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脂肪肉瘤:分子遗传学与治疗学

Liposarcoma: molecular genetics and therapeutics.

作者信息

Conyers Rachel, Young Sophie, Thomas David M

机构信息

Sarcoma Genomics & Genetics, Peter MacCallum Cancer Centre, 12 St Andrews Place, East Melbourne, VIC 3002, Australia.

出版信息

Sarcoma. 2011;2011:483154. doi: 10.1155/2011/483154. Epub 2010 Dec 27.

DOI:10.1155/2011/483154
PMID:21253554
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3021868/
Abstract

Sarcomas are a group of heterogeneous tumours with varying genetic basis. Cytogenetic abnormalities range from distinct genomic rearrangements such as pathognomonic translocation events and common chromosomal amplification or loss, to more complex rearrangements involving multiple chromosomes. The different subtypes of liposarcoma are spread across this spectrum and constitute an interesting tumour type for molecular review. This paper will outline molecular pathogenesis of the three main subtypes of liposarcoma: well-differentiated/dedifferentiated, myxoid/round cell, and pleomorphic liposarcoma. Both the molecular basis and future avenues for therapeutic intervention will be discussed.

摘要

肉瘤是一组具有不同遗传基础的异质性肿瘤。细胞遗传学异常范围从明显的基因组重排,如特征性的易位事件和常见的染色体扩增或缺失,到涉及多条染色体的更复杂重排。脂肪肉瘤的不同亚型分布在这个范围内,构成了一个有趣的分子研究肿瘤类型。本文将概述脂肪肉瘤三种主要亚型的分子发病机制:高分化/去分化型、黏液样/圆形细胞型和多形性脂肪肉瘤。将讨论其分子基础以及未来治疗干预的途径。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dda8/3021868/4843ded88985/SRCM2011-483154.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dda8/3021868/e4cae7400988/SRCM2011-483154.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dda8/3021868/30dcbae13eec/SRCM2011-483154.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dda8/3021868/4843ded88985/SRCM2011-483154.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dda8/3021868/e4cae7400988/SRCM2011-483154.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dda8/3021868/30dcbae13eec/SRCM2011-483154.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dda8/3021868/4843ded88985/SRCM2011-483154.003.jpg

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本文引用的文献

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Clin Cancer Res. 2010 Oct 15;16(20):4958-67. doi: 10.1158/1078-0432.CCR-10-0317. Epub 2010 Aug 20.
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Deregulation of the PI3K and KRAS signaling pathways in human cancer cells determines their response to everolimus.
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