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A circuitous route to therapy resistance
Date:6/26/2013

thor of the publication.

If direct NAD+ production is blocked, malignant glioma cells, unlike normal astrocytes, increase production of QRPT. This enzyme breaks down quinolinic acid into NAD+. Therapies involving the anticancer drug temozolomide, radiation, or oxidative stress were found to lead to increased levels of QRPT in tumors. The higher the degree of malignancy of the gliomas that were investigated, the more QRPT they contained. Brain tumors that recurred after combined radiotherapy-chemotherapy had a poorer prognosis when the cancer cells produced high levels of quinolinic acid.

The researchers also discovered that the tumor cells are not capable of forming quinolinic acid on their own. Instead, the substance is produced by immune cells called microglia, which migrate in large quantities into gliomas. Microglia cells may constitute up to 50 percent of the total cell content of a glioma.

In these cases, only the tumor cells contain QRPT; healthy astrocytes do not. Hence only the tumor cells are capable of breaking down quinolinic acid into NAD+. "The malignant transformation of astrocytes appears to be linked to their ability to use quinolinic acid as an alternative source of NAD+ and thus develop resistance against radiotherapy and chemotherapy," says Michael Platten. "A link between microglia and the malignancy of gliomas has been known for some time now we may have found a possible cause. The key enzyme for the alternative NAD+ supply is QRPT. An agent directed against this enzyme might help suppress therapy resistance in brain cancer. This might enable us to achieve better outcomes in treating malignant brain tumors using existing methods."


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Contact: Dr. Sibylle Kohlstädt
s.kohlstaedt@dkfz.de
Helmholtz Association of German Research Centres
Source:Eurekalert

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