Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027627 (metastases)
 103,950 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Bone scintigraphy with 99mTc-polyphosphate or 99mTc-pyrophosphate was carried out in 54 children suspected of bone disease. Signs of skeletal metastases were recognized in 13 children by scintigraphy whereas X-ray examination showed lesions in only 10 of these. In 5 children with primary osteosarcoma, three cases of fibrous dysplasia, and 4 cases of osteomyelitis, the lesions were clearly demonstrated by scintigraphy. Abnormal accumulation of radioactivity in soft tissue lesions was observed in primary adrenal neuroblastoma, Hodgkin's granuloma, and metastatic Burkitt's lymphoma. Several cases are reported, and the value of bone scintigraphy in children is discussed.
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PMID:Bone scintigraphy in children. 18 23

The case of a 33-year-old woman with Burkitt's lymphoma is presented. This is the third case that has been reported from India. The primary involvement was in the mandible. Endoxan was administered without response. Radiotherapy was resorted to as the second choice of treatment, but metastases developed rapidly in other organs. The patient survived for only 3 months after a diagnostic biopsy.
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PMID:Burkitt's lymphoma. 105 44

Specific host-graft interactions, as well as intrinsic properties of transferred cell, determine tumorigenicity in xenogeneic systems. We compared the growth characteristics of human B-lymphoid cell lines in SCID mice with the well characterized growth pattern in nude mice and observed striking differences in malignancy in the respective hosts. Two cell lines derived from the same individual, the Epstein-Barr-virus(EBV)-positive Burkitt's lymphoma BL 60 (BL) and the autologous EBV-immortalized lymphoblastoid cell line IARC 277 (LCL) were used. In addition, we tested somatic cell hybrids (HYB) of both cell lines, which despite the LCL-like differentiation phenotype show the de-regulated c-myc expression pattern of the parental BL line, assumed to be a critical factor in BL pathogenesis. Subcutaneously (s.c.) injected BL cells produced local progressively growing tumor masses at the injection site without distant metastases in both nude and SCID mice. Although both mouse strains possess the same genetic background (BALB/c) and differ only in the B-cell sub-set, the growth patterns of the LCL and hybrids were completely different. In contrast to the regressive behaviour of LCL and hybrids in nude mice, these lines show invasive and disseminated progressive growth in SCID mice. Peripheral lymph nodes an thymic tissue were preferentially colonized, whereas mucosal-associated lymphoid tissue (Peyer's patches and appendix) and spleen were not infiltrated. The preferential migration of lymphocytes to certain tissues is termed homing in a syngeneic system and mediated by homing receptors and vascular addressins. The "homing" of LCL and hybrids into lymphoid SCID mouse tissue suggests a strong interaction with the endothelial cells of the host. Detailed phenotypic analysis of BL, LCL and 3 different hybrids was performed using an antibody panel against differentiation and adhesion markers. Overall dominance of the LCL phenotype was observed in the hybrids, as indicated by cytology, tumor growth, dissemination and the pattern of surface-marker expression. The c-myc activation in hybrids does not appear to influence growth behavior.
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PMID:Local growth of a Burkitt's lymphoma versus disseminated invasive growth of the autologous EBV-immortalized lymphoblastoid cells and their somatic cell hybrids in SCID mice. 130 26

The abdomen is the most frequent site of involvement in nonendemic Burkitt's lymphoma (small noncleaved cell). Some authors have proposed a role for extensive surgical resection or "second look" laparotomy in these patients. We retrospectively reviewed our series of 53 patients with Burkitt's lymphoma (1977 to 1990) to assess the role of surgery in their treatment. Patients were 2.5 to 21 years of age (median, 9.5 years) and 44 were males. The primary site of disease was the abdomen (38), head and neck (12), axilla (1), and bone marrow (2). Twenty-four of the 38 patients with abdominal primaries underwent laparotomy. Twelve of these patients presented with acute abdominal symptoms (right lower quadrant pain or intestinal obstruction) and at exploration underwent resection of the primary tumor. Ten of these 12 patients achieved grossly complete excision of tumor (9 had disease limited to the ileocecal area and adjacent mesentery and one had exophytic tumor adherent to the liver, which was excised). Of note, only 1 of these 12 patients had metastatic disease outside of the abdomen. The remaining 12 patients who underwent laparotomy had an incisional biopsy performed. Of the 14 patients who did not have a laparotomy, the diagnosis was made by bone marrow biopsy (6), and/or cytology of pleural fluid or ascites (6), lymph node biopsy (1), testicular biopsy (1), tibial biopsy (1), and percutaneous biopsy (1). Murphy staging for these 38 patients was: stage II (10), stage III (19), stage IV (5), and B cell acute lymphoblastic leukemia (ALL) (4). All patients received cyclophosphamide-containing combination chemotherapy regimens and stage III/IV/B cell ALL patients received central nervous system (CNS) prophylaxis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The role of surgery in abdominal Burkitt's lymphoma. 156 24

