Gangliogliomas are generally benign WHO grade I tumors; the presence of anaplastic changes in the glial component is considered to represent WHO grade III (anaplastic ganglioglioma). Criteria for WHO grade II have been suggested, but are not established. Malignant transformation of spinal ganglioglioma has been seen in only a select few cases. Poor prognostic factors for adults with gangliogliomas include older age at diagnosis, male sex, and malignant histologic features.

Ganglioglioma is a rare, slow-growing primary central nervous system (CNS) tumor which most frequently occurs in the temporal lobes of children and young adults.

Pediatric ependymomas are similar in nature to the adult form of ependymoma in that they are thought to arise from radial glial cells lining the ventricular system. However, they differ from adult ependymomas in which genes and chromosomes are most often affected, the region of the brain they are most frequently found in, and the prognosis of the patients. Children with certain hereditary diseases, such as neurofibromatosis type II (NF2), have been found to be more frequently afflicted with this class of tumors, but a firm genetic link remains to be established. Symptoms associated with the development of pediatric ependymomas are varied, much like symptoms for a number of other pediatric brain tumors including vomiting, headache, irritability, lethargy, and changes in gait. Although younger children and children with invasive tumor types generally experience less favorable outcomes, total removal of the tumors is the most conspicuous prognostic factor for both survival and relapse.

Symptoms present 1–36 months before diagnosis, and can vary depending on age, tumor grade, and location. Increased intracranial pressure can induce vomiting, headache, irritability, lethargy, changes in gait, and in children less than 2, feeding problems, involuntary eye movements, and hydrocephalus are often noticeable. Seizures occur in about 20% of pediatric patients. Loss of cognitive function and even sudden death could occur if the tumor is located at a crucial location for CSF flow. Pediatric ependymomas most often occur in the posterior cranial fossa, in contrast with adult ependymomas which usually occur along the spine. Ependymomas present as low-density masses on CT scans, and are hyperintense on T2-weighted MRI images.

Embryonal tumor is a mass of rapidly growing cells. It is believed that it begins in embryonic (fetal) tissue. Embryonal tumors may be benign or malignant, and include neuroblastomas and Wilms tumors. Also called embryoma. Embryomas have been defined as: "Adult neoplasms expressing one or more embryo-exclusive genes", in: "Embryoma Gene Networks", http://www.embryomas.net

Embryomas can appear in the lungs.

It is not a precise term, and it is not commonly used in modern medical literature. Embryomas have been defined as: "Adult neoplasms expressing one or more embryo-exclusive genes".

The most common cancers in children are (childhood) leukemia (32%), brain tumors (18%), and lymphomas (11%). In 2005, 4.1 of every 100,000 young people under 20 years of age in the U.S. were diagnosed with leukemia, and 0.8 per 100,000 died from it. The number of new cases was highest among the 1–4 age group, but the number of deaths was highest among the 10–14 age group.

In 2005, 2.9 of every 100,000 people 0–19 years of age were found to have cancer of the brain or central nervous system, and 0.7 per 100,000 died from it. These cancers were found most often in children between 1 and 4 years of age, but the most deaths occurred among those aged 5–9. The main subtypes of brain and central nervous system tumors in children are: astrocytoma, brain stem glioma, craniopharyngioma, desmoplastic infantile ganglioglioma, ependymoma, high-grade glioma, medulloblastoma and atypical teratoid rhabdoid tumor.

Other, less common childhood cancer types are:

- Neuroblastoma (6%, nervous system)

- Wilms tumor (5%, kidney)

- Non-Hodgkin lymphoma (4%, blood)

- Childhood rhabdomyosarcoma (3%, many sites)

- Retinoblastoma (3%, eye)

- Osteosarcoma (3%, bone cancer)

- Ewing sarcoma (1%, many sites)

- Germ cell tumors (5%, many sites)

- Pleuropulmonary blastoma (lung or pleural cavity)

- Hepatoblastoma and hepatocellular carcinoma (liver cancer)

Childhood cancer (also known as pediatric cancer) is cancer in a child. In the United States, an arbitrarily adopted standard of the ages used are 0–14 years inclusive, that is, up to 14 years 11.9 months of age. However, the definition of childhood cancer sometimes includes adolescents between 15–19 years old. Pediatric oncology is the branch of medicine concerned with the diagnosis and treatment of cancer in children.

