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A paraganglioma is a rare neuroendocrine neoplasm that may develop at various body sites (including the head, neck, thorax and abdomen). When the same type of tumor is found in the adrenal gland, they are referred to as a pheochromocytoma .
Tumors of the paraganglionic tissues are known as paragangliomas, though this term tends to imply the nonchromaffin type, and can occur at a number of sites throughout the body. Chromaffin paragangliomas are issued from chromaffin cells, and are known as pheochromocytomas .
It can be the source of paraganglioma. [8]The organ of Zuckerkandl is of pathological significance in the adult as a common extra-adrenal site of pheochromocytoma though the most common extra-adrenal site is in the superior para-aortic region between the diaphragm and lower renal poles.
A gangliocytic paraganglioma is a rare tumour that is typically found in the duodenum and consists of three components: (1) ganglion cells, (2) epithelioid cells (paraganglioma-like) and, (3) spindle cells (schwannoma-like).
The criteria in 2024 included all patients with paraganglioma and all patients with unilateral pheochromocytoma aged under 60. [46] The most recent data indicates that there are 25 pheochromocytoma susceptibility genes; however, just 12 are recognized as part of a well-known syndrome. [ 9 ]
Ganglioneuroma (occasionally called a "ganglioma") is a rare and benign tumor of the autonomic nerve fibers arising from neural crest sympathogonia (undifferentiated cells of the sympathetic nervous system). [1]
M8680/3 paraganglioma, malignant M8681/1 Sympathetic paraganglioma M8682/1 Parasympathetic paraganglioma M8683/0 Gangliocytic paraganglioma (C17.0) M8690/1 Glomus jugulare tumor, NOS (C75.5) Jugular/jugulotympanic paranglioma; M8691/1 Aortic body tumor (C75.5) Aortic/aorticopulmonary paraganglioma; M8692/1 Carotid body tumor/paraganglioma (C75.4)
Mutations in the genes encoding alpha subunits of hypoxia-inducible factors (HIF-alpha) have not previously been identified in any cancer. [4]In the Pacak–Zhuang syndrome, patients have somatic gain of function mutations in the genes encoding for HIF2A, leading to prolonged HIF-2α activity and, thus, an increase in its half-life. [5]