Pathology of mouse models of intestinal cancer: Consensus report and recommendations

Gregory P. Boivin, Kay Washington, Kan Yang, Jerrold M. Ward, Theresa P. Pretlow, Robert Russell, David G. Besselsen, Virginia L. Godfrey, Thomas C Doetschman, William F. Dove, Henry C. Pitot, Richard B. Halberg, Steven H. Itzkowltz, Joanna Groden, Robert J. Coffey

Research output: Contribution to journalArticle

369 Citations (Scopus)

Abstract

The marked diversity in the phenotype of intestinal neoplasia in murine models offers opportunities to model many characteristics of human CRC, including tumor progression, metastasis, gross morphology, and histology. However, the lack of a consistent model of metastasis is of particular concern in developing mouse models of human CRC. AOM-treated mice consistently develop metastasis, but the absence of control by known genetic mutations under carcinogen treatment makes this model system less desirable. The Smad3-/-, PI(3)Kγ-/-,90 and Apc1638N/+ mutants are the only mouse models reported to develop colonic adenocarcinomas that metastasize to the lymph nodes and liver, which are common metastatic sites of human CRCs. However, there has been difficulty reproducing this observation in similar strains from different laboratories. Neoplastic lesions in mice with specific genetic alterations often do not parallel the phenotype of human cancer. Lastly, the role of intestinal pathogens and their contribution to the inflammatory response and tumor initiation is generally underappreciated. Despite these limitations, mouse models are invaluable in approximating the pathogenesis of human intestinal cancer and thus provide an in vivo platform for identifying therapeutic targets and developing new strategies for prevention and treatment.

Original languageEnglish (US)
Pages (from-to)762-777
Number of pages16
JournalGastroenterology
Volume124
Issue number3
DOIs
StatePublished - Mar 1 2003
Externally publishedYes

Fingerprint

Intestinal Neoplasms
Pathology
Neoplasm Metastasis
Neoplasms
Phenotype
Carcinogens
Histology
Adenocarcinoma
Therapeutics
Lymph Nodes
Mutation
Liver

ASJC Scopus subject areas

  • Gastroenterology

Cite this

Boivin, G. P., Washington, K., Yang, K., Ward, J. M., Pretlow, T. P., Russell, R., ... Coffey, R. J. (2003). Pathology of mouse models of intestinal cancer: Consensus report and recommendations. Gastroenterology, 124(3), 762-777. https://doi.org/10.1053/gast.2003.50094

Pathology of mouse models of intestinal cancer : Consensus report and recommendations. / Boivin, Gregory P.; Washington, Kay; Yang, Kan; Ward, Jerrold M.; Pretlow, Theresa P.; Russell, Robert; Besselsen, David G.; Godfrey, Virginia L.; Doetschman, Thomas C; Dove, William F.; Pitot, Henry C.; Halberg, Richard B.; Itzkowltz, Steven H.; Groden, Joanna; Coffey, Robert J.

In: Gastroenterology, Vol. 124, No. 3, 01.03.2003, p. 762-777.

Research output: Contribution to journalArticle

Boivin, GP, Washington, K, Yang, K, Ward, JM, Pretlow, TP, Russell, R, Besselsen, DG, Godfrey, VL, Doetschman, TC, Dove, WF, Pitot, HC, Halberg, RB, Itzkowltz, SH, Groden, J & Coffey, RJ 2003, 'Pathology of mouse models of intestinal cancer: Consensus report and recommendations', Gastroenterology, vol. 124, no. 3, pp. 762-777. https://doi.org/10.1053/gast.2003.50094
Boivin GP, Washington K, Yang K, Ward JM, Pretlow TP, Russell R et al. Pathology of mouse models of intestinal cancer: Consensus report and recommendations. Gastroenterology. 2003 Mar 1;124(3):762-777. https://doi.org/10.1053/gast.2003.50094
Boivin, Gregory P. ; Washington, Kay ; Yang, Kan ; Ward, Jerrold M. ; Pretlow, Theresa P. ; Russell, Robert ; Besselsen, David G. ; Godfrey, Virginia L. ; Doetschman, Thomas C ; Dove, William F. ; Pitot, Henry C. ; Halberg, Richard B. ; Itzkowltz, Steven H. ; Groden, Joanna ; Coffey, Robert J. / Pathology of mouse models of intestinal cancer : Consensus report and recommendations. In: Gastroenterology. 2003 ; Vol. 124, No. 3. pp. 762-777.
@article{aa5d6619c2ef43559b6bffd93b9b6ec4,
title = "Pathology of mouse models of intestinal cancer: Consensus report and recommendations",
abstract = "The marked diversity in the phenotype of intestinal neoplasia in murine models offers opportunities to model many characteristics of human CRC, including tumor progression, metastasis, gross morphology, and histology. However, the lack of a consistent model of metastasis is of particular concern in developing mouse models of human CRC. AOM-treated mice consistently develop metastasis, but the absence of control by known genetic mutations under carcinogen treatment makes this model system less desirable. The Smad3-/-, PI(3)Kγ-/-,90 and Apc1638N/+ mutants are the only mouse models reported to develop colonic adenocarcinomas that metastasize to the lymph nodes and liver, which are common metastatic sites of human CRCs. However, there has been difficulty reproducing this observation in similar strains from different laboratories. Neoplastic lesions in mice with specific genetic alterations often do not parallel the phenotype of human cancer. Lastly, the role of intestinal pathogens and their contribution to the inflammatory response and tumor initiation is generally underappreciated. Despite these limitations, mouse models are invaluable in approximating the pathogenesis of human intestinal cancer and thus provide an in vivo platform for identifying therapeutic targets and developing new strategies for prevention and treatment.",
author = "Boivin, {Gregory P.} and Kay Washington and Kan Yang and Ward, {Jerrold M.} and Pretlow, {Theresa P.} and Robert Russell and Besselsen, {David G.} and Godfrey, {Virginia L.} and Doetschman, {Thomas C} and Dove, {William F.} and Pitot, {Henry C.} and Halberg, {Richard B.} and Itzkowltz, {Steven H.} and Joanna Groden and Coffey, {Robert J.}",
year = "2003",
month = "3",
day = "1",
doi = "10.1053/gast.2003.50094",
language = "English (US)",
volume = "124",
pages = "762--777",
journal = "Gastroenterology",
issn = "0016-5085",
publisher = "W.B. Saunders Ltd",
number = "3",

