Oral bacteria in pancreatic cancer: mutagenesis of the p53 tumour suppressor gene.

Oral bacteria in pancreatic cancer: mutagenesis of the p53 tumour suppressor gene.
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胰腺癌中的口腔细菌:p53 抑癌基因的突变。

DOI:
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发表时间:
2015
影响因子:
1.4
通讯作者:
Mesut Öğrendik
Mesut Öğrendik
中科院分区:
医学4区
文献类型:
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作者:
Mesut Öğrendik

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胰腺外分泌癌是全球癌症死亡的第四大原因。这种疾病在慢性胰腺炎患者中的患病率很高。口腔消化系癌多见于牙周炎患者。这些发现表明,这种类型的癌症可能有一些细菌起源。这项研究假设,在口腔细菌中发现的肽基精氨酸脱氨酶(PAD)酶可能是胰腺癌患者发生P53点突变的原因。牙龈卟啉单胞菌、中间普雷沃特氏菌、连翘坦纳氏菌和齿密螺旋体都具有PAD酶,在胰腺癌患者中也检测到了P53精氨酸突变。此外,Pro等位基因p53Arg72-Pro是该癌发生的危险因素。抗P。与健康对照组相比,胰腺癌患者的牙龈抗体效价更高。如果能在P53精氨酸突变的患者身上检测到牙龈假单胞菌的DNA或抗体,就可以检验上述假说。如果这一假说属实,它可能会揭示胰腺癌的真正原因,而胰腺癌是一种致命的疾病。为了证实这一假设,有必要进行进一步的研究。
Carcinoma of exocrine pancreas is the fourth leading cause of cancer deaths, worldwide. The prevalence of this disease is very high in patients with chronic pancreatitis. Orodigestive cancers are frequently seen in patients with periodontitis. These findings suggest that this type of cancer may have some bacterial origins. This study hypothesizes that the peptidyl arginine deaminase (PAD) enzymes found in oral bacteria may be responsible for the p53 point mutations that occur in patients with pancreatic cancer. Porphyromonas gingivalis, Prevotella intermedia, Tannerella forsythia, and Treponema denticola possess the PAD enzyme, and p53 arginine mutations have been detected in patients with pancreatic cancer. Moreover, the Pro allele p53Arg72-Pro is a risk factor for the development of this cancer. Anti-P. gingivalis antibody titers have been found to be higher in patients with pancreatic cancer as compared to healthy controls. The hypothesis in question can be tested if the DNA of P. gingivalis or the antibodies against P. gingivalis can be detected in patients with the p53 arginine mutation.If this hypothesis is true, it could reveal the real cause of pancreatic cancer, which is a fatal disease. Further studies are necessary in order to confirm this hypothesis.
DOI: 10.1093/carcin/bgs112
发表时间: 2012-05-01
期刊: CARCINOGENESIS
影响因子: 4.7
作者:
Ahn, Jiyoung;Segers, Stephanie;Hayes, Richard B.
通讯作者: Hayes, Richard B.