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Cited by 2,051Cancer-related Molecular PathwaysCell death mechanisms and regulationDNA Repair Mechanisms

The DOI matches its Crossref record; 5 of the 5 references it cites were found in a registry or an index.

Tumor spectrum analysis in p53-mutant mice

Jacks, Tyler, Remington, Lee, Williams, Bart O., Schmitt, Earlene M., Halachmi, Schlomit, Bronson, Roderick T., Weinberg, Robert A.·1994·Current Biology
DOI 10.1016/s0960-9822(00)00002-6
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Abstract

Background The p53 tumor suppressor gene is mutated in a large percentage of human malignancies, including tumors of the colon, breast, lung and brain. Individuals who inherit one mutant allele of p53 are susceptible to a wide range of tumor types. The gene encodes a transcriptional regulator that may function in the cellular response to DNA damage. The construction of mouse strains carrying germline mutations of p53 facilitates analysis of the function of p53 in normal cells and tumorigenesis.Results In order to study the effects of p53 mutation in vivo, we have constructed a mouse strain carrying a germline disruption of the gene. This mutation removes approximately 40% of the coding capacity of p53 and completely eliminates synthesis of p53 protein. As observed previously for a different germline mutation of p53, animals homozygous for this p53 deletion mutation are viable but highly predisposed to malignancy. Heterozygous animals also have an increased cancer risk, although the distribution of tumor types in these animals differs from that in homozygous mutants. In most cases, tumorigenesis in heterozygous animals is accompanied by loss of the wild-type p53 allele.Conclusion We reaffirm that p53 function is not required for normal mouse development and conclude that p53 status can strongly influence tumor latency and tissue distribution.

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Citations

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Research works printed but not linked: 29

  1. Hollstein, 1991, p53 mutations in human cancers, Science, 253, 49, 10.1126/science.1905840 · DOI · Paper page
  2. Malkin, 1990, Germ line p53 mutations in a familial syndrome of breast cancer, sarcomas, and other neoplasms, Science, 250, 1233, 10.1126/science.1978757 · DOI · Paper page
  3. Malkin, 1993, p53 and the Li-Fraumeni syndrome, Cancer Genet Cytogenet, 66, 83, 10.1016/0165-4608(93)90233-C · DOI
  4. Kastan, 1991, Participation of p53 protein in the cellular response to DNA damage, Cancer Res, 51, 6304
  5. Yin, 1992, Wild-type p53 restores cell-cycle control and inhibits gene amplification in cells with mutant p53 alleles, Cell, 70, 937, 10.1016/0092-8674(92)90244-7 · DOI
  6. Livingstone, 1992, Altered cell cycle arrest and gene amplification potential accompany loss of wild-type p53, Cell, 70, 923, 10.1016/0092-8674(92)90243-6 · DOI
  7. Clarke, 1993, Thymocyte apoptosis induced by p53-dependent and independent pathways, Nature, 362, 849, 10.1038/362849a0 · DOI
  8. Kern, 1991, Identification of p53 as a sequence-specific DNA binding protein, Science, 252, 1708, 10.1126/science.2047879 · DOI
  9. Wu, 1993, The p53-mdm-2 autoregulatory feedback loop, Genes Dev, 7, 1126, 10.1101/gad.7.7a.1126 · DOI · Paper page
  10. Kern, 1992, Oncogenic forms of p53 inhibit p53-regulated gene expression, Science, 256, 827, 10.1126/science.1589764 · DOI
  11. Seto, 1992, Wild-type p53 binds to the TATA-binding protein and represses transcription, Proc Natl Acad Sci USA, 89, 12028, 10.1073/pnas.89.24.12028 · DOI
  12. Zambetti, 1992, Wild-type p53 mediates positive regulation of gene expression through a specific DNA sequence element, Genes Dev, 6, 1143, 10.1101/gad.6.7.1143 · DOI
  13. Mansour, 1988, Disruption of the proto-oncogene int-2 in mouse embryo-derived stem cells: a general strategy for targeting mutations to non-selectable genes, Nature, 336, 348, 10.1038/336348a0 · DOI · Paper page
  14. Wade-Evans, 1985, Precise epitope mapping of the murine transformation-associated protein, p53, EMBO J, 4, 699, 10.1002/j.1460-2075.1985.tb03686.x · DOI
  15. Hinds, 1989, Mutation is required to activate the p53 gene for cooperation with the ras oncogene and transformation, J Virol, 63, 739, 10.1128/JVI.63.2.739-746.1989 · DOI
  16. Dittmer, 1993, Gain of function mutations in p53, Nature Genet, 4, 42, 10.1038/ng0593-42 · DOI · Paper page
  17. Wolf, 1984, Reconstitution of p53 expression in a non-producer Ab-MuLV-transformed cell line by transfection of a functional p53 gene, Cell, 38, 119, 10.1016/0092-8674(84)90532-4 · DOI
  18. Von Boehmer, 1988, The developmental biology of T lymphocytes, Ann Rev Immunol, 6, 309, 10.1146/annurev.immunol.6.1.309 · DOI
  19. Capecchi, 1989, Altering the genome by homologous recombination, Science, 244, 1288, 10.1126/science.2660260 · DOI
  20. Lane, 1993, A death in the life of p53, Nature, 362, 786, 10.1038/362786a0 · DOI
  21. Debbas, 1993, Wild-type p53 mediates apoptosis by E1A, which is inhibited by E1B, Genes Dev, 7, 546, 10.1101/gad.7.4.546 · DOI
  22. Lowe, 1993, p53-dependent apoptosis modulates the cytoxicity of anticancer agents, Cell, 74, 957, 10.1016/0092-8674(93)90719-7 · DOI
  23. Jacks, 1992, Effects of an Rb mutation in the mouse, Nature, 359, 295, 10.1038/359295a0 · DOI
  24. Clarke, 1992, Requirement for a functional Rb-1 gene in murine development, Nature, 359, 328, 10.1038/359328a0 · DOI
  25. Lee, 1992, Mice deficient for Rb are nonviable and show defects in neurogenesis and haematopoiesis, Nature, 359, 288, 10.1038/359288a0 · DOI
  26. Hanahan, 1989, Transgenic mice as probes into complex systems, Science, 246, 1265, 10.1126/science.2686032 · DOI
  27. Bienz, 1984, Analysis of the gene coding for the murine cellular tumour antigen p53, EMBO J, 3, 2179, 10.1002/j.1460-2075.1984.tb02110.x · DOI
  28. Tybulewicz, 1991, Neonatal lethality and lymphopenia in mice with a homozygous disruption of the c-abl proto-oncogene, Cell, 65, 1153, 10.1016/0092-8674(91)90011-M · DOI
  29. Gossler, 1986, Transgenesis by means of blastocyst-derived embryonic stem cell lines, Proc Natl Acad Sci USA, 83, 9065, 10.1073/pnas.83.23.9065 · DOI

