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Biomedical subjects

J Bras

Publications and source records attributed to J Bras.

At least 19 recordsLinked to original sources
PubMed2006

Different susceptibility of osteosarcoma cell lines and primary cells to treatment with oncolytic adenovirus and doxorubicin or cisplatin.

Despite improvements in treatment regimens for osteosarcoma (OS) patients, survival rate has not increased over the last two decades. New treatment modalities are therefore warranted. Preclinical results with conditionally replicative adenoviruses (CRAds) to treat OS are promising. One type of CRAd that was effective against OS cells is Ad5-Delta24RGD. In other types of cancer, CRAds have been shown to interact synergistically with chemotherapeutic agents. Chemotherapy for OS often includes doxorubicin and cisplatin. Therefore, we explored combination treatment of OS cell lines and primary OS cell cultures with Ad5-Delta24RGD and doxorubicin or cisplatin. On OS cell lines, combination treatment was additive to synergistic. Surprisingly, however, on seven of eight primary OS samples no such combination effects were observed. In contrast, in many cases chemotherapy even inhibited CRAd-mediated cell killing. The inhibitory effect of doxorubicin on Ad5-Delta24RGD in primary OS cells appeared to correlate with slow cell growth rate; reduced viral replication and absence of chemotherapy-induced G2 cell cycle arrest. Our results point to the possibility that, at least for OS, virotherapy and chemotherapy should best not be performed simultaneously. In general, our work underscores the importance of testing new genetic anticancer agents and treatment regimens on primary cancer specimens.

Adenoviridae↗
PubMed2001

The role of fine-needle aspiration cytology in children with persistent or suspicious lymphadenopathy.

PURPOSE: The aim of this study was (1) To determine the value of fine-needle aspiration cytology (FNAC) in children with persistent or suspicious peripheral lymphadenopathy and (2) to analyze whether a history of previous malignancy influenced the accuracy of FNAC. METHODS: A retrospective study in an Academic Children's Hospital of 73 FNACs of peripheral lymph nodes in 64 patients (35 boys and 29 girls; median age, 9 years; range, 15 months to 20 years) was performed between 1992 and 1997. Eleven patients were excluded because aspirated material appeared inadequate. Outcome was compared with results of subsequent surgical biopsies, clinical follow-up, or both. Patients were divided into group A "de novo" lymphadenopathy (n = 39) and group B lymphadenopathy and a history of previous malignancy (n = 23). RESULTS: Group A: FNAC showed a benign diagnosis in 25 cases, a malignancy in 13, and was inconclusive in 1. Outcome was false-negative in 2 and false-positive in 1. Sensitivity and specificity were 86% and 96%, respectively. FNAC helped avoid additional surgical procedures in 27 cases (61%). However, if FNAC showed malignant lymphoma, open biopsy was inevitable (8 of 13) to establish proper classification. Group B: FNAC showed a benign diagnosis in 10 cases and a malignancy in 13. Outcome was false-negative in 1, and false-positive in 1. Sensitivity and specificity were 92% and 90%, respectively. FNAC helped avoid additional surgical diagnostic procedures in 25 cases (86%). CONCLUSIONS: (1) Fine-needle aspiration cytology is a rapid, simple and accurate diagnostic procedure to differentiate between benign and malignant peripheral lymphadenopathy in children. FNAC can avoid open biopsy in at least 60% of cases. (2) A history of previous malignant disease does not influence the accuracy of the test.

Adolescent↗
PubMed1998

Carney's triad.

The purpose of this study is to provide an overview of cases of Carney's triad and to discuss the clinical implications of this diagnosis. A search was made of the English-language literature for original articles, reviews and abstracts addressing Carney's triad. A new patient was described and added to the number of known patients. In literature 40 patients were found with a complete or incomplete triad. There exists no agreement on the pathology and possible common origin of these tumours. Directions are given for diagnostics and therapy. The diagnosis of Carney's triad has specific clinical implications that make a good knowledge of this syndrome mandatory.

Adult↗
PubMed1997

Allelotype of pediatric rhabdomyosarcoma.

An allelotype covering all autosomes was constructed for the embryonal form of childhood rhabdomyosarcoma (ERMS) in order to identify regions encompassing tumorsuppressor genes (TSG) involved in ERMS. Thusfar most studies were focussed on chromosome 11p15.5, which frequently shows loss of heterozygozity (LOH) in embryonal tumors like RMS and Wilms' tumor (WT). In this study we show that, besides LOH of chromosome 11p15.5 (72%), LOH of chromosome 16q was present in 54% of the tumors analysed. Delineation of these two regions shows that the smallest region of overlap (SRO) for chromosome 11 was between D11S988 and D11S922. This region, estimated to be 7 cM and 3-5 Mb, is also the location of the putative Wilms' tumor WT2 TSG. It contains several genes including IGF2 and potential tumorsuppressor genes like H19 and p57kip2, which might contribute to the carcinogenesis of RMS. Analysis of chromosome 16q LOH defined the SRO between D16S752 and D16S413. LOH of chromosome 16 is also found in other tumors, including WT. Our data suggest that genes involved in the development of RMS and WT may not only be similar for chromosome 11 but also for chromosome 16.

