AlM To investigate lor the first time p16/CDKN2 gene expres-sion at proten level in human gastric cancer.p16/CDKN2 gene is a newly identidied lumor suppresser gene and has been shown to be deleted,mutated,or rearrange...AlM To investigate lor the first time p16/CDKN2 gene expres-sion at proten level in human gastric cancer.p16/CDKN2 gene is a newly identidied lumor suppresser gene and has been shown to be deleted,mutated,or rearranged in numerous human tumors.Recently,homozygous deletion of the p16/CDKN2 gene has been reported in gastric cancer cell Iines with high Irequency,but none In surgical specimens ol gastric adenocarcinomas by Southern blot and SSCP analysis.METHODS The expression level ol p16 protein was analyzed informalin-loxed,paraffin-embedded tissue sections from 30 cases of gastric carcinomas and 20 cases of nomal gastric mucosa us-Ing a sensitive and specifie immunochemical technique with protein A-gold probe.RESULTS In normal controls all the samples expressed p16protein,the mean percenlage ol p16 protein-positive cells was 72.55%±17.22%(42%to 100%),whereas in cacer cases itwas 54.9%±28.9%which was much lower than that of nomalconlrols(P<0.05).Among cancer cases 23.33%(7/30)of specimens showed reduced expression of p16 protein and 10%(3/30)expressed no p16 protein.In additron,overexpression olp16 protein was also observed in one case.CONCLUSION Abnormal expression oi p16 protein 1s involvedIn gastric carcinoma and immunochemical technique may accu-rately reveal the expression of p16 protein,thus being more uselul In clinical sludies.展开更多
Objective: The molecular mechanism of prostate cancer is poorly understood. The aim of the study was to investigate the prevalence and prognostic value of promoter hypermethylation of retinoic acid receptor beta (RARB...Objective: The molecular mechanism of prostate cancer is poorly understood. The aim of the study was to investigate the prevalence and prognostic value of promoter hypermethylation of retinoic acid receptor beta (RARB) and p16 among benign prostatic hyperplasia (BPH) and prostate cancer patients. Methods: In this case-control study, 63 patients were included in three groups; 21 with BPH as the control group, 21 with prostate cancer and good prognostic factors (based on prostate-specific antigen, Gleason score and stage) as good prognosis group, and 21 with prostate cancer and poor prognostic features as poor prognosis group. The prostate biopsy specimen of each individual was examined for hypermethylation of RARB and p16 promoters by methylation specific PCR (MSPCR). Results: Seven (33.3%) patients with good prognosis and 15 (71.4%) patients with poor prognosis were positive for RARB methylation, which were significantly higher than controls (P <0.0001). p16 promoter methylation was shown in 19.0% and 47.6% patients with good and poor prognosis, respectively. The RARB and p16 promoter methylation in the poor prognosis group was significantly higher than that in the good prognosis group (P =0.02 for RARB and P<0.0001 for p16). Conclusion: Hypermethylation of RARB and p16 promoters may predict prognosis in prostate cancer.展开更多
Objective To study on the CDKN2/P16gene in prim ary osteosarcoma.Method By using molecular biological methods that inclued genome DNA extraction from p araffined tissue and PCR-SSCP analy sis technique,we studied alte...Objective To study on the CDKN2/P16gene in prim ary osteosarcoma.Method By using molecular biological methods that inclued genome DNA extraction from p araffined tissue and PCR-SSCP analy sis technique,we studied alternations of CDKN2/P16gene in 25primary osteosarcomas.Results(1)The deletions frequency in differen tiation degree of osteosarcomas was①bone brood cell,16.7%;②cartilage brood cell,12.5%;③Fiber brood cell:20%,(P >0.05).(2)The deletion frequency in male patie nts was 17.6%,female pa-tients 12.5%,(P >0.05).(3)In early metastatic osteosarcomas t he deletion rate was 33.3%,which was significantly higher than that of th e control group with the rate of 10.5%(P <0.05).(4)The deletion rate was 16%and the muta tions were not found.Conclusion(1)The deletion rate was 16%and the mutatio ns were not found.This suggests that the deletions of CDKN2/P16gene were closely related to the genesis of primary osteosarcoma and that the main type of the alternation of CDKN2/P16gene was deletion.(2)In early metastatic osteosaarcomas the deletion rate was 33.3%,which was significantly higher than that of the c ontrol group with the rate of 10.5%.T his indicates to great extend that the deletions of CDKN2/P16gene were closely related to the metastat ic ability.(3)The deletions frequency had no signi ficant relationship with differentiation degree of oste osarcomas,so was with the sex of the p atient.展开更多
