ReviewPeerJ2026
Multilayered analysis of cisplatin resistance mechanisms in bladder cancer: from the cell membrane to organelles.
Review in PeerJ, 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.
- The 2025 paradigm shift in urothelial carcinoma pharmacotherapy: from chemotherapy to ADCs and ICIs.Frontiers in cell and developmental biology · 2026Review
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.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Bladder cancer (BCa) is one of the most common malignancies of the urinary tract worldwide. Cisplatin-based combination chemotherapy remains a cornerstone of treatment for muscle-invasive and advanced disease and has substantially improved clinical outcomes, yet primary and acquired resistance frequently leads to treatment failure and disease recurrence. Classical mechanisms, including altered drug uptake and efflux and detoxification by glutathione or metallothioneins, account for only part of this phenotype. Recent work in BCa increasingly points to cisplatin resistance as a multilayered cellular adaptation involving coordinated changes in drug handling, stress responses, and cell-death control. Drawing primarily on studies published between January 2020 and April 2025, while incorporating selected foundational studies from the preceding decade, this review maps cisplatin resistance in BCa within a structured "cell membrane and tumor microenvironment-cytoplasm-nucleus and chromatin-organelles" framework. Particular emphasis is placed on the interaction of epithelial-mesenchymal transition and cancer stem cell programs with stromal and immune signals at the membrane level; on metabolic rewiring, ferroptosis regulation, and stress-activated signaling cascades in the cytoplasm; on reinforced DNA damage response pathways and RNA- or chromatin-directed epigenetic remodeling in the nucleus; and on the resetting of apoptotic, autophagic, and mitophagic thresholds at the organelle level. Across these compartments, recurrent regulatory nodes and signaling axes are outlined, and areas are delineated where mechanisms are supported by convergent
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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.