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)

Several studies have evaluated cancer risk associated with occupational and environmental exposure to dichlorodiphenyltrichloroethane (DDT). Results are mixed. To further inquire into human carcinogenicity of DDT, we conducted a mortality follow-up study of 4,552 male workers, exposed to DDT during antimalarial operations in Sardinia, Italy, conducted in 1946 to 1950. Detailed information on DDT use during the operations provided the opportunity to develop individual estimates of average and cumulative exposure. Mortality of the cohort was first compared with that of the Sardinian population. Overall mortality in the cohort was about as expected, but there was a deficit for death from cardiovascular disease and a slight excess for nonmalignant respiratory diseases and lymphatic cancer among the unexposed subcohort. For internal comparisons, we used Poisson regression analysis to calculate relative risks of selected malignant and nonmalignant diseases with the unexposed subcohort as the reference. Cancer mortality was decreased among DDT-exposed workers, mainly due to a reduction in lung cancer deaths. Birth outside from the study area was a strong predictor of mortality from leukemia. Mortality from stomach cancer increased up to 2-fold in the highest quartile of cumulative exposure (relative risk, 2.0; 95% confidence interval, 0.9-4.4), but no exposure-response trend was observed. Risks of liver cancer, pancreatic cancer, and leukemia were not elevated among DDT-exposed workers. No effect of latency on risk estimates was observed over the 45 years of follow-up and within selected time windows. Adjusting risks by possible exposure to chlordane in the second part of the antimalarial operations did not change the results. In conclusion, we found little evidence for a link between occupational exposure to DDT and mortality from any of the cancers previously suggested to be associated.
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PMID:Cancer mortality among men occupationally exposed to dichlorodiphenyltrichloroethane. 1623 Apr 25

Arylamine carcinogens and drugs are N-acetylated by cytosolic N-acetyltransferase (NAT), which uses acetyl-coenzyme A as a cofactor. NAT plays an initial role in the metabolism of these arylamine compounds. 2-Aminofluorene is one of the arylamine carcinogens which have been demonstrated to undergo N-acetylation in laboratory animals and humans. Our previous study showed that human cancer cell lines (colon cancer, colo 205; liver cancer, Hep G2; bladder cancer, T24; leukemia, HL-60; prostate cancer, LNCaP; osteogenic sarcoma, U-2 OS; malignant melanoma, A375.S2) displayed NAT activity, which was affected by aloe-emodin in human leukemia cells. The purpose of this study was to determine whether aloe-emodin could affect the enzyme activity and gene expression of NAT at the mRNA and protein levels in malignant human melanoma A375.S2 cells. The results showed that aloe-emodin inhibited NAT1 activity (decreased N-acetylation of 2-aminofluorene) in intact cells in a dose-dependent manner. The effect of aloe-emodin on NAT1 at the protein level was determined by Western blotting and the mRNA levels were examined by polymerase chain reaction (PCR) and cDNA microarray. These results clearly indicate that aloe-emodin inhibits the mRNA expression and enzyme activity of NAT1 in A375.S2 cells.
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PMID:Effect of inhibition of aloe-emodin on N-acetyltransferase activity and gene expression in human malignant melanoma cells (A375.S2). 1631 33

The objective of the present study was to investigate the association between human T-lymphotropic virus type-1 (HTLV-1) infection and cancer risk in a longitudinal study. The study population consisted of 2729 atomic bomb survivors in Nagasaki Prefecture, Japan, who had no previous history of cancer at baseline. The baseline survey, including analysis of antibody to HTLV-1, took place during 1985-1987 and follow-up was performed until the end of 2001. There were 553 incident cases of malignant neoplasms during the observation period. After adjustment for sex, age and other variables, HTLV-1 infection was not associated with the risk of developing cancers of all sites, excluding adult T-cell leukemia (rate ratio 1.0, 95% confidence interval [CI] 0.76-1.4), stomach, colon and rectum, lung, female breast or other minor sites, but was associated with increased risk of liver cancer (rate ratio 2.1, 95%CI 1.0-4.6). The point estimate of the rate ratio for thyroid cancer was 3.0, but this was not significantly higher than 1 because of the small number of events (n = 11) and low prevalence of HTLV-1 seropositivity. These findings support the idea that HTLV-1 infection is not associated with an increased general cancer risk. Confounding by hepatitis C virus (HCV) and the interaction between HTLV-1 and HCV may explain the increased risk of liver cancer among HTLV-1 carriers. Further follow-up may be required to determine if HTLV-1 carriers are at increased risk of thyroid cancer.
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PMID:Human T-cell lymphotropic virus type-1 infection and risk of cancer: 15.4 year longitudinal study among atomic bomb survivors in Nagasaki, Japan. 1673 33

