Article in Molecular cancer therapeutics, 2026. 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.
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
5 · Who and what money
Authors and funding
15 authors.
Kaiting JiangDepartment of Hematology, Oncology and Cancer Immunology, Charité - Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin Berlin, Germany.ORCID 0009-0000-3282-5953
Marieluise KirchnerCore Unit Proteomics, Berlin Institute of Health at Charité - Universitätsmedizin Berlin and Max-Delbrück-Center for Molecular Medicine, Berlin, Germany.ORCID 0000-0002-7049-534X
Frederik HerzbergDepartment of Hematology, Oncology and Cancer Immunology, Charité - Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin Berlin, Germany.ORCID 0009-0000-7338-7849
Yan ZhaoDepartment of Hematology, Oncology and Cancer Immunology, Charité - Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin Berlin, Germany.ORCID 0000-0002-3087-4767
Amelie GasperDepartment of Hematology, Oncology and Cancer Immunology, Charité - Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin Berlin, Germany.ORCID 0009-0003-5247-9498
Francis BaumgartnerDepartment of Hematology, Oncology and Cancer Immunology, Charité - Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin Berlin, Germany.ORCID 0000-0003-0768-1956
Paul JungDepartment of Hematology, Oncology and Cancer Immunology, Charité - Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin Berlin, Germany.ORCID 0000-0002-6447-450X
Jan BrauneDepartment of Hematology, Oncology and Cancer Immunology, Charité - Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin Berlin, Germany.ORCID 0000-0003-2026-2641
Veronika SchulzeDepartment of Hematology, Oncology and Cancer Immunology, Charité - Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin Berlin, Germany.ORCID 0009-0004-0823-1660
Konstandina IsaakidisDepartment of Hematology, Oncology and Cancer Immunology, Charité - Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin Berlin, Germany.ORCID 0009-0002-7451-6889
Philipp MertinsCore Unit Proteomics, Berlin Institute of Health at Charité - Universitätsmedizin Berlin and Max-Delbrück-Center for Molecular Medicine, Berlin, Germany.ORCID 0000-0002-2245-528X
Jan KrönkeDepartment of Hematology, Oncology and Cancer Immunology, Charité - Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin Berlin, Germany.ORCID 0000-0002-4649-0506
Matthias WirthDepartment of Hematology, Oncology and Cancer Immunology, Charité - Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin Berlin, Germany.ORCID 0000-0002-8340-0872
Ulrich KellerDepartment of Hematology, Oncology and Cancer Immunology, Charité - Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin Berlin, Germany.ORCID 0000-0002-8485-1958
Stefan HabringerDepartment of Hematology, Oncology and Cancer Immunology, Charité - Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin Berlin, Germany.ORCID 0000-0002-3976-9592
Funding
Berliner Krebsgesellschaft HAFF202130 MMCharité - Universitätsmedizin Berlin (Medical School - Charité - University Medicine Berlin) Promotionsstipendium IChinese Scholarship Council ScholarshipDeutsche Forschungsgemeinschaft (DFG) KE 222/10-1 (project number 494535244)Deutsche Krebshilfe (German Cancer Aid) and project number 70111944)Deutsche Krebshilfe (German Cancer Aid) (project number 70114425Deutsche Krebshilfe (German Cancer Aid) project number 70114724Deutschen Konsortium für Translationale Krebsforschung (DKTK) Young Investigator GrantElse Kröner-Fresenius-Stiftung (EKFS) 2022_EKEA.94
6 · The paper itself
Abstract
Epigenetic aberrations are key drivers of multiple myeloma, yet targeted therapies exploiting epigenetic alterations have not been established. By integrating clinical and molecular datasets of patients with multiple myeloma with an unbiased genetic in vivo screen, we identified KAT8 regulatory NSL complex subunit 2 (KANSL2) as a histone posttranslational modification-associated candidate oncogene. High expression of KANSL2 was associated with adverse prognosis in patients with multiple myeloma. Genetic gain- and loss-of-function models identified a protective role of KANSL2 toward genotoxic stress. By transcriptomics, proteomics, and quantitative acetylome profiling, we identified a KANSL2-dependent specific molecular program targetable by acetylation-related modifiers. High KANSL2 levels increased sensitivity to the histone deacetylase (HDAC) inhibitor panobinostat and bromodomain and extra-terminal motif (BET) inhibitor OTX-015 and their combination. Ex vivo drug response profiling in samples from patients with relapsed/refractory multiple myeloma confirmed that high KANSL2 expression is associated with selective multiple myeloma cell killing by HDAC and BET inhibitors. Collectively, these findings position KANSL2 as a mediator of chemotherapy resistance and actionable biomarker for response to drugs targeting its epigenetic program.
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.
The Histone Modifier KANSL2 Is an Actionable Biomarker in Multiple Myeloma. · full record | OpenQuestion