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Metadata

Authors
Jacks, T., Remington, L., Williams, B. O., Schmitt, E. M., Halachmi, S., Bronson, R. T., & Weinberg, R. A.
Affiliations
  • Massachusetts Institute of Technology (US)
  • Tufts University (US)
  • Whitehead Institute for Biomedical Research (US)
Corresponding author
Jacks, Tyler
ORCID
Venue
Current Biology
Publisher
Elsevier BV
Published
1994-01
Volume
4
Issue
1
Pages
1-7
ISSN
0960-9822 (ISSN-L)
DOI
10.1016/s0960-9822(00)00002-6
OpenAlex
W2088740611
Cited by
2,051
References
5
Citations by year
2026: 17 · 2025: 33 · 2024: 51 · 2023: 46 · 2022: 35 · 2021: 58 · 2020: 63 · 2019: 44 · 2018: 61 · 2017: 57 · 2016: 66 · 2015: 51 · 2014: 75 · 2013: 72 · 2012: 102
FWCI
17.41
Type
journal article
Language
en
Open access
closed
Licence
www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations
  • Current Biology (publishedVersion)
  • PubMed (publishedVersion)
  • The Mouseion at the JAXlibrary (Jackson Laboratory) (submittedVersion)
Funders
  • National Institutes of Health (5r35ca039826-10)
  • National Cancer Institute (5R35 CA39826)
Topics
  • Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
Keywords
p53, tumor suppressor, germline mutations, p53 knockout mice, tumor spectrum, tumor latency, heterozygous carriers, cancer susceptibility, DNA damage response, transcriptional regulation
MeSH terms
Alleles, Animals, Base Sequence, Chimera, Chromosome Deletion, Crosses, Genetic, DNA Damage, Female, Humans, Male, Mice, Inbred C57BL, Mice, Transgenic, Molecular Sequence Data, Neoplasms, Experimental, Polymerase Chain Reaction, Genes, p53, Tumor Suppressor Protein p53, Li-Fraumeni Syndrome, Sequence Deletion, DNA Primers, Mice

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