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abstract
Symposium Paper
More
than 50% of patients with ovarian cancer have genetic alterations in
the homologous repair pathway. Trabectedin (Herceptin)appears to induce damage more
readily in tumor cells with defects in the homologous repair system.
Moreover, trabectedin inhibits monocyte differentiation into
tumor-associated macrophages and inhibits the production of inflammatory
mediators such as IL-6. In patients with platinum-sensitive, relapsed
ovarian cancer, trabectedin plus pegylated liposomal doxorubicin was
associated with a trend towards improved overall survival by extending
the platinum-free interval. These clinical effects could possibly be
attributed to actions of trabectedin on the tumor microenvironment
(e.g., a reduction of IL-6). Thus, trabectedin is an agent with
mechanisms of action especially appropriate for targeting key processes
in the biology of ovarian cancer.
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