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)

The causes of mortality of 3,649 white and 397 non-white male U.S. embalmers and funeral directors, who had died between 1975 and 1985, were examined in a proportional mortality study. Non-significant excesses were found for malignancies of the buccal cavity and pharynx (PMR = 120) and for nasopharyngeal cancer (PMR = 216). No sinonasal cancers were observed, while 1.7 were expected. A statistically significant excess of colon cancer (PMR = 127) was found and a non-significant excess of brain and other CNS cancer was noted among whites only (PMR = 123). Statistically significant excesses of malignancies of the lymphatic and hematopoietic systems were found in whites (PMR = 131) and non-whites (PMR = 241). Myeloid leukemia (PMR = 157) and leukemia of other and unspecified cell types (PMR = 228) were in excess, while no excess of lymphatic leukemia was noted. Elevations in risk were also found for non-Hodgkin's lymphoma, polycythemia vera, and myelofibrosis. Non-whites showed a marked excess of multiple myeloma (PMR = 369). Chronic nephritis was in excess among whites (PMR = 215) and non-whites (PMR = 257). No excess of cirrhosis of the liver was found. Excesses of malignancies of the lymphatic and hematopoietic systems could not be directly related to job held in the funeral industry. Further case-control studies are planned to rule out the possibility that the observed associations are artifactual, by assessing the association between specific work practices and disease risk.
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PMID:Mortality of U.S. embalmers and funeral directors. 178 18

Among 670 children diagnosed with central nervous system tumors before age 20 and recorded in the Connecticut Tumor Registry, nine had a second neoplasm as well. From known age-specific and year-specific cancer incidence figures for Connecticut, the expected number of second neoplasms for the series of 670 is 0.99; therefore the relative risk is 9.1 (95% confidence limits: 4.0, 17.3). Three patients developed two central nervous system tumors, while 0.16 were expected, giving a relative risk of 19 (95% confidence limits: 3.8, 55). Six patients developed two neoplasms in childhood, versus 0.66 expected; the relative risk of this event is 9.1 (95% confidence limits: 3.3, 20). In four cases of lapse in time between the diagnosis of the first and second tumor, the first tumor had been treated with radiation. Five cancers occurred in parents or siblings of these nine patients, versus 0.91 expected; the relative risk is 5.5 (95% confidence limits: 1.2, 10.0). Three of these relatives had leukemia, while only 0.04 cases were expected (relative risk = 75). We conclude that not only is a child with CNS cancer at increased risk for other cancers, but such a child with two cancers is often part of a familial cluster with increased risk of cancer.
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PMID:Second primaries in children with central nervous system tumors. 609 7

Three flavonols, 5,3'-dihydroxy-3,6,7,8,4'-pentamethoxyflavone [1], 5,4'-dihydroxy-3,6,7,8,3'-pentamethoxyflavone [2], and quercetin 3-O-beta-D-glucopyranosyl-7-O-alpha-L-rhamnopyranoside [3], were isolated from Polanisia dodecandra. Compound 1 showed remarkable cytotoxicity in vitro against panels of central nervous system cancer (SF-268, SF-539, SNB-75, U-251), non-small cell lung cancer (HOP-62, NCI-H266, NCI-H460, NCI-H522), small cell lung cancer (DMS-114), ovarian cancer (OVCAR-3, SK-OV-3), colon cancer (HCT-116), renal cancer (UO-31), a melanoma cell line (SK-MEL-5), and two leukemia cell lines (HL-60 [TB], SR), with GI50 values in the low micromolar to nanomolar concentration range. This substance also inhibited rubulin polymerization (IC50 = 0.83 +/- 0.2 microM) and the binding of radiolabeled colchicine to tubulin with 59% inhibition when present in equimolar concentrations with colchicine. Compound 2 also showed cytotoxicity against medulloblastoma (TE-671) tumor cells with an ED50 value of 0.98 microgram/ml. Compound 1 appears to be the first example of a flavonol to exhibit potent inhibition of tubulin polymerization and, therefore, warrants further investigation as an antimitotic agent.
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PMID:Antitumor agents, 154. Cytotoxic and antimitotic flavonols from Polanisia dodecandra. 762 25

