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Liposarcoma

Liposarcomas are the most common subtype of soft tissue sarcomas, accounting for at least 20% of all sarcomas in adults. Soft tissue sarcomas are rare neoplasms with over 150 different histological subtypes or forms. Liposarcomas arise from the precursor lipoblasts of the adipocytes in adipose tissues. Adipose tissues are distributed throughout the body, including such sites as the deep and more superficial layers of subcutaneous tissues as well as in less surgically accessible sites like the retroperitoneum and visceral fat inside the abdominal cavity.

Etymology
"fatty tumor" (plural lipomata), 1830, medical Latin, from Greek lipos "fat" (n.), from PIE root *leip- "to stick, adhere", also used to form words for "fat", + -oma. 1650s, "fleshy excrescence", (plural liposarcomata), Medical Latin, from Latinized form of Greek sarkoma "fleshy substance" (Galen), from sarkoun "to produce flesh, grow fleshy", from sarx (genitive sarkos) "flesh", + -oma. ==Forms of liposarcomas==
Forms of liposarcomas
Liposarcomas are generally large tumors (>10 cm) but can be of almost any size. They occur mainly in adults with only 0.7% of cases occurring in those 5 cm), and painless but highly malignant adipocyte tumors. They occur primarily in individuals >50 years old chest wall, pelvic cavity, pulmonary pleurae, pericardium, and spine. mixed with areas containing undifferentiated cells. The undifferentiated component of these tumors most often consists of spindle-shaped cells, with 25% of cases showing cells with an epithelioid cell morphology. These tumors have at least some foci with a histopathology similar to high-grade myxofibrosarcoma type histiocytomas, a tumor formerly termed malignant myxoid fibrous histiocytoma. Genetics PLS neoplastic cells contain various gene and chromosome abnormalities: the TP53 gene is deleted or mutated in 17–60% of cases; the RB1 gene is deleted in 60% of cases; and the Neurofibromin 1 gene is lost by inactivating mutations in 8% of cases or in rarer cases by a deletion around its location in band 11.2 on the long arm of chromosome 12. These cells can also show gains in the genetic material around: bands 12–15 on the short arm of chromosome 5; band 21 on the short arm of chromosome 1; and band 22 on the long arm of chromosome 7. The alterations in gene copy numbers induced by these abnormalities are similar to those seen in the myxofibrosarcoma type of the histiocytomas. The role(s) of these changes in gene copy numbers in promoting PLS has not been defined. Thus, PLS is unlike other liposarcomas in that its neoplastic cells have a complex genome without characteristic genomic alterations or identifiable genes that drive the disease. Detection of alterations in the expression of the TP53, RB1, and neurofibromin 1 genes, as well as other, less commonly altered genes in PLS (e.g. PIK3CA, tyrosine-protein kinase SYK, PTK2B, EPHA5, and ERBB4), may help support but do not clearly define a tumor as being PLS.) was first described in a large 2009 study of the liposarcomas. While initially regarded as a possible variant of the myxoid liposarcomas with pleomorphic features, the World Health Organization (2020) classified it as a new and distinct form of the liposarcomas. This classification was based on findings that the myxoid pleomorphic liposarcomas, while having histopathological features that were similar to myxoid liposarcomas, had clinical and, most importantly, critical genetic and molecular features that differed from the myxoid as well as the other three liposarcoma forms. Pathology On histopathologic analyses, MPL tumors consist of areas resembling conventional myxoid liposarcoma; these areas, which represent 30–50% of the total tumor areas, have an abundant myxoid matrix, a well-developed capillary vasculature, bland cells that are round and/or slightly spindle-shaped, vacuolated lipoblasts, and multinucleated cells shaped like small flowers. However, these areas also contain a scattering of highly pleomorphic cells that show greater degrees of nuclear enlargement and irregularity than the cells seen myxoid liposarcoma tumors. Other areas of MPL tumors are more cellular and consist of rapidly growing and highly pleomorphic lipoblasts. a 2021 review found that there were no consensus recommendations for the standard of care for MPL with respect to radiation and chemotherapy regimens (when used either alone or combined with surgery) for treating these tumors. ==Histopathology of liposarcomas==
Histopathology of liposarcomas
File:Osseous formation in a well-differentiated liposarcoma.jpg|Fig. 1 Micrograph of bone formation in a liposarcoma tumor Image:Dedifferentiated liposarcoma - intermed mag.jpg|Fig. 2 Micrograph of a dedifferentiated liposarcoma tumor Image:Myxoid liposarcoma (01).jpg|Fig. 3 Lower-power micrograph of myxoid liposarcoma tumor File:Myxoid liposarcoma (06).JPG|Fig. 4 Higher-power micrograph of myxoid liposarcoma tumor ==Medical imaging==
Medical imaging
Medical ultrasonography and magnetic resonance imaging (MRI) of liposarcomas are helpful and often essential in determining their extent, surgical accessibility, and relationship to any observed organ dysfunctions. Since ultrasonography is usually unable to distinguish a liposarcoma from a benign lipoma, MRI is the initial imaging of choice to provide evidence relative to making this distinction. In myxoid liposarcoma, it shows low signal intensity mass with high signal intensity foci on T1-weighted MRI images. The mass shows high signal intensity on T2-weighted images. This is because it contains predominantly mucoid substance (accounts for low signal intensity on T1) and small amount of mature fat (accounts for high signal intensity on T1). The mass is well-defined, lobulated, multiloculated, or oval in shape without any infiltration into surrounding structures. Scrotal ultrasonography of liposarcoma mimicking a lipoma.jpg|Fig. 6 Ultrasonography of a liposarcoma mimicking a lipoma. This homogeneous high-echoic mass has the same appearance as a lipoma. HG mixoid liposarcoma, MRI, 2019, 10, 09.png|Fig. 7 MRI of myxoid liposarcoma of high grade, in the left axillary region of 40-year-old man, highlighted by its white color, in this horizontal section of the tumor. ==Society and culture==
Society and culture
Notable casesChad Brown (19612014), a poker player, died from liposarcoma • Richard Feynman (1918–1988), a theoretical physicist, died following surgery to address the disease. • Rob Ford (19692016), former Toronto mayor and Toronto city councillor, died of pleomorphic liposarcoma. • Hokie Gajan (19592016), former running back for the New Orleans Saints and radio color commentator for the team, died from liposarcoma. • Charlie Davies (born 1986), former soccer player for the Philadelphia Union of Major League Soccer, diagnosed with liposarcoma in 2016. • Mark Strand (19342014), former US Poet Laureate and Pulitzer Prize-winner, died from liposarcoma. ==See also==
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