ArticleLeukemia2020
ATM activity in T cells is critical for immune surveillance of lymphoma in vivo.
Article in Leukemia, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 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
9 citing papers in PubMed, 18 citations in OpenAlex.
- Oxidative Stress Early After Hematopoietic Stem Cell Transplant.Transplantation and cellular therapy · 2025Article
- T-cell Lymphoblastic Lymphoma Presenting as a Pituitary Mass.JCEM case reports · 2023Article
- Galectin-9 blockade synergizes with ATM inhibition to induce potent anti-tumor immunity.International journal of biological sciences · 2023Article
- Mouse models of diffuse large B cell lymphoma.Frontiers in immunology · 2023Review
- SHMT2 inhibition disrupts the TCF3 transcriptional survival program in Burkitt lymphoma.Blood · 2022Article
- DNA-PKcs kinase activity stabilizes the transcription factor Egr1 in activated immune cells.The Journal of biological chemistry · 2021Article
- Synthetic Lethality in Cancer Therapeutics: The Next Generation.Cancer discovery · 2021Review
- Review
- Update on DNA-Double Strand Break Repair Defects in Combined Primary Immunodeficiency.Current allergy and asthma reports · 2020Review
Corrections and comments
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Authors and funding
33 authors at 11 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The proximal DNA damage response kinase ATM is frequently inactivated in human malignancies. Germline mutations in the ATM gene cause Ataxia-telangiectasia (A-T), characterized by cerebellar ataxia and cancer predisposition. Whether ATM deficiency impacts on tumor initiation or also on the maintenance of the malignant state is unclear. Here, we show that Atm reactivation in initially Atm-deficient B- and T cell lymphomas induces tumor regression. We further find a reduced T cell abundance in B cell lymphomas from Atm-defective mice and A-T patients. Using T cell-specific Atm-knockout models, as well as allogeneic transplantation experiments, we pinpoint impaired immune surveillance as a contributor to cancer predisposition and development. Moreover, we demonstrate that Atm-deficient T cells display impaired proliferation capacity upon stimulation, due to replication stress. Altogether, our data indicate that T cell-specific restoration of ATM activity or allogeneic hematopoietic stem cell transplantation may prevent lymphomagenesis in A-T patients.
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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.