Extensive characterization of genetic alterations in a series of human colorectal cancer cell lines

Gayet, Jacqueline; Zhou, Xiaoping; Duval, Alex; Rolland, Sandra; Hoang, Jean-Marc; Cottu, Paul; Hamelin, Richard

doi:10.1038/sj.onc.1204611

Cited by 158 publications

(135 citation statements)

References 45 publications

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“…Our data regarding CRCs were consistent with those reported in the literature, 38,44,45 except for the low frequency of 18q LOH (25%), which may have resulted from our choice of marker for use in the current analysis. LOH in MEN1, which is located within 11q13, had not been investigated previously and was found in one-third of all cases examined.…”

Section: Discussionsupporting

confidence: 89%

Genetic alterations in poorly differentiated endocrine carcinomas of the gastrointestinal tract

Pizzi

Azzoni

Bassi

et al. 2003

Cancer

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The length scales of film thickness nonuniformities, commonly observed in polymer colloid (i.e., latex) films, are predicted. This prediction is achieved by investigating the stability behavior of drying latex films. A linear stability analysis is performed on a base solution representing a uniformly drying latex film containing a surfactant. The analysis identifies film thickness nonuniformities over two length scales: long (millimeter) range (from lubrication theory) and short (micrometer) range (from nonlubrication theory). Evaporation and surfactant desorption into the bulk film are identified as the primary destabilizing mechanisms during drying. Experimental evidence through direct visualization and atomic force microscopy confirm the existence of nonuniformities over both length scales, which are shown to be functions of parameters such as initial particle volume fraction, surfactant amount, and desorption strength, while being independent of drying rate. © 2008 American Institute of Chemical Engineers AIChE J, 2008

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Section: Discussionsupporting

confidence: 89%

Genetic alterations in poorly differentiated endocrine carcinomas of the gastrointestinal tract

Pizzi

Azzoni

Bassi

et al. 2003

Cancer

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“…Cell line LoVo was chosen on the basis of literature data indicating that LoVo cells harbor a K-ras point mutation at codon 13. [23][24][25] As a control cell line, HT29 (91072201 ECACC, Porton Down, UK) cell with WT K-ras were selected. 26 They were grown in Advanced Eagle's minimum essential medium (Gibco) supplemented with 2% fetal bovine serum (Gibco), 2 mM L-glutamine, 1 mM sodium pyruvate and 350 mg l À1 gentamicin and 1 ml l À1 crystacillin.…”

Section: Colorectal Tumor Cell Linementioning

confidence: 99%

MicroRNAs targeting mutant K-ras by electrotransfer inhibit human colorectal adenocarcinoma cell growth in vitro and in vivo

et al. 2010

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Mutations of K-ras have been found in 30-60% of colorectal carcinomas and are believed to be associated with tumor initiation, tumor progression and metastasis formation. Therefore, silencing of mutant K-ras expression has become an attractive therapeutic strategy for colorectal cancer treatment. The aim of our study was to investigate the effect of microRNA (miRNA) molecules directed against K-ras (miRNA-K-ras) on K-ras expression level and the growth of colorectal carcinoma cell line LoVo in vitro and in vivo. In addition, we evaluated electroporation as a gene delivery method for transfection of LoVo cells and tumors with plasmid DNA encoding miRNA-K-ras (pmiRNA-K-ras). Results of our study indicated that miRNAs targeting K-ras efficiently reduced K-ras expression and cell survival after in vitro electrotransfection of LoVo cells with pmiRNA-K-ras. In vivo, electroporation has proven to be a simple and efficient delivery method for local administration of pmiRNA-K-ras molecules into LoVo tumors. This therapy shows pronounced antitumor effectiveness and has no side effects. The obtained results demonstrate that electrogene therapy with miRNA-K-ras molecules can be potential therapeutic strategy for treatment of colorectal cancers harboring K-ras mutations.

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“…Germline mutational analysis of hMLH1 and hMSH2 genes in family FGC#1 and FGC#24 which had MSI gastric carcinoma in the proband, was performed by denaturing gradient gel electrophoresis (DGGE) as described in [20]. …”

Section: Dggementioning

confidence: 99%

E-Cadherin (CDH1) and p53 rather than SMAD4 and Caspase-10 germline mutations contribute to genetic predisposition in Portuguese gastric cancer patients

Oliveira

Ferreira

Nabais

et al. 2004

European Journal of Cancer

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Approximately 30% of all hereditary diffuse gastric cancer (HDGC) families carry CDH1 germline mutations. The other two thirds remain genetically unexplained and are probably caused by alterations in other genes. Using polymerase chain reaction (PCR)/single-strand conformation polymorphism (SSCP)/sequencing, we screened 32 Portuguese families with a history of gastric cancer and 23 patients with early onset gastric cancer for CDH1 germline mutations. In probands negative for CDH1 mutations, we screened genes involved in hereditary cancer syndromes in which gastric cancer may be one of the component tumours, namely p53 (Li-Fraumeni Syndrome) and hMLH1 and hMSH2 (HNPCC). We also screened in these patients for mutations in Caspase-10, a gene inactivated in sporadic gastric cancer, and SMAD4, a gene whose inactivation in mice is associated with signet-ring cell carcinoma of the stomach. One of the families fulfilling the HDGC criteria harboured a CDH1 germline mutation, and one of the families with incomplete criteria harboured a p53 germline mutation. No mutations were identified in hMLH1 and hMSH2, and only sequence variants were found in SMAD4 and Caspase-10. The present work reports for the first time CDH1 germline mutations in Portuguese gastric cancer families, and highlights the need for p53 mutation screening in families lacking CDH1 germline mutations, in a country with one of the highest incidences of gastric cancer in the world. No evidence was found for a role of germline mutations in SMAD4 and Caspase-10 in families lacking CDH1 mutations.

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Extensive characterization of genetic alterations in a series of human colorectal cancer cell lines

Cited by 158 publications

References 45 publications

Genetic alterations in poorly differentiated endocrine carcinomas of the gastrointestinal tract

Genetic alterations in poorly differentiated endocrine carcinomas of the gastrointestinal tract

MicroRNAs targeting mutant K-ras by electrotransfer inhibit human colorectal adenocarcinoma cell growth in vitro and in vivo

E-Cadherin (CDH1) and p53 rather than SMAD4 and Caspase-10 germline mutations contribute to genetic predisposition in Portuguese gastric cancer patients

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