Worldwide, it is estimated that childhood cancer has an incidence of more than 175,000 per year, and a mortality rate of approximately 96,000 per year. In developed countries, childhood cancer has a mortality of approximately 20% of cases. In low resource settings, on the other hand, mortality is approximately 80%, or even 90% in the world's poorest countries. In many developed countries the incidence is slowly increasing, as rates of childhood cancer increased by 0.6% per year between 1975 and 2002 in the United States and by 1.1% per year between 1978 and 1997 in Europe.

Acrospiroma (also known as hidradenoma) is a cutaneous condition, primarily occurring in adult women, that is a form of benign adnexal neoplasm closely related to poroma.

A common symptom of laryngeal papillomatosis is a perceptual change in voice quality. More specifically, hoarseness is observed. As a consequence of the narrowing of the laryngeal or tracheal parts of the airway, shortness of breath, chronic cough and stridor (i.e. noisy breathing which can sound like a whistle or a snore), can be present. As the disease progresses, occurrence of secondary symptoms such as dysphagia, pneumonia, acute respiratory distress syndrome, failure to thrive, and recurrent upper respiratory infections can be diagnosed. In children, symptoms are usually more severe and often mistaken for manifestations of other diseases such as asthma, croup or bronchitis. Therefore, diagnosis is usually delayed.

Ovine pulmonary adenocarcinoma (OPA), also known as ovine pulmonary adenomatosis, or jaagsiekte, is a chronic and contagious disease of the lungs of sheep and goats. OPA is caused by a retrovirus called jaagsiekte sheep retrovirus (JSRV).

The disease has a long incubation period, and therefore signs usually occur in adult animals (over 2 years of age). Clinical signs resemble a non-specific progressive pneumonia, including poor body condition and, particularly after exercise, respiratory difficulty. Unless a concurrent lung infection is present, affected sheep continue to eat. The only sign specific to OPA is a watery nasal discharge, consisting of lung fluid produced by the affected lung tissue; lifting the hind legs of the animal above the level of its head will cause large volumes of this fluid to flow from the nostrils.

There are no reliable tests for the diagnosis of OPA in live animals which are suitable for use on farms, so diagnosis can only be confirmed at necropsy (post-mortem examination). On necropsy, lungs are interspersed with multifocal tumors. Some of these are small discrete nodules and others will involve the entire half of a lung lobule. JSRV acutely transforms the lung epithelia into cancerous cells, with type-2 pneumocytes and club cells being the likely target for JSRV transformation. The tumors have overactive secretory functions, which are a hallmark of OPA.

The retroviral antigen levels of JSRV are very high in OPA tumors and can be detected in the lung secretions of infected sheep. It is thought that infected animals secrete the virus before showing signs, so the virus is easily spread within flocks.

Laryngeal papillomatosis, also known as recurrent respiratory papillomatosis, is a rare medical condition that leads to audible changes in voice quality and narrowing of the airway. It is caused by type 6 and 11 human papillomavirus (HPV) infections of the throat, in which benign tumors or papillomas form on the larynx or other areas of the respiratory tract. Laryngeal papillomatosis is initially diagnosed through indirect laryngoscopy upon observation of growths on the larynx and can be confirmed through a biopsy. Treatment for laryngeal papillomatosis aims to remove the papillomas and limit their recurrence. Due to the recurrent nature of the virus, repeated treatments usually are needed. Laryngeal papillomatosis is primarily treated surgically, though supplemental nonsurgical and/or medical treatments may be considered in some cases. The evolution of laryngeal papillomatosis is highly variable. Though total recovery may be observed, it is often persistent despite treatment. The number of new cases of laryngeal papillomatosis cases is at approximately 4.3 cases per 100 000 children and 1.8 cases per 100 000 adults annually.

