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)

The diagnosis of malignant histiocytosis is usually based upon typical light microscopic features of the neoplasm. Supplementary cytochemical and immunologic features have been suggested as typical of malignant histiocytosis. The present study was prompted by an unusual erythropagocytic hepatocellular carcinoma having immunologic and cytochemical markers suggesting mononuclear phagocytic origin. Twenty-four neoplasms of unquestionable epithelial origin were prospectively evaluated for activity of alpha-naphthyl acetate esterase, a cytochemical marker useful in distinguishing between the non-Hodgkin's lymphomas and malignant histiocytosis. The epithelial tumors represented a broad spectrum of tissue origins and consistently demonstrated alpha-naphthyl acetate esterase activity. Thus, erythrophagocytosis and alpha-naphthyl acetate esterase positivity may be misleading in the unusual instance in which the histopathologic differential diagnosis includes malignant histiocytosis and epithelial neoplasia. Ultrastructural assessment is useful in the exclusion of poorly differentiated carcinoma.
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PMID:Expression of monocytic--histiocytic cytochemical markers in epithelial neoplasia. 22 45

Plasma and 24-h urinary adenosine 3':5'-monophosphate (cyclic AMP) and guanosine 3':5'-monophosphate (cyclic GMP) were measured by radioimmunoassay in 12 normal subjects, 33 patients with six types of non-neoplastic disease (cholelithiasis, peptic ulcer, coronary heart disease, hypertension, regional ileitis, and cirrhosis), and 34 patients with five types of disseminated neoplastic disease (acute myelocytic leukemia; Hodgkin's disease; and metastatic cancer of the lung, colon, and breast). In patients with non-neoplastic disease, cyclic nucleotide values in plasma and urine did not differ significantly (P greater than 0.05) from those in normal subjects. In patients with disseminated cancer, cyclic AMP values in plasma and urine likewise did not differ significantly from those in normal subjects. Plasma cyclic GMP, in contrast, was significantly elevated in all five types of cancer patients, and urinary cyclic GMP was significantly elevated (five times the normal mean) in patients with acute myelogenous leukemia and Hodgkin's disease.
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PMID:Plasma and urine cyclic guanosine 3':5'-monophosphate in disseminated cancer. 22 52

Long-term monolayer cell cultures have been prepared from tumor nodules in spleens removed from 28 patients with Hodgkin's disease and from 84 spleens that did not have tumors from Hodgkin's disease patients, normal adult spleens, and human fetal spleens and thymuses. After 5 to 20 serial passages in culture, cells from nine of the Hodgkin's disease monolayers underwent morphologic change in vitro with transition from a spindle and reticular pattern of replication to polygonal and round cells that propagated in mosaic arrays. Four of such Hodgkin's disease monolayer cell lines were injected subcutaneously into 43 nude, athymic mice. In 36 animals (84%), neoplasms developed at the inoculation site that werel ocally destructive, capable of pulmonary metastasis, and eventually fatal to the recipients. Transplanted tumors were not observed in 18 athymic mice injected with cultures prepared from normal human adult spleen and fetal spleen and thymus, nor were tumors seen in 16 similar animals that received fresh, noncultured Hodgkin's disease tumor tissue. On microscopic examination, xenografts derived from Hodgkin's disease cultures were pleomorphic malignant neoplasms composed of large, undifferentiated cells, resembling reticulum cell sarcoma. These neoplasms did not involve the lymphoreticular organs of mice. Chromosome studies indicated that the transplanted neoplasms were composed of human cells with an aneuploid karyotype and that monolayer cultures prepared from the heterotransplants contained a karyotype similar to that of the cultured cells prior to passage in mice. The ability of these Hodgkin's disease cell lines to produce invasive tumors with human karyotypes in nude mice is evidence of the neoplastic nature of the monolayer cells and their relationship to the malignant cell of the human disorder.
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PMID:Growth of cultured cells from patients with Hodgkin's disease and transplantation into nude mice. 26 39

