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PubMed2004

Iatrogenic Kaposi's sarcoma and HCV infection.

Iatrogenic Kaposi's sarcoma develops in patients undergoing immunosuppressive treatment and is considered to be induced by activation of latent HHV8. In most cases the first manifestation of Kaposi's sarcoma develops after 1 year from when the drug was first administered. In a recent study from Italy on HHV8 positivity in patients with Kaposi's sarcoma, it was found that 52% of the control group were positive (Masini C., et al. G Ital Dermatol Venereol 1999; 134: 315-320). For this reason we could expect a larger number of cases of iatrogenic Kaposi's sarcoma given the number of patients who undergo immunosuppressive treatment for one reason or another. Thus, we have to look to a contemporaneous presence of other factors that co-operate with the HHV8. We present a case of a 49-year-old woman, HHV8 and HCV positive, who develops a Kaposi's sarcoma after 9 months of steroid therapy (methylprednisolone 16 mg/die). The low dose of steroids prescribed to our patient and the fact that the first skin manifestation developed after a shorter period than average from the start of therapy do not explain the acute onset of an extensive Kaposi's sarcoma even taking into account the HHV8 positive status. Both HHV8 and HCV produce proteins, such as IL6 and IL8 which are able to control cell growth. It can be supposed that the contemporaneus presence of the two viruses created a sinergy for the onset of the Kaposi's sarcoma.

Female↗
PubMed1977

Oncogenicity of avian leukosis viruses of different subgroups and of mutants of sarcoma viruses.

Leukosis viruses of seven subgroups were tested for oncogenicity in chickens susceptible to virus infection and to development of lymphoid leukosis (LL) tumors. All subgroup A viruses and the subgroup B virus tested produced a high incidence of LL and other related neoplasms. Viruses of subgroup C and RAV-61 of subgroup F produced a low level of LL. The RAV-50 of subgroup D produced osteopetrosis. In these tests, the viruses of subgroup E and G and one virus of subgroup F were not pathogenic, possibly because infection was not established in the chickens, the chickens were not susceptible to tumor development by these viruses, or the viruses lacked oncogenicity. All temperature-sensitive mutants of Rous sarcoma virus produced sarcomas, but the level varied. One nontransforming mutant produced sarcomas, and the other three tested produced LL. All three mutants that cause cells to grow as colonies in agar produced a high incidence of sarcomas. Thus, sarcoma viruses, by back-mutation, may lose the ability to transform cells in vitro, to make cells grow in agar colonies, or to induce sarcomas in vivo, yet they retain the ability to produce LL. Conversely, it was previously shown that leukosis viruses may be changed into viruses that transform cells in vitro and produce sarcomas in vivo by suitable passage in chicks.

Animals↗
PubMed1978

Comparison of the expression of the src gene of Rous sarcoma virus in vitro and in vivo.

We have compared the polypeptide products of the src gene of several strains of Rous sarcoma virus produced by in vitro translation of heat-denatured 70S virion RNA in the nuclease-treated reticulocyte lysate with those present in chick cells transformed by these viruses. We have done this by immunoprecipitation, using sera from rabbits injected at birth with Schmidt-Ruppin Rous sarcoma virus. In vitro translation results in the synthesis of at least nine polypeptides which appear to be encoded by the src gene. These range in size from 17,000 to 60,000 daltons. The sera from tumor-bearing rabbits precipitated these polypeptides arising from the in vitro translation of RNA from Schmidt-Ruppin Rous sarcoma virus of both subgroup A and subgroup D and from one stock of Prague Rous sarcoma virus of subgroup C. In each case, all of this family of related polypeptides could be precipitated except the smallest, the 17,000-dalton polypeptide. No precipitation of analogous polypeptides resulting from the translation of RNA from other strains of Rous sarcoma virus was observed. Cells transformed by these three strains of Rous sarcoma virus contain easily detectable amounts of a polypeptide, p60src, essentially identical to the 60,000-dalton in vitro product. With one exception, they do not contain significant amounts of polypeptides analogous to the smaller in vitro products which can be precipitated by these sera. Cells transformed by one stock of Schmidt-Ruppin Rous sarcoma virus of subgroup A did contain a 39,000-dalton polypeptide, which was related, by peptide mapping, to the 60,000-dalton polypeptide and was similar in size to a precipitable in vitro product. The 60,000-dalton polypeptide present in transformed cells appeared to be phosphorylated 10 to 25 min after its synthesis, metabolically very stable, and not derived from a precursor polypeptide. All immunoprecipitates from transformed cells which contained p60src also contained an 80,000-dalton phosphoprotein. This polypeptide is unrelated to p60src, as determined by peptide mapping, and may well be a host cell polypeptide which is specifically associated with p60src.

