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PubMed1996

The clinicopathologic spectrum of myxoid and round cell liposarcoma. A study of 95 cases.

BACKGROUND: The prognosis of patients with myxoid liposarcoma (ML) or round cell liposarcoma (RCL) has never been adequately defined. METHODS: We evaluated the clinical and pathologic features of 95 patients with biopsy proven ML or RCL examined at the Mayo Clinic between 1971 and 1992. Routine hematoxylin and eosin stained slides of all cases were reviewed. Morphologic variable evaluated included percent of round cell differentiation, percent of lipoblastic differentiation, and presence of tumor necrosis. Clinical follow-up was available for 86 patients (range: 6 months-23.4 years; mean: 7.2 years; median: 5.9 years). Flow cytometry for determination of DNA ploidy was performed on paraffin embedded tissue available from 46 cases. Survival analyses for the 86 patients with adequate clinical follow-up were performed by the Kaplan-Meier test using the approximate chi-square statistic for the log rank test. RESULTS: Age at diagnosis ranged from 16 to 81 years (median: 44 years). The extremities were involved in 91 cases, the retroperitoneum in 3 cases, and the perineum in 1 case. The single most common location was the thigh (61 cases). Histologically, round cell differentiation was present in 41 cases (43%) ranging from 5% to 100% of the tumor volume. Only one case of "pure" RCL was used in the study. Spontaneous tumor necrosis was noted in 4 cases. By flow cytometry, 38 tumors were diploid, 6 were aneuploid, and 1 was tetraploid. The data from 1 case was uninterpretable. Thirty patients (35%) developed metastasis; 27 (31%) died from the disease. CONCLUSIONS: With multivariate analysis, age ( > 45 years), percent of round cell differentiation ( > or = 25%), and the presence of spontaneous tumor necrosis are significantly associated with a poor prognosis. No correlation was observed between DNA ploidy (i.e., diploid vs. aneuploid) and percent of round cell differentiation or clinical outcome.

Adipocytes↗
PubMed1999

Identification of genes differentially expressed in TLS-CHOP carrying myxoid liposarcomas.

Myxoid liposarcomas (MLS) carry a t(12;16) or, more rarely, a t(12;22) resulting in fusion of the transcription factor gene CHOP on chromosome 12 with TLS/FUS on chromosome 16 or EWS on chromosome 22. The chimeric TLS-CHOP or EWS-CHOP proteins most probably function as abnormal transcription factors, causing transcriptional de-regulation of several target genes and relaxation of functions critical for growth and differentiation control. A PCR-based subtractive hybridization technique was used to identify genes that are differentially expressed in TLS-CHOP-carrying MLS but not in normal fat tissue. Six myxoid-liposarcoma-associated transcripts, MLAT, were isolated. The genes identified as MLAT can be divided into 2 groups. MLAT1, 2 and 6 show high similarity to glia-derived nexin, neuronatin and the RET oncogene, respectively, all normally involved in development of tissues of neural origin. MLAT3 to MLAT5 represent new genes.

CCAAT-Enhancer-Binding Proteins↗
PubMed1996

Genomic PCR detects tumor cells in peripheral blood from patients with myxoid liposarcoma.

Myxoid liposarcoma (MLS) is the most common subtype of liposarcoma. The cytogenetic hallmark of MLS is the pathognomonic t(12;16)(q13;p11), present in more than 85% of cases. The translocation leads to the fusion of the CHOP and FUS genes at 12q13 and 16p11, respectively, and the generation of a FUS/CHOP hybrid protein. The presence of a tumor-specific chimeric gene makes it possible to identify MLS cells by polymerase chain reaction (PCR). We have analyzed peripheral blood samples obtained during a 10-year period at diagnosis of primary and/or recurrent disease in 19 MLS patients with t(12;16) and in one MLS patient with t(12;22;20), resulting in the fusion of the CHOP and EWS genes. Nested PCR on genomic DNA from blood samples amplified FUS/CHOP hybrid fragments in three patients and EWS/CHOP in the patient with t(12;22;20). There was no obvious association between PCR findings and clinical outcome, but larger series are needed to draw any firm conclusions.

