| First Author | de Visser KE | Year | 2005 |
| Journal | Cancer Cell | Volume | 7 |
| Issue | 5 | Pages | 411-23 |
| PubMed ID | 15894262 | Mgi Jnum | J:98942 |
| Mgi Id | MGI:3580757 | Doi | 10.1016/j.ccr.2005.04.014 |
| Citation | de Visser KE, et al. (2005) De novo carcinogenesis promoted by chronic inflammation is B lymphocyte dependent. Cancer Cell 7(5):411-23 |
| abstractText | Chronic inflammation predisposes tissue to cancer development; however, regulatory mechanisms underlying recruitment of innate leukocytes toward developing neoplasms are obscure. We report that genetic elimination of mature T and B lymphocytes in a transgenic mouse model of inflammation-associated de novo epithelial carcinogenesis, e.g., K14-HPV16 mice, limits neoplastic progression to development of epithelial hyperplasias that fail to recruit innate immune cells. Adoptive transfer of B lymphocytes or serum from HPV16 mice into T and B cell-deficient/HPV16 mice restores innate immune cell infiltration into premalignant tissue and reinstates necessary parameters for full malignancy, e.g., chronic inflammation, angiogenic vasculature, hyperproliferative epidermis. These findings support a model in which B lymphocytes are required for establishing chronic inflammatory states that promote de novo carcinogenesis. |
