Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019829 (Hodgkin's disease)
 30,247 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Interleukin-6 (IL-6) was demonstrated to be a strong autocrine or paracrine plasmocytoma cell growth factor in humans. Using a bioassay, high serum IL-6 (S-IL-6) levels were correlated with disease severity in plasma cell dyscrasias. Since other cytokines could interfere with the bioassays, we developed a specific radioimmunoassay to study S-IL-6 levels in 102 patients with monoclonal gammopathy (MG). S-IL-6 level was studied by a double antibody radioimmunoassay using a rabbit polyclonal anti-IL-6 antibody and a human recombinant IL-6 as the standard. The lowest value of the standard significantly different from zero was found to be 78 pg/ml. Within-run and between-run precisions were characterized by a mean coefficient of variation of 3.72 and 5.5%, respectively. The mean analytical recovery was found to be 113% and the immunochemical identity of IL-6 standard and S-IL-6 was shown by dilution tests. IL-6 was detected in all tested sera. Sera from 66 healthy volunteers and 43 patients with acute leukemia or malignant lymphoma were tested as controls. In healthy subjects, S-IL-6 values were 294 +/- 86 pg/ml. MG were classified as multiple myeloma (MM), macroglobulinemia, and MG of undetermined significance (MGUS). The distribution of S-IL-6 levels in patients with MG was significantly higher than in healthy subjects but lower than in patients with acute leukemia or Hodgkin's lymphoma. Results obtained in 55 patients with MM were related to other biological parameters. S-IL-6 levels correlated with bone-marrow plasmacytosis (P less than .0005), serum-lactate dehydrogenase (S-LDH; P less than .005), serum beta 2 microglobulin (S -beta 2m; P less than .01), and serum calcium (S-Ca; P less than .025) and inversely correlated with haemoglobin (P less than .025). Our results indicate that 1) radioimmunoassay is suitable for the measurement of human IL-6 in serum; 2) high S-IL-6 levels are observed in a small number of patients with MG; and 3) S-IL-6 level correlates with tumour cell mass in patients with overt MM.
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PMID:Radioimmunoassay for the measurement of serum IL-6 and its correlation with tumour cell mass parameters in multiple myeloma. 154 13

This prospective study was designed to determine the efficacy of iodized talc pleurodesis in patients with pleural effusions. Thirty-four patients underwent this treatment (three bilaterally) between October 1, 1989, and March 31, 1991. All patients had to have complete or nearly complete lung reexpansion after tube thoracostomy with fluid drainage less than 100 ml in 24 hours. A slurry containing 5 gm of talc and 3 gm of thymol iodide was instilled into the pleural space through the chest tube. Chest tubes were removed after complete reexpansion and clearing of the effusions, usually in 3 to 5 days. The patients' ages ranged from 26 to 88 years (average 50 years). Eighteen patients had lung carcinoma, two had mesothelioma, and one each had carcinoma of the ovary, breast, or anorectum, multiple myeloma, schwannoma, or Hodgkin's lymphoma. Two patients had an unknown adenocarcinoma primary and five other patients had acquired immunodeficiency syndrome. One patient had congestive heart failure. Nineteen patients had left, 12 had right, and three had bilateral pleural effusions. The effusion was serosanguineous in 26 and serofibrinous in eight patients. Serial chest radiography showed complete response in all patients. The period of follow-up ranged from 1 to 21 (average 4.9) months, with no recurrences. Twenty-three patients have died during the follow-up period, and there was no sign that reaccumulated pleural effusion existed in any, despite clinical evidence of systemic tumor progression. These observations indicate that intrapleural instillation of a slurry of iodized talc is a safe, adequate, and effective treatment for control of neoplastic or benign pleural effusions.
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PMID:Iodized talc pleurodesis for the treatment of pleural effusions. 156 70

