Patel Rashi Bharat, Li Ting, Liao Zhichao, Jaldeepbhai Jivani Aakash, Perera H A Pavanika N V, Muthukuda Sujani Kaushalya, Dhirubhai Dholiya Hardeep, Singh Vaibhav, Du Xiaoling, Yang Jilong
International Medical School, Tianjin Medical University, Tianjin 300061, China.
Department of Bone and Soft Tissue Tumor, Tianjin Medical University Cancer Institute & Hospital, Tianjin 300060, China.
Stem Cell Investig. 2017 Mar 15;4:21. doi: 10.21037/sci.2017.02.09. eCollection 2017.
Liposarcomas (LPS) are among the most common soft tissue sarcomas, originating from adipocytes. Treatment for LPS typically involves surgical resection and radiation therapy, while the use of conventional cytotoxic chemotherapy for unresectable or metastatic LPS remains controversial. This review summarizes the results of recent translational research and trials of novel therapies targeting various genetic and molecular aberrations in different subtypes of LPS. Genetic aberrations such as the 12q13-15 amplicon, genetic amplification of , and point mutations in , and , as the fusion of are involved in the pathogenesis LPS and represent potential therapeutic candidates. Tyrosine kinase inhibitors targeting MET, AXL, IGF1R, EGFR, VEGFR2, PDGFR-β and Aurora kinase are effective in certain types of LPS. Abnormalities in the PI3K/Akt signaling pathway deregulation of and its partner , and the interaction between calreticulin (CRT) and CD47 are also promising therapeutic targets. These promising new approaches may help to supplement existing treatments for LPS.
脂肪肉瘤(LPS)是最常见的软组织肉瘤之一,起源于脂肪细胞。LPS的治疗通常包括手术切除和放射治疗,而对于不可切除或转移性LPS使用传统的细胞毒性化疗仍存在争议。本综述总结了近期针对LPS不同亚型中各种基因和分子异常的转化研究及新疗法试验的结果。诸如12q13 - 15扩增子、 、 的基因扩增、 、 和 中的点突变以及 融合等基因异常参与了LPS的发病机制,并代表了潜在的治疗靶点。靶向MET、AXL、IGF1R、EGFR、VEGFR2、PDGFR-β和Aurora激酶的酪氨酸激酶抑制剂在某些类型的LPS中有效。PI3K/Akt信号通路的异常、 及其伴侣 的失调以及钙网蛋白(CRT)与CD47之间的相互作用也是有前景的治疗靶点。这些有前景的新方法可能有助于补充现有的LPS治疗方法。