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PubMed2003

[Synovial sarcoma in clinical practice--description of selected cases].

UNLABELLED: Clinically, synovial sarcoma becomes apparent as a growing mass. Initial presentation and the course may be variable. We discuss 4 characteristic patients. CASE 1: A 37 year-old female patient presented with a mass in her thigh after two consecutive resections of a malignant hemangioendothelioma. HISTOLOGY: Biphasic synovial sarcoma (G II). CASE 2: A tumor was enucleated in the adductors of a 42 year-old female patient. HISTOLOGY: Biphasic synovial sarcoma (G I). 2 years later local tumor recurrence (G I) occurred. Treatment was provided by wide resection and radiotherapy. CASE 3: Resection of a suspected neurinoma in the thigh of a 34 year-old male patient. HISTOLOGY: Biphasic synovial sarcoma, positive margins. CASE 4: A 74 year- old female patient receiving anticoagulants was symptomatic due to intracranial tumor hemorrhage of a metastasis of a previously unknown synovial sarcoma of her popliteal fossa. The primary tumor was initially misdiagnosed as Baker's cyst, causing a deep vein thrombosis. HISTOLOGY: Angioinvasive synovial sarcoma (G II). Survival: 11 months. THERAPY: Wide resection and postoperative irradiation in cases 1-3. Indication for the irradiation in case 2 and 3 was due to the inadequate operation. An amputation was performed in case 4 because of infiltration of the neurovascular structures. CONCLUSION: The presentation of synovial sarcoma does not differ from other soft tissue sarcomas. Patients should be treated in specialized centers to reduce inadequate operations. Outcome and rate of metastatic disease suggest the need for improved adjuvant treatment modalities.

Adult↗
PubMed1983

Combination chemotherapy with Clostridium perfringens phospholipase C and cytosine antimetabolites: complementary inhibition directed at membrane lipids.

Tumor cell membranes were susceptible to the action of Clostridium perfringens phospholipase C, and this was reflected by inhibition of cellular replication in culture. The differential susceptibility of two neoplastic cell lines to this enzyme was studied in detail. The growth of sarcoma 180 cells cultured in Fischer's medium was markedly inhibited by phospholipase C; whereas, in contrast, cultured L1210 leukemia cells were relatively resistant to the cytotoxic effects of this enzyme. The differential sensitivity of these two neoplastic cell lines to phospholipase C was corroborated by dye-exclusion tests. Thus, leukemia L1210 cells exposed to a concentration of 0.2 mg of phospholipase C per ml of Fischer's medium for 30 min at 37 degrees C were able to exclude Trypan Blue; whereas, only about 21% of sarcoma 180 cells treated under identical conditions were able to exclude the dye. That the cytotoxicity of phospholipase C to sarcoma 180 was the result of hydrolysis of phospholipids of the plasma membrane was supported by measurements of the rate of hydrolysis of radioactivity from the phospholipid of neoplastic cells prelabeled with [3H]choline. Eighty-two percent of incorporated radioactive choline was released from sarcoma 180 cells treated with phospholipase C in Fischer's medium, whereas, only 20% of the label from [3H]choline was solubilized from L1210 leukemia cells treated with the enzyme under similar conditions. Scanning electron microscopy revealed significant damage to sarcoma 180 cells exposed to phospholipase C in Fischer's medium, which was characterized by alterations in size and shape of cells, disappearance of microvilli, and appearance of fistulas in cell membranes; relatively resistant L1210 leukemic cells did not appear to be markedly damaged by comparable enzyme treatment. Exposure of leukemia L1210 cells to phospholipase C in Puck's saline A increased the sensitivity of these cells to enzymatic action. Under these conditions, a comparable amount of phospholipid was hydrolyzed from surface membranes of sarcoma 180 and leukemia L1210 cells, and the degree of membrane damage appeared to be similar, as measured by the capacity of the tumor cell lines to exclude Trypan Blue and by scanning electron microscopy. The extensive damage to membranes by hydrolysis of phospholipids was not accompanied by a change in the degree of specific binding of [3H]concanavalin A(ConA).(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1989

Conservative treatment for lower gynecological tract malignancies in children and adolescents: the Institut Gustave-Roussy experience.

