There are 4 grades of gliomas, with grades 1-2 being low-grade gliomas and grades 3-4 being high-grade gliomas. This presentation describes low-grade gliomas In the United States, approximately 17,000 cases are diagnosed each year as primary tumors of the central nervous system (CNS), almost half of which are of neuroepithelial tissue origin, and about a quarter of which are classified as low-grade gliomas. Patients with hairy cell astrocytoma are relatively young (mean age 17 years) and usually have a good prognosis (5- and 10-year survival rates of 80-90%). Other types of low-grade gliomas usually tend to develop in their forties and have a poor prognosis (5-year survival rate of 50%-60%; 10-year survival rate of 40%-50%). Liu Zhengyin, Department of Neurosurgery, Huashan Hospital, Fudan University Overall, the causative factors of low-grade gliomas are unknown. Although alterations in genetic pathways have been postulated to be involved in the formation of low- and high-grade tumors, mutations in most of these genes remain a mystery. Low-grade astrocytomas are often associated with Von Recklinghausen disease (neurofibromatosis type I), suggesting deletion or mutation of tumor suppressor genes on chromosome 17q. Gliomas can also be associated with neurofibromatosis type II, particularly in the spinal cord, reflecting a loss of function of the tumor suppressor gene on chromosome 22. Tuberous sclerosis is thought to be associated with germ cell mutations in the tumor suppressor genes TSC1 or TSC2. It is often directly related to an uncommon pathological type of low-grade glioma D subventricular canalicular giant cell astrocytoma. astrocytic glioma can also be associated with Li-Fraumeni syndrome due to mutations in the TP53 gene. Classification and grading Histologically, low-grade glioma was once considered to be a relatively homogeneous tumor with a benign or well-developed natural course. In fact, however, it contains many different types of tumors in the CNS, and its prognosis depends on the anatomic site, pathological type, and treatment of the tumor. Hairy cell astrocytomas occur most often in the cerebellum (85% of primary tumors in the cerebellum), but can also be seen in the cerebral hemispheres. These tumors are often cystic in nature and are more common in children and young patients. Although some features suggest a malignant tendency (enhancement on imaging, microscopic nuclear schizophrenia and microvascular hyperplasia), the presence of biphasic cell populations composed of dense bipolar cells and Rosenthal fibers, multipolar cells with microcyst formation, and granulosa identifies a hairy cell astrocytoma. In addition, there are some uncommon subtypes of low-grade gliomas, such as pleomorphic yellow astrocytomas (PXAs), subventricular ventricular meningiomas, and subventricular giant cell astrocytomas. As with hairy cell astrocytomas, these tumors are usually well-defined, slow-growing, and rarely malignant. Broadly speaking, most low-grade gliomas in adults can be divided into three groups: astrocytomas, oligodendrogliomas, and mixed oligodendroglial astrocytomas. The typical low-grade astrocytoma has an indistinct border, infiltrates and spreads to adjacent brain tissue, and is either parenchymal or cystic in nature. Histologically, low-grade astrocytomas exhibit increased cell numbers and microcyst formation without the features of homogeneous anisotropy, necrosis, and endothelial cell proliferation. Differentiation from reactive gliosis is sometimes difficult, especially in the case of small tissue specimens. The tumor has several histologic subtypes, with the obese cell type more often undergoing early transformation to high-grade glioma (mesenchymal astrocytoma or glioblastoma). The typical oligodendroglioma is characterized by a moderate number of cells, a round nucleus, and a perinuclear hollow halo (so-called omelet-like changes) with a fine wire meshwork of vessels and calcifications. Secondly, Scherer structural changes (formation of perineuronal satellite nodules with extension along white matter fiber bundles, submural and paravascular) are common. Based on this criterion, Mork et al. found oligodendroglioma to account for 4.2% of all primary brain tumors in a Norwegian cancer registry and study. Coons et al. and Daumas-Duport et al. noted that a significant number of diffuse fibrous astrocytomas actually consist of mesenchymal oligodendroglioma cells with neuraxial and fibrillary reactive glial proliferation, with the latter two acting as a background to encapsulate the former. A retrospective analysis of 153 cases of “pure” oligodendrogliomas revealed two types of growth patterns: type III tumors consisted of isolated invasive tumor cells; type II tumors consisted of solid tumor tissue and isolated invasive tumor cells. It was also found that type III tumors are more likely to be misdiagnosed as diffuse fibrous astrocytomas, which have slow growth and longer survival, whereas type II tumors are more likely to have neurological dysfunction, enhanced lesions and neovascularization, and have shorter survival. They found that it was difficult to distinguish diffuse astrocytomas from oligodendrogliomas and oligodendrocytic tumors. They found that in the diagnosis of oligodendroglioma, it is not necessary to have classical oligodendrocytes or vascular beds, but it is important to identify the components of oligodendrocytes, such as: small round cells, glial fibrous oligodendrocytes and protoplasmic astrocytes. At the same time, they noted a tendency to misclassify oligodendrogliomas as mesenchymal astrocytomas or glioblastomas multiforme in diagnosis, and that nearly 25% of gliomas are actually oligodendrogliomas or mixed oligodendrocytomas when measured by their modified criteria. The distinction between simple oligodendrogliomas and mixed oligodendrocytic astrocytomas is another diagnostic challenge, and Coons et al. found that it was difficult to agree between investigators on the definition of mixed oligodendrocytic-astrocytic tumors. The most obvious difficulty is that the multiple cellular morphologies of high-grade tumors make the typical cytologic features of oligodendrocytes ambiguous, so that these tumors are often misdiagnosed as mesenchymal astrocytomas or glioblastomas. Moreover, even in tumors with a distinct oligodendroglial component, it is difficult to determine the amount of fibrous or obese astrocytes and make a correct diagnosis of mixed oligodendroglioma. They proposed a feasible criterion for the definition of mixed oligodendroglial astrocytoma, namely: an obvious oligodendroglial component with a well-differentiated fibrous and/or obese cellular component. Currently, the most commonly used grading standard is the WHO-established grading system for grading tumors of astrocytic and oligodendrocytic origin. While it is generally accepted that the following pathological features are important in high-grade gliomas: cellular anisotropy, degree of mitosis, microvascular formation or endothelial cell proliferation, and tumor necrosis, the importance of aggressive features in low-grade gliomas is unclear. For example, elevated proliferation indices (MIB-1, Ki67, and PCNA) suggest a poor prognosis for patients with oligodendrogliomas and astrocytomas. However, it remains unclear whether these features can be used as independent factors in determining tumor prognosis when other prognostic factors are taken into account. Malignant transformation is a common form of progression and treatment failure in low-grade gliomas. Recurrence of low-grade gliomas after multiple surgeries often presents with nuclear anisotropy, polychromatin, and increased mitotic activity, suggesting transformation to a mesenchymal tumor. Several recurrences are associated with enhanced imaging and evidence of microvascular proliferation and necrosis, suggesting glioblastoma. The time frame for transformation from low-grade glioma to mesenchymal glioma is large, averaging 4-5 years, while progression from mesenchymal glioma to glioblastoma is usually rapid (1-2 years).