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Introduction: Tumor immunology is important in cancer progression, but poorly understood. Few data evaluate the effects of B lymphocytes on cancer. In our model of murine pancreatic cancer in obesity, we have observed fewer circulating B lymphocytes, reduced B lymphocyte gene expression, and fewer tumor infiltrating B lymphocytes in the tumor microenvironment of obese mice. These mice also had larger tumors than control mice. These observations suggest that decreased B lymphocytes, as seen in obesity, permit accelerated pancreatic cancer growth. We therefore hypothesized that B lymphocyte activity inhibits the growth of murine pancreatic cancer. Methods: Seven-month old C57 Bl/6J mice were studied. Splenic lymphocytes were extracted by pressure injection and B lymphocytes isolated by nylon wool microfiltration. The B lymphocytes were activated with 10μg/ml LPS. For time course evaluation, B cells were incubated for 18, 24, 42, and 48 hours before collection of the supernatant media. For concentration evaluation, B cells were seeded at 1.5x106, 3x106, and 6x106 cells/ml and incubated for 24 hours. 50μl of the conditioned media was collected and added to 5000 PAN02 murine pancreatic cancer cells. After 20 hours of growth, a standard MTT assay was performed to evaluate proliferation. Student’s t-test and ANOVA were used to compare results, with a p value <0.05 considered significant.Results: B lymphocyte conditioned media significantly inhibited PAN02 proliferation in both a time- and concentration-dependent fashion relative to control (Figure). Conclusion: These data show that B lymphocyte conditioned media inhibited PAN02 proliferation in both a time- and concentration dependent fashion. We conclude that B lymphocytes play an important role in the tumor immunology of pancreatic cancer.