Epigenetics of colorectal cancer: biomarker and therapeutic potential

Nature Reviews Gastroenterology & Hepatology, Journal Year: 2020, Volume and Issue: 17(2), P. 111 - 130

Published: Jan. 3, 2020

Language: Английский

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Single-cell RNA sequencing highlights the role of inflammatory cancer-associated fibroblasts in bladder urothelial carcinoma

Nature Communications, Journal Year: 2020, Volume and Issue: 11(1)

Published: Oct. 8, 2020

Although substantial progress has been made in cancer biology and treatment, clinical outcomes of bladder carcinoma (BC) patients are still not satisfactory. The tumor microenvironment (TME) is a potential target. Here, by single-cell RNA sequencing on 8 BC samples 3 para samples, we identify 19 different cell types the microenvironment, indicating high intra-tumoral heterogeneity. We find that cells down regulated MHC-II molecules, suggesting downregulated immunogenicity may contribute to formation an immunosuppressive microenvironment. also monocytes undergo M2 polarization region differentiate. Furthermore, LAMP3 + DC subgroup be able recruit regulatory T cells, potentially taking part TME. Through correlation analysis using public datasets containing over 3000 role for inflammatory cancer-associated fibroblasts (iCAFs) progression, which significantly related poor prognosis. Additionally, characterize network depending iCAFs. These results could help elucidate protumor mechanisms Our provide deep insight into immunology essential resource drug discovery future.

Language: Английский

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Longitudinal molecular trajectories of diffuse glioma in adults

Nature, Journal Year: 2019, Volume and Issue: 576(7785), P. 112 - 120

Published: Nov. 20, 2019

Language: Английский

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Spatial omics and multiplexed imaging to explore cancer biology

Nature Methods, Journal Year: 2021, Volume and Issue: 18(9), P. 997 - 1012

Published: Aug. 2, 2021

Language: Английский

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The multi-factorial nature of clinical multidrug resistance in cancer

Drug Resistance Updates, Journal Year: 2019, Volume and Issue: 46, P. 100645 - 100645

Published: Sept. 1, 2019

Language: Английский

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Mechanisms generating cancer genome complexity from a single cell division error

Science, Journal Year: 2020, Volume and Issue: 368(6488)

Published: April 16, 2020

Genomic havoc from one fateful mistake Many human tumors display scrambled genomes that arise two distinct mutational processes. The first, the chromosome breakage-fusion-bridge (BFB) cycle, produces gene amplification and genomic instability. second, chromothripsis, generates massive, clustered rearrangements in or a few chromosomes. Umbreit et al. hypothesized these processes are mechanistically related tested this idea by recreating essential steps of BFB cycle cultured cells (see Perspective Paiano Nussenzweig). They found chromothripsis arises cascade events begins with aberrant bridge formation during mitosis, followed fragmentation, DNA damage, missegregation, micronuclei. propose model explains how single cell division error (chromosome formation) can generate many hallmark features cancer genomes. Science , issue p. 240 ; see also eaba0712

Language: Английский

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Next-generation cancer organoids

Nature Materials, Journal Year: 2021, Volume and Issue: 21(2), P. 143 - 159

Published: Aug. 12, 2021

Language: Английский

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Integrating genetic and non-genetic determinants of cancer evolution by single-cell multi-omics

Nature Reviews Genetics, Journal Year: 2020, Volume and Issue: 22(1), P. 3 - 18

Published: Aug. 17, 2020

Language: Английский

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Immunological impact of cell death signaling driven by radiation on the tumor microenvironment

Nature Immunology, Journal Year: 2019, Volume and Issue: 21(2), P. 120 - 134

Published: Dec. 23, 2019

Language: Английский

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Cell Death in the Origin and Treatment of Cancer

Molecular Cell, Journal Year: 2020, Volume and Issue: 78(6), P. 1045 - 1054

Published: June 1, 2020

Cell death, or, more specifically, cell suicide, is a process of fundamental importance to human health. Throughout our lives, over million cells are produced every second. When organismal growth has stopped, balance division, similar number must be removed. This achieved by activation molecular mechanisms that have evolved so can destroy themselves. The first clues regarding the nature one these came from studying genes associated with cancer, in particular gene for BCL-2. Subsequent studies revealed mutations or other defects inhibit death allow accumulate, prevent removal damaged DNA, and increase resistance malignant chemotherapy. Knowledge this mechanism allowed development drugs kill cancer directly activating machinery synergizing conventional chemotherapy as well targeted agents achieve improved outcomes patients. theory, established 1800s, posits all organisms composed derived (reviewed Mazzarello, 1999Mazzarello P. A unifying concept: history theory.Nat. Biol. 1999; 1: E13-E15Crossref PubMed Google Scholar). Since then, it became apparent only multicellular get cancers expand when rate at which divide greater than they die. What surprising die, whether normal cells, seldom because injured killed cells. Rather, most die activate programmed purpose (Kerr et al., 1972Kerr J.F. Wyllie A.H. Currie A.R. Apoptosis: basic biological phenomenon wide-ranging implications tissue kinetics.Br. J. Cancer. 1972; 26: 239-257Crossref Scholar, Vaux 1994Vaux D.L. Haecker G. Strasser A. An evolutionary perspective on apoptosis.Cell. 1994; 76: 777-779Abstract Full Text PDF Scopus (675) been observed long time, but was initially largely reported context necrosis hypoxic areas growing tumors (Thomlinson Gray, 1955Thomlinson R.H. Gray L.H. histological structure some lung possible radiotherapy.Br. 1955; 9: 539-549Crossref also therapy radiation were designed cause comes cost causing many (Ballantyne, 1975Ballantyne A.J. 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Köntgen Proapoptotic relative Bim certain responses, leukocyte homeostasis, preclude autoimmunity.Science. 286: 1735-1738Crossref (1233) Puthalakath 2007Puthalakath O'Reilly L.A. Gunn Kelly P.N. Huntington N.D. Hughes P.D. McKimm-Breschkin Motoyama al.ER Bim.Cell. 129: 1337-1349Abstract (941) Induction regulated microRNA cluster mir-17-92 (Ventura 2008Ventura Young A.G. Winslow M.M. Lintault Meissner Erkeland S.J. Newman Bronson R.T. Crowley Stone al.Targeted deletion reveals overlapping functions miR-17 92 miRNA clusters.Cell. 2008; 132: 875-886Abstract (1193) Xiao 2008Xiao Srinivasan Calado Patterson H.C. Henderson Kutok J.L. Rajewsky Lymphoproliferative disease autoimmunity miR-17-92 expression lymphocytes.Nat. 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Language: Английский

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