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PubMed1992

Identification of surgical biopsy borders by use of india ink.

Separation of surgical biopsy borders from artifactual borders created during trimming of biopsy specimens is necessary to avoid misinterpretation of histologic borders. Misinterpretation of a contaminated trimming border as a surgical border may lead to additional surgery and excessive removal of normal tissue. Likewise, a neoplasm may regrow locally or metastasize if a surgical border infiltrated with neoplastic cells is falsely assumed to be an artifactual trimming border. The use of India ink for distinguishing between surgical biopsy borders and artifactual borders was evaluated. Ten normal tissue specimens from 8 types of tissue (skin, small intestine, urinary bladder, bone, muscle, lung, large intestine, and uterus) were obtained from freshly euthanatized dogs. The specimens were painted with India ink and examined for adherence of the ink to the cut surface of the specimen. Adherence of the ink was observed in all specimens with the exception of the cut surface of the lung. Twenty-five biopsy specimens from dogs with clinical cases of disease were similarly painted with India ink and evaluated. Twenty-two were identified as neoplastic and 3 as inflammatory lesions. Wedges of tissue were obtained from the center of the biopsy specimens to purposely create borders that contained neoplastic tissue. These positive controls were painted with India ink to evaluate the effect of the ink on the histologic appearance of the neoplastic cells. Distortion or alteration of the cellular architecture was not observed in any of the normal specimens, specimens from dogs with clinical cases, or positive controls. The use of India ink for delineation of biopsy borders is a simple technique that presents few technical difficulties.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1991

Effusion cytology.

Cytologic evaluation is the best way to detect the presence of malignancy in body cavity fluids. Although a positive diagnosis is highly reliable, a negative result does not rule out a malignant cause. Adenocarcinomas, well-differentiated squamous carcinomas, small-cell carcinomas, malignant melanomas, large-cell lymphomas, and acute leukemias are accurately classified when present in effusions. The definitive diagnosis of malignant mesothelioma, small-cell lymphomas, and chronic leukemias, and subclassification of sarcomas and poorly differentiated neoplasms are difficult and may require additional diagnostic techniques. With a few exceptions, the exact causes of benign effusions cannot be determined by cytologic methods.

Ascitic Fluid↗

PubMed1986

The morphologic categorization of cell death induced by mild hyperthermia and comparison with death induced by ionizing radiation and cytotoxic drugs.

This paper presents a summary of the morphological categorization of cell death, results of two in vivo studies on the cell death induced by mild hyperthermia in rat small intestine and mouse mastocytoma, and a comparison of the cell death induced by hyperthermia, radiation and cytotoxic drugs. Two distinct forms of cell death, apoptosis and necrosis, can be recognized on morphologic grounds. Apoptosis appears to be a process of active cellular self-destruction to which a biologically meaningful role can usually be attributed, whereas necrosis is a passive degenerative phenomenon that results from irreversible cellular injury. Light and transmission electron microscopic studies showed that lower body hyperthermia (43 degrees C for 30 min) induced only apoptosis of intestinal epithelial cells, and of lymphocytes, plasma cells, and eosinophils. In the mastocytoma, hyperthermia (43 degrees C for 15 min) produced widespread tumor necrosis and also enhanced apoptosis of tumor cells. Ionizing radiation and cytotoxic drugs are also known to induce apoptosis in a variety of tissues. It is attractive to speculate that DNA damage by each agent is the common event which triggers the same process of active cellular self-destruction that characteristically effects selective cell deletion in normal tissue homeostasis.

Animals↗

PubMed1986

Extensive deposition of eosinophil peroxidase in Hodgkin's and non-Hodgkin's lymphomas.

To determine whether occult eosinophil degranulation occurs in lymphomas, the authors performed immunohistologic and cytochemical studies on cryostat sections from 25 consecutive lymph node biopsies. A glucose-oxidase immunohistochemical technique was employed with a murine monoclonal antibody specific for human eosinophil peroxidase (EPO). In 7 cases of Hodgkin's disease, 3 cases of T-immunoblastic sarcoma, and 1 case of small cleaved follicular center cell lymphoma with sclerosis, there was extensive and striking extracellular deposition of EPO in a granular and fibrillar pattern within the connective tissue. Similar degranulation of eosinophils was not observed in any of the benign lymph node specimens or other B-cell lymphomas. It is concluded that eosinophils extensively degranulate and release EPO in some types of lymphoma.

