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AACR: EGFR Involved in KRAS-Driven Pancreatic Cancer

Also, GLV-1h153 facilitates uptake of radioiodine, offering imaging and therapeutic value

THURSDAY, Sept. 15 (HealthDay News) -- The epidermal growth factor receptor EGFR gene is involved in the development of KRAS-pancreatic cancer; and the vaccinia virus construct GLV-1h153 may be a promising oncolytic agent for the treatment and monitoring of pancreatic cancer, according to two experimental studies presented at the American Association for Cancer Research International Conference on Frontiers in Basic Cancer Research, held from Sept. 14 to 18 in San Francisco.

Barbara M. Grüner, from the Technical University Munich in Germany, and colleagues investigated the effects of EGFR on KRAS-driven pancreatic cancer development in genetically-engineered mouse models. Mice with pancreatic-specific deletion of EGFR were compared with KRAS mouse models for pancreatic cancer. Contrary to KrasG12D control mice, KrasG12D;EgfrΔ/Δ mouse models of induced pancreatitis did not develop pancreatic intraepithelial neoplasia. In KrasG12D;EgfrΔ/Δ mice, initiating events were still detectable, but progression to ductal-like structures did not occur.

Dana Haddad, M.D., Ph.D., from the Memorial Sloan-Kettering Cancer Center in New York City, and colleagues investigated the feasibility and parameters of systemic virotherapy together with radiotherapeutic response of pancreatic cancer xenografts treated with GLV-1h153. GLV-1h153 was injected systemically or intratumorally into pancreatic cancer xenografts in nude mice and 124I-positron emissions tomography (PET) was used image tumors. PET signal intensity correlated with antitumor response. Colonization of tumors with GLV-1h153 facilitated uptake of radioiodine at potentially therapeutic doses. Combining GLV-1h153 with 131I led to enhanced tumor kill compared to either treatment alone.

"GLV-1h153 provided insights into tumor biological activity and facilitated enhanced tumor kill when combined with systemic targeted radiotherapy," Haddad and colleagues write.

Press Release - Grüner
Press Release - Haddad
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