Gene Organization of the Pregnancy-Specific Glycoprotein Region on Human Chromosome 19: Assembly and Analysis of a 700-kb Cosmid Contig Spanning the Region

Olsen, Anne S.; Teglund, Stephan; Nelson, David Lee; Gordon, Laurie; Copeland, Alex; Georgescu, Anca Meda; Carrano, A.V.; Hammarström, Sten

doi:10.1006/geno.1994.1555

Cited by 52 publications

(30 citation statements)

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“…Located at chromosome 19q13.2 within the cluster of CEA-related genes (Olsen et al, 1994), CEACAM1 is the most conserved member with one known gene in humans . This gene gives rise to alternatively spliced mRNA species with isoforms differing mostly in their cytoplasmic domains.…”

Section: Introductionmentioning

confidence: 99%

CEACAM1 impedes thyroid cancer growth but promotes invasiveness: a putative mechanism for early metastases

Winer

et al. 2006

Oncogene

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Section: Introductionmentioning

confidence: 99%

CEACAM1 impedes thyroid cancer growth but promotes invasiveness: a putative mechanism for early metastases

Winer

et al. 2006

Oncogene

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“…The whole-genome mapping projects (Chumakov et al 1995;Hudson et al 1995) have produced contigs in 22q11 that differ from Collins et al (1995), and discrepancies can often be traced to problems with low copy repeats. The high-resolution YAC and cosmid map of chromosome 16 and 19 contains multigene families and noncoding repetitive sequences that also required special attention during contig assembly (see Olsen et al 1994;Ashworth et al 1995;Doggett et al 1995). The existence of low copy repeats such as those described here may interfere with production of sequence-ready maps and genomic DNA sequence in several regions of the human genome, and may require more detailed mapping methods to be applied.…”

Section: Discussionmentioning

confidence: 99%

“…For instance, Stallings et al (1992) noted that repetitive sequences had resulted in apparent false overlaps in a cosmid contig on chromosome 16. A region of low copy repeats was also found on chromosome 19, but a modified fingerprinting method was able to resolve cosmids in this region (Olsen et al 1994). Repetitive DNA also leads to yeast artificial chromosome (YAC) instability (Neil et al 1990), which hampers the YAC mapping strategy.…”

mentioning

confidence: 99%

The Organization of the γ-Glutamyl Transferase Genes and Other Low Copy Repeats in Human Chromosome 22q11

Collins¹,

Mungall²,

Badcock³

et al. 1997

Genome Res.

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A clone map consisting of YACs, cosmids, and fosmids has been constructed covering low copy repeat regions of human chromosome 22q11. A combination of clone restriction digest analysis, single-copy landmark content analysis, HindIII–Sau3AI fingerprinting, and sequencing of PCR products derived from clones was required to resolve the map in this region. Seven repeat-containing contigs were placed in 22q11, five containing γ-glutamyl transferase (GGT) sequences described previously. In one case, a single interval at the resolution of the YAC map was shown to contain at least three GGT sequences after higher resolution mapping. The sequence information was used to design a rapid PCR/restriction digest technique that distinguishes the GGT loci placed in the YAC map. This approach has allowed us to resolve the previous cDNA and mapping information relating to GGT and link it to the physical map of 22q11.[The sequence data described in this paper have been submitted to EMBL under accession nos. Z93342 (gene 11; EMBL identification no. HSGGT11), Z93343 (gene 12; EMBL no. HSGGT12), Z93344(gene 1; EMBL no. HSGGT1A), Z93345 (gene 2; EMBL no. HSGGT2A), Z93346(gene 3; EMBL no. HSGGT3A), Z93347 (gene 3-like; EMBL no. HSGGT3L), andZ93348 (gene 6; EMBL no. HSGGT6).]

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“…Carcinoembryonic antigen is part of the large immunoglobulin-like CEA gene family comprising as many as 31 genes , all located on chromosome 19q13.2 in humans (Olsen et al, 1994). Twenty of these genes are expressed in a variety of normal and tumor epithelial, hematopoietic cells and in placenta .…”

Section: Introductionmentioning

confidence: 99%

Deletion of the carcinoembryonic antigen-related cell adhesion molecule 1 (Ceacam1) gene contributes to colon tumor progression in a murine model of carcinogenesis

et al. 2006

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Carcinoembryonic antigen-related cell adhesion molecule 1 (CEACAM1) is a glycoprotein that is part of the carcinoembryonic antigen and the immunoglobulin superfamilies. We have shown that it functions as a tumor suppressor and that this function depends upon the presence of the longer CEACAM1 cytoplasmic domain. In this report, we describe the generation of a Ceacam1À/À mouse. The Ceacam1À/À colon exhibits increased in vivo proliferation relative to the wild-type counterpart with a corresponding decreased expression of the p21Cip1 and p27Kip1 Cyclin D kinase inhibitors. The colonic villi undergo decreased apoptosis. Out of 35 litters of mice, no spontaneous tumors in any tissues normally expressing CEACAM1 were found over the lifespan of the animals, suggesting that CEACAM1 may not be involved in initiation of tumor development. However, when mice are treated with azoxymethane to induce colonic tumors, we find that Ceacam1À/À mice developed a significantly greater number of tumors than their littermate controls. Moreover, the tumor size was greater in the knockout mice relative to that in the wild-type mice. These results indicate that deletion of CEACAM1 favors progression of colon tumorigenesis.

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Gene Organization of the Pregnancy-Specific Glycoprotein Region on Human Chromosome 19: Assembly and Analysis of a 700-kb Cosmid Contig Spanning the Region

Cited by 52 publications

References 0 publications

CEACAM1 impedes thyroid cancer growth but promotes invasiveness: a putative mechanism for early metastases

CEACAM1 impedes thyroid cancer growth but promotes invasiveness: a putative mechanism for early metastases

The Organization of the γ-Glutamyl Transferase Genes and Other Low Copy Repeats in Human Chromosome 22q11

Deletion of the carcinoembryonic antigen-related cell adhesion molecule 1 (Ceacam1) gene contributes to colon tumor progression in a murine model of carcinogenesis

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