Background Schwannoma is the tumor arising mainly from the cranial and spinal nerves. Bilateral vestibular schwannoma is the hallmark of neurofibromatosis type 2 （NF2）. The NF2 gene has been cloned with comprehensiv...Background Schwannoma is the tumor arising mainly from the cranial and spinal nerves. Bilateral vestibular schwannoma is the hallmark of neurofibromatosis type 2 （NF2）. The NF2 gene has been cloned with comprehensive analysis of its mutations in schwannoma. However, most studies focused on vestibular schwannoma. There are differences in proliferation of tumor cell and uhrastructure between vestibular and spinal schwannomas. It is unknown whether genetic alterations in vestibular schwannoma are different from those in non-vestibular schwannoma. We analyzed the loss of heterozygosity （LOH） on chromosome 22 in patients with sporadic schwannoma including vestibular and spinal schwannomas and correlated this genetic alteration with tumor proliferation. Methods In 54 unrelated patients without clinical NF1 or NF2, 36 patients had sporadic vestibular schwannoma, and 18 dorsal spinal root schwannoma. Four highly polymorphic linkage to NF2 gene microsatellite DNA markers （D22S264, D22S268, D22S280, CRYB2） were used to analyze LOH. The proliferative index was evaluated by Ki-67 and proliferative cell nuclear antigen （PCNA） immunostaining. Student＇s t test was used to analyze the difference of the proliferative index between schwannoma with LOH and that without LOH. The difference of the frequency of LOH in vestibular and spinal schwannomas was investigated by the chi-square test. Results Twenty-three schwannomas （42. 6% , 23/54） showed allele loss. The frequency of LOH in vestibular schwannoma was significantly higher than that in spinal schwannoma （ X^2 = 5.14, P 〈 0.05 ）. The proliferative index of schwannoma with LOH was significantly higher than that without LOH （tki-67 = 2. 97, P= 0. 0045 ; tPCNA =2.93, P =0. 0051）. Conclusions LOH on chromosome 22 is a frequent there is a correlation between LOH on chromosome 22 event in the tumorigenesis of sporadic schwannoma. And, and proliferative activity in schwannoma. The frequency of LOH in vestibular schwannoma is significantly different from 展开更多
Fifteen loci on chromosome 9p and 17 were analyzed to clarify the involvement of loss of heterozygosity (LOH) in hepatocellular carcinoma (HCC) in Chinese patients positive for hepatitis B (HBV) and/or hepatitis C (HC...Fifteen loci on chromosome 9p and 17 were analyzed to clarify the involvement of loss of heterozygosity (LOH) in hepatocellular carcinoma (HCC) in Chinese patients positive for hepatitis B (HBV) and/or hepatitis C (HCV) infection Expression of tumor suppressor genes (TSG) of p53, p16, and p15 gene was found to correlate with a deletion of these genes Methods Immunohistochemistry and PCR-based microsatellite polymorphism analysis techniques were used Results A high frequency of LOH was detected on chromosome 9p24 at locus D9S54 (61 8%) and 9p21, concentrated at loci D9S1747 (52 4%) and D9S1752 (51 8%) On chromosome 17, high frequent LOH was concentrated on 17p at the p53 gene locus (53 8%) and locus D17S520 (52 8%) p53 protein expression was increased in HCC, which correlated with p53 gene loss Expression of p16 and p15 protein decreased in HCC when LOH occurred at locus D9S1752 (p15 gene locus) or at locus D9S1747 and D9S1748 (p16 gene is located between these 2 loci) LOH at the p53 gene and p15 gene loci was closely associated with HBV and HCV co-infection in HCC No significant relationship between LOH and HCC clinico-pathological outcomes was observed Conclusion High frequency LOH occurs on chromosomes 9p and 17 in HCC in Chinese patients Such sites may contain several putative tumor suppressor genes critically involved in the development and/or progression of HCC Deletion of p53, p16, or p15 tumor suppressor genes may cause abnormal expression of the protein product of these genes HBV and/or HCV infection may be closely associated with LOH p53 and/or p15 gene expression展开更多
