ArticleOncogene2017
Defective replication stress response inhibits lymphomagenesis and impairs lymphocyte reconstitution.
Article in Oncogene, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 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
12 citing papers in PubMed, 18 citations in OpenAlex.
- Case Report: Post-transplant lymphoproliferative disorder after kidney transplantation in a child with schimke immuno-osseous dysplasia.Frontiers in immunology · 2026Article
- Identifying and validating SMARCAL1 as a prognostic and immunotherapy predictive biomarker for NSCLC.Discover oncology · 2025Article
- DNA fork remodeling proteins, Zranb3 and Smarcal1, are uniquely essential for aging hematopoiesis.Aging cell · 2024Article
- Stress-triggered hematopoietic stem cell proliferation relies on PrimPol-mediated repriming.Molecular cell · 2022Article
- Critical DNA damaging pathways in tumorigenesis.Seminars in cancer biology · 2022Review
- T-cell receptor signaling in Schimke immuno-osseous dysplasia is SMARCAL1-independent.Frontiers in immunology · 2022Article
- Time for remodeling: SNF2-family DNA translocases in replication fork metabolism and human disease.DNA repair · 2020Review
- IL-33 Is a Cell-Intrinsic Regulator of Fitness during Early B Cell Development.Journal of immunology (Baltimore, Md. : 1950) · 2019Article
- DNA damage tolerance in stem cells, ageing, mutagenesis, disease and cancer therapy.Nucleic acids research · 2019Review
- MicroRNA-21 is Required for Hematopoietic Cell Viability After Radiation Exposure.International journal of radiation oncology, biology, physics · 2019Article
- Smarcal1 and Zranb3 Protect Replication Forks from Myc-Induced DNA Replication Stress.Cancer research · 2019Article
- Functions of SMARCAL1, ZRANB3, and HLTF in maintaining genome stability.Critical reviews in biochemistry and molecular biology · 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
8 authors at 1 institution in 1 country.
Funding
Abstract
DNA replication stress promotes genome instability in cancer. However, the contribution of the replication stress response to the development of malignancies remains unresolved. The DNA replication stress response protein SMARCAL1 stabilizes DNA replication forks and prevents replication fork collapse, a cause of DNA breaks and apoptosis. While the fork regression/remodeling functions of SMARCAL1 have been investigated, its in vivo functions in replication stress and cancer are unclear. Using a gamma radiation (IR)-induced replication stress T-cell lymphoma mouse model, we observed a significant inhibition of lymphomagenesis in mice lacking one or both alleles of Smarcal1. Notably, a quarter of the Smarcal1-deficient mice did not develop tumors. Moreover, hematopoietic stem/progenitor cells (HSPCs) and developing thymocytes in Smarcal1-deficient mice showed increased DNA damage and apoptosis during the proliferation burst following IR and an impaired ability to repopulate the thymus after IR. Additionally, mice lacking Smarcal1 showed significant HSPC defects when challenged to respond to other replication stress stimuli. Thus, our data reveal the critical function of the DNA replication stress response and, specifically, Smarcal1 in hematopoietic cell survival and tumor development. Our results also provide important insight into the immunodeficiency observed in individuals with mutations in SMARCAL1 by suggesting that it is an HSPC defect.
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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.