ArticleOncogene2005
Cdt1 transgenic mice develop lymphoblastic lymphoma in the absence of p53.
Article in Oncogene, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
47 citing papers in PubMed, 84 citations in OpenAlex.
- Overexpression of CDT1 inhibits cell cycle progression at S phase by interacting with the mini-chromosome maintenance complex and causes DNA damage.FEBS open bio · 2026Article
- CDC45 promotes the stemness and metastasis in lung adenocarcinoma by affecting the cell cycle.Journal of translational medicine · 2024Article
- Review
- Identification of CDT1 as a prognostic marker in human lung adenocarcinoma using bioinformatics approaches.PeerJ · 2023Article
- Critical DNA damaging pathways in tumorigenesis.Seminars in cancer biology · 2022Review
- Small Molecule Inhibitor Targeting CDT1/Geminin Protein Complex Promotes DNA Damage and Cell Death in Cancer Cells.Frontiers in pharmacology · 2022Article
- Long non-coding RNAs in Epstein-Barr virus-related cancer.Cancer cell international · 2021Review
- CDT1 Is a Novel Prognostic and Predictive Biomarkers for Hepatocellular Carcinoma.Frontiers in oncology · 2021Article
- Article
- TGFβ1 Cell Cycle Arrest Is Mediated by Inhibition of MCM Assembly in Rb-Deficient Conditions.Molecular cancer research : MCR · 2019Article
- [Long non-coding RNA and lymphoma].Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi · 2017Article
- Targeting mitotic pathways for endocrine-related cancer therapeutics.Endocrine-related cancer · 2017Review
- Strategic role of the ubiquitin-dependent segregase p97 (VCP or Cdc48) in DNA replication.Chromosoma · 2017Review
- Regulation and Function of Cdt1; A Key Factor in Cell Proliferation and Genome Stability.Genes · 2016Review
- Replication fork instability and the consequences of fork collisions from rereplication.Genes & development · 2016Review
- Met promotes the formation of double minute chromosomes induced by Sei-1 in NIH-3T3 murine fibroblasts.Oncotarget · 2016Article
- Replication origins: determinants or consequences of nuclear organization?Current opinion in genetics & development · 2016Review
- MINCR is a MYC-induced lncRNA able to modulate MYC's transcriptional network in Burkitt lymphoma cells.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- DNA replication origin activation in space and time.Nature reviews. Molecular cell biology · 2015Review
- Replication stress and cancer.Nature reviews. Cancer · 2015Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
The exact duplication of chromosomal DNA during each cell cycle ensures the correct inheritance of genetic material from mother to daughter cells. In eukaryotic cells, DNA replication can occur only when the origin of DNA replication is accurately marked by a group of proteins termed licensing proteins. One such protein is Cdt1, which is recruited first to the origin of DNA replication followed by cell division cycle 6 (Cdc6) and mini-chromosome maintenance proteins (Mcms). We previously reported that NIH3T3 cells overexpressing Cdt1 readily formed tumors in mice. To further investigate its oncogenic mechanism, we generated transgenic mice expressing Cdt1 in thymocytes. Our studies demonstrated that T-cell-directed Cdt1 transgenic mice showed normal T-cell development. However, such transgenic mice developed thymic lymphoblastic lymphoma when crossed with p53 null mice. Furthermore, tumor cells derived from NIH3T3 cells overexpressing Cdt1 displayed numerical and structural chromosomal aberrations in the form of ploidy, double minutes, translocation, inversion, chromosome end-to-end fusion and robertsonian mutation. Collectively, our studies suggest that Cdt1 overexpression most likely contributes to tumorigenecity by causing genomic instability.
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Identifiers
What OpenQuestion holds
Registered trials
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.