Abstract
Most of the cancer cells arrested in the microcirculation during hematogenous metastasis are rapidly killed; one major mechanism is surface-membrane rupture, associated with the mechanical deformation of cancer cells in capillaries.
The feasibility of increasing the susceptibility of cancer cells to lethal, deformation-associated trauma by doxorubicin, was tested in an in vitro mechanical model system, by filtering suspensions of L1210 leukemia cells through 8-μm pore-size Nuclepore® membranes, with or without prior incubation with 10-7M doxorubicin.
The results showed that mechanically-induced loss of cancer cells immediately after filtration was increased from 18 to 55% in cells previously exposed to doxorubicin for 48 h. The results indicate the feasibility of chemotherapeutic enhancement of the mechanical killing-action of the microvasculature as a potential rate-regulator of hematogenous metastasis.
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Weiss, L., Bernacki, R.J., Elkin, G. et al. Effects of doxorubicin on the sensitivity of L1210 leukemia cells to deformation-associated trauma. Cell Biophysics 18, 57–67 (1991). https://doi.org/10.1007/BF02990515
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DOI: https://doi.org/10.1007/BF02990515