Glioblastoma
Glioblastoma, also known as glioblastoma multiforme (GBM), is the most aggressive cancer that begins within the brain. Initially, signs and symptoms of glioblastoma are non-specific. They may include headaches, personality changes, nausea, and symptoms similar to those of a stroke. Worsening of symptoms often is rapid. This may progress to unconsciousness.
The cause of most cases is unclear. Uncommon risk factors include genetic disorders such as neurofibromatosis and Li–Fraumeni syndrome, and previous radiation therapy. Glioblastomas represent 15% of brain tumors. They can either start from normal brain cells or develop from an existing low-grade astrocytoma. The diagnosis typically is made by a combination of CT scan, MRI scan, and tissue biopsy.
There is no clear way to prevent the disease. Typically, treatment involves surgery, after which chemotherapy and radiation therapy are used. The medication temozolomide is used frequently as part of chemotherapy. High dose steroids may be used to help reduce swelling and decrease symptoms. It is unclear whether trying to remove all or simply most of the cancer is better.
Despite maximum treatment, the cancer usually recurs. The most common length of survival following diagnosis is 12 to 15 months, with fewer than 3% to 5% of people surviving longer than five years. Without treatment, survival is typically three months. It is the most common cancer that begins within the brain and the second most common brain tumor, after meningioma. About 3 per 100,000 people develop the disease a year. It most often begins around 64 years of age and occurs more commonly in males than females. Immunotherapy is being studied.
Common symptoms include seizure, headaches, nausea and vomiting, memory loss, changes to personality, mood or concentration, and localized neurological problems.
N6-Methyladenosine
Considering the versatile functions of mA in various physiological processes, it is thus not surprising to find links between mA and numerous human diseases; many originated from mutations or single nucleotide polymorphisms (SNPs) of cognate factors of mA. The linkages between mA and numerous cancer types have been indicated in reports that include stomach cancer, prostate cancer, breast cancer, pancreatic cancer, kidney cancer, mesothelioma, sarcoma, and leukaemia. The impacts of mA on cancer cell proliferation might be much more profound with more data emerging. The depletion of METTL3 is known to cause apoptosis of cancer cells and reduce invasiveness of cancer cells, while the activation of ALKBH5 by hypoxia was shown to cause cancer stem cell enrichment. mA has also been indicated in the regulation of energy homeostasis and obesity, as FTO is a key regulatory gene for energy metabolism and obesity. SNPs of "FTO" have been shown to associate with body mass index in human populations and occurrence of obesity and diabetes. The influence of FTO on pre-adipocyte differentiation has been suggested. The connection between mA and neuronal disorders has also been studied. For instance, neurodegenerative diseases may be affected by mA as the cognate dopamine signalling was shown to be dependent on FTO and correct mA methylation on key signalling transcripts. The mutations in HNRNPA2B1, a potential reader of mA, have been known to cause neurodegeneration. The IGF2BP1–3, a novel class of mA reader, has oncogenic functions. IGF2BP1–3 knockdown or knockout decreased MYC protein expression, cell proliferation and colony formation in human cancer cell lines. The ZC3H13,a member of the m6A methyltransferase complex, markedly inhibited the colorectal cancer cells growth when knocked down.