According to the SEER cancer statistics, 1,658,370 persons will develop new cancers in 2015 and 589,430 will die from cancer. Compared to this, the number of new primary brain tumors (BT), 22,850 or 1.4%, is relatively small.Cognitive domain of learning however, if one adds metastases from other cancers to the brain, the number of BT increases significantly. Primary BT will claim 15,320 lives in 2015, 2.6% of all cancer deaths.Cognitive domain of learning the incidence of BT shows a peak in childhood followed by a decline till 25 years. After this, there is a continuous increase with advancing age.Cognitive domain of learning cancer is second only to accidents as a cause of death in children and adolescents, 1 to 19 years old. It causes 10.5% of all deaths. In that age group, BT, with an average annual age-adjusted

cognitive domain of learning

Incidence rate of 5.42 per 100,000, are the most frequent neoplasm, accounting for about 18% of all cancers. The second most common cancer in that age group is leukemia.Cognitive domain of learning the CNS is among the three leading sites of cancer mortality in the first three decades of life. The most frequent BT (all ages) is meningioma (35.6%) followed by glioblastoma (15.4%).Cognitive domain of learning

Is an autosomal dominant condition that affects the brain, skin, kidneys, lungs, heart, and other organs. It is characterized by several major and minor features that are used as diagnostic criteria.Cognitive domain of learning major features are cortical tubers, subependymal nodules, subependymal giant cell astrocytomas (SEGA), hypomelanotic skin macules, shagreen patches, retinal nodular hamartomas, ungual or periungual fibromas, cardiac rhabdomyomas, pulmonary lymphangiomyomatosis, and renal angiomyolipomas.Cognitive domain of learning minor features include dental pits, intraoral fibromas, multiple renal cysts, “confetti” (hypopigmented) skin lesions, nonrenal hamartomas, and retinal achromatic patches.Cognitive domain of learning the diagnosis of TSC can be established if 2 major or one major and 2 minor criteria are present. TSC patients have seizures, intellectual disability, ADHD, and other neuropsychiatric disorders.Cognitive domain of learning

The cortical tubers are abnormal, broad (potato-like), firm gyri. They represent focal malformations of cortical development, similar to some forms of cortical dysplasia, and have an abnormal cytoarchitecture which includes large, often bizarre pyramidal cells in a background of gliosis.Cognitive domain of learning tubers are epileptogenic. The segas consist of variable size, often large or giant astrocytes and have frequent calcifications. Despite their cellular atypia, they are slowly growing tumors but can cause hydrocephalus because they are located at the foramina of monro.Cognitive domain of learning

TSC is caused by mutations of two genes, TSC1 on 9q34 which encodes hamartin and TSC2 on 16p13.3 which encodes tuberin. Hamartin and tuberin form a functional complex which suppresses the activity of the mammalian target of rapamycin (mtor), a serine/threonine kinase that plays a central role in multiple processes involved in brain development, including neuronal proliferation, neuronal growth, and axon formation.Cognitive domain of learning rapamycin is an antibiotic, antifungal and immunosuppressant. It is also a potent antagonist of mtor. Overactivatin of mtor signaling (caused by mutations of TSC1 and TSC2 and other regulatory proteins) leads to cortical malformations, including tubers, focal cortical dysplasia type iib, ganglioglioma, and hemimegalencephaly.Cognitive domain of learning the latter is a mosaic disorder with mtor hyperactivation present in one hemisphere. MTOR hyperactivation is evident in pathological specimens from these disorders, which have been grouped under the umbrella term "mtoropathy".Cognitive domain of learning the key features of mtoropathies are abnormal cortical cytoarchitecture, abnormal cells (dysplastic neurons and balloon cells), intractable seizures, and cognitive abnormalities.Cognitive domain of learning mtor overactivation has also been demonstrated in neurofibromatosis 1, sturge-weber syndrome, cowden syndrome, PMSE (polyhydramnios, megalencephaly, symptomatic epilepsy), and proteus syndrome.Cognitive domain of learning treatment with mtor inhibitors (rapamycin, everolimus) causes regression of segas and other TSC lesions.