期刊文献+

胰腺癌的分子病理学研究进展 被引量:4

Progression on molecular pathology of pancreatic cancer
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摘要 胰腺癌是一种致死性极高的恶性肿瘤,且治疗效果不佳,预后极差。近年来基础实验分子技术的发展为胰腺癌发生分子机制的研究提供了平台。更好的明确胰腺癌的分子病理特点对于胰腺癌的早期诊断、治疗和预后具有重大意义。笔者对胰腺癌分子病理学的最新研究进展进行综述。 Pancreatic cancer is a highly lethal malignancy that responds poorly to current treatments and therefore has a dismal survival rate. Current progress in experimental molecular techniques has enabled detailed understanding of the molecular processes of pancreatic cancer development. Understanding of the molecular pathology should promote the development of new methodology for early diagnosis of pancreatic cancer, facilitate improvement in current approaches for pancreatic cancer treatment and improve its prognosis. Here, the authors present the current knowledge about the molecular alterations found in pancreatic cancer.
出处 《中国普通外科杂志》 CAS CSCD 北大核心 2014年第9期1253-1257,共5页 China Journal of General Surgery
基金 辽宁省科技计划资助项目(2006225001-10)
关键词 胰腺肿瘤/病因学 病理过程 信号传导 综述文献 Pancreatic Neoplasms/etiol Pathologic Processes Signal Transduction Review
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参考文献42

  • 1Chu D, Kohlmann W, Adler DG. Identification and screening of individuals at increased risk for pancreatic cancer with emphasis on known environmental and genetic factors and hereditary syndromes[J].JOP, 2010, 11(3):203-212.
  • 2Collins MA, Pasca di Magliano M. Kras as a key oncogene and therapeutic target in pancreatic cancer[J]. Front Physiol, 2014, 4:407.
  • 3Hong SM, Park JY, Hruban RH, et al. Molecular signatures of pancreatic cancer[J]. Arch Pathol Lab Med, 2011,135(6):716-727.
  • 4Lohr M, Kloppel G, Maisonneuve P, et al. Frequency of K-ras mutations in pancreatic intraductalneoplasias associated with pancreatic ductal adenocarcinoma and chronic pancreatitis: a meta- analysis[J]. Neoplasia, 2005, 7(1): 17-23.
  • 5Chen H, Tu H, Meng ZQ, et al. K-ras mutational status predicts poor prognosis in unresectable pancreatic cancer[J]. Eur J SurgOncol, 2010, 36(7):657-662.
  • 6Laheru D, Shah P, Rajeshkumar NV, et al. Integrated preclinical and clinical development of S-trans, trans-Farnesyhhiosalicylic Acid (FTS, Salirasib) in pancreatic cancer[J]. Invest New Drugs, 2012, 30(6):2391-2399.
  • 7Wedon S, Klemp M, Gladhaug IP, et al. Long-term follow-up of patients with resected pancreatic cancer following vaccination against mutant K-ras[J]. Int J Cancer, 2011,128(5): 1120-1128.
  • 8杨卫华,王春友,朱求实,阎雷,许州.胰腺癌中p16基因甲基化改变及其蛋白表达分析[J].中国普通外科杂志,2007,16(5):446-450. 被引量:6
  • 9Jeong J, Park YN, Park JS, et al. Clinical significance of p16 protein expression loss and aberrant p53 protein expression in pancreatic cancer[J]. Yonsei Med J, 2005, 46(4):519-525.
  • 10Chang DT, Chapman CH, Norton JA, et al. Expression of pl6(1NK4A) but not hypoxia markers or poly adenosine diphosphate-ribose polymerase is associated with improved survival in patients with pancreatic adenocarcinoma[J]. Cancer, 2010, 116(22):5179-5187.

