Identification of a 1-Mb common region at 16q24.1-24.2 deleted in hepatocellular carcinoma

Bando, Koichi; Nagai, Hisaki; Matsumoto, Satoshi; Koyama, Masaaki; Kawamura, Naoki; Tajiri, Takashi; Onda, Masahiko; Emi, Mitsuru

doi:10.1002/(sici)1098-2264(200005)28:1<38::aid-gcc5>3.0.co;2-a

Cited by 24 publications

(16 citation statements)

References 25 publications

(29 reference statements)

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“…In ovarian cancer, an association between a poor clinical outcome and the copy number loss of D16S3026 detected by QuMA has been reported (27). Furthermore, a significant association between an allelic imbalance at (41) reported that an allelic imbalance at 16q24.1-24.2 was frequently observed in hepatocellular carcinoma. These results imply that regions distal to 16q23 may code the candidate tumor suppressor genes in various malignant tumors.…”

Section: Discussionmentioning

confidence: 99%

Comparative Study between DNA Copy Number Aberrations Determined by Quantitative Microsatellite Analysis and Clinical Outcome in Patients with Stomach Cancer

Suzuki

Egami²,

Sasajima³

et al. 2004

Clinical Cancer Research

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Purpose: We detected the relative DNA copy numbers (RCNs) at target loci in patients with stomach cancer with quantitative microsatellite analysis. We additionally clarified the relationship between DNA copy number aberrations and the clinical outcome of the patients.Experimental Design: Fresh frozen samples were obtained from 30 patients who had undergone surgery for stomach cancer. Seven microsatellite loci in chromosomes 8q, 16q, and 20q and one gene-specific locus (ZNF217) were selected as the target loci. The DNA copy number was obtained relatively to a pooled reference consisting of six microsatellite primer sets selected from the regions where few aberrations have been reported in comparative genomic hybridization analysis. On the basis of the TaqMan PCR system, the internal probes used were carrying donor (6-carboxyfluorescein) and acceptor (6-carboxytetramethylrhodamine) fluorescent molecules complementary to CA repeats in the microsatellite markers and to one gene-specific oligomer in the gene-specific marker.Results: Chromosome 8q gain, 20q gain, and 16q loss were detected in 18 (60.0%), 8 (26.7%), and 13 (43.3%) cases, respectively. Gains in the RCNs of D8S1801 and D8S1724 were most frequently found (36.7%). There was a significant correlation between the loss of D16S3026 and reduced survival duration (P ‫؍‬ 0.0158), and the simultaneous aberrations of D8S1801 gain and D16S3026 loss (double marker positive) was significantly associated with reduced survival duration (P ‫؍‬ 0.0008). According to Cox proportional hazards model, the double marker positive was a significant and independent factor indicating an unfavorable prognostic factor (relative risk, 17.176; 95% confidence interval, 2.782-106.026; P ‫؍‬ 0.0022).Conclusion: RCN aberrations in tumor tissues determined by quantitative microsatellite analysis enable identification of the prognostic factors that correlate with clinical outcome of the patients with stomach cancer.

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Section: Discussionmentioning

confidence: 99%

Comparative Study between DNA Copy Number Aberrations Determined by Quantitative Microsatellite Analysis and Clinical Outcome in Patients with Stomach Cancer

Suzuki

Egami²,

Sasajima³

et al. 2004

Clinical Cancer Research

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“…MAP1-LC3 (ATG8 homolog) is localized to 16q24.1, a locus that is frequently deleted in liver, 10,11 breast, 12,13 prostate, 14 and ovarian 15,16 cancers. The HsGSA7 gene (ATG7 ortholog) is at 3p25.2, a region frequently deleted in lung cancers.…”

