Controversies in clinical cancer dormancy.
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Controversies in clinical cancer dormancy. / Uhr, Jonathan W; Pantel, Klaus.
in: P NATL ACAD SCI USA, Jahrgang 108, Nr. 30, 30, 2011, S. 12396-12400.Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung
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TY - JOUR
T1 - Controversies in clinical cancer dormancy.
AU - Uhr, Jonathan W
AU - Pantel, Klaus
PY - 2011
Y1 - 2011
N2 - Clinical cancer dormancy is defined as an unusually long time between removal of the primary tumor and subsequent relapse in a patient who has been clinically disease-free. The condition is frequently observed in certain carcinomas (e.g., breast cancer), B-cell lymphoma, and melanoma, with relapse occurring 5-25 y later. Clinical data suggest that a majority of breast cancer survivors have cancer cells for decades but can remain clinically cancer-free for their lifetime. Thus, there is a major effort to characterize the molecular mechanisms responsible for inducing tumor cell dormancy using experimental models or studying the early phases of cancer growth in humans. Many molecules and signaling pathways have been characterized and have led to concepts that dominate the field, such as the possible role of innate and adaptive immunity in immune surveillance and initiation and maintenance of dormancy. However, recent clinical data do not support many of these concepts. Several areas need further study to determine their relevance to clinical cancer dormancy. We suggest hypotheses that may contribute to elucidation of the mechanisms underlying the dormant state.
AB - Clinical cancer dormancy is defined as an unusually long time between removal of the primary tumor and subsequent relapse in a patient who has been clinically disease-free. The condition is frequently observed in certain carcinomas (e.g., breast cancer), B-cell lymphoma, and melanoma, with relapse occurring 5-25 y later. Clinical data suggest that a majority of breast cancer survivors have cancer cells for decades but can remain clinically cancer-free for their lifetime. Thus, there is a major effort to characterize the molecular mechanisms responsible for inducing tumor cell dormancy using experimental models or studying the early phases of cancer growth in humans. Many molecules and signaling pathways have been characterized and have led to concepts that dominate the field, such as the possible role of innate and adaptive immunity in immune surveillance and initiation and maintenance of dormancy. However, recent clinical data do not support many of these concepts. Several areas need further study to determine their relevance to clinical cancer dormancy. We suggest hypotheses that may contribute to elucidation of the mechanisms underlying the dormant state.
KW - Animals
KW - Humans
KW - Male
KW - Female
KW - Time Factors
KW - Mice
KW - Recurrence
KW - Immunity, Innate
KW - Adaptive Immunity
KW - Breast Neoplasms/immunology/pathology
KW - Cancer Vaccines/pharmacology
KW - Homeostasis/immunology
KW - Models, Immunological
KW - Neoplasms/immunology/pathology/therapy
KW - Animals
KW - Humans
KW - Male
KW - Female
KW - Time Factors
KW - Mice
KW - Recurrence
KW - Immunity, Innate
KW - Adaptive Immunity
KW - Breast Neoplasms/immunology/pathology
KW - Cancer Vaccines/pharmacology
KW - Homeostasis/immunology
KW - Models, Immunological
KW - Neoplasms/immunology/pathology/therapy
M3 - SCORING: Journal article
VL - 108
SP - 12396
EP - 12400
JO - P NATL ACAD SCI USA
JF - P NATL ACAD SCI USA
SN - 0027-8424
IS - 30
M1 - 30
ER -
