Article in Cancer research communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
2 · The registry
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.
Eunhee YiDepartment of Physiology, College of Human Medicine, Michigan State University, East Lansing, Michigan.ORCID 0000-0002-7839-7795
Amit D GujarDepartment of Neurosurgery, School of Medicine, Yale University, New Haven, Connecticut.ORCID 0000-0003-0689-6680
Dacheng ZhaoDepartment of Neurosurgery, School of Medicine, Yale University, New Haven, Connecticut.ORCID 0009-0007-1968-2063
Kentaro SuinaDepartment of Neurosurgery, School of Medicine, Yale University, New Haven, Connecticut.ORCID 0000-0001-7805-5480
Xue JinDepartment of Neurosurgery, School of Medicine, Yale University, New Haven, Connecticut.ORCID 0000-0003-4214-6238
Katharina PardonDepartment of Pediatric Oncology/Hematology, Charité-Universitätsmedizin Berlin, Berlin, Germany.ORCID 0009-0001-5048-3261
Qinghao YuDepartment of Pediatric Oncology/Hematology, Charité-Universitätsmedizin Berlin, Berlin, Germany.ORCID 0000-0002-2151-9624
Larisa KagermazovaDepartment of Biochemistry and Molecular Pharmacology, Institute for Systems Genetics, NYU Langone Health, New York, New York.ORCID 0009-0004-7494-284X
Emmanuel E KorsahDepartment of Physiology, College of Natural Science, Michigan State University, East Lansing, Michigan.ORCID 0009-0009-8695-6639
Noah A DusseauDepartment of Physiology, College of Natural Science, Michigan State University, East Lansing, Michigan.ORCID 0009-0008-2243-1318
Jef D BoekeDepartment of Biochemistry and Molecular Pharmacology, Institute for Systems Genetics, NYU Langone Health, New York, New York.ORCID 0000-0001-5322-4946
Anton G HenssenDepartment of Pediatric Oncology/Hematology, Charité-Universitätsmedizin Berlin, Berlin, Germany.ORCID 0000-0003-1534-778X
Roel G W VerhaakDepartment of Neurosurgery, School of Medicine, Yale University, New Haven, Connecticut.ORCID 0000-0003-2773-0436
Funding
eDyNAmiC - STANFORDOT2CA278688 · NCI · STANFORD UNIVERSITY · PI PAUL S MISCHEL · 2022 to 2026
$7.7M
Extrachromosomal DNA as a Targetable Mechanism in GlioblastomaR01CA237208 · NCI · YALE UNIVERSITY · PI VERHAAK, ROEL GW · 2020 to 2024
$2.5M
eDyNAmiC - NYUOT2CA278666 · NCI · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI Jef D BOEKE · 2022 to 2026
$1.9M
eDyNAmiC - YALEOT2CA278649 · NCI · YALE UNIVERSITY · PI Roel GW Verhaak · 2022 to 2026
$1.6M
Advancing Ultra Long-read Sequencing and Chromatin Interaction Analyses for Chromosomal and Extrachromosomal Structural Variation Characterization in CancerR33CA236681 · NCI · JACKSON LABORATORY · PI VERHAAK, ROEL GW, WEI, CHIA-LIN · 2020 to 2020
$1.4M
Modeling Tumor Evolution in GliomaR21NS114873 · NINDS · JACKSON LABORATORY · PI VERHAAK, ROEL GW · 2019 to 2020
$520k
Cancer Research UK (CRUK) 398299703Deutsche Krebshilfe (German Cancer Aid) 70114107Elsa U. Pardee Foundation (EUPF)European Research Council (ERC) 949172National Cancer Institute (NCI) CGCATF-2021/100012National Cancer Institute (NCI) CGCATF-2021/100016National Cancer Institute (NCI) CGCATF-2021/100018National Cancer Institute (NCI) OT2CA278649National Cancer Institute (NCI) OT2CA278666National Cancer Institute (NCI) OT2CA278688National Institutes of Health (NIH) R01CA237208National Institutes of Health (NIH) R21NS114873National Institutes of Health (NIH) R33CA236681NCI NIH HHS OT2 CA278649NCI NIH HHS OT2 CA278666NCI NIH HHS OT2 CA278688NCI NIH HHS R01 CA237208NCI NIH HHS R33 CA236681NINDS NIH HHS R21 NS114873
6 · The paper itself
Abstract
Extrachromosomal DNA (ecDNA), a major focal oncogene amplification mode found across cancer, has recently regained attention as an emerging cancer hallmark, with a pervasive presence across cancers. With technical advancements such as high-coverage sequencing and live-cell genome imaging, we can now investigate the behaviors and functions of ecDNA. However, we still lack an understanding of how to eliminate ecDNA. We observed depletion of cells containing ecDNA during lentiviral but not transposon-based transduction, whereas we sought to investigate the mechanism of ecDNA behavior. This discovery may provide critical information on utilizing a lentiviral system in emerging ecDNA research. Additionally, this observation suggests specific sensitivities for cells with ecDNA. SIGNIFICANCE: ecDNA is an essential factor in cancer progression. We found that a group of cancer cells with ecDNA is selectively depleted after lentiviral infection. This finding provides promise for ecDNA-specific targeting, suggests the need for caution in using lentivirus, and offers alternative ways to study ecDNA.
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.
Selective Depletion of Cancer Cells with Extrachromosomal DNA via Lentiviral Infection. · full record | OpenQuestion