Delays in development of some physical, psychological and behavioral skills; progressive enlargement of the head (macrocephaly), seizures, spasticity, and in some cases also hydrocephalus, idiopathic intracranial hypertension, and dementia.

Alexander disease, also known as fibrinoid leukodystrophy, is a progressive and fatal neurodegenerative disease. It is a rare genetic disorder and mostly affects infants and children, causing developmental delay and changes in physical characteristics.

This illness has a minimum incubation period of 7 months with a maximum of 12 months. This disease results in mortality of adult animals.

Clinical signs of TME include the characteristic behavioural changes such as confusion, loss of cleanliness, and aimless circling. An affected animal shows signs of weight loss, might develop matted fur, hindquarter ataxia, and its tail arched over its back. Seizures may very rarely occur. Near-death stages include the animal showing signs of drowsiness and unresponsiveness.

Currently, no tests are available to detect signs of this illness in live animals. However, veterinary pathologists can confirm this illness by microscopic examination of the brain tissue in animals suspected to have died of this disease, where they expect to detect areas of distinct sponge-like formations, or by the identification of the prion protein in these tissue samples.

Bilateral hilar lymphadenopathy is a bilateral enlargement of the lymph nodes of pulmonary hila. It is a radiographic term that describes the enlargement of mediastinal lymph nodes and is most commonly identified by a chest x-ray.

A prenatal diagnosis was made by Kleijer et al. in 1979 by measuring beta-galactosidase and neuraminidase activities in cultured amniotic fluid cells.

Transmissible mink encephalopathy (TME) is a rare sporadic disease that affects the central nervous system of ranch-raised mink. It is classified as a transmissible spongiform encephalopathy, believed to be caused by proteins called prions. This disease is only known to affect adult mink.

Galactosialidosis is a lysosomal storage disease.This condition is rare and most cases have been in the juvenile/adult group of patients. An infantile form has been described.

T-cell leukemia describes several different types of lymphoid leukemia which affect T cells.

Types include:

- Large granular lymphocytic leukemia

- Adult T-cell leukemia/lymphoma

- T-cell prolymphocytic leukemia

In practice, it can be hard to distinguish T-cell leukemia from T-cell lymphoma, and they are often grouped together.

Symptomatic presentation usually occurs between 6 and 24 months of age, but the majority of cases have been documented in children less than 1 year of age. The infantile form involves multiple organ systems and is primarily characterized by hypoketotic hypoglycemia (recurring attacks of abnormally low levels of fat breakdown products and blood sugar) that often results in loss of consciousness and seizure activity. Acute liver failure, liver enlargement, and cardiomyopathy are also associated with the infantile presentation of this disorder. Episodes are triggered by febrile illness, infection, or fasting. Some cases of sudden infant death syndrome are attributed to infantile CPT II deficiency at autopsy.

This exclusively myopathic form is the most prevalent and least severe phenotypic presentation of this disorder. Characteristic signs and symptoms include rhabdomyolysis (breakdown of muscle fibers and subsequent release of myoglobin), myoglobinuria, recurrent muscle pain, and weakness. It is important to note that muscle weakness and pain typically resolves within hours to days, and patients appear clinically normal in the intervening periods between attacks. Symptoms are most often exercise-induced, but fasting, a high-fat diet, exposure to cold temperature, or infection (especially febrile illness) can also provoke this metabolic myopathy. In a minority of cases, disease severity can be exacerbated by three life-threatening complications resulting from persistent rhabdomyolysis: acute kidney failure, respiratory insufficiency, and episodic abnormal heart rhythms. Severe forms may have continual pain from general life activity. The adult form has a variable age of onset. The first appearance of symptoms usually occurs between 6 and 20 years of age but has been documented in patients as young as 8 months as well as in adults over the age of 50. Roughly 80% cases reported to date have been male.

