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Results for “Muscle Neoplasms”

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PubMedDate not supplied

Primary extranodal lymphoma of skeletal muscles: a report of four cases.

Approximately one-fourth of non-Hodgkin's lymphomas originate in extranodal sites. True primary involvement of soft tissues is quite uncommon and only a few well-documented cases are reported in the literature. We report four cases of primary skeletal muscle lymphoma. Three of the four cases presented with a diffuse large B-cell lymphoma. The clinical history of two cases confirmed that soft tissue masses should be promptly biopsied, since the differential diagnosis comprises benign lesions, as well as sarcoma, primary or metastatic carcinoma, melanoma and lymphoma. As lymphomas have to be treated primarily according to the tumour histology and disease extent, treatment of primary skeletal muscle lymphomas must be planned with these factors in mind. For patients presenting with diffuse large cell histology, a CHOP-like regimen alone or a combined modality with radiotherapy seem to be proper approaches.

Aged↗
PubMed2002

Remission of lymphoma after drug withdrawal in rheumatoid arthritis.

A 63-year-old man with rheumatoid arthritis presented with pain and swelling of his right buttock. Imaging and tissue biopsy revealed a diffuse large B-cell, non-Hodgkin's lymphoma. The disease-modifying drugs he was taking, cyclosporin and methotrexate, were stopped, and the lymphoma resolved spontaneously without the use of chemotherapy.

Arthritis, Rheumatoid↗
PubMed1999

[Intramuscular myxoma. A case of myxoma of the spinal erector muscle].

A case of intramuscular myxoma, extended in the lumbar erector spinae muscles, is reported. This soft tissue tumor is rare, about one hundred observations are indexed in the literature. The clinical findings are nonspecific, magnetic resonance imaging reveals few characteristics, and finally a histological examination is required, after surgical removal, to pinpoint the diagnosis. Recurrence is uncommon, but a systematic follow-up is necessary.

Female↗
PubMed2000

Inhibition of the interferon-gamma/signal transducers and activators of transcription (STAT) pathway by hypermethylation at a STAT-binding site in the p21WAF1 promoter region.

Expression of the cyclin-dependent kinase inhibitor p21WAF1 can be up-regulated by activation of signal transducers and activators of transcription (STAT) proteins in response to IFN-gamma. In this study, we examined CpG methylation at the p21WAF1 promoter region in rhabdomyosarcomas (RMSs) using Southern blot analysis with the methylation-sensitive restriction enzyme HpaII. Sis-inducible element (SIE)-1, a STAT-responsive element located upstream of the p21 WAF1 CpG island, was completely methylated at an internal CpG in 13 of 26 (50%) primary RMS tumors and 2 of 5 RMS cell lines. In contrast, all normal tissues examined showed a partial methylation pattern at SIE-1. Complete methylation within SIE-1 strongly correlated with decreased p21WAF1 mRNA expression in RMS. We further studied the effects of SIE-1 hypermethylation on p21WAF1 induction by STAT activation. CpG methylation within SIE-1 significantly inhibited binding of activated STAT1 in electrophoretic mobility shift assays and abrogated STAT-mediated transcription activation in response to IFN-gamma in luciferase reporter gene assays. Activation of STAT1 in response to IFN-gamma resulted in increased p21WAF1 expression and growth suppression in RMS cells containing unmethylated SIE-1 but failed to induce p21WAF1 or growth inhibition in RD and A673 cells, both of which were completely methylated within SIE-1. However, demethylation at SIE-1, induced by a demethylating agent 5-aza-2'-deoxycytidine, reactivated p21WAF1 expression and restored the responsiveness to IFN-gamma in RD cells. Our results indicate a mechanism by which altered DNA methylation in the p21 WAF1 promoter region, by precluding STAT1 binding to SIE-1, directly inhibits the p21WAF1 induction and cell growth regulation through the IFN-gamma/STAT signaling pathway in RMS cells.

Antimetabolites, Antineoplastic↗
PubMed2002

Aberrant expression of HMGA2 in uterine leiomyoma associated with loss of TSC2 tumor suppressor gene function.

Unregulated proliferation of mesenchymal cells in leiomyomas, lipomas, hamartomas,and other diseases has been linked to the high mobility group (HMGA) family of DNA architectural proteins. HMGA genes are primarily expressed during embryonal development and silenced in adult tissues but can become reactivated in neoplasia as a result of chromosomal rearrangements. Although the genetic data suggesting a role for HMGA proteins in tumorigenesis are compelling, the biological role of these proteins in mesenchymal proliferation and differentiation is incompletely defined. Uterine myometria and spontaneous leiomyomas from the Eker rat, which carries a germ-line mutation in the tuberous sclerosis complex-2 (Tsc2) tumor suppressor gene, were analyzed for genetic defects in and expression of the Tsc2 and HMGA proteins. Eker leiomyomas exhibited a 50% incidence of loss of the wild-type Tsc2 allele and an almost uniform loss of protein expression, implicating loss of function of the Tsc2 gene in these tumors. Concomitantly, HMGA2 protein, which was completely absent in normal myometria, was expressed in 16 of 19 Eker leiomyomas. HMGA1 was expressed in both leiomyoma and normal myometria. No structural alterations were observed at the HMGA2 locus in either primary rat leiomyomas or leiomyoma-derived cell lines that expressed HMGA2. These data support a role for HMGA2 in the development of smooth muscle neoplasms and suggest HMGA2 expression is a point of convergence between the human disease and the Eker rat model. Furthermore, these data indicate that aberrant HMGA2 expression can result from dysfunction of the Tsc2 tumor suppressor gene, in the absence of structural alterations involving the HMGA2 locus.