Section: Autophagy In Cancer and Agingmentioning

confidence: 99%

Autophagy, Mitochondrial Quality Control, and Oncogenesis

Jin¹

2006

Autophagy

153

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“…1,2 In addition, a number of other autophagy genes are also localized in chromosomal regions that are frequently lost in human cancers. For example, MAP1LC3 (ATG8 homolog) is localized at 16q24.1, a locus that is frequently deleted in liver, 3,4 breast, 5 prostate 6 and ovarian 7,8 cancers, whereas HsGSA7 (ATG7 homolog) (3p25.2) is commonly deleted in lung cancers. 9 Conversely, functional analysis indicated that ectopic expression of Beclin 1 protein in breast cancer cells, such as MCF-7, increases autophagy levels and results in inhibition of cell proliferation, reduction of clonigenicity and tumorigenesis.…”

Section: Autophagy and Tumor Suppressionmentioning

confidence: 99%

p53, Autophagy and Tumor Suppression

Jin¹

2005

Autophagy

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Previously published online as an Autophagy E-publication: http://www.landesbioscience.com/journals/autophagy/abstract.php?id=2051 KEY WORDSp53, autophagy, tumor suppression, Beclin 1, mTOR, apoptosis, necrosis ABBREVIATIONS atg autophagy-related mTOR mammalian target of rapamycin Addenda p53, Autophagy and Tumor Suppression ABSTRACT Autophagy was recently established as a novel tumor suppression mechanism, which stimulated a wave of investigations that were aimed at understanding exactly how autophagy prevents tumorigenesis, as well as to determine to what extent autophagy is implicated in human cancers. Autophagy might exert its tumor suppression function at the subcellular level by removing defective cytoplasmic components, such as damaged mitochondria. In addition, it might function at the cellular level by helping in the orderly removal of damaged cells. Previous studies indicated that autophagy is compromised in human breast, ovarian and prostate cancers. Recent research revealed that autophagy is activated by p53, a critical tumor suppressor that is involved in most, if not all, tumorigenesis. This study places autophagy in a broader context of human cancers. Future work elucidating the role of autophagy in the p53 circuit and p53 function might provide more insight into tumorigenesis and targeted cancer chemotherapy. AUTOPHAGY AND TUMOR SUPPRESSIONThe role of autophagy in tumor suppression was first suggested by the fact that the Beclin 1 gene, the human orthologue of an essential yeast autophagy gene, atg6 (autophagyrelated), is commonly deleted in human breast, ovarian and prostate cancers. 1,2 In addition, a number of other autophagy genes are also localized in chromosomal regions that are frequently lost in human cancers. For example, MAP1LC3 (ATG8 homolog) is localized at 16q24.1, a locus that is frequently deleted in liver, 3,4 breast, 5 prostate 6 and ovarian 7,8 cancers, whereas HsGSA7 (ATG7 homolog) (3p25.2) is commonly deleted in lung cancers. 9 Conversely, functional analysis indicated that ectopic expression of Beclin 1 protein in breast cancer cells, such as MCF-7, increases autophagy levels and results in inhibition of cell proliferation, reduction of clonigenicity and tumorigenesis. 2 Finally, Beclin 1 heterozygous knockout mice exhibit reduced autophagy levels and develop various tumors, 10,11 providing genetic evidence that compromised autophagy plays a causal role in tumorigenesis. Together, these observations strongly support the view that autophagy is a bona fide tumor suppression mechanism.Exactly how autophagy suppresses tumor development is less clear. Autophagy is a membrane trafficking process leading to lysosomal degradation of cytoplasmic components, a process that is highly conserved from yeast to humans. 12,13 Autophagy might serve a surveillance function at the subcellular level by selectively removing damaged cytoplasmic components, in particular damaged mitochondria-the major intracellular source of ROS (reactive oxygen species) which could damage nuclear DNA, cause mutati...

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Identification of a 1-Mb common region at 16q24.1-24.2 deleted in hepatocellular carcinoma

Cited by 24 publications

References 25 publications

Comparative Study between DNA Copy Number Aberrations Determined by Quantitative Microsatellite Analysis and Clinical Outcome in Patients with Stomach Cancer

Comparative Study between DNA Copy Number Aberrations Determined by Quantitative Microsatellite Analysis and Clinical Outcome in Patients with Stomach Cancer

Autophagy, Mitochondrial Quality Control, and Oncogenesis

p53, Autophagy and Tumor Suppression

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