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)

The effect of chronic administration of 2,2'-dihydroxy-di-n-propylnitrosamine (DHPN) was studied in randombred guinea pigs. DHPN, dissolved in olive oil, was injected sc into 40 animals at a dose of 250 mg/kg body weight/week for 30 weeks, and the animals were observed until their death or termination of the experiment at the end of 40 weeks. Of the 32 guinea pigs that survived more than 20 weeks of DHPN treatment, 23 developed angiosarcoma of the liver between 22 and 40 weeks. Metastases to lungs, spleen, and peripancreatic lymph nodes were observed in 8 animals. Other tumors included hepatocellular carcinoma (1 animal), cholangiocarcinoma (1 animal), chronic myeloid leukemia (1 animal), acinar cell adenoma of pancreas (1 animal), and acinar cell carcinoma of pancreas (1 animal). In addition, megalocytic change of hepatic cells with intranuclear inclusions, pelliosis hepatis, and cholangiomatous lesions were also encountered frequently in the livers.
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PMID:Induction of malignant vascular tumors of the liver in guinea pigs treated with 2,2'-dihydroxy-di-n-propylnitrosamine. 18 51

Spontaneous human lymphocyte-mediated cytotoxicity (SLMC) against tumour-cell targets was examined in a series of patients with localized or malignant disease, both treated and untreated, and patients with untreated chronic lymphocytic leukemia (CLL). The level of SLMC was assessed by means of two previously established assay systems; the xenogeneic assay involving the mouse mastocytoma line P815, and the allogeneic assay in which the human chronic myelogenous leukemia-derived line, K562, was used. The assay systems involve the use of Ficoll-Isopaque-separated, iron-plus-magnetism-purified lymphocytes in an overnight 51chromium release assay, and reflect the cytotoxic ability of human non-T, complement receptor-, Fc receptor-positive lymphocytes. In the present paper, lymphocytes from all normal donors tested showed significant activity in the SLMC assay, with some variation from day to day. This variation was markedly reduced when different normal donors were tested on the same day and under identical experimental conditions. In contrast, lymphocytes from many patients with malignant disease had decreased SLM activity, and this decrease was highly significant in patients with treated or untreated metastatic disease, or untreated CLL. This was also the case when the data were expressed relative to the number of cytotoxic cells in the normal control population, or in comparison to the relative SLMC activity of lymphocytes from patients with other conditions. Markedly decreased SLMC was observed in some patients in spite of normal T and B lymphocyte proportions, or the presence of the ability to mount a vigorous delayed hypersensitivity reaction to PPD. A comparison of the xenogeneic and allogeneic assays showed that the same information with respect to whether SLMC was normal or abnormal was obtained with both assays in the majority of cases. The significance of the data is discussed with respect to the possible role of SLMC in vivo and the relevance of SLMC to the assessment of specific cell-mediated cytotoxicity in malignant disease.
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PMID:Spontaneous human lymphocyte-mediated cytotoxicity againts tumour target cells. I. The effect of malignant disease. 82 77

Elevation of transcobalamin I and serum vitamin B12 levels has usually been associated with increased granulocytic proliferation, such as occurs in chronic myelogenous leukemia. Two patients with metastatic cancer had extremely high serum vitamin B12 and transcobalamin I levels--greater than those seen in even the most intense granulocytic proliferation--that were not explainable by leukocytosis. The subjects' serum vitamin B12 levels were 18,750 and 21,221 pg per milliliter (normal, 471 plus or minus 174 pg per milliliter, mean plus or minus S.D.) and unsaturated vitamin B12 binding capacity 158,750 and 5,400 pg per milliliter (normal, 1153 plus or minus 313 pg per milliliter) respectively. The abnormally elevated serum binder was shown to be identical with transcobalamin balamin I in every respect. Levels of transcobalamin II and serum third binder were normal. The cause of the binder abnormality is unknown, but factors other than granulocyte proliferation may control or contribute to the production or accumulation of transcobalamin I.
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PMID:Extreme elevation of serum transcobalamin I in patients with metastatic cancer. 105 6

A human Philadelphia-chromosome positive chronic myeloid leukemia-blast crisis (CML-BC) cell line BV173 proliferated in the hematopoietic tissues, infiltrated various organs and caused the death of immunodeficient SCID mice. Leukemia spreading was assessed with diminished number of bone marrow cells and caused splenomegaly. The leukemic colonies grew from single cell suspension of bone marrow, spleen and peripheral blood. Bcr-abl m-RNA was detectable in bone marrow, spleen, peripheral blood, liver, lungs and brain. Dying mice demonstrated severely hypoplastic bone marrow, splenomegaly and massive metastases in the liver and kidneys. The survival time of animals was dependent on the number of inoculated leukemia cells.
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PMID:A model of Ph' positive chronic myeloid leukemia-blast crisis cell line growth in immunodeficient SCID mice. 128 28

Speciation and carcinogenesis result from genomic instability at the gametic or at the somatic levels. After an infinity of trials they occur, by chromosome rearrangements, in single individuals or in single cells and evolve by similar chromosomal or clonal evolutions. Loss of heterozygosity for the first event is essential in both processes: in evolution, a chromosomal rearrangement, a pericentric inversion or a Robertsonian fusion, must become homozygous to ensure a reproductive barrier for a new species; Knudson's two-event sequence is a similar situation in cancer. Position effect is equally important: we have shown overexpression of the SOD1 gene in the orangutan phylum probably by an intrachromosomal rearrangement; the t(9;22) in CML acts by typical position effect. Parental imprinting underlies the evolution of genome function and the unset of certain cancers. Evolution and malignancy are interweaved by viruses and oncogenes since the dawn of life. Cancer uses its intelligence to expand and to destroy the other tissues, using subtle metabolic pathways and a variety of tricks to metastasize other cells. It always wins but saws the branch on which it sits. Mankind also grows exponentially, killing thousands of other species, poisoning the oceans and soft waters, polluting the atmosphere, all for his egoistic needs. Man also travels and metastasizes other Earths. He modifies his genome or that of other species, and develops new technologies for his reproduction. He can destroy the planet in an eyeblink. To be or not to be the malignant primate, that will be the dilemma for the 21st Century.
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PMID:The malignant primate? 180 19

