Background:AZD1152, the prodrug for AZD1152-hydroxyquinazoline pyrazol anilide (HQPA), is a selective inhibitor of Aurora B kinase activity. Preclinical evaluation of AZD1152 has been reported in several human cancer models. The potentiality of this compound in combination therapy warrants further investigation in solid tumours.Experimental design:This study explored the effects of AZD1152-HQPA in colon and pancreatic tumour cells. The antitumour properties of AZD1152, either as single agent or in combination with chemotherapeutics, were evaluated in each study model. The efficacy and the toxicity of AZD1152 alone and in combination with gemcitabine were validated in pancreatic tumour xenograft model.Results:AZD1152-HQPA treatment resulted in a dramatic increase of chromosome number, modification of cell cycle and induction of apoptosis. The most effective combination was that with chemotherapeutics given soon after AZD1152 in both tumour cell types. The effectiveness of the sequential schedule of AZD1152 with gemcitabine was confirmed in nude mice bearing MiaPaCa-2 tumours, showing inhibition of tumour volumes and delaying of tumour growth after the interruption of the treatments.Conclusion:Here we show that AZD1152-HQPA enhances oxaliplatin and gemcitabine effectiveness in colon and pancreatic cancer, respectively. First, we provide advances into administration schedules and dosing regimens for the combination treatment in in vivo pancreatic tumour.
A study was undertaken to attempt to quantify the alleged inhibitory effect of the serum of cancer patients on in‐vitro lymphocyte transformation. The sera of ten cancer patients, ten patients with non‐neoplastic diseases, and ten healthy controls were separately tested in short‐term tissue cultures of donor lymphocytes. All cultures were grown in triplicate and repeated on three different occasions. Lymphocyte transformation was measured by radioactive thymidine uptake. There was no significant difference between the lymphocyte transformation occurring in the presence of the serum of cancer patients and of that found in the serum of healthy controls. Under the conditions of this study, we have been unable to confirm the presence of a decreased response to phytohemagglutinin by normal lymphocytes grown in cultures with sera of cancer patients.
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