Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023418 (leukemia)
 93,477 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 76-year-old man with spontaneous rupture of a hemangiosarcoma of the spleen, together with a review of 49 previously reported patients with splenic hemangiosarcoma are presented. Twenty-three were women and 27 were men. All but 3 were adults. Fiften were 50-59 years of age. The symptomatology was nonspecific. Three patients developed microangiopathic hemolytic anemia. Spontaneous rupture occurred in 17 cases (34%). Metastases occurred in 42 cases; they were primarily hematogenous and most often in the liver. Lymph node involvement, however, was present in 13 cases. The prognosis of untreated splenic hemangiosarcoma is poor. Three of 25 patients survived a year or more after the initial onset of symptoms. Splenectomy before rupture is advisable, since 5 of 19 patients survived at least 1-5 years. It is suggested that hemangiosarcoma be considered in patients with: 1) splenomegaly without evidence of malignant lymphoma or leukemia, 2) splenomegaly with microangiopathic hemolytic anemia, and 3) unexplained intraperitoneal hemorrhage.
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PMID:Hemangiosarcoma of spleen with spontaneous rupture. 116 82

It is well known that MPSV induces myeloproliferative syndrome (MPS) in mice. Intravenous one shot inoculation of myeloproliferative sarcoma virus (MPSV) with Friend murine leukemia virus (F-MuLV) as a helper in newborn Jar-2 rats (on the second neonatal day) yielded hematopoietic malignancies in all the treated rats (25/25 rats) after 2 weeks' latency. MPS appeared from the 14th day in 14 rats. In the midst of the myeloproliferative field of the spleen and bone marrow, myeloblastic or myeloblastic-erythroblastic foci were observed. From 19th day, acute myeloblastic leukemia occurred in 3 rats and erythroleukemia in 8 rats. MPSV induced first MPS which remained as such or later developed into acute leukemia. Myelofibrosis as seen in mice was not observed. In addition, hemangiosarcoma of the brain, spinal cord and spleen appeared in 15 rats from the 24th day, and were often multiple. MPSV can yield the tumor only in newborn rats, and target cells of MPSV are not only hematopoietic cells but also endothelial cells of the brain, spinal cord and occasionally spleen.
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PMID:Histopathologic studies on myeloproliferative sarcoma virus (MPSV) induced leukemias and hemangiosarcoma in Jar-2 rats. 245 78

The authors report a new case of primary angiosarcoma of the spleen and, after a review of the literature, they discuss its clinical, diagnostic and therapeutic problems. Primary angiosarcoma of the spleen is a very rare tumor. The diagnosis should be suspected in the case of a patient with splenomegaly and unexplained anemia, with no evidence of lymphoma, leukemia or myelofibrosis. In 30% of cases, the tumor presents in the form of spontaneous rupture of the spleen. The prognosis is very poor, as it is a highly malignant tumor, even more so in the presence of early metastases with or without spontaneous rupture of the organ. Splenectomy prior to rupture could increase the survival. Patients with or without metastatic disease may be treated by combination chemotherapy, which still remains empirical and palliative.
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PMID:[Primary angiosarcoma of the spleen. Apropos of a new case]. 261 17

To evaluate the effects of continuous low-level ionizing radiation on humans, the follow-up data (1980-85) on Japanese thorotrast-exposed patients were analyzed. The patients were 241 war-wounded military personnel registered with and cared for by the Ministry of Health and Welfare since 1979. During this period, a total of 1144 person-years, 94 patients died. Compared with the expected number of deaths calculated from age- and cause-specific death rates in Japan during the same period, the thorotrast-exposed patients were at three times greater risk of death from all causes (P less than 0.001), had 47 times the risk of liver cancer (P less than 0.001), 12 times the risk of leukemia (P less than 0.05), and 20 times the risk of liver cirrhosis (P less than 0.001). Age at time of thorotrast injection, drinking and smoking habits had little effect on these statistics. Analyses of 30 autopsied patients with liver cancer showed statistically significantly increases in hemangiosarcoma and cholangiocarcinoma. The thorotrast-exposed patients' estimated risk of liver cancer by histological type was 21 times that of the general population for hepatocellular carcinoma, 303 times that for cholangiocarcinoma and 3129 times that for hemangiosarcoma.
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PMID:Increased risk of death in thorotrast-exposed patients during the late follow-up period. 282 75

A primary angiosarcoma, which formed multiple ventricular pericardial and myocardial nodules without atrial involvement, occurred in the heart of an 80-year old Caucasian female and caused death within three weeks of the onset of symptoms. There were neither cutaneous lesions to suggest Kaposi's sarcoma nor serological evidence of infection by Human T-cell Leukemia Virus and the rapidly fatal course of the patient's illness was similar to that of the typical atrial cardiac angiosarcoma. The distinction between primary cardiac angiosarcoma and Kaposi's sarcoma affecting the heart is discussed.
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PMID:Generalised angiosarcoma of the heart. 313 59