Alleles↗
PubMed1997

Malignant astrocytoma-derived region of common amplification in chromosomal band 17p12 is frequently amplified in high-grade osteosarcomas.

Recently, we reported a new amplification event that involves marker D17S67 in 17p12 in three malignant astrocytomas of patients with a very short survival. The amplified region may contain an oncogene implicated in astrocytoma tumorigenesis. To determine the extent of the amplified regions, we constructed a yeast artificial chromosome contig spanning the D17S67 region and tested the amplification status of markers that map to the contig. We determined a commonly amplified region between markers D17S1311 and D17S1875 with a maximal length of 1,630 kb. By using marker 745R, from within the commonly amplified region, we screened 60 high-grade astrocytomas but could not detect additional tumors with the amplification event. This suggests that the incidence of the amplification event in high-grade astrocytoma is low (5%). It has recently been shown by comparative genomic hybridization that amplification of 17p11-p12 is a frequent event in high-grade osteosarcomas, occurring in 20-30% of cases. Since the commonly amplified region is within 17p12, we tested 745R in 20 osteosarcomas, including 6 lung metastases, and detected amplification in 9 cases (45%). Marker 745R was found to be amplified in 4 of the 6 lung metastases (66%). From this frequent involvement and the association with clinically aggressive astrocytomas we conclude that for both tumor types presence of the amplification event seems to correlate with aggressive clinical behaviour.

Astrocytoma↗
PubMed1996

[Iodobenzylguanide-131 therapy as first choice in non-metastasized neuroblastoma].

Three children with a localized pelvic neuroblastoma are presented. Because of progression and clinical signs of compression of adjacent structures therapy was necessary. Targeted radiotherapy with 131I-MIBG was used as the first mode of therapy. This new strategy proved to be feasible, effective and non-toxic. Application of 131I-MIBG as first-line therapy should be considered more often in neuroblastoma patients.

3-Iodobenzylguanidine↗
PubMed1996

Microsatellite instability in childhood rhabdomyosarcoma is locus specific and correlates with fractional allelic loss.

Replication errors (RERs) were initially identified in hereditary nonpolyposis colon cancer and other tumors of Lynch syndrome II. Mutations in genes involved in mismatch repair give rise to a mutator phenotype, resulting in RERs. The mutator phenotype is thought to predispose to malignant transformation. Here we show that in the embryonal form of childhood rhabdomyosarcoma, RERs also occur, but in contrast to hereditary nonpolyposis colon cancer, only a subset of the microsatellite loci analyzed show RERs. The occurrence of RERs is strongly correlated with increased fractional allelic loss (P < 0.001), suggesting that the occurrence of RERs is a secondary phenomenon in rhabdomyosarcoma. Coincidental loss of genes involved in mismatch repair, possibly due to their proximity to tumor suppressor genes involved in tumor progression of embryonal form of childhood rhabdomyosarcoma, could explain the observed phenomenon.

Alleles↗
PubMed1996

Diffuse sclerosing osteomyelitis and florid osseous dysplasia.

The literature on diffuse sclerosing osteomyelitis of the mandible has included at least two groups of lesions: (1) those from which bacterial infectious agents are rarely isolated (chronic-tendoperiostitis); and (2) those from which bacteria are readily isolated (true diffuse sclerosing osteomyelitis). The latter should be distinguished from secondarily infected florid osseous dysplasia. In this article the features of 16 patients with sclerotic jawbone lesions associated with symptoms of infection are analyzed. Eleven patients showed a large area of sclerosis of the mandible that was not restricted to the alveolar process and was surrounding an infectious focus. The histologic pattern revealed a deposition of reactive bone. These lesions are considered to represent true diffuse sclerosing osteomyelitis. The remaining five patients showed sclerotic lesions restricted to the alveolar process in one or more quadrants of the jaws. Apart from inflammation and reactive changes, histologic pattern revealed a fibroblastic stroma with bone and cementum-like structures that are formed by metaplasia. These lesions are considered to represent secondarily infected florid osseous dysplasia.

Adolescent↗
PubMed1995

Chronic congestive heart failure is associated with a phenotypic shift of intramyocardial endothelial cells.