Between 1972 and 1986, 37 patients with lower genital tract malignancies were treated with intracavitary or interstitial brachytherapy. Thirteen patients presented with clear cell adenocarcinoma, 14 patients with embryonal rhabdomyosarcoma, 6 patients with endodermal sinus tumor, 3 patients with sarcoma, and 1 patient with an undifferentiated tumor. FIGO classification was: Stage I, 16%; Stage II, 47%; and Stage III, 37%. Treatment policy included initial exploratory laparotomy with lymph node biopsy and ovarian transposition, chemotherapy (except in clear cell adenocarcinoma) and/or external radiotherapy prior to interstitial brachytherapy. Chemotherapy consisted of a combination of VAC-Ad (V = vincristine, A = D actinomycin, C = cyclophosphamide, Ad = adriamycin) in rhabdomyosarcoma and sarcomas, and MAC-Ad (M = methotrexate) in endodermal sinus tumor. External radiotherapy was used in seven patients: in one to reduce a bulky clear cell adenocarcinoma (20 Gy) and in six for pelvic nodal involvement (45 Gy). Brachytherapy techniques depended on tumor site and extent, and on the anatomy of the patients. Vulvar tumors were implanted with iridium-192 wires by an afterloading plastic tube technique. Cervical and vaginal tumors were treated with individually tailored moulded vaginal applicators loaded with either cesium-137 or iridium-192, with or without interstitial implants by plastic tube or guide gutter technique. Computerized dosimetry allowed calculation of treatment volumes and doses delivered on the tumor and adjacent critical organs. The prescribed dose (including external radiotherapy) was 60-75 Gy with 1-3 brachytherapy applications of a low dose rate (0.2 Gy/hr). Six patients are dead: one from chemotherapy complication, three of metastases (two sarcomas, one endodermal sinus tumor) and two of pelvic failures and metastases (two clear cell adenocarcinoma). The overall disease free 5-year survival is 72%. Actuarial 5-year local control is 84%, but including salvage is 94%: three (two rhabdomyosarcoma, one clear cell adenocarcinoma) of the five local failures were salvaged by surgery, chemotherapy and/or brachytherapy. Metastases occurred in six patients, one (sarcoma) salvaged by chemotherapy and external radiotherapy. Complications requiring surgery occurred in five patients: two hydronephroses, one urethral stricture, one ileo-cecal obstruction, and one vesicovaginal fistula. Twelve of the 17 patients (71%) over 12 years of age are normally menstruating. Two patients have produced three normal children. This multidisciplinary management of lower gynecological tract tumors including brachytherapy is both conservative and effective.

Adenocarcinoma↗
PubMed2004

Granulocytic sarcoma of the testis.

Granulocytic sarcoma is a rare tumor composed of neoplastic blood cells, typically occurring during the course of, or before the onset of, acute nonlymphoblastic leukemia. We present a case of a 37-year-old man with acute testicular pain who was found to have a testicular mass diagnosed as granulocytic sarcoma (GS). Because GS virtually always progresses to leukemia, he underwent postoperative radiotherapy and chemotherapy. He was free of disease 6 months after treatment. This case highlights a rare hematologic cancer that urologists and pathologists should be aware of because it can present as a testicular mass.

Adult↗
PubMed1975

Cellular uptake of soluble and aggregated ferritin: distinction between pinocytosis and phagocytosis.

Cellular uptake of ferritin amounting to 0-5 mug/mg cell protein or more can be measured colorimetrically on the basis of ferritin-iron content. 131I-serum albumin, soluble ferritin and aggregated ferritin used in equimolar concentrations are taken up differently by Sarcoma SI80 cells in culture. The net uptakes in 2 h at 37 degrees C are 0-065, 4-3 and 24-7 mug/mg cell protein or 0-93, 8-0 and 45-7 mumol, respectively. Albumin uptake is not inhibited by a 26-fold molar ferritin excess but is significantly inhibited by a 43-fold excess. The transport mechanism of the ferritins differs from that of albumin in that it is significantly inhibitable by 2 times 10(-4) M monoiodoacetate. Soluble ferritin contains small aggregates which are removed by filtration through Millipore membranes of 0-05, 0-1 and 0-22 mum. When the 0-1-mum filtrate is re-examined, uptake is no longer inhibited by iodoacetate. Since it can be inferred from other work that albumin is taken up by pinocytosis and ferritin aggregates by phagocytosis, the difference in susceptibility to inhibition is proposed as a way to distinguish pinocytosis from phagocytosis. Ferritin may form larger visible aggregates in culture medium. The transport mechanism of this aggregated ferritin differs from that of soluble unfiltered ferritin in that it causes concomitant enhancement of albumin uptake. Albumin transported by virtue of this effect becomes partially susceptible to iodoacetate. Thus, in addition to a distinction between pinocytosis and phagocytosis, our data single out 2 forms of albumin transport and 3 forms of ferritin transport.