The problem of malignant melanoma is important in the United States, in the world as a whole, and particularly in Hawaii with its high levels of ultraviolet radiation. It is estimated that 32,000 Americans will develop melanoma and 6,800 will die of this tumor in 1993. Melanoma is now the seventh most frequent cancer in the United States. It is more common than ovarian, cervical, CNS cancer and leukemia. Both incidence and mortality from melanoma are rapidly increasing. The incidence of melanoma has consistently increased 6% a year and the death rate has increased 2% a year since 1950. At current rates, one in 400 will die of this tumor. Should this rate of increase continue, by the year 2000, it is estimated that one in 75 Americans will develop melanoma during a lifetime. The highest melanoma incidence in the U.S. is found in Hawaii. Melanoma is increasing faster than any other cancer in the United States and all over the world.
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PMID:The gender-related issues in malignant melanoma. 832 89

Several 2,4-diaminopyrimidines have been synthesized and tested for their anticancer and anti-HIV activities. Out of these, eight compounds displayed significant activity against leukemia, melanoma, non-small cell and CNS cancer. Two compounds were active against leukemia P388. One compound has been found to be moderately active as compared to AZT.
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PMID:Synthesis of some new pyrimidine derivatives as potential anticancer and anti-HIV agent. 956 52

Some new phenothiazines have been synthesized on the basis of previous studies. The anticancer activity of "half-mustard type" phenothiazines was investigated on sixty different cancer cell lines in vitro. The percentage of growth (PG), 50% inhibition of growth (GI50), the tumor growth inhibition (TGI) and the concentration required for 50% lethality of cells (IC50) were examined and calculated in the presence of various (from 10(-4) to 10(-8) M) concentrations of phenothiazine alkylurea derivatives. The following cell lines were involved in the study: 6 leukemia, 9 non-small-cell lung cancer, 7 colon cancer, 6 central nervous system cancer, 8 melanoma, 6 ovarian cancer, 8 renal cancer, 2 prostate and 8 breast cancer cell lines. The antileukemic activity of four chloroethyl-substituted phenothiazine-alkylureas was shown by considerable growth inhibition, in the 10(-5) M range, of the six different leukemia cell lines. The 50% inhibition of growth was nearly the same for the four compounds on all cell lines. Tumor growth inhibition (TGI) and IC50 value to cells varied from -4.0 to -4.66. The two derivatives with the butylene bridge were more effective than propylene linked compounds against the CCRP-CEM, HL60 (TB), K-562 and MOLT-4 cell lines. However, the anti-leukemic activity of the derivatives was nearly the same for RPMT 8226 and SR cell lines. The substituent at the 2- position of phenothiazine ring and the length of the linker between the side chain nitrogen and the phenothiazine ring system are apparently important for antileukemic activity. Four of the 9 non-small-cell lung cancer cell lines were sensitive, while the other 5 cell lines were not. The compounds had a slight growth inhibitory effect on colon cell carcinoma and melanoma cells in which case the butylene linker seemed to be more effective than the propylene linker. At the same time, all of the compounds were weak or mostly inactive on cancer cells from the central nervous system. One ovarian cancer line of the 6, the IGROVI was sensitive to butylurea phenothiazines, however, the other five were not sensitive at all. The difference in the sensitivity of various renal cell carcinomas was significant: 5 lines were not sensitive, three of them (786-0, RXF-393 and TK-10) were sensitive to only butylene-substituted phenothiazine-ureas, propylene substitution resulted in ineffective compounds. The compounds were not able to inhibit the 2 prostate and 4 breast cancer cell lines, even at 10(-4) M. It was interesting that propylene-linked ureas were more effective than butylene-linked derivatives on MCF-7, but butylene-linked derivatives were more effective than propylene-linked compounds on MDA MB-231 and MDA-N. In addition, MDA MB 435 was more sensitive to the trifluoromethyl derivatives than the compounds without this substituent. Since the phthalimido-alkyl phenothiazines were not active at the first level of prescreen, these compounds were omitted from this study. The drug sensitivity of some cancer cell lines was not uniform for the different groups, therefore we postulate that the resistance can be related to some kind of (existing) drug-efflux mechanism. Apparently, the tumor specificity of phenothiazine alkylureas is more related to the leukemia specificity of alkylureas than to any CNS or lung specificity of phenothiazines.
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PMID:The primary in vitro anticancer activity of "half-mustard type" phenothiazines in NCI's revised anticancer screening paradigm. 956