BACKGROUND: There is evidence that patients with chronic congestive heart failure have endothelial cell-related abnormalities of the peripheral circulation and the coronary microvasculature. For that reason, we have studied the phenotypic expression of endothelial cells in hearts of patients with congestive heart failure. METHODS AND RESULTS: We studied cardiac explants (n = 19) and autopsy hearts (n = 5) of patients with chronic congestive heart failure caused by either a dilated cardiomyopathy (n = 12) or ischemic heart disease (n = 12) and compared them with normal hearts (n = 12). The antigenic expression obtained with several endothelial cell markers (factor VIII-related antigen, EN-4, Ulex europaeus agglutinin-1 (UEA-1), PAL-E, endoglin, and endothelin) and adhesion molecules (intercellular adhesion molecule [ICAM], vascular cell adhesion molecule [VCAM], or E-selectin) was compared by use of immunohistochemical techniques. On the basis of the initial findings, the number of PAL-E- and EN-4-positive vessels was counted. The incidence of PAL-E-positive vessels per area was quantified and related to the percentage of heart muscle cells and the total number of vessels per area. In control hearts, endothelial cells rarely were positive for PAL-E. In hearts of patients with ischemic cardiomyopathies, there was distinct staining with this marker. Hearts of patients with dilated cardiomyopathies showed a marked increase in the number of PAL-E-positive endothelial cells. Vessels with a muscular media were PAL-E-negative. Two-sample analysis revealed a statistically significant difference between hearts with dilated cardiomyopathies and ischemic cardiomyopathies (P < .01), between hearts with dilated cardiomyopathies and control hearts (P < .01), and between hearts with ischemic cardiomyopathies and control hearts (P < .01). Endoglin and ICAM were positive but nondiscriminating. Endothelin, VCAM, and E-selectin were negative. CONCLUSIONS: A phenotypic shift in endothelial antigen expression of the coronary microvasculature occurs in both ischemic hearts and hearts with dilated cardiomyopathies, as revealed by PAL-E, compared with control hearts. The change may relate to compensatory mechanisms in long-standing chronic heart failure.

Adult↗
PubMed1994

Cellular hemangioma and angioblastoma of the spine, originally classified as hemangioendothelioma. A confusing diagnosis.

STUDY DESIGN: The authors report two cases of vascular tumors of the spine, classified originally as benign and malignant hemangioendothelioma, and after revision, as cellular hemangioma and angioblastomatosis, respectively. OBJECTIVES: Problems in interpretation of the confusing term hemangioendothelioma and treatment modalities for vascular tumors of the spine are discussed. SUMMARY OF BACKGROUND DATA: Hemangioendothelioma is a confusing term and is often used to cover bewilderment at the biological behavior of a vascular tumor. Its spectrum ranges, depending the references used, from benign to malignant and can mistakenly include benign lesions like cellular hemangioma and angioblastoma (solitary and multicentric). METHODS: Of two patients with a cellular tumor of the spine, the clinicopathologic data and modes of treatment are reviewed. The relevant literature is discussed. RESULTS: In the first case, the diagnosis of benign cellular hemangioendothelioma was changed to cellular hemangioma. In the second case, the original diagnosis of malignant hemangioendothelioma with metastasis to liver and lungs was changed to angioblastomatosis, most probably benign. In both cases, a correct interpretation of the initial diagnosis or proper diagnosis would have influenced the mode of treatment. CONCLUSION: Avoid the confusing term hemangioendothelioma. If a vascular lesion is benign, it should be classified as a variant of hemangioma. If malignant as angiosarcoma, use a separate category, in which lesions like angioblastoma and angioblastomatosis can be put until their nature has been clarified.

Adult↗
PubMed1994

Through knee amputation with gastrocnemius musculocutaneous flap. 6 cases of tibial osteosarcoma followed for 3 (1-6) years.

6 cases of proximal tibial osteosarcoma were operated on by through knee amputation using a long dorsal gastrocnemius musculocutaneous flap; the usual anterior flap could not be used because of tumor size and the location of the biopsy tract. The only complication was one wound dehiscence which healed. The stump was of good quality in all patients. At follow-up, the patients walked without walking aids.

Adolescent↗
PubMed1994

A comparison of nutritional profiles of patients with alcohol-related pancreatitis and cirrhosis.

