Comparative genomic hybridization of esophageal squamous cell carcinoma

Yen, Ching‐Yu; M.D., Yann-Jang Chen; Chen, Jung‐Ta; Hsia, Jiun-Yi; Chen, Po‐Min; Liu, Jin-Hwang; Fan, Frank S.; Chiou, Tzeon‐Jye; Wang, Weishu; Lin, Chi‐Hung

doi:10.1002/1097-0142(20011201)92:11<2769::aid-cncr10118>3.0.co;2-m

Cited by 69 publications

(12 citation statements)

References 36 publications

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“…Previous studies show frequent allele losses on chromosomes 9 and 18 by both loss of heterozygosity (LOH) (Aoki et al, 1994;Mori et al, 1994;Shibagaki et al, 1994;Wang et al, 1996;Muzeau et al, 1997;Naidoo et al, 1999;Karkera et al, 2000;Yang et al, 2004) and comparative genomic hybridization (CGH) studies (Pack et al, 1999;Tada et al, 2000;Yen et al, 2001Yen et al, , 2003. These results suggest that tumor suppressor genes (TSGs) associated with esophageal tumorigenesis may be located on these chromosomes.…”

Section: Introductionmentioning

confidence: 94%

Tumor suppressive role of a 2.4 Mb 9q33–q34 critical region and DEC1 in esophageal squamous cell carcinoma

Yang

Leung

et al. 2004

Oncogene

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The key genes involved in the development of esophageal squamous cell carcinoma (ESCC) remain to be elucidated. Previous studies indicate extensive genomic alterations occur on chromosome 9 in ESCC. Using a monochromosome transfer approach, this study provides functional evidence and narrows down the critical region (CR) responsible for chromosome 9 tumor suppressing activity to a 2.4 Mb region mapping to 9q33-q34 between markers D9S1798 and D9S61. Interestingly, a high prevalence of allelic loss in this CR is also observed in primary ESCC tumors by microsatellite typing. Allelic loss is found in 30/ 34 (88%) tumors and the loss of heterozygosity (LOH) frequency ranges from 67 to 86%. Absent to low expression of a 9q32 candidate tumor suppressor gene (TSG), DEC1 (deleted in esophageal cancer 1), is detected in four Asian ESCC cell lines. Stably expressing DEC1 transfectants provide functional evidence for inhibition of tumor growth in nude mice and DEC1 expression is decreased in tumor segregants arising after long-term selection in vivo. There is 74% LOH in the DEC1 region of ESCC primary tumors. This study provides the first functional evidence for the presence of critical tumor suppressive regions on 9q33-q34. DEC1 is a candidate TSG that may be involved in ESCC development.

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Section: Introductionmentioning

confidence: 94%

Tumor suppressive role of a 2.4 Mb 9q33–q34 critical region and DEC1 in esophageal squamous cell carcinoma

Yang

Leung

et al. 2004

Oncogene

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“…Several studies explored that miR-145 or miR-143 played a tumor-suppressive role in various cancers [11], [12], [13], [14], [15], [16], [17], [18]. A large body of evidence detected by comparative genomic hybridization has established that 5q is a frequent loss segment in esophageal cancer with a loss frequency from 18% to 75% [19], [20], [21], [22], [23], [24], [25], [26]. Accordingly, the miR-143/miR-145 cluster located in 5q33 might be deleted or down-regulated in esophageal cancer.…”