The findings of the studies summarized in this report provide some understanding of the possible role of dosimetry in the different response of the rats and mice to benzene in the long-term bioassay studies. The more sensitive species, the mice, definitely has a higher capacity to metabolize benzene and to metabolize it to more of the putative toxic metabolites than do rats. A major finding of these studies is that in three different animal species, from mice to monkeys, the metabolic pathways leading to production of the putative toxic metabolites appear to be low-capacity, high-affinity pathways that are saturated at relatively low-exposure concentrations. This does not prove, but suggests, that the same may be true in humans. If the total formation of the putative toxic metabolites is predictive of the toxicity of benzene, then the animal studies suggest that calculations of the risk associated with low dose exposures based on the results of animal studies conducted at high doses would underestimate the toxicity of benzene. The current report concerns only dosimetry. Another problem in assessing the risk to humans from benzene exposure is the fact that the animal models do not respond to benzene in the same way as humans. The major concern for humans exposed to benzene, based on epidemiology studies, is the risk of developing acute myelogenous leukemia (Rinksy, 1987). The cancers developed by the rodents on the long-term bioassay studies were at other sites (liver, lung, Zymbal's gland, lymph tissue, ovaries, and mammary gland). There is as yet no good animal model for benzene-induced leukemia. However, it has been suggested that benzene may also increase the incidence of Hodgkin's disease, malignant lymphoma, multiple myeloma and lung cancer in humans, although a statistical basis for this is lacking (Askoy, 1985). It is not unreasonable to assume that whatever form of cancer is induced, the induction is most likely through the reactive metabolites produced from benzene. Therefore, the dosimetry of these metabolites is pertinent. Our studies indicate that benzene metabolite dosimetry data obtained in animals provides data relevant to the estimation of human risks.
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PMID:Benzene dosimetry in experimental animals: relevance for risk assessment. 162 Jul 20

The incidence of lymphoid malignancies (acute leukemias and myelomatosis excluded) during 1969-1987 in the County of Uppsala was calculated on the basis of the regional cancer register and local registers from the only oncological, hematological, dermatological and pathological departments in this well-defined geographical area. Of the 774 patients included, 639 had histopathological specimens available, all of which were re-examined. Seventy-nine patients were diagnosed on the basis of bone marrow investigations (greater than 70% re-examined, all had a low-grade non-Hodgkin's lymphoma = NHL) and 54 on fine-needle aspiration biopsies (not re-examined). Seventy-nine of the lymphoma diagnoses were based on autopsy specimens. The overall age standardized incidence was 16.2/100,000/year (NHL: 13.6, Hodgkin's disease = HD: 1.5) according to the Swedish 1970 census (according to world standard population: 10.2); male: 20.9 (12.9) and female: 12.4 (7.9). The annual change in trend was +3.0% +/- 2.6 (NHL: +3.6% +/- 2.4, HD: no change). The omission of the 54 'fine needle cases' led to an overall incidence of 15.0 (9.7) and an annual change in trend of +3.5% +/- 1.9. Among the histopathological specimens, an NHL was found in 524 patients and HD in 69. In 46 registered patients, the diagnosis malignant lymphoma was wrong. The diagnosis changed to NHL in 43 patients registered as HD.
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PMID:Lymphoma incidence in a Swedish county during 1969-1987. 162 46

A 52 year old male presenting chronic myeloid leukemia (CML) Philadelphia chromosome positive (Ph) four years after the diagnosis of a non Hodgkin's lymphoma is described. The patient had received high total doses of alkylating drugs (cyclophosphamide and chlorambucil) as part of chemotherapy treatment for a diffuse mixed lymphoma. At four years of diagnosis of the lymphoma the appearance of hepatosplenomegaly, leukocytosis with myeloma and basophilia and thrombocytosis were observed. These alterations augmented progressively until a cytogenetic study of the bone marrow two years late established the diagnosis of CML upon demonstrating the presence of the Ph chromosome with no other karyotypic anomalies being observed. The explorations carried out at that time confirmed that the lymphoma continued to be in remission. The CML initially responded to treatment with busulphan. However, following a year and a half the disease evolved to a phase of acceleration and the patient died a few weeks later due to pneumonia with no signs indicative of lymphoma activity having been detected since the diagnosis of the CML.
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PMID:[Chronic myeloid leukemia after chemotherapy treatment for non-Hodgkin's lymphoma]. 163 10