A carcinogenic role of inorganic arsenic has been suspected for nearly a century. Exposure to inorganic arsenic compounds occurs in some occupational groups, e.g., among smelter workers and workers engaged in the production and use of arsenic containing pesticides. Substantial exposure can also result from drinking water in certain areas and the use of some drugs. Tobacco and wine have had high As concentrations due to the use of arsenic containing pesticides. Inorganic arsenic compounds interfere with DNA repair mechanisms and an increased frequency of chromosomal aberrations have been observed among exposed workers and patients. Epidemiological data show that inorganic arsenic exposure can cause cancer of the lung and skin. The evidence of an etiologic role of arsenic for angiosarcoma of the liver is highly suggestive; however, the association between arsenic and cancer of other sites needs further investigation. No epidemiological data are available on exposure to organic arsenic compounds and cancer. Animal carcinogenicity studies involving exposure to various inorganic and organic arsenic compounds by different routes have been negative, with the possible exception of some preliminary data regarding lung cancer and leukemia. Some studies have indicated an increased mortality from lung cancer in populations living near point emission sources of arsenic into the air. The role of arsenic cannot be evaluated due to lack of exposure data. Epidemiological data suggest that the present WHO standard for drinking water (50 micrograms As/l.) provides only a small safety margin with regard to skin cancer.
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PMID:The carcinogenicity of arsenic. 702 36

The modified steroidal alkylating agent, 3 beta-hydroxy-13 alpha-amino-13,17-seco-5 alpha-androstane-17-oic-13,17-lactam[p-[bis(2-chloroethyl)amino]-phenyl]acetate showed excellent activity in treatment of there murine solid tumors. Colon 26-bearing CD2F1 mice lived twice as long as controls with tumor free survivors at the end of the 70-day observation period. CD8F1 mammary tumor growth was suppressed greater than 90% compared to controls. B16 melanoma-bearing B6D2F1 mice lived 50% longer than controls. This agent had previously been shown to be active in treatment of the Theagenion-Bahner angiosarcoma, the T8 Guerin tumor, L1210 leukemia and P388 leukemia.
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PMID:Activity of 3 beta-hydroxy-13 alpha-amino-13,17-seco-5 alpha-androstane-17-oic-13,17-lactam(p-(bis(2-chloroethyl)amino)-phenyl) acetate(NSC 290205) in murine solid tumors. 706 63

An overview of published information on occupational cancer and recorded ongoing occupational cancer research in developing countries is presented. The main cancers reported, of possible occupational origin, are skin carcinoma, leukemia due to exposure to benzene, asbestos-caused mesothelioma, vinyl chloride-induced hepatic angiosarcoma, carcinoma of bilharzial urinary bladder, stomach cancer reportedly associated with nitrogen fertilizers, lung cancer of nickel smelters, and nasopharyngeal and pulmonary carcinoma in workers exposed to the dust of hard wood. The difficulties of developing efficient occupational cancer prevention are discussed. Some options are analyzed regarding legislative, technological, environmental, medical, administrative, and educational cancer control applicable under conditions of developing countries.
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PMID:Problems of occupational carcinogenesis in developing countries. 734 83

Mortality through 1988 was studied for 5,932 male employees who worked between January 1, 1946 and December 31, 1967 at a New Jersey plastics manufacturing and research and development facility. The cohort was followed for an average of 32 years and included 1,859 deaths. Potential exposures included asbestos, formaldehyde, and polyvinyl chloride (PVC). Mortality rates for the cohort were compared to both U.S. and state mortality rates, and analyses were also performed by lagging duration of employment. Based on U.S. rates, mortality among hourly males (n = 3,853) from all cancers was similar to expected [standardized mortality ratio (SMR), 102; 95% confidence interval (CI), 92-114]. Excess mortality among hourly workers was seen for pancreatic cancer (SMR, 146; 95% CI, 95-216) and "malignancies of other parts of the respiratory system" (SMR, 373; 95% CI, 121-870). The latter excess was due entirely to five deaths from pleural mesothelioma. There were no deaths identified due to nasal cavity or nasopharyngeal cancers, or angiosarcoma of the liver. Mortality from leukemia among research and development workers (n = 1,421) was significantly elevated (SMR, 265; 95% CI, 115-524) and related to assignment to process development. This study verifies the excess of pancreatic cancer among workers at the facility seen in earlier studies and observes excesses of mesothelioma due to asbestos exposure and leukemia in process development workers.
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PMID:Mortality among workers at a plastics manufacturing and research and development facility: 1946-1988. 748 91

Mutations in the receptor for the epidermal growth factor provide valuable insight into mechanisms of growth control. Oncogenic mutants of this receptor tyrosine kinase cause erythroid leukemia, fibrosarcoma, angiosarcoma, glioblastoma, and melanoma. Mutations in the avian protooncogene occur by retroviral mechanisms. Deletion of the ligand-binding domain results in erythroblastosis, while additional mutations in cytoplasmic structures broaden the disease potential to other cell types. A carboxyl-terminal structure of erbB oncogenes modulates growth responses in a complex, cell-specific manner; this tissue-specificity region appears to promote growth in erythroblasts and to produce trans-dominant inhibition in fibroblasts. Human glioblastoma multiforme frequently contains receptor mutations that are reminiscent of avian oncogenes. In hereditary melanoma of Xiphophorus, aberrant regulation of transcription by a recombinant promoter determines tissue-specific tumorigenesis. The diversity of oncogenic mutations raises important questions concerning the roles of several receptor structures. The extracellular domain inhibits the receptor when unoccupied by ligand, for example, through a mechanism that is unknown. The auto-phosphorylation sites are dispensable for transformation, so their function in neoplastic growth is unclear. The carboxyl-terminal region promotes or blocks transformation in different tissues, suggesting complex regulation by unknown cellular factors. These issues are critical to understanding of the mechanisms of receptor activation and tissue tropism for this family of oncogenes.
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PMID:Tissue-specific transformation by oncogenic mutants of epidermal growth factor receptor. 771 Nov 15


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