Adult↗
PubMed2001

Sonographic appearance of primary liver liposarcoma.

Primary malignant mesenchymal tumors of the liver are extremely rare. We report a case of a primary liposarcoma in the right hepatic lobe of a 50-year-old man. Sonography showed a poorly defined, lobulated, infiltrating echogenic tumor with shadowing. Within the tumor were hyperechoic and hypoechoic foci thought to represent areas of hemorrhage and necrosis. Color Doppler sonography showed the mass to be avascular. A low-attenuation mass of fat density was confirmed on CT. The resected tumor was reasonably well circumscribed, with demonstrable infiltration of the liver parenchyma. Histologic analysis showed liposarcoma with high-grade sarcomatous features.

Humans↗
PubMed1978

Ultrastructural observations in pleomorphic liposarcoma.

An ultrastructural study of pleomorphic liposarcoma with an unusual clinical presentation is described. A 69-year-old Caucasian female presented with recurrent superficial phlebitis of left leg, which responded only partially to conventional therapy. Following investigations, a mass was excised. Diagnosis of pleomorphic liposarcoma was made on microscopic examination. Numerous lipid droplets in the cytoplasm and often within intranuclear extensions of cytoplasm were seen on oil red O stain of frozen sections. Ultrastructural features are quite distinctive. The cells varied from small to often large pleomorphic cells with numerous lipid spaces without limiting membrane, large pleomorphic nuclei, and an abundance of cytoplasmic organelles. Centrioles were very prominent, in close proximity to nuclei, and collections of autophagocytic inclusions. Intercellular collagen was immature and scant. These features are compared to ultrastructural features of malignant fibrous histiocytoma, pleomorphic rhabdomyosarcoma, and cardiac myxoma, indicating that ultrastructural features are distinctive and help differentiate similar soft tissue tumors.

Aged↗
PubMed1981

Computed tomography in liposarcoma.

Seventeen cases with proven liposarcoma were evaluated by computed tomography (CT) to assess the specificity and value of this radiographic modality. A specific diagnosis of liposarcoma could be made in only four cases (22%). Despite its relative nonspecificity, CT proved extremely useful in the clinical evaluation of this tumor and evidenced considerable superiority to other radiographic methods. In several cases, CT was the only radiographic modality to demonstrate the presence of the lesion. The use of CT gained additional important information in approximately 50% of the cases studied.

Adult↗
PubMed1987

Liposarcoma of the musculoskeletal system.

Two hundred eleven cases with the diagnosis of liposarcoma of the musculoskeletal system were reviewed. The mean age at diagnosis was 52.9 years. The primary site was the proximal lower extremity in 52%. Myxoid-type liposarcoma was most frequent (60%). Metastasis was observed in 45%. One hundred two patients without prior treatment or distant spread at diagnosis were studied separately. Recurrence was noted in 26%. The median survival time was 7.5 years, with a 5-year survival of 59% and a 10-year survival of 45%. Significant variation in survival time was related to histologic grade, Enneking's stage, tumor size, and histologic type.

Adolescent↗
PubMed1994

Myxoid liposarcoma. Experience with chemotherapy.