Several important new agents are effecting the management of non-Hodgkin lymphoma (NHL) and multiple myeloma. The two selected for review in this article include a biologic-response modifier and a new chemotherapeutic agent. The biologic-response modifiers offer entirely new approaches to these diseases. The most extensively tested agent currently has been recombinant alpha-interferon (alpha-IFN). The IFN are active, albeit weak, remission-induction agents for low-grade NHL and some T-cell lymphomas, but they appear to be ineffective as single agents in most intermediate-grade or high-grade NHL and myeloma. However, an emerging pattern in follicular lymphomas and myeloma is that alpha-IFN in combination with chemotherapy may lead to more complete and durable clinical responses and the increased prospect of prolonged disease control. Fludarabine, a new chemotherapeutic agent, is a promising drug with demonstrated activity in low-grade lymphomas that parallels its impressive activity in chronic lymphocytic leukemia.
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PMID:New agents for the treatment of multiple myeloma and non-Hodgkin lymphoma. 163 66

In this study, we investigated a possible association between the degree of macrophage activation - as measured by serum neopterin concentrations - and disturbances of iron metabolism, determined by the concentrations of ferritin and serum iron, in patients with malignant disorders. Additionally we evaluated correlations between these factors and the degree and type of anaemia. Seventy-three patients, who suffered from non-Hodgkin's lymphoma (NHL) (n = 43), Hodgkin's disease (n = 11), myeloma or monoclonal gammopathy of unknown significance (n = 9), myelodysplastic syndrome (n = 1), and solid tumours (n = 9), were examined. Mean neopterin levels were raised in all groups, patients with NHL showing the highest concentrations. Ferritin but not neopterin concentrations were higher in males than in females. A significant correlation was found between neopterin and ferritin concentrations (p less than 0.01). Considering only female patients the strength of the correlation was the same (p less than 0.02). In addition, we found inverse correlations of neopterin with haemoglobin and iron concentrations (all p less than 0.01). Similar relationships existed in patients during follow-up. Our results support the hypothesis of an association between the degree of activation of macrophages and the development of anaemia by a shift or iron towards the storage sites.
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PMID:Association between the activation of macrophages, changes of iron metabolism and the degree of anaemia in patients with malignant disorders. 164 56

Epstein-Barr viral DNA (EBV DNA) has been detected in 20 to 58% of Hodgkin's disease tumors analyzed by Southern blotting or polymerase chain reaction (PCR). Because patients with Hodgkin's disease are generally immunodepressed, it is possible that the EBV is not directly involved in the pathogenesis of Hodgkin's disease but is merely detectable by molecular techniques because of reactivation of a latent infection. The purpose of this study was to determine if EBV DNA could be detected in an even higher percentage of cases of Hodgkin's disease, including acquired immunodeficiency syndrome (AIDS)-related Hodgkin's disease, by using newly designed, PCR amplification primers, and to compare the incidence of EBV DNA with the incidence of another common, latent virus (cytomegalovirus) in Hodgkin's disease tissue. The PCR was performed on DNA extracted from cells from 15 benign hyperplastic lymph nodes and from 15 cryopreserved cases of Hodgkin's disease, including 2 cases of AIDS-related Hodgkin's disease. For negative controls, PCR was also performed without template DNA and on genomic DNA from E. coli, calf thymus, a murine myeloma, and from a human cell line. After 32 cycles of amplification, a 225 base-pair amplification product comigrating with an EBV-positive control was detected in none of the negative controls but was present in 14 out of 15 cases (93%) of Hodgkin's disease, including both cases of AIDS-related Hodgkin's disease, and in 2 out of 15 cases of benign lymphoid hyperplasia. By contrast, cytomegalovirus DNA was undetectable by PCR in any of our specimens. We conclude that in our study set, the PCR procedure detected EBV-DNA but not cytomegalovirus DNA in a high percentage of cases of Hodgkin's disease, including two cases of AIDS-related Hodgkin's disease. These findings strengthen the hypothesis that EBV may be involved in the pathogenesis of Hodgkin's disease and AIDS-related Hodgkin's disease.
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PMID:Frequent detection of Epstein-Barr viral deoxyribonucleic acid and absence of cytomegalovirus deoxyribonucleic acid in Hodgkin's disease and acquired immunodeficiency syndrome-related Hodgkin's disease. 166 51

