Neural stem cells(NSCs) and imprinted genes play an important role in brain development. On historical grounds, these two determinants have been largely studied independently of each other. Recent evidence suggests, h...Neural stem cells(NSCs) and imprinted genes play an important role in brain development. On historical grounds, these two determinants have been largely studied independently of each other. Recent evidence suggests, however, that NSCs can reset select genomic imprints to prevent precocious depletion of the stem cell reservoir. Moreover, imprinted genes like the transcriptional regulator Zac1 can fine tune neuronal vs astroglial differentiation of NSCs. Zac1 binds in a sequence-specific manner to pro-neuronal and imprinted genes to confer transcriptional regulation and furthermore coregulates members of the p53-family in NSCs. At the genome scale, Zac1 is a central hub of an imprinted gene network comprising genes with animportant role for NSC quiescence, proliferation and differentiation. Overall, transcriptional, epigenomic, and genomic mechanisms seem to coordinate the functional relationships of NSCs and imprinted genes from development to maturation, and possibly aging.展开更多
Summary: In situ hybridization was applied to locate and detect the expression of p57 KIP2 in hydatidiform mole (5 cases of partial hydatidiform mole and 18 cases of complete hydatidiform mole) and normal villi (23...Summary: In situ hybridization was applied to locate and detect the expression of p57 KIP2 in hydatidiform mole (5 cases of partial hydatidiform mole and 18 cases of complete hydatidiform mole) and normal villi (23 cases). The positive signals of p57 KIP2 expression were analyzed by HPIAS-1000 Image-Analysis System. p57 KIP2 was highly expressed in normal villi but showed distinct low expression in hydatidiform mole (P<0.01). Furthermore, the locus of low expression of p57 KIP2 accorded with the place where lesion of trophoblast occurred. Detection of p57 KIP2 made it possible to study the genetics of hydatidiform mole at the transcriptional level. Low expression of p57 KIP2 could be a molecular marker in hydatidiform mole and a target for therapy.展开更多
AIM: To investigate the expression of p57kip2 and its relationship with clinicopathology, PCNA and p53 in primary hepatocellular carcinoma (HCC). METHODS: Expression of p57kip2, PCNA and p53 in tumor tissues from 32 p...AIM: To investigate the expression of p57kip2 and its relationship with clinicopathology, PCNA and p53 in primary hepatocellular carcinoma (HCC). METHODS: Expression of p57kip2, PCNA and p53 in tumor tissues from 32 patients with HCC and 10 liver tissues of normal persons was detected with Elivision immunohistochemical technique. RESULTS: The p57kip2 protein positive-expression rate in HCC was 56.25%, lower than that in normal tissues (100%, P<0.05). The reduced expression of p57kip2 protein correlated significantly with moderate or low differentiation of tumor cells (P = 0.007 <0.05), high clinical stage (P= 0.041 <0.05) and poor prognosis (P= 0.036 <0.05), but did not correlate significantly with metastasis, tumor size, level of AFP and age (P>0.05). The PCNA positive-expression rate was 56.25%, which was correlated significantly with the expression of p57kip2 (P= 0.025<0.05). The p53 positive-expression rate was 46.88%, which was not correlated significantly with the expression of p57kip2 (P>0.05). CONCLUSION: There is a marked loss or absence of p57kip2 expression and high expression of PCNA in HCC, which are involved in carcinogenesis and development of HCC. The p57kip2 and p53 may induce apoptosis via different mechanisms.展开更多
AIM: To investigate the effects of p57^kip2, cyclinE protein and proliferating cell nuclear antigen (PCNA) on occurrence and progression of human pancreatic cancer. METHODS: The expression of p57^kip2, cyclinE pro...AIM: To investigate the effects of p57^kip2, cyclinE protein and proliferating cell nuclear antigen (PCNA) on occurrence and progression of human pancreatic cancer. METHODS: The expression of p57^kip2, cyclinE protein and PCNA in tumor tissues and adjacent tissues from 32 patients with pancreatic cancer was detected by SP immunohistochemical technique. RESULTS: The positive expression rate of p57^kip2 protein in tumor tissues was 46.9%, which was lower than that in adjacent pancreatic tissues (χ^2 = 5.317, P〈0.05). p57^kip2 protein positive expression remarkably correlated with tumor cell differentiation (P〈0.05), but not with lymph node metastasis (P〉0.05). The positive expression rate of cyclinE protein in tumor tissues was 68.8%, which was higher than that in adjacent