Self-healing papular mucinosis is a skin condition caused by fibroblasts producing abnormally large amounts of mucopolysaccharides, and may present in adult and juvenile forms. The juvenile variant is also called self-healing juvenile cutaneous mucinosis.

Tauopathy belongs to a class of neurodegenerative diseases associated with the pathological aggregation of tau protein in neurofibrillary or gliofibrillary tangles in the human brain. Tangles are formed by hyperphosphorylation of a microtubule-associated protein known as tau, causing it to aggregate in an insoluble form. (These aggregations of hyperphosphorylated tau protein are also referred to as paired helical filaments). The precise mechanism of tangle formation is not completely understood, and it is still controversial as to whether tangles are a primary causative factor in the disease or play a more peripheral role. Primary tauopathies, i.e., conditions in which neurofibrillary tangles (NFT) are predominantly observed, include:

- Primary age-related tauopathy (PART)/Neurofibrillary tangle-predominant senile dementia, with NFTs similar to AD, but without plaques.

- Chronic traumatic encephalopathy, including dementia pugilistica

- Progressive supranuclear palsy

- Corticobasal degeneration

- Frontotemporal dementia and parkinsonism linked to chromosome 17

- Lytico-Bodig disease (Parkinson-dementia complex of Guam)

- Ganglioglioma and gangliocytoma

- Meningioangiomatosis

- Postencephalitic parkinsonism

- Subacute sclerosing panencephalitis

- As well as lead encephalopathy, tuberous sclerosis, Hallervorden-Spatz disease, and lipofuscinosis

Neurofibrillary tangles were first described by Alois Alzheimer in one of his patients suffering from Alzheimer's disease (AD), which is considered a secondary tauopathy. AD is also classified as an amyloidosis because of the presence of senile plaques.

The degree of NFT involvement in AD is defined by Braak stages. Braak stages I and II are used when NFT involvement is confined mainly to the transentorhinal region of the brain, stages III and IV when there's also involvement of limbic regions such as the hippocampus, and V and VI when there's extensive neocortical involvement. This should not be confused with the degree of senile plaque involvement, which progresses differently.

In both Pick's disease and corticobasal degeneration, tau proteins are deposited as inclusion bodies within swollen or "ballooned" neurons.

Argyrophilic grain disease (AGD), another type of dementia, is marked by an abundance of argyrophilic grains and coiled bodies upon microscopic examination of brain tissue. Some consider it to be a type of Alzheimer's disease. It may co-exist with other tauopathies such as progressive supranuclear palsy and corticobasal degeneration, and also Pick's disease.

Huntington's disease (HD): a neurodegenerative disease caused by a CAG tripled expansion in the Huntington gene is the most recently described tauopathy (Fernandez-Nogales et al. Nat Med 2014). JJ Lucas and co-workers demonstrate that, in brains with HD, tau levels are increased and the 4R/3R balance is altered. In addition, the Lucas study shows intranuclear insoluble deposits of tau; these "Lucas' rods" were also found in brains with Alzheimer's disease.

Tauopathies are often overlapped with synucleinopathies, possibly due to interaction between the synuclein and tau proteins.

The non-Alzheimer's tauopathies are sometimes grouped together as "Pick's complex" due to their association with frontotemporal dementia, or frontotemporal lobar degeneration.

ADULT syndrome features include ectrodactyly, syndactyly, excessive freckling, lacrimal duct anomalies, dysplastic nails, hypodontia, hypoplastic breasts and nipples, hypotrichosis, hypohidrosis, broad nasal bridge, midfacial hypoplasia, exfoliative dermatitis, and xerosis. The lack of facial clefting and ankyloblepharon are important because they exist in ectrodactyly–ectodermal dysplasia–cleft syndrome (EEC) but not in ADULT syndrome.