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PubMed1989

Fibrosarcoma of the mandible following supravoltage irradiation. Report of a case.

Supravoltage irradiation is commonly thought not to be carcinogenic. Several recent studies question this concept, as does our case report. A 50-year-old woman with stage 1 squamous carcinoma of the left side of the tongue was treated in 1973 with 73 Gy of supravoltage irradiation. Twelve years later a painful, ulcerated lesion that eventually was shown to be fibrosarcoma developed in the contralateral mandible. The fibrosarcoma in this case fulfills all criteria for diagnosing radiation-induced neoplasia and demonstrates that supravoltage irradiation, like other forms of irradiation, can cause malignancy. The occasional occurrence of sarcoma should be recalled during follow-up of patients treated with supravoltage radiation. Similarly, the possibility of radiation-induced tumors should be considered in planning treatment for younger patients with tumors that can be treated equally well by surgery or irradiation.

Carcinoma, Squamous Cell↗
PubMed1998

Pulsing of dendritic cells with cell lysates from either B16 melanoma or MCA-106 fibrosarcoma yields equally effective vaccines against B16 tumors in mice.

BACKGROUND AND OBJECTIVES: Dendritic cells (DC) pulsed in vitro with a variety of antigens have proved effective in producing specific antitumor effects in vivo. Experimental evidence from other laboratories has confirmed that shared antigens can be encountered in histologically distinct tumors. In our experiments, we set out to evaluate the immunotherapeutic potential of vaccines consisting of DC pulsed with MCA-106 fibrosarcoma or B16 melanoma cell lysates and to determine whether a cross-reactivity exists between the two tumors. METHODS: DC were prepared from the bone marrow of C57BL/6 (B6) mice by culturing progenitor cells in murine granulocyte-macrophage colony-stimulating factor (GM-CSF). They were separated into three equal groups and were either pulsed with B16 melanoma cell lysates (BDC), pulsed with tumor extract from the syngeneic fibrosarcoma MCA-106 (MDC), or left unpulsed (UDC). DC were then used to immunize three groups of mice, with all mice receiving two weekly intravenous (IV) doses of 1 x 10(6) DC from their respective preparations on days -14 and -7. A fourth group of control mice were left untreated. On day 0, all mice were challenged with subcutaneous injections of 1 x 10(5) B16 and 1 x 10(5) MCA tumor cells, administered in the left and right thighs, respectively. After the inoculations, the mice were monitored closely with respect to tumor growth and survival. RESULTS: The MDC mice developed specific cellular immunity directed against not only MCA-106 tumor cells, but also against B16 melanoma, as measured through chromium-release assays of splenocyte preparations, while remaining ineffective at killing both L929 fibroblasts and CT26 tumor cells. By day 30 after tumor inoculations, control mice manifested the largest B16 tumor volumes at a mean of 2185 mm3, followed by the UDC, MDC, and BDC groups at 92 mm3 (P=0.00008), 3 mm3 (P=0.000002), and 2 mm3 (P=0.00004), respectively. The survival data mirrored this pattern, with control animals displaying the shortest mean survival time (37.1+/-4.0 days), followed by UDC (44.8+/-6.6), MDC (56.2 +/-14.7), and BDC (56.4+/-18.3) animals. No significant differences were noted between MCA-106 and B16 cell lysate-pulsed DC vaccines with respect to their abilities to inhibit B16 tumor growth and to prolong survival. These findings were confirmed using a B16 pulmonary metastasis model. Likewise, vaccination with interferon-gamma gene-modified MCA-106 tumor cells was shown to be effective at protecting against a subsequent subcutaneous B16 tumor challenge in 3 of 4 mice observed. CONCLUSIONS: These results demonstrate that immunization with antigen-pulsed DC confers cellular immunity, retards tumor growth, and prolongs the survival of tumor-challenged mice. The ability of MCA-106 cell lysate-pulsed DC vaccines to inhibit the growth of subcutaneous B16 tumors also suggests the presence of shared tumor-associated antigens between these two histologically distinct tumors.

Animals↗
PubMed1996

Juvenile fibrosarcoma of the temporal bone.

