Oncogenes and Tumor Suppressor Genes Involved in Human Lung Carcinogenesis

Harris, Curtis C.; Reddel, Roger R.; Modali, Rama; Lehman, Teresa A.; Iman, Deborah S.; McMenamin, Mary G.; Sugimura, Haruhiko; Weston, Ainsley; Pfeifer, Andréa

doi:10.1007/978-1-4613-0637-5_29

Cited by 5 publications

(3 citation statements)

References 58 publications

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“…Oncogene expression (abundance of mRNA) increased by up to 20% in cells cultured in medium containing 10,000 pM biotin compared to medium containing 250 pM biotin; oncogene expression decreased by up to 47% in cells cultured in medium containing 25 pM biotin compared to medium containing 250 pM biotin. Biotin-dependent expression of oncogenes is physiologically meaningful, given the important roles of the gene products in signal transduction, gene expression, and cell proliferation and differentiation [45][46][47][48][49][50][51].…”

Section: Oncogenesmentioning

confidence: 99%

Regulation of gene expression by biotin☆ (review)

Rodriguez-Melendez

Zempleni

2003

The Journal of Nutritional Biochemistry

143

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Section: Oncogenesmentioning

confidence: 99%

Regulation of gene expression by biotin☆ (review)

Rodriguez-Melendez

Zempleni

2003

The Journal of Nutritional Biochemistry

143

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“…In this study, to identify genes aberrantly hypermethylated and transcriptionally silenced in NSCLCs, we performed modi®ed MS-RDA using two squamous lung cancer cell lines and normal human bronchial epithelial cells, considering that squamous cell carcinomas arise from the bronchial epithelia (Harris et al, 1991;Sekido et al, 1998).…”

Section: Introductionmentioning

confidence: 99%

Silencing of HTR1B and reduced expression of EDN1 in human lung cancers, revealed by methylation-sensitive representational difference analysis

et al. 2001

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Aberrantly hypermethylated genes in human lung cancers were searched for by a genome scanning technique, methylation-sensitive-representational di erence analysis (MS-RDA). A total of 59 DNA fragments were isolated as those methylated more heavily in either/both of two lung squamous cell carcinoma cell lines, EBC-1 and LK-2, than in a primary culture of normal human bronchial epithelium, NHBE. Thirty-four DNA fragments, whose hypermethylation was con®rmed in primary squamous cell carcinomas, were sequenced. By database searches, 17 of them were shown to be located within 2 kb of putative CpG islands, and ®ve of the 17 DNA fragments had transcribed regions of known genes in their vicinities. By RT ± PCR of the ®ve genes in the carcinoma cell lines and NHBE, decreased expression of HTR1B (5-hydroxytryptamine receptor 1B) and EDN1 (endothelin-1) was observed. Sequencing after bisul®te modi®ca-tion showed that the CpG island in the promoter region of HTR1B was hypermethylated, while that of EDN1 was not. Demethylation and re-expression of HTR1B were observed after treatment of LK-2 cells with 5-aza-2'-deoxycytidine. In primary lung cancers, decreased mRNA expression of HTR1B was observed in 11 of 20 cases, and that of EDN1 was in 16 of 20 cases. Immunohistochemical analysis of endothelin-1 con®rmed that its immunoreactivity was reduced in squamous cell carcinoma cells compared with that in normal bronchial epithelial cells. Considering that endothelin-1 induces apoptosis in melanoma cells and that silencing of endothelin receptor B is observed in prostate cancers, its reduced expression was speculated to confer a growth advantage to lung cancer cells. MS-RDA was shown to isolate DNA fragments that are hypermethylated and silenced, such as HTR1B, and those whose expressions are altered and the methylation statuses outside the promoter region are altered, such as EDN1. Oncogene (2001) 20, 7505 ± 7513.

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“…Recent elucidation of molecular and chromosomal changes during the sequential progression of carcinogenesis (SPC) for colorectal cancer (Feron and Vogelstein, 1990) has established a paradigm that indicates the need for continued focus upon preneoplastic stages of other cancers in which the SPC has not been so clearly delineated. Many activated oncogenes and chromosomal abnormalities have been described in overt human non-small lung cancer (NSCLC; Harris et al, 1991), but when these activations and abnormalities occur during the SPC is not known. Serial examination of tissues during the preneoplastic stages of the SPC is needed, and this is not possible in humans.…”

Section: Introductionmentioning

confidence: 99%

A step section method for full histopathological assessment of carcinogen‐affected target tissue during respiratory carcinogenesis

Hammond

Teplitz

Benfield

1993

Microscopy Res & Technique

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Studies of carcinogenesis that are not limited to overt neoplasms but also involve evaluations of preneoplastic stages require histopathological assessment of the entire carcinogen-affected tissue so that the true nature and sequence of the progressive process can be determined. The customary serial sectioning approach achieves this goal, but at an inordinate logistic cost. In studies of hamster bronchial carcinogenesis, a step section method was compared to a quasi-random approach and to the customary serial section method. The step section method achieved the same diagnostic completeness as serial sectioning, but at a two orders of magnitude reduction in costs.

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Oncogenes and Tumor Suppressor Genes Involved in Human Lung Carcinogenesis

Cited by 5 publications

References 58 publications

Regulation of gene expression by biotin☆ (review)

Regulation of gene expression by biotin☆ (review)

Silencing of HTR1B and reduced expression of EDN1 in human lung cancers, revealed by methylation-sensitive representational difference analysis

A step section method for full histopathological assessment of carcinogen‐affected target tissue during respiratory carcinogenesis

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