title: Loss of RASSF1A expression in colorectal cancer and its association with K-ras status.
abstract: BACKGROUND
  The RAS-association domain family 1 A (RASSF1A) is a classical member of RAS effectors regulating cell proliferation and apoptosis. Loss of RASSF1A expression may shift the balance towards a growth-promoting effect without the necessity of activating K-ras mutations. Its potential association with K-ras mutations in colorectal cancer (CRC) is unclear.
  
  
  METHODS
  RASSF1A expression was examined in normal mucosa, adenoma, and tumor tissues of colon and rectum, respectively. We examined the association of RASSF1A expression, mutations of K-ras, and EGFR status in 76 primary CRCs. The relationship between clinicopathological characteristics and RASSF1A expression was also analyzed.
  
  
  RESULTS
  RASSF1A expression level decreased progressively in normal mucosa, adenoma and, tumor tissues, and the loss of RASSF1A expression occurred more frequently in tumor tissues. Of 76 primary CRCs, loss of RASSF1A expression and/or K-ras mutations were detected in 77% cases. Loss of RASSF1A expression was more frequent in K-ras wild-type than in mutation cases (63% versus 32%, P = 0.011).
  
  
  CONCLUSIONS
  Our study indicates that loss of RASSF1A may be involved in pathogenesis of CRC, its expression was found predominantly in K-ras wild-type CRCs, suggesting that it may be another way of affecting RAS signaling, in addition to K-ras mutations.
authors.affiliation: Department of Medical Oncology, Cancer Center, The State Key Laboratory of Biotherapy, West China Hospital, West China Medical School, Sichuan University, 37 Guo Xue Xiang, Chengdu, Sichuan 610041, China.
authors.forename: Dan
authors.initials: D
authors.lastname: Cao
authors.forename: Ye
authors.initials: Y
authors.lastname: Chen
authors.forename: Yuan
authors.initials: Y
authors.lastname: Tang
authors.forename: Xing-Chen
authors.initials: XC
authors.lastname: Peng
authors.forename: Hang
authors.initials: H
authors.lastname: Dong
authors.forename: Long-Hao
authors.initials: LH
authors.lastname: Li
authors.forename: Ke
authors.initials: K
authors.lastname: Cheng
authors.forename: Jun
authors.initials: J
authors.lastname: Ge
authors.forename: Ji-Yan
authors.initials: JY
authors.lastname: Liu
mesh_terms: D000236:Adenoma / Q000378:metabolism / Q000473:pathology; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D001483:Base Sequence; D015179:Colorectal Neoplasms / Q000235:genetics* / Q000378:metabolism* / Q000473:pathology; D004252:DNA Mutational Analysis; D066246:ErbB Receptors / Q000235:genetics; D005260:Female; D006801:Humans; D007150:Immunohistochemistry; D007413:Intestinal Mucosa / Q000378:metabolism / Q000473:pathology; D008297:Male; D008875:Middle Aged; D008969:Molecular Sequence Data; D011518:Proto-Oncogene Proteins / Q000235:genetics*; D016283:Proto-Oncogene Proteins p21(ras); D025521:Tumor Suppressor Proteins / Q000378:metabolism*; D018631:ras Proteins / Q000235:genetics*
chemical_list: C117307:KRAS protein, human; D011518:Proto-Oncogene Proteins; C411762:RASSF1 protein, human; D025521:Tumor Suppressor Proteins; D066246:ErbB Receptors; D016283:Proto-Oncogene Proteins p21(ras); D018631:ras Proteins