Avian Sarcoma Viruses↗
PubMed1981

Comparison between the viral transforming gene (src) of recovered avian sarcoma virus and its cellular homolog.

Recovered avian sarcoma viruses are recombinants between transformation-defective mutants of Rous sarcoma virus and the chicken cellular gene homologous to the src gene of Rous sarcoma virus. We have constructed and analyzed molecular clones of viral deoxyribonucleic acid from recovered avian sarcoma virus and its transformation-competent progenitor, the Schmidt-Ruppin A strain of Rous sarcoma virus. A 2.0-megadalton EcoRI fragment containing the entire src gene from each of these clones was subcloned and characterized. These fragments were also used as probes to isolate recombinant phage clones containing the cellular counterpart of the viral src gene, termed cellular src, from a lambda library of chicken deoxyribonucleic acid. The structure of cellular src was analyzed by restriction endonuclease mapping and electron microscopy. Restriction endonuclease mapping revealed extensive similarity between the src regions of Rous sarcoma virus and recovered avian sarcoma virus, but striking differences between the viral src's and cellular src. Electron microscopic analysis of heteroduplexes between recovered virus src and cellular src revealed a 1.8-kilobase region of homology. In the cellular gene, the homologous region was interrupted by seven nonhomologous regions which we interpret to be intervening sequences. We estimate the minimum length of cellular src to be about 7.2 kilobases. These findings have implications concerning the mechanism of formation of recovered virus src and possibly other cell-derived retrovirus transforming genes.

Alpharetrovirus↗
PubMed1996

Mixed low grade and high grade endometrial stromal sarcoma of uterus: differences on immunohistochemistry and chromosome in situ hybridisation.

A case of a 64 year old woman with a tumour of the uterus is reported. The patient presented with postmenopausal bleeding and subsequently underwent total hysterectomy and bilateral salpingo-oophorectomy. Sections of the tumour showed a low grade endometrial stromal sarcoma coexisting with areas consistent with high grade sarcoma. The sarcoma cells, in both the low and high grade areas, were positive for vimentin and negative for desmin and cytokeratin on immunohistochemistry. While the sarcoma cells in the low grade region showed immunoreactivity for oestrogen and progestogen receptors, those in the high grade region did not. Using chromosome in situ hybridisation, the low grade portion of the sarcoma was diploid for chromosomes X, 11, 12, and 17, whereas the more anaplastic areas were aneuploid for these chromosomes. This case may represent an example of high grade endometrial stromal sarcoma arising by dedifferentiation from a low grade stromal sarcoma. Adequate sampling is important in identifying such anaplastic changes as the origin of the tumour will affect patient management.

Chromosome Aberrations↗
PubMed1996

Pulmonary capillary blood volume in patients with probable pulmonary Kaposi's sarcoma.

BACKGROUND: An increase in pulmonary capillary blood volume secondary to angiogenesis has been described in Kaposi's sarcoma. The value of the pulmonary capillary blood volume as an early marker of pulmonary Kaposi's sarcoma was evaluated. METHODS: In a prospective study 45 HIV positive patients (nine asymptomatic for Kaposi's sarcoma, 29 with cutaneous or mucocutaneous Kaposi's sarcoma, and seven with pulmonary Kaposi's sarcoma), underwent pulmonary function tests and determination of transfer capacity for carbon monoxide (TLCO) with its components, pulmonary capillary volume and membrane factor. RESULTS: Total lung capacity (TLC), TLCO, and its components were similar in the three groups. TLCO was normal in patients with pulmonary Kaposi's sarcoma and no changes in membrane factor or pulmonary capillary volume were observed. CONCLUSION: Pulmonary function tests and pulmonary capillary volume alone are not useful for identifying patients with pulmonary Kaposi's sarcoma.

