ArticleCurrent cancer drug targets2026
Pharmacological Evaluation of
Article in Current cancer drug targets, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- Phytochemicals in overcoming venetoclax resistance in acute myeloid leukemia: mechanistic insights and therapeutic potential.Annals of hematology · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors.
Funding
Abstract
introductionBreast Cancer (BC) is one of the most prevalent malignant tumors in women. The incidence of estrogen receptor-positive (ER
aimsThe objectives of the present study were to explore the impact of different APR extracts on the proliferation, migration, and invasion of ER+BC and to investigate their possible mechanism at the molecular level.
methodsVarious extracts of APR were prepared in different solvents, such as petroleum ether, ethyl acetate, n-butanol, and water. ER
resultsAPR-EA demonstrated anti-proliferative, anti-migratory, and anti-invasive effects on the ER+ T47D cell line. Thus, APR-EAE might inhibit the expression of P-PI3K/PI3K and PAkt/ Akt proteins, which subsequently represses the expression of ERα. This inhibition affects the downstream expression of the proteins CDK4 and Bcl-2, which are linked to cell growth and apoptosis.
conclusionAdditionally, APR-EA might increase the expression of P21 and Bax proteins, which are associated with cell cycle arrest and apoptosis. Overall, these effects contribute to the anti-ER+ breast cancer properties of APR-EA.
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Registered trials
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