Brain Cancer

Brain Cancer

Brain tumors present a particular challenge as the risk of harming healthy brain tissue can severely limit doctors' ability to use surgery, radiation or other treatments. Still, researchers are making steady progress to extend survival and improve patients' quality of life. For example, recent genetic discoveries have led to the identification of distinct sub-types of brain tumors, allowing doctors to personalize care to individual patients and providing potential targets for new treatments.
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2017

New tumor-treating fields device extends survival in patients with glioblastoma

New tumor-treating fields device extends survival in patients with glioblastoma

A landmark clinical trial finds that using a novel technology called tumor-treating fields (TTF) – in combination with temozolomide – improves survival for patients with newly diagnosed glioblastoma, compared to temozolomide alone. TTF utilizes low-intensity electrical fields, which are delivered through the skin from a device that patients wear on their head. The electrical fields are thought to slow cancer growth by blocking cell division. Based on this research, the FDA expands approval of the first TTF device (Optune) for use in patients with newly diagnosed glioblastoma in addition to recurrent glioblastoma.

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JAMA 2017;318:2306-2316
FDA Premarket Approval
Adding chemotherapy slows growth of certain gliomas

Adding chemotherapy slows growth of certain gliomas

A large phase III study demonstrates that adding temozolomide (Temodar) chemotherapy to standard radiation after surgery for anaplastic glioma improves survival and delays disease progression by as long as two years for patients with tumors that do not have a genetic change called 1p19q codeletion (loss of chromosome arms 1p and 19q). This approach had been standard treatment for patients with 1p19q codeletions, but the evidence had been unclear for tumors without this abnormality. These findings establish adjuvant chemotherapy and radiation as a new standard treatment for these aggressive cancers, which typically arise in younger adults.

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Lancet 2017;390:1645-1653
More aggressive treatment proves beneficial for elderly patients with glioblastoma

More aggressive treatment proves beneficial for elderly patients with glioblastoma

 A major study shows that a more aggressive course of treatment that includes a shorter, more convenient course of radiation treatment along with temozolomide (Temodar) chemotherapy improves survival, compared to radiation alone, in older patients with glioblastoma. The survival benefit is greatest among patients with a genomic biomarker, called the methylation of the O6-methylguanine-DNA methyltransferase (MGMT) gene, which is known to predict better outcomes in glioblastoma. Importantly, the impact on patients’ quality of life was similar, regardless of whether they had chemotherapy and radiation or radiation alone. These findings help inform treatment decision-making, which is especially challenging for older patients who are typically frail and have more complex health needs to consider.

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N Engl J Med 2017;376:1027-1037

2016

A new standard of care for high-risk, low-grade gliomas

A new standard of care for high-risk, low-grade gliomas

Badge indicating that research was paid for using federal funds

A federally-funded clinical trial shows that adding a chemotherapy regimen called PCV (procarbazine, CCNU, and vincristine) to radiation therapy slows cancer growth of grade 2 glioma and extends survival by a median of 5 years. Grade 2 gliomas are a rare, slow-growing type of brain tumor that occur most often in young people. As a result of this study, PCV chemotherapy after radiation therapy is now the standard of care for high-risk, low-grade gliomas.

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JCO 2014; 32(Suppl. 15): 2000
N Engl J Med 2016; 374:1344-1355

2010

Nine-gene test can predict glioblastoma outcome

Nine-gene test can predict glioblastoma outcome

Badge indicating that research was paid for using federal funds

Researchers identify a set of nine genes that predict the likelihood that a glioblastoma tumor will respond to therapy. The research is used to create a test called DecisionDX-GBM. If validated in future trials, this test has the potential to help doctors choose the most effective therapy for a patient, and could be used to help identify new treatments targeting tumors that do not respond to standard therapies.

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Neuro-Oncology 2010; 12(1): 49–57

2009

Gene mutations linked to tumor aggressiveness

Gene mutations linked to tumor aggressiveness

Scientists learn that brain tumors with an alteration in the IDH1 or IDH2 genes are less aggressive than those without this mutation – a finding that may eventually enable some patients to safely undergo less intense therapy. The study also offers researchers a potential new clue regarding how some tumors form in the first place. The IDH1 and IDH2 genes are located on a pathway that governs the metabolic function of cells, and mutations to these genes may enable abnormal, or cancerous, cells to form. Continued research may guide future development of targeted therapies that interfere with the IDH1 and IDH2 genes in order to halt tumor growth.

