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A brain tumour is a lump of abnormal cells growing in your brain. Your brain controls all the parts of your body and its functions and produces your thoughts. Depending on where it is, a tumour in your brain can affect these functions.

Benign tumours are not cancerous. But a benign brain tumour may cause damage just by being there and pressing on your brain or nearby structures. This can be life-threatening, or affect other parts of your body, and may need urgent treatment.

Brain tumours have a range of symptoms, depending on where the tumour is, how big it is and what type of tumour it is. Some symptoms may also be caused by the treatments used to manage the tumour. Slow growing brain tumours may not have any symptoms to start with.

The symptoms of brain tumours in children include persistent headaches, recurrent vomiting, behavioural changes, abnormal eye movements and balance/coordination problems. There may be blurred or double vision or a child may hold their head in an abnormal position.

There is no definite link between mobile phones and brain tumours. Researchers continue to investigate the potential causes of brain tumours, including whether certain genes are important riskfactors. Read more about brain tumour research at Cure Brain Cancer Foundation.

Brain tumours are usually given a grade from 1 to 4, based on how the cells look. This can also suggest how quickly the tumour may grow. A pathologist works out the grade by looking at the cells under a microscope.

If you are diagnosed with a brain tumour, your doctor will discuss your treatment options with you. Treatment aims to either remove the tumour completely, slow its growth or relieve symptoms by shrinking the tumour.

Chemotherapy drugs for brain cancer are usually either swallowed, or given through a drip inserted into your vein (intravenously). They travel through the bloodstream killing cells that grow quickly, such as cancer cells.

If you are diagnosed with a brain tumour or brain cancer, it can be overwhelming. Connecting with, or reading about, other people who are going through or who have gone through the same thing can be helpful, as can talking to a counsellor. Finding out more information about your condition or treatments may also help you to cope.

A traumatic brain injury is a type of acquired brain injury that occurs following an impact to the head, causing damage to the brain tissue. These head injuries can be classified as either penetrating or non-penetrating. Long-term effects may range from mild to severe, depending on the patient.

We share a virtual laboratory at the University of Toronto with other University Health Network scientists and clinicians, allowing us to share ideas, resources and equipment as we study the molecular basis of brain tumour progression. This multidisciplinary approach has facilitated outstanding basic and applied molecular neuro-oncology research, scientific publications and translational research.

To stay on the forefront of brain tumour studies, lab staff attends weekly research conferences where progress is evaluated, new models are discussed and research is compared with clinical data. Labatt BTRC members also engage in a weekly seminar series that reviews the latest cancer research.

The BTRC aims to cure children and adults with brain tumours, while progressing towards more predictable clinical control of the condition. By determining how brain tumours form on a molecular level, our team is in a unique position to develop new scientific and clinical therapies.

Dr. Seunggu Han is an ABMS board certified neurological surgeon and an associate clinical professor in the department of neurological surgery at Stanford. He currently practices in Salinas and Santa Cruz, California. His interests include surgical neuro-oncology, traumatic brain injury, and quality improvement in surgery.

Brain tumors can be cancerous (malignant) or noncancerous (benign). When benign or malignant tumors grow, they can cause the pressure inside your skull to increase. This can cause brain damage, and it can be life-threatening.

Being exposed to certain chemicals, such as those you might find in a work environment, can increase your risk for brain cancer. The National Institute for Occupational Safety and Health keeps a list of potentially cancer-causing chemicals found in workplaces.

People who have been exposed to ionizing radiation have an increased risk of brain tumors. You can be exposed to ionizing radiation through high-radiation cancer therapies. You can also be exposed to radiation from nuclear fallout.

A small piece of the tumor is obtained during a biopsy. A specialist called a neuropathologist will examine it. The biopsy will identify if the tumor cells are benign or malignant. It will also determine whether the cancer originated in your brain or another part of your body.

While the location of some tumors allows for safe removal, other tumors may be located in an area that limits how much of the tumor can be removed. Even partial removal of brain cancer can be beneficial.

Risks of brain surgery include infection and bleeding. Clinically dangerous benign tumors are also surgically removed. Metastatic brain tumors are treated according to guidelines for the type of original cancer.

Seeking treatment early can prevent complications that can occur as a tumor grows and puts pressure on the skull and brain tissue. It may also help prevent malignant tumors from spreading to other tissues in the brain.