Antibodies, Monoclonal↗

PubMedDate not supplied

Fine needle aspiration cytology of undifferentiated small cell ("anaplastic") hepatoblastoma. A case report.

Cytologic features of a rare case of small cell undifferentiated ("anaplastic") hepatoblastoma are presented. The tumor cells were primitive and closely resembled the group of "small blue cell" pediatric neoplasms--neuroblastoma, lymphoma, Ewing's sarcoma and rhabdomyosarcoma. This particular subtype of hepatoblastoma is the least common and is associated with the worst prognosis.

Biopsy, Needle↗

PubMed1997

Experience with ifosfamide and etoposide combination chemotherapy in extensive-disease small-cell lung cancer.

BACKGROUND: Ifosfamide, an isomeric analogue of cyclophosphamide, has significant activity against many human tumors including lung cancer, testicular cancer, lymphoma and sarcoma, and may be superior to its analogue. Herein, we report our preliminary experience using ifosfamide and etoposide (IE) combination chemotherapy in previously untreated patients with extensive-disease (ED) small-cell lung cancer (SCLC). METHODS: Patients with histologically or cytologically confirmed SCLC, measurable or assessable ED, no previous chemotherapy or thoracic irradiation, younger than 70 years of age, Eastern Cooperative Oncology Group (ECOG) performance status (PS) of 0-3, and adequate marrow, liver, and renal functions were eligible for treatment which consisted of ifosfamide 2.0 g/m2/d given intravenously (i.v.) for 3 days with mesna 400 mg/m2/dose i.v. administered 0, 4, and 8 hours after the daily administration of ifosfarnide, and etoposide 80 mg/m2/d i.v. given for 3 days in every 4 weeks for a maximum of 6 cycles. RESULTS: Between January 1994 and February 1995, 10 patients were enrolled into the treatment. All were men with a mean age of 63 +/- 6 years. Five patients had an ECOG PS of 0 or 1, 4 patients of 2, and 1 patient of 3. A total of 45 cycles of IE were given. The mean number of cycles per patient was 4.5 +/- 2.1. Six patients completed 6 courses of therapy. Thirty-two of 45 cycles (71%) of IE were given at full doses, while the remaining 13 cycles (29%) were given at 75% of doses. Nine patients were assessable for response. Eight patients had a partial remission and one patient had stable disease. The overall response rate was 89%. The median survival was 8 months (range, 0 to 23 months) and the median failure-free survival duration was 5.5 months (range, 0 to 18 months). The 1- and 2-year survival rates were 30% and 0%, respectively. Myelotoxicity was the most important toxicity, particularly neutropenia, while thrombocytopenia and anemia were mild. Five of 10 patients (50%) experienced grade 4 neutropenia, which occurred in 2 patients during the first course of IE and resulted in one patient death from early sepsis. Other nonhematologic toxicities were mild. CONCLUSIONS: Our preliminary experience demonstrates that ifosfamide is an active drug against SCLC and combination chemotherapy with IE results in similar response rate and median survival, but probably higher myelotoxicity than reported studies in patients with ED SCLC.

Aged↗

PubMed2000

Clear cell sarcoma arising in the transverse colon.

A case of clear cell sarcoma (CCS) arising in the transverse colon is presented. The tumor consisted of sheets or small nests of epithelioid malignant cells possessing pleomorphic nuclei with one or more prominent nucleoli and ample clear or slightly eosinophilic cytoplasm. Some of the tumor cells contained various amounts of melanin pigments that were confirmed by histochemical and ultrastructural examinations. Immunohistochemical examination showed a positive immunoreactivity for HMB45 and S-100 protein. A metastatic nodule, which was found 9 months after surgery, showed similar histological findings to those of the primary one but lacked melanin pigments. Reverse transcriptase- polymerase chain reaction using total ribonucleic acid obtained from metastatic nodule demonstrated the presence of EWS-ATF-1 fusion gene. Based on these findings, the present case tumor is a CCS of the colon.

Aged↗

PubMedDate not supplied

Increased c-myc oncogene expression in Ewing's sarcoma: correlation with Ki67 proliferation index.