二级参考文献43

  • 1Yasui W,Yokozaki H,Fujimoto J,et al.Genetic and epigenetic alterations in multistep carcinogenesis of the stomach[J].Gastroenterol,2000,35(12):111-115.
  • 2Kamb A,Gruis NA,Wearer-Feldhaus J,et al.A cell cycle regulator potentially involved in genesis of many tumor types[J].Science,1994,264(5157):436-440.
  • 3Jones PA,Laird PW.Cancer epigenetics comes of age[J].Nat Genet,1999,21(2):163-167.
  • 4Herman J G,Graff J R,Myohanen S,et al.Methylation-specific PCR:A novel PCR assay for methylation status of CpG island[J].Proc Natl Acad Sci USA,1996,93(18):9821-9826.
  • 5Ueki T,Toyota M,Sohn T,et al.Hypermethylation of multiple genes in pancreatic adenocarcinoma[J].Cancer Res,2000,60(7):1835-1839.
  • 6Sato N,Ueki T,Fukushima N,et al.Aberrant methylation of CpG islands in intraductal papillary muci-nous neoplasms of the pancreas[J].Gastroenterology,2002,123(1):365-372.
  • 7Naka T,Kabayashi M,Ashida K,et al.Aberrant p16INK4 expression related to clinical stage and prognosis in patients with pancreatic cancer[J].Int J Oncol,1998,12(5):1111-1116.
  • 8Hu Y X,Watanabe H,Ohtsubo K,et al.Frequent loss of p16 expression and its correlationwith clinicopathological parameters in pancreatic carcinorma[J].Ciln Cancer Res,1997,3(9):1473-1477.
  • 9Herman J G,Merlo A,Mao L,et al.Inactivation and CAKN/p16/MTS1 gene is frequently associated with aberrant DNA methylation in all common human[J].Cancer Research,1995,55(20):4525.
  • 10Gonzale-Znlueta M,Bender CM,Yang AS,et al.Methylation of the 5'CpG island of the p16/CDKN2 tumor suppressor gene in normal and transformed tissues correlates with gene silencing[J].Cancer Res-earch,1995,55(20):4531.

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  • 1DeSantis CE, Lin CC, Mariotto AB, et al. Cancer treatment andsurvivorship statistics, 2014[J]. CA Cancer J Clin, 2014,64(4):252-271.
  • 2Heard ME, Simmons CD, Simmen FA, et al. Kruppel-like factor9 deficiency in uterine endometrial cells promotes ectopic lesionestablishment associated with activated notch and hedgehogsignaling in a mouse model of endometriosis[J]. Endocrinology,2014,155(4):1532-1546.
  • 3Ohguchi H, Tanaka T, Uchida A, et al. Hepatocyte nuclear factor4alpha contributes to thyroid hormone homeostasis by cooperativelyregulating the type 1 iodothyronine deiodinase gene with GATA4and Kruppel-like transcription factor 9[J], Mol Cell Biol, 2008,28(12):3917-3931.
  • 4Ying M, Sang Y, Li Y, et al. Kruppel-Like Family of TranscriptionFactor 9, a Differentiation-Associated Transcription Factor,Suppresses Notch 1 Signaling and Inhibits Glioblastoma-InitiatingStem Ce!ls[J], Stem Cells, 2011(1):20-31.
  • 5Pabona JM, Velarde MC, Zeng Z, et al. Nuclear receptor co-regulator Kriippel-like factor 9 and prohibitin 2 expression inestrogen-induced epithelial cell proliferation in the mouse uterus[J].J Endocrinol, 2009, 200(1):63-73.
  • 6Pabona JM, Simmen FA, Nikiforov MA, et al. Kruppel-like factor 9and progesterone receptor coregulation of decidualizing endometrialstromal cells: implications for the pathogenesis of endometriosis[J].J Clin Endocrinol Metab, 2012,97(3):E376-392.
  • 7Fu DZ, Cheng Y, He H, et al. The fate of Kruppel-like factor9-positive hepatic carcinoma cells may be determined by theprogrammed cell death protein 5[J], Int J Oncol, 2014,44(1): 153-160.
  • 8Shen P, Sun J, Xu G, et al. KLF9, a transcription factor inducedin flutamide-caused cell apoptosis, inhibits AKT activation andsuppresses tumor growth of prostate cancer cells[J]. Prostate, 2014,74(9):946-958.
  • 9Huang Y, Ju B, Tian J, et al. Ovarian cancer stem cell-specific geneexpression profiling and targeted drug prescreening[J]. Oncol Rep,2014,31(3):1235-1248.
  • 10Ying M, Tilghman J, Wei Y, et al. Kruppel-like factor-9 (KLF9)inhibits glioblastoma sternness through global transcriptionrepression and integrin a6 inhibition[J]. J Biol Chem, 2014,289(47):32742-32756.

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