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.

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.

Treatment consists of wide resection or amputation. Metastases are rare at presentation but may occur in up to 30% of patients during the disease course. Prognosis is excellent, with overall survival of 85% at 10 years, but is lower when wide surgical margins cannot be obtained. This tumor is insensitive to radiation so chemotherapy is not typically used unless the cancer has metastasized to the lungs or other organs.

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).

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.

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.

This is a very rare neoplasm accounting for approximately 0.0003% of all tumors and about 2.5% of all external ear neoplasms. There is a wide age range at initial presentation, although the mean age is about 50 years of age. Females are affected slightly more often (1.5:1).

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

- Nerve sheath tumor

- Brain tumor

- Arachnoid cyst

- Optic nerve glioma

Adamantinoma (from the Greek word "adamantinos", meaning "very hard") is a rare bone cancer, making up less than 1% of all bone cancers. It almost always occurs in the bones of the lower leg and involves both epithelial and osteofibrous tissue.

The condition was first described by Fischer in 1913.

An odontogenic tumor is a neoplasm of the cells or tissues that initiate odontogenic processes.

Examples include:

- Adenomatoid odontogenic tumor

- Ameloblastoma, a type of odontogenic tumor involving ameloblasts

- Calcifying epithelial odontogenic tumor

- Keratocystic odontogenic tumor

- Odontogenic myxoma

- Odontoma

Neoplasm is an abnormal growth of tissue which, if it forms a mass, is commonly referred to as a tumor. This abnormal growth (neoplasia) usually but not always forms a mass.

ICD-10 classifies neoplasms into four main groups: benign neoplasms, in situ neoplasms, malignant neoplasms, and neoplasms of uncertain or unknown behavior. Malignant neoplasms are also simply known as cancers and are the focus of oncology.

Prior to the abnormal growth of tissue, as neoplasia, cells often undergo an abnormal pattern of growth, such as metaplasia or dysplasia. However, metaplasia or dysplasia does not always progress to neoplasia. The word is from Ancient Greek νέος- "neo" "new" and πλάσμα "plasma" "formation, creation".

Ceruminous adenocarcinoma is a malignant neoplasm derived from ceruminous glands of the external auditory canal. This tumor is rare, with several names used in the past. Synonyms have included cylindroma, ceruminoma, ceruminous adenocarcinoma, not otherwise specified (NOS), ceruminous adenoid cystic carcinoma (ACC), and ceruminous mucoepidermoid carcinoma.

Neoplastic tumors are often heterogeneous and contain more than one type of cell, but their initiation and continued growth is usually dependent on a single population of neoplastic cells. These cells are presumed to be clonal – that is, they are derived from the same cell,

and all carry the same genetic or epigenetic anomaly – evident of clonality. For lymphoid neoplasms, e.g. lymphoma and leukemia, clonality is proven by the amplification of a single rearrangement of their immunoglobulin gene (for B cell lesions) or T cell receptor gene (for T cell lesions). The demonstration of clonality is now considered to be necessary to identify a lymphoid cell proliferation as neoplastic.

It is tempting to define neoplasms as clonal cellular proliferations but the demonstration of clonality is not always possible. Therefore, clonality is not required in the definition of neoplasia.

Vascular tissue neoplasms, like neoplasms of all tissues, are classified to benign and malignant ones, according to their biological behavior.

Most malignant vascular tumors are considered sarcomas, a major histological group of tumors, arising from transformed cells of mesenchymal origin.

- Hemangiosarcoma

- Hemangiopericytoma

- Kaposi's Sarcoma

- Hemangioblastoma

- Lymphangiosarcoma

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.

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.

Glandular and epithelial neoplasm is a grouping of tumors arising from the glands and epithelium.

An example is adenoma.

Age and gender have an effect on the incidence of these lesions; they are more prevalent in women than men (though still common in both genders), and they appear more frequently with age. Due to the standard of medical care and screening in developed countries, it is increasingly rare for primary hyperparathyroidism to present with accompanying bone disease. This is not the case in less developed nations, however, and the two conditions are more often seen together.

Trichoepithelioma is a neoplasm of the adnexa of the skin. Its appearance is similar to basal cell carcinoma.

One form has been mapped to chromosome 9p21.

An muscle tissue neoplasm is a neoplasm derived from muscle.

An example is myoma.

Squamous-cell thyroid carcinoma (SCTC) is rare malignant neoplasm of thyroid gland which shows tumor cells with distinct squamous differentiation. The incidence of SCTC is less than 1% out of thyroid malignancies.

An odontogenic keratocyst is a rare and benign but locally aggressive developmental cyst. It most often affects the posterior mandible. It most commonly presents in the third decade of life.

In the WHO/IARC classification of head and neck pathology, this clinical entity had been known for years as the odontogenic keratocyst; it was reclassified as keratocystic odontogenic tumour (KCOT) from 2005 to 2017. In 2017 it reverted to the earlier name, as the new WHO/IARC classification reclassified OKC back into the cystic category. The WHO/IARC classification no longer considers it a neoplasm, because the evidence supporting that hypothesis (for example, clonality) is considered insufficient. However, this is an area of hot debate within the head and neck pathology community, and some pathologists still regard OKC as a neoplasm despite the reclassification.

A urogenital neoplasm is a tumor of the urogenital system.

Types include:

- Cancer of the breast and female genital organs: (Breast cancer, Vulvar cancer, Vaginal cancer, Cervical cancer, Uterine cancer, Endometrial cancer, Ovarian cancer)

- Cancer of the male genital organs (Carcinoma of the penis, Prostate cancer, Testicular cancer)

- Cancer of the urinary organs (Renal cell carcinoma, Bladder cancer)

Carcinosarcomas are malignant tumors that consist of a mixture of carcinoma (or epithelial cancer) and sarcoma (or mesenchymal/connective tissue cancer). Carcinosarcomas are rare tumors, and can arise in diverse organs, such as the skin, salivary glands, lungs, the esophagus, pancreas, colon, uterus and ovaries.

Four main hypotheses have been proposed for the cellular origins of carcinosarcoma, based largely on the pathology of the disease. First, the collision tumor hypothesis, which proposes the collision of two independent tumors resulting in a single neoplasm, based on the observation that skin cancers and superficial malignant fibrous histiocytomas are commonly seen in patients with sun-damaged skin; second, the composition hypothesis, which suggests that the mesenchymal component represents a pseudosarcomatous reaction to the epithelial malignancy; third, the combination hypothesis, which suggests that both the epithelial and mesenchymal components of the tumor arise from a common pluripotential stem cell that undergoes divergent differentiation; and fourth, the conversion/divergence hypothesis, which argues that the sarcomatous component of the tumor represents a metaplastic sarcomatous transformation of the epithelial component. Despite the remaining uncertainty on the mechanisms that generate these tumors, recent immunohistochemical, ultrastructural, and molecular genetic studies suggest and favor the notion of monoclonality in carcinosarcoma. In addition, identical p53 and KRAS mutations have been identified in both epithelial and mesenchymal components of carcinosarcoma, findings that suggest an early alteration in the histogenesis of the tumor with late transformation or degeneration of the epithelial component into the sarcomatous component.