ArticleOncology letters2019
Article in Oncology letters, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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
2 citing papers in PubMed, 3 citations in OpenAlex.
- Elevated TNF-α level is correlated with NF-κB/p65 activation in patients with sporadic colorectal cancer.Molecular and clinical oncology · 2026Article
- Is Curcumin the Answer to Future Chemotherapy Cocktail?Molecules (Basel, Switzerland) · 2021Review
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 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Philadelphia chromosome-positive acute lymphoblastic leukemia (Ph+ ALL), is characterized by the t(9;22)(q34q11) that generates the BCR-ABL protein with uncontrolled tyrosine kinase activity. Recently, a connection between BCR-ABL signaling with NF-κB activation mediated by CK2 has been hypothesized. Approximately 95% of patients with Ph+ ALL have the BCR-ABLp190 isoform, which causes aggressive leukemia with a high rate of chemotherapy resistance. Therefore, the use of compounds that could improve the efficacy of chemotherapy drugs is of particular interest. Curcumin is an active chemical in turmeric with antineoplastic potential; it regulates protein-kinases by modulating downstream molecular pathways. The present study evaluated the effect of curcumin in combination with the chemotherapeutic drugs vincristine, imatinib and daunorubicin in the human OP-1 cell line. Several doses of the chemotherapy drugs were examined, and the effects were evaluated following 12, 24 and 48 h of exposure. The interaction between the chemotherapy drugs and curcumin was determined by the dose-effect curve, which generated a combination index (CI); these data were represented in isobolograms. In addition, the individual effect of each drug was compared with its effect in combination with curcumin on cell viability, apoptosis degree, NF-κB activation and gene expression changes. The present study observed that curcumin potentiates the efficacy of vincristine and imatinib, generating an additive/synergistic effect in a dose- and time-dependent manner. These combinations significantly increased the apoptosis degree, decreased the activation of NF-κB and the expression of its regulated genes. Conversely treatment with daunorubicin + curcumin combination produced an antagonistic/additive effect in a dose-dependent manner, and this combination significantly increased the apoptosis degree. However, this effect seems not to be associated with NF-κB activity, as no significant changes were observed in its activation or in the expression of the genes that it regulates. The results of the present study demonstrate that curcumin may be used as an adjuvant agent for chemotherapy in patients with Ph+ ALL.
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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.