha-fodrin with that of human alpha-spectrin indicated that alpha-fodrin has a similar 106-amino-acid repeating structure, which is homologous with alpha-spectrin repeats 7-15. Repeats 10 and 11 are anomalous in sequence and structure from other repeats. A comparison of nucleic acid and amino acid homologies between alpha-spectrin and the alpha-fodrin of several vertebrates indicated that human non-erythroid alpha-fodrin and the common alpha-subunit of erythroid and non-erythroid cells of non-mammalian vertebrates are closely related (90%-96% amino acid homology), whereas alpha-fodrin is only distantly related to the erythroid-specific alpha-spectrin subunit of mammals (55%-59% amino acid homology). These data suggest that mammalian erythroid alpha-spectrin evolved by duplication and rapid divergence from an ancestral alpha-fodrin-like gene.

Amino Acid Sequence↗