The Expressions And Significances Of ICAD,Ki-67 And PTEN In Nasal Polyps

Objectives: To explore the molecular mechanism of nasal polyps' pathogenesis via examining the expression of Inhibitor of Caspase-activated Dnase(ICAD) , Ki-67 antigen and Phosphatase and Tensin Homolog deleted on Chromosome 10(PTEN) in human nasal polyps(NP). Furthermore, by researching the relationship between the expressive intensity of ICAD, Ki-67 and PTEN and the recrudescent rate of postoperative patients, to find a molecule-level approach which can prejudge the possibility of recrudescence.Methods: Choosing randomly 40 cases from the preserved blocks of nasal polyps patients who were followed at least 12 months after FESS operation. 6 cases of normal uncinate process mucosa were served as contrast. With polyclonal anti-human DFF45(ICAD), monoclonal anti-human Ki-67 nuclear antigen and monoclonal anti- human PTEN, immunohistochemistry SP method was used to examine the expression of ICAD, Ki-67 及 PTEN in every case. Beige or puce granules appearing in NP cells were regarded as positive signal. Every case was observed randomly for five eyeshots (microscope ×400).The results were judged by semi-quantificational integral standard. All the data were disposed by statistics.Results: Of the 40 NP cases, ICAD positive were 27, positive rate was 67. 5 % (27/40), cytoplasm coloration, the main location was in gland epitheliumcells. Of the contrast, ICAD positive was none. Ki-67 positive were 23, positive rate was 57. 5% (23/40), caryon coloration, the main location was in the epidermis cells of polyps. One of the contrast was positive, positive rate was 16.67% (1/6) . PTEN positive were 21, positive rate was 52.5% (21/40) .cytoplasm coloration, the main location was in the epidermis cells of polyps. All of the contrast were positive, positive rate was 100%(6/6). The expressive intensity of ICAD^ PTEN between NP and normal mucosa were statistical different (P<0. 05) . Contrarily, there was no statistical difference in the expressive intensity of Ki-67 between NP and normal mucosa (P>0. 05) .The expressive intensity of ICAD^ PTEN between different clinical classifications of NP showed statistical difference (P<0. 05) . However, the expressive intensity of Ki-67 between different classifications of NP didn' t have statistical difference(P>0. 05) .There was a positive correlation between co-expressive intensity of ICAD and Ki —67 and NP classifications differentiated by type and stage (R ' .=0.607, P<0. 005) . Being completely contrary, for PTEN, it was a negative correlation(R ' s= -0. 629, P<0. 005). Furthermore, between the co-expressive intensity of ICAD and Ki —67 and the recrudescence rate of postoperative patients , a positive linear correlation was presented(R=0. 9589, t=4, 7778, P<0. 05 ) .For PTEN, it showed a negative linear correlation (R=-0.9991, t=33. 30, P<0. 001) .Conclusions: ICAD plays an important role in the genesis and development of the glands of NP. There is an obvious PTEN gene mutation and/or obstruction of gene expression in NP epidermis cells. In the pathogenesis of NP, the heightening of cell proliferative potential of NP probably acts as a subordinate role, the principal factor is that normal apoptosis is restrained. There is a positive correlation between the classifications of NP and the depressed extent of apoptosis. Examining ICAD^ Ki-67 andPTEN synchronously can be considered as a credible method by which we can forecast the probability of postoperative recrudescence of individual NP patient.