Combined Inactivation of MYC and K-Ras Oncogenes Reverses Tumorigenesis in Lung Adenocarcinomas and Lymphomas Dual-Oncogene Inhibition Model
2008

Inhibition of MYC and K-Ras Oncogenes Reverses Tumor Growth in Lung Cancer

Sample size: 51 publication 10 minutes Evidence: high

Author Information

Author(s): Tran Phuoc T., Fan Alice C., Bendapudi Pavan K., Koh Shan, Komatsubara Kim, Chen Joy, Horng George, Bellovin David I., Giuriato Sylvie, Wang Craig S., Whitsett Jeffrey A., Felsher Dean W.

Primary Institution: Stanford University School of Medicine

Hypothesis

How do MYC and K-rasG12D oncogenes cooperate for tumor initiation and maintenance?

Conclusion

The combined inactivation of MYC and K-rasG12D oncogenes can lead to significant tumor regression in lung adenocarcinomas and lymphomas.

Supporting Evidence

  • MYC-induced lung tumors did not regress completely upon MYC inactivation.
  • K-rasG12D-induced lung tumors regressed completely upon oncogene inactivation.
  • Combined inactivation of MYC and K-rasG12D resulted in more frequent complete lung tumor regression.
  • Stat3 and Stat5 phosphorylation persisted in non-regressing MYC-induced lung tumors.

Takeaway

This study shows that turning off two cancer genes at the same time can help shrink tumors in the lungs and lymph nodes.

Methodology

The study used double conditional transgenic mouse models to investigate the effects of MYC and K-rasG12D inactivation on tumor growth.

Limitations

The study primarily focuses on specific mouse models, which may not fully replicate human cancer biology.

Statistical Information

P-Value

p<0.0001

Statistical Significance

p<0.0001

Digital Object Identifier (DOI)

10.1371/journal.pone.0002125

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