ReviewCells2026
Acquired Chemoresistance in Colorectal Cancer: Therapy-Induced Signalling Adaptation, Cellular Plasticity and Mechanism-Guided Therapeutic Strategies.
Review in Cells, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The effectiveness of chemotherapy in colorectal cancer (CRC) is significantly reduced by acquired chemoresistance to 5-fluorouracil (5-FU), oxaliplatin and irinotecan. This structured narrative review synthesises mechanistic, preclinical, translational and clinical evidence underlying resistance to these agents. Distinct drug-specific molecular mechanisms can underlie acquired chemoresistance, whereas shared adaptive survival processes support treatment persistence and may, in some settings, contribute to the emergence of stable acquired resistance. 5-FU resistance is associated with factors such as altered thymidylate synthase activity, drug catabolism, nucleotide metabolism and apoptosis avoidance, whereas resistance to oxaliplatin involves enhanced deoxyribonucleic acid (DNA) repair, detoxification, reduced platinum accumulation and metabolic adaptation. Irinotecan resistance can involve reduced
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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.