ArticleJournal of virology1997
Mutation of Tp53 contributes to the malignant phenotype of Abelson virus-transformed lymphoid cells.
Article in Journal of virology, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
24 citing papers in PubMed, 32 citations in OpenAlex.
- Extra centrosomes delay DNA damage-driven tumorigenesis.Science advances · 2024Article
- Forward and Reverse Genetics of B Cell Malignancies: From Insertional Mutagenesis to CRISPR-Cas.Frontiers in immunology · 2021Review
- DNA damage responses in murine Pre-B cells with genetic deficiencies in damage response genes.Cell cycle (Georgetown, Tex.) · 2020Article
- Forced expression of cyclin-dependent kinase 6 confers resistance of pro-B acute lymphocytic leukemia to Gleevec treatment.Molecular and cellular biology · 2011Article
- Article
- Changes in p19Arf localization accompany apoptotic crisis during pre-B-cell transformation by Abelson murine leukemia virus.Journal of virology · 2008Article
- Loss of p53 impedes the antileukemic response to BCR-ABL inhibition.Proceedings of the National Academy of Sciences of the United States of America · 2006Article
- Inhibition of TFII-I-dependent cell cycle regulation by p53.Molecular and cellular biology · 2005Article
- p16(Ink4a) interferes with Abelson virus transformation by enhancing apoptosis.Journal of virology · 2004Article
- Active Akt and functional p53 modulate apoptosis in Abelson virus-transformed pre-B cells.Journal of virology · 2004Article
- Rapid, stabilizing palindrome rearrangements in somatic cells by the center-break mechanism.Molecular and cellular biology · 2003Article
- Absence of p53 complements defects in Abelson murine leukemia virus signaling.Journal of virology · 2003Article
- Review
- P53 is necessary for the apoptotic response mediated by a transient increase of Ras activity.Molecular and cellular biology · 2002Article
- Modeling Philadelphia chromosome positive leukemias.Oncogene · 2001Review
- Mink cell focus-forming murine leukemia virus killing of mink cells involves apoptosis and superinfection.Journal of virology · 2001Article
- Analysis of p53 inactivation in a human T-cell leukemia virus type 1 Tax transgenic mouse model.Journal of virology · 2001Article
- The absence of Msh2 alters abelson virus pre-B-cell transformation by influencing p53 mutation.Molecular and cellular biology · 2000Article
- Loss of heterozygosity at the Ink4a/Arf locus facilitates Abelson virus transformation of pre-B cells.Journal of virology · 2000Article
- Mink cell focus-forming murine leukemia virus infection induces apoptosis of thymic lymphocytes.Journal of virology · 2000Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Abelson murine leukemia virus transforms pre-B cells in vitro and induces rapid-onset pre-B-cell lymphoma in vivo. Expression of an active v-Abl protein tyrosine kinase is required for the oncogenic functions of the virus. Despite the strong growth-stimulatory signal provided by v-Abl, the virus-induced tumors are clonal or oligoclonal, and changes in the growth and oncogenic potential of in vitro transformants occur during the derivation of the cell lines. Both of these features suggest that v-Abl expression must be complemented by changes in expression of one or more cellular genes for cells to acquire a fully malignant phenotype. Such genes could include other oncogenes or tumor suppressor genes. Among the latter is Tp53, a gene mutated in many spontaneous cancers. To determine if mutation of the Tp53 tumor suppressor gene plays a role in Abelson virus transformation, conformation-specific monoclonal antibodies were used to examine p53 expression in a panel of Abelson virus-transformed pre-B cells. Expression of mutant forms of p53 was detected in over 40% of the isolates. Sequence analysis revealed the presence of point mutations affecting the highly conserved central portion of the protein. These mutations interfered with the ability of p53 to activate transcription from a promoter containing p53-responsive elements and to induce apoptosis in response to DNA damage. In addition, cells expressing mutant forms of p53 induced a higher frequency of tumors with a more rapid course compared to transformants expressing wild-type p53. These data suggest that Tp53 is one important cellular gene involved in malignant transformation by Abelson virus.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.