Azides↗
PubMed1985

Isolation of a line of immortal chicken embryo fibroblasts after transfection with the nuclei of Rous sarcoma virus-transformed Chinese hamster cells.

Secondary cultures of chicken embryo fibroblasts were transfected with purified nuclei from lysed cells of a clonal line of temperature-sensitive Rous sarcoma virus (tsRSV)-transformed Chinese hamster fibroblasts. After propagation for 3 months an established cell line designated ChR32 was obtained in one chicken cell culture. The cells of this line have been propagated so far for 18 months, whereas normal chicken embryo fibroblasts died after 2 months. The established cells were heteroploid with a diploid modal number of macrochromosomes and two Z chromosomes. No Chinese hamster chromosomes could be identified. Southern blot analysis of DNA from the uncloned ChR32 cells and the clones provided evidence that these established cells were, in fact, clonal in origin and contained full-length RSV proviruses and no defective proviruses. Furthermore, they contained, at the 3' end proviral-cellular junction, Bg/II, HpaI, KpnI, SacI, and XbaI fragments of the same size as the Chinese hamster donor cells, suggesting that the cellular sequence adjacent to the provirus is of Chinese hamster origin. The cells after establishment were able to grow continuously at 37 degrees or 41 degrees C and produce a large amount of ts sarcoma virus particles. A corollary finding was that these virus particles were non-leaky for the transforming function at the non-permissive temperature.

Animals↗
PubMed1998

[Liposomal DNA transfection of human sarcoma cells with p53 alterations].

An vital assay allows to optimize liposomal transfection for human tumor cells via FACS. Various cationic lipids were tested to analyse the reporter gene expression (green fluorescent protein, GFP) in different soft tissue sarcoma (STS) cells with known genetic alterations. Furthermore, the cellular uptake of fluorescence-labeled oligodeoxynucleotides (ODN's) was determined. The results obtained with two self-established sarcoma cell lines (LMS6-93, US8-93) were compared with ATCC sarcoma cell lines (Saos-2, A-204, RD) and fibroblast cells. We found maximal 37% cells expressing GFP 24 h post-transfection. All mesenchymal (tumor) cells but not fibroblast cells could be transfected in a cell-specific and lipid-dependent manner. In kinetic studies highest transfection rates were determined between 24 and 48 h, whereas the GFP expression is downregulated after 72 h. Furthermore, we found transfectability is p53 mutation-independent and a relative low toxicity of the new lipids (Lipotaxi and Clonfectin) in comparison to other lipids (Lipofectin, Lipofectamine). By a cell sorting system sarcoma cell lines expressing the reporter gene could be enriched up to 84% of the living cell population. Labeled ODN's were taken up more efficiently (> 90%) when they were mixed with lipids before, but ODN's alone were incorporated into sarcoma cells only in a low percentage (< 10%) and concentration. STS cell cultures showed also a relative high ODN uptake compared with cell lines. We propose the liposomal transfection strategy as an efficient method which can be applied to adherent-growing tumor cells. The method allows simultaneously to study transfection rates, apoptosis and cell cycle alterations in vitro. Furthermore, in future, extension on ex vivo and in vivo transgene expression (xenotransplanted sarcomas) will be evaluated.

Gene Expression Regulation, Neoplastic↗
PubMed1996

Ewing's sarcoma of the skull in an infant. A case report and review.

A 1-year-old female infant presented with a large 7-8 cm Ewing's sarcoma of the left parietal calvarium. It deeply indented the subjacent hemisphere. Wide surgical excision was followed by chemotherapy but not radiation. The patient was clinically free of tumor when she expired 9 months later of sepsis. Though primary Ewing's sarcoma of the skull is said to be relatively rare, we have tabulated 37 cases of this disorder, including the present one (we excluded mandibular tumors (> 100 cases) since they are not usually treated by neurosurgeons). The mean age was 11 years and of those available to follow-up, three quarters were tumor-free 6 months to 7 years postsurgery. The remainder survived an average of 21 months. Ewing's tumors of the calvarium generally grant a favorable prognosis following surgery and/or radiation and chemotherapy. Those at the base of the brain may be more difficult to eradicate. In addition to primary Ewing's tumors, metastases to the skull and the brain from other primary sources in the skeleton have been documented in several reports.

