Molecular studies of loss of heterozygosity in Chinese sporadic retinoblastoma patients

Zhang, Xiao L.; Fu, Weiling; Zhao, Hong; Zhou, Lai X.; Huang, Jiling; Wang, Jiang H.

doi:10.1016/j.cccn.2005.02.013

Cited by 13 publications

(8 citation statements)

References 8 publications

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“…From this perspective, the miR-17–92 cluster might act as a tumor suppressor. Consistent with this hypothesis, loss of heterozygosity or deletion of the 13q31–32 region is observed in multiple types of tumors, including squamous cell carcinoma of the larynx [24], retinoblastoma [25], hepatocellular carcinoma [26], breast cancer [27], and nasopharyngeal carcinoma [28,29]. Copy number loss was observed frequently for the microRNAs of the miR-17–92 cluster in breast cancers (21.9%), ovarian cancers (16.5%), and melanomas (20.0%) [30].…”

Section: Can Mir-17–92 Prevent Runaway Myc-e2f Activation?mentioning

confidence: 84%

“…miR-17–92 –mediated E2F1 inhibition would attenuate the hypothetical positive feedback loop of c-myc –E2F activity. The absence of the miR-17–92 –mediated dampening of proliferative signals could be tumorigenic, and this might explain the deletions in the 13q31–32 region in multiple types of tumors [24,25,28]. miR-17–92 induction would also limit apoptosis under normal proliferative conditions.…”

Section: Mir-17–92 As An Integrator Of Proliferative Versus Apoptoticmentioning

confidence: 99%

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“Myc’ed Messages”: Myc Induces Transcription of E2F1 while Inhibiting Its Translation via a microRNA Polycistron

Coller¹,

Forman²,

Legesse‐Miller³

2007

PLoS Genet

111

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The recent revelation that there are small, noncoding RNAs that regulate the expression of many other genes has led to an exciting, emerging body of literature defining the biological role for these molecules within signaling networks. In a flurry of recent papers, a microRNA polycistron induced by the oncogenic transcription factor c-myc has been found to be involved in an unusually structured network of interactions. This network includes the seemingly paradoxical transcriptional induction and translational inhibition of the same molecule, the E2F1 transcription factor. This microRNA cluster has been implicated in inhibiting proliferation, as well as inhibiting apoptosis, and promoting angiogenesis. Consistent with its seemingly paradoxical functions, the region of the genome in which it is encoded is deleted in some tumors and overexpressed in others. We consider the possibility that members of this polycistronic microRNA cluster help cells to integrate signals from the environment and decide whether a signal should be interpreted as proliferative or apoptotic.

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Section: Can Mir-17–92 Prevent Runaway Myc-e2f Activation?mentioning

confidence: 84%

Section: Mir-17–92 As An Integrator Of Proliferative Versus Apoptoticmentioning

confidence: 99%

“Myc’ed Messages”: Myc Induces Transcription of E2F1 while Inhibiting Its Translation via a microRNA Polycistron

Coller¹,

Forman²,

Legesse‐Miller³

2007

PLoS Genet

111

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“…But losses are not confined to the RB1 gene on 13q. LOH is seen at a number of other loci on this chromosome, notably D13S265 at 13q31-q32 (9 of 14 informative tumors), suggestive of another tumor suppressor gene in this region (Zhang et al, 2005). The minimal region of loss (MRL) in CGH studies also extends beyond 13q14 (19 of 179 tumors; Fig.…”

Section: Recurrent Changes On 13qmentioning

confidence: 96%

One hit, two hits, three hits, more? Genomic changes in the development of retinoblastoma

