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The tumor microenvironment (TME) is the cellular environment in which the tumor exists, including surrounding blood vessels, immune cells, fibroblasts, bone marrow-derived inflammatory cells, lymphocytes, signaling molecules and the extracellular matrix (ECM).〔(【引用サイトリンク】title=NCI Dictionary of Cancer Terms )〕 The tumor and the surrounding microenvironment are closely related and interact constantly. Tumors can influence the microenvironment by releasing extracellular signals, promoting tumor angiogenesis and inducing peripheral immune tolerance, while the immune cells in the microenvironment can affect the growth and evolution of cancerous cells, such as in immuno-editing. The tumor microenvironment contributes to tumour heterogeneity. == History == The importance of a stromal microenvironment, especially “wound” or regenerating tissue, has been recognized since the late 1800s. The interplay between the tumor and its microenvironment was part of Stephen Paget's 1889 "seed and soil" theory, in which he postulated that metastases of a particular type of cancer ("the seed") often metastasizes to certain sites ("the soil") based on the similarity of the original and secondary tumor sites.〔The Lancet, Volume 133, Issue 3421, 23 March 1889, Pages 571-573〕 Its role in blunting an immune attack awaited the discovery of adaptive cellular immunity. In 1960, Klein and colleagues found that in mice, primary methylcholanthrene-induced sarcomas exhibited an antitumor immune response mediated by lymph node cells to cancer cells derived from the primary tumor. This immune response did not however affect the primary tumor. The primary tumor instead established a microenvironment that is functionally analogous to that of certain normal tissues, such as the eye.〔 Later, mice experiments by Halachmi and Witz showed that for the same cancer cell line, greater tumorigenicity was evident ''in vivo'' than the same strain inoculated ''in vitro''. Unambiguous evidence for the inability in humans of a systemic immune response to eliminate immunogenic cancer cells was provided by Boon’s 1991 studies of antigens that elicit specific CD8+ T cell responses in melanoma patients. One such antigen was MAGE-A1. The coexistence of a progressing melanoma with melanoma-specific T cells implicitly does not involve immunoediting, but does not exclude the possibility of TME immune suppression.〔 The discovery of melanoma-specific T cells in patients led to the strategy of adoptively transferring large numbers of ''in vitro-''expanded tumor-infiltrating lymphocytes (TILs) which has proven that the immune system has the potential to control cancer. However, adoptive T cell therapy (ACT) with TILs has not had the dramatic success of ACT with virus-specific CD8+ T cells. The TME of solid cancers appears to be fundamentally different to that of the leukemias, in which clinical ACT trials with chimeric antigen receptor T cells have demonstrated efficacy.〔 抄文引用元・出典: フリー百科事典『 ウィキペディア（Wikipedia）』 ■ウィキペディアで「Tumor microenvironment」の詳細全文を読む スポンサード リンク
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