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Molecular target-based therapy of pancreatic cancer

Irina V Lebedeva1, Devanand Sarkar, Zao-Zhong Su

  • 1Department of Pathology, Herbert Irving Comprehensive Cancer Center, Columbia University, College of Physicians and Surgeons, New York, New York 10032, USA.

Cancer Research
|February 21, 2006
PubMed

Insights

Targeting K-ras mutations in pancreatic cancer with a dual approach combining gene therapy and K-ras inhibition shows promise. This strategy effectively suppresses tumor growth and induces cancer cell death.

Area of Science:

  • Oncology
  • Molecular Biology
  • Gene Therapy

Background:

  • Pancreatic cancer is a complex disease with limited effective therapies.
  • Kirsten-ras (K-ras) oncogene mutations are frequent (approx. 90%) early events in pancreatic cancer.
  • K-ras is a potential molecular target for pancreatic cancer treatment.

Purpose of the Study:

  • To investigate the efficacy of a dual molecular targeted therapy for K-ras mutant pancreatic cancer.
  • To evaluate the combined effects of mda-7/interleukin-24 (IL-24) gene therapy and K-ras inhibition.

Main Methods:

  • Utilized a bipartite adenovirus expressing mda-7/IL-24 and a K-ras antisense (AS) gene.
  • Investigated the combination of mda-7/IL-24 adenovirus with pharmacologic/genetic K-ras or downstream signaling inhibitors.
  • Assessed tumor growth suppression, apoptosis induction, and translational regulation of mda-7/IL-24 mRNA.

Main Results:

  • The combined therapy (mda-7/IL-24 + K-ras AS gene) suppressed growth and induced apoptosis in K-ras mutant pancreatic cancer cells.
  • Simultaneous blockade of K-ras or extracellular regulated kinase 1/2 (ERK1/2) signaling with mda-7/IL-24 therapy also inhibited tumor cell growth and survival.
  • Therapeutic effects correlated with the reversal of a translational block on mda-7/IL-24 mRNA.

Conclusions:

  • A dual molecular targeted therapy combining oncogene inhibition and cancer-specific gene expression is a promising strategy.
  • This approach has potential for effectively treating pancreatic cancer by targeting K-ras mutations and inducing apoptosis.

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