Characterization of Short Tandem Repeats from Thirty-One Human Telomeres

Rosenberg, Marjorie; Hui, Lester; Ma, Junli; Nusbaum, H. C.; Clark, Kevin; Robinson, Louise; Dziadzio, Laura; Swain, Pamela; Keith, Tim P.; Hudson, Thomas J.; Biesecker, Leslie G.; Flint, Jonathan

doi:10.1101/gr.7.9.917

Cited by 37 publications

(31 citation statements)

References 31 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In fact, the most distal 285 kb of chromosome 16p has been completely sequenced (Flint et al 1997a). To develop a telomeric clone that met our criteria for a unique telomere clone, we used primers for a chromosome 16p STS, 16PTEL05 (D16S3400) (Rosenberg et al 1997), which lies within 300 kb of the end of the chromosome to identify RG191K2. The appropriate telomeric location of BAC RG191K2 was confirmed by FISH; the probe shows strong signals on 16p with no cross-hybridization to other sites.…”

Section: Resultsmentioning

confidence: 99%

“…For 4p and 16q, we have converted our previous telomere clones into larger format BAC clones to provide more robust FISH signals for analysis. For 4p, we used end sequence from a subtelomeric repeat clone (GS10K2) isolated with the telomeric STS, 4PTEL02 (D4S3359) (Rosenberg et al 1997), to identify GS118B13, a unique 4p telomere clone. The unique 16q telomere clone (PAC GS191P24) was identified using primers developed from the telomeric sequence, 16QTEL013 (GenBank accession no.…”

Section: Resultsmentioning

confidence: 99%

“…RH mapping has been used previously to define the physical map for the telomeric regions of many human chromosomes (Rosenberg et al 1997). RH mapping is useful, as either polymorphic or nonpolymorphic STSs can be mapped and placed on a physical map by estimating the distance between markers (Cox et al 1990;Stewart et al 1997).…”

Section: Discussionmentioning

confidence: 99%

“…Chromosome-specific (unique sequence) DNA for each telomere is located proximal to the subtelomeric repeats, about 100-300 kb from the end of the chromosome (National Institutes of Health et al 1996;Flint et al 1997b). Extensive half-YAC cloning has been carried out from the TTAGGG telomeric repeat to the unique telomere sequence and targeted efforts at cloning human telomeres have succeeded in identifying unique sequences at most telomeres (National Institutes of Health et al 1996;Riethman 1997;Rosenberg et al 1997). However, the distance between these telomere clones and the most distal marker on previously published physical and genetic maps is largely unknown.…”

mentioning

confidence: 99%

See 3 more Smart Citations

Characterization of Physical Gap Sizes at Human Telomeres

Lese¹,

Fantes²,

Riethman³

et al. 1999

Genome Res.

View full text Add to dashboard Cite

Genome-wide physical and genetic mapping efforts have not yet fully addressed the problem of closure at the telomeric ends of human chromosomes. Targeted efforts at cloning human and mouse telomeres have succeeded in identifying unique sequences at most telomeres, but gap sizes between these telomere clones and the distal markers on integrated genetic/physical maps remain largely unknown. As telomeric regions are known to be the most gene-rich regions of the human genome, filling these gaps should have a high priority in completion of the Human Genome Project. We reported previously a first generation set of unique sequence probes for human telomeric regions. Of 41 human telomere regions, 33 were represented by unique clones with a known distance (Յ300 kb) from the end of the chromosome; clones for the remaining eight telomeric regions had not yet been identified and were represented by the most distal markers on the integrated genetic/physical map. We have identified unique telomere clones for four of the remaining telomeres, 9p, 12p, 15q, and 16p. To determine the telomeric gap size for these chromosomes and five other human telomeres, interphase FISH analysis was performed to measure the distance between each telomere clone and the corresponding most distal marker. These studies provide distance estimates ranging from <100 kb to >1 Mb, thus defining the physical mapping task for filling telomeric gaps.

show abstract

Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

See 2 more Smart Citations

Characterization of Physical Gap Sizes at Human Telomeres

Lese¹,

Fantes²,

Riethman³

et al. 1999

Genome Res.