BACKGROUND: Myxoid liposarcoma (ML) is the most common type of liposarcoma. It has been classified as an intermediate grade tumor with a definite metastatic potential but a relatively indolent natural history. Little is known about its sensitivity to chemotherapy. METHOD: The authors reviewed their experience with chemotherapy in ML from 1986 to 1992. The patient population was identified through a search of the database maintained by the Department of Melanoma-Sarcoma Medical Oncology of the M.D. Anderson Cancer Center. RESULTS: Forty-four patients each with a histologically confirmed diagnosis of ML were identified. Twenty-one were treated with chemotherapy. The median age was 45 years (31-69 years); there were 14 men and 7 women. The ML in 19 patients was in the lower extremity, one in the head and neck, and one pelvic. The median size of the primary tumor was 15 cm (range, 7-48 cm) in maximum dimension. Of the 18 patients who received doxorubicin- and dacarbazine-based chemotherapy as a frontline regimen [median of 3 (2-9) cycles] and were evaluable for response, 8 (1 completed response, 7 partial responses) achieved an objective response (44%, 95% confidence interval 21-67%). Two of the remaining three patients who were also treated with a similar regimen were not evaluable for response (one received chemotherapy postoperatively, and the other received concomitant radiation and doxorubicin), and the third patient received ifosfamide as frontline chemotherapy because of a significant cardiac history. Seven patients received chemotherapy in the neoadjuvant setting, 13 for recurrent or metastatic disease, and 1 postoperatively after complete tumor resection. At the last follow-up, 10 patients were alive with no evidence of disease, 3 were alive with disease, and 8 had died. The median follow-up was 51 months (range, 6-199 months) from diagnosis. CONCLUSION: The authors conclude that doxorubicin- and dacarbazine-based chemotherapy is effective in the treatment of ML.

Adult↗
PubMed2003

Fine-needle aspiration smears from lipomatous hemangiopericytoma need not be confused with myxoid liposarcoma.

Lipomatous hemangiopericytoma (LHPC) is a rare benign soft tissue tumor that may mimic soft tissue sarcoma clinically. Despite the fact that LHPC shares most of the histologic features with solitary fibrous tumor, it may be occasionally misdiagnosed as myxoid liposarcoma or some other type of spindle-cell sarcoma. While some studies have addressed the histological features and origin of LHPC, no reports of cytological findings have been published. The author describes the cytological features of LHPC in two patients with correlations to histological and clinical findings. One of aspirates was misdiagnosed as being myxoid liposarcoma, while the other one was correctly diagnosed by a combination of FNAB and core needle biopsy (CNB). Cytological evaluation of LHPC can be problematic due to its rarity and to its similarity with other spindle-cell or fatty tumors. Correct diagnosis requires an awareness of cytologic features of this rare tumor and the use of ancillary studies.

Adipocytes↗
PubMed2001

Ectopic sequences from truncated HMGIC in liposarcomas are derived from various amplified chromosomal regions.

The HMGIC gene codes for an architectural transcription factor frequently rearranged by translocation in lipomas and other benign mesenchymal tumors. In sarcomas, malignant tumors of mesenchymal origin, the gene is also found to be rearranged, but in addition amplified and overexpressed. Here we report the sequence, chromosomal localization, and expression patterns of 11 novel ectopic sequences fused to exons 2 and 3 of HMGIC in seven different sarcoma samples. In addition, we identified a number of variant transcripts observed previously in benign tumors. Consistent with the suggested role of HMGIC in adipocytic differentiation, most of the novel ectopic sequences were observed in well-differentiated liposarcomas. These tumors are known to have complex marker chromosomes containing amplified segments from several chromosomes. Five novel sequences were derived from 12q14-q15, where HMGIC resides, two from 1q24, a region frequently amplified in these types of tumors, two from 11q14, and one from chromosome 2. All except one of the aberrant transcripts encoded truncated proteins with intact DNA-binding domains (AT hooks) but lacking the C-terminal acidic region, a target for constitutive phosphorylation by protein kinase CK2. Some of the ectopic sequences were transcribed in other tissues, and most of the ectopic sequences also showed recurrent amplification in liposarcomas.

Amino Acid Sequence↗
PubMed1992

Rearrangement of the transcription factor gene CHOP in myxoid liposarcomas with t(12;16)(q13;p11).

