Tailoring glioblastoma therapies: 1 size does not fit all

February 06, 2008

An upcoming G&D paper from Dr. Azad Bonni and colleagues at Harvard Medical School lends new insight into how the unique genetic signature of glioblastoma tumors affects treatment efficacy - a finding with promising hope for the therapeutic targeting of the leading cause of cancer-related deaths in the young and middle-aged population.

Dr. Bonni's group found that the transcription factor STAT3 has either a tumor promoting or tumor suppressive effect depending upon the genetic profile of the glioblastoma tumor.

Glioblastomas are the most common and aggressive type of adult brain cancer, with an annual incidence of approximately 13,000 in the United States, and an expected median survival rate of just over a year. STAT3 is a cytokine-activated transcription factor that has been previously reported to play a pro-oncogenic role in tumor development. Thus, much effort has been aimed at the development of STAT3 inhibitors as chemotherapeutic agents.

Dr. Bonni and colleagues now report that STAT3 can function as either a tumor suppressor or an oncoprotein. Using a mouse model system of two common genetic mutations in glioblastomas - PTEN deficiency or EGFRvIII activation -- the researchers show that PTEN regulates STAT3 tumor suppressor function, while STAT3 cooperates with the EGFRvIII oncoprotein to promote tumor growth.

Thus, the researchers convincingly demonstrate a need for effective therapies tailored to the unique genetic thumbprint of individual glioblastoma tumors. "These findings may change the way we approach not only glioblastoma but other types of cancer as well", says Azad Bonni, senior author of the study.
-end-


Cold Spring Harbor Laboratory

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