文摘Background Schwannoma is the tumor arising mainly from the cranial and spinal nerves. Bilateral vestibular schwannoma is the hallmark of neurofibromatosis type 2 （NF2）. The NF2 gene has been cloned with comprehensive analysis of its mutations in schwannoma. However, most studies focused on vestibular schwannoma. There are differences in proliferation of tumor cell and uhrastructure between vestibular and spinal schwannomas. It is unknown whether genetic alterations in vestibular schwannoma are different from those in non-vestibular schwannoma. We analyzed the loss of heterozygosity （LOH） on chromosome 22 in patients with sporadic schwannoma including vestibular and spinal schwannomas and correlated this genetic alteration with tumor proliferation. Methods In 54 unrelated patients without clinical NF1 or NF2, 36 patients had sporadic vestibular schwannoma, and 18 dorsal spinal root schwannoma. Four highly polymorphic linkage to NF2 gene microsatellite DNA markers （D22S264, D22S268, D22S280, CRYB2） were used to analyze LOH. The proliferative index was evaluated by Ki-67 and proliferative cell nuclear antigen （PCNA） immunostaining. Student＇s t test was used to analyze the difference of the proliferative index between schwannoma with LOH and that without LOH. The difference of the frequency of LOH in vestibular and spinal schwannomas was investigated by the chi-square test. Results Twenty-three schwannomas （42. 6% , 23/54） showed allele loss. The frequency of LOH in vestibular schwannoma was significantly higher than that in spinal schwannoma （ X^2 = 5.14, P 〈 0.05 ）. The proliferative index of schwannoma with LOH was significantly higher than that without LOH （tki-67 = 2. 97, P= 0. 0045 ; tPCNA =2.93, P =0. 0051）. Conclusions LOH on chromosome 22 is a frequent there is a correlation between LOH on chromosome 22 event in the tumorigenesis of sporadic schwannoma. And, and proliferative activity in schwannoma. The frequency of LOH in vestibular schwannoma is significantly different from
基金ThisworkwassupportedbytheResearchGrantCommittee HongKong (No CU95 6 6 1/UPG)
文摘Fifteen loci on chromosome 9p and 17 were analyzed to clarify the involvement of loss of heterozygosity (LOH) in hepatocellular carcinoma (HCC) in Chinese patients positive for hepatitis B (HBV) and/or hepatitis C (HCV) infection Expression of tumor suppressor genes (TSG) of p53, p16, and p15 gene was found to correlate with a deletion of these genes Methods Immunohistochemistry and PCR-based microsatellite polymorphism analysis techniques were used Results A high frequency of LOH was detected on chromosome 9p24 at locus D9S54 (61 8%) and 9p21, concentrated at loci D9S1747 (52 4%) and D9S1752 (51 8%) On chromosome 17, high frequent LOH was concentrated on 17p at the p53 gene locus (53 8%) and locus D17S520 (52 8%) p53 protein expression was increased in HCC, which correlated with p53 gene loss Expression of p16 and p15 protein decreased in HCC when LOH occurred at locus D9S1752 (p15 gene locus) or at locus D9S1747 and D9S1748 (p16 gene is located between these 2 loci) LOH at the p53 gene and p15 gene loci was closely associated with HBV and HCV co-infection in HCC No significant relationship between LOH and HCC clinico-pathological outcomes was observed Conclusion High frequency LOH occurs on chromosomes 9p and 17 in HCC in Chinese patients Such sites may contain several putative tumor suppressor genes critically involved in the development and/or progression of HCC Deletion of p53, p16, or p15 tumor suppressor genes may cause abnormal expression of the protein product of these genes HBV and/or HCV infection may be closely associated with LOH p53 and/or p15 gene expression
