Association of MIF-173 gene polymorphism with inflammatory bowel disease in Chinese Han population

Fei, Bao-Ying; Huo-xiang, LV; Yang, J. T.; Ye, Zai-yuan

doi:10.1016/j.cyto.2007.10.010

Cited by 39 publications

(31 citation statements)

References 26 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…MIF gene polymorphism is studied in many different inflammatory diseases. The association between the MIF -173 C/C genotype and predisposition to ulcerative colitis was also found on the Chinese people (19). The C/C genotype is frequently seen in patients with pancolitis, although no genotype difference has been found to be associated with ulcerative colitis (20).…”

Section: Discussionmentioning

confidence: 86%

Evaluation of MIF -173 G/C Polymorphism in Turkish Patients with Ankylosing Spondylitis

et al. 2016

View full text Add to dashboard Cite

Background: Ankylosing spondylitis (AS) is a chronic inflammatory disease mainly affecting the spine and sacroiliac joints. Macrophage migration inhibitory (MIF) factor is a regulatory cytokine that inhibits random immune cell migration. MIF gene promoter polymorphisms play a role in the progression of several inflammatory disorders. Aims: To investigate the relationship between the MIF gene -173 G/C single-nucleotide polymorphism (SNP) and AS.

show abstract

Section: Discussionmentioning

confidence: 86%

Evaluation of MIF -173 G/C Polymorphism in Turkish Patients with Ankylosing Spondylitis

et al. 2016

View full text Add to dashboard Cite

show abstract

“…It sug gested that MIF-173 CC genotype could be associated with susceptibility to UC. However CC genotype was not related to clinical features in patients with UC in Chinese Han population [17] .…”

Section: Mif-173 Genementioning

confidence: 99%

“…Two cases were positive in the Bat26 locus by SSLP: one was an LGD case, and the other was a case of carcinoma, which also had abnormal exon 6 of p53 gene. Another nine microsatellite loci, [TGFbRII (A) (10), IGFIIR (G) (8), IGFIIR (CT) (5), TGFbRII (GT) (3), BAX (G) (8), hMSH3 (A) 8, hMSH6 (C) (8), TCF4 (A) (9) and DPC4 (CA) (17)] were negative in all cases. The p53 gene mutations and microsatellite instability may be one of the mechanisms for higher risk of carcinogenesis in UC [42] .…”

Section: P53 Genementioning

confidence: 99%

“…These differences in expression are likely to be due to differences in transcription factor interaction with the MIF-173 element. AP-4 transcription factor is a particular candidate [1,17] based on the promoter sequence analysis.…”

Section: Mif-173 Genementioning

confidence: 99%

“…MIF-173 SNP was genotyped by tetra-primer amplification refractory mutation system (ARMS) and RFLP-PCR was also performed in 142 healthy subjects and 98 patients with IBD [17] . There were no discrepancies between the results obtained by tetra-primer ARMS and RFLP-PCR.…”

Section: Mif-173 Genementioning

confidence: 99%

See 2 more Smart Citations

Epidemiology and gene markers of ulcerative colitis in the Chinese

Yun

Xu²,

Pan³

2009

WJG

View full text Add to dashboard Cite

Inflammatory bowel disease (IBD) includes two similar yet distinct conditions called ulcerative colitis (UC) and Crohn's disease (CD). These diseases affect the digestive system and cause the inflammation of intestinal tissue, form sores and bleed easily. Most children with IBD are diagnosed in late childhood and adolescence. However, both UC and CD have been reported as early as in infancy. Most information pertaining to the epidemiology of IBD is based upon adult studies. Symptoms include abdominal pain, cramping, fatigue and diarrhea.

show abstract

Mechanisms by which inflammation may increase intestinal cancer risk in inflammatory bowel disease

O'Connor

Lapointe

Beck

et al. 2010

Inflammatory Bowel Diseases

130

View full text Add to dashboard Cite

Patients with ulcerative colitis and Crohn's disease are at increased risk of developing intestinal cancers via mechanisms that remain incompletely understood. However, chronic inflammation and repeated events of inflammatory relapse in inflammatory bowel disease (IBD) expose these patients to a number of signals known to have tumorigenic effects including persistent activation of the nuclear factor-kappaB and cyclooxygenase-2/prostaglandin pathways, release of proinflammatory mediators such as tumor necrosis factor-alpha and interleukin-6, and enhanced local levels of reactive oxygen and nitrogen species. These inflammatory signals can contribute to carcinogenesis via 3 major processes: 1) by increasing oxidative stress, which promotes DNA mutagenesis thus contributing to tumor initiation; 2) by activating prosurvival and antiapoptotic pathways in epithelial cells, thereby contributing to tumor promotion; and 3) by creating an environment that supports sustained growth, angiogenesis, migration, and invasion of tumor cells, thus supporting tumor progression and metastasis. The present review integrates clinical and basic research observations in an attempt to provide a comprehensive understanding of how inflammatory processes may contribute to intestinal cancer development in IBD patients.

show abstract

Association of MIF-173 gene polymorphism with inflammatory bowel disease in Chinese Han population

Cited by 39 publications

References 26 publications

Evaluation of MIF -173 G/C Polymorphism in Turkish Patients with Ankylosing Spondylitis

Evaluation of MIF -173 G/C Polymorphism in Turkish Patients with Ankylosing Spondylitis

Epidemiology and gene markers of ulcerative colitis in the Chinese

Mechanisms by which inflammation may increase intestinal cancer risk in inflammatory bowel disease

Contact Info

Product

Resources

About