ArticleTranslational oncology2020
PIK3CA and KRAS Amplification in Esophageal Adenocarcinoma and their Impact on the Inflammatory Tumor Microenvironment and Prognosis.
Article in Translational oncology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 33 citations in OpenAlex.
- SMARCA2 and SMARCA4-deficiency is associated with a distinct molecular and microenvironmental subtype of esophageal adenocarcinoma.Scientific reports · 2026Article
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- Single-cell transcriptomic profiling combined with Mendelian randomization illuminates molecular drivers of bladder cancer.Molecular genetics and genomics : MGG · 2026Article
- Clinical Trials Update in Resectable Esophageal Cancer.Cancers · 2026Review
- Common oncogenic mutations in colorectal cancer: drivers of carcinogenesis and potential therapeutic targets.Frontiers in pharmacology · 2026Review
- The Interplay Between Esophageal Adenocarcinoma and Its Tumor Microenvironment: Toward Innovative Therapies.Cells · 2025Review
- Genomic Variations in Esophageal Squamous Cell Carcinoma and Esophageal Adenocarcinoma.Cureus · 2023Article
- Network and pathway-based analysis of candidate genes associated with esophageal adenocarcinoma.Journal of gastrointestinal oncology · 2023Article
- Combined score of Y chromosome loss and T-cell infiltration improves UICC based stratification of esophageal adenocarcinoma.Frontiers in oncology · 2023Article
- Integrin beta1 (ITGB1) as a prognostic marker in esophageal adenocarcinoma.Scientific reports · 2022Article
- Characterizing isoform switching events in esophageal adenocarcinoma.Molecular therapy. Nucleic acids · 2022Article
- The combination of gene hyperamplification and PD-L1 expression as a biomarker for the clinical benefit of tislelizumab in gastric/gastroesophageal junction adenocarcinoma.Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association · 2022Article
- Comparative genomic analysis of esophageal squamous cell carcinoma and adenocarcinoma: New opportunities towards molecularly targeted therapy.Acta pharmaceutica Sinica. B · 2022Review
- The Use of miRNAs in Predicting Response to Neoadjuvant Therapy in Oesophageal Cancer.Cancers · 2022Review
- Diffusion kernel-based predictive modeling of KRAS dependency in KRAS wild type cancer cell lines.NPJ systems biology and applications · 2022Article
- Exome sequencing identifies novel somatic variants in African American esophageal squamous cell carcinoma.Scientific reports · 2021Article
- Analytic validation and clinical utilization of the comprehensive genomic profiling test, GEM ExTraOncotarget · 2021Article
- GATA binding protein 6 (GATA6) is co-amplified with PIK3CA in patients with esophageal adenocarcinoma and is linked to neoadjuvant therapy.Journal of cancer research and clinical oncology · 2021Article
- Molecular profiles of response to neoadjuvant chemoradiotherapy in oesophageal cancers to develop personalized treatment strategies.Molecular oncology · 2021Article
- Identification and Validation of PIK3CA as a Marker Associated with Prognosis and Immune Infiltration in Renal Clear Cell Carcinoma.Journal of oncology · 2021Article
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Authors and funding
12 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Gene amplifications of PIK3CA or KRAS induce a downstream activation of the AKT-mTOR or RAF-ERK-pathways. Interactions of the active AKT pathway have been implicated in the inflammatory tumor microenvironment. Nothing is known about these interactions or prognostic power in esophageal adenocarcinoma (EAC). We retrospectively analyzed a large cohort of 685 EAC considering KRAS and PIK3CA gene amplification using fluorescence in situ hybridization (FISH) and immunohistochemistry. These results were correlated with clinical and molecular data as well as the inflammatory tumor microenvironment. Amplifications of KRAS were seen in 94 patients (17.1%), PIK3CA amplifications in 23 patients (5.0%). KRAS amplifications significantly correlated with nodal positive patients and poorer overall survival (OS) in the subgroup without neoadjuvant treatment (p = 0.004), coamplifications of Her2 (p = 0.027), and TP53 mutations (p = 0.016). PIK3CA amplifications significantly correlated with a high amount of tumor infiltrating T cells (p = 0.003) and showed a tendency to better OS (p = 0.068). A correlation with checkpoint makers (PD-L1, LAG3, VISTA, TIM3, IDO) could not be revealed. Our findings are the first to link the KRAS amplified genotype with lymphonodal positivity and poor prognosis and the PIK3CA-amplified genotype with a T cell-rich microenvironment in EAC. Future studies must show whether these two genotype subgroups can be therapeutically influenced. A dual inhibition of MEK and SHP2T could be effective in the subgroup of KRAS amplified EACs and an immune checkpoint blockade may prove to be particularly promising in the subgroup of PIK3CA-amplified EACs.
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Registered trials
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