Chemotherapy, Adjuvant↗
PubMed1982

[Clinical x-ray characteristics and growth kinetics of Ewing's tumor].

The clinico-roentgenological peculiarities of the course of Ewing's sarcoma depending on tumor localisation were studied in 66 patients (29 in diaphysis and 37 in metaphysis). Tumor growth rates versus localisation (43 cases) and end results (55 cases) wee compared. The malignancy and growth rate of diaphysic tumors appeared to be higher. This was matched by lower survival rates. Statistical data on growth rates of tumor and survival are presented.

Adolescent↗
PubMed1984

Binding and cytotoxicity of Ricinus communis lectins to HeLa cells, Sarcoma 180 ascites tumor cells and erythrocytes.

The binding of Ricinus communis lectins to HeLa cells, Sarcoma 180 ascites tumor cells and human erythrocytes was studied in detail. Scatchard plots of binding of 125I-lectins to these cells gave biphasic lines except for HeLa cells at 0 degree C. The association constants of lectins for the three cell types at 37 degrees C were lower than those at 0 degree C. The numbers of total binding sites were estimated to be 7 to 16 X 10(7) per HeLa cell, 3 to 4 X 10(7) per Sarcoma 180 ascites tumor cell and 0.4 to 1 X 10(6) per erythrocyte. A fraction, 16 to 27% of the total amount of cell-bound lectin at 37 degrees C, appeared to be bound irreversibly as judged by non-removal on washing with 0.1 M lactose, whereas no lectin was irreversibly bound at 0 degree C. In the case of erythrocytes, no lectin became irreversibly bound even at 37 degrees C. The toxicity of lectins on HeLa cells and Sarcoma 180 ascites tumor cells was investigated. The toxicity of ricin D was 50 times for Sarcoma 180 ascites tumor cells and 140 times for HeLa cells as much as that for castor bean hemagglutinin. As to the sensitivities of both cell types to these lectins, it became apparent that Sarcoma 180 ascites tumor cells were more susceptible than HeLa cells.

Animals↗
PubMed1999

Adults with Ewing's sarcoma/primitive neuroectodermal tumor: adverse effect of older age and primary extraosseous disease on outcome.

OBJECTIVE: To assess outcome and prognostic factors for survival of adults with Ewing's sarcoma/primitive neuroectodermal tumor (PNET). BACKGROUND: Ewing's sarcoma/PNET is a disease of childhood rarely seen in adults. Accordingly, there is a relative paucity of published literature pertaining to outcome for adults with this disease. METHODS: Between 1979 and 1996, 37 patients with newly diagnosed Ewing's sarcoma/PNET were evaluated and treated at the Adult Sarcoma Program at Dana-Farber Cancer Institute and Brigham & Women's Hospital. Twenty-six patients had localized disease at presentation and 11 had metastatic disease. All but two patients received multiagent chemotherapy. Local treatment consisted of surgery (7 patients), surgery and radiation therapy (19), radiation therapy (6), or no local treatment (5). Median follow-up for living patients was 100 months (range 8 to 199). RESULTS: The 5-year survival rate for the group overall was 37%+/-9%. The 5-year local control rate was 85%+/-7%. Significant favorable predictors for survival on univariate analysis included localized disease at presentation, primary origin in bone, primary size <8 cm, and a favorable objective response to chemotherapy. Patients with localized disease had a 5-year survival rate of 49%+/-11% compared with 0% for those with metastatic disease at presentation. Multivariate analysis showed three significant independent predictors for death: metastatic disease at presentation, primary origin in extraosseous tissue versus bone, and age 26 years or older. CONCLUSION: Adult patients with Ewing's sarcoma/PNET at highest risk for death are those who are older than 26 years and have metastatic disease or an extraosseous primary tumor. The development of novel therapies should target these high-risk groups.

Adolescent↗
PubMed1990

Fiberoptic bronchoscopy and sputum examination for diagnosis of pulmonary disease in AIDS patients in Stockholm.

