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Quality of Cancer-Related Information on New Media (2014-2023): Systematic Review and Meta-Analysis

Background: New media have become vital sources of cancer-related health information. However, concerns about the quality of that information persist. Objective: This study aims to identify characteristics of studies considering cancer-related information on new media (including social media and artificial intelligence chatbots); analyze patterns in information quality across different platforms, cancer types, and evaluation tools; and synthesize the quality levels of the information. Methods: We systematically searched PubMed, Web of Science, Scopus, and Medline databases for peer-reviewed studies published in English between 2014 and 2023. The validity of the included studies was assessed based on risk of bias, reporting quality, and ethical approval, using the Joanna Briggs Institute Critical Appraisal and the STROBE (Strengthening the Reporting of Observational Studies in Epidemiology) checklists. Features of platforms, cancer types, evaluation tools, and trends were summarized. Ordinal logistic regression was used to estimate the associations between the conclusion of quality assessments and study features. A random-effects meta-analysis of proportions was conducted to synthesize the overall levels of information quality and corresponding 95% CIs for each assessment indicator. Results: A total of 75 studies were included, encompassing 297,519 posts related to 17 cancer types across 15 media platforms. Studies focusing on video-based media (odds ratio [OR] 0.02, 95% CI 0.01-0.12), rare cancers (OR 0.32, 95% CI 0.16-0.65), and combined cancer types (OR 0.04, 95% CI 0.01-0.14) were statistically less likely to yield higher quality conclusions compared to those on text-based media and common cancers. The pooled estimates reported moderate overall quality (DISCERN 43.58, 95% CI 37.80-49.35; Global Quality Score 49.91, 95% CI 43.31-56.50), moderate technical quality (Journal of American Medical Association Benchmark Criteria 46.13, 95% CI 38.87-53.39; Health on the Net Foundation Code of Conduct 49.68, 95% CI 19.68-79.68), moderate-high understandability (Patient Education Material Assessment Tool for Understandability 66.92, 95% CI 59.86-73.99), moderate-low actionability (Patient Education Materials Assessment Tool for Actionability 37.24, 95% CI 18.08-58.68; usefulness 48.86, 95% CI 26.24-71.48), and moderate-low completeness (34.22, 95% CI 27.96-40.48). Furthermore, 27.15% (95% CI 21.36-33.35) of posts contained misinformation, 21.15% (95% CI 8.96-36.50) contained harmful information, and 12.46% (95% CI 7.52-17.39) contained commercial bias. Publication bias was detected only in misinformation studies (Egger test: bias –5.67, 95% CI –9.63 to –1.71; P=.006), with high heterogeneity across most outcomes (I²>75%). Conclusions: Meta-analysis results revealed that the overall quality of cancer-related information on social media and artificial intelligence chatbots was moderate, with relatively higher scores for understandability but lower scores for actionability and completeness. A notable proportion of content contained misleading, harmful, or commercially biased information, posing potential risks to users. To support informed decision-making in cancer care, it is essential to improve the quality of information delivered through these media platforms. Trial Registration: PROSPERO CRD420251058032; https://www.crd.york.ac.uk/PROSPERO/view/CRD420251058032

Cell-free epigenomes enhanced fragmentomics-based model for early detection of lung cancer

Clin Transl Med. 2025 Feb;15(2):e70225. doi: 10.1002/ctm2.70225.

ABSTRACT

BACKGROUND: Lung cancer is a leading cause of cancer mortality, highlighting the need for innovative non-invasive early detection methods. Although cell-free DNA (cfDNA) analysis shows promise, its sensitivity in early-stage lung cancer patients remains a challenge. This study aimed to integrate insights from epigenetic modifications and fragmentomic features of cfDNA using machine learning to develop a more accurate lung cancer detection model.

METHODS: To address this issue, a multi-centre prospective cohort study was conducted, with participants harbouring suspicious malignant lung nodules and healthy volunteers recruited from two clinical centres. Plasma cfDNA was analysed for its epigenetic and fragmentomic profiles using chromatin immunoprecipitation sequencing, reduced representation bisulphite sequencing and low-pass whole-genome sequencing. Machine learning algorithms were then employed to integrate the multi-omics data, aiding in the development of a precise lung cancer detection model.

RESULTS: Cancer-related changes in cfDNA fragmentomics were significantly enriched in specific genes marked by cell-free epigenomes. A total of 609 genes were identified, and the corresponding cfDNA fragmentomic features were utilised to construct the ensemble model. This model achieved a sensitivity of 90.4% and a specificity of 83.1%, with an AUC of 0.94 in the independent validation set. Notably, the model demonstrated exceptional sensitivity for stage I lung cancer cases, achieving 95.1%. It also showed remarkable performance in detecting minimally invasive adenocarcinoma, with a sensitivity of 96.2%, highlighting its potential for early detection in clinical settings.

CONCLUSIONS: With feature selection guided by multiple epigenetic sequencing approaches, the cfDNA fragmentomics-based machine learning model demonstrated outstanding performance in the independent validation cohort. These findings highlight its potential as an effective non-invasive strategy for the early detection of lung cancer.

KEYPOINTS: Our study elucidated the regulatory relationships between epigenetic modifications and their effects on fragmentomic features. Identifying epigenetically regulated genes provided a critical foundation for developing the cfDNA fragmentomics-based machine learning model. The model demonstrated exceptional clinical performance, highlighting its substantial potential for translational application in clinical practice.

PMID:39909829 | PMC:PMC11798665 | DOI:10.1002/ctm2.70225

RBM45 reprograms lipid metabolism promoting hepatocellular carcinoma via Rictor and ACSL1/ACSL4

Oncogene, Published online: 01 December 2023; doi:10.1038/s41388-023-02902-4

RBM45 reprograms lipid metabolism promoting hepatocellular carcinoma via Rictor and ACSL1/ACSL4
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