De novo carcinogenesis promoted by chronic inflammation is B lymphocyte dependent

Karin E. De Visser, Lidiya V. Korets, Lisa M. Coussens

Research output: Contribution to journalArticlepeer-review

642 Scopus citations


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.

Original languageEnglish (US)
Pages (from-to)411-423
Number of pages13
JournalCancer Cell
Issue number5
StatePublished - May 2005
Externally publishedYes

ASJC Scopus subject areas

  • Oncology
  • Cancer Research


Dive into the research topics of 'De novo carcinogenesis promoted by chronic inflammation is B lymphocyte dependent'. Together they form a unique fingerprint.

Cite this