For diagnosing pulmonary disease on 82 occasions in 68 patients (64 males) aged 39 (23-73) years infected with HIV-1 we used flexible fiberoptic bronchoscopy (FFB) with bronchoalveolar lavage (BAL) or washing with or without transbronchial lung biopsy (TBB) and brushing. A clinical diagnosis of lower respiratory tract disease was obtained in 68/82 episodes (83%). An etiological diagnosis was reached by FFB in 59/82 episodes (72%). Pneumocystis carinii (PC), the dominating pathogen causing pneumonia in 54/82 episodes (66%), was detected by FFB in 51/54 (94%). In spite of being isolated in bronchoscopy material in 36/82 episodes (44%) cytomegalovirus (CMV) seemed to be the cause of pneumonia only in 2/36 (5%) episodes. Except PC and CMV, only bacteria (including mycobacteria) were found as infectious etiological agents. Kaposi's sarcoma and pulmonary edema were diagnosed in one patient each. For detection of PC in 37 episodes we compared staining of BAL fluid with indirect immunofluorescence (IF) using monoclonal antibodies (MoAB) with staining of BAL material by silver methenamine (Grocott). Staining with IF MoAB alone of BAL fluid only seemed to be even more sensitive than silver methenamine staining of BAL, TBB and brushing material. When using IF MoAB staining of BAL fluid, TBB and brushing added nothing to the result, except in the patient with Kaposi's sarcoma, diagnosed by TBB. Sputum investigation using IF MoAB for detection was increasingly adopted during the study time. It was very useful (sensitivity approximately 74%) and reduced the number of required FFBs.

Acquired Immunodeficiency Syndrome↗
PubMed1975

Polyamine metabolism in normal and in virus-transformed chick embryo fibroblasts.

The effect of transformation by Rous sarcoma virus on the ornithine decarboxylase levels of chick embryo fibroblasts was studied. Infection with Rous sarcoma virus resulted in increased ornithine decarboxylase activity which preceded morphological alterations by at least 24 hr. The ornithine decarboxylase levels of normal controls, unlike those in Rous sarcoma virus-infected cells, declined with age, so that the enzyme activity of transformed cells was increased twentyfold 5 days postinfection. Infection with a temperature-sensitive mutant of Rous sarcoma virus, T5, stimulated ornithine decarboxylase activity of chick embryo fibroblasts at the permissive (37 degrees) but not at the nonpermissive (42 degrees) temperature. The ornithine decarboxylase activity of T5-infected cells shifted from 42 degrees to 37 degrees increased within 2 hr and reached the levels of wild-type, Schmidt-Ruppin-17A-transformed cells in 11 hr. When T5-transformed fibroblasts were shifted to the nonpermissive temperature, ornithine decarboxylase activity decreased fivefold within 4 hr and paralleled the levels of normal controls in 11 hr. Shifting of temperatures of incubation caused comparable alterations in cellular putrescine but not in spermine or spermidine content.

Avian Sarcoma Viruses↗
PubMedDate not supplied

Aspiration biopsy cytology of primary bone lesions.

Fine needle aspiration cytology of 79 primary bone lesions was done, and the clinical and radiologic features were correlated with cytopathology. Seventy-four of these cases were primary malignant bone tumors, two cases each were tumor-like or inflammatory lesions, and one case was a benign bone tumor. Osteosarcoma (37.7%) and Ewing's sarcoma (15.6%) were the most common primary lesions. Correlation with histopathology was possible in 37 cases, and an accuracy rate of 94.1% was achieved. There was an 89% correlation between radiologic and cytologic diagnoses. It was concluded that in this oncology center a working diagnosis based on cytology was possible in almost all cases after correlating with the radiologic findings. However, when there was a discrepancy between the clinical, radiologic and cytologic diagnoses, an open biopsy was mandatory.

Adolescent↗
PubMed1992

Phenotypic and functional analysis of lymphocytes infiltrating paediatric tumours, with a characterization of the tumour phenotype.

