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Liu, T.* ; Larionova, I.* ; Litviakov, N.* ; Riabov, V.* ; Zavyalova, M.V.* ; Tsyganov, M.* ; Buldakov, M.* ; Song, B.* ; Moganti, K.* ; Kazantseva, P.* ; Slonimskaya, E.* ; Kremmer, E. ; Flatley, A. ; Klüter, H.* ; Cherdyntseva, N.V.* ; Kzhyshkowska, J.*

Tumor-associated macrophages in human breast cancer produce new monocyte attracting and pro-angiogenic factor YKL-39 indicative for increased metastasis after neoadjuvant chemotherapy.

OncoImmunology 7:e1436922 (2018)
Verlagsversion DOI PMC
Open Access Hybrid
Creative Commons Lizenzvertrag
It is undeniably one of the greatest findings in biology that (with some very minor exceptions) every cell in the body possesses the whole genetic information needed to generate a complete individual. Today, this concept has been so thoroughly assimilated that we struggle to still see how surprising this finding actually was: all cellular phenotypes naturally occurring in one person are generated from genetic uniformity, and thus are per definition epigenetic. Transcriptional mechanisms are clearly critical for developing and protecting cell identities, because a mis-expression of few or even single genes can efficiently induce inappropriate cellular programmes. However, how transcriptional activities are molecularly controlled and which of the many known epigenomic features have causal roles remains unclear. Today, clarification of this issue is more pressing than ever because profiling efforts and epigenome-wide association studies (EWAS) continuously provide comprehensive datasets depicting epigenomic differences between tissues and disease states. In this commentary, we propagate the idea of a widespread follow-up use of epigenome editing technology in EWAS studies. This would enable them to address the questions of which features, where in the genome, and which circumstances are essential to shape development and trigger disease states.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Schlagwörter Angiogenesis ; Breast Cancer ; Chemotaxis ; Chitinase-like Protein ; Monocyte ; Neoadjuvant Chemotherapy ; Tumor-associated Macrophage ; Ykl-39; Base-resolution Analysis; Dna-methylation; Wide Association; Transcription Factors; Mammalian Genome; Cells; System; Enhancers; Cancer; Genes
Sprache englisch
Veröffentlichungsjahr 2018
HGF-Berichtsjahr 2018
ISSN (print) / ISBN 2162-4011
e-ISSN 2162-402X
Zeitschrift OncoImmunology
Quellenangaben Band: 7, Heft: 6, Seiten: , Artikelnummer: e1436922 Supplement: ,
Verlag Taylor & Francis
Verlagsort Philadelphia
Begutachtungsstatus Peer reviewed
Institut(e) Institute of Molecular Immunology (IMI)
POF Topic(s) 30504 - Mechanisms of Genetic and Environmental Influences on Health and Disease
Forschungsfeld(er) Immune Response and Infection
PSP-Element(e) G-501793-001
DOI 10.1080/2162402X.2018.1436922
WOS ID WOS:000432214900028
Scopus ID 85043680918
PubMed ID 29872578
Erfassungsdatum 2018-06-11
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