title: Dormant tumor cells as a therapeutic target?
abstract: 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.
authors.affiliation: INSERM, U837, E3 Institut de Recherche sur le Cancer de Lille, Lille, France. brunoquesnel@hotmail.com
authors.forename: Bruno
authors.initials: B
authors.lastname: Quesnel
mesh_terms: D000818:Animals; D015703:Antigens, CD / Q000378:metabolism; D018122:B7-1 Antigen / Q000378:metabolism; D060890:B7-H1 Antigen; D006801:Humans; D007167:Immunotherapy / Q000379:methods; D051379:Mice; D018365:Neoplasm, Residual / Q000276:immunology; D009369:Neoplasms / Q000276:immunology / Q000473:pathology / Q000628:therapy*; D014411:Neoplastic Stem Cells / Q000502:physiology; D019139:Tumor Escape
chemical_list: D015703:Antigens, CD; D018122:B7-1 Antigen; D060890:B7-H1 Antigen; C423236:CD274 protein, human