According to a Dutch source juvenile pilocytic astrocytoma occurs at a rate of 2 in 100,000 people. Most affected are children ages 5–14 years. According to the National Cancer Institute more than 80% of astrocytomas located in the cerebellum are low grade (pilocytic grade I) and often cystic; most of the remainder are diffuse grade II astrocytomas.

Tumors of the optic pathway account for 3.6-6% of pediatric brain tumors, 60% of which are juvenile pilocytic astrocytomas. Astrocytomas account for 50% of pediatric primary central nervous system tumors. About 80-85% of cerebellar astrocytomas are juvenile pilocytic astrocytomas.

Recent genetic studies of pilocytic astrocytomas show that some sporadic cases have gain in chromosome 7q34 involving the BRAF locus.

In reported cases of the tumor over the last 25 years, the number of affected females with astroblastoma is significantly higher than the number of affected males. Sughrue et al. confirmed this trend, stating that 70% of the cases with clearly stated gender were female (100 cases total). While several publications support a genetic predisposition to females, the underlying reasons are still unknown.

At this point, no literature has indicated whether environmental factors increase the likelihood of astroblastoma. Although cancer in general is caused by a variety of external factors, including carcinogens, dangerous chemicals, and viral infections, astroblastoma research has not even attempted to classify incidence in this regard. The next few decades will aid in this understanding.

Grade I pilocytic astrocytoma and cerebellar gliomas are not associated with recurrence after complete resection. Grade II astrocytomas and cerebellar gliomas are more likely to recur after surgical removal. Pilomyxoid astrocytomas may behave more aggressively than classic pilocytic astrocytoma.

After complete surgical removal, in cases of progressive/recurrent disease or when maximal surgical removal has been achieved, chemotherapy and/or radiation therapy will be considered by the medical team.

After complete surgical removal, a SEGA tumor does not grow back. They do not metastasize to other parts of the body. However, the patient is still at risk for, and often develops, new tumors arising from subependymal nodules elsewhere in the ventricular system.

Based on a survey of >800, surgical removal of the entire involved kidney plus the peri-renal fat appeared curative for the majority of all types of mesoblastic nephroma; the patient overall survival rate was 94%. Of the 4% of non-survivors, half were due to surgical or chemotherapeutic treatments. Another 4% of these patients suffered relapses, primarily in the local area of surgery rare cases of relapse due to lung or bone metastasis.. About 60% of these recurrent cases had a complete remission following further treatment. Recurrent disease was treated with a second surgery, radiation, and/or chemotherapy that often vincristine and actinomycin treatment. Removal of the entire afflicted kidney plus the peri-renal fat appears critical to avoiding local recurrences. In general, patients who were older than 3 months of age at diagnosis or had the cellular form of the disease, stage III disease, or involvement of renal lymph nodes had a higher recurrence rate. Among patients with these risk factors, only those with lymph node involvement are recommended for further therapy.

It has been suggested that mesoblastic nephroma patients with lymph node involvement or recurrent disease might benefit by adding the ALK inhibitor, crizotinib, or a tyrosine kinase inhibitor, either larotrectinib or entrectinib, to surgical, radiation, and/or chemotherapy treatment regimens. These drugs inhibit NTRK3's tyrosine kinase activity. Crizotinib has proven useful in treating certain cases of acute lymphoblastic leukemia that are associated with the "ETV6-NTRK3" fusion gene while larotrectinib and entrectinib have been useful in treating various cancers (e.g. a metastatic sarcoma, papillary thyroid cancer, non-small-cell lung carcinoma, gastrointestinal stromal tumor, mammary analog secretory carcinoma, and colorectal cancer) that are driven by mutated, overly active tyrosine kinases. Relevant to this issue, a 16-month-old girl with infantile fibrosarcoma harboring the "ETV6–NTRK3" fusion gene was successfully trated with larotrectinib. The success of these drugs, howwever, will likely depend on the relative malignancy-promoting roles of ETV6-NTRK3 protein's tyrosine kinase activity, the lose of ETV6-related transcription activity accompanying formation of ETV6-NTRK3 protein, and the various trisomy chromosomes that populate mesoblastic nephroma.