}

TY - JOUR

T1 - Pathology of mouse models of intestinal cancer

T2 - Consensus report and recommendations

AU - Boivin, Gregory P.

AU - Washington, Kay

AU - Yang, Kan

AU - Ward, Jerrold M.

AU - Pretlow, Theresa P.

AU - Russell, Robert

AU - Besselsen, David G.

AU - Godfrey, Virginia L.

AU - Doetschman, Thomas C

AU - Dove, William F.

AU - Pitot, Henry C.

AU - Halberg, Richard B.

AU - Itzkowltz, Steven H.

AU - Groden, Joanna

AU - Coffey, Robert J.

PY - 2003/3/1

Y1 - 2003/3/1

N2 - The marked diversity in the phenotype of intestinal neoplasia in murine models offers opportunities to model many characteristics of human CRC, including tumor progression, metastasis, gross morphology, and histology. However, the lack of a consistent model of metastasis is of particular concern in developing mouse models of human CRC. AOM-treated mice consistently develop metastasis, but the absence of control by known genetic mutations under carcinogen treatment makes this model system less desirable. The Smad3-/-, PI(3)Kγ-/-,90 and Apc1638N/+ mutants are the only mouse models reported to develop colonic adenocarcinomas that metastasize to the lymph nodes and liver, which are common metastatic sites of human CRCs. However, there has been difficulty reproducing this observation in similar strains from different laboratories. Neoplastic lesions in mice with specific genetic alterations often do not parallel the phenotype of human cancer. Lastly, the role of intestinal pathogens and their contribution to the inflammatory response and tumor initiation is generally underappreciated. Despite these limitations, mouse models are invaluable in approximating the pathogenesis of human intestinal cancer and thus provide an in vivo platform for identifying therapeutic targets and developing new strategies for prevention and treatment.

AB - The marked diversity in the phenotype of intestinal neoplasia in murine models offers opportunities to model many characteristics of human CRC, including tumor progression, metastasis, gross morphology, and histology. However, the lack of a consistent model of metastasis is of particular concern in developing mouse models of human CRC. AOM-treated mice consistently develop metastasis, but the absence of control by known genetic mutations under carcinogen treatment makes this model system less desirable. The Smad3-/-, PI(3)Kγ-/-,90 and Apc1638N/+ mutants are the only mouse models reported to develop colonic adenocarcinomas that metastasize to the lymph nodes and liver, which are common metastatic sites of human CRCs. However, there has been difficulty reproducing this observation in similar strains from different laboratories. Neoplastic lesions in mice with specific genetic alterations often do not parallel the phenotype of human cancer. Lastly, the role of intestinal pathogens and their contribution to the inflammatory response and tumor initiation is generally underappreciated. Despite these limitations, mouse models are invaluable in approximating the pathogenesis of human intestinal cancer and thus provide an in vivo platform for identifying therapeutic targets and developing new strategies for prevention and treatment.

UR - http://www.scopus.com/inward/record.url?scp=0037370137&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0037370137&partnerID=8YFLogxK

U2 - 10.1053/gast.2003.50094

DO - 10.1053/gast.2003.50094

M3 - Article

C2 - 12612914

AN - SCOPUS:0037370137

VL - 124

SP - 762

EP - 777

JO - Gastroenterology

JF - Gastroenterology

SN - 0016-5085

IS - 3

ER -