Most myxoid liposarcomas (MLS) are characterized cytogenetically by a t(12;16)(q13;p11). It is reasonable to assume that this translocation corresponds to the consistent rearrangement of one or two genes in 12q13 and/or 16p11, and that the loci thus affected are important in the normal control of fat cell differentiation and proliferation. We have used Southern blot technique to test whether a gene of the CCAAT/enhancer binding protein (C/EBP) family, CHOP, which maps to 12q13 and is assumed to be involved in adipocyte differentiation, could be the 12q gene in question. Using a cDNA probe that spans the CHOP coding region, we detected one rearranged and one wild type allele in nine of nine MLS with t(12;16). Using PCR generated, site-specific probes corresponding to the non-coding exons 1 and 2 and intron 2 of CHOP, rearrangements in five of seven tumors mapped to the 2.4 and 1.6 kbp PstI fragments that contain the first two exons and introns of the gene and the upstream promoter region. In contrast to the findings in MLS, no tumor without a t(12;16) exhibited aberrant CHOP restriction digest patterns. These tumors included one highly differentiated liposarcoma with abnormal karyotype but no involvement of 12q13, seven lipomas with various cytogenetic aberrations of 12q13-15, two uterine leiomyomas with t(12;14) (q14-15;q23-24), and one hemangiopericytoma and one chondroma, both of which also had 12q13 changes.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1993

The 12q13-q15 translocation breakpoints in pleomorphic adenoma and clear-cell sarcoma of tendons and aponeuroses are different from that in myxoid liposarcoma.

The transcription factor gene CHOP was recently shown to be rearranged in myxoid liposarcoma with t(12;16)(q13;p11). We have analyzed whether the CHOP gene is the target of rearrangements in pleomorphic adenoma and clear-cell sarcoma of tendons and aponeuroses with chromosome abnormalities of 12q13-q15. Restriction fragment analysis showed that the CHOP gene and its flanking sequences were not rearranged in any of these tumor types, indicating that the 12q translocation breakpoints in pleomorphic adenoma and clear-cell sarcoma are different from that in myxoid liposarcoma.

Adenoma↗
PubMed1994

Complex composition and co-amplification of SAS and MDM2 in ring and giant rod marker chromosomes in well-differentiated liposarcoma.

Extra abnormal chromosomes (rings and giant rods) containing chromosome 12 sequences are characteristic of well-differentiated liposarcoma (WDLPS). By whole chromosome painting we found in 6 WDLPS that minimally 5 chromosomes had contributed to the formation of the extra abnormal chromosomes. To the constant chromosome 12 contribution, sequences were variably added from chromosomes 1, 4, and 16. Material from chromosomes 1, 4, and 12 was identified by painting in interphase nuclear projections ("blebs") and in micronuclei consistent with the concept that blebs are precursors to micronuclei. The complexity of the mechanisms generating the extra abnormal chromosomes in WDLPS was also attested to by the diversity and, in some cases, intricacy of the patterns of fluorescence. To begin to fathom the function of the extra abnormal chromosomes we examined the amplification of genes, including SAS, MDM2, and GADD153/CHOP, known to be in the region 12q13-14. SAS and MDM2 demonstrated constant co-amplification. GADD153/CHOP, which is critically rearranged in myxoid liposarcoma, was not amplified in WDLPS.

Aged↗
PubMed2001

Analysis of the molecular species generated by MDM2 gene amplification in liposarcomas.

MDM2 gene is overexpressed in several tumors and its product may be processed into different isoforms, some of which have been demonstrated to possess transforming activity. In a panel of liposarcomas characterized by displaying 4 different combinations of mdm2/p53 immunoreactivity, molecular analysis of amplified MDM2 gene revealed a coexistence of mutated full-length MDM2 messenger RNAs, an out-of-frame splicing mRNA and finally aberrant spliced forms. Two of the latter are reported here for the first time. The molecular differences in this heterogeneous mRNA population seem to mirror distinct functional aspects of the altered encoded mdm2 proteins. In fact, besides the deleted transcripts defective in their ability to bind p53 and known to possess a transforming activity, here we describe both mutated full-length forms and deleted transcripts that still maintain the ability to bind p53 but, based on their mdm2+/p53+ immunophenotype, probably fail to signal its degradation. These aberrant forms, which are responsible for the accumulation and inactivation of p53, can contribute, together with the p53 independent transforming forms, to liposarcoma transforming pathway.

