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)

We report here sensitive and specific measurement of immune responses of patients with certain kinds of carcinoma toward the physically and chemically well defined T antigen isolated from healthy human erythrocytes. Over 90% of adenocarcinoma tissues tested possess T-specific immunoreactive structures as determined with human antisera, in contrast to healthy tissues and benign lesions. Adenocarcinoma patients recognize the carcinoma-associated T antigen as foreign. Delayed-type skin hypersensitivity reaction to T antigen (DTHR-T) was positive in all 25 lung adenocarcinoma patients tested, in 88% of 101 patients with ductal, in 43% of 30 patients with lobular or tubular breast carcinoma and in 9/9 patients with adenocarcinoma of body cavities. Patients of all Stages reacted positively. All 7 patients with small cell lung carcinoma and 3/5 with malignant melanoma had a positive DTHR-T. None of 17 patients with malignant brain tumors, leukemia or Hodgkin's disease, sarcoma or thyroid carcinoma reacted. The DTHR-T was specific in that all 77 healthy persons and 48/49 with other diseases, including 23/24 with non-cancer lung disease were negative; one patient with organizing interstitial pneumonitis was positive. This points to a possible source of false positive reactions. 91% of 149 patients with histologically benign breast disease had a negative DTHR-T; the histology of some of the positive ones was reexamined, 2 proved to have carcinoma in situ.
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PMID:Patients' immune response to breast and lung carcinoma-associated Thomsen-Friedenreich (T) specificity. 617 52

The experimental and clinical effects of ACNU so far recorded in Japan are reviewed. ACNU was highly effective in leukemia L-1210 and in other types of leukemias, ascites tumors, and solid tumors of mice and rats. On the basis of the results of phase I study, the maximum clinically tolerable single dose of ACNU was 101.8-135.7 mg/m2 at a time, and the total acceptable dose was 300-600 mg. The desirable interval between doses was 6-8 weeks. Phase II study revealed that ACNU seemed to be effective against small-cell carcinoma of the lung, brain tumors, Hodgkin's disease, and chronic myelocytic leukemia. In the treatment of small-cell carcinoma of the lung ACNU reduced the rate of brain metastasis and prolonged the survival of patients.
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PMID:Experimental and clinical effect of ACNU in Japan with emphasis on small-cell carcinoma of the lung. 624 13

In 139 patients with breast or lung carcinoma, malignant melanoma, and Hodgkin's or non-Hodgkin's lymphoma, JC and BK virus serology (hemagglutination inhibition) and urinary polyomavirus excretion (cytology and immunofluorescence microscopy) were studied. Overall, 18 of 70 patients with paired sera (26%) had titer increases against JC or BK virus, and 11 of 114 patients (10%) had evidence for urinary excretion. The infection rate was highest in patients with Hodgkin's or non-Hodgkin's lymphoma (approximately 40%). Serum HAI antibody titers against JC and BK viruses appeared similar to age-matched controls in each patient group--with the exception of decreased BK titers at diagnosis in patients with resected malignant melanoma and increased JC virus antibody titers at diagnosis in patients with poor-prognosis non-Hodgkin's lymphoma (IC-2). The biologic significance of these observations remains to be determined. Initial antibody titers against JC or BK virus were not of prognostic value for subsequent survival in any of the tested patient groups. Both nonspecific immunotherapy and aggressive, multidrug chemotherapy had surprisingly little effect on serum HAI titers to JC or BK virus. Patients with poor-prognosis non-Hodgkin's lymphoma appear especially suitable for further investigation of JC and BK virus infections. Study of nonbrain, nonurinary-tract tissues may disclose other parenchymal sites of polyomavirus replication in these patients.
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PMID:Survey of human polyomavirus (JCV, BKV) infections in 139 patients with lung cancer, breast cancer, melanoma, or lymphoma. 630 68

Lymphocyte response to PHA was depressed in 9 of 14 cases of Hodgkin's disease (HD) and in 4 of 14 cases of lung carcinoma (LC). This depression was caused in one-third of the HD cases and in one-half of the LC cases by an excess of prostaglandin synthesis.
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PMID:Suppressor cells in Hodgkin's disease and lung carcinoma. 645 11

The mechanism of the depression of cell-mediated immunity (CMI) in patients with Hodgkin's disease (HD) and lung carcinoma (LC) was investigated before any treatment. In 9 patients out of 14 with HD and in 4 patients out of 14 with LD, a depressed lymphocyte reactivity to phytohaemagglutinin (PHA) was observed. In 3 out of 9 patients with HD and in 2 out of 4 patients with LC who exhibited a depressed lymphocyte response to PHA, suppression caused by adherent cells and mediated by prostaglandins was evidenced. No relationship was found between this mechanism of suppression and depression of CMI in vivo as judged by skin tests to common recall antigens.
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PMID:Role of adherent suppressor cells in the depression of cell-mediated immunity in Hodgkin's disease and lung carcinoma. 645 31

The epipodophyllotoxin derivatives VM 26 and VP 16-213 are currently entering phase III studies. The mechanism of their action is incompletely understood, but the greatest lethal effect is experienced in the late S and G2 phases. In transplanted tumors both drugs have shown marked schedule dependency and human studies also support this. As a single agent VP 16-213 is among the most active drugs in small-cell carcinoma of the lung. Significant clinical activity (> 20% response frequency) has been observed for both drugs in Hodgkin's disease, non-Hodgkin lymphomas and possibly in other more rare tumors (monocytic leukemia, hepatoma and teratoma). Although further clinical studies of both drugs would be ideal, it seems possible at present to justify a discontinuation of VM-26 in order to concentrate the efforts on VP 16-213. Further studies are needed to define optimal dose and schedule and place in combination chemotherapy.
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PMID:The epipodophyllotoxin derivatives VM-26 and VP-16-213, 1976-1979, a review. 700 63