D.H. designed, conducted and analysed experiments and contributed to all aspects of the study, in particular confocal and in vivo multi-photon imaging of glioma network activity, proliferation, and invasion, immunofluorescence, immunochemistry, cranial window implantation, tumour implantation, quantification and analysis of the data, data interpretation, writing the code, TCGA data and RNA-expression data analysis. D.H. initially discovered the intrinsically rhythmic cells. D.H. and F.W. wrote the manuscript with the input of all co-authors. D.C.H. performed sample preparation and transcriptional analyses. D.C.H., V.V. and E.J. provided conceptual and methodological input and data interpretation. V.V. and S.K.T. performed electrophysiological recordings under the supervision of T. Kuner. S.H. and A.J. conducted brain organoid experiments under the supervision of P.K. D.D.A and S. Weil performed cranial window implantation and tumour injections and provided conceptual input. L.H. and T. Kessler performed bioinformatic analysis of RNA-expression data. T. Kessler provided conceptual input. A.K. provided the KCa3.1-knockout constructs. P.S. and A.H. provided staining of human paraffin sections under the supervision of F.S. M.O.B. provided MRI and subsequent analysis. M.A.K. and M.R. provided conceptual input. J.M.M., Y.Y. and E.R. performed tumour injections. S. Wendler and C.L. performed cell culture work, C.L. and C.M. performed immunostaining. K.F. and O.G. provided the Twitch-3A vector. M.O. provided in vivo Ca2+ imaging data and conceptual input. G.S. performed in vivo Ca2+ imaging. M.S. provided conceptual input for network analyses. W.W. provided conceptual input, performed data interpretation and supervised RNA-expression data analysis. F.W. conceptualized and supervised all aspects of the study and performed data interpretation.

Ca2+ imaging in vivo and in the newly developed in vitro model. Awake in vivo multiphoton Ca2+ imaging of gliomas growing in the brain under a chronic cranial window in mice. Glioblastoma cells were transduced with the GCaMP6s Ca2+ sensor using lentiviral vectors. In vitro Ca2+ imaging was performed in the monolayer assay where tumour cells were stained with the Rhod-2AM Ca2+ sensor and imaged using confocal microscopy. Recordings demonstrate the dynamics as well as the robust and frequent nature of Ca2+ transients in the in vivo and in vitro model, indicative of intercellular Ca2+ communication in these tumours.

Periodic glioblastoma cells in vivo. Awake in vivo multiphoton Ca2+ imaging of glioblastoma cells growing in the brain under a chronic cranial window in mice. Tumour cells were transduced with the Twitch3 Ca2+ sensor using lentiviral vectors. The representative recording demonstrates autonomous rhythmic Ca2+ activity of a periodic cell that triggers Ca2+ activity in regionally connected tumour cells.

Periodic glioblastoma cells in the in vitro monolayer assay. Ca2+ imaging in the in vitro monolayer assay of tumour cells stained with the Rhod-2AM Ca2+ sensor using confocal microscopy. The representative recordings demonstrate autonomous rhythmic Ca2+ activity of a periodic cell. Gap junction inhibition with MFA blocks the transmission of the autonomous activity to regionally connected tumour cells but does not affect the autonomous Ca2+ activity of periodic cells itself.

Ca2+ imaging mixing experiment. Ca2+ imaging in the in vitro monolayer assay of tumour cells stained with the Rhod-2AM Ca2+ sensor (displayed in red) using confocal microscopy. Recording of S24 wild-type cell monoculture shows vivid global Ca2+ activity. Recording of S24 KCa3.1 knockout cell monoculture shows strongly reduced global Ca2+ activity and no intrinsically rhythmic activity. Mixing 10% S24 wild-type cells (GFP negative) with 90% S24 KCa3.1 knockout cells (GFP positive, green) fully recovers the effect of the KCa3.1 knockout on global Ca2+ activity and the S24 wild-type cells show an unusually high fraction of periodic cells.

Glioma Ca2+ imaging before and after TRAM-34 treatment in vivo. Awake in vivo multiphoton Ca2+ imaging of GCaMP6s-labeled glioblastoma cells before and 1h after single TRAM-34 treatment. TRAM-34 treatment markedly reduced the tumour autonomous rhythmic Ca2+ activity and thereby the overall Ca2+ signaling in the tumour. 041b061a72