Molecular pathways in cancer-related inflammation
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Ac cu mu la ti ng evi den ce shows that chro nic in fl am ma tion is as so cia ted to in crea sed ri sk of can cer.An in fl am ma to ry com po ne nt is pre se nt al so in the mic roen vi ron me nt of tu mou rs epi de mio lo gi cal ly un re la ted to in fl am ma tion.Exten si ve in ves ti ga tio ns over the pa st de ca de ha ve un co ve red ma ny of the im por ta nt mec ha nis tic pat hways un der lyi ng can ce r-re la ted in fl am ma tion.Pat hways lin ki ng in fl am ma tion and can cer ha ve been iden ti fi ed: an in trin sic one (dri ven by ge ne tic even ts that cau se neop la sia) and an extrin sic one (dri ven by in fl am ma to ry con di tio ns whi ch pre dis po se to can cer).Smoul de ri ng in fl am ma tion is a com po ne nt of the tu mour mic roen vi ron me nt and is a re cog ni zed hal lma rk of can cer.Key or ches tra to rs at the in tersec tion of the in trin sic and extrin sic pat hways in clu de tran scrip tion fac to rs (e.g.Nuc lear Fac tor kap pa-B, NFκB) that mo du la te the in fl am ma to ry res pon se throu gh so lub le me dia to rs (cyto ki nes, che mo ki nes) and cel lu lar com po nen ts (e.g.tu mo r-as so cia ted mac rop ha ges), pro mo ti ng tu mo ri gene sis.NFκB aids in the pro li fe ra tion and sur vi val of ma lig na nt cel ls, pro mo tes an gio ge ne sis and me tas ta sis, sub ver ts adap ti ve im mu ni ty, and al te rs res pon ses to hor mo nes and che mot he ra peu tic agen ts.Emer gi ng evi den ce al so sug ges ts that per sis te nt in fl am ma tion pro mo tes ge ne tic in sta bi li ty.Thus, can ce r-re la ted in fl am ma tion rep re sen ts a tar get for in no va ti ve diag nos tic and the ra peu tic stra te gies.Key wor ds: can ce r-re la ted in fl am ma tion; cyto ki nes; che mo ki nes; mac rop ha ges
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Persistent inflammation contributes to the development of several diseases, such as insulin resistance, dementia, rheumatoid arthritis, atherosclerosis, and cancer.
“Chronic inflammation is an underlying cause of several pathological disorders including insulin resistance, dementia, rheumatoid arthritis, atherosclerosis, and cancer [1, 2].”
From Edible blue-green algae reduce the production of pro-inflammatory cytokines by inhibiting NF-κB pathway in macrophages and splenocytes (2013) · cites this paper as [2]
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- Authors
- Del Prete, A., Allavena, P., Santoro, G., Fumarulo, R., Corsi, M. M., & Mantovani, A.
- Affiliations
- IRCCS Humanitas Research Hospital (IT)
- University of Bari Aldo Moro (IT)
- University of Milan (IT)
- Venue
- Biochemia Medica
- Published
- 2011
- Volume
- 21
- Issue
- 3
- Pages
- 264-275
- ISSN
- 1330-0962 (ISSN-L)
- 1846-7482
- OpenAlex
- W2090098587
- Cited by
- 181
- References
- 22
- Citations by year
- 2026: 4 · 2025: 4 · 2024: 15 · 2023: 12 · 2022: 11 · 2021: 15 · 2020: 16 · 2019: 15 · 2018: 18 · 2017: 11 · 2016: 18 · 2015: 13 · 2014: 12 · 2013: 14 · 2012: 2
- FWCI
- 0.81
- Type
- journal article
- Language
- en
- Open access
- diamond
- doi.org
- Licence
- cc-by
- Locations
- Biochemia Medica (publishedVersion, cc-by)
- PubMed (publishedVersion)
- University of Zagreb University Computing Centre (SRCE) (submittedVersion, other-oa)
- Institutional Research Information System (Università degli Studi di Brescia) (submittedVersion, other-oa)
- CINECA IRIS Institutional Research Information System (University of Bari Aldo Moro) (submittedVersion)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Immune cells in cancer
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › NF-κB Signaling Pathways
- Health Sciences › Medicine › Pharmacology › Inflammatory mediators and NSAID effects
- Keywords
- tumor inflammation, tumor microenvironment, NF-κB signaling, chronic inflammation, tumor-associated macrophages, cytokines and chemokines, angiogenesis, metastasis, immune evasion, genomic instability, carcinogenesis, therapeutic target, biomarkers, chemoprevention, chemosensitization, tumor suppressor, oncogenes
- MeSH terms
- Animals, Humans, Inflammation, Models, Biological, Neoplasms, Oncogenes, Risk Factors, Signal Transduction
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