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How Signaling Molecules Regulate Tumor Microenvironment: Parallels to Wound Repair
P. Gál, L. Varinská, L. Fáber, Š. Novák, P. Szabo, P. Mitrengová, A. Mirossay, P. Mučaji, K. Smetana,
Jazyk angličtina Země Švýcarsko
Typ dokumentu časopisecké články, přehledy
Grantová podpora
NV15-28933A
MZ0
CEP - Centrální evidence projektů
Digitální knihovna NLK
Plný text - Článek
Zdroj
NLK
Directory of Open Access Journals
od 1997
Free Medical Journals
od 1997
PubMed Central
od 2001
Europe PubMed Central
od 2001
ProQuest Central
od 1997-01-01
Open Access Digital Library
od 1997-01-01
Medline Complete (EBSCOhost)
od 2009-03-01
Health & Medicine (ProQuest)
od 1997-01-01
- MeSH
- buněčné mikroprostředí MeSH
- cytokiny metabolismus MeSH
- galektiny metabolismus MeSH
- hojení ran MeSH
- imunitní systém cytologie imunologie metabolismus MeSH
- keloid metabolismus patologie MeSH
- lidé MeSH
- mezibuněčné signální peptidy a proteiny metabolismus MeSH
- nádorové kmenové buňky metabolismus patologie MeSH
- nádorové mikroprostředí * MeSH
- nádory imunologie metabolismus patologie MeSH
- rány a poranění imunologie metabolismus patologie MeSH
- signální transdukce * MeSH
- zvířata MeSH
- Check Tag
- lidé MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- přehledy MeSH
It is now suggested that the inhibition of biological programs that are associated with the tumor microenvironment may be critical to the diagnostics, prevention and treatment of cancer. On the other hand, a suitable wound microenvironment would accelerate tissue repair and prevent extensive scar formation. In the present review paper, we define key signaling molecules (growth factors, cytokines, chemokines, and galectins) involved in the formation of the tumor microenvironment that decrease overall survival and increase drug resistance in cancer suffering patients. Additional attention will also be given to show whether targeted modulation of these regulators promote tissue regeneration and wound management. Whole-genome transcriptome profiling, in vitro and animal experiments revealed that interleukin 6, interleukin 8, chemokine (C-X-C motif) ligand 1, galectin-1, and selected proteins of the extracellular matrix (e.g., fibronectin) do have similar regulation during wound healing and tumor growth. Published data demonstrate remarkable similarities between the tumor and wound microenvironments. Therefore, tailor made manipulation of cancer stroma can have important therapeutic consequences. Moreover, better understanding of cancer cell-stroma interaction can help to improve wound healing by supporting granulation tissue formation and process of reepithelization of extensive and chronic wounds as well as prevention of hypertrophic scars and formation of keloids.
Department of Pharmacology Faculty of Medicine Pavol Jozef Šafárik University 040 11 Košice Slovakia
Citace poskytuje Crossref.org
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- $a Gál, Peter $u Department for Biomedical Research, East-Slovak Institute of Cardiovascular Diseases, Inc., 040 11 Košice, Slovakia. pgal@vusch.sk. Department of Pharmacology, Faculty of Medicine, Pavol Jozef Šafárik University, 040 11 Košice, Slovakia. pgal@vusch.sk. Department of Pharmacognosy and Botany, Faculty of Pharmacy, Comenius University, 832 32 Bratislava, Slovakia. pgal@vusch.sk.
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- $a How Signaling Molecules Regulate Tumor Microenvironment: Parallels to Wound Repair / $c P. Gál, L. Varinská, L. Fáber, Š. Novák, P. Szabo, P. Mitrengová, A. Mirossay, P. Mučaji, K. Smetana,
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- $a It is now suggested that the inhibition of biological programs that are associated with the tumor microenvironment may be critical to the diagnostics, prevention and treatment of cancer. On the other hand, a suitable wound microenvironment would accelerate tissue repair and prevent extensive scar formation. In the present review paper, we define key signaling molecules (growth factors, cytokines, chemokines, and galectins) involved in the formation of the tumor microenvironment that decrease overall survival and increase drug resistance in cancer suffering patients. Additional attention will also be given to show whether targeted modulation of these regulators promote tissue regeneration and wound management. Whole-genome transcriptome profiling, in vitro and animal experiments revealed that interleukin 6, interleukin 8, chemokine (C-X-C motif) ligand 1, galectin-1, and selected proteins of the extracellular matrix (e.g., fibronectin) do have similar regulation during wound healing and tumor growth. Published data demonstrate remarkable similarities between the tumor and wound microenvironments. Therefore, tailor made manipulation of cancer stroma can have important therapeutic consequences. Moreover, better understanding of cancer cell-stroma interaction can help to improve wound healing by supporting granulation tissue formation and process of reepithelization of extensive and chronic wounds as well as prevention of hypertrophic scars and formation of keloids.
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