A rare combination of ocular melanoma with chronic myeloid leukemia was registered in a 61-year-old woman. The case history was not properly assessed in due time, therefore, the reason of ophthalmectomy was not identified leading to misdiagnosis. Neither chemotherapy nor radiation treatment was administered that permitted the author to establish a metachronous character of the primary malignancies. Melanoma was also uncommon for spindle cell components prone to late dissemination, specific alveoli resembling nevoid structures. There were metastases to the spleen.
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PMID:[Ocular melanoma associated with lymphocytic leukemia]. 337

The results of three phase II clinical trials with three new analogues belonging to the family of nitrosoureas are reported. One of the studied agents, chlorozotocine (CZT) is American, while the other two, RFCNU and RPCNU, are French. All three drugs have a sugar radical. CZT proved effective mainly in a few cases of leukemia and in one case of blastic transformation of chronic myelocytic leukemia. RFCNU was shown to be effective in 8% of digestive tumors, in 1 out of 7 pancreatic cancers and in 3 out of 10 hepatic and pulmonary metastases from an undiscovered primary adenocarcinoma. As for RPCNU, it's action resembles that of RFCNU: tumor regression lasting for over three years was obtained in a patient with hepatic metastases from a digestive carcinoma; in another patient a regression rate exceeding 50% was seen in pulmonary metastases from a rectal tumor. One of the significant results of our study is the apparent tissular specificity of responses according to the agent given: CZT is more often efficient on the lymphatic localizations of the studied tumors (4/5 responses); RFCNU and RPCNU often proved active on hepatic metastases (17% responses). Digestive tolerance was excellent with CZT and RFCNU and not quite as satisfactory for RPCNU. As predicted by our experimental study, platelet toxicity is both less common and less severe with RFCNU than with CZT and RPCNU.
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PMID:[Phase II study of 3 new nitrosoureas, 1 American (chlorozotocin) and 2 French (RFCNU and RPCNU)]. 629 62

An improved method for the detection of deoxythymidine kinase (TK) in human sera is reported. The method which utilizes 125I-iododeoxyuridine (IdUrd) as a substrate was used to measure TK in sera from patients with different diseases. Sera collected during the acute stage of infectious mononucleosis were found to contain elevated levels of TK, in most cases 10-40 times the normal value. The serum TK activity disappeared gradually and reached a normal level within 4 weeks. Sera from patients with other viral infections contained in most cases normal serum TK levels except in connection with measles, rubella, varicella, herpes simplex virus and cytomegalovirus infections. Additional studies revealed that sera from patients with different types of advanced lymphomas, acute leukemias, chronic granulocytic leukemia and lung cancer of the small-cell type with metastases, contained high TK levels which fluctuated in parallel with alterations in activity of the disease. The TK activity in sera from patients with both mononucleosis and tumor disease was characterized by electrophoresis and by its ability to utilize cytidine triphosphate as the phosphate donor. The results showed that the serum TK has the same properties as the human cytosolar TKI, except in connection with varicella.
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PMID:Application of an in vitro assay for serum thymidine kinase: results on viral disease and malignancies in humans. 669 95

Young gibbons that were experimentally inoculated with cell-free gibbon ape leukemia virus (GaLV) and developed peristent viremia subsequently developed chronic granulocytic leukemia (CGL) with associated multifocal bone lesions and metastases. An 8-month-old gibbon inoculated with 10(5) tissue culture infectious virus (TCIV) developed acute myeloproliferative disease with associated bone lesions after a latency of 5 months, while a 9-month-old gibbon inoculated with 10(3) TCIV developed CGL after and 11-month latency. The clinical symptoms associated with the onset of leukemia were an increased number of leukocytes which were predominantly mature granulocytes, development of anemia, and multifocal bone lesions. Terminally, the animals had elevated immature granulocytes in the blood, cellular bone marrow with a predominant number of immature granulocytes, and hepatosplenomegaly. The gibbon with CGL had metastatic growth in the spleen and lung. Two 14-month-old gibbons that were inoculated with 10(3) TCIV and developed persistent neutralizing antibody to the virus infection remained free of hematopoietic disease, as did uninoculated animals. The fact that only animals with persistent viremia developed leukemia supports the oncogenicity of GaLV in gibbons.
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PMID:Oncogenicity of gibbon type-C myelogenous leukemia virus. 676 82

Over a period of 4 years, 241 patients with advanced cancer were treated with mecaphane alone in 11 hospitals. Effective objective responses were obtained in 100 patients (41.4%). The response was most conspicuous in chronic granulocytic leukemia, with remission in 37 of 40 patients; in Hodgkin's disease and lymphosarcoma response rates were 60% and 47.3%, respectively. Mecaphane had an analgesic action in metastatic osteolytic bone cancer, and two patients with such metastases even attained recalcification of the osteolytic destructive lesions. The common toxic manifestations of mecaphane were leukopenia (33.6%), gastrointestinal upsets (28.2%), and thrombocytopenia (12.8%). It is concluded, therefore, that mecaphane could be a good antitumor agent in clinical use. It is less expensive and can be taken orally. Further trials of this drug are recommended.
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PMID:Clinical studies on the antitumor action of mecaphane. 730 33


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