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Identifying Rational Immunotherapy Combinations for Glioblastoma: A Progress Report

Surabhi Dangi-Garimella, PhD
Leading global experts believe that for immunotherapy to work in glioblastoma—which has an estimated 5-year survival rate of 33% in the United States—combination treatments are the way forward.
Leading global experts believe that for immunotherapy to work in glioblastoma (GBM)—which has an estimated 5-year survival rate of 33% in the United States—combination treatments are the way forward. This was the most important takeaway from one of the sessions that kicked off the 2018 American Society of Clinical Oncology (ASCO) Annual Meeting in Chicago, Illinois.

Chairing the session was Amy B. Heimberger, MD, professor, Department of Neurosurgery, The University of Texas MD Anderson Cancer Center. During her presentation, Heimberger provided the audience with a flavor for potential strategies that can be tapped to induce antitumor immune-induction in glioblastoma.

“What are key steps necessary for an optimal antitumor immune therapeutic response in brain tumors?” she asked, considering that glioblastomas are highly immunosuppressive.

How do we overcome lack of T-cell infiltration in the tumor? She shared the results of a successful single patient strategy in a patient with recurrent multifocal glioblastoma received chimeric antigen receptor (CAR) T cells targeting the tumor-associated antigen interleukin-13 receptor alpha 2 (IL13Rα2). Multiple intracranial infusions of the IL13Rα2 CAR T cells in the resected tumor cavity, as well as in the ventricular system, resulted in a regression of intracranial and spinal tumors in that patient—a response that was sustained for 7.5 months.1

The CAR domain has several limitations, Heimberger pointed out: the lack of tumor-specific antigens, antigen escape, and in vivo persistence and generation of a product in a timely fashion.

“All these limitations need to be addressed to view the efficacy of CAR T cells in GBM," she said.

Her laboratory has developed a small molecule inhibitor against STAT3—another key driver of GBMs. The researchers developed a small-molecule inhibitor called WP1066, which, they found, can block M2 macrophages. The drug has minimal toxicity, but it is lipophilic, meaning it is difficult for the drug to dissolve in the blood stream. The team had to be innovative in its approach: the researchers spray-dried the drug with methocellulose. A phase 1 trial of WP1066 is ongoing in patients with GBM refractory to treatment.

Another approach to treating GBM is via viral vaccines, and Michael Platten, MD, Mannheim University Hospital, German Cancer Research Center, provided the audience with an overview of where the field stands.

His team has developed a novel method to detect the immunological presentation of the mutated antigen in tumor tissue of brain tumor patients.

“We don’t know what the relevance of whole tumor vaccines is,” Platten said, and explained that several unknowns remain, including:
  • How do you select appropriate target antigens?
  • What are the appropriate biomarkers?
  • How do you bring the vaccine in context with immunotherapeutics/checkpoint blockade agents?
There are 3 categories of antigens in GBMs, he noted:
  • Tumor-associated antigens: shared antigens; have low immunogenicity and potential for side effects
  • Viral antigens: usually not endogenous; heterogenous if exogenously expressed
  • Tumor antigen: specific but not a strong immune response.


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