pancreatic tissues (χ^2 = 4.063, P〈0.05). CyclinE protein positive expression significantly correlated with tumor cell differentiation and lymph node metastasis (P〈0.05). The positive expression rate of PCNA in the tumor tissues was 71.9%, which was higher than that in adjacent pancreatic tissues (χ^2 = 5.189, P〈0.05). PCNA positive expression remarkably correlated with tumor cell differentiation and lymph node metastasis (P〈0.05). CONCLUSION: The decreased expression of p57^kip2 and/or overexpression of cyclinE protein and PCNA may contribute to the occurrence and progression of pancreatic cancer. p57^kip2, cyclinE protein, and PCNA play an important role in occurrence and progression of pancreatic cancer.展开更多
AIM: To investigate the effects of inhibiting factor of cellcycle regulation p57kip2, retinoblastinoma protein (Rb protein)and proliferating cell nuclear antigen (PCNA) in the genesisand progression of human pancreati...AIM: To investigate the effects of inhibiting factor of cellcycle regulation p57kip2, retinoblastinoma protein (Rb protein)and proliferating cell nuclear antigen (PCNA) in the genesisand progression of human pancreatic cancer.METHODS: The expression of p57kip2, Rb protein and PCNAin tumor tissues and adjacent tissues of 32 patients withpancreatic cancer was detected with SP immunohistochemicaltechnique.RESULTS: p57kip2 protein positive-expression rate in tumortissues of pancreatic cancer was 46.9 %, which was lowerthan that in adjacent pancreatic tissues (75.0 %) (x2=5.317,P<0.05), p57kip2 protein positive-expression correlatedsignificantly with tumor cell differentiation (well-differentiationversus moderate or low-differentiation, P<0.05) but did notcorrelate significantly with lymph node metastasis (lymph nodemetastasis versus non-lymph node metastasis, P>0.05); Rbgene protein positive-expression rate in tumor tissues was50.0 %, which was also lower than that in adjacent pancreatictissues (78.1%) (x2=5.497, P<0.05); PCNA positive-expression rate was 71.9 %, being higher than that inadjacent pancreatic tissues (43.8 %) (x2=5.189, P<0.05),PCNA positive-expression also correlated significantly withtumor cell differentiation and lymph node metastasis (well-differentiation versus moderate or low- differentiation, lymphnode metastasis versus non-lymph node metastasis, P<0.05).Rb protein positive-expression rate in the tumor tissues ofp57kip2 protein positive-expression group was 53.3 %; andRb protein positive-expression rate in the tumor tissues ofp57kip2 protein negative-expression group was 47.1%. Therewas no significant relationship between the two groups(r=0.16507, P>0.05).CONCLUSION: The decreased expression of p57kip2, Rbprotein or over-expression of PCNA protein might contributeto the genesis or progression of pancreatic cancer, p57kip2,Rb protein and PCNA may play an important role in genesisand progression of pancreatic cancer.展开更多
文摘Neural stem cells(NSCs) and imprinted genes play an important role in brain development. On historical grounds, these two determinants have been largely studied independently of each other. Recent evidence suggests, however, that NSCs can reset select genomic imprints to prevent precocious depletion of the stem cell reservoir. Moreover, imprinted genes like the transcriptional regulator Zac1 can fine tune neuronal vs astroglial differentiation of NSCs. Zac1 binds in a sequence-specific manner to pro-neuronal and imprinted genes to confer transcriptional regulation and furthermore coregulates members of the p53-family in NSCs. At the genome scale, Zac1 is a central hub of an imprinted gene network comprising genes with animportant role for NSC quiescence, proliferation and differentiation. Overall, transcriptional, epigenomic, and genomic mechanisms seem to coordinate the functional relationships of NSCs and imprinted genes from development to maturation, and possibly aging.
文摘Summary: In situ hybridization was applied to locate and detect the expression of p57 KIP2 in hydatidiform mole (5 cases of partial hydatidiform mole and 18 cases of complete hydatidiform mole) and normal villi (23 cases). The positive signals of p57 KIP2 expression were analyzed by HPIAS-1000 Image-Analysis System. p57 KIP2 was highly expressed in normal villi but showed distinct low expression in hydatidiform mole (P<0.01). Furthermore, the locus of low expression of p57 KIP2 accorded with the place where lesion of trophoblast occurred. Detection of p57 KIP2 made it possible to study the genetics of hydatidiform mole at the transcriptional level. Low expression of p57 KIP2 could be a molecular marker in hydatidiform mole and a target for therapy.