A series of 3-amino-1,2,4-benzotriazine-1,4-dioxide derivatives 1 have been synthesized and evaluated for their cytotoxic activity in vitro against human leukemia cell lines: Molt-4, K562, HL60, human liver cancer cell Hep-G2, human prostate cancer cell PC-3 in hypoxia. Most of the compounds showed more potent activity than TPZ. Compounds 1i and 1m displayed encouraging superior activity against Molt-4 and HL-60 cell lines. Three potential derivatives received the test of the activity in hypoxia and in normoxia against Molt-4 and HL-60 cell lines and showed obvious hypoxia selectivity. Further mechanism study revealed that the cytotoxic activities of compounds 1i and 1k in Molt-4 cells might be mediated by modulation of p53 protein expression and mitochondrial membrane potential (DeltaPsi(m)).
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PMID:Synthesis and hypoxic-cytotoxic activity of some 3-amino-1,2,4-benzotriazine-1,4-dioxide derivatives. 1677 9

The literature provides evidence that metabolic nitric oxide (NO) release mediates the cytotoxic activities (against human leukemia and prostate cancer xenografts in mice) of JS-K, a compound of structure R(2)N-N(O)=NO-Ar for which R(2)N is 4-(ethoxycarbonyl)piperazin-1-yl and Ar is 2,4-dinitrophenyl. Here we present comparative data on the potencies of JS-K and 41 other O(2)-arylated diazeniumdiolates as inhibitors of HL-60 human leukemia cell proliferation, as well as in the NCI 51-cell-line screen for six of them. The data show JS-K to be the most potent of the 42 in both screens and suggest that other features of its structure and metabolism besides NO release may contribute importantly to its activity. Results with control compounds implicate JS-K's arylating ability, and the surprisingly low IC(50) value of the N-(ethoxycarbonyl)piperazine byproduct of NO release suggests a role for the R(2)N moiety. In addition to the above-mentioned in vivo activities, JS-K is shown here to be carcinostatic in a rat liver cancer model.
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PMID:Antitumor activity of JS-K [O2-(2,4-dinitrophenyl) 1-[(4-ethoxycarbonyl)piperazin-1-yl]diazen-1-ium-1,2-diolate] and related O2-aryl diazeniumdiolates in vitro and in vivo. 1682 95

Cancer mortality data collected by the Guam Cancer Registry for the period 1998 through 2002 were analyzed by cancer site, age, and ethnicity. Ethnicity and site specific age-adjusted cancer mortality rates for Guam were calculated utilizing Guam 2000 census data, the US 2000 standard population and compared to U.S. 2002 age-adjusted cancer mortality rates. Age-adjusted cancer mortality rates for ethnic populations represented on Guam, except those of leukemia and non-Hodgkins lymphoma, were high in relation to other population groups and higher than U.S. averages. Some highlights include: 1. Chamorros had high age-adjusted mortality rates for mouth and pharynx (15.5 vs. 2.7 [corrected] U.S.), nasopharynx (9.1 vs. 0.2 U.S.), lung and bronchus (66.9 vs. 54.9 U.S.), colon-rectum-anus (28.6 vs. 19.7 U.S.), breast (32.0 vs. 28.0 U.S.) and prostate cancer (40.9 vs. 27.9 U.S.); 2. Chamorros (6.4 vs. 2.5 U.S.) and Micronesians (6.3) had high and nearly identical age-adjusted mortality rates for cancer of the mouth and pharynx when nasopharyngeal cancers were excluded; 3. Micronesians had the highest mortality rate for liver cancer over all ethnicities documented (43.5 vs. 4.9 U.S.); 4. Asians had the highest mortality rates for pancreatic (12.5 vs. 10.5 U.S.) and cervical cancer (8.5 vs. 2.6 U.S.); 5. Caucasians had the highest mortality rates for leukemia (19.9 vs. 7.5 U.S.) and Non-Hodgkin's lymphoma (17.6 vs. 7.6 U.S.). Suggestions are made for further research on both explaining and ameliorating cancer mortality disparities among ethnic groups on Guam.
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PMID:Ethnic disparities in cancer mortality among residents of Guam. 1705 33

Novel aminophenol analogues were synthesized based on the structure of fenretinide (N-(4-hydroxyphenyl)retinamide, 5), which is a potent anticancer agent. Our findings showed that the anticancer activities of 5 were due to the side chain attached to the aminophenol moiety. A p-octylaminophenol (p-OAP) provided the most potent anticancer activity among p-alkylaminophenols examined. In this study, we investigated anticancer activities against various cancer cell lines by the new aminophenols, p-dodecylaminophenol (1), p-decylaminophenol (2), N-(4-hydroxyphenyl)dodecananamide (3), and N-(4-hydroxyphenyl)decananamide (4), which exhibits a side chain as long as 5. Cell growth of breast cancer (MCF-7, MCF-7/Adr(R)), prostate cancer (DU-145), and leukemia (HL60) cells was suppressed by 1 and 2 in a fashion dependent on the length of the alkyl chain attached to the aminophenol. In contrast, 3 and 4 were extremely weak. Compound 5 was less potent than 1. Cell growth of liver cancer (HepG2) was not markedly affected by these compounds. In addition, apoptosis of HL60 cells was induced by 1 and 2 in a chain length-dependent manner, but not by 3 and 4. Incorporation of compounds into HL60 cells was in the order 1>2=3>4. These results indicated that anticancer activities for 1 and 2 are correlated with their incorporation into cancer cells and their capability to induce apoptosis, but not for 3 and 4. Compound 1, a potent anticancer agent with potency strikingly greater than 5, may potentially be useful in clinic.
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PMID:Potent anticancer activities of novel aminophenol analogues against various cancer cell lines. 1709 29

