ArticleOncogene2012
Mcm2 deficiency results in short deletions allowing high resolution identification of genes contributing to lymphoblastic lymphoma.
Article in Oncogene, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 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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Who cites it
29 citing papers in PubMed, 45 citations in OpenAlex.
- Ptpn1 deficiency collaborates with a NUP98::HOXD13 fusion gene to generate B cell precursor acute lymphoblastic leukemia.Journal of immunology (Baltimore, Md. : 1950) · 2026Article
- MBD3 increased expression by BRD4 and facilitated castration-resistant prostate cancer cell proliferation by inhibiting PTEN.Discover oncology · 2026Article
- Expression and prognostic value of MCM2 in type B thymomas.BMC cancer · 2025Article
- Unwinding Helicase MCM Functionality for Diagnosis and Therapeutics of Replication Abnormalities Associated with Cancer: A Review.Molecular diagnosis & therapy · 2024Review
- Multi-omics analysis identifies RFX7 targets involved in tumor suppression and neuronal processes.Cell death discovery · 2023Article
- MCM2 in human cancer: functions, mechanisms, and clinical significance.Molecular medicine (Cambridge, Mass.) · 2022Review
- Replication stress generates distinctive landscapes of DNA copy number alterations and chromosome scale losses.Genome biology · 2022Article
- Mcm2 hypomorph leads to acute leukemia or hematopoietic stem cell failure, dependent on genetic context.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2022Article
- Transcription factor RFX7 governs a tumor suppressor network in response to p53 and stress.Nucleic acids research · 2021Article
- Tumor Spheroids of an Aggressive Form of Central Neurocytoma Have Transit-Amplifying Progenitor Characteristics with Enhanced EGFR and Tumor Stem Cell Signaling.Experimental neurobiology · 2021Article
- A Tumor Suppressor Enhancer ofBlood cancer discovery · 2021Article
- Expression and Prognostic Value of MCM Family Genes in Osteosarcoma.Frontiers in molecular biosciences · 2021Article
- MCMs in Cancer: Prognostic Potential and Mechanisms.Analytical cellular pathology (Amsterdam) · 2020Review
- A unique mutator phenotype reveals complementary oncogenic lesions leading to acute leukemia.JCI insight · 2019Article
- Resting cells rely on the DNA helicase component MCM2 to build cilia.Nucleic acids research · 2019Article
- Article
- Examining transcriptional changes to DNA replication and repair factors over uveal melanoma subtypes.BMC cancer · 2018Article
- The transcription factor Rfx7 limits metabolism of NK cells and promotes their maintenance and immunity.Nature immunology · 2018Article
- DNA replication stress restricts ribosomal DNA copy number.PLoS genetics · 2017Article
- Dormant origins as a built-in safeguard in eukaryotic DNA replication against genome instability and disease development.DNA repair · 2017Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Mini-chromosome maintenance (Mcm) proteins are part of the replication-licensing complex that is loaded onto chromatin during the G1-phase of the cell cycle and required for initiation of DNA replication in the subsequent S-phase. Mcm proteins are typically loaded in excess of the number of locations that are used during S-phase. Nonetheless, partial depletion of Mcm proteins leads to cancers and stem cell deficiencies. Mcm2 deficient mice, on a 129Sv genetic background, display a high rate of thymic lymphoblastic lymphoma. Here array comparative genomic hybridization is used to characterize the genetic damage accruing in these tumors. The predominant events are deletions averaging less than 0.5 Mbp, considerably shorter than observed in prior studies using alternative mouse lymphoma models or human tumors. Such deletions facilitate identification of specific genes and pathways responsible for the tumors. Mutations in many genes that have been implicated in human lymphomas are recapitulated in this mouse model. These features, and the fact that the mutation underlying the accelerated genetic damage does not target a specific gene or pathway a priori, are valuable features of this mouse model for identification of tumor suppressor genes. Genes affected in all tumors include Pten, Tcfe2a, Mbd3 and Setd1b. Notch1 and additional genes are affected in subsets of tumors. The high frequency of relatively short deletions is consistent with elevated recombination between nearby stalled replication forks in Mcm2-deficient mice.
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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.