Aims Oesophageal adenocarcinoma (EAC) tumorigenesis has been linked primarily to loss‐of‐function mutations in tumour suppressor genes. Knowledge of specific oncogenes that drive tumour progression, and their relationship to outcomes, is limited. High mobility group AT‐hook 2 (HMGA2) has been reported to be amplified in a subset of EACs, but the clinicopathological and prognostic implications of HMGA2 expression in EAC are unknown. Methods and results We performed HMGA2 immunohistochemistry and fluorescence in‐situ hybridization (FISH) in EAC to determine its clinicopathological and prognostic significance. Ninety‐one primary EAC resections without neoadjuvant treatment were identified and immunohistochemistry for HMGA2 was performed. The presence or absence of nuclear staining was evaluated and correlated with predetermined clinicopathological parameters and patient outcomes. A selected subset of tumours was subjected to FISH to identify alterations at the HMGA2 locus. HMGA2 expression was present in 25 of 91 (27.4%) tumours. HMGA2‐expressing cells were present in solid, poorly differentiated areas of the tumours at the invasive front, or as single infiltrating cells. FISH showed that three to four copies of HMGA2 are frequently present in EAC irrespective of HMGA2 protein expression and that high level HMGA2 amplification is a rare event. HMGA2 expression was associated with numerous adverse clinicopathological parameters, including higher T‐ and N‐stage, the presence of lymphovascular invasion and with a worse recurrence‐free and overall survival. Conclusion Our data suggest that HMGA2 is regulated in EAC primarily through non‐chromosomal‐level alterations that lead to increased HMGA2 expression. HMGA2‐positive EAC correlates with adverse pathological features and worse patient outcomes.