Patients suffering from malignant disease will probably develop some metabolic abnormality of electrolytes. Hypernatremia is defined as an elevation of serum natrium over 150 mEq/l and caused by decrease of water intake, low level of ADH secretion and impaired response of kidney to ADH. Hyponatremia below 135 mEq/l of serum natrium is caused by SI-DAH, sick cell syndrome and increased loss of natrium from the kidney. On the other hand, hyperkalemia is defined as an elevation of serum kalium over 5.0 mEq/l and caused by acute tumor cell lysis syndrome, adrenal and renal insufficiency. Hypokalemia is caused by kalium loss from kidney and hypersecretion of mineral corticoid. Hypercalcemia is found in the high frequency among patients with malignant disease. Hypercalcemia is defined as an elevation of serum calcium over 11.0 mg/dl, although the most important aspect is the level of ionized calcium. The excess calcium causes defective urinary concentration with polydipsia, nausea and vomiting leading to volume depletion. At serum calcium levels about 13.8 mg/dl, there may be rapid deterioration or renal function, dehydration, coma and cardiac arrhythmias. Hypercalcemia is rarely the first manifestation of cancer. There are three principle pathogenic causes of malignant hypercalcemia, 1) hypercalcemia is a feature of several hematological cancers, including Burkitt's lymphoma, T cell leukemia, but most commonly with myeloma. The hypercalcemia in these myeloma patients is due to the secretion of an osteoclast activator, a lymphokine by the myeloma cells. 2) all patients with bony metastases have biochemical evidence of increased bone resorption. However, not all patients with bony metastases develop hypercalcemia. Probably the hypercalcemia is due partially to increased renal tubular reabsorption of calcium, mediated by a humoral factor, with activity similar to that of parathormone. 3) hypercalcemia in the patients without bony metastases is due to increased bone resorption caused by the ectopic secretion by the tumor. Mildly symptomatic patients will benefit from modest salt loading. They are dehydrated and replacement of the extracellular fluid is the first line of treatment. This may require 4-10 l normal saline/24 h. In addition, frusemide will increase calcium excretion. Calcitonin may be given subcutaneously or intravenously to refuse the mobilisation of calcium from bone. Glucocorticoids are unhelpful, but will prolong the effect of calcitonin. A diphosphonate is also useful.
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PMID:[Palliative therapy in cancer. 4. Palliation of the symptoms from a malignant tumor. (2)]. 169 56

A Burkitt's lymphoma (BL, EBV +, 8/22 translocation), the EBV immortalized lymphoblastoid cell line from the same individual (LCL) and somatic cell hybrids (HYB) between both cell lines were inoculated in immunedeficient scid mice. Subcutaneous injected BL cells produced local tumor masses without distant metastases. In contrast LCL and hybrids show invasive and disseminated growth. Peripheral lymph nodes and thymic tissue were preferentially colonized. A detailed phenotypic analysis of BL, LCL and 3 different hybrids was performed using differntiation and adhesion molecules. The preferential "homing" of LCL and hybrids seem to be correlated with the expression of the lymphocyte homing receptor (CD44). The growth of LCL in scid mice shows, that additional genetic alterations are not necessary to cause a malignant phenotype. Activation of myc seem to play a minor role, because hybrids mimic the LCL phenotype and distribution pattern.
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PMID:[Invasive, metastatic growth of lymphoblastoid B cells in immunodeficient SCID mice]. 172 38

Using culture techniques, we have been able to grow occult tumor cells from the bone marrow from cancer patients and have developed a new malignant lymphoid cell line, OMA-BL-1, from the bone marrow of a 17-year-old patient with recurrent Burkitt's lymphoma. The tumor cells grew rapidly in vitro in suspension culture, and very aggressively in vivo in athymic nude mice with metastases to the liver and abdominal cavity. The morphological, chromosomal, immunophenotypic and molecular biologic characteristics of fresh uncultured tumor cells from the patient and tumor cells grown in culture and in athymic nude mice were very similar. The cells were positive for Epstein-Barr virus-associated nuclear antigens (EBNA) and chromosome analysis of the cells revealed an atypical chromosomal abnormality of 45,X,-X,i(8q), HSR(18)(q21),t(8;14)(q24;q32). Southern analysis demonstrated that c-myc was rearranged and amplified in these cells. Immunophenotypic analysis of the cells using flow cytometry showed monoclonal B cells expressing a surface IgG-kappa isotype. The tumor cells grown in nude mice had a significant decrease in CD24 expression when compared to cultured tumor cells. Electron microscopy of the fresh and cultured cells revealed Herpes virus, most likely Epstein-Barr virus, particles. This cell line has been maintained in culture for over 18 months. The aggressive growth and metastatic properties of this cell line in athymic nude mice make it a potentially useful experimental model to study the biology of human lymphoma.
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PMID:Characterization of a newly established human Burkitt's lymphoma cell line, OMA-BL-1. 184 32