Highly active antiretroviral therapy (HAART) has dramatically reduced the incidence of acquired immunodeficiency syndrome (AIDS) and increased AIDS survival time, but little is known about its impact on cancer. Data from adults in the San Francisco, California, AIDS surveillance registry were computer matched with the California Cancer Registry. Age-, sex-, and race-adjusted standardized incidence ratios (SIRs) were computed, and proportional hazards models evaluated the effect of HAART use on cancer incidence and cancer survival time. Among 14,210 adults with AIDS diagnosed in 1990-2000, 482 non-AIDS-defining cancers were diagnosed. Compared with rates for the general population, significantly increased cancer incidence rates were observed for anal (SIR = 13.4), Hodgkin's lymphoma (SIR = 11.5), liver (SIR = 3.6), oral cavity and pharynx (SIR = 2.6), respiratory (SIR = 2.6), leukemia (SIR = 2.4), skin melanoma (SIR = 2.4), and prostate (SIR = 1.7) cancers. Risk of liver cancer was lower with HAART use (relative hazard (RH) = 0.32). Risk of anal cancer increased after 1995 (RH = 2.9). Respiratory cancer (RH = 0.40) and Hodgkin's lymphoma (RH = 0.17) showed increased cancer survival time with HAART use, while anal cancer survival may have been slightly decreased (RH = 1.4). The impact of HAART on non-AIDS-defining cancer incidence rates and survival is not uniform, and the mechanism(s) responsible for these differences should be investigated further.
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PMID:The impact of highly active antiretroviral therapy on non-AIDS-defining cancers among adults with AIDS. 1734 4

Two new flavonoids - 3'-formyl-4',6'-dihydroxy-2'-methoxy-5'-methylchalcone (FMC) and (2S)-8-formyl-5-hydroxy-7-methoxy-6-methylflavanone (FMF) - isolated from the buds of Cleistocalyx operculatus, were investigated for their antioxidant and anticancer activity. Total antioxidant activity and reducing ability were measured. 1,1-diphenyl-2-picrylhydrazyl (DPPH) radical and superoxide anion radical scavenging assays were carried out to evaluate the antioxidant potential of the two compounds. The antioxidant activity of the two compounds increased in a concentration-dependent manner. FMC and FMF at a concentration of 500 microM inhibited lipid peroxidation by 64.3 +/- 2.5% and 60.3 +/- 2.3%, respectively, an antioxidant activity approximately similar to that of 500 microM alpha-tocopherol (66.3 +/- 2.5%). Similarly, the effect of FMC and FMF on reducing power increased in a concentration-dependent manner. In DPPH radical scavenging assays, the IC50 values of FMC and FMF were 50.2 +/- 2.8 microM and 75.8 +/- 2.5 microM, respectively. Moreover, FMC and FMF scavenged the superoxide generated by the phenazine methosulfate (PMS)/reduced beta-nicotinamide adenine dinucleotide (NADH) nitroblue tetrazolium (NBT) system, with IC50 values of 56.3 +/- 2.3 microM and 317.5 +/- 2.9 microM, respectively. The anticancer activity of the two compounds were determined in five human cancer cell lines, SMMC-7721 (liver cancer), 8898 (pancreatic cancer), K562 (chronic leukaemia), HeLa (tumour of cervix uteri) and 95-D (high metastic lung carcinoma). FMC and FMF showed broad-spectrum anticancer activity against all the human cancer cell lines tested. The results obtained in the current study indicate that the two flavonoids could be a potential source of natural antioxidant and anticancer agents. To our knowledge, this is the first report on bioactivity of FMC and FMF.
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PMID:Antioxidant and anticancer activity of 3'-formyl-4', 6'-dihydroxy-2'-methoxy-5'-methylchalcone and (2S)-8-formyl-5-hydroxy-7-methoxy-6-methylflavanone. 1743 Jun 39

Suppressor of cytokine signaling (SOCS) is a new family of proteins produced in cells. It may play an important role in classic negative feedback loop to regulate cytokine signal transduction. SOCS-1 was observed and confirmed firstly. Expression of SOCS-1 can inhibit cytokine signal transduction of some cytokines, such as IL-6, LIF, OSM, INF-gamma, GH, and so on, many immune responses are regulated by them in vivo. Abnormal expression of SOCS-1 is closely related to some human diseases. It plays an important role in the development of leukemia, rheumatoid arthritis, liver cirrhosis and liver cancer. In this review, the advances of research on the relationship between SOCS-1 and cytokine, and its correlation with some diseases were summarized.
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PMID:[Progress of study on suppressor of cytokine signaling-1 - review]. 1749 65


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