In an effort to develop a clinically useful approach to overcoming P-glycoprotein-mediated multidrug resistance (MDR1), we evaluated combined chemosensitization with verapamil and quinine in a multidrug-resistant (MDR) human myeloma cell line model. In clonogenic assay, verapamil was used at concentrations from 0.1 to 1.0 micrograms/mL, bracketing the plasma levels achieved by oral administration and high-dose intravenous (IV) infusion, respectively. The dose of quinine was held constant at 1.0 micrograms/mL, a plasma concentration readily achieved by oral administration. At each dose level of verapamil tested, the combination with quinine proved more effective than either drug individually in reversing resistance to doxorubicin and vinblastine and synergistic chemosensitizing interaction was observed. Verapamil at 0.1 microgram/mL combined with quinine was capable of restoring sensitivity to doxorubicin fully and reduced resistance to vinblastine as effectively as verapamil alone at 1.0 micrograms/mL. Furthermore, the combination of 1.0 mumol verapamil with 10 mumols quinine increased accumulation and retention of anthracycline in the resistant cells to a greater extent than did either drug individually (P less than .001) and inhibited drug efflux as effectively as verapamil alone at 10 mumols. Our findings suggest that combined chemosensitization with verapamil and quinine may prove useful for overcoming MDR1 in patients with drug-refractory B-cell neoplasms such as multiple myeloma or non-Hodgkin's lymphomas.
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PMID:Synergistic inhibition by verapamil and quinine of P-glycoprotein-mediated multidrug resistance in a human myeloma cell line model. 167 Jul 60

Verapamil was evaluated as a chemosensitizer for reversing multidrug resistance in multiple myeloma both in vitro and in clinical trials. Bone marrows from 59 myeloma patients in relapse were evaluated for several resistance parameters: expression of p-glycoprotein (MDR1), doxorubicin (Adriamycin) and vincristine sensitivity, and the ability of added verapamil to reduce resistance to the cytotoxic agents. We found that verapamil was capable of sensitizing myeloma cells that exhibited resistance to doxorubicin and vincristine in vitro, but did not enhance sensitivity of cells that were drug sensitive (P less than .001). Myeloma cells expressing MDR1 immunohistochemically tended to be more doxorubicin resistant in vitro than MDR1-negative cells. In the clinical trials, 22 patients with myeloma refractory to vincristine-Adriamycin-dexamethasone (VAD) were treated with VAD plus high-dose intravenous verapamil (Ve). Among the 22 patients treated with VAD/Ve, five achieved a partial remission (23%). The median relapse-free survival for the VAD/Ve responders was 5.4 months and their overall survival from the start of VAD/Ve was better than that of the nonresponders. Among the subset of 10 patients whose myeloma cells were MDR1 positive, four responded clinically (40%), whereas none of five patients with MDR1-negative myeloma cells achieved remission with VAD/Ve. We also observed that myeloma cells from three of four VAD/Ve clinical responders exhibited in vitro chemosensitization with verapamil, whereas in vitro verapamil chemosensitization was seen in only one of six clinical nonresponders. Our observations demonstrate that clinical reversal of multidrug resistance can be achieved in some patients with VAD-refractory myeloma with the use of verapamil. In addition to their value in drug development, in vitro tests of MDR1 expression and of chemosensitizers plus cytotoxic drugs on the patients' bone marrow myeloma cells may identify patients who will respond clinically to chemosensitizer-containing regimens. We anticipate that chemosensitizer regimens capable of inhibiting multidrug resistance will play an increasing role in the treatment of hematologic malignancies, including B-cell neoplasms such as multiple myeloma and the non-Hodgkin's lymphomas.
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PMID:Multidrug-resistant myeloma: laboratory and clinical effects of verapamil as a chemosensitizer. 167 18


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