Liposarcoma: Advances in Cellular and Molecular Genetics Alterations and Corresponding Clinical Treatment

Abstract

Liposarcoma is a malignant tumor of mesenchymal origin with significant tissue diversity. It is composed of adipocytes with different degrees of differentiation and different degrees of heteromorphosis. It is not sensitive to traditional radiotherapy and chemotherapy and has a poor prognosis. In recent years, with the rapid development of basic immunology, molecular genetics and tumor molecular biology, the histological classification of liposarcoma has become increasingly clear. More and more new methods and technologies, such as gene expression profile analysis, the whole genome sequencing, miRNA expression profile analysis and RNA sequencing, have been successfully applied to liposarcoma, bringing about a deeper understanding of gene expression changes and molecular pathogenic mechanisms in the occurrence and development of liposarcoma. This study reviews the present research status and progress of cellular and molecular alterations of liposarcoma and corresponding clinical treatment progress.

Diagnosis and Prognosis of Retroperitoneum Liposarcoma: a single Asian center cohort of 57 cases

“…WDLPS is the most common retroperitoneal LPS, accounting for 40-45% of all LPS. [2,[7][8][9] Gene ampli cation in 12q12-21 and 10p11-14 is often spotted in WDLPS and DLPS, and DLPS has an additional gene ampli cation in 6q23 and 1p32. [8,10] Also, WDLPS has about 10% probability to convert into DLPS, a more invasive subtype of LPS.…”

“…[2,[7][8][9] Gene ampli cation in 12q12-21 and 10p11-14 is often spotted in WDLPS and DLPS, and DLPS has an additional gene ampli cation in 6q23 and 1p32. [8,10] Also, WDLPS has about 10% probability to convert into DLPS, a more invasive subtype of LPS. [8] Approximately 95% of MLPS patients have a t(12;16)(q13;p11) reciprocal chromosomal translocation resulting in an in-frame fusion of fused in sarcoma (FUS) to DNA damage inducible transcript 3 (DDIT3), and the remaining 5% patients exhibit a t(12;22)(q13;q12) translocation.…”

“…[8,10] Also, WDLPS has about 10% probability to convert into DLPS, a more invasive subtype of LPS. [8] Approximately 95% of MLPS patients have a t(12;16)(q13;p11) reciprocal chromosomal translocation resulting in an in-frame fusion of fused in sarcoma (FUS) to DNA damage inducible transcript 3 (DDIT3), and the remaining 5% patients exhibit a t(12;22)(q13;q12) translocation. [8,11] For PLPS, the rarest case among all subtypes, there is so far no constant chromosomal aberration or molecular alternation reported.…”

“…[8] Approximately 95% of MLPS patients have a t(12;16)(q13;p11) reciprocal chromosomal translocation resulting in an in-frame fusion of fused in sarcoma (FUS) to DNA damage inducible transcript 3 (DDIT3), and the remaining 5% patients exhibit a t(12;22)(q13;q12) translocation. [8,11] For PLPS, the rarest case among all subtypes, there is so far no constant chromosomal aberration or molecular alternation reported. [8] Diagnosis of LPS is currently highly dependent on pathological ndings, with CT or magnetic resonance imaging (MRI) responsible for the majority of pre-surgical diagnoses.…”

“…[8,11] For PLPS, the rarest case among all subtypes, there is so far no constant chromosomal aberration or molecular alternation reported. [8] Diagnosis of LPS is currently highly dependent on pathological ndings, with CT or magnetic resonance imaging (MRI) responsible for the majority of pre-surgical diagnoses. [11,12] Since many liposarcomas can be asymptotic before diagnosis, and symptoms, if there are any, are mainly nonspeci c such as abdominal pain or distention, pre-operative diagnosis for LPS is di cult.…”