De novo carcinogenesis promoted by chronic inflammation is B lymphocyte dependent

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

Research output: Contribution to journalArticle

506 Citations (Scopus)

Abstract

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
Volume7
Issue number5
DOIs
StatePublished - May 2005
Externally publishedYes

Fingerprint

Carcinogenesis
B-Lymphocytes
Inflammation
T-Lymphocytes
Neoplasms
Adoptive Transfer
Epidermis
Transgenic Mice
Hyperplasia
Leukocytes
Serum

ASJC Scopus subject areas

  • Cancer Research
  • Cell Biology
  • Oncology

Cite this

De novo carcinogenesis promoted by chronic inflammation is B lymphocyte dependent. / De Visser, Karin E.; Korets, Lidiya V.; Coussens, Lisa.

In: Cancer Cell, Vol. 7, No. 5, 05.2005, p. 411-423.

Research output: Contribution to journalArticle

De Visser, Karin E. ; Korets, Lidiya V. ; Coussens, Lisa. / De novo carcinogenesis promoted by chronic inflammation is B lymphocyte dependent. In: Cancer Cell. 2005 ; Vol. 7, No. 5. pp. 411-423.
@article{1f8166489cb24f4e88d0b3f60c5ea126,
title = "De novo carcinogenesis promoted by chronic inflammation is B lymphocyte dependent",
abstract = "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.",
author = "{De Visser}, {Karin E.} and Korets, {Lidiya V.} and Lisa Coussens",
year = "2005",
month = "5",
doi = "10.1016/j.ccr.2005.04.014",
language = "English (US)",
volume = "7",
pages = "411--423",
journal = "Cancer Cell",
issn = "1535-6108",
publisher = "Cell Press",
number = "5",

}

TY - JOUR

T1 - De novo carcinogenesis promoted by chronic inflammation is B lymphocyte dependent

AU - De Visser, Karin E.

AU - Korets, Lidiya V.

AU - Coussens, Lisa

PY - 2005/5

Y1 - 2005/5

N2 - 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.

AB - 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.

UR - http://www.scopus.com/inward/record.url?scp=19344365408&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=19344365408&partnerID=8YFLogxK

U2 - 10.1016/j.ccr.2005.04.014

DO - 10.1016/j.ccr.2005.04.014

M3 - Article

C2 - 15894262

AN - SCOPUS:19344365408

VL - 7

SP - 411

EP - 423

JO - Cancer Cell

JF - Cancer Cell

SN - 1535-6108

IS - 5

ER -