Section: Introductionmentioning

confidence: 99%

The Cluster of miR-143 and miR-145 Affects the Risk for Esophageal Squamous Cell Carcinoma through Co-Regulating Fascin Homolog 1

et al. 2012

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MicroRNAs (miRNAs), 18–24 nt non-coding RNAs, are thought to play important roles in cell proliferation, differentiation, apoptosis, and development. Recent studies suggest that some of the known microRNAs map to a single genomic locale within a single polycistronic transcript. But the roles of the cluster remain to be known. In order to understand the role and mechanism of a cluster of miR-143 and miR-145 in esophageal squamous cell carcinoma (ESCC), the association of mature miR-143 and miR-145 expression with the risk for esophageal cancer was evaluated in ESCC patients with a case-control study, and target protein regulated by mature miRNA was analyzed in ESCC cell lines with 3′UTR luciferase reporter assay. The expression levels of miR-143 and miR-145 were determined in 110 pairs of esophageal cancer tissues and adjacent normal tissues using real-time reverse transcription PCR. The relative expression of miR-143 and miR-145 were statistically different between cancer tissues and matched controls. The combined expression of miR-143 and miR-145 was significantly associated with the risk for esophageal cancer. Meanwhile, the reduced expression of two miRNAs in tumor patient was supposed to have a trend of lymph node metastases. The co-expression pattern of miR-143 and miR-145 was analyzed with Pearson correlation. It showed a significant correlation between these two miRNAs expression both in tissues and tumor cell lines. 3′UTR luciferase reporter assay indicated that Fascin Homolog 1 (FSCN1) could be co-regulated by miR-143 and miR-145. The protein level of FSCN1 showed no significant linear correlation with miR-143 and miR-145 expression in ESCC cell lines with Western blotting analysis. In conclusion, since miR-143 and miR-145 could regulate oncogenic FSCN1 and take part in the modulation of metastases, the result suggested the combination variable of miR-143 and miR-145 as a potential biomarker for earlier diagnosis and prognosis of esophageal cancer.

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“…Another loss of heterozygosity (LOH) study in lung cancer showed that frequently deleted regions at 3p include 3p24–26, 3p21.3, 3p21.1–21.2, 3p14.2, and 3p12–13 [28] . In esophageal squamous cell carcinoma (ESCC), deletion of 3p is also a frequent allelic imbalance detected by CGH [29] - [31] , LOH [32] , and genome-wide genotyping [33] . Using SNP-MassArray, several commonly deleted regions in ESCC have been identified, including 3p26.3, 3p22, 3p21.3, and 3p14.2 [33] .…”

Section: Frequently Deleted Minimal Regions At 3p In Human Cancersmentioning

confidence: 99%

Tumor suppressor genes on frequently deleted chromosome 3p in nasopharyngeal carcinoma

Chen¹,

Fu²,

Zhang³

et al. 2012

Chin J Cancer

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Nasopharyngeal carcinoma (NPC) is among the most common malignancies in southern China. Deletion of genomic DNA, which occurs during the complex pathogenesis process for NPC, represents a pivotal mechanism in the inactivation of tumor suppressor genes (TSGs). In many circumstances, loss of TSGs can be detected as diagnostic and prognostic markers in cancer. The short arm of chromosome 3 (3p) is a frequently deleted chromosomal region in NPC, with 3p21.1–21.2 and 3p25.2–26.1 being the most frequently deleted minimal regions. In recent years, our research group and others have focused on the identification and characterization of novel target TSGs at 3p, such as RASSF1A, BLU, RBMS3, and CHL1, in the development and progression of NPC. In this review, we summarize recent findings of TSGs at 3p and discuss some of these genes in detail. A better understanding of TSGs at 3p will significantly improve our understanding of NPC pathogenesis, diagnosis, and treatment.

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Comparative genomic hybridization of esophageal squamous cell carcinoma

Cited by 69 publications

References 36 publications

Tumor suppressive role of a 2.4 Mb 9q33–q34 critical region and DEC1 in esophageal squamous cell carcinoma

Tumor suppressive role of a 2.4 Mb 9q33–q34 critical region and DEC1 in esophageal squamous cell carcinoma

The Cluster of miR-143 and miR-145 Affects the Risk for Esophageal Squamous Cell Carcinoma through Co-Regulating Fascin Homolog 1

Tumor suppressor genes on frequently deleted chromosome 3p in nasopharyngeal carcinoma

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