ArticleBlood cancer journal2014
Synergistic cytotoxicity of gemcitabine, clofarabine and edelfosine in lymphoma cell lines.
Article in Blood cancer journal, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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
12 citing papers in PubMed, 19 citations in OpenAlex.
- Systematic and Quantitative Investigation of Newly Synthesized Proteins Reveals Distinct Ion Homeostasis and Mitochondrial Changes between Cuproptosis and Ferroptosis in Human Cells.Analytical chemistry · 2026Article
- Participation of lipids in the tumor response to photodynamic therapy and its exploitation for therapeutic gain.Journal of lipid research · 2025Review
- High activity of the new myeloablative regimen of gemcitabine/clofarabine/busulfan for allogeneic transplant for aggressive lymphomas.Bone marrow transplantation · 2024Article
- Caffeic acid phenethyl ester reverses doxorubicin resistance in breast cancer cells via lipid metabolism regulation at least partly by suppressing the Akt/mTOR/SREBP1 pathway.The Kaohsiung journal of medical sciences · 2023Article
- Tumour cells are sensitised to ferroptosis via RB1CC1-mediated transcriptional reprogramming.Clinical and translational medicine · 2022Article
- The autophagy protein Ambra1 regulates gene expression by supporting novel transcriptional complexes.The Journal of biological chemistry · 2020Article
- The PARP inhibitor olaparib enhances the cytotoxicity of combined gemcitabine, busulfan and melphalan in lymphoma cells.Leukemia & lymphoma · 2017Article
- Romidepsin enhances the cytotoxicity of fludarabine, clofarabine and busulfan combination in malignant T-cells.Leukemia research · 2016Article
- Comparison of the cytotoxicity of cladribine and clofarabine when combined with fludarabine and busulfan in AML cells: Enhancement of cytotoxicity with epigenetic modulators.Experimental hematology · 2015Article
- Dysregulated choline metabolism in T-cell lymphoma: role of choline kinase-α and therapeutic targeting.Blood cancer journal · 2015Article
- Article
- Targeting the hallmarks of cancer with therapy-induced endoplasmic reticulum (ER) stress.Molecular & cellular oncologyReview
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
Abstract
Treatments for lymphomas include gemcitabine (Gem) and clofarabine (Clo) which inhibit DNA synthesis. To improve their cytotoxicity, we studied their synergism with the alkyl phospholipid edelfosine (Ed). Exposure of the J45.01 and SUP-T1 (T-cell) and the OCI-LY10 (B-cell) lymphoma cell lines to IC10-IC20 levels of the drugs resulted in strong synergistic cytotoxicity for the 3-drug combination based on various assays of cell proliferation and apoptosis. Cell death correlated with increased phosphorylation of histone 2AX and KAP1, decreased mitochondrial transmembrane potential, increased production of reactive oxygen species and release of pro-apoptotic factors. Caspase 8-negative I9.2 cells were considerably more resistant to [Gem+Clo+Ed] than caspase 8-positive cells. In all three cell lines [Gem+Clo+Ed] decreased the level of phosphorylation of the pro-survival protein AKT and activated the stress-activated protein kinase/c-Jun N-terminal kinase (SAPK/JNK) stress signaling pathway, which in J45.01 cells resulted in the phosphorylation and heterodimerization of the transcription factors ATF2 and c-Jun. The observed rational mechanism-based efficacy of [Gem+Clo+Ed] based on the synergistic convergence of several pro-death and anti-apoptotic signaling pathways in three very different cell backgrounds provides a powerful foundation for undertaking clinical trials of this drug combination for the treatment of lymphomas.
Identifiers
What OpenQuestion holds
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.