An amplification of the MDM2 and CDK4 genes respectively in the atypical lipomatous tumor/well-differentiated liposarcoma areas was detected by fluorescence in situ hybridization (FISH) analysis, and translocations of the CHOP and FUS genes were detected by FISH analysis in the myxoid/round cell liposarcoma areas.
An amplification of the MDM2 and CDK4 genes respectively in the atypical lipomatous tumor/well-differentiated liposarcoma areas was detected by fluorescence in situ hybridization (FISH) analysis, and translocations of the CHOP and FUS genes were detected by FISH analysis in the myxoid/round cell liposarcoma areas.
An established myxoid liposarcoma avian chorioallantoic membrane model was used for <i>in vivo</i> confirmation of the preclinical <i>in vitro</i> results.<b>Results:</b> A comprehensive subset of myxoid liposarcoma specimens showed elevated expression and phosphorylation levels of various IGF-IR/PI3K/Akt signaling effectors.
An established myxoid liposarcoma avian chorioallantoic membrane model was used for <i>in vivo</i> confirmation of the preclinical <i>in vitro</i> results.<b>Results:</b> A comprehensive subset of myxoid liposarcoma specimens showed elevated expression and phosphorylation levels of various IGF-IR/PI3K/Akt signaling effectors.
An established myxoid liposarcoma avian chorioallantoic membrane model was used for <i>in vivo</i> confirmation of the preclinical <i>in vitro</i> results.<b>Results:</b> A comprehensive subset of myxoid liposarcoma specimens showed elevated expression and phosphorylation levels of various IGF-IR/PI3K/Akt signaling effectors.
An established myxoid liposarcoma avian chorioallantoic membrane model was used for <i>in vivo</i> confirmation of the preclinical <i>in vitro</i> results.<b>Results:</b> A comprehensive subset of myxoid liposarcoma specimens showed elevated expression and phosphorylation levels of various IGF-IR/PI3K/Akt signaling effectors.
An established myxoid liposarcoma avian chorioallantoic membrane model was used for <i>in vivo</i> confirmation of the preclinical <i>in vitro</i> results.<b>Results:</b> A comprehensive subset of myxoid liposarcoma specimens showed elevated expression and phosphorylation levels of various IGF-IR/PI3K/Akt signaling effectors.
By the use of patient-derived and established cell lines from liposarcoma, as well as specimens from patient biopsies, we found that HMGA1 is involved in the progression of dedifferentiated and myxoid liposarcoma.
C/EBPzeta, also known as GADD153, CHOP10, and DDIT3 has been found associated with the development of myxoid liposarcoma and the progression of melanoma.
Chromosomal translocations of t(12,16) (q13;p11) and t(12;22) (q13;q12), rendering gene fusions of DDIT3 (previously CHOP) with FUS and EWSR1, have been found to be characteristic of myxoid liposarcoma, and were identifiable in more than 95% cases.
Circumstantial evidence suggests that genetic changes may lead to tumor progression within the myxoid liposarcoma tumors (MLTs) carrying non-random chromosomal translocation t(12;16).
Described here is the use of detecting TLS/FUS-CHOP fusion transcripts to confirm the diagnosis of a myxoid liposarcoma by nested reverse transcription-polymerase chain reaction assay using archival formalin-fixed, paraffin-embedded tissues of a young man with a benign-looking myxoid tumor on his upper extremity, which is often misdiagnosed clinically or histopathologically as a benign tumor.
Described here is the use of detecting TLS/FUS-CHOP fusion transcripts to confirm the diagnosis of a myxoid liposarcoma by nested reverse transcription-polymerase chain reaction assay using archival formalin-fixed, paraffin-embedded tissues of a young man with a benign-looking myxoid tumor on his upper extremity, which is often misdiagnosed clinically or histopathologically as a benign tumor.
Despite high expression of immunogenic cancer-testis antigens, synovial sarcoma (SS) and myxoid/round cell liposarcoma (MRCL) have a cold tumor microenvironment (TME), with few infiltrating T cells and low expression of major histocompatibility complex class I (MHC-I).
Distinct chromosomal translocations have been identified in several myxoid sarcomas, including t(12;16)(q13;p11) FUS-DDIT3 in myxoid liposarcoma, t(7;16)(q34;p11) FUS-CREB3L2 in low-grade fibromyxoid sarcoma, and t(9;22)(q31;q12) EWSR1-NR4A3 in extraskeletal myxoid chondrosarcoma.