AIM To investigate the relationship between the expression of p16 gene and the gastric carcinogenesis,depth of invasion and lymph node metastases, and to evaluate the deletion and mutation of exon 2 in p16 gene in gas...AIM To investigate the relationship between the expression of p16 gene and the gastric carcinogenesis,depth of invasion and lymph node metastases, and to evaluate the deletion and mutation of exon 2 in p16 gene in gastric carcinoma.METHODS The expression of P16 protein was examined by streptavidin-peroxidase conjugated method (S-P); the deletion and mutation of p16 gene were respectively examined by polymerase chain reaction (PCR) and polymerase chain reaction single-strand conformation polymorphism analysis (PCR-SSCP) in gastric carcinoma.RESULTS Expression of P16 protein was detected in 96.25% (77/80) of the normal gastric mucosa, in 92.00% (45/50) of the dysplastic gastric mucosa and in 47.54% (58/122) of the gastric carcinoma. The positive rate of P16 protein expression in gastric carcinoma was significantly lower than that in normal gastric mucosa and dysplastic gastric mucosa (P＜0.05). The positive rate of P16 protein expression in mucoid carcinoma 10.00% (1/ 10) was significantly lower than that in poorly differentiated carcinoma 51.22% ( 21/ 41 ),undifferentiated carcinoma 57.69% (15/26) and signet ring cell carcinoma 62.50% (10/ 16) (P＜0.05). The positive rate of p16 protein in 30 cases paired primary and lymph node metastatic gastric carcinoma: There was 46.67% (14/30) in primary gastric carcinoma, 16.67% (5/30) in lymph node metastatic gastric carcinoma. The positive rate of lymph node metastatic carcinoma was significantly lower than that of primary carcinoma (P＜0.05). There was of p16 gene mutation in exon 2, but 5 cases displayed deletion of p16 gene in exon 2 in the 25 primary gastric carcinomas.CONCLUSIONS The expression loss of P16 protein related to the gastric carcinogenesis, gastric carcinoma histopathological subtypes and lymph metastasis. The mutation of p16 gene in exon 2 may not be involved in gastric carcinogenesis. But the deletion of p16 gene in exon 2 may be involved in gastric carcinogenesis.展开更多
文摘AlM To investigate lor the first time p16/CDKN2 gene expres-sion at proten level in human gastric cancer.p16/CDKN2 gene is a newly identidied lumor suppresser gene and has been shown to be deleted,mutated,or rearranged in numerous human tumors.Recently,homozygous deletion of the p16/CDKN2 gene has been reported in gastric cancer cell Iines with high Irequency,but none In surgical specimens ol gastric adenocarcinomas by Southern blot and SSCP analysis.METHODS The expression level ol p16 protein was analyzed informalin-loxed,paraffin-embedded tissue sections from 30 cases of gastric carcinomas and 20 cases of nomal gastric mucosa us-Ing a sensitive and specifie immunochemical technique with protein A-gold probe.RESULTS In normal controls all the samples expressed p16protein,the mean percenlage ol p16 protein-positive cells was 72.55%±17.22%(42%to 100%),whereas in cacer cases itwas 54.9%±28.9%which was much lower than that of nomalconlrols(P<0.05).Among cancer cases 23.33%(7/30)of specimens showed reduced expression of p16 protein and 10%(3/30)expressed no p16 protein.In additron,overexpression olp16 protein was also observed in one case.CONCLUSION Abnormal expression oi p16 protein 1s involvedIn gastric carcinoma and immunochemical technique may accu-rately reveal the expression of p16 protein,thus being more uselul In clinical sludies.