Salivary obstruction may result from growth of a malignant tumor in the vicinity of the salivary gland, as well as result from sialolithiasis. Lymphomas of all types, including Hodgkin disease, lymphosarcoma, and reticulum cell sarcoma frequently are diagnosed in the region of the head and neck. The biopsy of a suspected tumor should be done by multiple needle biopsies. Open biopsies should be avoided to prevent seeding and spreading. When the diagnosis of malignant lymphoma is made, the tumor must be classified histologically and the extent of disease must be determined and staged for proper treatment. Treatment should consist of radiation and chemotherapy. Surgery is of little value. Malignant lymphomas usually are disseminated widely and end fatally.
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PMID:Malignant lymphoma and salivary obstruction. 27 57

Familial non-Hodgkin lymphoma (NHL) cases were classified according to the histologic criteria (modified) of Rappaport, to determine the extent of morphologic similarities of the tumors. In four families affected members had different tumor histologies that may be observed in an individual patient as the lymphoma progresses. In two families, the affected relatives had tumors of seemingly discordant histology. These tumors may nonetheless be etiologically related as indicated by the pattern of laboratory abnormalities, especially immunologic, in affected as well as unaffected members. The 20 cases had a reversal of the sex ratio (M/F) usually seen in NHL: 0.5 instead of 1.3. Other tumors observed in these families included primary hepatocellular carcinoma, pulmonary adenocarcinoma, Hodgkin disease, and acute lymphocytic leukemia - all of which have been associated with inborn or acquired immunodeficiency states.
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PMID:Familial non-Hodgkin lymphoma: histologic diversity and relation to other cancers. 27 64

The latency period, success rate, and minimal cell inoculum size required for transplantation of continuously passaged human tumor lines into congenitally athymic (nude) mice, antilymphocyte serum (ALS)-treated congenitally athymic (nude) mice, and congenitally athymic-asplenic (lasat) mice were compared. The 11 tumor lines studied included examples of breast adenocarcinoma, transitional cell carcinoma, osteosarcoma, fibrosarcoma, Hodgkin's disease, malignant melanoma, and rhabdomyosarcoma. Of these 11 tumor lines, 3 were successfully transplanted into nude mice, compared to 5 of 10 tumor lines in ALS-treated nude mice and 9 of 11 lines in lasat mice. Moreover, the latency period was shorter and the minimal cell inoculum size was lower for lasat mice than for either nude or ALS-treated nude mice. Despite this enhancement of heterotransplantation into lasat mice and despite the growth of large local masses, no evidence of distant metastases was found.
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PMID:Enhancement of heterotransplanted human tumor graft survival in nude mice treated with antilymphocyte serum and in congenitally athymic-asplenic (Lasat) mice. 27 31

We investigated whether human adenovirus type 4 (Ad4) might cause cancer in humans. Cell culture and animal model studies indicated that Ad4-induced human tumors should contain Ad4 DNA sequences. Thus Ad4 DNA was labeled in vitro (sp act, approximately 10(7) 3H counts/min/microgram) and hybridized in liquid phase with DNA extracted from human tumors. No viral sequences were detected in 31 squamous cell carcinomas of the lung, 5 adenocarcinomas of the lung, 4 oat cell carcinomas of the lung, 4 carcinomas of the stomach, 10 carcinomas of the colon, 3 carcinomas of the kidney, 3 carcinomas of the breast, 2 carcinomas of the ovary, and 6 Hodgkin's lymphomas. Reconstruction experiments with added Ad4 DNA indicated that the probe detected about 1 copy of 5% of the Ad4 genome per tumor cell. Therefore, these data were strong evidence (but did not prove) that none of these particular tumors were induced by Ad4.
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PMID:Analysis of human cancer DNA for DNA sequences of human adenovirus type 4. 28 75

Spontaneous sister chromatid exchanges and banded karyotypes were studied in blood lymphocytes from 96 individuals: seven patients with chronic myelogenous leukemia, 15 normal controls, and five "cancer families" comprising 12 cancer patients, 40 tumor-free blood relatives and 22 spouses. The families had: malignant melanoma; Epstein-Barr virus-associated malignancies and a birth defect syndrome; non-Hodgkin lymphoma and diverse carcinomas; Hodgkin's lymphoma and adenocarcinomas; and acute myelogenous leukemia. In addition to the Philadelphia chromosome in chronic myelogenous leukemia patients, karyotypic abnormalities, especially breaks and fragments, were found in 29% of cancer family members, but were inconsistent and usually attributable to radiotherapy. Mean sister chromatid exchange values were normal in chronic myelogenous leukemia, but low (by t-test) in tumor patients and their blood relatives in cancer-prone families. In tumor patients, mean sister chromatid exchange levels fell as age increased. After adjusting for this age effect, no significant differences remained among groups. In patients at high risk of cancer (because they have chronic myelogenous leukemia or a strong family history of cancer), spontaneous sister chromatid exchange rates were not a marker of cancer risk.
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PMID:Sister chromatid exchanges and chromosomes in chronic myelogenous leukemia and cancer families. 28 71

