Chromosomes in human-mouse and human-(human-mouse)hybridomas wereanalysed by G-banding methods.It was found that most human chromosomes,exceptNo.13 and X,Y,were retained.The frequencies of chromosomes No.1,3,4,5,6,17,...Chromosomes in human-mouse and human-(human-mouse)hybridomas wereanalysed by G-banding methods.It was found that most human chromosomes,exceptNo.13 and X,Y,were retained.The frequencies of chromosomes No.1,3,4,5,6,17,19,21 and 22 were higher than those of other chromosomes in each hybridoma clone.The myeloma cell lines X63-Ag8.653 and SHM-D33 were also analysed.The morphologyof marker chromosomes was apparently different between hybridomas.There were 7 kindsof marker chromosomes in human-mouse hybridomas and 16 kinds of markerchromosomes in human-(human-mouse)hybridomas.Clones that retained humanchromosome No.1 were more stable and clones that did not retain human chromosomeNo.14 were still capable of secreting human immunoglobulin.Clones that retained humanchromosome No.2 did not secret human k light chain McAb while clones that retainedhuman chromosomes No.2 and No.22 only secreted λ light chain.展开更多
OBJECTIVE: To investigate the loss of heterozygosity (LOH) on chromosomal arms 13q and 14q in nasopharyngeal carcinoma (NPC) using 21 microsatellite polymorphic markers and to study whether there is a correlation betw...OBJECTIVE: To investigate the loss of heterozygosity (LOH) on chromosomal arms 13q and 14q in nasopharyngeal carcinoma (NPC) using 21 microsatellite polymorphic markers and to study whether there is a correlation between LOH and clinicopathologic parameters and/or Epstein-Barr virus (EBV) infection in NPC. METHODS: Sixty cases of NPC were studied using polymerase chain reaction based microsatellite analysis with genescan and genotyping techniques. RESULTS: LOH was detected on 13q in 78% of NPC tumors, high frequency LOH loci (more than 30%) clustered to 13q12.3-q14.3 and 13q32. On chromosome 14q, LOH was detected in 80% of NPC tumors; high frequency LOH loci clustered to 14q11-q13, 14q21-q24 and 14q32. High frequency LOH at 13q31-q32 correlated with a lower level of EBV infection; LOH on chromosome 14q was closely associated with poor differentiation of NPC tumor cells. CONCLUSION: Our results suggest that in NPC, LOH on chromosome 13q and 14q are common genetic events, and putative tumor suppressor genes (TSG) residing in these regions may be involved in tumorigenesis.展开更多
The effects of selected DNA repair inhibitors on the frequency of human cytomegalovirus (HCMV)-induced chromosome aberrations in human peripheral blood lymphocytes (PBLs) were evaluated. Trealment of HCMV-infected PBL...The effects of selected DNA repair inhibitors on the frequency of human cytomegalovirus (HCMV)-induced chromosome aberrations in human peripheral blood lymphocytes (PBLs) were evaluated. Trealment of HCMV-infected PBLs with camptothecin (0.05 to 0.3μg/ml), an inhibitor of topoisomerase I, for 30 hr resulted in a significant (P<0.01) synergistic enhancement of the frequency of HCMV-induced chromosome damage, on the other hand, a significant increase in the frequency of chromosome damage was not noted for infected PBLs treated with either 3-aminobenzamide (3-AB) (3 to 30μg/ml), an inhibitor of poly (ADP-ribose) poiymerase, ur novobiocin 3 to 30 |ig/ml) an inhibitor of topoiso-merase I or excision repair processes for 30 hr. chromatid-type breaks including chromosome exchanges were the predominant type of chromosome aberrations observed in the HCMV-infected cells treated with camptothecin suggesting that HCMV infection is associated