Adult↗
PubMed1978

Radiation-induced soft-tissue and bone sarcoma.

From the records of Memorial Hospital of the past 50 years, 47 cases with an established diagnosis of radiation-induced sarcoma were identified and divided into two groups: the first included 20 cases of soft-tissue sarcoma arising from irradiated tissues, and the second comprised 27 cases of bone sarcoma arising from normal bones in the irradiated field. Medians for the latent periods from irradiation to diagnosis of bone and soft-tissue sarcoma were 11 and 12, years, respectively. In bone sarcomas, the latent period was longer after larger radiation doses and children appeared to be more susceptible to cancer induction than adults. Criteria for establishing the diagnosis of radiation-induced sarcoma and the magnitude of the risk of bone sarcoma are discussed.

Adolescent↗
PubMedDate not supplied

From the archives of the AFIP: Imaging of synovial sarcoma with radiologic-pathologic correlation.

Synovial sarcoma is the fourth most common type of soft-tissue sarcoma, accounting for 2.5%-10.5% of all primary soft-tissue malignancies worldwide. Synovial sarcoma most often affects the extremities (80%-95% of cases), particularly the knee in the popliteal fossa, of adolescents and young adults (15-40 years of age). Despite its name, the lesion does not commonly arise in an intraarticular location but usually occurs near joints. Histologic subtypes include monophasic, biphasic, and poorly differentiated; the cytogenetic aberration of the t(X;18) translocation is highly specific for synovial sarcoma. Although radiographic features of these tumors are not pathognomonic, findings of a soft-tissue mass, particularly if calcified (30%), near but not in a joint of a young patient, are very suggestive of the diagnosis. Cross-sectional imaging features are vital for staging tumor extent and planning surgical resection; they also frequently reveal suggestive appearances of multilobulation and marked heterogeneity (creating the "triple sign") with hemorrhage, fluid levels, and septa (creating the "bowl of grapes" sign). Two features associated with synovial sarcoma that may lead to an initial mistaken diagnosis of a benign indolent process are slow growth (average time to diagnosis, 2-4 years) and small size (< 5 cm at initial presentation); in addition, these lesions may demonstrate well-defined margins and homogeneous appearance on cross-sectional images. Synovial sarcoma is an intermediate- to high-grade lesion, and, despite initial aggressive wide surgical resection, local recurrence and metastatic disease are common and prognosis is guarded. Understanding and recognizing the spectrum of appearances of synovial sarcoma, which reflect the underlying pathologic characteristics, improve radiologic assessment and are important for optimal patient management.

Arthrography↗
PubMed2026

BRD9 Degraders Unleash GBAF Chromatin Remodeling Activity in Synovial Sarcoma.

UNLABELLED: Synovial sarcoma incorporates the SS18::SSX fusion oncoprotein into GLTSCR1-containing BRG1/BRM and associated factors (GBAF) complexes, which confers a dependency on the GBAF subunit BRD9. However, synovial sarcoma clinical trials with multiple BRD9 degraders failed to achieve clinically impactful remissions. In this study, we identified a mechanistic framework to explain these results. BRD9 depletion served to blunt proliferation in synovial sarcoma harboring minimal genomic alterations, rare in trial participants. In cultured cells, xenografts, and recombinant-purified complexes, BRD9 loss did not affect GBAF assembly. Although BRD9 degradation in synovial sarcoma reduced GBAF enrichment at target loci, BRD9-less complexes maintained or increased chromatin accessibility and associated gene transcription. Biochemical assays with purified recombinant GBAF demonstrated increased nucleosome sliding in the absence of BRD9. Together, these findings show that BRD9 restrains GBAF activity, with BRD9 degradation increasing enzymatic remodeling and target gene expression by fusion oncoprotein-distributed GBAFs in synovial sarcoma. This subtle epigenetic disturbance creates a low hurdle for synovial sarcoma to surpass, limiting the therapeutic efficacy of BRD9 degraders. SIGNIFICANCE: BRD9 represses the GBAF chromatin remodeling complex, which causes enhanced rather than disrupted SS18::SSX complex activity following BRD9 degradation and explains the lack of efficacy of pharmacological BRD9 degraders in synovial sarcoma.

