The Molecular Basis of the Liposarcoma Disease

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Researchers attempt to identify molecular changes that cause the development of liposarcomas. This knowledge is important for the prevention and treatment of this disease. An important characteristic of this sarcoma is the presence of giant rod chromosomes and supernumerary ring (Miettinen, 2010, p. 115). This attribute is particularly typical of well-differentiated liposarcoma (Miettinen, 2010, p. 115). Moreover, this chromosome includes different oncogenes such as HMGA2, MDM2, OS1, and some others. In particular, the amplification of MDM2 is associated with an increased risk of liposarcoma. In addition to that, CDK4 is also amplified during this disease (Conyers, Young, & Thomas 2011, p. 3). Researchers pay attention to the important role that this gene plays in the cell cycle. Overall, it is believed that well-differentiated liposarcoma can be trigged by different molecular mechanisms. This is one of the main challenges that have not been overcome yet.

Furthermore, it is possible to speak about myxoid liposarcoma that occurs primarily in deep soft tissues (Pfeifer 2006, p. 209). It is characterized by the fusion of the FUS-CHOP gene. Additionally, FUS can be fused with EBP protein. Researchers conjecture that these translocations also lead to the formation of oncogenes (Conyers, Young, & Thomas 2011, p. 3). One should note that mice that have fused FUS-CHOP gene can also have liposarcomas.

Currently, researchers rely on such as a technique as interphase FISH (fluorescence in situ hybridization) since it is useful for detecting possible translocations of genes (Pfeifer 2006, p. 209). Moreover, the patients, who have myxoid liposarcoma, have PIK3CA mutations (Conyers, Young, & Thomas 2011, p. 3). These are some of the main findings. Nevertheless, it is difficult to identify a single underlying cause of this disease.

Finally, one can speak about pleomorphic liposarcoma. This disorder is also accompanied by genetic modifications. In particular, it is possible to mention the loss of such chromosomes as 13p14 and 12p13 (Conyers, Young, & Thomas 2011, p. 5). However, the main limitation is that pleomorphic liposarcoma is not very widespread, and there are not many molecular studies of this disease. At present, researchers try to develop effective mouse models because such models can help them better understand the pathogenesis of this disease. On the whole, by understanding the molecular basis of liposarcomas, researchers can develop more effective treatments of this disease. For example, one can speak about MDM2 inhibitors. These are some of the main benefits that can be identified.

References

Conyers, R, Young, S & Thomas, D 2011, ‘Liposarcoma: Molecular Genetics and Therapeutics’, Sarcoma, vol. 20, no. 1, pp. 1-13. Web.

Miettinen, M 2010, Modern Soft Tissue Pathology: Tumors and Non-Neoplastic Conditions, Cambridge University Press, Cambridge. Web.

Pfeifer, J 2006, Molecular Genetic Testing in Surgical Pathology, Lippincott Williams & Wilkins, New York. Web.

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