High-grade non-Hodgkins B-cell lymphoma is one of the principle malignancies that occurs in individuals infected with the human immunodeficiency virus (HIV-1). Immunoblastic lymphomas that arise in immunosuppressed transplant patients have been described as both monoclonal and polyclonal, and occur in association with Epstein-Barr virus (EBV) infection. To test whether polyclonal lymphoma occurred in patients with AIDS we studied tumors from multiple sites in three patients who died with widespread AIDS-associated large cell or large cell immunoblastic lymphoma. All biopsy specimens contained invasive lymphoma. Tumor cells were mature IgM-positive immunoblasts by immunohistochemical analysis, with the same B-cell phenotype observed in all tumor sites. Only a minority of sites from all patients analyzed were monoclonal as measured by immunoglobulin gene rearrangements, with one case having several foci of monoclonal disease with other histologically identical metastases showing no evidence of monoclonal proliferation. Similar to the transplant-associated polyclonal B-cell proliferations. EBV gene sequences were present in multiple sites from one autopsy. In the other two autopsies, polyclonal B-cell proliferations occurred in the absence of EBV involvement except at one site, where a minor clone of EBV-infected cells was found. In contrast to HIV-associated Burkitt's lymphoma, no c-myc rearrangements were found at any site. These studies describe the occurrence of polyclonal lymphoma in AIDS and suggest that EBV-negative polyclonal lymphoma may be a distinct disease entity unique to HIV-infected individuals.
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PMID:AIDS-associated polyclonal lymphoma: identification of a new HIV-associated disease process. 184 89

Studies on normal bone marrow and Daudi Burkitt lymphoma cells were performed to determine the efficacy of selective, in vitro chemopurging with methylprednisolone (MP). We found that MP reduces the number of lymphoma cells without significant damage to bone marrow cells. This information is important because we need to improve the existing in vitro purging regimens used to cleanse autologous marrows of metastatic disease before transplantation into cancer patients who have received high-dose chemotherapy. Normal human bone marrow (NBM) and Daudi lymphoma cells were treated in parallel with various purging regimens, NBM death was evaluated using soft-agar culture, while Daudi cell death was evaluated using one-week liquid culture. A protocol of 2.0 mg/mL of MP for four hours demonstrated optimal selectivity. When treatment was followed by cryopreservation, a 1.7 log purge of Daudi cells was increased to 2.3 logs while preserving 36% of committed NBM precursors. We repeated these experiments on a simulated contaminated marrow to model closely the mixture of normal and malignant cells found in advanced, metastatic disease. We evaluated this mixed system by flow cytometric immunoanalysis using the two-color CD10/CD20 markers to detect residual, viable Daudi cells. Our initial results were reproducible in this mixed-cell system, further supporting the evidence for effective in vitro purging of bone marrow using MP.
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PMID:Assessment of methylprednisolone purging efficacy on Daudi burkitt lymphoma cells from normal bone marrow. 189 5

Human B-cell tumors have been established in athymic, BALB/c mice using the EBV-positive Burkitt lymphoma cell line Namalwa. One-hundred-one of 104 animals (97%) developed tumors 10-14 days following s.c. injection of a mixture of 20 x 10(6) Namalwa and 5 X 10(6) irradiated human fibrosarcoma (HT-1080) cells. Tumors developed at the site of injection and reached approximately 300 mm2 (product of cross-sectional diameters) after 21 days; no metastases were found. Histological analysis showed that tumors consisted solely of lymphoid cells. Immunofluorescence assays demonstrated that while 85% of the tumor cells retained reactivity with the monoclonal B-cell antibody BA-1, 96% retained reactivity with antibody BA-2 and 43% with BA-3. A similar reactivity profile was observed with cultured Namalwa cells. Tumors were passaged serially 10 times without significant change in BA-1, BA-2, or BA-3 reactivity. Indirect immunofluorescence demonstrated that antibody BA-2 reached tumor cells within 2 h following i.p. injection; antigen modulation was not observed. These results demonstrate the suitability of this B-cell model for testing the in vivo efficacy and stability of anti-B-cell immunoconjugates.
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PMID:Establishment of a human B-cell tumor in athymic mice. 310 70


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