What are the specific symptoms of glioma in the later stage

For each of us, once we suffer from glioma, a series of negative effects will occur. This will cause serious harm to our body and make us negative. In order to minimize these negative effects, we need to focus on understanding the symptoms of glioma. What are the specific symptoms of glioma in the later stage?

Gliomas are the most common and lethal intracranial tumors in adults. Due to their highly invasive nature, complete neurosurgical resection is impossible, and the presence of residual tumors leads to recurrence and malignant progression. In general, most low-grade gliomas (grades I, II, and III) will progress to high-grade gliomas (grade IV, also known as glioblastoma multiforme, GBM). Despite improvements in current treatment standards, the survival rate of glioma patients has remained unchanged over the past decades, especially for patients with aggressive gliomas (with an average survival time of only 12 to 18 months). Recent high-throughput technologies have enabled extensive characterization of genomic status, including but not limited to genetic variations, methylation modifications, and gene expression regulation. Large-scale data collection and comprehensive data analysis (such as the Cancer Genome Atlas) have revealed the mutational landscape of low-grade or high-grade gliomas, but molecular changes during malignant progression have rarely been addressed. Precision medicine in cancer proposes that genomic features of tumors can provide a basis for personalized targeted therapy. The Chinese Glioma Genome Atlas (CGGA) project, launched in 2012, is a comprehensive and coordinated effort to accelerate our understanding of the molecular basis of gliomas, especially secondary glioblastomas, by applying high-throughput biotechnology and bioinformatics. The project aims to classify and discover major genomic changes that drive glioma progression and describe detailed genomic features of a large Chinese glioma cohort. Using the CGGA database, we have developed several methods to stratify patients and clarify diagnostic accuracy. In particular, we studied a cohort of 485 diffuse glioma patients from CGGA and found that PTPRZ1-Met (ZM, an oncogenic fusion gene) fusions were present in 26.7% of sGBMs. In addition, we discovered a new single-target Met kinase inhibitor that is effective in treating ZM-positive patients. This case illustrates the driver role of ZM fusions and provides a new avenue for precision therapy of gliomas. To share this valuable resource, the CGGA portal was established as an open access platform for interactive exploration of multidimensional glioma genomics datasets. DNA methylation microarray (149 samples), messenger RNA (mRNA) microarray (305) and sequencing (375), microRNA microarray (198) data, and matched clinical data are currently available. This database significantly lowers the barrier between complex genomic data and glioma researchers who want fast, intuitive, and high-quality access to data resources, and enables researchers to translate these unmeasured data sources into biological insights and clinical applications. Importantly, it has been demonstrated that making the data freely available will enable researchers around the world to quickly make the data available to the research community. We believe that CGGA will provide a practical database for cancer biologists, clinicians, and of course, patients themselves.

Headaches are mostly caused by increased intracranial pressure. As the tumor grows, the intracranial pressure gradually increases, compressing and pulling on pain-sensitive structures in the brain such as blood vessels, dura mater and certain cranial nerves, causing headaches. Most of the headaches are throbbing and distending pains, mostly in the frontal, temporal or occipital regions. For superficial tumors in one cerebral hemisphere, the headache may be mainly on the affected side. It is intermittent at first, then gradually worsens and lasts longer.

Vomiting is caused by stimulation of the medullary vomiting center or the vagus nerve, which leads to decreased vision. Increased intracranial pressure can cause papilledema, and long-term treatment can lead to secondary atrophy of the optic nerve and decreased vision. The compression and traction of the abducens nerve often causes paralysis and diplopia. Therefore, for glioma patients, once diagnosed, they must receive regular treatment as soon as possible to avoid the continuous deterioration of the disease, thereby increasing the difficulty and risk of treatment. Many patients are difficult to treat later because they did not receive timely treatment when the disease was discovered, which caused the disease to continue to worsen.

Visual impairment: including changes in vision, visual field and fundus. Due to increased intracranial pressure, optic disc edema occurs or the optic nerve is directly compressed by a tumor. Over time, the optic nerve can atrophy and affect vision, resulting in vision loss or even blindness. The cause of optic disc edema is increased intracranial pressure, which restricts the return of lymph in the lymphatic sheath around the optic nerve, increases ocular venous pressure, and causes venous congestion. In addition, there may be dizziness, diplopia, mental symptoms, epileptic seizures, neck stiffness, decreased corneal reflex, and changes in vital signs such as breathing and blood pressure. In severe cases, motor nerves can be compressed, causing limb movement disorders and language disorders.