Cancer-related inflammation.
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TLDR
The molecular pathways of this cancer-related inflammation are now being unravelled, resulting in the identification of new target molecules that could lead to improved diagnosis and treatment.Citations
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Interleukin-17 produced by tumor microenvironment promotes self-renewal of CD133 + cancer stem-like cells in ovarian cancer
TL;DR: The data indicate that IL-17 contributed to ovarian cancer malignancy through promoting the self-renewal of CD133+CSLCs and that IL -17 and its signaling pathway might serve as therapeutic targets for the treatment of ovarian cancer.
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TLR-signaling and proinflammatory cytokines as drivers of tumorigenesis.
Kirill V. Korneev,Kamar-Sulu N. Atretkhany,M. S. Drutskaya,Sergei I. Grivennikov,Dmitry V. Kuprash,Dmitry V. Kuprash,Sergei A. Nedospasov +6 more
TL;DR: The role of Toll-like receptor (TLR) 4 signaling in cancer and contributions of proinflammatory cytokine signaling (whose expression may be driven by TLR-mediated signals) to tumor-promoting microenvironment are discussed.
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Toll-Like Receptor 4 Activation in Cancer Progression and Therapy
Alja Oblak,Roman Jerala +1 more
TL;DR: Research of the role and mechanisms of TLR4 activation in cancer may provide novel antitumor vaccine adjuvants as well asTLR4 inhibitors that could prevent inflammation-induced carcinogenesis.
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Type and location of tumor-infiltrating macrophages and lymphatic vessels predict survival of colorectal cancer patients.
Annika Ålgars,Heikki Irjala,Heikki Irjala,Samuli Vaittinen,Samuli Vaittinen,Heikki Huhtinen,Jari Sundström,Jari Sundström,Marko Salmi,Raija Ristamäki,Sirpa Jalkanen +10 more
TL;DR: The results of this work suggest that the type of macrophages, number of lymphatic vessels and their location contribute to the clinical behavior of colorectal cancer in a disease stage‐specific manner.
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Small molecule immunomodulation: the tumor microenvironment and overcoming immune escape.
TL;DR: Two promising classes of immunomodulatory small molecule inhibitors are focused on: colony stimulating factor-1 receptor (CSF-1R) and focal adhesion kinase (FAK), which present a unique opportunity to attenuate immune escape of tumors and potentiate the effectiveness of immunotherapy and traditional cytotoxic therapy.
References
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Journal ArticleDOI
Inflammation and cancer
Lisa M. Coussens,Zena Werb +1 more
TL;DR: It is now becoming clear that the tumour microenvironment, which is largely orchestrated by inflammatory cells, is an indispensable participant in the neoplastic process, fostering proliferation, survival and migration.
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Inflammation and cancer: back to Virchow?
TL;DR: A rationale for the use of cytokine and chemokine blockade, and further investigation of non-steroidal anti-inflammatory drugs, in the chemoprevention and treatment of malignant diseases is provided.
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Involvement of chemokine receptors in breast cancer metastasis.
Anja Müller,Bernhard Homey,Hortensia Soto,Nianfeng Ge,Daniel Catron,Matthew E. Buchanan,Terri McClanahan,Erin Murphy,Wei Yuan,Stephan N. Wagner,Jose Luis Barrera,Alejandro Mohar,Emma Verastegui,Albert Zlotnik +13 more
TL;DR: It is reported that the chemokine receptors CXCR4 and CCR7 are highly expressed in human breast cancer cells, malignant breast tumours and metastases and their respective ligands CXCL12/SDF-1α and CCL21/6Ckine exhibit peak levels of expression in organs representing the first destinations of breast cancer metastasis.
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Macrophage polarization: tumor-associated macrophages as a paradigm for polarized M2 mononuclear phagocytes
Alberto Mantovani,Silvano Sozzani,Silvano Sozzani,Massimo Locati,Paola Allavena,Antonio Sica +5 more
TL;DR: These functionally polarized cells, and similarly oriented or immature dendritic cells present in tumors, have a key role in subversion of adaptive immunity and in inflammatory circuits that promote tumor growth and progression.
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Nuclear factor-kappaB in cancer development and progression.
TL;DR: This article showed that NF-kappaB provides a mechanistic link between inflammation and cancer, and is a major factor controlling the ability of both pre-neoplastic and malignant cells to resist apoptosis-based tumour-surveillance mechanisms.