Its presence is associated with either pilocytic astrocytoma (more common) or Alexander's disease (a rare leukodystrophy). They are also seen in the context of fucosidosis.

Pilocytic astrocytoma is the most common primitive tumor in pediatric patients.

A Rosenthal fiber is a thick, elongated, worm-like or "corkscrew" eosinophilic (pink) bundle that is found on H&E staining of the brain in the presence of long-standing gliosis, occasional tumors, and some metabolic disorders.

SCTC exhibits a highly aggressive phenotype, thus prognosis of that malignancy is extremely poor. The overall survival is less than 1 year in most of cases.

Fibrillary astrocytomas also called low grade or diffuse astrocytomas, are a group of primary slow growing brain tumors. They typically occur in adults between the ages of twenty and fifty.

The cause of oligodendrogliomas is unknown. Some studies have linked oligodendroglioma with a viral cause. A 2009 Oxford Neurosymposium study illustrated a 69% correlation between NJDS gene mutation and the tumor initiation shown by Kevin Smith. A single case report has linked oligodendroglioma to irradiation of pituitary adenoma.

Subependymal giant cell astrocytoma (SEGA, SGCA, or SGCT) is a low-grade astrocytic brain tumor (astrocytoma) that arises within the ventricles of the brain. It is most commonly associated with tuberous sclerosis complex (TSC). Although it is a low-grade tumor, its location can potentially obstruct the ventricles and lead to hydrocephalus.

Endodermal sinus tumor (EST), also known as yolk sac tumor (YST), is a member of the germ cell tumor group of cancers. It is the most common testicular tumor in children under 3, and is also known as infantile embryonal carcinoma. This age group has a very good prognosis. In contrast to the pure form typical of infants, adult endodermal sinus tumors are often found in combination with other kinds of germ cell tumor, particularly teratoma and embryonal carcinoma. While pure teratoma is usually benign, endodermal sinus tumor is malignant.

Most treatments involve some combination of surgery and chemotherapy. Treatment with cisplatin, etoposide, and bleomycin has been described.

Before modern chemotherapy, this type of neoplasm was highly lethal, but the prognosis has significantly improved since.

When endodermal sinus tumors are treated promptly with surgery and chemotherapy, fatal outcomes are exceedingly rare.

The tumor is rare, affecting adults in the 4th decade most commonly. Patients are usually younger than those who present with a lipoma. There is a slight male predominance. Hibernoma are most commonly identified in the subcutaneous and muscle tissue of the head and neck region (shoulders, neck, scapular), followed by thigh, back, chest, abdomen, and arms. In rare cases hibernoma may arise in bone tissue, however it is an incidental finding.

Fibrillary astrocytomas arise from neoplastic astrocytes, a type of glial cell found in the central nervous system. They may occur anywhere in the brain, or even in the spinal cord, but are most commonly found in the cerebral hemispheres. As the alternative name of "diffuse astrocytoma" implies, the outline of the tumour is not clearly visible in scans, because the borders of the neoplasm tend to send out tiny microscopic fibrillary tentacles that spread into the surrounding brain tissue. These tentacles intermingle with healthy brain cells, making complete surgical removal difficult. However, they are low grade tumors, with a slow rate of growth, so that patients commonly survive longer than those with otherwise similar types of brain tumour, such as glioblastoma multiforme.

Congenital mesoblastic nephroma, while rare, is the most common kidney neoplasm diagnosed in the first three months of life and accounts for 3-5% of all childhood renal neoplasms. This neoplasm is generally non-aggressive and amenable to surgical removal. However, a readily identifiable subset of these kidney tumors has a more malignant potential and is capable of causing life-threatening metastases. Congenital mesoblastic nephroma was first named as such in 1967 but was recognized decades before this as fetal renal hamartoma or leiomyomatous renal hamartoma.

