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An 8-year-old, spayed, female domestic shorthair was diagnosed with a vaccine-associated fibrosarcoma and treated with full course radiation therapy, aggressive surgery, and postoperative chemotherapy. Histopathologic examination confirmed that excision of the tumor was complete. The cat was doing well 278 days after initial presentation.
Murine fibrosarcoma cell lines transduced with retroviral vectors containing the murine interleukin 6 (IL-6) gene constitutively secreted IL-6. When injected s.c. into normal mice these IL-6-secreting tumors exhibited reduced tumorigenicity. This reduced tumorigenicity was not seen in nude or irradiated mice, implicating a T-cell-dependent, radiosensitive host response activated by the cytokine. Subcutaneous IL-6-secreting tumor did not retard the growth of distant deposits of wild-type tumor in the same host. However, animals rejecting IL-6-secreting tumors exhibited resistance to later challenge with wild-type tumor. When injected i.v. in an experimental metastasis model the IL-6-secreting tumors failed to or were extremely inefficient in giving rise to pulmonary nodules; this was observed in both normal and immunoincompetent mice, implicating a second, nonimmune mechanism affecting the growth of the tumor modified to secrete IL-6.
Matrix metalloproteinase 9 (MMP-9) has been purified as an inactive zymogen of M(r) 92,000 (proMMP-9) from the culture medium of HT 1080 human fibrosarcoma cells. The NH2-terminal sequence of proMMP-9 is Ala-Pro-Arg-Gln-Arg-Gln-Ser-Thr-Leu-Val-Leu-Phe-Pro, which is identical to that of the 92-kDa type IV collagenase/gelatinase. The zymogen can be activated by 4-aminophenylmercuric acetate, yielding an intermediate form of M(r) 83,000 and an active species of M(r) 67,000, the second of which has a new NH2 terminus of Met-Arg-Thr-Pro-Arg-(Cys)-Gly-Val-Pro-Asp-Leu-Gly-Arg-Phe-Gln-Thr- Phe-Glu. Immunoblot analyses demonstrate that this activation process is achieved by sequential processing of both NH2- and COOH-terminal peptides. TIMP-1 complexed with proMMP-9 inhibits the conversion of the intermediate form to the active species of M(r) 67,000. The proenzyme is fully activated by cathepsin G, trypsin, alpha-chymotrypsin, and MMP-3 (stromelysin 1) but not by plasmin, leukocyte elastase, plasma kallikrein, thrombin, or MMP-1 (tissue collagenase). During the activation by MMP-3, proMMP-9 is converted to an active species of M(r) 64,000 that lacks both NH2- and COOH-terminal peptides. In addition, HOCl partially activates the zymogen by reacting with an intermediate species of M(r) 83,000. The enzyme degrades type I gelatin rapidly and also cleaves native collagens including alpha 2 chain of type I collagen, collagen types III, IV, and V at undenaturing temperatures. These results indicate that MMP-9 has different activation mechanisms and substrate specificity from those of MMP-2 (72-kDa gelatinase/type IV collagenase).
We report about two patients with fibrosarcoma of the soft tissues of the face. We discuss the problems of biological viability of the tumor, of the diagnostics and of the etiological factors, and about the therapy. The prognosis depends on the localisation, the degree of malignancy of the tumor and the therapy.
The changes in sialoglycoconjugates synthesis after administration of 14C-glucose to fibrosarcoma bearing rats were studied. After 1 hr treatment 14C-glucose tumor bearing rat synthesized hexosamine which contained more radioactivity when compared to sialic acid. On fractionation of lipoproteins, low density lipoproteins (LDL) contained more sialic acid. This was further confirmed by separating the lipoproteins, as more radioactivity incorporation was observed in the LDL fraction. It is noteworthy that inspite of the tumor, high density lipoproteins (HDL) did not show any change.
