Journal
CANCER LETTERS
Volume 267, Issue 1, Pages 10-17Publisher
ELSEVIER IRELAND LTD
DOI: 10.1016/j.canlet.2008.02.055
Keywords
tumor dormancy; B7-H1; PD-L1; stem cell; NK; cytotoxic T cells; imatinib
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Tumor dormancy is characterised by the persistence of residual tumor cells for long periods. Recurrence from minimal residual disease is a major cause of cancer death. Thus, understanding how cancer cells become and remain dormant, may lead to new strategies to prevent relapse. Evidence has emerged that a balance exists between host and dormant tumor cells. Cross-talk between tumor cells and their micro-environment, angiogenesis, and anti-tumor immune response participate in the control of dormant tumor cells. Tumor cells have several mechanisms of maintaining equilibrium, and immune escape, including expression of immuno-regulatory molecules (e.g., increased expression of B7.1 and B7-H1); epigenetic modifications (e.g., silencing of the SOCS1 gene, de-regulating the JAK/STAT pathway); and autocrine loops. These new findings offer new opportunities to design specific treatments, to modify the balance in favor of the host immune response. (C) 2008 Elsevier Ireland Ltd. All rights reserved.
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