Oligodendrogliomas are generally felt to be incurable using current treatments. However compared to the more common astrocytomas, they are slowly growing with prolonged survival. In one series, median survival times for oligodendrogliomas were 11.6 years for grade II and 3.5 years for grade III.

However, such figures can be misleading since they do not factor in the types of treatment nor the genetic signature of the tumors. A recent study analyzed survival based on chromosomal deletions and the effects of radiation or chemotherapy as treatment, with the following results (both low-grade and anaplastic oligodendrogliomas): 1p/19q deletion with radiation = 121 months (mean), 1p/19q deletion with chemotherapy = over 160 months (mean not yet reached), no 1p/19q deletion with radiation = 58 months (mean), and no 1p/19q deletion with chemotherapy = 75 months (mean). Another study divided anaplastic oligodendrogliomas into the following four clinically relevant groups of histology with the following results: combined 1p/19q loss = median survival was >123 months (not yet reached), 1p loss only = median survival was 71 months, 1p intact with TP53 mutation = median survival 71 months, and 1p intact with no TP53 mutation = median survival was 16 months.

Because of the indolent nature of these tumors and the potential morbidity associated with neurosurgery, chemotherapy and radiation therapy, most neurooncologists will initially pursue a course of watchful waiting and treat patients symptomatically. Symptomatic treatment often includes the use of anticonvulsants for seizures and steroids for brain swelling. PCV chemotherapy (Procarbazine, CCNU and Vincristine) has been shown to be effective and was the most commonly used chemotherapy regimen used for treating anaplastic oligodendrogliomas, but is now being superseded by a newer drug: Temozolomide. Temozolomide is a common chemotherapeutic drug to which oligodendrogliomas appear to be quite sensitive. It is often used as a first line therapy, especially because of its relatively mild side effects when compared to other chemotherapeutic drugs.

Nevertheless, a retrospective study on 1054 patients with anaplastic oligodendroglioma, presented during the 2009 ASCO Annual Meeting, suggests that PCV therapy may be superior in efficacy to the newer temozolomide therapy. Median time to progression for patients with 1p19q co-deletion was longer following PCV alone (7.6 years) than with temozolomide alone (3.3 years); median overall survival was also longer with PCV treatment versus temozolomide treatment (not reached, vs. 7.1 years).

The standard dosing schedule of temozolomide is 5 consecutive days of daily dosing during 28-day cycles. However, different dosing schedules may produce better results, such as continuous daily dosing using lower amounts of drug (e.g. 21-day dosing during 28-day cycles). As an example of an altered dosing schedule, promising results have been shown using lower daily doses on each day for 7 weeks, followed by a 4-week off periods. Regarding the duration of dosing, for oligodendrogliomas the duration prescribed by oncologists varies considerably and seems to range from 6 cycles to over 32 cycles (i.e. over 3 years). In one study, researchers compared patients who received temozolomide for at least 12 months on the 5/28 day cycle, dividing such patients into two groups: "short term" patients receiving temozolomide for 12-18 cycles and those "long term" patients receiving 19 or more cycles (range was 19 to 32 cycles). Researchers found that there was a statistically significant advantage for "long term" treatment (median progression free survival for "short term" patients was 95 weeks (follow up of 73 weeks), but for "long term" patients the median progression free survival was not yet reached (follow up of 134 weeks)).

Because of their diffusely infiltrating nature, oligodendrogliomas cannot be completely resected and are not curable by surgical excision. If the tumor mass compresses adjacent brain structures, a neurosurgeon will typically remove as much of the tumor as he or she can without damaging other critical, healthy brain structures. Surgery may be followed up by chemotherapy, radiation, or a mix of both, but recent studies suggest that radiation does not improve overall survival (even when age, clinical data, histological grading, and type of surgery are considered). However, a recent long-term study does affirm that radiation combined with adjuvant chemotherapy is significantly more efficacious for anaplastic oligodendroglioma patients with 1p 19q co-deleted tumors and has become the new standard of care. However, it is possible that radiotherapy may prolong the overall time to progression for non-deleted tumors.

