Author
Jinsong Liu
Bio: Jinsong Liu is an academic researcher from University of Texas MD Anderson Cancer Center. The author has contributed to research in topics: Somatic cell & Embryonic stem cell. The author has an hindex of 3, co-authored 3 publications receiving 123 citations.
Papers
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TL;DR: Evidence is reviewed that suggests somatic cells may have a previously overlooked endogenous embryonic program that can be activated to dedifferentiate somatics cells into stem cells of various potencies for tumor initiation, and a unified dualistic model is proposed to demonstrate the origin of human tumors.
117 citations
TL;DR: The increase in ploidy explains not only normal embryogenesis for well-differentiated tumors but also “somatic embryogenesis” for undifferentiated tumors, and the concept of the ‘life code’ may provide a simple theoretical framework to guide the immense efforts to understand cancer and fight this disease.
72 citations
TL;DR: Giant cells link McClintock's heredity to both early embryogenesis and tumor origin, the most fundamental mechanism on how both germ and soma for coping with environmental stresses for the survival across the tree of life which evolved over millions of years on Earth.
16 citations
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01 Apr 2014
TL;DR: This study identifies a core set of neurodevelopmental TFs (POU3F2, SOX2, SALL2, and OLIG2) essential for GBM propagation and reconstructs a network model that highlights critical interactions and identifies candidate therapeutic targets for eliminating TPCs.
Abstract: Developmental fate decisions are dictated by master transcription factors (TFs) that interact with cis-regulatory elements to direct transcriptional programs. Certain malignant tumors may also depend on cellular hierarchies reminiscent of normal development but superimposed on underlying genetic aberrations. In glioblastoma (GBM), a subset of stem-like tumor-propagating cells (TPCs) appears to drive tumor progression and underlie therapeutic resistance yet remain poorly understood. Here, we identify a core set of neurodevelopmental TFs (POU3F2, SOX2, SALL2, and OLIG2) essential for GBM propagation. These TFs coordinately bind and activate TPC-specific regulatory elements and are sufficient to fully reprogram differentiated GBM cells to "induced" TPCs, recapitulating the epigenetic landscape and phenotype of native TPCs. We reconstruct a network model that highlights critical interactions and identifies candidate therapeutic targets for eliminating TPCs. Our study establishes the epigenetic basis of a developmental hierarchy in GBM, provides detailed insight into underlying gene regulatory programs, and suggests attendant therapeutic strategies. PAPERCLIP:
614 citations
379 citations
TL;DR: Historical and contemporary evidence is presented that the key actuators of this process—of tumorigenesis, metastasis, and therapy resistance—are polyploid giant cancer cells.
Abstract: Cancer led to the deaths of more than 9 million people worldwide in 2018, and most of these deaths were due to metastatic tumor burden. While in most cases, we still do not know why cancer is lethal, we know that a total tumor burden of 1 kg-equivalent to one trillion cells-is not compatible with life. While localized disease is curable through surgical removal or radiation, once cancer has spread, it is largely incurable. The inability to cure metastatic cancer lies, at least in part, to the fact that cancer is resistant to all known compounds and anticancer drugs. The source of this resistance remains undefined. In fact, the vast majority of metastatic cancers are resistant to all currently available anticancer therapies, including chemotherapy, hormone therapy, immunotherapy, and systemic radiation. Thus, despite decades-even centuries-of research, metastatic cancer remains lethal and incurable. We present historical and contemporary evidence that the key actuators of this process-of tumorigenesis, metastasis, and therapy resistance-are polyploid giant cancer cells.
125 citations
TL;DR: The increase in ploidy explains not only normal embryogenesis for well-differentiated tumors but also “somatic embryogenesis” for undifferentiated tumors, and the concept of the ‘life code’ may provide a simple theoretical framework to guide the immense efforts to understand cancer and fight this disease.
72 citations