Hepatocellular carcinoma (HCC) is characterised by a robust resistance to therapy, resulting in the very poor prognosis usually seen in patients with unresectable HCC. A thorough understanding of the molecular and cellular pathogenesis of HCC is of paramount importance for the identification of more effective treatment options. As hypoxia in tumours is associated with the malignant phenotype, molecules involved in the hypoxic response are being investigated as potential targets for cancer therapy. One key hallmark of human HCC is the hypervascularisation and arterialisation of the tumour’s blood supply. Hypoxia being a strong inducer of neo-angiogenesis, it was hypothesised over 20 years ago that reduced oxygen levels in human HCC are a crucial feature of this deadly disease. However, while there is a considerable body of literature espousing the presumed functional relevance of hypoxia in HCC, direct measurements of oxygen partial pressures or O₂ concentrations in human HCCs have yet to be performed. This narrative review seeks to demonstrate how overinterpretation of in vitro experiments and incorrect citations have resulted in HCCs being perceived as severely hypoxic tumours.

肝细胞癌 (HCC) 的特点是对治疗有强烈的抵抗力，导致通常在不可切除的 HCC 患者中看到的非常差的预后。彻底了解 HCC 的分子和细胞发病机制对于确定更有效的治疗方案至关重要。由于肿瘤中的缺氧与恶性表型相关，因此正在研究参与缺氧反应的分子作为癌症治疗的潜在靶标。人类 HCC 的一个关键标志是肿瘤血液供应的过度血管化和动脉化。缺氧是新血管生成的强诱导剂，20 多年前就假设人类 HCC 中氧水平降低是这种致命疾病的关键特征。然而，_{人类 HCC 中的2}种浓度尚未进行。这篇叙述性综述旨在证明对体外实验的过度解释和不正确的引用如何导致 HCC 被视为严重缺氧的肿瘤。