A case of juvenile fibrosarcoma arising from the head and neck region is described. This type of tumour should be considered as a separate entity different from the fibrosarcoma in adults because of the different clinical behaviour. The symptomatology, the radiographic features and the literature data are reviewed.

Child, Preschool↗
PubMed1996

Multiple inflammatory fibrosarcoma of the abdominal cavity in a child.

Inflammatory fibrosarcoma is a rare condition in childhood. In the abdominal location, its behaviour is often aggressive and potentially metastasizing. We report a case of a 3-year-old female with abdominal inflammatory fibrosarcoma who relapsed after 1 month from radical surgery. Chemotherapy was ineffective, and we registered a brief stabilisation of disease only with alpha-IFN. Our case confirms the potential malignancy of this tumour and its resistance to treatment. It is noteworthy that the therapy with alpha-IFN improved the quality of life in this child for 4 months.

Abdominal Neoplasms↗
PubMed1998

Prenatal sonographic appearance of congenital fibrosarcoma.

Congenital fibrosarcoma is a rare soft tissue sarcoma. A 22-year-old woman in the 22nd week of her first pregnancy underwent sonographic examination, which revealed a soft tissue swelling of the fetus's left thigh. The pregnancy was terminated, and congenital fibrosarcoma was diagnosed by pathologic examination. To our knowledge, this is the first published report of the intrauterine sonographic observation of this tumor in a fetal extremity.

Adult↗
PubMed1996

Frequent occurrence of p53 mutations in rhabdomyosarcoma and leiomyosarcoma, but not in fibrosarcoma and malignant neural tumors.

We have analyzed soft-tissue sarcomas (STS) molecularly for mutations in the tumor-suppressor gene p53 and immunohisto-chemically for expression of p53 and mdm2 proteins. In this study, tumor samples from 3 groups of soft-tissue sarcomas, i.e., fibrosarcomas, myogenic sarcomas and malignant neural tumors (MNT), were investigated. The methods applied encompass immunohistochemistry on 198 tumor samples using p53 antibodies (DO-1 and DO-7) and an mdm2 antibody (IF-2). Out of these, 100 samples were subjected to non-radioactive PCR-SSCP-sequencing analysis. Immunohistochemical detection rate for p53 (range of 57% to 67%) and for mdm2 proteins (range of 19 to 44%) was similar in all 3 groups. In higher tumor grades, an increased rate of immunopositivity was found for p53 but not for mdm2. Investigation of p53 mutational status revealed 6 mutations in myogenic sarcomas but none in malignant neural tumors or fibrosarcomas, suggesting different roles of p53 in the 3 STS groups. Interestingly, a G-->A transition in codon 245 (a CpG site) was found in 3 myogenic sarcomas. Our results and those of others suggest p53 codon 245 as a mutational hotspot in sarcomas, as recognized in carcinomas.

Base Sequence↗
PubMed1998

HT-1080 fibrosarcoma cell matrix degradation and invasion are inhibited by the matrix-associated serine protease inhibitor TFPI-2/33 kDa MSPI.

The urokinase-urokinase receptor system plays a dominant role in the degradation and invasion of extracellular matrix (ECM) by tumor cells. In this system, urokinase bound to its cell receptor converts plasminogen to plasmin, a broad-spectrum serine protease that participates in the degradation and invasion of connective tissues by tumor cells. In this study, we evaluated whether these activities of plasmin are inhibited by a newly characterized human 32 kDa recombinant serine protease inhibitor called trypsin/tissue factor pathway inhibitor-2 (rTFPI-2). We found that rTFPI-2 dose-dependently inhibited fluid-phase plasmin as well as plasmin generated on the ECM and/or the cell surface of HT-1080 fibrosarcoma cells. The degradation of radiolabeled matrix as well as Matrigel invasion by these tumor cells is also inhibited by rTFPI-2 in a dose-dependent fashion. We have reported that rTFPI-2 is identical to 33 kDa extracellular matrix-associated serine protease inhibitor (33 kDa MSPI), whereas the 31 and 27 kDa MSPIs are under-glycosylated forms of the 33 kDa MSPI. We therefore evaluated the ability of MSPIs from the ECM of dermal fibroblasts to inhibit plasmin and found that the plasmin activity was effectively blocked by the MSPIs. We have also evaluated whether the HT-1080 cells synthesize and secrete the MSPIs and found that the synthesis and secretion of the MSPIs was undetectable in these cells. Collectively, our results suggest that rTFPI-2/33 kDa MSPI inhibits plasmin on the tumor cell and ECM surfaces as well as the degradation and invasion of matrix by HT-1080 fibrosarcoma cells.

