瘦素、雌激素及其受体与肺腺癌临床相关性研究

doi:10.3760/cma.j.issn.1673422X.2015.09.003

摘要/Abstract

摘要： 目的探讨瘦素、雌激素及雌激素受体（ER）在肺腺癌中的表达及意义。方法对58例肺腺癌（肺腺癌组）、63例肺鳞状细胞癌（肺鳞状细胞癌组）及50例正常肺组织（正常对照组）标本，用免疫组织化学法检测瘦素和ER的表达，同时检测患者静脉血中雌激素水平，比较瘦素、雌激素及ER在肺腺癌与肺鳞状细胞癌、正常组织中表达的差异，分析其与肺腺癌临床病理学特征间的相关性。结果瘦素、雌激素及ER在肺腺癌组中阳性率分别为65.5%、36.2%、58.6%，在肺鳞状细胞癌组中的阳性率分别为33.3%、15.9%、30.2%，两组比较差异有统计学意义（χ2=4.324, P＜0.050; χ2=5.372, P＜0.050; χ2=5.718, P＜0.050）；三者在正常对照组中的阳性率分别为24.0%、4.0%和0，与肺腺癌组比较差异有统计学意义（χ2= 7.126, P＜0.010; χ2= 9.683, P＜0.005; χ2=22.308, P＜0.005）。瘦素、雌激素及ER与肺腺癌肿瘤临床分期(χ2=0.001, P=0.950; χ2=0.061, P=0.900; χ2=0.178, P=0.750)、原发灶大小(χ2=0.023, P=0.900; χ2=0.001, P=0.950; χ2=0.001, P=0.950)无关。结论瘦素、雌激素及ER在肺腺癌组织中均呈现高表达，与肺腺癌的发生、发展和临床类型可能存在一定相关性，与肺腺癌临床病理学特征间无明显相关性。

Abstract: ObjectiveTo study the expressions and significances of leptin, estrogen and estrogen receptor (ER) in pulmonary squamous carcinoma and adenocarcinoma. MethodsThe expressions of leptin and estrogen receptor were detected in 58 cases of lung adenocarcinoma and 63 cases of pulmonary squamous cell carcinoma and 50 cases of normal lung tissue samples by immunohistochemical menthod, the levels of estrogen were also detected in patients with venous blood at the same time. Comparison of differential expression of leptin, estrogen and estrogen receptor in lung adenocarcinoma and lung squamous cell carcinoma, normal tissues, and explore their relationships with lung adenocarcinoma. ResultsLeptin, estrogen and estrogen receptor positive rates in lung adenocarcinoma group were 65.5%, 36.2% and 58.6% respectively, and 33.3%, 15.9%, 30.2% in lung squamous cell carcinoma group. There were a statistical difference between the two groups (χ2=4.324, P<0.050; χ2=5.372, P<0.050; χ2=5.718, P<0.050). In the normal control group the positive rates were 24.0%, 4.0% and 0 respectively, and there was a statistical difference compared with lung adenocarcinoma group (χ2=7.126, P<0.010; χ2=9.683, P<0.005; χ2=22.308, P<0.005). In lung adenocarcinoma group, leptin, estrogen and estrogen receptor positive rate have no relationships with tumor stage (χ2=0.001, P=0.950; χ2=0.061, P=0.900; χ2=0.178, P=0.750) and primary tumor size (χ2=0.023, P=0.900; χ2=0.001, P=0.950; χ2=0.001, P=0.950). ConclusionLeptin, estrogen and ER were expressed highly in adenocarcinoma of lung tumor. The expressions of leptin, estrogen and ER may associated with the carcinogenesis, development and clinical type of adenocarcinoma of lung.

郭嘉漪, 章龙珍, 杨成喜. 瘦素、雌激素及其受体与肺腺癌临床相关性研究[J]. 国际肿瘤学杂志, 2015, 42(8): 649-.

GUO Jia-Yi, ZHANG Long-Zhen, YANG Cheng-Xi. The clinical significance research between leptin, estrogen, estrogen receptor and lung adenocarcinoma[J]. Journal of International Oncology, 2015, 42(8): 649-.

参考文献

1］ Mendonsa AM, Chalfant MC, Gorden LD, et al. Modulation of the leptin receptor mediates tumor growth and migration of pancreatic cancer cells［J］. PLoS One, 2015, 10(4): e0126686. ［2］ Schmidt S, Monk JM, Robinson LE, et al. The integrative role of leptin, oestrogen and the insulin family in obesityassociated breast cancer: potential effects of exercise［J］. Obes Rev, 2015, 16(6): 473487. ［3］ Howell A, Pippen J, Elledge RM, et al. Fulvestrant versus anastrozole for the treatment of advanced breast carcinoma: a prospectively planned combined survival analysis of two multicenter trials［J］. Cancer, 2005, 104(2): 236239. ［4］ Dardeno TA, Chou SH, Moon HS, et al. Leptin in human physiology and therapeutics［J］. Front Neuroendocrinol, 2010, 31(3):377393. ［5］ Marquez Garban DC, Chen HW, Fishbein MC, et al. Estrogen recepyor signaling pathways in human nonsmall cell lung cancer［J］. Steroids, 2007, 72(2):135143. ［6］ Garofalo C, Surmacz E. Leptin and cancer［J］. J Cell Physiol, 2006, 207(1): 1222. ［7］ Miycahi Y, Funahashi T, Tanka S, et al. High expression of leptin receptor mRNA in breast cancer tissues predicts poor prognosis for patients with, but not low, serum leptin levels［J］. Int J Cancer, 2006, 118(6): 14141419. ［8］ Cao R, Brakenhiclm E, Wahlestedt C, et al. Leptin induces vascular permeability and synergistically stimulates angiogenesis with PGF2 and VEGF［J］. Proc Natl Acad Sci USA, 2001, 98(11): 63906395. ［9］ Bouloumié A, Drexler HC, Lafontan M, et al. Leptin, theproduct of Ob gene, promotes angiogenesis［J］. Circ Res, 1998, 83(10): 10591066. ［10］ Somasundar P, Mcfadden DW, Hileman SM, et al. Leptin is a growth factor in cancer［J］. J Surg Res, 2004, 116(2): 337349. ［11］ Unsal M, Kara N, Karakus N, et al. Effects of leptin and leptin receptor gene polymorphisms on lung cancer［J］. Tumour Biol, 2014, 35(10): 102311026. ［12］ Tanaka M, Nakaya S, Kumai T, et al. Effects of estrogen on serum leptin levels and leptin mRNA expression in adipose tissue in rate［J］. Horm Res, 2001, 56(34): 98104. ［13］ Pinilla L, Seoane LM, Gonzalea L, et al. Regulation of serum leptin levels by gonadal function in rate［J］. Eur J Endocrinol, 1999, 140(5): 468473. ［14］ Kristensen K, Pedersen SB, Richelsen B. Regulation of leptin by steroid hormones in rat adipose tissue［J］. Biophys Biophys Res Commun, 1999, 259(3): 624630. ［15］ Baig M, Rehman R, Tariq S, et al. Serum leptin levels in polycystic ovary syndrome and its relationship with metabolic and hormonal profile in pakistani females［J］. Int J Endocrinol, 2014, 2014: 132908.