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An evolutionary explanation for the perturbation of the dynamics of metastatic tumors induced by surgery and acute inflammation.

Carmona Bayonas A - Cancers (Basel) (2011)

Bottom Line: The postsurgical patterns of progression include unexpected features such as distant interactions and variable rhythms.The paper proposes that distant interactions are an extension of the ecological events at the local level.This notion explains the evolutionary basis for tumor dormancy, and warns against the teleological view of tumorigenesis as a process directed towards the maximization of a concrete trait such as aggressiveness.

View Article: PubMed Central - PubMed

Affiliation: Department of Hematology and Medical Oncology, Hospital Morales Meseguer, Murcia, Spain. alberto.carmonabayonas@gmail.com.

ABSTRACT
Surgery has contributed to unveil a tumor behavior that is difficult to reconcile with the models of tumorigenesis based on gradualism. The postsurgical patterns of progression include unexpected features such as distant interactions and variable rhythms. The underlying evidence can be summarized as follows: (1) the resection of the primary tumor is able to accelerate the evolution of micrometastasis in early stages, and (2) the outcome is transiently opposed in advanced tumors. The objective of this paper is to give some insight into tumorigenesis and surgery-related effects, by applying the concepts of the evolutionary theory in those tumor behaviors that gompertzian and tissular-centered models are unable to explain. According to this view, tumors are the consequence of natural selection operating at the somatic level, which is the basic mechanism of tumorigenesis, notwithstanding the complementary role of the intrinsic constrictions of complex networks. A tumor is a complicated phenomenon that entails growth, evolution and development simultaneously. So, an evo-devo perspective can explain how and why tumor subclones are able to translate competition from a metabolic level into neoangiogenesis and the immune response. The paper proposes that distant interactions are an extension of the ecological events at the local level. This notion explains the evolutionary basis for tumor dormancy, and warns against the teleological view of tumorigenesis as a process directed towards the maximization of a concrete trait such as aggressiveness.

No MeSH data available.


Related in: MedlinePlus

How to “construct and deconstruct” a multicellular organism. (a) The regulation of the asymmetric division of stem cells is an evolutionary trade-off between terminal differentiation and proliferation. The origin of multicellularity entailed large increases in signal transduction pathways, to guarantee and regulate these hierarchies. So, unregulated cell proliferation constitutes a pathological state. (b) Genetic instability is linked to the appearance of ecological interactions, and it makes tumorigenesis different from other processes such as embryological development, and other emergent phenomena of gene regulatory networks. Notice that the reverse process of “metazoan evolution” is cancer.
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f2-cancers-03-00945: How to “construct and deconstruct” a multicellular organism. (a) The regulation of the asymmetric division of stem cells is an evolutionary trade-off between terminal differentiation and proliferation. The origin of multicellularity entailed large increases in signal transduction pathways, to guarantee and regulate these hierarchies. So, unregulated cell proliferation constitutes a pathological state. (b) Genetic instability is linked to the appearance of ecological interactions, and it makes tumorigenesis different from other processes such as embryological development, and other emergent phenomena of gene regulatory networks. Notice that the reverse process of “metazoan evolution” is cancer.

Mentions: Interestingly, one of these mechanisms of diversion is the expression of pyruvate kinase M2 isoform, a fetal isoenzyme that is regulated by phosphorylation when proliferation signaling pathways are active [31]. This regulation reduces the flux of pyruvate into mitochondria, slowing the rate of the TCA cycle before the exposure to hypoxic conditions. The emission of large amounts of lactate as a result of anaerobic glycolysis reduces the microenvironmental pH with further selective consequences. In particular, the activation of HIF-1α induces several cell programs including the beginning of a new type of competition based on neoangiogenesis (Figure 2).


An evolutionary explanation for the perturbation of the dynamics of metastatic tumors induced by surgery and acute inflammation.

Carmona Bayonas A - Cancers (Basel) (2011)

How to “construct and deconstruct” a multicellular organism. (a) The regulation of the asymmetric division of stem cells is an evolutionary trade-off between terminal differentiation and proliferation. The origin of multicellularity entailed large increases in signal transduction pathways, to guarantee and regulate these hierarchies. So, unregulated cell proliferation constitutes a pathological state. (b) Genetic instability is linked to the appearance of ecological interactions, and it makes tumorigenesis different from other processes such as embryological development, and other emergent phenomena of gene regulatory networks. Notice that the reverse process of “metazoan evolution” is cancer.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3756398&req=5

f2-cancers-03-00945: How to “construct and deconstruct” a multicellular organism. (a) The regulation of the asymmetric division of stem cells is an evolutionary trade-off between terminal differentiation and proliferation. The origin of multicellularity entailed large increases in signal transduction pathways, to guarantee and regulate these hierarchies. So, unregulated cell proliferation constitutes a pathological state. (b) Genetic instability is linked to the appearance of ecological interactions, and it makes tumorigenesis different from other processes such as embryological development, and other emergent phenomena of gene regulatory networks. Notice that the reverse process of “metazoan evolution” is cancer.
Mentions: Interestingly, one of these mechanisms of diversion is the expression of pyruvate kinase M2 isoform, a fetal isoenzyme that is regulated by phosphorylation when proliferation signaling pathways are active [31]. This regulation reduces the flux of pyruvate into mitochondria, slowing the rate of the TCA cycle before the exposure to hypoxic conditions. The emission of large amounts of lactate as a result of anaerobic glycolysis reduces the microenvironmental pH with further selective consequences. In particular, the activation of HIF-1α induces several cell programs including the beginning of a new type of competition based on neoangiogenesis (Figure 2).

Bottom Line: The postsurgical patterns of progression include unexpected features such as distant interactions and variable rhythms.The paper proposes that distant interactions are an extension of the ecological events at the local level.This notion explains the evolutionary basis for tumor dormancy, and warns against the teleological view of tumorigenesis as a process directed towards the maximization of a concrete trait such as aggressiveness.

View Article: PubMed Central - PubMed

Affiliation: Department of Hematology and Medical Oncology, Hospital Morales Meseguer, Murcia, Spain. alberto.carmonabayonas@gmail.com.

ABSTRACT
Surgery has contributed to unveil a tumor behavior that is difficult to reconcile with the models of tumorigenesis based on gradualism. The postsurgical patterns of progression include unexpected features such as distant interactions and variable rhythms. The underlying evidence can be summarized as follows: (1) the resection of the primary tumor is able to accelerate the evolution of micrometastasis in early stages, and (2) the outcome is transiently opposed in advanced tumors. The objective of this paper is to give some insight into tumorigenesis and surgery-related effects, by applying the concepts of the evolutionary theory in those tumor behaviors that gompertzian and tissular-centered models are unable to explain. According to this view, tumors are the consequence of natural selection operating at the somatic level, which is the basic mechanism of tumorigenesis, notwithstanding the complementary role of the intrinsic constrictions of complex networks. A tumor is a complicated phenomenon that entails growth, evolution and development simultaneously. So, an evo-devo perspective can explain how and why tumor subclones are able to translate competition from a metabolic level into neoangiogenesis and the immune response. The paper proposes that distant interactions are an extension of the ecological events at the local level. This notion explains the evolutionary basis for tumor dormancy, and warns against the teleological view of tumorigenesis as a process directed towards the maximization of a concrete trait such as aggressiveness.

No MeSH data available.


Related in: MedlinePlus