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Alfacell Provides Shareholder Update
Date:6/19/2009

emotherapy out of the cells, so anything that will interfere with this function may allow more drug to come into the cells and cause death of the cancer. Another major master controller gene known as nfkB is also known to be elevated when normal cells turn into mesothelioma cells, and high levels of this gene have been associated with resistance to chemotherapy. In order to investigate whether Onconase specifically targets these three genes, we added Onconase to three mesothelioma cell lines at a dose which is achievable in humans, and then using molecular biology techniques including polymerase chain reaction, measured the levels of the MDR and nfkB genes after treatment with the drug. Striking decreases in all of these genes in the mesothelioma cell lines were seen after treatment with Onconase validating the hypothesis that one of the mechanisms of action of Onconase is to decrease resistance to chemotherapy. Moreover, these data in cell lines are complemented by most recent animal study in mice bearing tumors of varying sensitivity to Cisplatin and Carbo Platinum. In all of the animal models, the addition of Onconase to Cisplatin significantly increased the tumor growth inhibition compared to Cisplatin or Onconase alone, and in the tumor model most resistant to platinum, Onconase addition to platinum increased tumor growth inhibition from 37% to 73%. These in vitro and in vivo data, which are presently being prepared for publication emphasize the uniqueness of Onconase in its ability to directly modulate chemotherapy sensitivity, and mandate a trial in non-small cell lung cancer to prospectively demonstrate increased tumor responses when Onconase is added to a standard lung cancer chemotherapy regimen." Another independent study in vivo is underway that may confirm Dr. Pass' in vitro study.

After much thought, consideration, and input from highly respected lung experts, we have decided our path moving forward would be t
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