Inflammation and necrosis promote tumour growth

By J. Vakkila, Michael Lotze. Nature reviews. Immunology, 2004

712 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/0f83c85b17ab3c6aa1a5c08df22edad1d7f6ee10

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Citations in the corpus

Immunity, Inflammation, and Cancer (2010, neutral): “Surgery results in activation of infection- or stress-sensing pathways, whereas chemo- and radiotherapy kill cancer cells mostly through necrosis, a proinflammatory form of cell death (Vakkila and Lotze, 2004).”
Role of systemic inflammatory response in predicting survival in patients with primary operable cancer. (2010, background): “In the last decade or so it has become clear that disease progression in cancer is dependent on a complex interaction of the characteristics of both the tumor and the host inf lammatory response [2–4].”
Molecular mechanisms of cell death in neurological diseases (2021, background): “Necrosis is observed in many pathological conditions, including myocardial infarction, stroke, several neurodegenerative diseases and in certain cancers, where factors released from necrotic malignant cells are likely to impact the tumour microenvironment [14, 141].”
Principles and Current Strategies for Targeting Autophagy for Cancer Treatment (2011, background): “Autophagy, immunity, and cancer Cancer in adults (69), but not in children (70), arises in the setting of chronic inflammation.”
Activated monocytes in peritumoral stroma of hepatocellular carcinoma foster immune privilege and disease progression through PD-L1 (2009, background): “Human tumor tissues can be anatomically classified into areas of intratumoral and peritumoral stroma, each with distinct compositions and functional properties (5, 7, 24, 25).”
Autophagy promotes tumor cell survival and restricts necrosis, inflammation, and tumorigenesis. (2006, background): “The inflammatory response to stress-mediated, oncogene-activated necrosis in tumors, by analogy to a wound healing response, may stimulate angiogenesis and tumor cell proliferation (Balkwill et al., 2005; Balkwill and Coussens, 2004; Vakkila and Lotze, 2004; Zeh and Lotze, 2005).”