Oligodendrogliomas, like all other infiltrating gliomas, have a very high (almost uniform) rate of recurrence and gradually increase in grade over time. Recurrent tumors are generally treated with more aggressive chemotherapy and radiation therapy. Recently, stereotactic surgery has proven successful in treating small tumors that have been diagnosed early.

Long-term survival is reported in a minority of patients. With aggressive treatment and close monitoring, it is possible to outlive the typical life expectancies for both low grade and high grade oligodendrogliomas. Westergaard's

study (1997) showed that patients younger than 20 years had a median survival of 17.5 years. Another study shows a 34% survival rate after 20 years. However, as discussed above, such figures can be misleading since they do not factor in the types of treatment nor the genetic signature of the tumors. Additionally, such historic data loses significance due to the relatively long survival of patients (compared to other types of brain tumors) and the introduction of newer treatment options over time.

Brain, other CNS or intracranial tumors are the ninth most common cancer in the UK (around 10,600 people were diagnosed in 2013), and it is the eighth most common cause of cancer death (around 5,200 people died in 2012).

Gliomatosis cerebri (infiltrative diffuse astrocytosis) is a rare primary brain tumor. It is commonly characterized by diffuse infiltration of the brain with neoplastic glial cells that affect various areas of the cerebral lobes. These malignancies consist of infiltrative threads that spread quickly and deeply into the surrounding brain tissue, or into multiple parts of the brain simultaneously, making them very difficult to remove with surgery or treat with radiation. Gliomatosis cerebi behaves like a malignant tumor that is very similar to Glioblastoma.

While gliomatosis cerebri can occur at any age, it is generally found in the third and fourth decades of life.

A solid pseudopapillary tumour (also known as solid pseudopapillary neoplasm or, more formally, solid pseudopapillary tumour/neoplasm of the pancreas) is a low-grade malignant neoplasm of the pancreas of architecture that typically afflicts young women.

A nervous system neoplasm is a tumor affecting the nervous system. Types include:

- Nerve sheath tumor

- Brain tumor

- Arachnoid cyst

- Optic nerve glioma

Epidemiological studies are required to determine risk factors. Aside from exposure to vinyl chloride or ionizing radiation, there are no known environmental factors associated with brain tumors. Mutations and deletions of so-called tumor suppressor genes, such as P53, are thought to be the cause of some forms of brain tumor. Inherited conditions, such as Von Hippel–Lindau disease, multiple endocrine neoplasia, and neurofibromatosis type 2 carry a high risk for the development of brain tumors. People with celiac disease have a slightly increased risk of developing brain tumors.

Although studies have not shown any link between cell phone or mobile phone radiation and the occurrence of brain tumors, the World Health Organization has classified mobile phone radiation on the IARC scale into Group 2B – possibly carcinogenic. Discounting claims that current cell phone usage may cause brain cancer, modern, third-generation (3G) phones emit, on average, about 1% of the energy emitted by the GSM (2G) phones that were in use when epidemiological studies that observed a slight increase in the risk for glioma – a malignant type of brain cancer – among heavy users of wireless and cordless telephones were conducted.

A germinoma is a type of germ cell tumor, which is not differentiated upon examination. It may be benign or malignant.

The prognosis for gliomatosis cerebri is generally poor. Surgery is not practical considering the extent of the disease, standard chemotherapy (nitrosourea) has been unsuccessful, and while brain irradiation can stabilize or improve neurologic function in some patients, its impact on survival has yet to be proven.

In 2014, Weill Cornell Brain and Spine Center launched an international registry for Gliomatosis Cerebri, where tissue samples can be stored for genomic study.