with the induction of single-strand DNA breaks. Furthermore, these findings suggest that HCMV infection does rol inflict dircc: DNA damage which is repaired through 3-AB- or novobiocinsensitive pathways.Human cytomegalovirus (HCMV) is a common pathogen which irferfs about 80% of the world's population causing, for the most part, persistent subcliniclil infeclions (Wellcr, 1971). A relatively small percentage of otherwise healthy immunologically competent people experience clinical HCMV disease (Cohen et al., 1985). Generalized HCMV infection, however, is the bane of individuals whose immune system is compromised (Schooley, 1990) Rubin, 1990). Molecular epidemiological studies strongly suggest that HCMV is one of the most frequent cause of congenital infections and that these infections result in a high incidence of birth defects and developmental abnormalities (Alford et al., 1990). Several studies (Nachtigal et al., 1978; Luleci et al., 1980; AbuBakar et al., 1988) have shown that HCMV infectior can result in an increase in the frequency of chromosome aberrations. Since the ability to cause chromosome damage may be significant in the induction of birth defects and possibly in HCMV-induced malignancy, we undertook the present investigation to evaluate the mechanisms by which HCMV may cause chromosome damage. In ths study, the effects of selected DNA repair inhibitors on the frequency of HCMV-induced chromosome aberrations were evaluated. The results indicae that the presence of camptothecin, but nut 3-aminobenzamidc (3-AB) ro novobiocin, results in a concentration-dependent increase in the frequent) of chromosome aberrations in HCMV-infected peripheral blood lymphocytes (PBLs). Accordingly, it is proposed that HCMV-induced chromosome damage in PBLs does not substantially involve DNA repair activities sensitive to inhibition of poly ADP-ribosylation or excision repair processes, but is related to camp of thccin-sersitive DNA repair, conceivably involving the activity of topoisomrrasc I .展开更多
目的探讨3号染色体短臂(3p14)等位基因杂合性丢失(loss of heterozygosity,LOH)与人卵巢癌发生及发展之间的相关性研究。方法采用聚合酶链反应并结合二核苷酸重复序列多态性方法.分别对31例卵巢癌及24例卵巢良性肿瘤患者的组织标本DNA中...目的探讨3号染色体短臂(3p14)等位基因杂合性丢失(loss of heterozygosity,LOH)与人卵巢癌发生及发展之间的相关性研究。方法采用聚合酶链反应并结合二核苷酸重复序列多态性方法.分别对31例卵巢癌及24例卵巢良性肿瘤患者的组织标本DNA中3p14上3个微卫星位点(D3S1234、D3S1300、D3S1312)杂合性丢失(LOH)进行检测,同时还随机地检测31 例卵巢癌中21例患者的血清DNA中3p14的LOH。结果31例卵巢癌组织DNA中21例(67.7%)至少在1个微卫星位点中出现杂合性丢失,11例卵巢癌患者(35.5%)有2个以上微卫星位点出现LOH。癌组织DNA中基因杂合性丢失频率与癌细胞分化程度呈正相关,与肿瘤病理类型及FIGO分期无关。24例卵巢良性肿瘤组织及血清DNA中均未出现3p位点上的杂合性丢失。21例卵巢癌血清DNA与肿瘤组织DNA3p14基因3个微卫星位点杂合性丢失率之间存在明显的相关性(P< 0 05)。结论鉴于人卵巢癌3p14出现杂合性丢失率与其癌细胞分化恶性程度相关以及卵巢癌患者血清DNA与癌组织DNA中3p14出现LOH相一致,故本文实验结果提示3p14 LOH的检测可能具有对卵巢癌患者的临床诊断潜在性价值。展开更多
文摘Chromosomes in human-mouse and human-(human-mouse)hybridomas wereanalysed by G-banding methods.It was found that most human chromosomes,exceptNo.13 and X,Y,were retained.The frequencies of chromosomes No.1,3,4,5,6,17,19,21 and 22 were higher than those of other chromosomes in each hybridoma clone.The myeloma cell lines X63-Ag8.653 and SHM-D33 were also analysed.The morphologyof marker chromosomes was apparently different between hybridomas.There were 7 kindsof marker chromosomes in human-mouse hybridomas and 16 kinds of markerchromosomes in human-(human-mouse)hybridomas.Clones that retained humanchromosome No.1 were more stable and clones that did not retain human chromosomeNo.14 were still capable of secreting human immunoglobulin.Clones that retained humanchromosome No.2 did not secret human k light chain McAb while clones that retainedhuman chromosomes No.2 and No.22 only secreted λ light chain.