Antineoplastic Agents↗
PubMed1998

Recurrent chromosome changes in two adult fibrosarcomas.

Cytogenetic analysis of two adult fibrosarcomas revealed clonal chromosomal rearrangements including unbalanced translocations between chromosomes 2 and 19, with the same segment, 2q21-qter, translocated onto 19p13 in one tumor and 19q13 in another; and partial monosomy of 10q due to add(10)(q22) and del(10)(q22q25) seen in one tumor each. This is the first description of nonrandom chromosomal changes in adult fibrosarcoma.

Adolescent↗
PubMed1999

Pulmonary fibrosarcoma in childhood: fiber-optic bronchoscopic diagnosis and review of the literature.

Primary pulmonary fibrosarcoma is a rare malignant tumor in childhood. In the absence of metastases, complete resection is curative. An 8-year-old boy suffered from unresolving pneumonia due to an obstructing lesion in the left main bronchus. Cytology of the bronchoalveolar lavage fluid and histology of bronchial biopsy revealed the diagnosis of pulmonary fibrosarcoma. The tumor did not respond to chemotherapy, and a total lobectomy with sleeve resection was performed with complete removal of the neoplasm. Two years after the operation the child has no evidence of disease.

Biopsy↗
PubMed1999

Immunogene therapy of murine fibrosarcoma using IL-15 gene with high translation efficiency.

We have recently found that translational efficiency is up-regulated by an alternative exon in IL-15 mRNA in mice. In a malignancy model using BALB/c mice and syngeneic Meth A fibrosarcoma (Meth A), we successfully applied immunological gene therapy with IL-15 protein using alternative IL-15 cDNA with high translational efficiency. Two expression vectors carrying the murine IL-15 gene were constructed for use in tumor immunotherapy, one utilizing IL-15 cDNA with alternative exon 5 and the second utilizing IL-15 cDNA with normal exon 5. The first vector induced the production of a large amount of IL-15 protein in Meth A cells, whereas tumor cells transfected by the second vector produced only a marginal level of IL-15 protein. Although cell growth of both transfectants in vitro remained unchanged, inoculation of clones transfected with normal IL-15 cDNA resulted in progressive tumor growth, while clones transfected with alternative IL-15 cDNA led to the rejection of the tumor. The clone producing high levels of IL-15 grew progressively in nude mice and mice treated with anti-CD4 monoclonal antibodies (mAb), whereas the growth of the transfectants was retarded in anti-CD8 mAb- or anti-asialo GM1 antibody-treated mice. Cured mice were shown to have generated immunity against a subsequent challenge with the wild type of Meth A but not against Meth 1 tumor cells, another type of fibrosarcoma derived from BALB/c mice. Thus, tumor therapy based on IL-15 gene transfection was effective against Meth A tumor cells, suggesting a possible application to human neoplasms.

Animals↗
PubMed1999

Search for novel proteins involved in the development of chemoresistance in colorectal cancer and fibrosarcoma cells in vitro using two-dimensional electrophoresis, mass spectrometry and microsequencing.

In search of novel mechanisms that may lead to the development of chemoresistance of malignant tumors of the large bowel we used two-dimensional electrophoresis to identify proteins that were overexpressed in colorectal and fibrosarcoma cell lines that were resistant towards mitoxantrone. This cytostatic drug is known to lead to atypical multidrug resistance, i.e., the classical mechanism of multidrug resistance (MDR) accompanied by the overexpression of P-glycoprotein (P-gp) is ineffective. Using mass spectrometry and microsequencing we found adenine phosphoribosyl transferase and breast cancer specific gene 1 (BCSG1) overexpressed in the resistant colorectal tumor cell line. In the chemoresistant fibrosarcoma cell line we found two proteins that were overexpressed. One was identified as Rho-guanine dinucleotide phosphate (Rho-GDP) dissociation inhibitor and the other had sequence homologies with yeast protein yer-7. The putative role of these proteins is discussed.