Abdominal Neoplasms↗
PubMed2002

The myxoid liposarcoma specific TLS-CHOP fusion protein localizes to nuclear structures distinct from PML nuclear bodies.

CHOP in 12q13, also called GADD153 or DDIT3, encodes a transcription factor of the C/EBP type. As a result of t(12;16) translocations, CHOP is rearranged and fused to TLS in 16p11 in about 90% of myxoid liposarcomas/round cell liposarcomas (MLS/RCLS). The TLS-CHOP protein consists of the N-terminal half of TLS juxtaposed to the N-terminal of the entire CHOP. It is capable of forming dimers with the natural dimer partners of CHOP. Here we report that recombinant TLS-CHOP-green fluorescence protein localizes to nuclear structures, similar to, but distinct from, PML nuclear bodies. The TLS-CHOP-green fluorescent protein nuclear structures are resistant to high salt concentration and nuclease treatment. Transfection of TLS-CHOP to normal fibroblasts causes a rapid down regulation and relocation of PML nuclear bodies. An abnormal extra nuclear localization of PML bodies was also found in TLS-CHOP carrying cell lines established from myxoid liposarcomas. Transfection of TLS-CHOP induced a rapid disappearance of PCNA. TLS-CHOP may disturb the nuclear machinery by binding and sequestering important factors from their natural sites.

Animals↗
PubMed2005

Myxoid liposarcoma FUS-DDIT3 fusion oncogene induces C/EBP beta-mediated interleukin 6 expression.

The myxoid/round cell liposarcoma oncogene FUS-DDIT3 is the result of a translocation derived gene fusion between the splicing factor FUS and DDIT3. In order to investigate the downstream targets of DDIT3, and the transforming effects of the FUS-DDIT3 fusion protein, we have introduced DDIT3-GFP and FUS-DDIT3-GFP constructs into a human fibrosarcoma cell line. The gene expression profiles of stable transfectants were compared to the original fibrosarcoma cell line by microarray analysis. We here report that the NFkappaB and C/EBP beta controlled gene IL6 is upregulated in DDIT3- and FUS-DDIT3-expressing fibrosarcoma cell lines and in myxoid liposarcoma cell lines. Strong expression of the tumor associated multifunctional cytokine interleukin 6 was confirmed both at mRNA and protein level. Knockdown experiments using siRNA against CEBPB transcripts showed that the effect of FUS-DDIT3 on IL6 expression is C/EBP beta dependent. Chromatin immunoprecipitation revealed direct interaction between the IL6 promoter and the C/EBP beta protein. In addition, the effect of DDIT3 and FUS-DDIT3 on the expression of other acute phase genes was examined using real-time PCR. We demonstrate for the first time that DDIT3 and FUS-DDIT3 show opposite transcriptional regulation of IL8 and suggest that FUS-DDIT3 may affect the synergistic activation of promoters regulated by C/EBP beta and NFkappaB.

Animals↗
PubMed1984

Malignant mesenchymoma of median nerve: combined nerve sheath sarcoma and liposarcoma.

A malignant mesenchymoma consisting of nerve sheath sarcoma and liposarcoma occurred in the right median nerve of a 29-year-old man who did not have stigmata of von Recklinghausen neurofibromatosis. It produced pain at the affected part, referred pain to the palm, and weakness of muscles supplied by branches of this nerve. The tumor was first excised 1 month after its initial manifestation, but recurred twice and eventually metastasized to the lung within 19 months. It is suggested that aberrant differentiation of the mesenchymal component of the neural crest, the ectomesenchymal structure, has created this combined sarcoma of nerve sheath and liposarcoma, forming a malignant mesenchymoma.

Adipose Tissue↗
PubMed1986

Liposarcoma arising within a cystosarcoma phyllodes.

A liposarcoma arising within a cystosarcoma phyllodes in a 17-year-old black female was treated by total mastectomy without the need of radiation and/or chemotherapy. The patient is alive and well with no evidence of recurrence or metastasis at 20 months recent follow-up. The clinicopathological features of malignant cystosarcoma phyllodes-liposarcoma are discussed.

Adolescent↗