The study of tumor necrosis factor beta gene polymorphism in lung cancer patients

Shimura, Tatsuo; Hagihara, Masao; Takebe, Kentaro; Munkhbat, Batmunkh; Odaka, Tatsuro; Kato, Harubumi; Nagamachi, Yukio; Tsuji, Kimiyoshi

doi:10.1002/1097-0142(19940215)73:4<1184::aid-cncr2820730410>3.0.co;2-y

Cited by 41 publications

(34 citation statements)

References 22 publications

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“…A NcoI RFLP exists in the first intron of TNFB (gene for TNF-b); the rare allele of which (TNFB*2) is associated with reduced TNF-b production (Messer et al, 1991). The homozygous common allele genotype (TNFB*1/ TNFB*1) seems to protect against lung cancer (Shimura et al, 1994), colorectal cancer (Park et al, 1998) and breast cancer (Park et al, 2002). Studies on gastric cancer have also shown a prolonged survival in patients with this genotype (Shimura et al, 1995), whereas no association with either susceptibility or survival was demonstrated in pancreatic cancer (Barber et al, 1999).…”

Section: Tumour Necrosis Factormentioning

confidence: 99%

Role of genetic polymorphisms in tumour angiogenesis

2002

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Angiogenesis plays a crucial role in the development, growth and spread of solid tumours. Pro-and anti-angiogenic factors are abnormally expressed in tumours, influencing tumour angiogenesis, growth and progression. Polymorphisms in genes encoding angiogenic factors or their receptors may alter protein expression and/or activity. This article reviews the literature to determine the possible role of angiogenesis-related polymorphisms in cancer. Further research studies in this potentially crucial area of tumour biology are proposed.

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Section: Tumour Necrosis Factormentioning

confidence: 99%

Role of genetic polymorphisms in tumour angiogenesis

2002

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“…Both TNFs bind to the TNF receptor and exert similar biological activities; TNF-α is derived from macrophages and TNF-from helper T-lymphocytes type I (Th1). The TNF-B A252G (formerly designated as LTα NcoI) G allele was reportedly associated with lung cancer risk [17], and poor prognosis of sarcoidosis [18]. The combination of TNF-A G-308A and TNF-B A252G was reported to have an association with asthma [19].…”

Section: Introductionmentioning

confidence: 99%

Subjects with TNF-A-857TT and -1031TT genotypes showed the highest Helicobacter pylori seropositive rate compared with those with other genotypes

Hamajima

Shibata

Katsuda³

et al. 2003

Gastric Cancer

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“…Designations of SNPs refer to the nucleotide position relative to transcriptional start site. Clade A is uniquely defined by LTA+10A, LTA+252G and LTA+723A; clade B is uniquely defined by LTA+80A and LTA+368C; and clade C is uniquely defined by LTA+438 (10) and LTA+495C. The frequencies of these main haplotype clades were 0.27, 0.46 and 0.27, respectively.…”

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confidence: 98%

“…An intronic SNP at LTA+252 is associated with susceptibility to myocardial infarction 4 , asthma 5,6 , bacterial sepsis 7,8 , cancer 9,10 and autoimmune diseases 11,12 . Haplotypes bearing the LTA+252G allele show relatively high levels of reporter gene expression 4 and LTA protein production by peripheral blood mononuclear cells in some 13,14 but not all 15,16 studies.…”

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confidence: 99%

Allele-specific repression of lymphotoxin-α by activated B cell factor-1

2004

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Genetic variation at the human LTA locus, encoding lymphotoxin-α, is associated with susceptibility to myocardial infarction, asthma and other diseases. By detailed haplotypic analysis of the locus, we identified a single-nucleotide polymorphism (SNP) at LTA+80 as a main predictor of LTA protein production by human B cells. We found that activated B-cell factor-1 (ABF-1) binds to this site in vitro and suppresses reporter gene expression, but only in the presence of the LTA+80A allele. Using haplotype-specific chromatin immunoprecipitation, we confirmed that ABF-1 is preferentially recruited to the low-producer allele in vivo. These findings provide a molecular model of how LTA expression may be genetically regulated by allele-specific recruitment of the transcriptional repressor ABF-1.Identifying human DNA polymorphisms that regulate gene expression is essential for understanding the genetic basis of common diseases but is technically challenging. Valuable insights into molecular mechanisms can be derived by in vitro analysis of protein-DNA binding and reporter gene expression, but we have limited tools to interrogate putative regulatory polymorphisms in vivo. Such analysis needs to consider natural chromatin structure and natural haplotypic combinations of polymorphisms. It also must be able to detect small differences in gene expression, which could be crucial for disease susceptibility if a physiologically important mediator is involved.We attempted to address these issues for LTA, an important early mediator of immune and inflammatory responses 1 . Regulation of LTA is finely calibrated to resist dangerous pathogens but not to cause inflammatory damage to the host, as seems to occur in bacterial sepsis 2 and a b Figure 1 LTA protein production is associated with LTA haplotype. (a) Haplotype structure at the LTA locus. SNPs present at an allele frequency >0.1 in the panel of 26 LCLs are shown (minor allele frequencies given in brackets) together with haplotypes (haplotype frequencies shown at the head of the columns). Designations of SNPs refer to the nucleotide position relative to transcriptional start site. Clade A is uniquely defined by LTA+10A, LTA+252G and LTA+723A; clade B is uniquely defined by LTA+80A and LTA+368C; and clade C is uniquely defined by LTA+438(10) and LTA+495C. The frequencies of these main haplotype clades were 0.27, 0.46 and 0.27, respectively. (b) Analysis of LTA production by haplotype pair. A scatter plot of LTA concentration in cell culture supernatant from the panel of LCLs is shown per 10 6 cells, plotted as a symbol representing each cell line together with the geometric mean (horizontal lines). A total of six replicate experiments were done. The cell lines heterozygous with respect to haplotypes A, B and C are shown categorized at a given time point according to the pair of haplotypes present in that cell line (A+B, A+C or B+C). At 24 h after stimulation, cells bearing haplotypes B+C or B+A were associated with significantly lower LTA concentrations than those bearing haploty...

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The study of tumor necrosis factor beta gene polymorphism in lung cancer patients

Abstract: Background. In recent years numerous reports have discussed the relationship between the human leukocyte antigen and lung cancer. However, the genetic background of lung cancer has not yet been precisely clarified.

Cited by 41 publications

References 22 publications

Role of genetic polymorphisms in tumour angiogenesis

Role of genetic polymorphisms in tumour angiogenesis

Subjects with TNF-A-857TT and -1031TT genotypes showed the highest Helicobacter pylori seropositive rate compared with those with other genotypes

Allele-specific repression of lymphotoxin-α by activated B cell factor-1

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