Comparison of the human versus murine cytomegalovirus immediate early gene promoters for transgene expression by adenoviral vectors.

Addison, Christina L.; Hitt, Mary; Kunsken, Derek; Graham, Frank L.

doi:10.1099/0022-1317-78-7-1653

Cited by 150 publications

(107 citation statements)

References 32 publications

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“…Neither injection of control virus nor any of the cyclin kinase inhibitor expressing viruses was able to completely block tumour progression (Figure 8). Intratumoural injection with AdBHGD1,3 resulted in a slight inhibition of tumour growth compared to phosphate bu ered saline (PBS) controls, as reported previously (Addison et al, 1997), possibly as a result of an anti-adenovirus immune response generated against infected cells. There was no signi®cant di erence in the delay of tumour progression observed between tumours injected with control virus versus the Ads expressing the various CKIs p18, p19, p21 and p27.…”

Section: The Ad Vector Expressing P16 Induces a Delay In Tumour Growtsupporting

confidence: 80%

“…Transgene expression is under the control of the murine cytomegalovirus MCMV IE promoter and the SV40 polyadenylation signal. Previously it was found that the MCMV IE promoter gave higher expression levels in murine cells when compared with those obtained with the HCMV IE promoter, and transgene expression directed by the two promoters was comparable in human cells (Addison et al, 1997). These Ad vectors directed e cient expression of the di erent transgenes in a variety of human and mouse cell lines.…”

Section: Ad Vectors Direct the Expression Of Cyclin Kinase Inhibitorsmentioning

confidence: 99%

“…The MT1A2 cell line was derived from these explanted PyMidT mammary adenocarcinoma cells (Addison et al, 1997), but MT1A2 cells are less tumorigenic than primary PyMidT cells. After a 24 h incubation of infected primary PyMidT cells to allow expression of the transgenes, syngeneic mice were injected s.c. with 5610 5 viable infected tumour cells and monitored for tumour development.…”

Section: Modulation Of Tumorigenicity By the Ckismentioning

confidence: 99%

“…The 293 cell line (human embryonic kidney Ad5E1-transformed) and the MT1A2 cell line (derived from a mammary adenocarcinoma obtained from a PyMidT transgenic mouse) (Addison et al, 1997) were cultured in minimal essential medium (MEM)-F11supplemented with 10% foetal bovine serum (FBS). MRC-5 cells (human ®broblast; ATCC CCL 171), A549 cells (human lung carcinoma; ATCC CCL 185), SKOV-3 cells (p53 negative human ovarian adenocarcinoma obtained from Hal Hirte, McMaster University) and HeLa cells (HPV-18 transformed cervical carcinoma) were maintained in a-MEM plus 10% FBS.…”

Section: Cell Culturementioning

confidence: 99%

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Comparison of the effectiveness of adenovirus vectors expressing cyclin kinase inhibitors p16INK4A, p18INK4C, p19INK4D, p21WAF1/CIP1 and p27KIP1 in inducing cell cycle arrest, apoptosis and inhibition of tumorigenicity

et al. 1999

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Cell cycle regulatory proteins are important candidates for therapeutic tumour suppressors. Adenovirus vectors were constructed to overexpress cyclin kinase inhibitors p16 INK4A , p18 INK4C , p19 INK4D , p21 WAF1/CIP1 and p27 KIP1 under the control of the murine cytomegalovirus immediate early gene promoter. These vectors directed the e cient expression of each of the cyclin kinase inhibitors and induced growth arrest, inhibited DNA synthesis, and prevented phosphorylation of the retinoblastoma protein (pRb) in cell lines expressing functional pRb. In pRbde®cient cells, expression of the cyclin kinase inhibitors was not e ective in inhibiting DNA replication or growth arrest. Interestingly, three of the cyclin kinase inhibitors, p16, p18 and p27 were found to induce apoptotic death in transduced HeLa and A549 cells. When the vectors were tested for their ability to inhibit tumorigenicity in a polyomavirus middle T antigen model of murine breast carcinoma, expression of the cyclin kinase inhibitors resulted in a delay in tumour formation that varied from several weeks for the p19 expressing vector to greater than 25 weeks for the p27 expressing vector. When tumours were injected directly with the adenovirus vectors expressing the cyclin kinase inhibitors, only treatment with the vector expressing p16 resulted in a delay in tumour growth.

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Section: The Ad Vector Expressing P16 Induces a Delay In Tumour Growtsupporting

confidence: 80%

Section: Ad Vectors Direct the Expression Of Cyclin Kinase Inhibitorsmentioning

confidence: 99%

Section: Modulation Of Tumorigenicity By the Ckismentioning

confidence: 99%

Section: Cell Culturementioning

confidence: 99%

See 2 more Smart Citations

Comparison of the effectiveness of adenovirus vectors expressing cyclin kinase inhibitors p16INK4A, p18INK4C, p19INK4D, p21WAF1/CIP1 and p27KIP1 in inducing cell cycle arrest, apoptosis and inhibition of tumorigenicity

et al. 1999

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“…However, the OBHRE promoter mediated strong b-gal expression in the tumour microenvironment, comparable to that driven by the CMV promoter. Since the CMV promoter has been recognized as one of the strongest promoters in an adenoviral context, 23 the induced activity of the OBHRE promoter observed in the tumour approaches the maximum as benchmarked by the CMV promoter. Interestingly, the OBHRE-mediated expression in the tumour model occurred predominantly at sites distal to blood vessels further supporting the physiological regulation within the tumour microenvironment.…”

Section: Hre-mediated Tumour Targetingmentioning

confidence: 99%