Sarcoma, Synovial↗
PubMed2004

Vascular endothelial growth factor expression is up-regulated by EWS-ETS oncoproteins and Sp1 and may represent an independent predictor of survival in Ewing's sarcoma.

PURPOSE: Tumor markers ideally allow monitoring and prediction of disease progression. In Ewing's sarcoma, a devastating childhood cancer, only a few reliable prognostic markers have been identified. To this end, we analyzed the expression of four tumor-promoting proteins, cyclin D1, HER2/Neu, Mdm2, and vascular endothelial growth factor (VEGF), in Ewing's sarcoma. EXPERIMENTAL DESIGN AND RESULTS: Thirty-one tissue samples from patients with Ewing's sarcoma were stained with antibodies against cyclin D1, HER2/Neu, Mdm2, or VEGF. Whereas no significant expression of HER2/Neu and Mdm2 was detected, positive cyclin D1 and VEGF staining was observed in 42% and 55% of all tumors, respectively. Importantly, VEGF expression was found to be an independent negative predictor of survival in Ewing's sarcoma patients, whereas cyclin D1 expression did not correlate with survival in these patients. Consistently, the Ewing's sarcoma-specific EWS-ETS oncoproteins were capable of activating both the cyclin D1 and VEGF promoters in transient transfections of tissue culture cells. Furthermore, this activation was enhanced by coexpression of the Sp1 transcription factor. Using a mammalian two-hybrid system, some evidence was obtained that this may involve a physical interaction between EWS-ETS and Sp1 proteins. CONCLUSIONS: Our data reveal that VEGF may serve as a prognostic marker in Ewing's sarcoma patients and provide a molecular mechanism by which VEGF and cyclin D1 expression is up-regulated in approximately half of all Ewing's sarcomas.

Antigens, Protozoan↗
PubMed2007

Expression of cellular FLICE inhibitory protein, caspase-8, and protease inhibitor-9 in Ewing sarcoma and implications for susceptibility to cytotoxic pathways.

PURPOSE: Ewing sarcoma is a common pediatric bone tumor with an unfavorable prognosis for metastatic or recurrent disease. Cellular immunotherapy may provide new treatment options and depends on the cytolytic death receptor and perforin/granzyme pathways. Expression of death receptor pathway inhibitor cellular FLICE inhibitory protein (cFLIP), initiator caspase-8, and granzyme B inhibitor protease inhibitor-9 (PI-9) have been reported to determine susceptibility to cell- and chemotherapy-mediated killing in several tumor types. Here, we have studied their in vitro and in vivo expression in Ewing sarcoma and the implications for susceptibility to cytotoxicity. EXPERIMENTAL DESIGN: Ewing sarcoma cell lines (n = 8) were tested for cFLIP, PI-9, and caspase-8 expression. Functional significance was tested by anti-Fas antibody (death receptor pathway) or natural killer cell (perforin/granzyme pathway) treatment. Immunohistochemistry was done on 28 sections from 18 patients. In half of the cases, sequential material, including metastases, was available. RESULTS: Although all tested Ewing sarcoma cell lines expressed cFLIP, resistance to CD95/Fas-mediated apoptosis was only observed in two cell lines lacking caspase-8 expression. PI-9 was expressed at low levels in four of eight Ewing sarcoma cell lines, but positive cell lines remained susceptible to perforin/granzyme-mediated killing. In primary Ewing sarcoma, including metastases, cFLIP was abundantly expressed in 18 of 18 patients. Caspase-8 was expressed in all patients but showed more intertumoral and intratumoral variation in both intensity and heterogeneity of staining. PI-9, in contrast, was undetectable. CONCLUSIONS: The expression patterns of cFLIP, caspase-8, and the absence of PI-9 provide a rationale to preferentially exploit the perforin/granzyme pathway in cytotoxic therapies against Ewing sarcoma.