Antineoplastic Agents↗
PubMed2000

MS-2 fibrosarcoma characterization by laser induced autofluorescence.

BACKGROUND AND OBJECTIVE: MS-2 fibrosarcoma implanted in BALB-CDF1 mice was investigated by frequency and time domain measurements of the autofluorescence (AF) radiation emitted upon excitation by a N(2) laser beam (337.1 nm). STUDY DESIGN/MATERIALS AND METHODS: AF spectra were obtained by using a spectrograph, a multichannel plate and an optical multichannel analyzer for the steady state detection. Time-resolved spectra were performed by means of a monochromator, a photomultiplier, and a digital signal analyzer. RESULTS: Spectral measurements show that the autofluorescence intensity of pathologic tissue is lower than that of healthy one in the 400- to 500- spectral region. In the same spectral range, we found the fluorescence decay to be the sum of a fast and a slow component. The lifetime of the fast component of tumoral tissue is significantly lower than that of healthy samples. CONCLUSION: Frequency and time domain measurements used in combination show that MS2-fibrosarcoma is characterized by the probable presence of the free form of NADH.

Animals↗
PubMed1976

Infantile fibrosarcoma.

The pathologic features and the behavior of 53 cases of infantile fibrosarcoma are presented. The tumor nearly always occurred during the first 2 years of life; 41 of the 53 cases occurred during the first, six during the second, and three each during the third and fourth year of life, respectively. Twenty of the 53 cases were present at birth. The tumor was more common in boys (60%) and affected chiefly the distal portions of the lower and upper extremities (72%). Most of the tumors grew rapidly and reached a large size within a few weeks or months. They were generally poorly circumscribed and infiltrated variously subcutaneous fat, muscle, fascia and tendons. Microscopically, they were composed of immature-appearing spindle-shaped cells and were marked by their high cellularity and prominent mitotic activity. Despite these features, follow-up information revealed a favorable clinical course, particularly as compared with the adult form of fibrosarcoma. Of the 48 patients with follow-up data, 31 were alive and well with no evidence of recurrence, eight were alive with recurrence, and one was alive following lobectomy for metastatic tumor. Of the living patients, 12 were treated with amputation, nine with radical or wide local excision, and 15 with simple excision. In two cases surgery was followed by chemotherapy, and in one, by radiotherapy. Eight of the 48 patients with follow-up had died, four of metastatic tumor (8.3%) and four of miscellaneous causes. Wide local excision appears to be the treatment of choice unless the size of the tumor and its anatomic location require amputation. Since late recurrent and metastatic lesions were encountered, long-term followup is necessary before one can safely assume that the patient has been cured.

Child, Preschool↗
PubMed1978

Single dose X-irradiation and concomitant hyperthermia on a murine fibrosarcoma.

The objectives of this study were to quantitate the effects of local tumor hyperthermia (LTH) and concomitant x-irradiation (RAD) on a moderately radioresistant murine fibrosarcoma in situ. Comparisons were made to the combined treatment response on the Ridgway osteogenic sarcoma, a radio sensitive tumor previously used in this laboratory and to establish the Meth-A fibrosarcoma as a model system for combined modality studies. 1.0 cm3 tumors were exposed to single doses of RAD ranging from 0.5-3.5 krad alone or 0.5-2.3 krad in combination with LTH (water bath at 43.1 +/- .05 C for 20 minutes) applied immediately postirradiation. LTH significantly enhanced the action of radiation as measured by tumor volume analysis, mean survival time and cures. The ratio of radiation doses vs. RAD + LTH required to produce an equivalent response ranged from 1.4 to 2.5 depending upon the endpoints evaluated. These findings are consistent with single dose studies on the radiosensitive Ridgway osteogenic sarcoma and suggest that the tumoricidal effectiveness of combination radiation and hyperthermia cannot be predicted on the basis of the radiation alone responsiveness of tumor.

