Amplification of DNA Sequences from Chromosome 19q13.1 in Human Pancreatic Cell Lines

Curtis, Lucy J.; Li, Yong; Gerbault‐Seureau, Michèle; Kuick, Rork; Dutrillaux, Anne-Marie; Goubin, Gérard; Fawcett, John J.; Cram, Scott; Dutrillaux, Bernard; Hanash, Sam; Muleris, Martine

doi:10.1006/geno.1998.5405

Cited by 48 publications

(62 citation statements)

References 32 publications

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“…In all, novel sequences were detected. Interestingly, some of these regions (1q41, 7p22, 8p11.23, 8q13.1, 8q22.3, 10q21.3, 10q24.32, 19q13.1, 20p11.23) have been described as amplified sequences in other human malignancies (Bruch et al, 1998;Curtis et al, 1998;Du Plessis et al, 1999;Larramendy et al, 2000;Pimkhaokham et al, 2000;Tang et al, 2002;Dai et al, 2003;Lukasova et al, 2004;Rao et al, 2004). The RLGS data does not allow us to discriminate between DNA copy number gains that have integrated at the location of the original sequence or extra DNA localized in extrachromosomal double minutes.…”

Section: Resultsmentioning

confidence: 99%

DNA copy number gains in head and neck squamous cell carcinoma

et al. 2005

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Gene amplification, a common mechanism for oncogene activation in cancer, has been used as a tag for the identification of novel oncogenes. DNA amplification is frequently observed in head and neck squamous cell carcinoma (HNSCC) and potential oncogenes have already been reported. We applied restriction landmark genome scanning (RLGS) to study gene amplifications and low-level copy number changes in HNSCC in order to locate previously uncharacterized regions with copy number gains in primary tumor samples. A total of 63 enhanced RLGS fragments, indicative of DNA copy number changes, including gains of single alleles, were scored. Enhanced sequences were identified from 33 different chromosomal regions including those previously reported (e.g. 3q26.3 and 11q13.3) as well as novel regions (e.g. 3q29, 8q13.1, 8q22.3, 9q32, 10q24.32, 14q32.32, 17q25.1 and 20q13.33). Furthermore, our data suggest that amplicons 11q13.3 and 3q26.3-q29 may be divided into possibly two and three independent amplicons, respectively, an observation supported by published microarray expression data.

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Section: Resultsmentioning

confidence: 99%

DNA copy number gains in head and neck squamous cell carcinoma

et al. 2005

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“…Three of these cell lines had high level ampli®cation of a series of overlapping NotI restriction fragments from 19q13.1 (Curtis et al, 1998). SU86.86 and AICPC-1 had ampli®cation of both OZF and AKT2, whilst PANC-1 only exhibited ampli®cation of AKT2 (Curtis et al, 1998). SU86.86 and AICP-1 were the only representatives of the 14 pancreatic carcinoma cell lines studied here, with ampli®cation of MLL2 as detected by both FISH and blotting methods.…”

Section: Discussionmentioning

confidence: 71%

“…FISH results in pancreatic carcinoma cell lines The karyotypes and CGH analysis of AICPC-1, AICPC-2, BxPC-3, HPAC, PANC-1, and SU.86.86 have been published previously (Curtis et al, 1998 noted along this hsr (see Figure 4a and Table 3). SU.86.86 cells have two normal chromosome 19s and one chromosome containing an hsr.…”

Section: Detection Of Mll2 Ampli®cations By Fish Analysismentioning

confidence: 72%

“…Similarly in several other cell lines, MLL2 was located near but was not disrupted by 19q13.1 translocations. DNA sequences from 19q13.1 have been shown to be ampli®ed in pancreatic carcinoma cell lines and primary pancreatic cancers and the corresponding genes overexpressed in pancreatic carcinomas (Cheng et al, 1996;Curtis et al, 1998;Ferbus et al, 1999;Hoglund et al, 1998). Of 12 pancreatic carcinoma cell lines analysed by both conventional cytogenetics and CGH, six showed ampli®cation of 19q13.1 (Curtis et al, 1998).…”

Section: Discussionmentioning

confidence: 99%

“…Of 12 pancreatic carcinoma cell lines analysed by both conventional cytogenetics and CGH, six showed ampli®cation of 19q13.1 (Curtis et al, 1998). Three of these cell lines had high level ampli®cation of a series of overlapping NotI restriction fragments from 19q13.1 (Curtis et al, 1998). SU86.86 and AICPC-1 had ampli®cation of both OZF and AKT2, whilst PANC-1 only exhibited ampli®cation of AKT2 (Curtis et al, 1998).…”

Section: Discussionmentioning

confidence: 99%

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MLL2, the second human homolog of the Drosophila trithorax gene, maps to 19q13.1 and is amplified in solid tumor cell lines

et al. 1999

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The Mixed Lineage Leukemia (MLL) gene is commonly involved in translocations in infantile leukemia and is ampli®ed in some cases of adult myeloid leukemia. A homolog of MLL denoted MLL2, which represents the second human homolog of the Drosophila trithorax gene, was characterized by assembling ESTs, the KIAA0304 cDNA clone, RT ± PCR fragments and a new clone isolated from a cDNA phage library and compared to the available genomic sequence. The MLL2 gene maps to 19q13.1, a region of frequent rearrangement or ampli®cation in solid tumors. MLL2 consists of an 8.5 ± 9 kb transcript and spans 20 kb of genomic DNA. The predicted MLL2 protein possesses all of the major domains de®ned in MLL and the two genes have a similar genomic structure. We ®nd that MLL2 is ampli®ed in two of 14 pancreatic carcinoma cell lines and one of ®ve glioblastoma cell lines and is a likely critical gene in 19q13.1 ampli®cations. It is also a candidate for chromosomal rearrangements involving this chromosome locus. MLL2 is one additional mammalian trithorax-group gene with involvement in human cancer.

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