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Article Synopsis
  • HPV8, a type of human papillomavirus linked to skin cancer, affects immune cell presence and inflammation in patients with epidermodysplasia verruciformis (EV).
  • The study found that HPV8 E6 significantly induces the chemokine CCL2, attracting monocytes and leading to a predominance of macrophages in the lesions, surpassing even pro-inflammatory cytokines like TNF-α.
  • Researchers highlighted a specific mechanism involving the C/EBPα/miR-203/p63 pathway in how HPV8 E6 influences CCL2 production, showing that HPV8's oncoproteins disrupt skin immune balance for viral persistence.
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Background: Matrix metalloproteinase-13 (MMP13) is a member of the endopeptidase matrix metalloproteinase family, which is involved in many normal physiological processes and even tumorigenesis. However, its co-carcinogenic signature in different cancers is not fully understood.

Methods: In this study, we first analyzed the expression of MMP13 in pan-cancer and its association with prognosis, immune infiltration, and cancer-related signaling pathways through integrated bioinformatics.

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Impacts of arsenic on Rad18 and translesion synthesis.

Toxicol Appl Pharmacol

November 2022

Department of Pharmaceutical Sciences, University of New Mexico Health Sciences Center, 1 University of New Mexico, Albuquerque, NM 87131, USA. Electronic address:

Arsenite interferes with DNA repair protein function resulting in the retention of UV-induced DNA damage. Accumulated DNA damage promotes replication stress which is bypassed by DNA damage tolerance pathways such as translesion synthesis (TLS). Rad18 is an essential factor in initiating TLS through PCNA monoubiquitination and contains two functionally and structurally distinct zinc fingers that are potential targets for arsenite binding.

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The WHO classified air pollution as a human lung carcinogen and polycyclic aromatic hydrocarbons (PAHs) are components of both indoor (e.g., tobacco smoke and cookstoves) and outdoor (e.

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Aberrant activation of the phosphoinositide 3-kinase (PI3K)/AKT/mTOR and Ras/mitogen-activated protein kinase (MAPK) pathways is a hallmark of hepatocarcinogenesis. In a subset of hepatocellular carcinomas (HCCs), PI3K/AKT/mTOR signaling dysregulation depends on phosphatidylinositol-4,5-bisphosphate 3-kinase, catalytic subunit alpha (PIK3CA) mutations, while RAS/MAPK activation is partly attributed to promoter methylation of the tumor suppressor Ras association domain-containing protein 1 (RASSF1A). To evaluate a possible cocarcinogenic effect of PIK3CA activation and RASSF1A knockout, plasmids expressing oncogenic forms of PIK3CA (E545K or H1047R mutants) were delivered to the liver of RASSF1A knockout and wild-type mice by hydrodynamic tail vein injection combined with sleeping beauty-mediated somatic integration.

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