文摘AIM: To investigate the expression of p57kip2 and its relationship with clinicopathology, PCNA and p53 in primary hepatocellular carcinoma (HCC). METHODS: Expression of p57kip2, PCNA and p53 in tumor tissues from 32 patients with HCC and 10 liver tissues of normal persons was detected with Elivision immunohistochemical technique. RESULTS: The p57kip2 protein positive-expression rate in HCC was 56.25%, lower than that in normal tissues (100%, P<0.05). The reduced expression of p57kip2 protein correlated significantly with moderate or low differentiation of tumor cells (P = 0.007 <0.05), high clinical stage (P= 0.041 <0.05) and poor prognosis (P= 0.036 <0.05), but did not correlate significantly with metastasis, tumor size, level of AFP and age (P>0.05). The PCNA positive-expression rate was 56.25%, which was correlated significantly with the expression of p57kip2 (P= 0.025<0.05). The p53 positive-expression rate was 46.88%, which was not correlated significantly with the expression of p57kip2 (P>0.05). CONCLUSION: There is a marked loss or absence of p57kip2 expression and high expression of PCNA in HCC, which are involved in carcinogenesis and development of HCC. The p57kip2 and p53 may induce apoptosis via different mechanisms.
文摘AIM: To investigate the effects of p57^kip2, cyclinE protein and proliferating cell nuclear antigen (PCNA) on occurrence and progression of human pancreatic cancer. METHODS: The expression of p57^kip2, cyclinE protein and PCNA in tumor tissues and adjacent tissues from 32 patients with pancreatic cancer was detected by SP immunohistochemical technique. RESULTS: The positive expression rate of p57^kip2 protein in tumor tissues was 46.9%, which was lower than that in adjacent pancreatic tissues (χ^2 = 5.317, P〈0.05). p57^kip2 protein positive expression remarkably correlated with tumor cell differentiation (P〈0.05), but not with lymph node metastasis (P〉0.05). The positive expression rate of cyclinE protein in tumor tissues was 68.8%, which was higher than that in adjacent pancreatic tissues (χ^2 = 4.063, P〈0.05). CyclinE protein positive expression significantly correlated with tumor cell differentiation and lymph node metastasis (P〈0.05). The positive expression rate of PCNA in the tumor tissues was 71.9%, which was higher than that in adjacent pancreatic tissues (χ^2 = 5.189, P〈0.05). PCNA positive expression remarkably correlated with tumor cell differentiation and lymph node metastasis (P〈0.05). CONCLUSION: The decreased expression of p57^kip2 and/or overexpression of cyclinE protein and PCNA may contribute to the occurrence and progression of pancreatic cancer. p57^kip2, cyclinE protein, and PCNA play an important role in occurrence and progression of pancreatic cancer.
文摘AIM: To investigate the effects of inhibiting factor of cellcycle regulation p57kip2, retinoblastinoma protein (Rb protein)and proliferating cell nuclear antigen (PCNA) in the genesisand progression of human pancreatic cancer.METHODS: The expression of p57kip2, Rb protein and PCNAin tumor tissues and adjacent tissues of 32 patients withpancreatic cancer was detected with SP immunohistochemicaltechnique.RESULTS: p57kip2 protein positive-expression rate in tumortissues of pancreatic cancer was 46.9 %, which was lowerthan that in adjacent pancreatic tissues (75.0 %) (x2=5.317,P<0.05), p57kip2 protein positive-expression correlatedsignificantly with tumor cell differentiation (well-differentiationversus moderate or low-differentiation, P<0.05) but did notcorrelate significantly with lymph node metastasis (lymph nodemetastasis versus non-lymph node metastasis, P>0.05); Rbgene protein positive-expression rate in tumor tissues was50.0 %, which was also lower than that in adjacent pancreatictissues (78.1%) (x2=5.497, P<0.05); PCNA positive-expression rate was 71.9 %, being higher than that inadjacent pancreatic tissues (43.8 %) (x2=5.189, P<0.05),PCNA positive-expression also correlated significantly withtumor cell differentiation and lymph node metastasis (well-differentiation versus moderate or low- differentiation, lymphnode metastasis versus non-lymph node metastasis, P<0.05).Rb protein positive-expression rate in the tumor tissues ofp57kip2 protein positive-expression group was 53.3 %; andRb protein positive-expression rate in the tumor tissues ofp57kip2 protein negative-expression group was 47.1%. Therewas no significant relationship between the two groups(r=0.16507, P>0.05).CONCLUSION: The decreased expression of p57kip2, Rbprotein or over-expression of PCNA protein might contributeto the genesis or progression of pancreatic cancer, p57kip2,Rb protein and PCNA may play an important role in genesisand progression of pancreatic cancer.