ArticleOncogene2025
ALKBH5 suppresses m
Article in Oncogene, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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
5 citing papers in PubMed.
- The Role of NMedComm · 2026Review
- Lactate metabolism and lactylation in cancer: from pathogenesis to therapeutic advances.Signal transduction and targeted therapy · 2026Review
- The methylation pattern of osimertinib resistance: prospects for diagnosis and treatment of NSCLC.Frontiers in oncology · 2026Review
- Context-dependent functions of ALKBH5: a mechanistic framework linking cellular stress responses, immune regulation, viral infection, and therapeutic vulnerabilities.Frontiers in immunology · 2026Review
- DNA, RNA, and histone methylation regulation enzymes and their crosstalk in colorectal carcinogenesis and progression: a review of molecular mechanisms, clinical implications, and future perspectives.Cellular & molecular biology letters · 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
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Colorectal cancer (CRC) is a severe health risk, and while Cetuximab is a key treatment, resistance due to KRAS mutations poses a challenge. The role of ALKBH5, often overexpressed in cancers, in KRAS-mutated CRC and its resistance to Cetuximab is not yet fully understood. This research initiates an inquiry from both cellular and animal experimental perspectives, investigating the potential of ALKBH5 to confer resistance to Cetuximab in colorectal cancer cells harboring KRAS mutations. We investigated ALKBH5 expression in clinical samples of CRC with varying responses to Cetuximab and KRAS statuses. Drug-resistant cell lines were developed using incremental drug concentrations, and the effects of ALKBH5 modulation on cell viability and proliferation were assessed using CCK-8 and clonogenic assays. The in vivo impact of ALKBH5 on drug resistance in KRAS-mutant cells was explored. Transcriptome sequencing of ALKBH5 knockdown cells pinpointed genes linked to Cetuximab resistance. We also examined ALKBH5's regulation of FOXM1 m
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Identifiers
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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.