A multifactorial study of 58 variables of alcohol, dietary and tobacco habits of 106 chronic alcoholic and normal subjects was conducted over 2 years. The alcoholic population included subjects with either calcifying chronic pancreatitis (CCP) or cirrhosis (Ci). A standardized, previously validated questionnaire was used to investigate dietary intakes, drinking and smoking habits. The patients with CCP consumed a richer diet than those with Ci, consisting mainly of saturated fats and animals proteins. Although the alcoholics with CCP drank the same total quantity of alcohol as the alcoholics with Ci, they drank it over a shorter time period (less than 20 years) before diagnosis. Differences in the nutritional profiles of the two groups indicate that the population with alcohol-related digestive diseases is made up of subjects with different drinking and eating habits. These behavioural differences with respect to dietary and alcohol intake indicate that the alcoholic patients with CCP or Ci belong to different subgroups.

Adult↗
PubMed1993

Monoclonal antibody to an external epitope of the human mdr1 P-glycoprotein.

A membrane glycoprotein, termed P-glycoprotein, has been shown to be responsible for cross-resistance to a broad range of structurally and functionally distinct cytotoxic agents. P-glycoprotein, encoded in humans by the mdr1 gene, functions as an energy-dependent efflux pump to exclude these cytotoxic agents from the resistant cell. In order to study the phenomenon of multidrug resistance in both normal and neoplastic cells, we have generated a mouse monoclonal antibody directed to an external epitope of the human P-glycoprotein. This monoclonal antibody, 4E3, is an IgG2a class antibody which specifically recognizes the human mdr1 P-glycoprotein but not the mdr3 gene product. The 4E3 monoclonal antibody immunoprecipitates both the glycosylated and nonglycosylated forms of P-glycoprotein under mild denaturation conditions. In addition, 4E3 can detect P-glycoprotein in immunocytochemical analysis of fixed tissue-cultured cells and in analysis of frozen sections of human tissue. Binding of the monoclonal antibody to multidrug-resistant cells does not significantly affect the intracellular accumulation or potentiate the cytotoxicity of daunomycin in multidrug-resistant cells. However, at high concentrations of antibody, 4E3 produces a mild potentiation of vinblastine and actinomycin cytotoxicity in multidrug-resistant cells. This monoclonal antibody will be useful both for analyzing P-glycoprotein expression in normal and neoplastic cells and for isolating live cells expressing the P-glycoprotein without significantly affecting the efflux functions of the transporter.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed1993

Allelic loss of chromosome 1p36 in neuroblastoma is of preferential maternal origin and correlates with N-myc amplification.

Neuroblastomas frequently have deletions of chromosome 1p and amplification of the N-myc oncogene. We analysed 53 neuroblastomas for the N-myc copy number, loss of heterozygosity (LOH) of chromosome 1p36 and the parental origin of the lost alleles. Allelic loss of 1p36 was found in 15 tumours. All N-myc amplified tumours belonged to this subset. In 13/15 tumours with LOH of 1p36 the lost allele was of maternal origin. This non-random distribution implies that the two alleles of the putative neuroblastoma suppressor gene on chromosome 1p36 are functionally different, depending on their parental origin. This is the first evidence as far as we know for genomic imprinting on chromosome 1p.

Adult↗
PubMed1992

Diffuse sclerosing osteomyelitis (chronic tendoperiostitis) of the mandible. An 11-year follow-up report.

Diffuse sclerosing osteomyelitis of the mandible is a disease that is characterized by a protracted course of recurrent pain, swelling of the cheek, and trismus. The cause of the lesion has been obscure for a long period of time. Recent research, however, pointed out that this disease is likely to be caused by overuse of the jaw musculature (chronic tendoperiostitis) and can be treated accordingly. The protracted course of the disease and the difficulty of treatment with an eventual positive outcome are illustrated by a case report of a 65-year-old man with an 11-year history of diffuse sclerosing osteomyelitis (chronic tendoperiostitis) of the mandible.

Aged↗
PubMed1992

Changes in masseter inhibitory reflex responses in patients with diffuse sclerosing osteomyelitis of the mandible.

Masticatory inhibitory mechanisms were studied in 10 patients treated for diffuse sclerosing osteomyelitis of the mandible. Their masseter inhibitory reflex responses were provoked electrically by mental nerve stimulation during maximal clenching of the teeth. The masseter inhibitory reflex was normal in two patients and significantly abnormal in eight patients. The two patients with a normal masseter inhibitory reflex were free of complaints, whereas, of the eight patients with an abnormal masseter inhibitory reflex, two were free of complaints and six had moderate to severe symptoms. In three patients, spasms and involuntary bursts of electromyographic activity were found. The abnormal masseter inhibitory reflex consisted of a loss of early and late components in four patients or a loss of the late component with a normal early one in four patients. These findings seem to support the hypothesis that diffuse sclerosing osteomyelitis of the mandible is a chronic tendoperiostitis caused by muscle overuse. It is suggested that this overuse is caused by central hyperexcitability of trigeminal motoneurons.

Adolescent↗