The DOI matches its Crossref record; 6 of the 6 references it cites were found in a registry or an index.
Inflammation Amplifier, a New Paradigm in Cancer Biology
Abstract
Tumor-associated inflammation can induce various molecules expressed from the tumors themselves or surrounding cells to create a microenvironment that potentially promotes cancer development. Inflammation, particularly chronic inflammation, is often linked to cancer development, even though its evolutionary role should impair nonself objects including tumors. The inflammation amplifier, a hyperinducer of chemokines in nonimmune cells, is the principal machinery for inflammation and is activated by the simultaneous stimulation of NF-κB and STAT3. We have redefined inflammation as local activation of the inflammation amplifier, which causes an accumulation of various immune cells followed by dysregulation of local homeostasis. Genes related to the inflammation amplifier have been genetically associated with various human inflammatory diseases. Here, we describe how cancer-associated genes, including interleukin (IL)-6, Ptgs2, ErbB1, Gas1, Serpine1, cMyc, and Vegf-α, are strongly enriched in genes related to the amplifier. The inflammation amplifier is activated by the stimulation of cytokines, such as TNF-α, IL-17, and IL-6, resulting in the subsequent expression of various target genes for chemokines and tumor-related genes like BCL2L11, CPNE7, FAS, HIF1-α, IL-1RAP, and SOD2. Thus, we conclude that inflammation does indeed associate with the development of cancer. The identified genes associated with the inflammation amplifier may thus make potential therapeutic targets of can…
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“It too plays a key role in inflammatory diseases including cytokine storm syndromes, autoimmune diseases and cancer (10, 11, 15, 41, 66–68)”
From IL-6 in inflammation, autoimmunity and cancer (2021) · cites this paper as [11]
In the citing paper
“Among them, IL-6 is a major player in chronic inflammatory diseases, autoimmune diseases, cancer and cytokine storm (1, 3, 10–26).”
From IL-6 in inflammation, autoimmunity and cancer (2021) · cites this paper as [11]
In the citing paper
“Moreover, the IL-6 Amp is related with various types of cancer, including hematologic malignancies, tumors in lung, and colorectal/intestinal, urinary/bladder/vulvar, breast, stomach and liver cancers (11).”
From IL-6 in inflammation, autoimmunity and cancer (2021) · cites this paper as [11]
In the citing paper
“Furthermore, many cancer-associated genes were identified as regulators or target genes of the IL-6 Amp (11).”
From IL-6 in inflammation, autoimmunity and cancer (2021) · cites this paper as [11]
In the citing paper
“Target molecules of the IL-6 Amp include EGFR, c-Myc, Pim1, VEGFα, hypoxia-inducible factor 1-alpha (HIF1-α), MMPs and many pro-inflammatory cytokines and growth factors involved in cell survival, proliferation, angiogenesis and metastasis (Fig. 3) (10, 11).”
From IL-6 in inflammation, autoimmunity and cancer (2021) · cites this paper as [11]
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Cited by
Sorted by citations
IL-6 in inflammation, autoimmunity and cancer
Hirano, T. (2021) · International Immunology · doi:10.1093/intimm/dxaa078 · Cited by 1,453
“Furthermore, many cancer-associated genes were identified as regulators or target genes of the IL-6 Amp (11).”
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Chronic inflammation, cancer development and immunotherapy
Wen, Y., Zhu, Y., Zhang, C., Yang, X., Gao, Y., Li, M., Yang, H., Liu, T., & Tang, H. (2022) · Frontiers in Pharmacology · doi:10.3389/fphar.2022.1040163 · Cited by 247
“…evidences demonstrate that tumorassociated inflammation could affect almost every stage of cancer: cancer development, metastasis, drug resistance and cancer recurrence by inducing genomic instability, driving selfrenewal of cancer stem-like cells (CSCs) and angiogenesis (Atsumi et al., 2014).”
Background
Metadata
- Authors
- Atsumi, T., Singh, R., Sabharwal, L., Bando, H., Meng, J., Arima, Y., Yamada, M., Harada, M., Jiang, J.-J., Kamimura, D., Ogura, H., Hirano, T., & Murakami, M.
- Affiliations
- Japan Science and Technology Agency (JP)
- ORCID
- Venue
- Cancer Research
- Published
- 2014-01-01
- Volume
- 74
- Issue
- 1
- Pages
- 8-14
- ISSN
- 0008-5472 (ISSN-L)
- 1538-7445
- OpenAlex
- W2101899879
- Cited by
- 217
- References
- 0
- Citations by year
- 2026: 7 · 2025: 13 · 2024: 18 · 2023: 13 · 2022: 16 · 2021: 14 · 2020: 12 · 2019: 18 · 2018: 18 · 2017: 20 · 2016: 20 · 2015: 33 · 2014: 14
- FWCI
- 2.40
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Cancer Research (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Japan Society for the Promotion of Science (24790472, 24249028, 26460574, 24390098)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Cytokine Signaling Pathways and Interactions
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › NF-κB Signaling Pathways
- Life Sciences › Immunology and Microbiology › Immunology › Immune cells in cancer
- Keywords
- tumor inflammation, chronic inflammation, carcinogenesis, NF-κB, STAT3, tumor microenvironment, cytokines, interleukin-6, cyclooxygenase-2, EGF receptor, GAS1, SERPINE1, c-Myc, VEGFα, HIF-1α, therapeutic target
- MeSH terms
- Animals, Humans, Inflammation, Neoplasms, Signal Transduction, Tumor Microenvironment
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