Tumour-infiltrating lymphocytes (TIL) of paediatric tumours obtained from 37 lesions of different histotype (12 osteosarcomas, 5 Wilms' tumours, 7 soft-tissue sarcomas, 5 neuroblastomas and 8 miscellaneous) were studied to establish their potential for therapy. Fresh isolated TIL were cultured for the first 2 weeks with low doses of interleukin-2 (IL-2) (20 Cetus U/ml) to select for "tumour-specific" lymphocytes potentially present in the neoplastic lesion, followed by culture with high doses of IL-2 (1000 Cetus U/ml) to achieve TIL expansion. TIL were grown with more than 10-fold expansion in only 9 cases (mean expansion: 58-fold, range 13.5-346). In 17 cases no viable cells were obtained. After 30 days of culture with IL-2 the proliferative ability of TIL declined sharply in the majority of cases and TIL became refractory to any further stimulus, including addition of IL-4, tumour necrosis factor alpha (TNF alpha) or interferon gamma, and activation with OKT3 in solid phase. In 20 out of 37 cases TIL were available for phenotypic and functional analysis. TIL after long-term culture were predominantly CD3+ but 2 cases of osteosarcoma showed a predominance of CD3+TcR gamma/delta cells. The CD4/CD8 ratio was more than 1 in 10 cases, without correlation with tumour histology, site of lesion or TIL growth. The number of CD16+ and CD25+ lymphocytes decreased progressively during culture, the latter concomitantly with a reduction of TIL growth rate. The lytic pattern of TIL against allogenic and autologous tumour (Auto-Tu) cells was variable, but specific lysis of Auto-Tu was seen in only one case (Wilms' tumour) after culture with TNF alpha and irradiated Auto-Tu cells. The immunohistochemical analysis of tumour lesions revealed a limited lymphocyte infiltrate, a low expression of histocompatibility leukocyte antigens (HLA) class I and of the adhesion molecules ICAM1, LFA3, and a significant production of transforming growth factor beta (TGF beta). These data indicate that TIL obtained from paediatric patients are difficult to expand at levels required for immunotherapy and lack a significant number of tumour-specific T lymphocytes. A low expression of immunomodulatory molecules on tumour cells or the production of suppressive factors may prevent activation and expansion of TIL in paediatric tumours.

Antigens, CD↗
PubMed1993

Genetic changes in lung cancer.

In an attempt to define the type and temporal sequences of somatic genetic changes that precede the onset of invasive lung cancer, and to search for biological markers useful in screening multiple primary tumors of the upper aerodigestive tract, we have performed a cytogenetic and genetic study using normal bronchial epithelium and primary tumor specimens of 68 patients undergoing pulmonary resection for early stage lung cancer, and normal bronchial epithelium of 5 controls with metastatic sarcomas. Of the 68 lung cancer cases, 31 had a single tumor and 37 displayed multiple synchronous or metachronous tumors. Cytogenetic alterations were observed in 59% (23/39) of the evaluable tumor specimens with complex rearranged karyotypes, particularly involving chromosomes 3 (70%), 17 (39%), 11 (26%), 8, 9, 12 (22%), and 7 (17%). Gene alterations were also detected including overexpression of epidermal growth factor receptor (EGFR) in 63% (36/57), HER2/NEU in 21% (12/56), and p53 mutations in 50% (12/24). The overall frequency of genetic changes (any type) in the tumors was 76% (52/68). In the normal bronchial mucosa, we identified a rearranged karyotype in 20% of the evaluable cases (13/63); particularly simple rearrangements involving chromosomes 3p (6 cases), 7 (6 cases), 17 (3 cases), 9, 11 (2 cases), 8 (1 case); as well as overexpression of EGFR in 39% (20/51) and of HER2/NEU in 14% (7/51). The overall frequency of genetic changes (any type) in the normal epithelium was 46% (30/65). The presence of a rearranged karyotype in the bronchial mucosa was associated with a rearranged karyotype in the tumor sample. Other statistically significant correlations were found between histopathologic and clinical features and the occurrence of the different cytogenetic and genetic changes both in tumors and in the normal bronchial mucosa. No genetic abnormalities were found in the bronchial epithelium of the 5 controls.

Biomarkers, Tumor↗
PubMed2004

Duodenocaval fistula: a late complication of retroperitoneal irradiation and vena cava replacement.

Duodenocaval fistula (DCF), an unusual pathology, is associated with a 40% mortality rate in the 36 patients previously reported. Although migrating or ingested foreign bodies, trauma, and peptic ulcer disease are often described etiologies, 11 patients have been described who developed DCF after resection of retroperitoneal tumors, 9 of whom also had postoperative radiotherapy. We report two patients who developed DCF after resection of retroperitoneal tumors followed by radiation therapy. The first patient, a 56-year-old female, presented with upper gastrointestinal hemorrhage requiring transfusion caused by a duodenoprosthetic caval fistula 7 years after successful resection of a retroperitoneal leiomyosarcoma and replacement of the inferior vena cava followed by radiation and chemotherapy. The second patient, a 37-year-old male who had previously undergone resection of a retroperitoneal sarcoma followed by external radiotherapy, developed massive upper and lower gastrointestinal bleeding secondary to a duodenocaval fistula. The etiology, diagnosis, and treatment of DCF are analyzed with an emphasis on DCF following resection and irradiation of retroperitoneal tumors. In most patients, "spontaneous" DCF have occurred as a late complication of high-dose radiation for carcinoma of the right kidney or retroperitoneal structures.

Adult↗