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Open AccessJournal ArticleDOI

EMT and inflammation: inseparable actors of cancer progression

TLDR
The interconnections between EMT programs and cellular and molecular actors of inflammation are described, and data linking the EMT/inflammation axis to metastasis is recapitulate.
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This article is published in Molecular Oncology.The article was published on 2017-07-01 and is currently open access. It has received 368 citations till now. The article focuses on the topics: Epithelial–mesenchymal transition & Cancer cell.

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Getting TANned: How the tumor microenvironment drives neutrophil recruitment.

TL;DR: Recent advances in understanding how guidance cues underlie neutrophil migration to primary and secondary tumor sites are reviewed and a cohesive view is provided on how both myeloid cell types shape TME‐associated extracellular matrix organization, which in turn contribute to tumor progression.
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Macrophages in pancreatic cancer: An immunometabolic perspective.

TL;DR: Recent advances in the understanding of macrophage origin, distribution and polarization are summarized and a thorough review of the role macrophages in PC carcinogenesis and development is provided, as well as the underlying molecular mechanism.
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Gut Microbiota and Colon Cancer: A Role for Bacterial Protein Toxins?

TL;DR: This review is focused on those toxins that, by mimicking carcinogens and cancer promoters, could represent a paradigm for bacterially induced carcinogenesis.
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The role of the epithelial-to-mesenchymal transition (EMT) in diseases of the salivary glands

TL;DR: The current state-of-the-art and latest findings regarding the link between EMT, inflammation, fibrosis and cancer are discussed, highlighting the most recent data on EMT-dependent tissue fibrosis during chronic inflammatory salivary glands conditions and salivARY glands tumors.
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Intrahepatic cholangiocarcinoma induced M2-polarized tumor-associated macrophages facilitate tumor growth and invasiveness

TL;DR: The results indicated that M2-polarized macrophages induced by ICC promote tumor growth and invasiveness through IL-10/STAT3-induced EMT and might be a potential therapeutic target for ICC.
References
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Journal ArticleDOI

Monocyte chemoattractant protein-1 (MCP-1): an overview.

TL;DR: This review will discuss the biological processes and the structure and function of CCL2, one of the key chemokines that regulate migration and infiltration of monocytes/macrophages.
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Evidence for a tumoral immune resistance mechanism based on tryptophan degradation by indoleamine 2,3-dioxygenase

TL;DR: It is shown that most human tumors constitutively express IDO, and that expression of IDO by immunogenic mouse tumor cells prevents their rejection by preimmunized mice, suggesting that the efficacy of therapeutic vaccination of cancer patients might be improved by concomitant administration of an IDO inhibitor.
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Circulating Breast Tumor Cells Exhibit Dynamic Changes in Epithelial and Mesenchymal Composition

TL;DR: A role for EMT in the blood-borne dissemination of human breast cancer is supported as both single cells and multicellular clusters, expressing known EMT regulators, including transforming growth factor (TGF)–β pathway components and the FOXC1 transcription factor.
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Epithelial-to-mesenchymal transition is dispensable for metastasis but induces chemoresistance in pancreatic cancer

TL;DR: This study functionally probes the role of EMT in PDAC by generating mouse models of PDAC with deletion of Snail or Twist, two key transcription factors responsible for EMT, and highlights the importance of combining EMT inhibition with chemotherapy for the treatment of pancreatic cancer.
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Epithelial-to-mesenchymal transition is not required for lung metastasis but contributes to chemoresistance

TL;DR: The potential of an EMT-targeting strategy, in conjunction with conventional chemotherapies, for breast cancer treatment is suggested, using a mesenchymal-specific Cre-mediated fluorescent marker switch system in spontaneous breast-to-lung metastasis models.
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