A myxoid liposarcoma is a malignant adipose tissue neoplasm of myxoid appearance histologically. Myxoid liposarcomas are the second-most common type of liposarcoma, representing 30–40% of all liposarcomas in the limbs, occurring most commonly in the legs, particularly the thigh, followed by the buttocks, retroperitoneum, trunk, ankle, proximal limb girdle, head and neck, and wrist. They occur in the intermuscular fascial planes or deep-seated areas. They present as a large, slow-growing, painless mass.The neoplastic cells in these neoplasms contain chromosomal translocations which create one of two fusion genes: the FUS-DDIT3 in ~90% and the EWSR1-DDIT3 fusion gene in up to 10% of myxoid liposarcoma cases. The FUS-DDIT3 fusion gene forms by a merger of part of the FUS FET gene family gene normally located at band 11.2 on the short (or "p") arm of chromosome 16 with part of the DDIT3 ETS transcription factor family gene normally located at band 13.3 on the long (or "q") arm of chromosome 12. This fusion gene is notated as t(12;16)(q13;p11). Preclinical studies, i.e. laboratory studies, suggest that the FUS-DDIT3 fusion gene may act as an oncogene to promote the development of myxoid liposarmas. The EWSR1-DDIT3 fusion gene forms by a merger of the EWSR1 FET gene family gene located at band 12.2 on the q arm of chromosome 22 with part of the DDIT3 gene. This fusion gene is notated as t(12;22)(q13;12). Additional images
See also
Lipoma
Trabectedin

References
External links
Myxoid liposarcoma: a rare soft-tissue tumor with a misleading benign appearance
Efficacy of first-line doxorubicin and ifosfamide in myxoid liposarcoma. 2012
This is a controversial point, some assign COX 1 as the major prostacyclin producing cyclooxygenase in the endothelial cells of the blood vessels.The series-3 prostaglandin PGH3 also follows the prostacyclin synthase pathway, yielding another prostacyclin, PGI3. The unqualified term prostacyclin usually refers to PGI2. PGI2 is derived from the ω-6 arachidonic acid. PGI3 is derived from the ω-3 EPA. Artificial synthesis
Prostacyclin can be synthesized from the methyl ester of prostaglandin F2α. After its synthesis, the drug is reconstituted in saline and glycerin.Because prostacyclin is so chemically labile, quantitation of their inactive metabolites, rather than the active compounds, is used to assess their rate of synthesis. History
During the 1960s, a UK research team, headed by Professor John Vane, began to explore the role of prostaglandins in anaphylaxis and respiratory diseases. Working with a team from the Royal College of Surgeons, Vane discovered that aspirin and other oral anti-inflammatory drugs work by inhibiting the synthesis of prostaglandins. This critical finding opened the door to a broader understanding of the role of prostaglandins in the body. A team at The Wellcome Foundation led by Salvador Moncada had identified a lipid mediator they called "PG-X," which inhibits platelet aggregation. PG-X, later known as prostacyclin, is 30 times more potent than any other then-known anti-aggregatory agent. They did this while searching for an enzyme that generates a fellow unstable prostanoid, Thromboxane A2In 1976, Vane and fellow researchers Salvador Moncada, Ryszard Gryglewski, and Stuart Bunting published the first paper on prostacyclin in  Nature.