AIMS AND BACKGROUND: Ewing's sarcoma is a highly malignant musculoskeletal tumor composed of small round cells. Although important results have been achieved with surgery associated with chemotherapy, recurrent disease is still a major problem. In order to define new prognostic factors useful for therapeutic decision-making, we conducted a study on 38 Ewing's sarcoma samples in which c-myc oncogene expression and Ki67 proliferation index were correlated with clinical outcome. METHODS AND STUDY DESIGN: Nineteen patients developed metastases during follow-up and 10 of these patients died. C-myc and Ki67 protein expression was evaluated by immunohistochemistry performed on 5 microm formalin-fixed and paraffin-embedded sections, while the c-myc mRNA transcript was localized using in situ hybridization. RESULTS: A statistically positive correlation was found between c-myc protein and Ki67 (P = 0.001) and c-myc mRNA and Ki67 expression (P = 0.047). The 38 patients were divided into two groups using as the cutoff 50% of Ki67-positive cells. The disease-free survival and overall survival estimates were 68% and 90%, respectively, in the group of patients with a percentage of Ki67-positive cells <50%, and 25% and 50%, respectively, in the group with a percentage of Ki67-positive cells > or = 50%. The difference between the survival curves was statistically significant (P <0.05 and P <0.01). Furthermore, relapsed patients had a high and uniform expression of c-myc protein and mRNA compared to disease-free patients. CONCLUSION: These results suggest a possible role of the c-myc oncogene and Ki67 antigen in the malignant progression of Ewing's sarcoma.

Adolescent↗

PubMed1995

Nuclear texture in poorly differentiated small round cell tumors. Image analysis study of fine needle aspiration material.

Gradient analysis and pattern spectrum decomposition based on mathematical morphology concepts were used to explore nuclear texture patterns in a pool of 108 cells obtained by fine needle aspiration of five undifferentiated small round cell tumors of childhood, including one case each of Wilms' tumor, neuroblastoma, lymphoblastic lymphoma, Ewing's sarcoma and rhabdomyosarcoma. The aim of the study was to determine the presumptive value of nuclear pattern to correctly allocate each isolated cell to each of the five patients. The cells were examples of five histogenetically different tumors, all undifferentiated and with a close microscopic resemblance to one another. High gradient structures (heterochromatin-euchromatin and nuclear membrane edges) were estimated by a difference-of-boxes filter, and pattern spectrum decomposition was obtained by successive openings and closings performed on the input gray tone image. One important feature of these procedures was that no prior selection by thresholding of the structures to be studied was required, thus obviating subjective bias. Percentages of correctly allocated cells by canonical analysis ranged from 70.0% (rhabdomyosarcoma) to 92.9% (Ewing's sarcoma). Although the five cases could be distinguished using seven texture variables, this does not imply generalization of the results for the differential diagnosis of these tumors. Nonetheless, the possibility that undifferentiated small round cells present distinctive nuclear patterns when studied by sensitive image analysis techniques is suggested by our results.

Biopsy, Needle↗

PubMed1994

The Ewing family of tumors--a subgroup of small-round-cell tumors defined by specific chimeric transcripts.

BACKGROUND: Precise diagnosis of small-round-cell tumors is often a challenge to the pathologist and the clinical oncologist. In Ewing's sarcomas and related peripheral primitive neuroectodermal tumors, a t(11;22) translocation or a (21,22) rearrangement is associated with hybrid transcripts of the EWS gene with the FLI1 or ERG gene. To investigate the diagnostic implication of this observation, we searched for these hybrid transcripts in tumors from patients with clinical and radiologic features of Ewing's sarcoma or peripheral primitive neuroectodermal tumors. METHODS: Samples of RNA from 114 tumors were reverse transcribed and subjected to the polymerase chain reaction with primers designed to amplify the relevant chimeric transcripts. All amplified products were sequenced. RESULTS: In-frame hybrid transcripts were observed in 89 cases. A hybrid transcript was found in 83 of 87 cases (95 percent) of Ewing's sarcoma or peripheral primitive neuroectodermal tumors. Samples of RNA from all of 12 tumors that had been proved to be other than Ewing's sarcoma or neuroectodermal tumors had no hybrid transcript. However, 6 of 15 undifferentiated tumors whose type was ambiguous (nonsecreting, poorly differentiated neuroblastoma or undifferentiated sarcoma) contained a hybrid transcript, suggesting that they might have to be reclassified. CONCLUSIONS: A subgroup of small-round-cell tumors identified as belonging to the Ewing family of tumors can be defined according to a specific molecular genetic lesion that is detectable by a rapid, reliable, and efficient method. This approach can be applied to small specimens obtained by fine-needle biopsies.