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N Engl J Med 2009; 360: 765-773

2007

Bevacizumab (Avastin) receives FDA approval for glioblastoma

Bevacizumab (Avastin) receives FDA approval for glioblastoma

Two early-stage trials suggest that giving the targeted therapy bevacizumab (Avastin), alone or with the chemotherapy drug irinotecan (Camptosar), may cause tumor shrinkage in patients with glioblastoma whose disease progresses after previous therapy. Based on these findings, the FDA grants accelerated (or early, conditional) approval for bevacizumab to treat glioblastoma. Bevacizumab is an "anti-angiogenic" drug, meaning it works by interfering with the development of blood vessels that tumors need to grow and spread. This marks the first new drug approved for treating brain tumors in a decade, and studies are ongoing to determine if initial treatment with bevacizumab improves overall survival.

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JCO 2009; 27(28): 4733-4740

2006

Molecular sub-classification of high-grade gliomas predicts prognosis

Molecular sub-classification of high-grade gliomas predicts prognosis

Using advanced molecular classification techniques to examine tumor samples, researchers discover distinct subtypes of high-grade astrocytoma tumors (a form of glioma). They find that each subtype has unique biological features that appear to influence the tumor's behavior and response to certain therapies. The findings pave the way for future research that may help personalize therapy for each tumor and patient, ensuring better outcomes and avoiding unnecessary side effects.

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Cancer Cell 2006; 9: 157–173
Chemically "illuminating" glioma tumors during surgery postpones recurrence

Chemically "illuminating" glioma tumors during surgery postpones recurrence

The use of 5-aminolevulinic acid, a substance that reacts with and illuminates malignant glioma cells, is shown to improve surgeons' ability to remove tumor tissue. Patients treated with this technique during surgery were significantly less likely to have any tumor growth after six months, compared to those who underwent conventional surgery.

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Cancer.Net; Brain Tumor: Treatment Options
Lancet Oncology 2006; 7(5): 392–401
Genetic mutations affect survival for oligodendroglioma

Genetic mutations affect survival for oligodendroglioma

Badge indicating that research was paid for using federal funds

Two studies find that patients with oligodendroglioma tumors (a form of glioma) that lack certain parts of chromosomes 1 and 19 are more sensitive to treatment and have better survival than patients whose tumors are not missing this genetic material. Follow-up data later show that these patients fare much better, living several years longer, when they receive chemotherapy and radiation together, rather than radiation alone. 

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JCO 2006; 24(18): 2707-2714
JCO 2006; 24(18): 2715-2722
JCO 2013; 31(3): 337-343
JCO 2013; 31(3): 344-350

2005

Researchers begin mapping the genome of glioblastoma

Researchers begin mapping the genome of glioblastoma

Badge indicating that research was paid for using federal funds

In 2005, the National Cancer Institute and the National Genome Research Institute launch The Cancer Genome Atlas Project, with the goal of mapping the genetic changes involved in glioblastoma and other cancers. In 2008, researchers report the identification of several key mutations – in the ERBB2, NF1 and TP53 genes – that are involved in triggering the development and spread of glioblastoma. It is hoped that these findings will help pinpoint new targets for drug therapies.

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Nature 2008; 455: 1061–1068
MGMT gene alteration predicts response to chemotherapy

MGMT gene alteration predicts response to chemotherapy

Researchers discover that patients with tumors carrying a specific alteration in a gene known as MGMT benefit from temozolomide (Temodar) therapy. The MGMT gene is involved in repairing DNA damage in cancer cells, including damage caused by chemotherapy. Tumors with a genetic alteration that silences this gene are unable to repair the damage caused by temozolomide, and therefore are more susceptible to the drug. On the other hand, tumors without this gene alteration are more resistant to the drug. Researchers continue to explore how to use this and other genetic information to identify which patients are most likely to benefit from chemotherapy.

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N Engl J Med 2005; 352: 997-1003

2003

Chemotherapy "wafer" active against malignant gliomas

Chemotherapy "wafer" active against malignant gliomas

Use of a surgically implanted biodegradable wafer containing the anticancer medication carmustine (BCNU) is found to delay tumor growth and improve overall survival in some patients with gliomas. The wafer provides continuous chemotherapy directly to the tumor site to kill remaining cancer cells and to prevent or slow regrowth of the cancer. Today it is used in patients with recurrent malignant glioma and newly diagnosed glioblastoma, a highly aggressive form of glioma.

More Information: 

Cancer.Net; Brain Tumor: Treatment Options
Neuro-Oncology 2003; 5(2): 79–88
Cancer: Journal for Clinicians 2010; 60(3): 166-193

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