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)

Eight cutaneous malignant melanomas occurred in 6 of 1405 patients with Hodgkin's disease, although the expected incidence rate was 0.77 (relative risk, 8; 95% confidence interval, 3 to 17). One melanoma was a thin, level II lesion less than 0.76 mm thick; the rest were mostly bulky, deeply invasive lesions despite close clinical surveillance. The melanomas spread aggressively; 3 of 6 patients died within 1 to 3 years. Two of the six patients developed a second primary malignant melanoma 1 year after the first. Two of six patients had biopsy-proven dysplastic nevus syndrome, a known precursor to cutaneous malignant melanoma, and an additional 3 patients had clinical evidence of dysplastic nevus syndrome. Histologically, the malignant melanomas showed a sparse inflammatory infiltrate, an abnormal host response seen previously in cutaneous melanomas developing in immunosuppressed patients. Dysplastic nevi may identify patients at highest risk who require modified medical management.
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PMID:Cutaneous malignant melanoma after Hodgkin's disease. 396 43

The risk of developing a second primary cancer was evaluated in approximately 19,000 persons with initial cancers of the lymphatic and hematopoietic system in Connecticut between 1935 and 1982. Significant excesses for all second cancers were observed among patients with leukemia (34%), Hodgkin's disease (70%), non-Hodgkin's lymphoma (25%), and multiple myeloma (24%). In general, the risk of second cancers was greater in males than in females, even for cohorts not showing an excess of surveillance-related prostate cancer. Among patients with leukemia, significant excesses of cancers of the lung, kidney/ureter, and prostate were noted; cutaneous melanoma was elevated only in males. These excesses did not persist in the small number of long-term survivors. Possible etiologic factors included tobacco smoking for lung and kidney cancers, medical surveillance artifact for prostate cancer, and immunosuppression for malignant melanoma and lung cancer. The large number and good prognoses of patients with chronic lymphocytic leukemia strongly influenced the pattern of second cancers when all leukemias were analyzed together; no evidence was found for an increased risk of second cancer in patients with acute lymphocytic leukemia. A disproportionate number of subsequent cancers, particularly those of the kidney and ureter, were diagnosed incidentally at autopsy. Patients with Hodgkin's disease displayed significant excesses of cancers of the buccal cavity and pharynx, lung, female breast, and thyroid. The latter 3 sites remained significantly elevated in long-term survivors (10 yr or more postdiagnosis), so that radiation therapy may have contributed to their development. Among persons with non-Hodgkin's lymphoma, cancers of the stomach, lung, brain, and connective tissue occurred excessively. The first 3 sites, plus cancers of the urinary bladder, remained elevated among long-term survivors. The brain cancer excess, not previously reported, may represent misclassification of central nervous system lymphoma. The risk of gastric cancer is reminiscent of similar findings in patients with both acquired and genetically determined immunodeficiency disorders. The alkylating agent, cyclophosphamide, used extensively in the treatment of non-Hodgkin's lymphoma, is known to cause bladder cancer in man.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Second cancer following lymphatic and hematopoietic cancers in Connecticut, 1935-82. 408 98

The results of complement fixation tests on 202 sera from people without cancer and from patients with cancer in 29 different areas of the body indicated that only those with nine varieties of advanced cancer (lip, mouth, oropharynx, nasopharynx, kidney, urinary bladder, prostate, cervix uteri, and vulva-all of 56 tested) gave positive specific reactions with nonvirion antigens induced by the DNA herpes simplex (HSV 1) and herpes genitalis (HSV 2) viruses. None of 57 people without cancer (including 10 with current and 18 with recurrent HSV 1 or HSV 2 infections), none of 81 patients with 20 other varieties of advanced cancer (gum, tongue, tonsil, salivary gland, accessory sinus, epiglottis, lung-bronchus, stomach, colon, breast, corpus uteri, ovary, testis, liver, thyroid, Wilms' embryonal kidney, melanoma, Hodgkin's disease, acute lymphocytic leukemia, and acute myelocytic leukemia), and none of four women with early malignant changes in the cervix uteri gave positive results. The seven patients with advanced cancer of the lip or oropharynx gave positive reactions with HSV 1 but not with HSV 2 nonvirion antigens (compatible with involvement of only HSV 1), all of the 13 women with advanced cancer of the cervix uteri and the one woman with advanced cancer of the vulva gave positive reactions with both HSV 1 and HSV 2 nonvirion antigens (compatible with involvement of only HSV 2), while among the 35 other positive patients only two (one with cancer of the kidney and one with cancer of the bladder) reacted with HSV 1 and not at all with HSV 2 nonvirion antigens. Positive sera failed to react with cells harvested at different times after high-multiplicity infection with the DNA vaccinia virus. Massive absorption of positive sera with trypsinized, uninfected human embryonic kidney cells failed to remove, or lower the titer of, the HSV 1 and HSV 2 nonvirion antibodies. All of these data taken together are interpreted as indicating that HSV 1 and HSV 2 play an etiologic role in certain human cancers, because they provide the kind of evidence by which virus-free experimental cancers can be proved to have been originally induced by such DNA viruses as polyoma, Simian Virus 40, or certain types of adenovirus.
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PMID:Herpes simplex and herpes genitalis viruses in etiology of some human cancers. 436 85

