Medulloblastomas affect just under two people per million per year, and affect children 10 times more than adults. Medulloblastoma is the second-most frequent brain tumor in children after pilocytic astrocytoma and the most common malignant brain tumor in children, comprising 14.5% of newly diagnosed cases. In adults, medulloblastoma is rare, comprising fewer than 2% of CNS malignancies.

The rate of new cases of childhood medulloblastoma is higher in males (62%) than females (38%), a feature which is not seen in adults. Medulloblastoma and other PNET`s are more prevalent in younger children than older children. About 40% of medulloblastoma patients are diagnosed before the age of five, 31% are between the ages of 5 and 9, 18.3% are between the ages of 10 and 14, and 12.7% are between the ages of 15 and 19.

The cumulative relative survival rate for all age groups and histology follow-up was 60%, 52%, and 47% at 5 years, 10 years, and 20 years, respectively. Patients diagnosed with a medulloblastoma or PNET are 50 times more likely to die than a matched member of the general population.

The most recent population-based (SEER) 5-year relative survival rates are 69% overall, but 72% in children (1–9 years) and 67% in adults (20+ years). The 20-year survival rate is 51% in children. Children and adults have different survival profiles, with adults faring worse than children only after the fourth year after diagnosis (after controlling for increased background mortality). Before the fourth year, survival probabilities are nearly identical. Longterm sequelae of standard treatment include hypothalamic-pituitary and thyroid dysfunction and intellectual impairment. The hormonal and intellectual deficits created by these therapies causes significant impairment of the survivors.

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.

For low-grade tumors, the prognosis is somewhat more optimistic. Patients diagnosed with a low-grade glioma are 17 times as likely to die as matched patients in the general population.

The age-standardized 10-year relative survival rate was 47%. One study reported that low-grade oligodendroglioma patients have a median survival of 11.6 years; another reported a median survival of 16.7 years.

The age-standardized 5-year relative survival rate is 23.6%. Patients with this tumor are 46 times more likely to die than matched members of the general population. It is important to note that prognosis across age groups is different especially during the first three years post-diagnosis. When the elderly population is compared with young adults, the excess hazard ratio (a hazard ratio that is corrected for differences in mortality across age groups) decreases from 10.15 to 1.85 at 1 to 3 years, meaning that the elderly population are much more likely to die in the first year post-diagnosis when compared to young adults (aged 15 to 40), but after three years, this difference is reduced markedly.

Typical median survival for anaplastic astrocytoma is 2–3 years. Secondary progression to glioblastoma multiforme is common. Radiation, younger age, female sex, treatment after 2000, and surgery were associated with improved survival in AA patients.

Gliomas are rarely curable. The prognosis for patients with high-grade gliomas is generally poor, and is especially so for older patients. Of 10,000 Americans diagnosed each year with malignant gliomas, about half are alive one year after diagnosis, and 25% after two years. Those with anaplastic astrocytoma survive about three years. Glioblastoma multiforme has a worse prognosis with less than a 12-month average survival after diagnosis, though this has extended to 14 months with more recent treatments.

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.

Among people with PXA who were able to have their tumors completely resected during surgery, there is a long-term survival rate of 90%. After incomplete resection, the long-term survival rate is higher than 50%. Morbidity is determined by the type and evolution of the tumor, with high-graded anaplastic tumors causing more fatalities.

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. It is the second most common central nervous system cancer after meningioma.

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.

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 3 months.

Increasing age (> 60 years of age) carries a worse prognostic risk. Death is usually due to widespread tumor infiltration with cerebral edema and increased intracranial pressure.

A good initial Karnofsky Performance Score (KPS) and MGMT methylation are associated with longer survival. A DNA test can be conducted on glioblastomas to determine whether or not the promoter of the "MGMT" gene is methylated. Patients with a methylated MGMT promoter have longer survival than those with an unmethylated MGMT promoter, due in part to increased sensitivity to temozolomide. This DNA characteristic is intrinsic to the patient and currently cannot be altered externally. Another positive prognostic marker for glioblastoma patients is mutation of the "IDH1" gene, which can be tested by DNA-based methods or by immunohistochemistry using an antibody against the most common mutation, namely IDH1-R132H.

More prognostic power can be obtained by combining the mutational status of "IDH1" and the methylation status of "MGMT" into a two-gene predictor. Patients with both "IDH1" mutations and "MGMT" methylation have the longest survival, patients with an "IDH1" mutation or "MGMT" methylation an intermediate survival and patients without either genetic event have the shortest survival.

Long-term benefits have also been associated with those patients who receive surgery, radiotherapy, and temozolomide chemotherapy. However, much remains unknown about why some patients survive longer with glioblastoma. Age of under 50 is linked to longer survival in glioblastoma multiforme, as is 98%+ resection and use of temozolomide chemotherapy and better Karnofsky performance scores. A recent study confirms that younger age is associated with a much better prognosis, with a small fraction of patients under 40 years of age achieving a population-based cure. The population-based cure is thought to occur when a population's risk of death returns to that of the normal population, and in GBM, this is thought to occur after 10 years.

UCLA Neuro-Oncology publishes real-time survival data for patients with this diagnosis. They are the only institution in the United States that shows how their patients are performing. They also show a listing of chemotherapy agents used to treat GBM tumors. Despite a poor prognosis, there is a small number of survivors who have been GBM free for more than 10–20 years.

According to a 2003 study, glioblastoma multiforme prognosis can be divided into three subgroups dependent on KPS, the age of the patient, and treatment.