Adolescent↗

PubMedDate not supplied

Anticancer efficacy of methioninase in vivo.

Therapeutics that are selective for cancer would have a high potential for efficacy. We have previously shown that the metabolic defect of enhanced methionine dependence is a broad cancer-selective target. Methionine depletion can completely arrest the growth of methionine-dependent tumor cells in vivo with a reversible pre-mitosis cell-cycle block. Dietary methionine depletion can partially arrest the growth of methionine-dependent rodent tumors in vivo. This report demonstrates that methioninase isolated from Pseudomonas putida can arrest rodent and human tumors in nude mice with no apparent toxic side effects. Methioninase injected i.p. arrested the growth of the Yoshida sarcoma in nude mice and greatly slowed the growth of the H460 human non-small-cell-lung carcinoma in nude mice. The effectiveness of methioninase against H460 was in contrast to 5-fluorouracil and vincristine, which were inactive against this tumor. The activity of the administered methioninase did not cause weight loss for up to 10 days treatment at 40-120 units/day indicating the possibility of low toxicity. In contrast, vincristine was highly toxic despite its ineffectiveness. Methioninase also induced a tumor-specific late cell-cycle block. The tumor-selective late cell-cycle block induced by methioninase should be able to be exploited to enhance the tumor specificity of antimitotic drugs and other agents in future experiments. Thus methioninase is a highly effective antitumor agent with a new tumor-selective mode of action with minimal toxicity, demonstrating potential clinical effectiveness against solid tumors.

Animals↗

PubMed2007

Extreme sensitivity to Yondelis (Trabectedin, ET-743) in low passaged sarcoma cell lines correlates with mutated p53.

Yondelis (Trabectedin, ET-743) is a marine anticancer agent currently in Phase II/III development in patients with advanced pretreated soft tissue sarcoma. In the present study, we generated a panel of low passaged tumor cell lines from samples explanted from chemonaive sarcoma patients with different tumor types. We assessed in vitro sensitivity/resistance to Trabectedin and doxorubicin in a panel of sarcoma cell lines and examined the correlation between molecular alterations in DNA repair genes and sensitivity to Trabectedin. We treated cell lines with Trabectedin and doxorubicin in both 96-h and clonogenic assays. In both assays, well-defined groups of resistant and sensitive cell lines were observed. Resistance to Trabectedin did not correlate with resistance to doxorubicin, indicating that the two drugs may have different mechanisms of resistance. p53 mutations and deletions correlated with extreme sensitivity (IC50 < 1 nM) to Trabectedin (P < 0.01). In a pair of isogenic cell lines differing only in the presence or absence of wild-type p53, the absence of p53 rendered cells threefold more sensitive to Trabectedin.

Cell Proliferation↗

PubMed1984

Diagnosis of soft tissue sarcomas.

Based on a review of 752 cases coded as soft tissue sarcomas, histologic features were analyzed for a differential diagnosis, dividing the sarcomas in the first diagnostic step into purely descriptive groups, regardless of biologic behavior: spindle cell, small cell, pleomorphic and myxoid varieties. The tumor categories mainly discussed in order were fibrosarcoma, leiomyosarcoma, malignant schwannoma, synovial sarcoma, malignant fibrous histiocytoma, embryonal and alveolar rhabdomyosarcoma, malignant neuroepithelioma , extraskeletal Ewing's sarcoma, and myxoid and other types of liposarcoma. The discussion was focused on the problems we were facing often in the histologic diagnosis of these tumors, emphasizing in particular those microscopic features which were helpful in differential diagnosis. Principal clinical features, important for an accurate diagnosis, were added to the histopathologic considerations in each item, together with prognosis of all these Japanese patients, regardless of the stages. Other benign and malignant lesions confused occasionally with the soft tissue sarcomas were also listed. With the aid of electron microscopy and immunohistochemistry, sometimes each differentiating feature can be identified but these methods are not always contributory to a diagnosis. Routine light microscopy with or without standard histochemical techniques remains essential to avoid pitfalls when attempting to diagnose the tumor.