文摘OBJECTIVE: To investigate the loss of heterozygosity (LOH) on chromosomal arms 13q and 14q in nasopharyngeal carcinoma (NPC) using 21 microsatellite polymorphic markers and to study whether there is a correlation between LOH and clinicopathologic parameters and/or Epstein-Barr virus (EBV) infection in NPC. METHODS: Sixty cases of NPC were studied using polymerase chain reaction based microsatellite analysis with genescan and genotyping techniques. RESULTS: LOH was detected on 13q in 78% of NPC tumors, high frequency LOH loci (more than 30%) clustered to 13q12.3-q14.3 and 13q32. On chromosome 14q, LOH was detected in 80% of NPC tumors; high frequency LOH loci clustered to 14q11-q13, 14q21-q24 and 14q32. High frequency LOH at 13q31-q32 correlated with a lower level of EBV infection; LOH on chromosome 14q was closely associated with poor differentiation of NPC tumor cells. CONCLUSION: Our results suggest that in NPC, LOH on chromosome 13q and 14q are common genetic events, and putative tumor suppressor genes (TSG) residing in these regions may be involved in tumorigenesis.
文摘The effects of selected DNA repair inhibitors on the frequency of human cytomegalovirus (HCMV)-induced chromosome aberrations in human peripheral blood lymphocytes (PBLs) were evaluated. Trealment of HCMV-infected PBLs with camptothecin (0.05 to 0.3μg/ml), an inhibitor of topoisomerase I, for 30 hr resulted in a significant (P<0.01) synergistic enhancement of the frequency of HCMV-induced chromosome damage, on the other hand, a significant increase in the frequency of chromosome damage was not noted for infected PBLs treated with either 3-aminobenzamide (3-AB) (3 to 30μg/ml), an inhibitor of poly (ADP-ribose) poiymerase, ur novobiocin 3 to 30 |ig/ml) an inhibitor of topoiso-merase I or excision repair processes for 30 hr. chromatid-type breaks including chromosome exchanges were the predominant type of chromosome aberrations observed in the HCMV-infected cells treated with camptothecin suggesting that HCMV infection is associated with the induction of single-strand DNA breaks. Furthermore, these findings suggest that HCMV infection does rol inflict dircc: DNA damage which is repaired through 3-AB- or novobiocinsensitive pathways.Human cytomegalovirus (HCMV) is a common pathogen which irferfs about 80% of the world's population causing, for the most part, persistent subcliniclil infeclions (Wellcr, 1971). A relatively small percentage of otherwise healthy immunologically competent people experience clinical HCMV disease (Cohen et al., 1985). Generalized HCMV infection, however, is the bane of individuals whose immune system is compromised (Schooley, 1990) Rubin, 1990). Molecular epidemiological studies strongly suggest that HCMV is one of the most frequent cause of congenital infections and that these infections result in a high incidence of birth defects and developmental abnormalities (Alford et al., 1990). Several studies (Nachtigal et al., 1978; Luleci et al., 1980; AbuBakar et al., 1988) have shown that HCMV infectior can result in an increase in the frequency of chromosome aberrations. Since the ability to cause chromosome damage may be significant in the induction of birth defects and possibly in HCMV-induced malignancy, we undertook the present investigation to evaluate the mechanisms by which HCMV may cause chromosome damage. In ths study, the effects of selected DNA repair inhibitors on the frequency of HCMV-induced chromosome aberrations were evaluated. The results indicae that the presence of camptothecin, but nut 3-aminobenzamidc (3-AB) ro novobiocin, results in a concentration-dependent increase in the frequent) of chromosome aberrations in HCMV-infected peripheral blood lymphocytes (PBLs). Accordingly, it is proposed that HCMV-induced chromosome damage in PBLs does not substantially involve DNA repair activities sensitive to inhibition of poly ADP-ribosylation or excision repair processes, but is related to camp of thccin-sersitive DNA repair, conceivably involving the activity of topoisomrrasc I .
基金Supported by the National Natural Science Foundation of China (30170394) the Special Fund for Promotion of Education Ministry of Science P.R.C (985) and "973"Foundation of China (001cb51010201).
