title: [Observations on expression of c-fos and c-myc genes and activity of PDGFBB autocrine loop in 67 human gliomas].
abstract: OBJECTIVE
  To investigate the variance of expression of c-fos and c-myc genes and the activity of platelet-derived growth factor (PDGF) BB autocrine loop in human gliomas as well as their relationship.
  
  
  METHODS
  In situ hybridization and immunohistochemistry were used to study 67 human glioma specimens of different grades.
  
  
  RESULTS
  The incidences, of positive expression for c-fos mRNA, c-fos protein, c-myc mRNA and c-myc protein were 100% (67/67), 100% (67/67), 85.1% (57/67) and 83.6% (56/67) respectively. There was significant positive correlation between the positive cell densities of c-fos mRNA (92.49 +/- 33.87) and c-fos protein (91.64 +/- 38.11), and of c-myc mRNA (72.70 +/- 40.56) and c-myc protein (71.49 +/- 41.11, r = 0.917 - 0.988, P < 0.001). All of them also increased correspondingly with the malignant degree of the tumors and level of PDGFB mRNA expression in the tumor cells (P < 0.05 - 0.01). Not only were the positive cell densities of PDGF alpha receptor (58.46 +/- 28.77), PDGF beta receptor (63.03 +/- 31.63) and phosphotyrosine protein (68.25 +/- 29.30) correlated positively with one another (r = 0.827 - 0.896, P < 0.001), but they also all correlated positively with the positive cell densities of PDGFB mRNA, c-fos mRNA, c-fos protein, c-myc mRNA and c-myc protein respectively (r = 0.615 - 0.888, P < 0.001).
  
  
  CONCLUSIONS
  The abnormally increased activity of the PDGFBB autocrine loop possibly upregulated the overexpression of c-fos and c-myc genes in glioma cells and suggested that c-fos and c-myc proteins probably played an important role as downstream response factors in the signaling pathway in which PDGFBB could induce gliocyte transformation and glioma development.
authors.affiliation: Department of Neuropathology, Neurology Institute, Tianjin Medical University General Hospital, Tianjin 300052.
authors.forename: S
authors.initials: S
authors.lastname: Yu
authors.forename: P
authors.initials: P
authors.lastname: Pu
authors.forename: D
authors.initials: D
authors.lastname: Jiang
authors.forename: Y
authors.initials: Y
authors.lastname: Cheng
authors.forename: T
authors.initials: T
authors.lastname: An
authors.forename: X
authors.initials: X
authors.lastname: Guan
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D000077214:Becaplermin; D002648:Child; D002675:Child, Preschool; D005260:Female; D015972:Gene Expression Regulation, Neoplastic; D005910:Glioma / Q000235:genetics / Q000378:metabolism / Q000473:pathology*; D006801:Humans; D007150:Immunohistochemistry; D017403:In Situ Hybridization; D008297:Male; D008875:Middle Aged; D019000:Phosphotyrosine / Q000378:metabolism; D010982:Platelet-Derived Growth Factor / Q000235:genetics* / Q000378:metabolism; D016760:Proto-Oncogene Proteins c-fos / Q000235:genetics* / Q000378:metabolism; D016271:Proto-Oncogene Proteins c-myc / Q000235:genetics* / Q000378:metabolism; D020574:Proto-Oncogene Proteins c-sis; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D020796:Receptor, Platelet-Derived Growth Factor alpha / Q000378:metabolism; D020797:Receptor, Platelet-Derived Growth Factor beta / Q000378:metabolism
chemical_list: D010982:Platelet-Derived Growth Factor; D016760:Proto-Oncogene Proteins c-fos; D016271:Proto-Oncogene Proteins c-myc; D020574:Proto-Oncogene Proteins c-sis; D012333:RNA, Messenger; D000077214:Becaplermin; D019000:Phosphotyrosine; D020796:Receptor, Platelet-Derived Growth Factor alpha; D020797:Receptor, Platelet-Derived Growth Factor beta