View full text Add to dashboard Cite

show abstract

“…23,24 When exon size was not exceeding 600 bp, both primers were chosen in flanking intronic sequences whereas for larger exons (Ͼ600 bp) one primer was chosen in exonic sequences and the other in a flanking intron. The subtelomeric markers have been described by Rosenberg et al 25 and Knight et al 26 All primer sequences are available on request. Oligonucleotides were obtained from Eurogentec (Seraing, Belgium), Genset (Paris, France), and Life Technologies (Cergy-Pontoise, France).…”

Section: Methodsmentioning

confidence: 99%

Homozygous deletion scanning in hepatobiliary tumor cell lines reveals alternative pathways for liver carcinogenesis

et al. 2003

View full text Add to dashboard Cite

Despite high rates of loss of heterozygosity affecting various chromosomes, the number of tumor suppressor genes (TSGs) found to be consistently involved in primary liver cancer is low. In the past decade, characterization of homozygous deletions (HDs) in tumors has become instrumental to identify new TSGs or to reveal the influence of a particular TSG on the development of a specific tumor type. We performed a detailed HD profiling at 238 critical loci on a collection of 57 hepatobiliary tumor cell lines (hepatocellular, cholangiocellular, and bile duct carcinomas, hepatoblastomas, and immortalized hepatocytes). We identified HDs at 9 independent loci, the analysis of which was extended to 17 additional hepatobiliary tumor cell lines. In total, 34 homozygous losses involving 9 distinct genes were detected in the 74 cell lines analyzed. Besides expected deletions at the p16-INK4A/p14-ARF, FHIT, AXIN1, and p53 genes, we detected HDs at the PTEN, NF2, STK11, BAX, and LRPDIT genes that were formerly not known to be implicated in human liver tumorigenesis. In conclusion, our data suggest that these genes may represent novel liver tumor suppressive targets. Additional tumorigenic pathways should be carefully considered in hepatocarcinogenesis. ( H epatocellular carcinoma (HCC), the main histologic form of primary liver cancer, is one of the most prevalent human tumors in the world. 1,2 Chronic infections of the liver by hepatitis B or hepatitis C viruses represent the dominant etiologies of HCC. 3 The historically recent spread of hepatitis C virus in human populations will result in a substantial increase in HCC incidence in developed countries and several epidemiologic surveys already have detected such a trend for the past 20 years in Japan, the United States, and Europe. 4,5 Until recently, chromosomal abnormalities occurring in HCC were defined poorly. We and others have performed allelotyping and comparative genomic hybridization studies to characterize the main chromosome targets in human liver tumorigenesis. 6-8 Only a handful of cancer genes are, however, consistently found mutated in this tumor type. p53 and AXIN1 genes are inactivated by somatic mutations in, respectively, 30% and 5% of cases, whereas p16-INK4A and SOCS1 are silenced through promoter hypermethylation in more than 50% of cases. 9-13 Finally, ␤-catenin, the only proto-oncogene previously found to be mutated in liver cancer, is activated in 20% of the samples. 14 The liver tumor-suppressive function of the product of the mannose-6-phosphate/insulinlike growth factor 2 receptor (IGF2/M6PR) gene is suspected but remains still controversial. 15,16 The past decade has seen the isolation of numerous tumor suppressor genes (TSGs) through the characterization of homozygous deletions (HDs) in primary tumors and cell lines. Although, HDs represent rare events, many of the TSG isolations, including WT1, p16-INK4A, BRCA2, FHIT, PTEN, SMAD4, and SNF5, were at least partly attributable to their detection. [17][18][19][20][21][22] In an attempt to

show abstract

The end of the beginning of chromosome ends†

Biesecker

2002

Am. J. Med. Genet.

Self Cite

View full text Add to dashboard Cite

Characterization of Short Tandem Repeats from Thirty-One Human Telomeres

Cited by 37 publications

References 31 publications

Characterization of Physical Gap Sizes at Human Telomeres

Characterization of Physical Gap Sizes at Human Telomeres

Homozygous deletion scanning in hepatobiliary tumor cell lines reveals alternative pathways for liver carcinogenesis

The end of the beginning of chromosome ends†

Contact Info

Product

Resources

About