The 5-year disease-free survival for age >5 years is 50-60%. Another report found a similar 5-year survival at about 65% with 51% progression-free survival. The 10-year disease-free survival is 40-50%. Younger ages showed lower 5 and 10-year survival rates. A 2006 study that observed 133 patients found 31 (23.3%) had a recurrence of the disease within a five-year period.

Most high-grade gliomas occur sporadically or without identifiable cause. However, a small proportion (less than 5%) of persons with malignant astrocytoma has a definite or suspected hereditary predisposition. The main hereditary predispositions are mainly neurofibromatosis type I, Li-Fraumeni syndrome, hereditary nonpolyposis colorectal cancer and tuberous sclerosis. Anaplastic astrocytomas have also been associated with previous exposure to vinyl chloride and to high doses of radiation therapy to the brain.

With treatment, pleomorphic xanthoastrocytomas are associated with a high rate of cure.

- Grade II pleomorphic xanthoastrocytomas are known to progress towards grade II tumors, which are more likely to recur after surgical removal.

- Grade III anaplastic pleomorphic xanthoastrocytomas may evolve and show signs of anaplasia, according to evidence in the medical literature.

Use of telomerase inhibitors such as Imetelstat seem to have very low toxicity compared to other chemotherapy. The only known side effect of most telomerase inhibitors is dose-induced neutropenia. Neuropsychological deficits can result from resection, chemotherapy, and radiation, as well as endocrinopathies. Additionally, an increase in gastrointestinal complications has been observed in survivors of pediatric cancers.

Based on a series of 493 neuroblastoma samples, it has been reported that overall genomic pattern, as tested by array-based karyotyping, is a predictor of outcome in neuroblastoma:

- Tumors presenting exclusively with whole chromosome copy number changes were associated with excellent survival.

- Tumors presenting with any kind of segmental chromosome copy number changes were associated with a high risk of relapse.

- Within tumors showing segmental alterations, additional independent predictors of decreased overall survival were N-myc amplification, 1p and 11q deletions, and 1q gain.

Earlier publications categorized neuroblastomas into three major subtypes based on cytogenetic profiles:

- Subtype 1: favorable neuroblastoma with near triploidy and a predominance of numerical gains and losses, mostly representing non-metastatic NB stages 1, 2 and 4S.

- Subtypes 2A and 2B: found in unfavorable widespread neuroblastoma, stages 3 and 4, with 11q loss and 17q gain without N-myc amplification (subtype 2A) or with N-myc amplification often together with 1p deletions and 17q gain (subtype 2B).

Virtual karyotyping can be performed on fresh or paraffin-embedded tumors to assess copy number at these loci. SNP array virtual karyotyping is preferred for tumor samples, including neuroblastomas, because they can detect copy neutral loss of heterozygosity (acquired uniparental disomy). Copy neutral LOH can be biologically equivalent to a deletion and has been detected at key loci in neuroblastoma. ArrayCGH, FISH, or conventional cytogenetics cannot detect copy neutral LOH.

Between 20% and 50% of high-risk cases do not respond adequately to induction high-dose chemotherapy and are progressive or refractory. Relapse after completion of frontline therapy is also common. Further treatment is available in phase I and phase II clinical trials that test new agents and combinations of agents against neuroblastoma, but the outcome remains very poor for relapsed high-risk disease.

Most long-term survivors alive today had low or intermediate risk disease and milder courses of treatment compared to high-risk disease. The majority of survivors have long-term effects from the treatment. Survivors of intermediate and high-risk treatment often experience hearing loss. Growth reduction, thyroid function disorders, learning difficulties, and greater risk of secondary cancers affect survivors of high-risk disease. An estimated two of three survivors of childhood cancer will ultimately develop at least one chronic and sometimes life-threatening health problem within 20 to 30 years after the cancer diagnosis.

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.

There are no precise guidelines because the exact cause of astrocytoma is not known.

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).

Oligodendrogliomas are incurable but slowly progressive malignant brain tumors. They can be treated with surgical resection, chemotherapy, radiotherapy or a combination. For some suspected low-grade (grade II) tumors, only a course of watchful waiting and symptomatic therapy is opted for. These tumors show a high frequency of co-deletions of the p and q arms of chromosome 1 and chromosome 19 respectively (1p19q co-deletion) and have been found to be especially chemosensitive with one report claiming them to be one of the most chemosensitive tumors. A median survival of up to 16.7 years has been reported for grade II oligodendrogliomas.

For low grade astrocytomas, removal of the tumor will generally allow functional survival for many years. In some reports, the five-year survival has been over 90% with well resected tumors. Indeed, broad intervention of low grade conditions is a contested matter. In particular, pilocytic astrocytomas are commonly indolent bodies that may permit normal neurologic function. However, left unattended these tumors may eventually undergo neoplastic transformation. To date, complete resection of high grade astrocytomas is impossible because of the diffuse infiltration of tumor cells into normal parenchyma. Thus, high grade astrocytomas inevitably recur after initial surgery or therapy, and are usually treated similarly as the initial tumor. Despite decades of therapeutic research, curative intervention is still nonexistent for high grade astrocytomas; patient care ultimately focuses on palliative management.

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.

Even after surgery, an oligoastrocytoma will often recur. The treatment for a recurring brain tumor may include surgical resection, chemo and radiation therapy. Survival time of this brain tumor varies - younger age and low-grade initial diagnosis are factors in improved survival time.