Immunogenic variant was induced from the methylcholanthrene induced fibrosarcoma (MCA-F) by in vitro treatment with the mutagen 1-methyl-3-nitro-1-nitrosoguanidine (MNNG). D-10 tumor cell which was cloned from MNNG treated MCA-F tumor cell was rejected by normal syngeneic C3H-HeJ mice but not by 650 rad irradiated immunosuppressed mice. Host which had rejected D-10 tumor growth, rejected parental MCA-F tumor cells. But active immunotherapy using D-10 tumor cell against MCA-F tumor cells. But active immunotherapy using D-10 tumor cell against MCA-F tumor bearing mice was not successful. Cytotoxic T cell (CTL) established from D-10 immunized spleen cells showed D-10 specific cytotoxic activity and not lysed parent MCA-F cells. CTL clone C-E-6 showed specific cytotoxic and proliferative activity against D-10 cell. In vivo tumor neutralizing assay also showed its specificity against D-10 tumor cell. Active immunotherapy and adoptive immunotherapy using immunogenic variant, D-10 was not successful. D-10 tumor cell possesses very strong neoantigen induced by MNNG treatment and parental MCA-F antigen.
The association between neoplasia and thrombosis has been well documented. We have studied the production of a procoagulant which is a factor X activator in a rat fibrosarcoma model. Extracts of excised tumor were assayed in a one stage clotting assay using normal and factor deficient human plasmas. The activity was not due to tissue factor, as acceleration of clotting was observed in FVII deficient plasma. No activity was noted in FX deficient plasma. The activator was capable of cleaving 125I-FX in the absence or presence of calcium. A radioimmunoassay (RIA) demonstrated a 5,100-fold increase in the levels of FX activation peptide after exposure to sarcoma extract. The FX activation occurs in the absence of calcium although the effect is greatly accelerated in the presence of 5 mM CaCl2. Using a two-stage amidolytic assay, functional activation of FX by the sarcoma was demonstrated. Inhibitor studies suggest that the sarcoma-derived procoagulant is a serine protease. The methylcholanthrene-induced rat sarcoma may serve as a useful model for investigating the regulation and effects of cancer procoagulants.
The authors describe a patient with a large retroperitoneal infantile fibrosarcoma that responded well to preoperative chemotherapy, which subsequently facilitated the complete surgical resection of the mass. The patient had an unusual site of metastasis presumed to be to a regional lymph node. The histology on initial core biopsies was not classic but showed a round cell, myxoid pattern. The presence of the t(12;15)(p13;q25) and the fusion transcript ETV6-NTRK3 by RTPCR facilitated the diagnosis.
A fibrosarcoma of the psoas in a 62-year-old woman manifested itself essentially by a febrile syndrome for approximately one year. It would appear that the first manifestation of the lesion occurred three years previously (lumbar pain). Careful clinical examination, numerous radiological studies and two exploratory laparotomies failed to reveal the site of the lesion. The latter was finally demonstrated by GaC67 gammagraphy. This case thus confirms the great value of this radioactive tracer in the diagnostic study of a febrile syndrome as a tumour syndrome. It would appear to be perhaps desirable, in this pathological context, to request a whole body study using GaC67 before proceeding to exploratory laparotomy.
Cepharanthine (Ce) is a biscoclaurine alkaloid extracted from Stephania cepharantha Hayata. In our previous study, Ce significantly enhanced thermosensitivity and thereby reduced thermotolerance in vitro, and intra-peritoneal injection of Ce slightly enhanced thermosensitivity in vivo. In the present study, we investigated Ce's effect in vitro on the pattern of cell death after heating and the effect of intra-tumoral injection of Ce on in vivo thermosensitivity using a mouse fibrosarcoma, FSa-II, and C3H/He mice. Ce significantly enhanced the in vitro thermosensitivity of FSa-II cells with heating at 44 degrees C, with increased Ce concentration. Time-lapse microscopic observation of individual cells confirmed that Ce treatment hastened both apoptosis (specifically, apoptotic budding) and necrosis (as indicated by staining with propidium iodide). Staining with annexin V-enhanced green fluorescent protein indicated that Ce used concomitantly with heating significantly increased the proportion of cells in the early stage of apoptosis. Ce combined with heating also significantly increased the proportion of cells with high intracellular caspase-3 activity, as detected by a substrate of caspase-3, PhiPhiLux-G1D2. The intra-tumoral injection of Ce, followed by heating at 44 degrees C, significantly delayed in vivo tumor growth, and this delay increased in a Ce concentration-dependent manner. Ce injected 30 min before heating delayed tumor growth more than Ce injected immediately before heating. These findings suggest the potential of Ce as a thermosensitizer to increase apoptosis of tumor cells.
