ArticleFrontiers in oncology2025
Genomic complexity in advanced gastric and esophageal adenocarcinomas: a case report of rare
Article in Frontiers in oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
Abstract
Fibroblast growth factor receptor 2 (FGFR2) alterations represent an emerging therapeutic target in gastroesophageal adenocarcinoma (GEA). Although FGFR2 amplifications and overexpression have been associated with poor prognosis and therapeutic resistance, the clinical significant FGFR2 fusions, which are exceedingly rare, is unknown. Herein we describe two cases of advanced gastroesophageal and gastric adenocarcinomas characterized by aggressive disease course, rapid progression despite standard first-line chemoimmunotherapy, and the presence of high-level FGFR2 amplification with concurrent WDR11-AS1-FGFR2 fusion detected by circulating tumor DNA (ctDNA) analysis. These cases highlight the genomic complexity and aggressive behavior of FGFR2-driven GEA, underscored by coexisting genetic alterations. The findings emphasize the importance of comprehensive genomic profiling, including both tissue and liquid. in order to capture intratumoral heterogeneity and evolving molecular events. Further investigation of FGFR2 fusion biology and combinatorial therapeutic strategies is warranted to address the clinical challenge of biomarker overlap and treatment resistance in GEA.
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.