ArticlePloS one2018
Molecular signatures in IASLC/ATS/ERS classified growth patterns of lung adenocarcinoma.
Article in PloS one, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.
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, 1 synthesis or guideline pooled it.
- Prognostic impact of the newly revised IASLC proposed grading system for invasive lung adenocarcinoma: a systematic review and meta-analysis.World journal of surgical oncology · 2024Pooled it
- IL4I1⁺ Macrophages and TDO2⁺ Myofibroblasts Drive AhR-Mediated Immunosuppression and Ferroptosis Resistance in Solid Predominant Lung Adenocarcinoma.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Single-cell and spatial transcriptomic characterization of pulmonary pleomorphic carcinoma.Communications biology · 2025Article
- Excessive MYC Orchestrates Macrophages induced Chromatin Remodeling to Sustain Micropapillary-Patterned Malignancy in Lung Adenocarcinoma.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Hypoxia drives the formation of lung micropapillary adenocarcinoma-like structure through hypoxia-inducible factor-1α.Scientific reports · 2024Article
- Article
- Article
- The Profiling of Apoptosis-Associated MicroRNA Expressions of the Lung Adenocarcinoma.Thoracic research and practice · 2023Article
- Therapeutic Targeting of Macrophage Plasticity Remodels the Tumor-Immune Microenvironment.Cancer research · 2022Article
- A lepidic gene signature predicts patient prognosis and sensitivity to immunotherapy in lung adenocarcinoma.Genome medicine · 2022Article
- Transcriptional patterns reveal tumor histologic heterogeneity and immunotherapy response in lung adenocarcinoma.Frontiers in immunology · 2022Article
- Mechanism of BIP-4 mediated inhibition of InsP3Kinase-A.Bioscience reports · 2021Article
- ITPKA induces cell senescence, inhibits ovarian cancer tumorigenesis and can be downregulated by miR-203.Aging · 2021Article
- Molecular differences across invasive lung adenocarcinoma morphological subgroups.Translational lung cancer research · 2020Article
- Infiltrative tumour growth pattern correlates with poor outcome in oesophageal cancer.BMJ open gastroenterology · 2020Article
- High expression of CXCL14 is a biomarker of lung adenocarcinoma with micropapillary pattern.Cancer science · 2020Article
- Identification of microRNAs involved in pathways which characterize the expression subtypes of NSCLC.Molecular oncology · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe current classification of human lung adenocarcinoma defines five different histological growth patterns within the group of conventional invasive adenocarcinomas. The five growth patterns are characterised by their typical architecture, but also by variable tumor biological behaviour.
aimsThe aim of this study was to identify specific gene signatures of the five adenocarcinoma growth patterns defined by the joint IASLC/ATS/ERS working group.
methodsTotal RNA from microdissected adenocarcinoma tissue samples of ten lepidic, ten acinar, ten solid, nine papillary, and nine micropapillary tumor portions was isolated and prepared for gene expression analysis. Differential expression of genes was determined using the R package "LIMMA". The overall significance of each signature was assessed via global test. Gene ontology statistics were analysed using GOstat. For immunohistochemical validation, tissue specimens from 20 tumors with solid and 20 tumors with lepidic growth pattern were used.
resultsMicroarray analyses between the growth patterns resulted in numerous differentially expressed genes between the solid architecture and other patterns. The comparison of transcriptomic activity in the solid and lepidic patterns revealed 705 up- and 110 downregulated non-redundant genes. The pattern-specific protein expression of Inositol-1,4,5-trisphosphate-kinase-A (ITPKA) and angiogenin by immunohistochemistry confirmed the RNA levels. The strongest differences in protein expression between the two patterns were shown for ITPKA (p = 0.02) and angiogenin (p = 0.113).
conclusionsIn this study growth pattern-specific gene signatures in pulmonary adenocarcinoma were identified and distinct transcriptomic differences between lung adenocarcinoma growth patterns were defined. The study provides valuable new information about pulmonary adenocarcinoma and allows a better assessment of the five adenocarcinoma subgroups.
Indexed as
Identifiers
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.