1996
DOI: 10.1007/978-1-4899-0274-0_7
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Role of Antibody Signaling in Inducing Tumor Dormancy

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Cited by 7 publications
(2 citation statements)
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“…The cancer dormancy field has worked based on three definitions that are not necessarily mutually exclusive and may be complementary. These have led to the working hypothesis that asymptomatic minimal residual disease (MRD) can be defined and explained by three potential scenarios: 1) angiogenic dormancy, an impaired angiogenic response maintaining tumor mass constant in size by balancing proliferation and cell death [1][2][3] ; 2) immune-mediated dormancy, in which proliferative tumor cell populations are constantly trimmed by cytotoxic immune cell responses that also maintain an equilibrium between cell death and proliferation [4][5][6][7][8][9][10][11][12][13] ; and 3) cellular dormancy, in which solitary DTCs or small cell clusters enter a prolonged growth arrest with no increase in cell death 19,[24][25][26][27] .…”
Section: Discussing Definitionsmentioning
confidence: 99%
See 1 more Smart Citation
“…The cancer dormancy field has worked based on three definitions that are not necessarily mutually exclusive and may be complementary. These have led to the working hypothesis that asymptomatic minimal residual disease (MRD) can be defined and explained by three potential scenarios: 1) angiogenic dormancy, an impaired angiogenic response maintaining tumor mass constant in size by balancing proliferation and cell death [1][2][3] ; 2) immune-mediated dormancy, in which proliferative tumor cell populations are constantly trimmed by cytotoxic immune cell responses that also maintain an equilibrium between cell death and proliferation [4][5][6][7][8][9][10][11][12][13] ; and 3) cellular dormancy, in which solitary DTCs or small cell clusters enter a prolonged growth arrest with no increase in cell death 19,[24][25][26][27] .…”
Section: Discussing Definitionsmentioning
confidence: 99%
“…In recent years our understanding of metastasis biology and cancer cell dormancy has advanced considerably. Current knowledge of how cancer dormancy proceeds has stemmed from pioneering work on angiogenesis [1][2][3] , immune regulation of equilibrium states and antibody signaling [4][5][6][7][8][9][10][11][12][13] , and on how micro-environmental and signaling mechanisms control cellular dormancy through growth arrest programs 14,15 . Key findings based on this body of work proposed that dormant cells might evade anti-proliferative therapies in a passive manner 16 .…”
Section: Introductionmentioning
confidence: 99%