Corson

Gallie

2007

Genes Chromosomes & Cancer

234

215

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The childhood eye cancer retinoblastoma is initiated by the loss of both alleles of the prototypic tumor suppressor gene, RB1. However, a large number of cytogenetic and comparative genomic hybridization (CGH) studies have shown that these M1 and M2 mutational events--although necessary for initiation--are not the only genomic changes in retinoblastoma. Some of these subsequent changes, which we have termed M3 to Mn, are likely crucial for tumor progression not only in retinoblastoma but also in other cancers. Moreover, genes showing genomic change in cancer are more stable markers and, therefore, possible therapeutic targets than genes simply differentially expressed. In this review, we provide the first comprehensive summary of the genomic evidence implicating gain of 1q, 2p, 6p, and 13q, and loss of 16q in retinoblastoma oncogenesis, including karyotype, CGH, and microarray CGH data. We discuss the search for candidate oncogenes and tumor suppressor genes within these regions, including the candidates (KIF14, MDM4, MYCN, E2F3, DEK, CDH11, and others), plus associations between genomic changes and clinical parameters. We also review studies of other regions of the retinoblastoma genome, the epigenetic changes of aberrant methylation of MGMT, RASSF1A, CASP8, and MLH1, and the roles microRNAs might play in this cancer. Although many candidate genes have yet to be functionally validated in retinoblastoma, work in this field lays out a molecular cytogenetic pathway of retinoblastoma development. Candidate cancer genes carry diagnostic, prognostic, and therapeutic implications beyond retinoblastoma.

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“…The primers were obtained as labeled primers with fluorescent dye at the 5-terminus (MWG Biotech, Ebersberg, Germany). LOH analysis was performed as described in our previous study (2). In brief, the 5-µl volume of microsatellite DNA amplification included 40 ng of DNA template, 1X Buffer, 200 µM dNTPs, 250 nM microsatellite primer, 2.5 mM MgCl 2 and 0.25 units of Taq DNA polymerase.…”

Section: Analysis Of Loss Of Heterozygositymentioning

confidence: 99%

Loss of heterozygosity analysis of microsatellites on multiple chromosome regions in dysplasia and squamous cell carcinoma of the esophagus

Liu

Zhang

Liu

et al. 2011

Experimental and Therapeutic Medicine

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Abstract. The objective of this study was to characterize the molecular events in the carcinogenesis of esophageal squamous cell carcinoma (ESCC) and to identify biomarkers for early detection of the disease. Matched precancerous and cancerous tissues resected from 34 esophageal cancer patients from Chongqing, southern China, were compared to evaluate the extent of loss of heterozygosity (LOH). Sixteen microsatellite markers on chromosome regions 3p, 4p, 5q, 8p, 9p, 9q, 11p, 13q and 17p were used for PCR-based LOH analysis. The overall frequency of LOH at the 16 microsatellite loci was significantly increased as the pathological status of the resection specimens changed from low-grade dysplasia (LGD) to high-grade dysplasia (HGD) and SCC (P<0.001). A total of 8 markers showed LOH in the LGD samples. In addition, heterozygosity was regained at 4 loci in the SCC samples of 4 patients, respectively, in comparison to the results for these loci in the HGD samples. The overall rate of LOH increased significantly with the deterioration of the lesions, indicating that tumorigenesis of the esophageal squamous epithelia is a progressive process involving accumulative changes in LOH. The 8 loci showing allelic loss in the LGD samples may be involved in the early-stage tumorigenesis of ESCC, and LOH analysis at these loci may help improve the early detection of this disease. Regain of heterozygosity found in certain patients suggests the possibility of genetic heterogeneity in the tumorigenesis of esophageal cancer.

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Molecular studies of loss of heterozygosity in Chinese sporadic retinoblastoma patients

Cited by 13 publications

References 8 publications

“Myc’ed Messages”: Myc Induces Transcription of E2F1 while Inhibiting Its Translation via a microRNA Polycistron

“Myc’ed Messages”: Myc Induces Transcription of E2F1 while Inhibiting Its Translation via a microRNA Polycistron

One hit, two hits, three hits, more? Genomic changes in the development of retinoblastoma

Loss of heterozygosity analysis of microsatellites on multiple chromosome regions in dysplasia and squamous cell carcinoma of the esophagus

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