PortalPublikationenMSH2 deficient mice are viable and susceptible to lymphoid t...

MSH2 deficient mice are viable and susceptible to lymphoid tumours

Standard

MSH2 deficient mice are viable and susceptible to lymphoid tumours. / Reitmair, A H; Schmits, R; Ewel, A; Bapat, B; Redston, M; Mitri, A; Waterhouse, P; Mittrücker, H W; Wakeham, A; Liu, B.

in: NAT GENET, Jahrgang 11, Nr. 1, 01.09.1995, S. 64-70.

Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung

Harvard

Reitmair, AH, Schmits, R, Ewel, A, Bapat, B, Redston, M, Mitri, A, Waterhouse, P, Mittrücker, HW, Wakeham, A & Liu, B 1995, 'MSH2 deficient mice are viable and susceptible to lymphoid tumours', NAT GENET, Jg. 11, Nr. 1, S. 64-70. https://doi.org/10.1038/ng0995-64

APA

Reitmair, A. H., Schmits, R., Ewel, A., Bapat, B., Redston, M., Mitri, A., Waterhouse, P., Mittrücker, H. W., Wakeham, A., & Liu, B. (1995). MSH2 deficient mice are viable and susceptible to lymphoid tumours. NAT GENET, 11(1), 64-70. https://doi.org/10.1038/ng0995-64

Vancouver

Reitmair AH, Schmits R, Ewel A, Bapat B, Redston M, Mitri A et al. MSH2 deficient mice are viable and susceptible to lymphoid tumours. NAT GENET. 1995 Sep 1;11(1):64-70. https://doi.org/10.1038/ng0995-64

Bibtex

@article{f65d398771374edf8581c8bb20e909ff,
title = "MSH2 deficient mice are viable and susceptible to lymphoid tumours",
abstract = "Alterations of the human MSH2 gene, a homologue of the bacterial MutS mismatch repair gene, co-segregate with the majority of hereditary non-polyposis colon cancer (HNPCC) cases. We have generated homozygous MSH2-/- mice. Surprisingly, these mice were found to be viable, produced offspring in a mendelian ratio and bred through at least two generations. Starting at two months of age homozygous-/- mice began, with high frequency, to develop lymphoid tumours that contained microsatellite instabilities. These data establish a direct link between MSH2 deficiency and the pathogenesis of cancer. These mutant mice should be good models to study the progression of tumours and also to screen carcinogenic and anti-cancer agents.",
keywords = "Animals, Base Sequence, Cell Transformation, Neoplastic, Colorectal Neoplasms, Hereditary Nonpolyposis, DNA Repair, DNA, Neoplasm, DNA, Satellite, DNA-Binding Proteins, Female, Fungal Proteins, Gene Targeting, Genotype, Humans, Lymphoid Tissue, Male, Meiosis, Mice, Mice, Knockout, Mice, Mutant Strains, Molecular Sequence Data, MutS Homolog 2 Protein, Precursor Cell Lymphoblastic Leukemia-Lymphoma, Species Specificity",
author = "Reitmair, {A H} and R Schmits and A Ewel and B Bapat and M Redston and A Mitri and P Waterhouse and Mittr{\"u}cker, {H W} and A Wakeham and B Liu",
year = "1995",
month = sep,
day = "1",
doi = "10.1038/ng0995-64",
language = "English",
volume = "11",
pages = "64--70",
journal = "NAT GENET",
issn = "1061-4036",
publisher = "NATURE PUBLISHING GROUP",
number = "1",

}

RIS

TY - JOUR

T1 - MSH2 deficient mice are viable and susceptible to lymphoid tumours

AU - Reitmair, A H

AU - Schmits, R

AU - Ewel, A

AU - Bapat, B

AU - Redston, M

AU - Mitri, A

AU - Waterhouse, P

AU - Mittrücker, H W

AU - Wakeham, A

AU - Liu, B

PY - 1995/9/1

Y1 - 1995/9/1

N2 - Alterations of the human MSH2 gene, a homologue of the bacterial MutS mismatch repair gene, co-segregate with the majority of hereditary non-polyposis colon cancer (HNPCC) cases. We have generated homozygous MSH2-/- mice. Surprisingly, these mice were found to be viable, produced offspring in a mendelian ratio and bred through at least two generations. Starting at two months of age homozygous-/- mice began, with high frequency, to develop lymphoid tumours that contained microsatellite instabilities. These data establish a direct link between MSH2 deficiency and the pathogenesis of cancer. These mutant mice should be good models to study the progression of tumours and also to screen carcinogenic and anti-cancer agents.

AB - Alterations of the human MSH2 gene, a homologue of the bacterial MutS mismatch repair gene, co-segregate with the majority of hereditary non-polyposis colon cancer (HNPCC) cases. We have generated homozygous MSH2-/- mice. Surprisingly, these mice were found to be viable, produced offspring in a mendelian ratio and bred through at least two generations. Starting at two months of age homozygous-/- mice began, with high frequency, to develop lymphoid tumours that contained microsatellite instabilities. These data establish a direct link between MSH2 deficiency and the pathogenesis of cancer. These mutant mice should be good models to study the progression of tumours and also to screen carcinogenic and anti-cancer agents.

KW - Animals

KW - Base Sequence

KW - Cell Transformation, Neoplastic

KW - Colorectal Neoplasms, Hereditary Nonpolyposis

KW - DNA Repair

KW - DNA, Neoplasm

KW - DNA, Satellite

KW - DNA-Binding Proteins

KW - Female

KW - Fungal Proteins

KW - Gene Targeting

KW - Genotype

KW - Humans

KW - Lymphoid Tissue

KW - Male

KW - Meiosis

KW - Mice

KW - Mice, Knockout

KW - Mice, Mutant Strains

KW - Molecular Sequence Data

KW - MutS Homolog 2 Protein

KW - Precursor Cell Lymphoblastic Leukemia-Lymphoma

KW - Species Specificity

U2 - 10.1038/ng0995-64

DO - 10.1038/ng0995-64

M3 - SCORING: Journal article

C2 - 7550317

VL - 11

SP - 64

EP - 70

JO - NAT GENET

JF - NAT GENET

SN - 1061-4036

IS - 1

ER -