Apoptosis↗
PubMed2026

RAS Pathway Activation and Microenvironmental Adaptation as Hallmarks of Myeloid Sarcoma.

UNLABELLED: Myeloid sarcoma, an aggressive extramedullary subtype of acute myeloid leukemia (AML), occurs in approximately 20% of patients and remains strikingly understudied in large-scale genomic and multiomic investigations. The key drivers of its tumor evolution are largely unknown; timely detection in asymptomatic patients poses a clinical challenge, and effective treatment options are limited, as patients are often excluded from clinical trials, rendering it a largely neglected disease entity. In this study, we demonstrate that myeloid sarcoma evolves from medullary AML but exhibits distinct site-specific clonal evolution. This is supported by unique transcriptional signatures of myeloid sarcoma, reflecting adaptation to the extramedullary microenvironment. We establish a proof of concept that circulating tumor DNA (ctDNA) sequencing captures the molecular composition of myeloid sarcoma, offering a potential noninvasive approach for molecular profiling of extramedullary AML. Our findings highlight marked differences between medullary AML and myeloid sarcoma, including universal molecular evolution and RAS pathway activation as disease hallmarks. SIGNIFICANCE: We provide a comprehensive multiomic characterization of myeloid sarcoma, identifying key molecular pathways that contribute to its development, and suggest ctDNA as a noninvasive method of detection. We identify RAS pathway activation and transcriptional adaptation to the solid tissue microenvironment as cardinal features of myeloid sarcoma, suggesting novel therapeutic avenues.

Sarcoma, Myeloid↗
PubMed2002

Gene therapy for sarcoma.

Soft tissue sarcomas are mesenchymal tumors which respond poorly to systemic therapy. Recent studies suggest a higher response rate with an increased doxorubicin dosage. However, this was parallel with a profound hematotoxicity in 75% of patients. Transfer of the human multidrug resistance 1 (MDR1) gene to normal hematopoietic stem cells and transplantation may significantly reduce the hematotoxicity of anthracyclin-based chemotherapy. To test this concept of supportive gene therapy in advance of a clinical study, we transduced mobilized peripheral blood progenitor cells (PBPC) with the retroviral vector SF91m3 containing the human MDR1 gene, transplanted these cells to immune-deficient mice, allowed 6 weeks for engraftment to occur and treated the animals with MDR1-based chemotherapy. In the MDR1-transduced group the human leukocytes were significantly protected from the toxicity of chemotherapy (p < 0.05). While the gene transfer rate was in the range of 10% and thus comparable to recent clinical trials, the gene expression was 59% of transduced cells and thus significantly higher than previously reported for less-advanced vectors. On the other hand, ifosfamide, a drug which has been used successfully for stem cell mobilization, is active in soft tissue sarcoma. Due to these favorable characteristics sarcoma is an attractive target to test the efficacy of MDR1 gene therapy in a clinical setting. Gene therapeutic strategies may also be used to directly target sarcoma cells, e.g. by transfer of suicide genes. We found that adenoassociated virus 2 (AAV-2) vectors efficiently transduce human HS-1 and HT1080 sarcoma cells (>90%) while other tumor cell lines and primary human PBPC were less susceptible. The thymidine kinase (TK) suicide gene was cloned into an AAV-2 vector and a complete kill of TK-transduced HS-1 and HT1080 cells was observed following exposure to aciclovir or ganciclovir (GCV), while >90% of mock-transduced HS-1 cells survived at these dosages. Transplantation of those sarcoma cells to nonobese diabetic (NOD)/LtSz-severe-combined immunodeficient (scid)/scid (NOD/SCID) mice resulted in a survival of >5 months in the AAV-TK-transduced/GCV-treated group, while the mice in the mock-transduced/GCV-treated group had died after 3 weeks. These data show that soft tissue sarcomas are a particularly suitable model system for the development and clinical testing of new gene therapeutic concepts.

