Colorectal cancer(CRC) is the second most common cancer in women and the third most common in men globally. CRC arises from one or a combination of chromosomal instability, Cp G island methylator phenotype, and micros...Colorectal cancer(CRC) is the second most common cancer in women and the third most common in men globally. CRC arises from one or a combination of chromosomal instability, Cp G island methylator phenotype, and microsatellite instability. Genetic instability is usually caused by aneuploidy and loss of heterozygosity. Mutations in the tumor suppressor or cell cycle genes may also lead to cellular transformation. Similarly, epigenetic and/or genetic alterations resulting in impaired cellular pathways, such as DNA repair mechanism, may lead to microsatellite instability and mutator phenotype. Non-coding RNAs, more importantly micro RNAs and long non-coding RNAs have also been implicated at various CRC stages. Understanding the specific mechanisms of tumorigenesis and the underlying genetic and epigenetic traits is critical in comprehending the disease phenotype. This paper reviews these mechanisms along with the roles of various non-coding RNAs in CRCs.展开更多
Biliary cystic tumors,such as cystadenomas and cystadenocarcinomas,are rare cystic tumors of the liver,accounting for less than 5% of all intrahepatic cysts of biliary origin.Biliary cystadenomas have been known to oc...Biliary cystic tumors,such as cystadenomas and cystadenocarcinomas,are rare cystic tumors of the liver,accounting for less than 5% of all intrahepatic cysts of biliary origin.Biliary cystadenomas have been known to occur predominantly in women (> 85%),and 38%-44% of biliary cystadenocarcinomas have occurred in males.We wrote this letter to comment on a brief article (World J Gasteroenterol 2011 January 21;17(3):361-365) regarding a case of intrahepatic biliary cystic neoplasm treated with surgery.The adenoma-carcinoma sequence is the possible mechanism of carcinogenesis.If the carcinogenesis of biliary cystadenocarcinoma occurs in the adenoma-carcinoma sequence,we believe that the male-to-female ratio of cystadenoma should be higher than the incidence rate that has been reported to date.展开更多
AIM：To investigate the patterns of cell proliferation in proximal and distal colons in normal rats and rats with1,2-dimethylhydrazine(DMH)induced carcinogenesis using the thymidine analogue bromodeoxyuridine.METHODS:...AIM：To investigate the patterns of cell proliferation in proximal and distal colons in normal rats and rats with1,2-dimethylhydrazine(DMH)induced carcinogenesis using the thymidine analogue bromodeoxyuridine.METHODS:Colonic crypt cell proliferation was immunohistochemically detected using the anti-bromodeoxyuridine Bu20a monoclonal antibody.RESULTS:Marked regional differences were found in both groups.Total labelling index(LI)and proliferative zone size in both normal(8.65±0.34vs7.2±0.45,27.74±1.07vs16.75±1.45)andDMH groups(13.13±0.46vs11.55±0.45,39.60±1.32vs35.52±1.58)were significantly higher in distal than in proximal colon(P<0.05).although the number of cells per proxmal crypt was greater(31.45±0.20vs34.45±0.39,42.68±0.53vs49.09±0.65,P<0.001).Crypt length,total LT and proliferative zone size all increased in both proximal and distal regions of DMH rats compared to normal controls(P<0.0001).In DMH-treated rat colon a shift of labelled cells to higher crypt cell positions was demonstrated distally whist a bi-directional shift was evident proximally(P<0.05).CONCLUSION:Our results show that changes in cell proliferation patterns,as assessed by bromodeoxyuridine uptake,can act as a reliable intermediate marker of colonic cancer formation.Observed differences between proliferation patterns in distal and proximal colon may be associated with the higher incidence of tumors in t he distal colon.展开更多
文摘Colorectal cancer(CRC) is the second most common cancer in women and the third most common in men globally. CRC arises from one or a combination of chromosomal instability, Cp G island methylator phenotype, and microsatellite instability. Genetic instability is usually caused by aneuploidy and loss of heterozygosity. Mutations in the tumor suppressor or cell cycle genes may also lead to cellular transformation. Similarly, epigenetic and/or genetic alterations resulting in impaired cellular pathways, such as DNA repair mechanism, may lead to microsatellite instability and mutator phenotype. Non-coding RNAs, more importantly micro RNAs and long non-coding RNAs have also been implicated at various CRC stages. Understanding the specific mechanisms of tumorigenesis and the underlying genetic and epigenetic traits is critical in comprehending the disease phenotype. This paper reviews these mechanisms along with the roles of various non-coding RNAs in CRCs.
文摘Biliary cystic tumors,such as cystadenomas and cystadenocarcinomas,are rare cystic tumors of the liver,accounting for less than 5% of all intrahepatic cysts of biliary origin.Biliary cystadenomas have been known to occur predominantly in women (> 85%),and 38%-44% of biliary cystadenocarcinomas have occurred in males.We wrote this letter to comment on a brief article (World J Gasteroenterol 2011 January 21;17(3):361-365) regarding a case of intrahepatic biliary cystic neoplasm treated with surgery.The adenoma-carcinoma sequence is the possible mechanism of carcinogenesis.If the carcinogenesis of biliary cystadenocarcinoma occurs in the adenoma-carcinoma sequence,we believe that the male-to-female ratio of cystadenoma should be higher than the incidence rate that has been reported to date.
文摘AIM：To investigate the patterns of cell proliferation in proximal and distal colons in normal rats and rats with1,2-dimethylhydrazine(DMH)induced carcinogenesis using the thymidine analogue bromodeoxyuridine.METHODS:Colonic crypt cell proliferation was immunohistochemically detected using the anti-bromodeoxyuridine Bu20a monoclonal antibody.RESULTS:Marked regional differences were found in both groups.Total labelling index(LI)and proliferative zone size in both normal(8.65±0.34vs7.2±0.45,27.74±1.07vs16.75±1.45)andDMH groups(13.13±0.46vs11.55±0.45,39.60±1.32vs35.52±1.58)were significantly higher in distal than in proximal colon(P<0.05).although the number of cells per proxmal crypt was greater(31.45±0.20vs34.45±0.39,42.68±0.53vs49.09±0.65,P<0.001).Crypt length,total LT and proliferative zone size all increased in both proximal and distal regions of DMH rats compared to normal controls(P<0.0001).In DMH-treated rat colon a shift of labelled cells to higher crypt cell positions was demonstrated distally whist a bi-directional shift was evident proximally(P<0.05).CONCLUSION:Our results show that changes in cell proliferation patterns,as assessed by bromodeoxyuridine uptake,can act as a reliable intermediate marker of colonic cancer formation.Observed differences between proliferation patterns in distal and proximal colon may be associated with the higher incidence of tumors in t he distal colon.
