Article in Cancer research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
0numbers the graph read from it
0cells of the map it votes in
2citing 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.
Etienne P DanisDepartment of Pediatrics, University of Colorado Anschutz Medical Campus, Aurora, Colorado.ORCID 0000-0002-5651-8111
Siddhartha S MitraDepartment of Pediatrics, University of Colorado Anschutz Medical Campus, Aurora, Colorado.ORCID 0000-0002-1829-7856
Adam L GreenDepartment of Pediatrics, University of Colorado Anschutz Medical Campus, Aurora, Colorado.ORCID 0000-0002-4469-2358
Nathan DahlDepartment of Pediatrics, University of Colorado Anschutz Medical Campus, Aurora, Colorado.ORCID 0000-0003-2555-1741
Rajeev Vibhakar *Department of Pediatrics, University of Colorado Anschutz Medical Campus, Aurora, Colorado.ORCID 0000-0002-5949-3896
Sujatha Venkataraman *Department of Pediatrics, University of Colorado Anschutz Medical Campus, Aurora, Colorado.ORCID 0000-0002-1512-284X
Funding
University of Colorado Cancer Center Support Grant - Lung Cancer Patient-Derived Xenografts with Autologous Human Immune SystemsP30CA046934 · NCI · UNIVERSITY OF COLORADO DENVER · PI James V Degregori · 1988 to 2026
$117.0M
Colorado REACH HubU01HL152405 · NHLBI · UNIVERSITY OF COLORADO DENVER · PI DUKE, RICHARD C · 2019 to 2022
$5.1M
Bruker 9.4T/ 20cm BioSpec MR Scanner for Colorado Animal Imaging Shared ResourcesS10OD023485 · OD · UNIVERSITY OF COLORADO DENVER · PI SERKOVA, NATALIE J. · 2017 to 2017
$2.0M
Multi-Modal Optical/ microCT system for Colorado Animal Imaging ResourceS10OD027023 · OD · UNIVERSITY OF COLORADO DENVER · PI SERKOVA, NATALIE J. · 2020 to 2020
$733k
Intra-tumor Heterogeneity in Colorectal Cancer Progression and Treatment ResponseK08CA190645 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI HARDIMAN, KARIN MARIE · 2016 to 2019
$700k
Anschutz Medical Campus, University of Colorado (CU AMC)Cancer League of Colorado (CLC)ChadTough Foundation (Chad Tough Foundation)Laya Arts AcademyMarc Jr FoundationMorgan Adams FoundationNCI NIH HHS K08 CA190645NCI NIH HHS P30 CA046934NHLBI NIH HHS U01 HL152405NIH HHS S10 OD023485NIH HHS S10 OD027023Olivia Caldwell FoundationU.S. Department of Defense (DOD) CA190645
6 · The paper itself
Abstract
Diffuse midline gliomas (DMG) are devastating brain tumors that occur primarily in children. The salient feature of these tumors is the presence of a H3K27M mutation (K27M), associated with the worst prognosis. Development of effective strategies for treating K27M+ DMG is desperately needed to help improve patient outcomes. In this study, we identified the cell surface antigen CD99 as notably expressed in DMGs, particularly in K27M+ DMGs. The increased expression of CD99 in K27M+ DMGs was a result of the oncohistone K27M mutation. In K27M+ DMG cells, CD99 inactivation impaired tumor growth by inducing cell differentiation. The development of a therapeutic anti-CD99 chimeric antibody, 10D1, with a membrane-proximal binding epitope enabled the evaluation of the antitumor efficacy of targeting CD99 in preclinical models of K27M+ DMGs. 10D1 suppressed DMG growth in vitro and in vivo by inducing apoptosis. When combined with radiation treatment, 10D1 exhibited improved antitumor efficacy and prolonged xenograft survival. Together, these findings provide a strong justification for the clinical development of 10D1 as a therapy for targeting CD99 to treat DMGs. SIGNIFICANCE: The H3K27M mutation in diffuse midline glioma increases CD99 expression to suppress apoptosis, inhibit differentiation, and induce radioresistance, supporting using the anti-CD99 antibody 10D1 in pediatric brain cancer trials.
Indexed as
12E7 AntigenAntibodies, MonoclonalBrain NeoplasmsGliomaAnimalsApoptosisCell Line, TumorFemaleHumansMiceMutationXenograft Model Antitumor Assays12E7 AntigenAntibodies, MonoclonalCD99 protein, human
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.
Development of an Anti-CD99 Antibody Enables Targeting of Diffuse Midline Glioma. · full record | OpenQuestion