Establishment and characterization of 12 uterine cervical-carcinoma cell lines: Common sequence variation in theE7 gene of HPV-16-positive cell lines

Ku, Ja Lok; Kim, Woo Ho; Park, Hyun Sook; Kang, Soon Beom; Park, Jae Gahb

doi:10.1002/(sici)1097-0215(19970717)72:2<313::aid-ijc19>3.0.co;2-g

Cited by 30 publications

(21 citation statements)

References 24 publications

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“…Most of these cell lines were isolated more than 10 years ago, however, and have been passaged many times in vitro in uncontrolled growth conditions. Therefore, they could have lost their phenotypic heterogeneity, like cervical cancer cell lines commonly observed in primary tumor lines (reviewed by Ku et al, 1997). The use of pancreatic carcinoma cell lines with a low passage number would solve this problem.…”

Section: Discussionmentioning

confidence: 99%

Establishment and characterization of four human pancreatic carcinoma cell lines

Yoon

Kim

et al. 2002

Cell and Tissue Research

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We characterized four pancreatic carcinoma cell lines (designated SNU-213, SNU-324, SNU-410, and SNU-494) established from histopathologically varied primary or liver metastatic tumor samples of Korean patients. Three cell lines grew as adherent monolayers and one as adherent and floating cell clumps. All lines had: (1) relatively high viability; (2) an absence of mycoplasma or bacterial contamination; (3) genetic heterogeneity as assessed by DNA-fingerprinting analysis; (4) an absence of MADH4 mutation. Among the lines, three lines had mutations in codon 12 in K- ras, two lines harbored p53 mutations within the DNA-binding domain; two lines had homozygous deletions in both p16 and p15 genes; and one line had a missense mutation. Two lines (SNU-324 and SNU-410) had genetic alterations in the TGFBR2 gene: the SNU-324 line had a -1-bp or +1-bp mutation in 10-bp polydeoxyadenine repeat tracts; the SNU-410 line had a genomic deletion in this gene. Mutation analysis of mismatch repair genes demonstrated that SNU-324 has two heterozygous missense mutations in different exons of the hMLH1 gene. In addition, this line showed microsatellite instability and harbored frameshift mutations in simple repeated sequences of the coding regions of the TGFBR2, BAX, and hMSH3 genes. These defects of microsatellite instability and mismatch repair genes suggest the possibility of a new mutator phenotype for pancreatic carcinogenesis. These cell lines should be very useful for studying the biology of pancreatic carcinoma, particularly those related to mutator phenotype and genetic alterations in the TGFBR2 gene.

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Section: Discussionmentioning

confidence: 99%

Establishment and characterization of four human pancreatic carcinoma cell lines

Yoon

Kim

et al. 2002

Cell and Tissue Research

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“…In another study, alterations at eight dinucleotide loci mapping to six different chromosomes were found in five out of 82 cervical cancers (Helland et al, 1997;Kersemaekers et al, 1998a). In another 51 cases, mutator phenotypes were detected in four cases (Ku J-L et al, 1977;Ku W-H et al, 1997). This instability affected to one or two alleles at one or few loci.…”

Section: Microsatellite Instability and Mutator Phenotypementioning

confidence: 93%

“…Human Yokota et al, 1989;Jones and Nakamura, 1992;Kohno et al, 1993;Karlsen et al, 1994;Mitra et al, 1994a;Mullokandov et al, 1996;Ku et al, 1997;Larson et al, 1997;Chu et al, 1998;Huettner et al, 1998;Kersemaekers et al, 1998b 4p16 27/66 40 Hampton et al, 1996;Mullokandov et al, 1996;Kersemaekers et al, 1998b 4q21-35 23/72 32 Mitra et al, 1994a;Mullokandov et al, 1996;Kersemaekers et al, 1998b 5p13-15 20/117 17 Ku et al, 1977;Mitra et al, 1994a;Mullokandov et al, 1996;Kersemaekers et al, 1998b 6p21.3-22 60 keratinocytes immortalized with HPV-16 DNA show LOH at 3p. The tumorigenicity of these cells in nude animals correlated very well with instability and loss of genetic material from human chromosome 3p (Montgomery et al, 1995;Steenbergen et al, 1996), 10p, 11q and 18q regions (Montgomery et al, 1995;Steenbergen et al, 1995Steenbergen et al, , 1996.…”

