ArticleOncotarget2014
Curaxin CBL0137 eradicates drug resistant cancer stem cells and potentiates efficacy of gemcitabine in preclinical models of pancreatic cancer.
Article in Oncotarget, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers, 1 of them a synthesis that pooled 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.
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
37 citing papers in PubMed, 1 synthesis or guideline pooled it, 59 citations in OpenAlex.
- Pooled it
- Chromatin adaptation and histone remodeling as mechanisms of PARP inhibitor resistance and therapeutic vulnerability.Frontiers in pharmacology · 2026Review
- Insights into FACT in Cancers with Targeted Therapeutic Implications.Molecular and cellular biology · 2026Review
- CBL0137 and NKG2A blockade: a novel immuno-oncology combination therapy for Myc-overexpressing triple-negative breast cancers.Oncogene · 2025Article
- Investigation of the mechanistic impact of CBL0137 on airway remodeling in asthma.BMC pulmonary medicine · 2025Article
- Activation and Evasion of the FEAR Pathway by RNA Viruses.bioRxiv : the preprint server for biology · 2025Article
- Chromatin as an old and new anticancer target.Trends in cancer · 2024Review
- Multiparameter ranking of carbazoles for anti-trypanosome lead discovery.Frontiers in drug discovery · 2024Article
- Comparison of cell response to chromatin and DNA damage.Nucleic acids research · 2023Article
- Targeting Features of Curaxin CBL0137 on Hematological Malignancies In Vitro and In Vivo.Biomedicines · 2023Article
- Human FACT subunits coordinate to catalyze both disassembly and reassembly of nucleosomes.Cell reports · 2022Article
- Review
- Kidney cancer biomarkers and targets for therapeutics: survivin (BIRC5), XIAP, MCL-1, HIF1α, HIF2α, NRF2, MDM2, MDM4, p53, KRAS and AKT in renal cell carcinoma.Journal of experimental & clinical cancer research : CR · 2021Review
- Dual Targeting of Chromatin Stability By The Curaxin CBL0137 and Histone Deacetylase Inhibitor Panobinostat Shows Significant Preclinical Efficacy in Neuroblastoma.Clinical cancer research : an official journal of the American Association for Cancer Research · 2021Article
- Stimulation of an anti-tumor immune response with "chromatin-damaging" therapy.Cancer immunology, immunotherapy : CII · 2021Article
- Exploring the Interaction of Curaxin CBL0137 with G-Quadruplex DNA Oligomers.International journal of molecular sciences · 2021Article
- Proteasomal Regulation of Mammalian SPT16 in Controlling Transcription.Molecular and cellular biology · 2021Article
- Effective inhibition of MYC-amplified group 3 medulloblastoma by FACT-targeted curaxin drug CBL0137.Cell death & disease · 2020Article
- Suppressor of Ty 16 promotes lung cancer malignancy and is negatively regulated by miR-1227-5p.Cancer science · 2020Article
- SSRP1 promotes colorectal cancer progression and is negatively regulated by miR-28-5p.Journal of cellular and molecular medicine · 2019Article
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
Abstract
Pancreatic ductal adenocarcinoma (PDA) continues to be one of the deadliest cancers due to the absence of effective treatment. Curaxins are a class of small molecules with anti-cancer activity demonstrated in different models of cancer in mice. The lead curaxin compound, CBL0137, recently entered Phase I clinical trials. Curaxins modulate several important signaling pathways involved in the pathogenesis of PDA through inhibition of chromatin remodeling complex FACT. FACT is overexpressed in multiple types of tumor, with one of the highest rate of overexpression in PDA (59%). In this study, the efficacy of CBL0137 alone or in combination with current standard of care, gemcitabine, was tested against different models of PDA in vitro and in mouse models. It was found that CBL0137 alone is a potent inducer of apoptosis in pancreatic cancer cell lines and is toxic not only for proliferating bulk tumor cells, but also for pancreatic cancer stem cells. In mice, CBL0137 was effective against several PDA models, including orthotopic gemcitabine resistant PANC-1 model and patient derived xenografts, in which CBL0137 anti-tumor effect correlated with overexpression of FACT. Moreover, we observed synergy of CBL0137 with gemcitabine which may be explained by the ability of CBL0137 to inhibit several transcriptional programs induced by gemcitabine, including NF-kappaB response and expression of ribonucleotide reductase, one of the targets of gemcitabine in cells. This data suggest testing of CBL0137 efficacy in Phase II trial in PDA patients alone and in combination with gemcitabine.
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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.