Leucocytes of normal persons and patients with acute and chronic granulocytic leukemia, chronic lymphocytic leukemia, and non-Hodgkin lymphoma were separated into subfractions by centrifugation in discontinuous Ficoll density gradient. Osmotic resistance was examined in hypotonic NaCl solutions with decreasing concentration and by determining LDH activity in the supernatant. Suspensions of myelocytes, polymorphnuclear granulocytes, and lymphocytes of normal persons and patients with chronic lymphocytic leukemia demonstrated the same osmotic resistance. Only myeloblasts were osmotically less fragile, and tumor cells of non-Hodgkin lymphoma more fragile.
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PMID:[Osmotic fragility in subfractions of leucocytes in hematological diseases (author's transl)]. 29 98

Group C human adenoviruses (Ads) of serotypes 1, 2, 5, and 6 infect most children and commonly cause latent infections of lymphoid tissues. Ads transform cells into a malignant-like phenotype; the oncogenic genetic information is in the left 8% of the viral genome, in the HindIII-G DNA fragment. We have investigated the molecular basis for group C Ad latent infections in human tonsils as well as whether these viruses are linked to human cancer. Tonsil or cancer DNAs and RNAs were assayed for Ad sequences by liquid-phase saturation-hybridization with in vitro-labeled Ad5 HindIII-G fragment. About 25% of the 52 tonsils analyzed contained DNA or RNA sequences specific to HindIII-G, indicating that Ad transforming sequences are expressed as RNA in tonsils. Southern blotting analysis of four tonsil DNAs revealed multiple copies of the complete Ad genome in a free state and provided evidence for an unusual form of the Ad genome, possibly Ad DNA integrated into cellular DNA. In assays of human cancers, no Ad sequences were detected in DNAs from 26 squamous cell carcinomas (Cas), 3 adenocarcinomas, 4 oat cell Cas, 5 stomach Cas, 5 small intestine Cas, 15 colon Cas, 6 rectum Cas, 5 Hodgkin and 6 non-Hodgkin lymphomas, and 2 breast Cas. Reconstruction experiments indicated that the HindIII-G probe could detect 1 copy per cell of 0.2-0.3% of the viral genome. No HindIII-G-specific sequences were detected in RNAs from 21 squamous cell Cas, 3 oat cell Cas, 2 stomach Cas, or 18 colon Cas. In six other experiments using the complete Ad2 genome as probe, no Ad sequences were found in DNAs from 6 lung Cas, 12 normal lung tissues, 33 gastrointestinal Cas, 19 normal gastrointestinal tissues, 6 Hodgkin lymphomas, 3 breast Cas, or 4 kidney Cas, at a sensitivity of about 1 copy per tumor cell of 5-10% of the Ad2 genome. All Ad-induced cancer cells should contain at least 1 copy of 1-6% of the viral genome, the minimal size of the transforming region, and probably should contain multiple copies of more of the genome. Therefore, our data are definitive evidence against group C Ads being the cause of the cancers tested, which represent about 50% of the cancer incidence in the United States. Of additional interest, we did not detect Ad2 sequences in RNAs from 7 human placentas, 12 normal lungs, or 19 normal gastrointestinal tissues (nor in 44 cancer or 23 tonsil RNAs). Thus, we did not confirm a recent report of the presence of Ad2 RNA in RNAs from human placentas; the possibility that a small population of cells in placenta expresses group C "related" sequences is not ruled out.
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PMID:Analysis of human tonsil and cancer DNAs and RNAs for DNA sequences of group C (serotypes 1, 2, 5, and 6) human adenoviruses. 29 48


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