Clonal evolution of acute myeloid leukemia highlighted by latest genome sequencing studies
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Xuehong Zhang1, Dekang Lv1, Yu Zhang1, Quentin Liu1,2,3,4 and Zhiguang Li1
1 Center of Genome and Personalized Medicine, Institute of Cancer Stem Cell, Cancer Center, Dalian Medical University, Dalian, China
2 State Key Laboratory of Oncology in South China, Cancer Center, Sun Yat-sen University, Guangzhou, China
3 Department of Hematology, The Third Affiliated Hospital, Sun Yat-sen University, Guangzhou, China
4 Institute of Hematology, Sun Yat-sen University, Guangzhou, China
Zhiguang Li, email:
Quentin Liu, email:
Keywords: acute myeloid leukemia, clonal evolution, cancer genome
Received: May 02, 2016 Accepted: July 11, 2016 Published: July 26, 2016
Decades of years might be required for an initiated cell to become a fully-pledged, metastasized tumor. DNA mutations are accumulated during this process including background mutations that emerge scholastically, as well as driver mutations that selectively occur in a handful of cancer genes and confer the cell a growth advantage over its neighbors. A clone of tumor cells could be superseded by another clone that acquires new mutations and grows more aggressively. Tumor evolutional patterns have been studied for years using conventional approaches that focus on the investigation of a single or a couple of genes. Latest deep sequencing technology enables a global view of tumor evolution by deciphering almost all genome aberrations in a tumor. Tumor clones and the fate of each clone during tumor evolution can be depicted with the help of the concept of variant allele frequency. Here, we summarize the new insights of cancer evolutional progression in acute myeloid leukemia.
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