The DOI matches its Crossref record; 5 of the 5 references it cites were found in a registry or an index.
An oncogenic form of p53 confers a dominant, gain-of-function phenotype that disrupts spindle checkpoint control
Open accessAbstract
Although it is well-established that p53 functions as a tumor suppressor gene, certain mutations exhibit gain-of-function activities that increase oncogenic transformation. We have found a common class of p53 missense mutation that exhibits a dominant, gain-of-function activity that generates genomic instability. Fibroblasts from Li–Fraumeni syndrome heterozygotes with such mutations generate polyploid cells when exposed to spindle depolymerizing agents. Expression of such mutant alleles in normal fibroblasts yields the same phenotype. This class of dominant, gain-of-function p53 mutation (p53 RSC , relaxed spindle checkpoint allele) does not require the transcriptional activation function of p53 for this behavior. Thus p53 mutations can contribute to progression of a cancer cell not only by absence of p53 tumor suppressor activity but also by the presence of an activity that promotes genetic instability.
Overview
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
Citations
Cites
p53 Mutations in Human Cancers
Hollstein, M., Sidransky, D., Vogelstein, B., & Harris, C. C. (1991) · Science · doi:10.1126/science.1905840 · Cited by 8,018
Mice deficient for p53 are developmentally normal but susceptible to spontaneous tumours
Donehower, L. A., Harvey, M., Slagle, B. L., McArthur, M. J., Montgomery, C. A., Butel, J. S., & Bradley, A. (1992) · Nature · doi:10.1038/356215a0 · Cited by 4,649
Crystal Structure of a p53 Tumor Suppressor-DNA Complex: Understanding Tumorigenic Mutations
Cho, Y., Gorina, S., Jeffrey, P. D., & Pavletich, N. P. (1994) · Science · doi:10.1126/science.8023157 · Cited by 2,551
The p53 proto-oncogene can act as a suppressor of transformation
Finlay, C. A., Hinds, P. W., & Levine, A. J. (1989) · Cell · doi:10.1016/0092-8674(89)90045-7 · Cited by 1,987
Uncoupling of S phase and mitosis induced by anticancer agents in cells lacking p21
Waldman, T., Lengauer, C., Kinzler, K. W., & Vogelstein, B. (1996) · Nature · doi:10.1038/381713a0 · Cited by 728
Cited by
Mutant p53 in Cancer: New Functions and Therapeutic Opportunities
Muller, P. A. J., & Vousden, K. H. (2014) · Cancer Cell · doi:10.1016/j.ccr.2014.01.021 · Cited by 1,545
Bcl10 Is Involved in t(1;14)(p22;q32) of MALT B Cell Lymphoma and Mutated in Multiple Tumor Types
Willis, T. G., Jadayel, D. M., Du, M.-Q., Peng, H., Perry, A. R., Abdul-Rauf, M., Price, H., Karran, L., Majekodunmi, O., Wlodarska, I., et al. (1999) · Cell · doi:10.1016/s0092-8674(00)80957-5 · Cited by 658
Blandino, G., Levine, A. J., & Oren, M. (1999) · Oncogene · doi:10.1038/sj.onc.1202314 · Cited by 441
Di Agostino, S., Strano, S., Emiliozzi, V., Zerbini, V., Mottolese, M., Sacchi, A., Blandino, G., & Piaggio, G. (2006) · Cancer Cell · doi:10.1016/j.ccr.2006.08.013 · Cited by 418
van Bokhoven, H., Hamel, B. C. J., Bamshad, M., Sangiorgi, E., Gurrieri, F., Duijf, P. H. G., Vanmolkot, K. R. J., van Beusekom, E., van Beersum, S. E. C., Celli, J., et al. (2001) · The American Journal of Human Genetics · doi:10.1086/323123 · Cited by 373
Metadata
- Authors
- Gualberto, A., Aldape, K., Kozakiewicz, K., & Tlsty, T. D.
- Venue
- Proceedings of the National Academy of Sciences
- Published
- 1998-04-28
- Volume
- 95
- Issue
- 9
- Pages
- 5166-5171
- ISSN
- 0027-8424 (ISSN-L)
- 1091-6490
- OpenAlex
- W2043964688
- Cited by
- 237
- References
- 5
- FWCI
- 13.22
- Type
- journal article
- Language
- en
- Open access
- green
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
How to cite
Cite CoChat for the checks on this page, and the paper for its own findings.
- This page
- CoChat. (2026). Citation check: An oncogenic form of p53 confers a dominant, gain-of-function phenotype that disrupts spindle checkpoint control. https://app.cochat.ai/papers/10.1073/pnas.95.9.5166
- The paper
- Gualberto, A., Aldape, K., Kozakiewicz, K., & Tlsty, T. D. (1998). An oncogenic form of p53 confers a dominant, gain-of-function phenotype that disrupts spindle checkpoint control. Proceedings of the National Academy of Sciences. https://doi.org/10.1073/pnas.95.9.5166
Data sources
Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.