53 patients with advanced and measurable cancerr were treated with vindesine in doses of 3 mg/m2 (pretreated) and 4 mg/m2 (non pretreated) i.v. once weekly. 48 patients are evaluable for response: of 14 patients with squamous cell carcinoma of the lung, 1 partial remission (PR), 1 minor response (MR) and 1 no change (NC) were observed. In 5 patients with large cell carcinoma of the lung: 1 NC. In 3 with adenocarcinoma of the lung: 1 MR. One patient with nasopharyngeal carcinoma had progressive disease. Stable disease was observed in a patient with carcinoma of the tongue and in a patient with adenocarcinoma of the esophagus. Four patients with colorectal carcinoma had progressive disease. One MR was observed in a patient with breast cancer, while all of the other 3 patients had progressive disease. One carcinoma of the penis was stable. One MR was observed in a patient with Hodgkin's disease. One PR was observed in a case with no-Hodgkin's lymphoma. A patient with acute leukemia had progressive disease. Among 9 patients with malignant melanoma, 3 had an MR and 1 patient had stable disease. A patient with fibrosarcoma had progressive disease. Observed toxicity included leukopenia, thrombocytopenia, anemia, paresthesias, constipation, jaw pain, nausea, stomatitis, alopecia, loss of taste, pruritus and skin rash, weakness and fatigue.
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PMID:[Phase-II-study with vindesine (desacetyl-vinblastine-amide-sulfate) in advanced malignant diseases]. 742 51

A phase II study of vindesine in 41 evaluable patients demonstrated the drug to be active in heavily pretreated patients with breast cancer, non-Hodgkin's lymphoma, and other tumors. There were two partial responses in 11 patients with breast cancer (18%) and five partial responses and one complete response in 11 patients with non-Hodgkin's lymphoma (40%). Other responses were seen in small cell carcinoma of the lung, ovarian carcinoma, and Hodgkin's disease. Prior vinca exposure did not adversely affect the response rate. Neutropenia was dose-limiting. Neurotoxic effects occurred in 10% of the patients. A high incidence of local tissue reactions at the injection site (27%) could be reduced by a careful administration technique. Vindesine should be studied further in combination with other agents.
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PMID:Phase II trial of vindesine in the treatment of lymphomas, breast cancer, and other solid tumors. 744 18

The bcl-2 gene product (bcl-2 protein, BCLP) prevents apoptotic cell death. Via a 14;18 chromosomal translocation, BCLP is overexpressed in most follicular lymphomas as well as some other non-Hodgkin's lymphomas, and it has also been documented in other nonlymphomatous malignancies. To address the possible prognostic value of this marker in predefined subsets of non-small cell lung carcinoma (NSCLC), the authors studied 126 T1N0M0 cases seen between the years 1986 to 1991 at our institution. Patients were treated by lobectomy (105 cases) or wedge excision (21 cases) with negative margins; neuroendocrine carcinomas of all grades were specifically excluded. The mean follow-up period was 39 months. Immunostaining for BCLP was done using a monoclonal antibody (clone no. 124; DAKO, Carpinteria, CA), and the avidin-biotin-peroxidase complex (ABC) technique. The study cases included 73 adenocarcinomas (ACs) as well as 40 squamous cell (SCC), five adenosquamous (ASC), and eight large cell/poorly differentiated (LCC) carcinomas. As assessed with the Kaplan-Meier method, overall survival was 64% at 5 years (66% AC vs 59% SC). BCLP was detected in 47 of 126 cases (37%) including 32 AC (44%), 10 SCC 925%), two ASC (40%), and three LCC (38%). No significant difference in 5-year survival was noted in a comparison of all cases with BCLP expression (63%) and those without (59%). There was, however, a significant difference in the survival of grade 1 BCLP(+) cases, when compared with grade 2 or 3 BCLP(+) cases (P = .01). A nonstatistically significant trend toward increased survival was observed in BCLP(+) SCC cases (66% 5-year survival in BCLP[+] vs 45% in BCLP[-] [P = .11]). Proportional hazards analysis failed to disclose significant independent risk factors. These data suggest that bcl-2 protein immunoreactivity has limited prognostic value in the pathological evaluation of NSCLC.
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PMID:Expression of bcl-2 protein in stage T1N0M0 non-small cell lung carcinoma. 759 Jun 97

We previously have reported on an experimental athymic mouse model in which regression of human Burkitt's lymphoma is induced by either coinjection with or intratumor inoculation of Epstein-Barr virus (EBV)-immortalized human B cells. In the current study, we were interested in determining whether the powerful antitumor effects of EBV-immortalized B cells could be effective against a variety of human tumors grown in athymic mice, including acute lymphocytic leukemia, malignant melanoma, acute promyelocytic leukemia, neuroblastoma, lung carcinoma, colon adenocarcinoma, Wilms tumor, Hodgkin's lymphoma, rhabdomyosarcoma and breast adenocarcinoma. We report here the results of experiments in nude mice that demonstrated the potent antitumor effect of EBV-immortalized B cells against human tumors derived from a variety of different tissues.
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PMID:Regression of experimental human leukemias and solid tumors induced by Epstein-Barr virus-immortalized B cells. 853 18


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