The Jamshidi-Swaim biopsy needle was utilized to perform 205 bone marrow biopsies, accompanied by simultaneous bone marrow aspirates, on patients with lymphoma, leukaemia, and a variety of solid tumours. There was no significant morbidity. There were 67 positive findings with biopsy and 42 with aspiration. The two techniques were complementary in Hodgkin's disease, non-Hodgkin's lymphoma, breast carcinoma, bronchogenic carcinoma, malignant melanoma, and in leukaemia. We have examined the bone marrow biopsies and aspirates with respect to the adequacy of the bone marrow biopsy specimen, the number of positive biopsies in the various categories of neoplasia, and the disparity of biopsy and aspirate, finding that 28 of the 67 positive biopsies (41.8%) had negative aspirates. These data and specimens obtained compared quite favourably with other series in which a modification of the Vim-Silverman needle was used.
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PMID:Comparison of the diagnostic value of bone marrow biopsy and bone marrow aspiration in neoplastic disease. 442 82

Epipodophyllotoxin VP 16213 (4-demethyl-epipodophyllotoxin-beta-D-ethylidene glucoside), given to 250 patients with various types of malignant disease, induced apparently complete remissions in four out of eight cases of acute monocytoid and acute myelomonocytoid leukaemia but only one complete regression and six incomplete remissions in 21 cases of reticulosarcoma. Incomplete regressions occurred in patients with Hodgkin's disease, lymphosarcoma, melanoma, and carcinoma of the breast, ovary, testis, bladder, kidney, and thyroid. Seemingly complete regressions of malignant pleural effusion occurred when the drug was given systemically. Toxic side effects interfered with treatment in 40 patients but stopped it in only nine. No signs of toxicity were seen in 114 patients and in 85 the side effects were negligible. VP 16213 represents an advance in the treatment of acute monocytoid leukaemia, which has been up till now insensitive to any drug.
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PMID:Epipodophyllotoxin VP 16213 in treatment of acute leukaemias, haematosarcomas, and solid tumours. 457 34

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

Indomethacin significantly enhances the depressed levels of lymphocyte proliferation to the mitogens phytohemagglutinin and concanavalin A in melanoma patients. We postulated that these results were related to an abnormality in prostaglandin E2 (PGE2)-mediated suppression, since this mechanism has previously has previously been demonstrated in patients with Hodgkin's lymphoma and with head and neck carcinoma. However, the results of three experimental approaches did not support this hypothesis. First, in vitro PGE2 production by cultured blood mononuclear cells was the same in 16 melanoma patients as in 45 normal controls (4.9 versus 4.7 ng/ml). Second, lymphocyte sensitivity to PGE2 for melanoma patients was essentially the same as that for normal controls, since exogenous doses of PGE2 inhibited the mitogen responses to the same degree. Third, another prostaglandin synthetase inhibitor (RO-205720), which is structurally unrelated to indomethacin, did not augment the mitogen response in these patients. Thus PGE2 cannot be implicated as a mediator of immunosuppression in melanoma patients. To further examine the immunomodulatory mechanism of indomethacin, we preincubated the drug with purified populations of either lymphocytes or monocytes, which were then recombined and tested for mitogen response. The results suggested that indomethacin had a direct effect on the responding T lymphocytes rather than an indirect effect on monocytes. These are the first studies demonstrating that indomethacin can act directly as a modulator of cellular immune function, independent of PGE2-mediated suppression.
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PMID:Immune modulatory effects of indomethacin in melanoma patients are not related to prostaglandin E2-mediated suppression. 628 58

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

Lipid-bound sialic acids were estimated in blood serum of 118 patients with tumors, of 13 donors and of 38 patients with non-tumoral diseases. Content of the sialic acids in blood serum of the patients with growing tumors constituted 23.1 +/- 1.1 mg/100 ml, which was 2-2.5-fold higher as compared with healthy donors (10.5 +/- 0.4 mg/100 ml) or with the patients with non-tumoral diseases (13.8 +/- 0.5 mg/100 ml). In the oncologic patients during the remission period the content of lipid-bound sialic acids in blood serum approached the normal level - 12.1 +/- 0.5 mg/100 ml. The highest level of the sialic acids was found in patients with lymphogranulomatosis II-IV step, with melanoma during the period of growth, with kidney tumor and with liver tissue primary tumor. Estimation of circulating lipid-bound sialic acids in the oncologic patients may serve as a test for evaluation of the tumor growth as well as of therapeutic treatment efficiency.
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PMID:[Circulating lipid-bound sialic acid levels in patients with malignant tumors]. 647 37

Fifty-six patients with advanced metastatic carcinoma of the breast, melanoma and lymphoma were treated with the new vinca alkaloid vindesine in a prospective Phase II study. The dose was 3 mg/M2 by I.V. bolus once a week for a minimum of two doses. Patients who failed to respond to four I.V. doses were treated with 48-h intravenous infusions at a dose of 1.5 mg/M2 per 24 h. Of the 26 evaluable patients with breast cancer, there were only two incomplete responses and four patients who experienced stabilization of disease. Of the 12 evaluable patients with melanoma, no responses were seen with four patients experiencing stabilization of disease. Of the 11 patients with non-Hodgkin's lymphomas, there was one complete remission which persisted for 26 months and two partial remissions. No additional responses were seen when the mode of administration was changed to 48-h infusion in three patients with breast cancer, five patients with melanoma and one patient with lymphoma. Significant toxicities included neutropenia in 24 patients and nausea and vomiting in two patients. There were no drug related deaths. Previously reported experience with vindesine in these tumors is reviewed as well.
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PMID:Vindesine in advanced breast cancer, lymphoma and melanoma. A Colorado Clinical Oncology Group study. 651 Dec 38


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