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Would you share the latest news on how genetics is influencing the treatment of brain cancer?
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MineshMehtaMD (Physician - Oncology - Radiation (Verified) ) - 07 / 05 / 2012
The unraveling of the human genome has led to the cancer genome atlas project, in which detailed genetic analysis of several cancers/tumors is being pursued. Glioblastoma was one of the early candidate tumors for this effort and the recent seminal publications outlining the genetic make-up of this tumor has provided us with several significant insights which can be summarized as follows:
A. Unlike some other tumors, GBM is characterized by multiple genetic modifications, and is rarely, if ever dependent on a “single driver mutation”. This makes the disease challenging to treat, as targeting one single abnormal gene or just one pathway is unlikely to result in a cure.
B. Considerable genetic heterogeneity exists even for this single histopathologic entity, implying multiple possible causative pathways, and variability in terms of response to treatment. This heterogeneity has now been explored in large datasets, allowing prognostic grouping of patients into 3 to 4 distinct classes; theories are emerging as to which pathways and drugs maybe best for the various classes, and clinical trials to test these theories are being pursued.
C. There are some preliminary data allowing us to understand an association between certain therapies and the presence/absence of certain molecular and genetic features which can be either prognostic, or sometimes even predictive markers for certain therapies; example sof this include MGMT methylation status, IDH mutation status, 1p19q deletion status, etc. The exact mechanisms underlying these findings are still being worked out, but the data are resulting in some degree of customization of therapy.
D. In certain lower grade gliomas, especially in children, targeted agents are already being pursued, with good early promising results.
A. Unlike some other tumors, GBM is characterized by multiple genetic modifications, and is rarely, if ever dependent on a “single driver mutation”. This makes the disease challenging to treat, as targeting one single abnormal gene or just one pathway is unlikely to result in a cure.
B. Considerable genetic heterogeneity exists even for this single histopathologic entity, implying multiple possible causative pathways, and variability in terms of response to treatment. This heterogeneity has now been explored in large datasets, allowing prognostic grouping of patients into 3 to 4 distinct classes; theories are emerging as to which pathways and drugs maybe best for the various classes, and clinical trials to test these theories are being pursued.
C. There are some preliminary data allowing us to understand an association between certain therapies and the presence/absence of certain molecular and genetic features which can be either prognostic, or sometimes even predictive markers for certain therapies; example sof this include MGMT methylation status, IDH mutation status, 1p19q deletion status, etc. The exact mechanisms underlying these findings are still being worked out, but the data are resulting in some degree of customization of therapy.
D. In certain lower grade gliomas, especially in children, targeted agents are already being pursued, with good early promising results.
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