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June 5, 2008Journal of VirologyOpen Access

In Vivo Potential Effects of Adenovirus Type 5 E1A and E1B on Lung Carcinogenesis and Lymphoproliferative Inflammation

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Population

Lung-specific transgenic mouse models generated from B6/SJL fertilized eggs bred to C57BL/6 mice

Comparison

Transgenic expression of Ad5 E1A and E1B… vs Nontransgenic mice derived from the same litters

Design

Preclinical

Follow-up

Up to 25 months

Authors

YYYongping YangCMColin McKerlieLZLu Zhan

Discussion

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Overview

Hypothesis-generating for Ad5 vector safety in humans; leaves open clinical translation of these animal oncogenesis findings.

Structured PICO

P
Population
Lung-specific transgenic mouse models (SPCE1A or SPCE1A E1B) generated from B6/SJL fertilized eggs bred to C57BL/6 mice
I
Intervention
Transgenic expression of Ad5 E1A and E1B oncogenes (or E1A alone) under the control of human pulmonary epithelial cell-specific promoter of surfactant protein C regulatory element (pSPC)
C
Comparator
Nontransgenic mice derived from the same litters
O
Outcome
Lung carcinogenesis and lymphoproliferative inflammationsurrogate

Latent Ad5 E1A and E1B oncogenes cooperate to induce lung carcinogenesis and lymphoproliferative inflammation in vivo by impairing p53 and apoptosis responses.

Limitations

  • Differences in tumor type between the transgenic mice and humans due to species difference (e.g., lack of small-cell lung cancer in the transgenic mice)

Cite This Study

Yang et al. (2008) studied this question.

synapsesocial.com/papers/6a8a50d74e1caf75feec6403https://doi.org/10.1128/jvi.00536-08
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