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Embryonic Origin and Subclonal Evolution of Tumor-Associated Macrophages Imply Preventive Care for Cancer.
Zhang, Xiao-Mei; Chen, De-Gao; Li, Shengwen Calvin; Zhu, Bo; Li, Zhong-Jun.
  • Zhang XM; Laboratory of Radiation Biology, Laboratory Medicine Center, Department of Blood Transfusion, The Second Affiliated Hospital, Army Military Medical University, Chongqing 400037, China.
  • Chen DG; Institute of Cancer, The Second Affiliated Hospital, Army Military Medical University, Chongqing 400037, China.
  • Li SC; Neuro-Oncology and Stem Cell Research Laboratory, Center for Neuroscience Research, CHOC Children's Research Institute, Children's Hospital of Orange County (CHOC), 1201 West La Veta Ave., Orange, CA 92868, USA.
  • Zhu B; Department of Neurology, University of California-Irvine School of Medicine, 200 S Manchester Ave., Ste 206, Orange, CA 92868, USA.
  • Li ZJ; Institute of Cancer, The Second Affiliated Hospital, Army Military Medical University, Chongqing 400037, China.
Cells ; 10(4)2021 04 14.
Article in English | MEDLINE | ID: covidwho-1408630
ABSTRACT
Macrophages are widely distributed in tissues and function in homeostasis. During cancer development, tumor-associated macrophages (TAMs) dominatingly support disease progression and resistance to therapy by promoting tumor proliferation, angiogenesis, metastasis, and immunosuppression, thereby making TAMs a target for tumor immunotherapy. Here, we started with evidence that TAMs are highly plastic and heterogeneous in phenotype and function in response to microenvironmental cues. We pointed out that efforts to tear off the heterogeneous "camouflage" in TAMs conduce to target de facto protumoral TAMs efficiently. In particular, several fate-mapping models suggest that most tissue-resident macrophages (TRMs) are generated from embryonic progenitors, and new paradigms uncover the ontogeny of TAMs. First, TAMs from embryonic modeling of TRMs and circulating monocytes have distinct transcriptional profiling and function, suggesting that the ontogeny of TAMs is responsible for the functional heterogeneity of TAMs, in addition to microenvironmental cues. Second, metabolic remodeling helps determine the mechanism of phenotypic and functional characteristics in TAMs, including metabolic bias from macrophages' ontogeny in macrophages' functional plasticity under physiological and pathological conditions. Both models aim at dissecting the ontogeny-related metabolic regulation in the phenotypic and functional heterogeneity in TAMs. We argue that gleaning from the single-cell transcriptomics on subclonal TAMs' origins may help understand the classification of TAMs' population in subclonal evolution and their distinct roles in tumor development. We envision that TAM-subclone-specific metabolic reprogramming may round-up with future cancer therapies.
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Full text: Available Collection: International databases Database: MEDLINE Main subject: Embryo, Mammalian / Tumor-Associated Macrophages / Neoplasms Limits: Humans Language: English Year: 2021 Document Type: Article Affiliation country: Cells10040903

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Full text: Available Collection: International databases Database: MEDLINE Main subject: Embryo, Mammalian / Tumor-Associated Macrophages / Neoplasms Limits: Humans Language: English Year: 2021 Document Type: Article Affiliation country: Cells10040903