The minimum LOH region defined on chromosome 17p13.3 in human hepatocellular carcinoma with gene content analysis

Zhao, Xing; He, Mei; Wan, Dafang; Yang, Yun; He, Yinghua; Lv, Han; Guo, Ming‐Lei; Huang, Yifan; Qin, Wenxin; Wang, Ming Wei; Chong, Wenming; Chen, Jianguo; Zhang, Lisheng; Yang, Ning; Xu, Baicheng; Wu, Mengchao; Zuo, Li; Gu, Jianren

doi:10.1016/s0304-3835(02)00622-5

Cited by 33 publications

(29 citation statements)

References 35 publications

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“…The FISH data for 17 EAC tumors are indicative of deletion of Ttsg in one tumor, of deletion of Tp53 in three EAC tumors, and of deletion of both Tp53 and Ttsg in 13 EAC tumors (Table III). 32 are mentioned in these reports, all located telomeric to TP53, around the band 17p13.3. It is a distinct possibility that the candidate tumor suppressor region (Ttsg) implicated by the present study may be analogous to that discussed in these human cancer studies.…”

Section: Ai In 12 Tumorsmentioning

confidence: 87%

“…28,29,31 The second frequently affected region is a telomeric-subtelomeric region of HSA1713.3 encompassing D17S1866, D17S831 and D17S1574, which corresponds to the minimum deleted regions in hepatocellular carcinoma. 26,32 A homozygous deletion fine-mapping study has demonstrated a third region of LOH involving D17S1174 in lung cancer. 28 The present study suggests that a potential tumor suppressor gene(s) with involvement in rat EAC development is located in a chromosome segment with approximate size of 0.5 Mb, including BACs CH230-8N1 and CH230-19F2 on RNO10.…”

Section: Ai In 12 Tumorsmentioning

confidence: 99%

“…As shown in Table VI, by comparing our candidate region in RNO10 with the corresponding region in HSA17p13. 3 28,32 (Table VI). In a reciprocal comparison approach, genes located in segments D, E as well as in the beginning of segment C may also be excluded, since they are located upstream of D17S379 and, thus, are outside of the suggested candidate region in the human studies.…”

Section: Ai In 12 Tumorsmentioning

confidence: 99%

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Analysis of chromosome 10 aberrations in rat endometrial cancer—evidence for a tumor suppressor locus distal to Tp53

Nordlander

Karlsson

et al. 2007

Intl Journal of Cancer

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We have recently shown in the BDII rat model of human endometrial adenocarcinoma (EAC), rat chromosome 10 (RNO10) is frequently involved in chromosomal aberrations. In the present study, we investigated the association between RNO10 deletions, allelic imbalance (AI) at RNO10q24 and Tp53 mutation in 27 rat EAC tumors. We detected chromosomal breakage accompanied by loss of proximal and/or gain of distal parts of RNO10 in approximately 2/3 of the tumors. This finding is suggestive of a tumor suppressor activity encoded from the proximal RNO10. Given the fact that Tp53 is located at RNO10q24-q25, we then performed Tp53 mutation analysis. However, we could not find a strong correlation between AI/deletions at RNO10q24 and Tp53 mutation. Instead, the observed patterns for AI, chromosomal breaks and deletions suggest that major selection was directed against a region located close to, but distal of Tp53. In different human malignancies a similar situation of AI at chromosome band 17p13.3 (HSA17p13.3) unassociated with TP53 mutation has been observed. Although RNO10 is largely homologous to HSA17, the conservation with respect to gene order among them is not extensive. We utilized publicly available draft DNA sequences to study intrachromosomal rearrangement during the divergence between HSA17 and RNO10. By using reciprocal comparison of rat and human genome data, we could substantially narrow down the candidate tumor suppressor region in rat from 3 Mb to a chromosomal segment of about 0.5 Mb in size. These results provide scientific groundwork for identification of the putative tumor suppressor gene(s) at 17p13.3 in human tumors. ' 2006 Wiley-Liss, Inc.Key words: BDII; endometrial adenocarcinoma; RNO10; 17p13.3; allelic imbalance; Tp53 mutation; tumor suppressor gene Endometrial cancer is the most frequently diagnosed female genital tract malignancy in the western world. 1 Endometrial adenocarcinoma (EAC) is the prevalent subtype, accounting for approximately 75% of the reported cases. 2 It has been clearly demonstrated that an inherited genetic predisposition plays a critical role in the development of many cases of EAC, as the risk for a woman to develop EAC is tripled when there is an affected firstdegree relative. 3,4 Molecular genetic analysis of uterine tumor biopsies have revealed alterations in a number of chromosomal regions harboring transforming genes, including tumor suppressor genes (e.g. TP53, PTEN and hMLH1) and oncogenes (e.g. K-RAS and c-ERBB2/neu). 1,5-9 However, the molecular genetic events underlying endometrial cancer tumorigenesis are still poorly understood.Females of the inbred BDII rat strain are genetically prone to spontaneously occurring hormone-related endometrial carcinoma, providing a suitable experimental model system for genetic analysis of inherited EAC in humans. 10,11 Cytogenetic and comparative genome hybridization (CGH) analyses of the tumors pointed to common deletions in the proximal part of rat chromosome 10 (RNO10) in the tumor material. 12 According to Knudson's two-hit theo...

