Disease relevance of Liposarcoma

• The human NAB2 gene has been localized to chromosome 12ql3.3-14.1, a region that is rearranged in several solid tumors, lipomas, uterine leiomyomata, and liposarcomas [1].
• Seven of 22 (32%) malignant fibrous histiocytomas and three liposarcomas contained SAS amplification [2].
• Our findings indicate that in liposarcomas TLS/FUS-CHOP fusion transcripts have variations at the junction of chimeric messages, which was the case for Ewing's sarcoma [3].
• Four MFHs and nine other types of sarcoma (four leiomyosarcomas, two chondrosarcomas, one liposarcoma, one fibrosarcoma, and one dermatofibrosarcoma protuberans) showed nuclear positivity for p53 [4].
• RASSF1A hypermethylation was detected in 17 of 84 (20%) STSs; however, methylation was more frequent in leiomyosarcomas (39%) compared to MFHs (6%; p < 0.015) and liposarcomas (18%) [5].

High impact information on Liposarcoma

• Fusion of the dominant negative transcription regulator CHOP with a novel gene FUS by translocation t(12;16) in malignant liposarcoma [6].
• No anti-OS antibody activity was found in sera from healthy individuals or patients with breast carcinoma, clear cell liposarcoma, or leukemia in this study [7].
• RESULTS: beta-Catenin physically interacted with fusion (FUS)/translocated in liposarcoma (TLS) and various RNA-binding proteins [8].
• We have conducted a clinical trial for treatment of patients with advanced liposarcoma by using the peroxisome proliferator-activated receptor-gamma ligand troglitazone, in which extensive correlative laboratory studies of tumor differentiation were performed [9].
• We report here the results of three patients with intermediate to high-grade liposarcomas in whom troglitazone administration induced histologic and biochemical differentiation in vivo [9].

Chemical compound and disease context of Liposarcoma

• Terminal differentiation of human liposarcoma cells induced by ligands for peroxisome proliferator-activated receptor gamma and the retinoid X receptor [10].
• Moreover, primary human liposarcoma cells can be induced to undergo terminal differentiation by treatment with the PPAR gamma ligand pioglitazone, suggesting that the differentiation block in these cells can be overcome by maximal activation of the PPAR pathway [10].
• CONCLUSIONS: In patients with large, high-grade, primary extremity liposarcoma; DOX is not associated with improved DSS and IF is associated with an improved DSS [11].
• These animals consistently show the accumulation of a glycoprotein material within the terminally differentiated adipocytes, a characteristic figure of liposarcomas associated with FUS-CHOP [12].
• Effect of treatment with interferon and cyclophosphamide on the growth of a spontaneous liposarcoma in rats [13].
• In the present study, we assessed the reproducibility of APB detection on frozen versus formalin-fixed, paraffin-embedded specimens from the same liposarcoma specimens and investigated the eventual stability of ALT in 103 different lesions from 40 adult patients followed during their disease [14].

Biological context of Liposarcoma

• Chimeric TLS/FUS-CHOP gene expression and the heterogeneity of its junction in human myxoid and round cell liposarcoma [3].
• The most common chromosomal translocation in liposarcomas, t(12;16)(q13;p11), creates the FUS-CHOP fusion gene [15].
• This subtype of liposarcoma contains the specific t(12;16) chromosomal translocation, which results in rearrangement of the TLS and CHOP genes that is clone specific at the DNA level [16].
• MDM2 and CDK4 gene amplification was detected in 2.8% and 5.6% of lipomas and 98.2% and 82.4% of liposarcomas, respectively [17].
• Significance of loss of heterozygosity of the RB1 gene during tumour progression in well-differentiated liposarcomas [18].

Anatomical context of Liposarcoma

• Furthermore, using FUS-CHOP fusion transcripts as targets in reverse transcription-PCR assays, we detected disseminated tumor cells in peripheral blood or bone marrow in 3 of 5 patients undergoing surgery for soft tissue liposarcoma [19].
• Human liposarcoma cell line, SW872, secretes cholesteryl ester transfer protein in response to cholesterol [20].
• Tyrosinase RNA was also detected in neoplastic samples including benign cutaneous nevi, lymph nodes involved by MM, breast carcinoma, liposarcoma, malignant lymphoma, and schwannoma [21].
• The results show a high incidence of cytosolic estrogen and glucocorticoid receptors in tumors of adipose tissue origin except in lipoma and well differentiated liposarcoma [22].
• The possible involvement in these tumors of the rare folate-sensitive fragile site 12q13.1 has been investigated in PHA-stimulated peripheral blood cells from three patients carrying the t(12;16)(q13;p11) in their liposarcoma cells and one patient with the t(3;12)(q28;q14) in his lipoma cells [23].

Gene context of Liposarcoma

• In contrast with the rare involvement of the TP53 gene in well differentiated liposarcoma, aberrations of the TP53 gene were observed in approximately 30% of cases of myxoid and round cell liposarcoma [24].
• Evaluation of MDM2 and CDK4 amplification by real-time PCR on paraffin wax-embedded material: a potential tool for the diagnosis of atypical lipomatous tumours/well-differentiated liposarcomas [17].
• We found that monensin treatment or energy depletion of the SW872 liposarcoma cells with 2-deoxyglucose and NaN3 had no effect on CETP-mediated selective uptake, demonstrating that endocytosis is not required [25].
• Translocated in liposarcoma (TLS) is a substrate for fibroblast growth factor receptor-1 [26].
• LRP was strongly expressed in MFH and unspecified sarcomas, but was low in liposarcomas [27].
• These results provide new insight into the mechanism of NFV-mediated induction of ER stress and cell death in liposarcomas and are the first to report targeting S2P for cancer therapy [28].

Analytical, diagnostic and therapeutic context of Liposarcoma

• Immunohistochemistry showed positivity of tumour cells for MDM2 in every tumour in both groups and for CDK4 in ten and seven inflammatory MFHs and dedifferentiated liposarcomas, respectively [29].
• We performed C-banding, fluorescence in situ hybridization, and immunostaining with anti-centromere antibodies in 8 cases of liposarcomas with supernumerary rings and large markers, including 5 ALP-WDLPS and 3 dedifferentiated-LPS and high-grade LPS [30].
• MATERIALS AND METHODS: In the human liposarcoma cell line, SW872, we analyzed the expression of S100A4 protein by immunohistochemistry and flow cytometry [31].
• Iodine-123 BMIPP and Ga-67 scintigraphy in liposarcoma [32].
• This case report describes the features of gadolinium-enhanced MRI in well-differentiated liposarcoma with histologic correlation and addresses the usefulness of this imaging technique in distinguishing well-differentiated liposarcoma from lipoma [33].

References