Animals↗
PubMedDate not supplied

Fine needle aspiration biopsy of primary renal synovial sarcoma. A case report.

BACKGROUND: Primary renal synovial sarcoma is a relatively recently described and characterized neoplasm, formerly designated embryonal sarcoma of the kidney, and has not been diagnosed before by fine needle aspiration biopsy cytology. We describe the cytologic features of a malignant biphasic neoplasm of the kidney that was subsequently diagnosed at nephrectomy and confirmed with molecular genetic analysis as a biphasic renal synovial sarcoma. CASE: A 38-year-old male presented with acute abdominal pain. Computed tomography (CT) demonstrated a 4.7-cm mass in the left kidney. No soft tissue or extrarenal masses were identified. A CT-guided fine needle aspiration biopsy revealed a malignant biphasic tumor characterized by minimally atypical tubular epithelium, immature spindle cells and foci of coagulative tumor necrosis. At nephrectomy, a necrotic, pseudo-encapsulated synovial sarcoma of the upper pole of the left kidney was identified and was additionally evaluated with immunohistochemistry and molecular genetic studies. The case is unique since biphasic synovial sarcomas have yet to be reported to occur in the kidney and fine needle aspiration biopsy findings of this renal neoplasm have never been reported to our knowledge. CONCLUSION: Synovial sarcoma should be a diagnostic consideration particularly in a young adult with a malignant spindle cell neoplasm of the kidney. The list of differential diagnoses should include sarcomatoid renal cell carcinoma, sarcomatoid transitional cell carcinoma of the renal pelvis, angiomyolipoma and monophasic or biphasic synovial sarcoma.

Adult↗
PubMed1993

Spontaneous histiocytic sarcoma with possible origin from the bone marrow and lymph node in Donryu and F-344 rats.

Ninety-five male and 96 female Donryu rats reared up to 120 wk of age and 244 male and 243 female F-344 rats used as untreated controls in 5 carcinogenicity studies were examined histopathologically to clarify the primary site of histiocytic sarcoma. Histiocytic sarcoma in Donryu rats was observed in 5 of 95 (5.3%) males and 4 of 96 (4.2%) females. In F-344 rats, 4 of 244 (1.6%) males and 3 of 243 (1.2%) females had the neoplasms. Histologically, sarcomas consisting of large pleomorphic histiocytic cells were seen in the bone marrow, liver, lymph node, spleen, and lung. Among 16 sarcomas observed, 15 had neoplastic lesions in the bone marrow, and 1 F-344 rat had the lesions only in the lymph nodes. Eleven (6 F-344 rats and 5 Donryu rats) of the 15 cases had the lesions in the liver, and 4 Donryu rats had no lesions in the liver but lesions in the lymph node and/or spleen, except for 1 case where the sarcoma occurred only in the bone marrow. Among the 11 cases with the lesions both in the liver and bone marrow, neoplastic lesions were found also in the lymph node, spleen, and/or lung, but the severity of neoplastic proliferation of these organs was not so marked as that in the bone marrow except for 2 cases. Although histiocytic sarcomas in rats are considered to originate from the liver, peritoneum, or subcutis, the present results strongly suggest that some histiocytic sarcomas in Donryu and F-344 rats may also originate from the bone marrow and lymph nodes.

Animals↗
PubMed1994

Kaposi's sarcoma of the head and neck in patients with acquired immunodeficiency syndrome.

