From the *Department of Epidemiology, Indiana University Richard M. Fairbanks School of Public Health at IUPUI; †Melvin Bren Simon Cancer Center, Indiana University, Indianapolis, IN; ‡Department of Biostatistics, Fay W. Boozman College of Public Health, University of Arkansas for Medical Sciences, Little Rock, AR; §Department of Molecular Biology, College of Life Sciences, Hebei United University, Tangshan, China; ∥Division of Epidemiology and Community Health, School of Public Health, and ¶Masonic Cancer Center, University of Minnesota, Minneapolis, MN.
Pancreas. 2014 Mar;43(2):281-6. doi: 10.1097/MPA.0b013e3182a7c829.
Accumulating evidence suggests that energy imbalance plays a role in pancreatic carcinogenesis. However, it remains unclear whether single-nucleotide polymorphisms (SNPs) in genes regulating energy homeostasis influence pancreatic cancer risk. We investigated this question in a case-control study conducted from 1994 to 1998.
Patients (n = 173) were ascertained from hospitals in the Twin Cities and Mayo Clinic, Minnesota. Control subjects (n = 476) were identified from the general population and frequency matched to patients by age and sex. Seven SNPs were evaluated in relation to pancreatic cancer using unconditional logistic regression.
After adjustment for confounders, the leucine/proline or proline/proline genotype of the neuropeptide Y (NPY) gene rs16139 was associated with a lower risk than the leucine/leucine genotype (odds ratio, 0.40 [95% confidence interval, 0.15-0.91]). Conversely, an increased risk was observed for the glycine/arginine or arginine/arginine genotype of the adrenoceptor β2, surface (ADRB2) gene rs1042713 as compared with the glycine/glycine genotype (odds ratio, 1.52 [95% confidence interval, 1.01-2.31]).
This study first reveals that SNPs in genes modulating energy intake (NPY) and energy expenditure (ADRB2) altered pancreatic cancer risk. If confirmed by other studies, our findings may shed new light on the etiology and prevention of pancreatic cancer.
越来越多的证据表明，能量失衡在胰腺癌发生中起作用。然而，调节能量平衡的基因中单核苷酸多态性（SNP）是否影响胰腺癌风险尚不清楚。我们在 1994 年至 1998 年进行的病例对照研究中调查了这个问题。
从明尼苏达州双子城和梅奥诊所的医院确定患者（n = 173）。对照受试者（n = 476）从一般人群中确定，并按年龄和性别与患者进行频率匹配。使用非条件逻辑回归评估与胰腺癌相关的 7 个 SNP。
在调整混杂因素后，神经肽 Y（NPY）基因 rs16139 的亮氨酸/脯氨酸或脯氨酸/脯氨酸基因型与较低的风险相关，而亮氨酸/亮氨酸基因型（比值比，0.40 [95%置信区间，0.15-0.91]）。相反，与甘氨酸/甘氨酸基因型相比，肾上腺素能受体β2、表面（ADRB2）基因 rs1042713 的甘氨酸/精氨酸或精氨酸/精氨酸基因型观察到风险增加（比值比，1.52 [95%置信区间，1.01-2.31]）。
本研究首次揭示了调节能量摄入（NPY）和能量消耗（ADRB2）的基因中的 SNP 改变了胰腺癌风险。如果其他研究得到证实，我们的发现可能为胰腺癌的病因和预防提供新的线索。
