Cytogenetic studies of esophageal squamous cell carcinomas in the northern Chinese population by comparative genomic hybridization

Fang, Wei; Ni, Jiang; Wu, Shanshan; Líu, Hao; Xu, Xin; Han, Yaling; Cai, Yan; Zhang, Jianwei; Chen, Xian-Jun; Hui, Pei; Lü, Ning; Liang, Jing; Wu, Min; Wang, Ming-Rong

doi:10.1016/s0165-4608(02)00586-1

Cited by 25 publications

(12 citation statements)

References 23 publications

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“…Amplification of chromosomal DNA is one of the mechanisms capable of activating genes whose overexpression contributes to development and progression of cancer. Several studies, including our report, have shown that gain in DNA copy number within the short arm of chromosome 5 (5p) occurred frequently in ESCC, non -smallcell lung cancers, and oral squamous cell carcinomas (1)(2)(3)(4), suggesting that chromosome 5p may harbor some target genes whose amplification rendered them oncogenic in these tumors.…”

Section: Introductionmentioning

confidence: 64%

Suppression of Anoikis by SKP2 Amplification and Overexpression Promotes Metastasis of Esophageal Squamous Cell Carcinoma

Wang

Ye³

et al. 2009

Molecular Cancer Research

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The gene of SKP2, located on chromosome 5p13, plays a critical role in cell cycle progression, especially at the G 1 -S transition, putatively through its control of several cell cycle regulator proteins including p27 kip1 , p21 cip1 , p57 kip2 , p130, cyclin E, and c-Myc. Previous studies in this laboratory revealed that gain of chromosome 5p was often seen in esophageal squamous cell carcinoma (ESCC). In the present study, we examined the amplification status and expression level of SKP2 in ESCC and investigated its clinicopathologic significance. Amplification and elevated expression of SKP2 correlated significantly with tumor stage and positive lymph node metastasis (P < 0.05). The SKP2 protein expression level as determined by immunohistochemical staining showed a significant inverse correlation with p27 protein. In vivo assay showed that inhibition of SKP2 expression also decreased tumor growth and lung metastasis of ESCC cells. At the molecular level, knockdown of SKP2 by RNA interference inhibited cell migration and invasion ability. Knockdown of SKP2 expression sensitized cancer cells to anoikis, and a wobble mutant of SKP2 that is resistant to SKP2 small interfering RNA can rescue this effect. Expression level of pAkt decreased after SKP2 knockdown. Treatment of cells with phosphoinositidyl 3-kinase inhibitor (LY294002) and constitutively activator (insulin-like growth factor I) had significant effects on the anoikis of SKP2 RNA interference cells. These results show for the first time that SKP2 is amplified and overexpressed in ESCC. Elevated expression of SKP2 protected cancer cells from anoikis, and this effect was mediated, at least in part, by the phosphoinositidyl 3-kinase-Akt pathway.

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Section: Introductionmentioning

confidence: 64%

Suppression of Anoikis by SKP2 Amplification and Overexpression Promotes Metastasis of Esophageal Squamous Cell Carcinoma

Wang

Ye³

et al. 2009

Molecular Cancer Research

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“…Gain of 1q is one of the commonest changes observed in both pediatric and adult malignant solid tumors. 27 It is present in over 50% of a wide range of malignant human tumors [28][29][30] such as breast carcinomas, 28,[31][32][33] esophageal squamous cell carcinomas, 34 retinoblastomas, 35,36 neuroblastomas 37 and leukemias among others.…”

Section: Discussionmentioning

confidence: 99%

Phyllodes tumors of the breast segregate in two groups according to genetic criteria

et al. 2007

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Phyllodes tumors are rare fibroepithelial tumors of the breast. The pathologic grading of phyllodes tumors based on the aspect of the stromal component, is divided into 2 or 3 grades according to the system used. To determine whether genetic markers could be of use for improving the classification of phyllodes tumors and to provide a better knowledge of the genetic alterations in these tumors, we analyzed chromosomal changes detected by comparative genomic hybridization (CGH) in comparison with histological data, in a series of 30 cases. Recurrent chromosome imbalances were observed in 55, 91 and 100% of benign, borderline and malignant phyllodes tumors, respectively. The mean number of chromosome changes was one in benign, six in borderline, and six in malignant phyllodes tumors. Most frequent genetic imbalances were þ 1q (12/30), À13q (7/30), À6q (9/30), þ 5 (9/30) and À10p (8/30). Gains of 1q, present in only one of nine benign tumors, were found in 11/21 (51%) borderline or malignant tumors. Losses of 13q have 13q14.2 as smallest region of overlap, suggesting that the RB1 gene could be the target of deletions. Amplifications of 12q14, involving the MDM2 locus, and of 8p24, involving the MYC gene, were observed in one case each. Borderline and malignant phyllodes tumors could not be differentiated on the basis of their genomic imbalances (presence and number of chromosomal changes, presence of 1q gain and/or 13q loss). Conversely, benign tumors could be significantly differentiated from the group composed of borderline and malignant tumors (Po0.01). This study reveals two distinct patterns of genomic imbalance in phyllodes tumors: benign, with none or a few chromosome changes and malignant, with numerous recurrent chromosomal changes, in particular 1q gain and 13q loss. Helpful additional pathological criteria for differentiating the two genetic groups of phyllodes tumors are the nuclear size and the mitotic rate. Modern Pathology (2007) 20, 435-444.

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“…[2][3][4]. This chromosome locus has also been reported to be amplified in carcinomas of the head and neck, breast, lung, ovary, bladder, etc.…”

Section: Introductionmentioning

confidence: 98%

Amplification and Overexpression ofCTTN(EMS1) Contribute to the Metastasis of Esophageal Squamous Cell Carcinoma by Promoting Cell Migration and Anoikis Resistance

et al. 2006

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Gain of chromosome 11q13 is a common event in esophageal squamous cell carcinoma (ESCC). The cortactin gene (CTTN, also EMS1), located at 11q13, plays a pivotal role in coupling membrane dynamics to cortical actin assembly. This gene has been implicated in the motility of several types of cells. In the present study, we found that the amplification and overexpression of the CTTN gene was associated with lymph node metastasis in ESCC. Functional analysis by small interfering RNA-mediated silencing of CTTN revealed that in addition to the effect on cell migration, CTTN influenced cell invasiveness by anoikis resistance. In vivo assay showed that inhibition of CTTN expression also decreased tumor growth and lung metastasis of ESCC cells. At the molecular level, we showed for the first time that the protective role of CTTN in anoikis resistance was correlated with the activation of the phosphatidylinositol 3-kinase/Akt pathway. Overall, the data suggest that CTTN is an oncogene in the 11q13 amplicon and exerts functions on tumor metastasis in ESCC.

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Cytogenetic studies of esophageal squamous cell carcinomas in the northern Chinese population by comparative genomic hybridization

Cited by 25 publications

References 23 publications

Suppression of Anoikis by SKP2 Amplification and Overexpression Promotes Metastasis of Esophageal Squamous Cell Carcinoma

Suppression of Anoikis by SKP2 Amplification and Overexpression Promotes Metastasis of Esophageal Squamous Cell Carcinoma

Phyllodes tumors of the breast segregate in two groups according to genetic criteria

Amplification and Overexpression ofCTTN(EMS1) Contribute to the Metastasis of Esophageal Squamous Cell Carcinoma by Promoting Cell Migration and Anoikis Resistance

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