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Tumor dormancy: quiescence or equilibrium? Volume 16, issue 5, septembre-octobre 2010

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Author
Unité Inserm 837, Équipe « Facteurs de résistance des cellules leucémiques », Institut de Recherche sur le Cancer de Lille ; et Service des maladies du sang, CHU de Lille

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 from experimental models that a balance exists between host, and dormant tumor cells which seem to persist in very small numbers. 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. Other experimental models indicate that dormant tumor cell population may be constituted of tumor stem cells that enter in quiescence. Quiescence may also be not restricted to stem cells and appears to be regulated through autophagy. This apparent multiplicity of mechanisms is puzzling and should be clarified by isolation of dormant tumor cells from patients. These new findings offer new opportunities to design specific treatments to target dormant tumor cells.