Based on the knowledge that cancer
cells grow indefinitely, the general belief is that senescence could
act as a barrier against tumor growth and has the potential of being
used as a cancer treatment.
According to findings published in the 19th January issue of the open-access journal PLoS Computational Biology, a collaboration between a cancer biologist from the University of Milano, Italy, and two physicists, from the National Research Council of Italy and from Cornell University, has shown that although cell senescence occurs spontaneously in melanoma cells, it does not stop their growth, which is sustained by a small population of cancer stem cells.
The study examines the association between melanoma and senescence, which is the normal process in which cells decline and eventually stop duplicating after reaching maturity.
The researchers observed the long-term evolution of melanoma cell populations by monitoring the number of senescent cells, and discovered a slowing in growth with the majority of the cells turning senescent after three months. However, growth did not stop and was eventually resumed at its initial rate until the senescent cells had nearly disappeared.
The researchers applied a mathematical model of the experimental data using the cancer stem cell hypothesis, in which a sub-group of cancer cells multiply indefinitely, and therefore remain unaffected by senescence. These cancer stem cells produce a larger population of cancer cells, which are only able to replicate a certain number of times. The results of the model achieved an indirect confirmation that cancer stem cells are present in melanoma, an issue that remains to be controversial in the cancer research community.
The researchers conclude that even though a large percentage of cancer cells are susceptible to senescence, inducing senescence is unlikely to provide a successful therapeutic strategy because these cells are not important for tumor growth. The say however, that the indirect evidence of cancer stem cells in melanoma could potentially enable the development of new strategies for the treatment of specific types of cancer.
However, the strong resistance to drug induced senescence that may be found in the cancer stem cells will present a major challenge. Based on this study, treatment of tumors would concentrate on targeting only these cancer stem cells, instead of every single cancerous cell.
According to findings published in the 19th January issue of the open-access journal PLoS Computational Biology, a collaboration between a cancer biologist from the University of Milano, Italy, and two physicists, from the National Research Council of Italy and from Cornell University, has shown that although cell senescence occurs spontaneously in melanoma cells, it does not stop their growth, which is sustained by a small population of cancer stem cells.
The study examines the association between melanoma and senescence, which is the normal process in which cells decline and eventually stop duplicating after reaching maturity.
The researchers observed the long-term evolution of melanoma cell populations by monitoring the number of senescent cells, and discovered a slowing in growth with the majority of the cells turning senescent after three months. However, growth did not stop and was eventually resumed at its initial rate until the senescent cells had nearly disappeared.
The researchers applied a mathematical model of the experimental data using the cancer stem cell hypothesis, in which a sub-group of cancer cells multiply indefinitely, and therefore remain unaffected by senescence. These cancer stem cells produce a larger population of cancer cells, which are only able to replicate a certain number of times. The results of the model achieved an indirect confirmation that cancer stem cells are present in melanoma, an issue that remains to be controversial in the cancer research community.
The researchers conclude that even though a large percentage of cancer cells are susceptible to senescence, inducing senescence is unlikely to provide a successful therapeutic strategy because these cells are not important for tumor growth. The say however, that the indirect evidence of cancer stem cells in melanoma could potentially enable the development of new strategies for the treatment of specific types of cancer.
However, the strong resistance to drug induced senescence that may be found in the cancer stem cells will present a major challenge. Based on this study, treatment of tumors would concentrate on targeting only these cancer stem cells, instead of every single cancerous cell.
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