ArticleMedical oncology (Northwood, London, England)2025
Mechanism of etoposide resistance in small cell lung cancer and the potential therapeutic options.
Article in Medical oncology (Northwood, London, England), 2025. 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.
- HIST1H4L promotes small cell lung cancer tumorigenesis by regulating the PI3K/Akt pathway and serves as a potential diagnostic biomarker.Frontiers in oncology · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
Abstract
Small cell lung cancer (SCLC) is a type of high-grade neuroendocrine malignancy with low gene mutation. Chemotherapy is the major treatment strategy, but long-term clinical application often leads to drug resistance. Etoposide is a first-line drug approved by the US Food and Drug Administration for SCLC treatment, but etoposide-resistance is a problem. In this study, a SCLC cell line with etoposide-acquired resistance, H1048-ER, was constructed through a concentration gradient increasing method, and its resistance to etoposide was investigated in vitro and in a zebrafish model. Through transcriptome sequencing, real-time reverse transcription-quantitative polymerase chain reaction, and bioinformatic analyses of H1048-ER vs. H1048 cells, 51 differentially expressed genes were found to be significantly enriched in "collagen degradation" and "MET/FAK signaling activation in ECM". Among them, six genes (COL11A1, COL26A1, COL4A3, COL4A4, LAMA4, and LAMC1) had strong correlations with the prognosis of lung cancer. They may be key factors in the acquired etoposide resistance of H1048-ER cells. H1048-ER cells showed cross-resistance to cisplatin but were sensitive to doxorubicin and temozolomide. Our study provides novel insights into etoposide resistance in SCLC and affords the potential treatment options after etoposide resistance.
Indexed as
Identifiers
40257680What 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.