Animals↗
PubMed1980

Definitions of osteosarcoma, chondrosarcoma, and fibrosarcoma of bone.

The current definition of osteosarcoma, based on the prescence of tumor osteoid, is unsatisfactory because it fails to identify some examples of chondroblastic, fibroblastic, and anaplastic osteosarcoma having no demonstrable tumor osteoid. The tumor cells in osteosarcoma, whether osteoblastic, chondroblastic, fibroblastic, or anaplastic, contain abundant alkaline phsophatase, whereas this enzyme is scanty or absent in condrosarcoma and fibrosarcoma. It is therefore proposed that these bone sarcomas are best defined according to the origin of the constituent tumor cells and their alkaline phosphatase content: osteosarcoma--a malignant tumor of osteoblasts (alkaline phosphatase positive); chondrosarcoma--a malignant tumor of chondroblasts (alkaline phosphatase negative); and fibrosarcoma--a malignant tumor of fibroblasts (alkaline phosphatase negative).

Alkaline Phosphatase↗
PubMed1980

Congenital fibrosarcoma: presence of a histiocytic component.

We describe the histologic and ultrastructural appearance of a massive soft-tissue tumor in the left lower extremity of a newborn girl. In its clinical presentation and morphologic features, this tumor corresponded to the entity currently known as congenital fibrosarcoma. The variability of histologic conformation of these lesions is emphasized. Ultrastructural study disclosed many cells with the subcellular morphology of elements of the histiocytic-macrophagic series. Whether these cells are viewed as an integral part of the tumor or as a secondary feature, their presence in a congenital fibrosarcoma is of interest for understanding of biologic behaviour of these uncommon tumors.

Female↗
PubMed1985

Chemotherapy for inoperable infantile fibrosarcoma.

Infantile fibrosarcoma, an uncommon disease of childhood, generally occurs in an extremity and despite high local recurrence rates is usually curable with surgical excision alone. Two patients whose tumors were unresectable because of extensive retroperitoneal involvement are reported. Treatment with doxorubicin, vincristine, and cyclophosphamide resulted in complete clinical responses in both patients. They remain alive and tumor free 2.5 and 4 years from diagnosis. Chemotherapy as a single modality appears to be effective in controlling unresectable infantile fibrosarcoma.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed2000

Protein kinase C isoforms involved in regulation of cell shape and locomotion of human fibrosarcoma HT1080 cells.

The role of protein kinase C (PKC) isoforms in the regulation of cell shape [switch between fibroblast-like and crescent shape (CS)] and of locomotion of human fibrosarcoma HT1080 cells has been investigated. The PKC activator phorbol myristate acetate (PMA) induced the transition of elongated fibroblast-like cells into CS cells and stimulated locomotion. Both responses to PMA were inhibited by the PKC inhibitor Ro 31-8220. Analysis of the time course showed that stimulation of shape changes (formation of CS cells) and locomotor activity (increase in the proportion and speed of locomoting cells) was maximal in the early phase of the response (up to 2.5 hr) and significantly decreased later (15 to 21 hr). CS formation and stimulated locomotion correlated closely with a marked redistribution from the cytosol to the membrane of PKC isoforms alpha, beta1 and gamma in the early phase (0.5 to 2 hr) following activation with PMA. The subsequent reduction of the proportion of CS cells and of cell locomotion correlated with down-regulation of these isoforms in the second phase (16 to 21 hr). In contrast, the total amount and distribution of PKC beta2 remained almost unchanged with 10(-8) M PMA up to 21 hr. Furthermore, changes in shape and locomotion did not correlate with the responses of PKC delta to PMA. Inhibition of PMA-stimulated locomotion by the more specific inhibitor Gö 6976 is consistent with a role of PKC alpha and beta1 in this response. Ro 31-8220 alone induced a moderate down-regulation of PKC isoforms alpha and delta, but it also inhibited the more pronounced down-regulation of these isoforms by PMA. Our results indicate that activation of PKC isoforms alpha, gamma and beta1, but not beta2 or delta, stimulates locomotion and formation of CS cells in human fibrosarcoma HT1080 cells.

Carbazoles↗