Exposure to asbestos and drinking large amounts of alcohol are associated with increased risk of glioma. Poor immune system function and exposure to mutagenic chemicals appear to be major factors in the development of this disabling and rarely curable brain cancer.
The most common sign of a malignant brain tumour is headaches, often with a sudden onset. Other signs include signs of increased intracranial pressure, including vomiting, ocular abnormalities and papilledema. Tumour markers, such as alpha-fetoprotein and neurofilament light, may be useful. Neurological examination often reveals signs of a new or worsening tumour. On MRI, the most common lesion in a glioma is a ring-enhancing ring, which also tends to cause increased intracranial pressure, as can the ring-enhancing boundary around an anaplastic astrocytoma.
Approximately 2,400 people per year in the United States are diagnosed with glioma. This makes up 0.3% of people in the US. Although glioma has a low annual incidence of diagnosis in the United States at 0.3% of all cancers, mortality is 0.4%, suggesting that glioma may still be a significant cause of morbidity and mortality in the United States.
The treatment of glioma has shifted from the traditional surgical management to a multimodality approach, with increased use of adjuvant or neoadjuvant treatments. The extent of surgical resection is only one of the factors in deciding how to plan and deliver therapy. The extent of surgery may also be performed in conjunction with additional concurrent or adjuvant treatments to induce a dramatic, rapid, and durable clinical response, which helps optimize neurologic and functional outcomes.
Glioma treatments can be divided into surgery, radiotherapy, chemotherapy, and targeted therapies. Surgical removal is not always curative, but the extent of resection can be increased by radiotherapy and chemotherapy, and also improved with targeted therapies. As an important component of cancer care, surgeons should take time to learn and understand the principles of cancer research and treatment.
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This analysis suggests that high-risk patients are the most likely to benefit from clinical trial enrollment. However, a reasonable number of patients must be included in clinical trials before they are considered for inclusion in high-risk patient treatment protocols.
Although thiosulfate does not influence the average overall survival time of people with malignant glioma, it has a beneficial effect on QoL during the initial phases of treatment. This effect was not observed at 1 or 2 years after treatment cessation.
Most gliomas develop from normal brain tissue. A primary cause of glioma is not always found in patients. Patients who have a family history of glioma do not have a primary cause of glioma. About 20 percent of pediatric patients with glioma have hereditary cancer syndromes with germline mutations in one of about 15 genes, with mutations in the p16 gene being the most common. About 40 percent of adult patients have one or more hereditary cancers. If cancer in an individual is known to be hereditary, it is generally thought that a germline mutation in one of these genes is responsible for susceptibility to that kind of cancer.
The most recent developments included the discovery of several novel agents with pharmacological activity, and many studies of the mechanisms of action of sodium thiosulfate in the CNS, including its effects on glutamate, ammonia and glycine. In addition, a new sodium thiosulfate-labeled compound for clinical trials was developed at DCE-CRC.
There is strong evidence for an inherited association of brain tumours. This association may arise as a consequence of the genetics of the tumour cell itself, the patient's genetic background, which may influence tumour behaviour, or may be modifiable in the same way that common disease does. Future large, prospective studies with genetic analysis should validate this finding.