Department of Radiology, University of Texas Health Science Center-San Antonio, 7703 Floyd Curl Dr, San Antonio, TX 78229, USA.
Radiology. 2011 Mar;258(3):673-93. doi: 10.1148/radiol.10100376.
Focal nodular hyperplasia (FNH), hepatocellular adenoma (HCA), and hepatocellular carcinoma (HCC) compose hepatocellular neoplasms that occur in adults. These tumors demonstrate characteristic epidemiologic and histopathologic features and clinical and imaging manifestations. HCAs are monoclonal neoplasms characterized by increased predilection to hemorrhage or rupture and occasional transformation to HCC. On the other hand, FNH is a polyclonal tumorlike lesion that occurs in response to increased perfusion and has an indolent clinical course. Up to 90% of HCCs occur in the setting of cirrhosis. Chronic viral hepatitis (hepatitis B and hepatitis C) infection and metabolic syndrome are major risk factors that can induce HCCs in nonfibrotic liver. Recent advances in pathology and genetics have led to better understanding of the histogenesis, natural history, and molecular events that determine specific oncologic pathways used by these neoplasms. HCAs are now believed to result from specific genetic mutations involving TCF1 (transcription factor 1 gene), IL6ST (interleukin 6 signal transducer gene), and CTNNB1 (β catenin-1 gene); FNHs are characterized by an "imbalance" of angiopoietin. While the β catenin signaling pathway is associated with well- and moderately differentiated HCCs, mutations involving p53 (tumor protein 53 gene), MMP14 (matrix metalloproteinase 14 gene), and RhoC (Ras homolog gene family, member C) are associated with larger tumor size, higher tumor grade with resultant shortened tumor-free survival, and poor prognosis. Fibrolamellar carcinoma (FLC), a unique HCC subtype, exhibits genomic homogeneity that partly explains its better overall prognosis. On the basis of recent study results involving cytogenetics and oncologic pathways of HCCs, novel drugs that act against molecular targets are being developed. Indeed, sorafenib (a multikinase inhibitor) is currently being used in the successful treatment of patients with advanced HCC. Characterization of genetic abnormalities and genotype-phenotype correlations in adult hepatocellular tumors provides better understanding of tumor pathology and biology, imaging findings, prognosis, and response to molecular therapeutics.
局灶性结节性增生 (FNH)、肝细胞腺瘤 (HCA) 和肝细胞癌 (HCC) 构成了成人发生的肝细胞肿瘤。这些肿瘤具有特征性的流行病学和组织病理学特征以及临床和影像学表现。HCA 是一种单克隆肿瘤,其特点是增加出血或破裂的倾向,偶尔会转化为 HCC。另一方面,FNH 是一种多克隆肿瘤样病变,发生于灌注增加时,具有惰性的临床病程。高达 90%的 HCC 发生在肝硬化的背景下。慢性病毒性肝炎 (乙型肝炎和丙型肝炎) 感染和代谢综合征是主要的危险因素,可导致非纤维化肝脏中的 HCC。病理学和遗传学的最新进展使人们更好地理解了这些肿瘤的组织发生、自然史和决定特定肿瘤学途径的分子事件。现在认为 HCA 是由涉及 TCF1(转录因子 1 基因)、IL6ST(白细胞介素 6 信号转导基因)和 CTNNB1(β 连环蛋白-1 基因)的特定基因突变引起的;FNH 的特征是血管生成素的“失衡”。虽然 β 连环蛋白信号通路与分化良好和中度分化的 HCC 相关,但涉及 p53(肿瘤蛋白 53 基因)、MMP14(基质金属蛋白酶 14 基因)和 RhoC(Ras 同源基因家族,成员 C)的突变与较大的肿瘤大小、较高的肿瘤分级、较短的无肿瘤生存期和较差的预后相关。纤维板层样癌 (FLC) 是一种独特的 HCC 亚型,具有基因组同质性,这在一定程度上解释了其较好的总体预后。基于 HCC 的细胞遗传学和肿瘤学途径的最新研究结果,正在开发针对分子靶点的新型药物。事实上,索拉非尼(一种多激酶抑制剂)目前正被用于成功治疗晚期 HCC 患者。成人肝细胞肿瘤的遗传异常和基因型-表型相关性的特征描述提供了对肿瘤病理学和生物学、影像学发现、预后以及对分子治疗的反应的更好理解。