Molecular classification of hepatocellular carcinoma: potential therapeutic implications.
Molecular classification of hepatocellular carcinoma: potential therapeutic implications.
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DOI：
10.2217/hep.15.26
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发表时间：
2015
期刊：
影响因子：
5
通讯作者：
Hoshida Y
中科院分区：
文献类型：
--
作者：
Goossens N;Sun X;Hoshida Y
肝细胞癌(肝细胞癌)肿瘤的基因组图谱揭示了常见或特定于疾病病因学、患者种族或地理区域的反复出现的分子异常，从而可以将肝细胞癌肿瘤分类为具有相似分子和临床特征的亚类。以前报道的基于转录组的分子亚类突出了几个共同的主题。侵袭性肿瘤以TP53失活突变和致癌信号通路激活为特征，并根据干性标志物的表达进一步细分。干性标志物阴性的侵袭性肿瘤表现出优先的转化生长因子-β激活。另一组侵袭性较弱的肿瘤包含以CTNNB1突变为特征的亚类，并伴有肝脏特异性WNT靶点的过度表达，如GLUL。选择性地针对肝细胞癌亚类特征的分子治疗表明，它们在丰富临床试验中的潜在反应者和指导肝细胞癌患者的治疗决策方面具有实用价值。
Genomic profiling of hepatocellular carcinoma (HCC) tumors has elucidated recurrent molecular aberrations common or specific to disease etiology, patient race or geographic regions, allowing the classification of HCC tumors into subclasses sharing similar molecular and clinical characteristics. Previously reported transcriptome-based molecular subclasses have highlighted several common themes. Aggressive tumors are characterized by TP53 inactivation mutations and activation of pro-oncogenic signaling pathways, and further subclassified according to expression of stemness markers. The stemness marker-negative aggressive tumors display preferential TGF-β activation. Another group of less aggressive tumors contains a subclass characterized by CTNNB1 mutations accompanied with overexpression of liver-specific WNT targets such as GLUL. Molecular therapies selectively targeting features of the HCC subclasses have suggested their utility in enriching potential responders in clinical trials and guiding therapeutic decision-making for HCC patients.