Chondrosarcoma↗

PubMed1985

Possible differential diagnosis of neuroblastoma from rhabdomyosarcoma and Ewing's sarcoma by using a panel of monoclonal antibodies.

The accurate diagnosis of malignant tumor type is essential to enable the correct therapeutic regimen to be followed and to predict a patient's prognosis. However, the differential diagnosis of "small-round-cell" tumors, represented by neuroblastoma, rhabdomyosarcoma, lymphoma/leukemia and Ewing's sarcoma, can occasionally be difficult by conventional morphological and biochemical methods. If tumor membrane markers were available, these could provide rapid and accurate diagnostic aids. In the present work, a panel of 9 monoclonal antibodies raised against hematopoietic cells (BA-1, BA-2, J-5 and B7/21), brain cells (UJ-13A, UJ-127-11 and anti-Thy-1), and neuroblastoma cells (HSAN1.2 and PI153/3) was used to analyze the membrane phenotypes of 12 neuroblastoma, 4 rhabdomyosarcoma and 3 Ewing's sarcoma cell lines and cells of 3 fresh bone marrow tumors. BA-1, UJ-127-11 and PI153/3 antibodies may be useful for the differential diagnosis of neuroblastoma from rhabdomyosarcoma and Ewing's sarcoma.

Antibodies, Monoclonal↗

PubMed1992

[Pilot phase II trial of high-dose etoposide combined with cisplatin in the treatment of refractory lung cancer].

The efficacy of combined high-dose etoposide with standard dose cisplatin was evaluated in patients who had refractory lung cancer after standard chemotherapy. Each patient was given etoposide at 500 mg/m2/day on day 1 to 3 continuously (total dose 1,500 mg/m2) and cisplatin at 80 mg/m2 on day 1. Fifteen patients (7 adenocarcinoma, 5 small cell lung cancer, 2 squamous cell lung cancer and 1 sarcoma, which latter was difficult to distinguish from giant cell carcinoma) were entered in this study. The overall response was 41.7% (5 of 12); five partial response, 6 no change, and 1 progressive disease. Three treatment-related deaths were observed; one resulted from sepsis and two from respiratory failure because of tumor progression. All of the patients developed severe myelosuppression; the mean nadir white blood cell count was 400, and the mean nadir platelet count was 24,000 in 28 evaluable courses. The range of maximum concentration of etoposide determined by HPLC was from 17.4 to 39.1 micrograms/ml. These results suggest that high-dose etoposide combined with a standard dose of cisplatin is effective against refractory lung cancer.

Adenocarcinoma↗

PubMed1992

Preclinical antitumour activity and animal toxicology studies of rhizoxin, a novel tubulin-interacting agent.

Rhizoxin is a 16-membered antifungal macrocyclic lactone isolated from the plant pathogenic fungus Rhizopus chinensis. The compound binds to tubulin, preventing microtubule formation, and inhibiting mitosis. It possesses antitumour activity in vivo against various preclinical murine models, both leukaemias and solid tumours model, as well as in vincristine- and doxorubicin-resistant leukaemia lines. In the present study, cytotoxic activity was observed in human tumour cell lines in vitro at very low concentrations (+/- 10(-10) M) particularly against melanoma, colon, renal, non-small cell and small cell lung cancer. In vivo antitumour activity was demonstrated in murine P388 and L1210 murine leukaemias, solid tumour models B16 melanoma and M5076 sarcoma, and in 5 out of 9 human solid tumour xenografts: LOX melanoma, MX-1 breast cancer, non-small cell lung cancer A549, and small cell lung cancers LXFS 605 and LXFS 650. The absence of cross-resistance to vinca alkaloids was confirmed in vivo against the vincristine-resistant P388 leukaemia subline and the vincristine-resistant human small cell lung cancer LXFS 650. In addition, the antitumour activity of rhizoxin was improved by prolonged or repeated drug administration indicating a schedule dependency. In animal toxicology studies, transient changes in erythrocyte and leukocyte numbers, local phlebitis, diarrhea, and spermatogenic arrest were observed. The LD10 value of rhizoxin after a single intravenous injection was 2.8 mg/kg (8.4 mg/m2). One-tenth of the mouse equivalent LD10 (0.84 mg/m2), the starting dose for clinical phase I studies, was considered to be safe in rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed2001

PNET-like features of synovial sarcoma of the lung: a pitfall in the cytologic diagnosis of soft-tissue tumors.