文摘Objective: The molecular mechanism of prostate cancer is poorly understood. The aim of the study was to investigate the prevalence and prognostic value of promoter hypermethylation of retinoic acid receptor beta (RARB) and p16 among benign prostatic hyperplasia (BPH) and prostate cancer patients. Methods: In this case-control study, 63 patients were included in three groups; 21 with BPH as the control group, 21 with prostate cancer and good prognostic factors (based on prostate-specific antigen, Gleason score and stage) as good prognosis group, and 21 with prostate cancer and poor prognostic features as poor prognosis group. The prostate biopsy specimen of each individual was examined for hypermethylation of RARB and p16 promoters by methylation specific PCR (MSPCR). Results: Seven (33.3%) patients with good prognosis and 15 (71.4%) patients with poor prognosis were positive for RARB methylation, which were significantly higher than controls (P <0.0001). p16 promoter methylation was shown in 19.0% and 47.6% patients with good and poor prognosis, respectively. The RARB and p16 promoter methylation in the poor prognosis group was significantly higher than that in the good prognosis group (P =0.02 for RARB and P<0.0001 for p16). Conclusion: Hypermethylation of RARB and p16 promoters may predict prognosis in prostate cancer.
文摘Objective To study on the CDKN2/P16gene in prim ary osteosarcoma.Method By using molecular biological methods that inclued genome DNA extraction from p araffined tissue and PCR-SSCP analy sis technique,we studied alternations of CDKN2/P16gene in 25primary osteosarcomas.Results(1)The deletions frequency in differen tiation degree of osteosarcomas was①bone brood cell,16.7%;②cartilage brood cell,12.5%;③Fiber brood cell:20%,(P >0.05).(2)The deletion frequency in male patie nts was 17.6%,female pa-tients 12.5%,(P >0.05).(3)In early metastatic osteosarcomas t he deletion rate was 33.3%,which was significantly higher than that of th e control group with the rate of 10.5%(P <0.05).(4)The deletion rate was 16%and the muta tions were not found.Conclusion(1)The deletion rate was 16%and the mutatio ns were not found.This suggests that the deletions of CDKN2/P16gene were closely related to the genesis of primary osteosarcoma and that the main type of the alternation of CDKN2/P16gene was deletion.(2)In early metastatic osteosaarcomas the deletion rate was 33.3%,which was significantly higher than that of the c ontrol group with the rate of 10.5%.T his indicates to great extend that the deletions of CDKN2/P16gene were closely related to the metastat ic ability.(3)The deletions frequency had no signi ficant relationship with differentiation degree of oste osarcomas,so was with the sex of the p atient.
基金the grant from the Teaching Committee of HunanProvince,No.97B095the"8th 5-year Plan"of Health Department of Hunan Province,No.9301
文摘AIM To investigate the relationship between the expression of p16 gene and the gastric carcinogenesis,depth of invasion and lymph node metastases, and to evaluate the deletion and mutation of exon 2 in p16 gene in gastric carcinoma.METHODS The expression of P16 protein was examined by streptavidin-peroxidase conjugated method (S-P); the deletion and mutation of p16 gene were respectively examined by polymerase chain reaction (PCR) and polymerase chain reaction single-strand conformation polymorphism analysis (PCR-SSCP) in gastric carcinoma.RESULTS Expression of P16 protein was detected in 96.25% (77/80) of the normal gastric mucosa, in 92.00% (45/50) of the dysplastic gastric mucosa and in 47.54% (58/122) of the gastric carcinoma. The positive rate of P16 protein expression in gastric carcinoma was significantly lower than that in normal gastric mucosa and dysplastic gastric mucosa (P＜0.05). The positive rate of P16 protein expression in mucoid carcinoma 10.00% (1/ 10) was significantly lower than that in poorly differentiated carcinoma 51.22% ( 21/ 41 ),undifferentiated carcinoma 57.69% (15/26) and signet ring cell carcinoma 62.50% (10/ 16) (P＜0.05). The positive rate of p16 protein in 30 cases paired primary and lymph node metastatic gastric carcinoma: There was 46.67% (14/30) in primary gastric carcinoma, 16.67% (5/30) in lymph node metastatic gastric carcinoma. The positive rate of lymph node metastatic carcinoma was significantly lower than that of primary carcinoma (P＜0.05). There was of p16 gene mutation in exon 2, but 5 cases displayed deletion of p16 gene in exon 2 in the 25 primary gastric carcinomas.CONCLUSIONS The expression loss of P16 protein related to the gastric carcinogenesis, gastric carcinoma histopathological subtypes and lymph metastasis. The mutation of p16 gene in exon 2 may not be involved in gastric carcinogenesis. But the deletion of p16 gene in exon 2 may be involved in gastric carcinogenesis.
