ArticleeLife2021
A non-genetic, cell cycle-dependent mechanism of platinum resistance in lung adenocarcinoma.
Article in eLife, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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
17 citing papers in PubMed, 26 citations in OpenAlex.
- Nitrogen Mustard Disrupts Bioenergetics and Activates Oxidative Stress-Induced Cell Death Pathways in Human Keratinocytes.Chemical research in toxicology · 2026Article
- A deep learning approach for time-consistent cell cycle phase prediction from microscopy data.PLoS computational biology · 2025Article
- A Mendelian randomization-based risk model using aging-related genes for prognosis in lung adenocarcinoma.Discover oncology · 2025Article
- LeGO-3D: 3D imaging of lung metastases and vascularisation using light sheet fluorescence microscopy.Npj imaging · 2025Article
- A concise guide to fluorescent cell cycle reporters for live-cell imaging.Frontiers in cell and developmental biology · 2025Review
- The Role of ADCY1 in Regulating the Sensitivity of Platinum-Based Chemotherapy in NSCLC.Pharmaceuticals (Basel, Switzerland) · 2024Article
- A comprehensive review of computational cell cycle models in guiding cancer treatment strategies.NPJ systems biology and applications · 2024Review
- Impact of the thyroid hormone T3 and its nuclear receptor TRα1 on colon cancer stem cell phenotypes and response to chemotherapies.Cell death & disease · 2024Article
- A Nexus between Genetic and Non-Genetic Mechanisms Guides KRAS Inhibitor Resistance in Lung Cancer.Biomolecules · 2023Article
- Ascites-Derived Organoids to Depict Platinum Resistance in Gynaecological Serous Carcinomas.International journal of molecular sciences · 2023Article
- Single-cell intracellular pH dynamics regulate the cell cycle by timing the G1 exit and G2 transition.Journal of cell science · 2023Article
- A Systems Biology Approach for Addressing Cisplatin Resistance in Non-Small Cell Lung Cancer.Journal of clinical medicine · 2023Article
- Emerging role of non-coding RNAs in resistance to platinum-based anti-cancer agents in lung cancer.Frontiers in pharmacology · 2023Review
- Mastering the use of cellular barcoding to explore cancer heterogeneity.Nature reviews. Cancer · 2022Review
- A mathematical model for cell cycle control: graded response or quantized response.Cell cycle (Georgetown, Tex.) · 2022Article
- A prognostic and therapeutic hallmark developed by the integrated profile of basement membrane and immune infiltrative landscape in lung adenocarcinoma.Frontiers in immunology · 2022Article
- Intravital imaging technology guides FAK-mediated priming in pancreatic cancer precision medicine according to Merlin status.Science advances · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
15 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We previously used a pulse-based in vitro assay to unveil targetable signalling pathways associated with innate cisplatin resistance in lung adenocarcinoma (Hastings et al., 2020). Here, we advanced this model system and identified a non-genetic mechanism of resistance that drives recovery and regrowth in a subset of cells. Using RNAseq and a suite of biosensors to track single-cell fates both in vitro and in vivo, we identified that early S phase cells have a greater ability to maintain proliferative capacity, which correlated with reduced DNA damage over multiple generations. In contrast, cells in G1, late S or those treated with PARP/RAD51 inhibitors, maintained higher levels of DNA damage and underwent prolonged S/G2 phase arrest and senescence. Combined with our previous work, these data indicate that there is a non-genetic mechanism of resistance in human lung adenocarcinoma that is dependent on the cell cycle stage at the time of cisplatin exposure.
Indexed as
Identifiers
What Socratic 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 Socratic graph.