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Section: Ai In 12 Tumorsmentioning

confidence: 87%

Section: Ai In 12 Tumorsmentioning

confidence: 99%

Section: Ai In 12 Tumorsmentioning

confidence: 99%

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Analysis of chromosome 10 aberrations in rat endometrial cancer—evidence for a tumor suppressor locus distal to Tp53

Nordlander

Karlsson

et al. 2007

Intl Journal of Cancer

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“…High frequency of LOH at 17p13.3 and relatively low frequency of TP53 mutation in cases of hepatocellular carcinomas (HCC), lung cancers and astrocytomas indicate the presence of other TSGs involved in the development of these tumors. We have found that one minimal LOH region described in HCC and located telomeric to TP53 (tumor protein p53) gene between markers D17S1866 and D17S1574 (Zhao et al, 2003) harbor three miRNAs: miR-22, miR-132 and miR-212, while between ENO3 and TP53 (Tsuchiya et al, 2000) we found miR-195 (Calin et al, 2004b).…”

Section: For Several Chromosomal Abnormalities No Culprit Protein Codmentioning

confidence: 75%

MicroRNAs and chromosomal abnormalities in cancer cells

Calin

Croce²

2006

Oncogene

236

183

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“…1,2 Our recent studies demonstrated that replication-deficient adenovirus-mediated gene transfer of HCCS1 significantly inhibited the growth of human hepatocarcinoma cells in vitro or in vivo (submitted for publication), suggesting that HCCS1 may behave as a negative regulator of cell proliferation. However, the possible mechanism of this regulation is unclear.…”

mentioning

confidence: 99%

HCCS1 overexpression induces apoptosis via cathepsin D and intracellular calcium, and HCCS1 disruption in mice causes placental abnormality

Gan

Zhao

et al. 2008

Cell Death Differ

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Hepatocellular carcinoma suppressor 1 (HCCS1) was discovered as a novel tumor suppressor gene. We recently observed that adenovirus-mediated gene transfer of HCCS1 leads to cytotoxicity to human hepatocarcinoma cells. Here, we have demonstrated that adenovirus-mediated overexpression of HCCS1 induces apoptosis in hepatocarcinoma cells and have further characterized the apoptotic cascade. The results showed that lysosomal cathepsin D is released into the cytosol in response to HCCS1 overexpression and consequently triggers Bax insertion into the mitochondrial membrane, which leads to the release of cytochrome c. In addition, HCCS1 overexpression can induce an increase in intracellular free Ca 2 þ concentration, which also results in cytochrome c release. The released cytochrome c activates downstream caspases, leading to the occurrence of the late stages of apoptosis. Moreover, we demonstrated that the disruption of HCCS1 in mice leads to embryonic lethality, accompanied by abnormal labyrinth architecture resulting from the excessive proliferation of trophoblast cells in the placenta. These results suggest that HCCS1 plays a role in apoptosis regulation and development.

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The minimum LOH region defined on chromosome 17p13.3 in human hepatocellular carcinoma with gene content analysis

Cited by 33 publications

References 35 publications

Analysis of chromosome 10 aberrations in rat endometrial cancer—evidence for a tumor suppressor locus distal to Tp53

Analysis of chromosome 10 aberrations in rat endometrial cancer—evidence for a tumor suppressor locus distal to Tp53

MicroRNAs and chromosomal abnormalities in cancer cells

HCCS1 overexpression induces apoptosis via cathepsin D and intracellular calcium, and HCCS1 disruption in mice causes placental abnormality

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