Kaposi's sarcoma is the most common neoplastic process in patients infected with the human immunodeficiency virus. Moreover, the occurrence of Kaposi's sarcoma in human immunodeficiency virus-infected patients advances their classification to having the acquired immunodeficiency syndrome. We reviewed the medical records of 48 patients with human immunodeficiency virus infection who had Kaposi's sarcoma documented on their initial visit to the hospital. The onset of Kaposi's sarcoma occurred independent of the Centers for Disease Control and Prevention classification of human immunodeficiency virus infection (modified to exclude Kaposi's sarcoma). This neoplasm developed more frequently in patients who acquired human immunodeficiency virus infection by sexual contact (75% of cases), but manifestations were not significantly different in any of the risk populations for human immunodeficiency virus infection. Kaposi's sarcoma lesions were unpredictable and either showed progression, remained static, or occasionally, regressed spontaneously. Moreover, the lesions were usually multifocal at presentation, with the head and neck (62.5% of cases) as the primary site of involvement. In this region cutaneous lesions predominated (66.7%), followed by mucosal (56.7%) and deep structure (13.3%) involvement. The majority of patients with acquired immunodeficiency syndrome Kaposi's sarcoma involving head and neck structures were asymptomatic (80% of cases). Mucosal lesions were associated with symptoms in 29.3% of cases, whereas cutaneous lesions had symptoms in 5% of cases.

Acquired Immunodeficiency Syndrome↗
PubMed1980

Lymphography in bone and soft tissue sarcomas. Experiences from three institutions.

The case material was collected from 3 Institutions with a total of 441 patients: 217 with primary bone tumor and 224 with soft tissue sarcomas. In the majority of patients lymphography was performed during the initial diagnostic workup. The lymphograms were interpreted as negative or positive for metastases. In bone tumors, the incidence of metastases was 21%, ranging from 28% for osteosarcoma to 18% for Ewing's sarcoma and 13% for chondrosarcoma. In tumors of the soft tissue, the frequency was somewhat higher (28%), with special regard to rhabdomyosarcoma (53%), anaplastic sarcoma (67%), neurogenic sarcoma (42%) and synovial sarcoma (35%). In the group of bone sarcomas, primary hematogenous spread was 3 times more frequent than lymphogenous spread, while in soft tissue sarcomas, with a higher incidence of lymphatic spread, this finding was inverted. In the more consistent tumor groups, the occurrence of lymphatic metastases indicated a significant worsening of the prognosis. In 96 patients, lymph node biopsies were performed and the radiologic histologic correlation gave evidence of a 97.7% overall diagnostic accuracy.

Bone Neoplasms↗
PubMed1996

Detection of herpesvirus-like DNA in the bronchoalveolar lavage fluid of patients with pulmonary Kaposi's sarcoma.

Pulmonary involvement is a clinically important form of visceral Kaposi's sarcoma in immunocompromised patients. Recently, herpesvirus-like deoxyribonucleic acid (DNA) sequences, defining a new herpesvirus termed "human herpesvirus 8" (HHV8) or "Kaposi's sarcoma-associated herpesvirus" (KSHV), were detected in Kaposi's sarcoma of acquired immune deficiency syndrome (AIDS) and non-AIDS patients. We describe the successful detection of HHV8 DNA in the bronchoalveolar lavage (BAL) fluid of patients with pulmonary Kaposi's sarcoma. Three immunocompromised patients, two HIV seropositive and one after kidney transplantation, suffered from respiratory symptoms and showed pulmonary infiltrates on chest radiography after development of biopsy proven Kaposi's sarcoma of the skin. Bronchoscopy revealed the typical Kaposi like livid endobronchial lesions. BAL fluid was analysed for the presence of HHV8 DNA using a nested polymerase chain reaction (PCR) assay. HHV8 DNA was detected in the BAL fluid of all three patients. In addition, HHV8 DNA could be detected in the skin biopsy tissue, lymph node, and peripheral blood mononuclear cells of these patients. Our data show that human herpesvirus 8 deoxyribonucleic acid can be detected in the bronchoalveolar lavage fluid of patients with pulmonary Kaposi's sarcoma. If further studies reveal a high specificity for human herpesvirus 8 deoxyribonucleic acid detection, this test will improve the tools for the diagnosis of pulmonary Kaposi's sarcoma without further need of biopsies.

Adult↗