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Role of natural and adaptive immunity in renal cell carcinoma response to VEGFR‐TKIs and mTOR inhibitor
Author(s) -
Santoni Matteo,
Berardi Rossana,
Amantini Consuelo,
Burattini Luciano,
Santini Daniele,
Santoni Giorgio,
Cascinu Stefano
Publication year - 2013
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/ijc.28503
Subject(s) - temsirolimus , cancer research , immune system , sirolimus , acquired immune system , angiogenesis , axitinib , immunology , pi3k/akt/mtor pathway , pazopanib , sunitinib , tumor microenvironment , biology , renal cell carcinoma , medicine , signal transduction , microbiology and biotechnology , discovery and development of mtor inhibitors
Angiogenesis and immunosuppression work hand‐in‐hand in the renal cell carcinoma (RCC) microenvironment. Tumor growth is associated with impaired antitumor immune response in RCC, which involves T cells, natural killer cells, dendritic cells (DCs) and macrophages. Vascular endothelial growth factor receptor (VEGFR), such as sorafenib, sunitinib, pazopanib and axitinib, and mammalian target of rapamycin (mTOR) inhibitors, such as temsirolimus and everolimus, do exert both antiangiogenic and immunomodulatory functions. Indeed, these agents affect neutrophil migration, as well as T lymphocyte‐DC cross‐talk, DC maturation and immune cell metabolism and reactivity. In this review, we overview the essential role of innate and adaptive immune response in RCC proliferation, invasion and metastasis and the relationship between tumor‐associated immune cells and the response to targeted agents approved for the treatment of metastatic RCC.