Oncogenes and tumor-suppressor genes.

Lehman, Teresa A.; Reddel, Roger R.; Peiifer, A M; Spillare, Elisa A.; Kaighn, M. Edward; Weston, Ainsley; Gerwin, Brenda I.; Harris, Curtis C.

doi:10.1289/ehp.9193133

Cited by 16 publications

(7 citation statements)

References 94 publications

(96 reference statements)

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“…These cells have also been widely used to define conditions under which various agents and oncogenes cause neoplastic transformation. 21-23 Our results show that chronic exposure to SWCNT causes malignant transformation in vitro and tumorigenicity in vivo upon injection of transformed cells into nude mouse. Such data strengthen the safety concern for CNT exposure and support the prudent adoption of prevention strategies and implementation of exposure control.…”

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confidence: 67%

Carbon Nanotubes Induce Malignant Transformation and Tumorigenesis of Human Lung Epithelial Cells

Luanpitpong²,

et al. 2011

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Carcinogenicity of carbon nanotubes is a major concern but has not been well addressed due to the lack of experimental models. Here, we show that chronic exposure to single-walled carbon nanotubes causes malignant transformation of human lung epithelial cells. The transformed cells induce tumorigenesis in mice and exhibit an apoptosis resistant phenotype characteristic of cancer cells. This study provides new evidence for carbon nanotube-induced carcinogenesis and indicates the potential role of p53 in the process.

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mentioning

confidence: 67%

Carbon Nanotubes Induce Malignant Transformation and Tumorigenesis of Human Lung Epithelial Cells

Luanpitpong²,

et al. 2011

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“…Bronchial epithelial cells were chosen in this study because they are a key target for Cr(VI)-induced tumorigenesis. BEAS-2B cells have been widely used in the literature to define conditions under which various agents and oncogenes cause neoplastic transformation [27] – [29] . They have been shown to exhibit similar characteristics and cellular responses to carcinogens as primary or normal lung cells [30] – [32] .…”

Section: Discussionmentioning

confidence: 99%

Multifunctional Role of Bcl-2 in Malignant Transformation and Tumorigenesis of Cr(VI)-Transformed Lung Cells

et al. 2012

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B-cell lymphoma-2 (Bcl-2) is an antiapoptotic protein known to be important in the regulation of apoptosis in various cell types. However, its role in malignant transformation and tumorigenesis of human lung cells is not well understood. We previously reported that chronic exposure of human lung epithelial cells to the carcinogenic hexavalent chromium Cr(VI) caused malignant transformation and Bcl-2 upregulation; however, the role of Bcl-2 in the transformation is unclear. Using a gene silencing approach, we showed that Bcl-2 plays an important role in the malignant properties of Cr(VI)-transformed cells. Downregulation of Bcl-2 inhibited the invasive and proliferative properties of the cells as well as their colony forming and angiogenic activities, which are upregulated in the transformed cells as compared to control cells. Furthermore, animal studies showed the inhibitory effect of Bcl-2 knockdown on the tumorigenesis of Cr(VI)-transformed cells. The role of Bcl-2 in malignant transformation and tumorigenesis was confirmed by gene silencing experiments using human lung carcinoma NCI-H460 cells. These cells exhibited aggressive malignant phenotypes similar to those of Cr(VI)-transformed cells. Knockdown of Bcl-2 in the H460 cells inhibited malignant and tumorigenic properties of the cells, indicating the general role of Bcl-2 in human lung tumorigenesis. Ingenuity Pathways Analysis (IPA) revealed potential effectors of Bcl-2 in tumorigenesis regulation. Additionally, using IPA together with ectopic expression of p53, we show p53 as an upstream regulator of Bcl-2 in Cr(VI)-transformed cells. Together, our results indicate the novel and multifunctional role of Bcl-2 in malignant transformation and tumorigenesis of human lung epithelial cells chronically exposed to Cr(VI).

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“…Accordingly, high frequencies of LOH on chromosome 17p have been reported in many types of cancer, including EC 25-27. The p53 gene and other possible tumor-suppressor genes are located on 17p, and as such, it is conceivable to consider that 17p's telomere may somehow be implicated in tumorogenesis 28. In addition, Finley et al 11 observed that the loss of 17p was the most common event in Barrett's esophagus, and that this loss was significantly associated with an overall telomere length shortening (r = 0.55; p<0.0001).…”

Section: Discussionmentioning

confidence: 99%

Constitutive Short Telomere Length of Chromosome 17p and 12q but not 11q and 2p Is Associated with an Increased Risk for Esophageal Cancer

Xing

Ajani

Chen

et al. 2009

Cancer Prevention Research

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Shortened telomere length may cause chromosomal instability in Barrett's esophagus and thus promote tumorigenesis. However, whether short telomere length in all chromosomes or just some of them is associated with increased esophageal cancer (EC) risk is largely unknown. To address this question, we examined the overall and chromosome-specific telomere lengths of 17p, 12q, 2p, and 11q and assessed their associations with EC risk. In a case-control study with 94 EC cases and 94 matched controls, the overall telomere length and the chromosome-specific telomere lengths of 17p, 12q, 2p, and 11q in peripheral blood lymphocytes were determined by a real-time PCR and a modified single telomere length analysis assay, respectively. Multivariate logistic regression analysis was used to assess the association between telomere length and EC risk. Compared with controls, EC patients had significantly shorter overall telomere lengths (P = 0.004) and chromosome-specific telomere lengths of 17p (P = 0.003) and 12q (P = 0.006) but not of 11q (P = 0.632) and 2p (P = 0.972). Furthermore, the multivariate logistic regression analysis showed that the short overall telomere length and chromosome-specific telomere lengths of 17p and 12q were associated with a dose-dependent increase in EC risk. Our study provides the first epidemiologic evidence that short telomere length of 17p and 12q plays an important role in esophageal carcinogenesis, suggesting that short telomere length of specific chromosomes is associated with the etiology of different cancer types.

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Oncogenes and tumor-suppressor genes.

Cited by 16 publications

References 94 publications

Carbon Nanotubes Induce Malignant Transformation and Tumorigenesis of Human Lung Epithelial Cells

Carbon Nanotubes Induce Malignant Transformation and Tumorigenesis of Human Lung Epithelial Cells

Multifunctional Role of Bcl-2 in Malignant Transformation and Tumorigenesis of Cr(VI)-Transformed Lung Cells

Constitutive Short Telomere Length of Chromosome 17p and 12q but not 11q and 2p Is Associated with an Increased Risk for Esophageal Cancer

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