Section: Loh At 3p and The Fhit Gene In CCmentioning

confidence: 99%

“…Overall, of 344 cases analysed for the presence of the mutator phenotype, only 28 displayed MI (8%), independently of the type of allele and number of chromosomes studied (Ku J-L et al, 1977;Larson et al, 1996;Helland, 1997;Ku W-H et al, 1997), which represents a small subset of the total number of CC cases.…”

Section: Microsatellite Instability and Mutator Phenotypementioning

confidence: 99%

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The molecular genetics of cervical carcinoma

1999

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In the pathogenesis of cervical carcinoma there are three major components, two of them related to the role of human papillomaviruses (HPV). First, the effect of viral E6 and E7 proteins. Second, the integration of viral DNA in chromosomal regions associated with well known tumour phenotypes. Some of these viral integrations occur recurrently at specific chromosomal locations, such as 8q24 and 12q15, both harbouring HPV18 and HPV16. And third, there are other recurrent genetic alterations not linked to HPV. Recurrent losses of heterozygosity (LOH) have been detected in chromosome regions 3p14–22, 4p16, 5p15, 6p21–22, 11q23, 17p13.3 without effect on p53, 18q12–22 and 19q13, all of them suggesting the alteration of putative tumour suppressor genes not yet identified. Recurrent amplification has been mapped to 3q+ arm, with the common region in 3q24–28 in 90% of invasive carcinomas. The mutator phenotype, microsatellite instability, plays a minor role and is detected in only 7% of cervical carcinomas. The development of cervical carcinoma requires the sequential occurrence and selection of several genetic alterations. The identification of the specific genes involved, and their correlation with specific tumour properties and stages could improve the understanding and perhaps the management of cervical carcinoma. © 1999 Cancer Research Campaign

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“…Appropriate amounts of ®ne neoplastic tissue fragments were seeded into 25-cm 2¯a sks. Tumour cells were initially cultured in AR5 medium, which has proved useful in establishing human cancer cell lines [18,19] and the composition of which was described previously [18]. After being established, the cultures were maintained in RPMI 1640 (Gibco/BRL, Grand Island, NY) supplemented with 10% heatinactivated fetal bovine serum.…”

Section: Methodsmentioning

confidence: 99%

Establishment and characterization of seven human renal cell carcinoma cell lines

Shin¹,

Ku²,

Kim³

et al. 2000

BJU International

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and their tumour tissues, mutations in the VHL gene were found. The SNU-267 line had a frameshift mutation in the p53 gene. A missense mutation of the TGF-bRII gene was detected in the SNU-1272 line and the corresponding tissue. Analysis of the repeat sequences showed one cell line (SNU-349) to have MSI and the other six to have microsatellite stability. As MSI is a hallmark of the inactivation of mismatch repair genes, the presence of hMSH2 and hMLH1 mutations was investigated in all seven cell lines. An inactivating homozygous single base-pair deletion of the hMLH1 gene was found only in the SNU-349 cell line and corresponding tissue. Moreover, a frameshift mutation within an 8-bp polyadenine repeat present in the hMSH3 coding region was found only in the MSI cell line and tumour tissue. Conclusion These newly established RCC cell lines should provide a useful in vitro model for studies related to human RCC. The SNU-349 cell line should be especially useful for studies of MSI and mismatch repair-defective RCCs.

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Establishment and characterization of 12 uterine cervical-carcinoma cell lines: Common sequence variation in theE7 gene of HPV-16-positive cell lines

Cited by 30 publications

References 24 publications

Establishment and characterization of four human pancreatic carcinoma cell lines

Establishment and characterization of four human pancreatic carcinoma cell lines

The molecular genetics of cervical carcinoma

Establishment and characterization of seven human renal cell carcinoma cell lines

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