Fine-needle aspiration (FNA) cytology of soft-tissue tumors is evolving. As more experience is gained, we are becoming aware of potential pitfalls. We describe 2 cases of synovial sarcoma of the lung, primary and metastatic, in patients who had FNA biopsy performed on a lung mass. The cytologic smears showed extremely cellular groups of malignant small round cells, intersected by small blood vessels, with numerous loose single cells, in a background of macrophages and mature lymphocytes. The tumors displayed monomorphic cells forming rosettes and displaying occasional mitoses. A diagnosis of neuroendocrine tumor/primitive neuroepithelial tumor (PNET) was suspected. Furthermore, this suspicion was supported by immunohistochemical stains, which showed positivity for a neuroendocrine marker, Leu 7 (case 1), and for a neural marker, CD 99 (O 13 or HBA 71) (both cases); and negativity for cytokeratins (case 1). The resection specimen of case 1 had mostly tightly packed small round cells, with occasional rosettes, similar to the FNA biopsy, and focal areas composed of spindle cells, organized in a focal fibrosarcoma-like and hemangiopericytoma-like pattern. A balanced translocation between chromosomes X and 18, demonstrated by both karyotyping and fluorescent in situ hybridization (FISH), enabled us to make a diagnosis of synovial sarcoma, which was histologically classified as poorly differentiated. Case 2 was a metastatic biphasic synovial sarcoma of the arm, with a prominent epithelial component. Synovial sarcoma, when composed mainly of small round cells on cytologic smears, is a great mimicker of neuroendocrine/PNET tumors, with light microscopic and immunohistochemical overlap. Awareness of this potential pitfall may aid in preventing a misdiagnosis. Its recognition is of major concern, especially for the poorly differentiated variant, because it is associated with a worse prognosis.

Adult↗

PubMed1996

Primary cutaneous Ewing's family sarcoma. Report of a case with immunostaining for glycoprotein p30/32 mic2.

The differential diagnosis of cutaneous small round cell malignancies is a relatively uncommon but recurrent problem that usually requires adjuvant techniques including special histochemical stains, immunohistochemistry (IHC), electron microscopy (EM), and cytogenetics (CG) to arrive at a definite answer. This report describes a case of a primary cutaneous malignancy that, after workup, fulfilled the criteria of extraskeletal Ewing's family sarcoma, which was corroborated by IHC with an antibody to glycoprotein p30/32 mic2 that is highly expressed in these neoplasms. The lesions consisted of a large nodular proliferation of poorly differentiated monotonous small round cells confined to the dermis and subcutaneous tissue. The cells had high nuclear to cytoplasmic (N/C) ratios, scattered prominent nucleoli, and indistinct cytoplasm. A periodic acid-Schiff (PAS) stain with and without diastase demonstrated abundant cytoplasmic glycogen. The glycogen was confirmed with EM, which did not show neurosecretory granules, but extensive sectioning of the tissue blocks demonstrated with light microscopy a single focus with pseudorosette formation. IHC was positive for monoclonal antibody (MAb) O13 to glycoprotein p30/32 mic2 and negative for lymphoid (CD45), neural (S-100, NF, GFAP), neuroendocrine (NSE), and muscle (MSA, desmin) markers. To the best of our knowledge, this is one of few reported cases of primary cutaneous (extraskeletal/extraosseous) Ewing's sarcoma (EEWS) and the first to use IHC with MAb O13, which recognizes the cell surface glycoprotein p30/32 mic2. This case further illustrates the continuum between EEWS and primitive peripheral neuroepithelioma and supports the unifying concept that these two entities are merely subtle morphologic variants of the same malignant neoplasm, which is better designated a Ewing's family sarcoma.

12E7 Antigen↗