Fibrosarcoma in childhood is a rare disease. An interesting new case involving the infratemporal fossa in a three-year-old girl is reported. The literature, the symptomatology and the diagnostic features are reviewed. The difficult management decisions and the thorny problem of reconstruction of head and neck malignancies in growing children are discussed. Suggestions are made for management of similar cases.
The Authors reported a case of inflammatory fibrosarcoma of the urachus in a 27-year old woman. Differential diagnosis, surgical therapy and prognosis were discussed.
Malignant mesenchymal tumours of the breast are relatively rare tumours that have yet to receive universal approval in terms of terminology. With classification based on histogenesis rapidly gaining acceptance, we present a case with histological features of both fibrosarcoma and malignant fibrous histiocytoma, with the former predominating. An unusual finding was the presence of large areas with haemangiopericytomatous appearance. The literature on changing concepts regarding classification of malignant mesenchymal tumours of the breast is reviewed.
Brain catecholamines (CA) were studied in discrete brain areas of benzo(a)pyrene (b(a)p) induced fibrosarcoma bearing mice. Dopamine (DA) and norepinephrine (NE) levels decreased significantly in different brain areas especially in corpus striatum and hypothalamus with the tumor progression, indicating an inverse relationship between brain DA and NE levels and tumor growth. Since impaired hormonal and immunological functions are manifestation of systemic alteration during tumor growth, it appears that during malignant growth an alteration of these brain CA may play an important role in the regulation of systemic alterations.
The cytologic appearance of a carcinosarcoma (malignant ameloblastoma and fibrosarcoma) of the maxilla in a 63-year-old man is described. On his first admission the diagnosis of malignant ameloblastoma was made on biopsy. After five surgical excisions, radiotherapy and chemotherapy, the diagnosis was changed to carcinosarcoma because the stromal cells of the tumor had become malignant. Aspiration biopsy cytology of the tumor, with a cystic lesion found at the left suborbital area, revealed malignant epithelial cells, indicating malignant ameloblastoma. Imprint smears of both surgically resected and autopsy material showed two types of malignant neoplastic cells, of epithelial and mesenchymal origin.
Meningeal Fibrosarcoma (MF) accounts only for 0.5% of the brain tumors. Since the clinical manifestations and radiologic findings are non-specific, the diagnosis can only be achieved by pathological examination of surgically removed specimens. MF are tumors that behave locally very aggressively and respond poorly to treatment, with reported median survivals ranging from 6 to 15 months. We report a new case of MF describing the peculiar onset as a slow growing mass in scalp with bone destruction and without neurological clinical findings.
The aim of the study was an evaluation of the activity of mast cells and mark activity tryptase and chymase and of protein levels in experimental fibrosarcoma, induced in rat skin. The experiments were carried out on 50 male Wistar rats. The cancer was induced in rats by one subcutaneous injection of 0.2 mg 3-methylcholanthrene in 0.25 ml of olive oil. Tissue material was fixed in Bouin's fluid. Immunohistochemical tryptase detecting reactions were performed--using specific antibodies and the ABC complex. The activities of tryptase and chymase and protein levels were determined in supernatant of 10% homogenate. We found a very significant growth of mast cell quantity in the connective tissue of tumours. We observed slight differences in the activity of examined enzymes in tumours of different mass.
Inflammatory myofibroblastic tumors (inflammatory fibrosarcomas) of the pancreas are extremely rare. We report a 29-year-old woman who underwent pancreatoduodenectomy for a 6-cm tumor of the pancreas head causing obstructive jaundice. Tumor involvement was local, without apparent metastasis. The tumor was composed of proliferating fibroblastic/or myofibroblast-like spindle cells and aggregates of chronic inflammatory cells in a fibromyxoid matrix. Immunohistochemical examination demonstrated reactivity only to vimentin. This tumor has often been found in the peritoneal cavity, the retroperitoneum, or the pelvic cavity, but only very rarely in the pancreas.