Animals↗
PubMed2002

Experimental study on mechanism and rarity of metastases in skeletal muscle.

OBJECTIVE: To investigate the reasons for the rarity of metastases in skeletal muscle. METHODS: By injecting tumor cells (Walker256 rat carcinosarcoma) through the iliac artery (experimental group) and the tail vein (control group), animal models of blood-borne metastases were established. The quadriceps femoris muscle and lungs were observed grossly and microscopically. Immunohistochemistry was applied to investigate the expression of vascular cell adhesion molecule-1 (VCAM-1) in the microvascular endothelium of these organs. Primary culture of rat skeletal muscle cells was established and conditioned medium (MCM) was collected. Effects of MCM on several tumor cell lines and the biochemical characteristics of skeletal muscle delivered tumor factor(s) were tested by MTT assay. Apoptosis and morphological examination were carried out to investigate the antitumor mechanisms of MCM. RESULTS: In the experimental group, there were no definite metastases observed in muscle cells. In the control group, lung metastases were present in the lungs of all rats that were sacrificed at the 14th day or died spontaneously (17 rats in all). There was no significant difference between the increase in VCAM-1 in quadriceps femoris muscle 7 days after iliac artery injection and that in lungs 7 days after tail vein injection (P > 0.05). In vitro studies showed that the proliferation of tumor cell lines of mouse SP2/0 myeloma, rat Walker256 carcinosarcoma or human chronic granulocytic leukemia K562, human acute lymphatic leukemia HL-60, LS-174-T colon adenocarcinoma, PC3-M prostatic carcinoma and lung giant cell carcinoma with different metastatic potency (PLA801-C with low metastatic potency, PLA801-D with high metastatic potency) was significantly inhibited when cultured with MCM (P < 0.01 - 0.05). Proliferation of malignant cells showed a dose-dependent decrease, to a certain degree. Proliferation of normal rabbit joint epiphysial disk cells (RGP-2) were not affected by MCM. Proliferation of lung giant cell carcinoma cells with high metastatic potency showed a significant decrease even when cultured in highly diluted MCM (6.25% of primary MCM), when compared with the strain of low metastatic potency. Following ultrafiltration, boiling at 100 degrees C, and treatment with trypsin, skeletal muscle delivered tumor factor(s) were found to be a low molecular weight (MW <or= 10.0 KDa) component which was trypsin resistant but not heat resistant. The factor(s) did not induce apoptosis in K562 cells but caused direct destruction of the cytoplasmic membrane. CONCLUSIONS: The rarity of metastases in skeletal muscles, generally accepted in the clinical setting, can be reproduced in an animal model. It does not seem to be related to VCAM-1 expression in the microvessels of these organs. Skeletal muscle delivered factor(s) play a key role in the mechanism of the rarity of metastases in skeletal muscle.

Animals↗
PubMed2003

[Non-traumatic myositis ossificans circumscripta in the teres major muscle].

A 49-year-old male presented with a painful progressive swelling in his right axillar region, without further complaints, which had been present for 2 weeks. On radiological examination a peripheral circumferential zone of mineralisation was seen in the right teres major muscle. An incision biopsy specimen showed a lesion of fibroblastic tissue in which areas of osteoid and fragmented lamellar bone tissue, without signs of malignancy. The diagnosis was myositis ossificans circumscripta. This is a rare benign ossifying lesion in skeletal muscles, mostly caused by a trauma and with an average age of occurrence between 20 and 30 years old. It must be differentiated from extra-skeletal osteosarcoma. The pathogenesis is unknown. Because it is a benign and self-limiting disorder, surgical excision is only necessary in case of mechanical hindrance. The patient's swelling partially regressed and he had no further complaints.

Axilla↗
PubMed2003

Development of rhabdomyosarcoma in HER-2/neu transgenic p53 mutant mice.

Rhabdomyosarcomas derive from the skeletal muscle lineage and harbor a variety of genetic and molecular lesions. However, it is not clear which molecular alterations have a pathogenetic role. We show that activation of the HER-2/neu oncogene coupled with inactivation of the oncosuppressor gene p53 causes rhabdomyosarcoma in mice. At the age of 11-21 weeks, all male mice carrying both genetic lesions developed embryonal rhabdomyosarcomas expressing desmin, myosin, and insulin-like growth factor-II, in the genitourinary tract. Our findings led to the hypothesis that the interaction between HER family genes and the p53 pathway might be involved in the origin of human rhabdomyosarcoma.

Alleles↗
PubMedDate not supplied

[Muscular angiomas].

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Hemangioma↗