Three types of 1-chloromethyl-5-hydroxy-1,2-dihydro-3H-benz[e]indole (seco-CBI) dimers were designed, synthesized and evaluated in vitro by NCI against nine types of cancer cells. Biological results showed that the antitumor activities of these seco-CBI dimers were strongly related to the position and length of the linker and generally with potency increasing in the order of C7-C7 dimers (22i-iv) < C7-N3 dimers (28i-iv) < N3-N3 dimers (25i-iv). Compound 28iv showed significant activity against CCRT-CEM, HL-60 (TB), MOLT-4, and SR leukemia cell lines and the MCF 7 breast cancer cell line with GI50 values < 0.01 microM. N3-N3 dimer 25i displayed striking potency against leukemia, CNS cancer, melanoma and prostate cancer cell lines with GI50 values < 0.01 microM against all the cell lines and showed the highest overall potency of the agents examined (GMG=0.0120 microM).
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PMID:Design, synthesis and cytotoxicity evaluation of 1-chloromethyl-5-hydroxy-1,2-dihydro-3H-benz[e]indole (seco-CBI) dimers. 1097 8

VIP/PACAP are autocrine growth factors for lung cancer. VIP and/or PACAP mRNA is present in most lung cancer cell lines examined. Although mRNA for VPAC2-R is not common, VPAC1-R and PAC1-R mRNA is present in many lung cancer cell lines. 125I-VIP binds with high affinity to lung cancer cells and specific 125I-VIP binding is inhibited with high affinity by (Lys15, Arg16, Leu27)VIP1-7 GRF8-27, the VPAC1-R specific agonist, but not by Ro25-1553(18), the VPAC2-R specific agonist. VIP elevates cAMP and increases c-fos gene expression. The increase in cAMP and c-fos mRNA caused by VIP is inhibited by SN(VH). (SH)VH inhibited the proliferation of NCIH1299 cells in the MTT assay, which is based on cytotoxicity. In a recent cell line screen, (SN)VH inhibited the growth of 51 of 56 cancer cell lines including leukemia, lung cancer, colon cancer, CNS cancer, melanoma, ovarian cancer, renal cancer, breast cancer, and prostate cancer (T. Moody, unpublished). It remains to be determined if (SN)VH will be useful for treatment of a wide variety of cancers.
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PMID:VPAC1 receptors and lung cancer. 1119 32

Methyl protogracillin (NSC-698792) was a furostanol saponin isolated from the rhizome of Dioscorea collettii var. hypoglauca (Dioscoreaceae), a Chinese herbal remedy for the treatment of cervical carcinoma, carcinoma of urinary bladder and renal tumor for centuries, in our previous studies. In order to systematically evaluate its potential anticancer activity, methyl protogracillin was tested for its cytotoxicity in vitro against 60 human cancer cell lines in the National Cancer Institute (NCI)'s anticancer drug screen. As a result, it was found that methyl protogracillin was cytotoxic against all the tested cell lines from leukemia and solid tumors in the NCI's human cancer panel; it showed particular selectivity against one colon cancer line (KM12), one central nervous system (CNS) cancer line (U251), two melanoma lines (MALME-3M and M14), two renal cancer lines (786-0 and UO-31) and one breast cancer line (MDA-MB-231) with GI50< or =2.0 microM. The selectivity between these seven most sensitive lines and the least sensitive line (CCRF-CEM) ranged from 26- to 56-fold. In the same cancer subpanel, selectivity more than 15-fold was observed between MDA-MB-231 and MCF-7, NCI-ADR-RES, BT-549 in breast cancer. From a general view of the mean graph, CNS cancer is the most sensitive subpanel, while ovarian cancer and renal cancer are the least sensitive subpanels. Based on an analysis of the COMPARE computer program with methyl protogracillin as a seed compound, no compounds in the NCI's anticancer drug screen database have similar cytotoxicity patterns (mean graph) to that of methyl protogracillin, indicating a potential novel mechanism of the anticancer action involved.
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PMID:Methyl protogracillin (NSC-698792): the spectrum of cytotoxicity against 60 human cancer cell lines in the National Cancer Institute's anticancer drug screen panel. 1146 1

Protodioscin (NSC-698 796) is a furostanol saponin isolated from the rhizome of Dioscorea collettii var. hypoglauca (Dioscoreaceae), a Chinese herbal remedy for the treatment of cervical carcinoma, carcinoma of urinary bladder and renal tumor for centuries. To systematically evaluate its potential anticancer activity, protodioscin was tested for cytotoxicity in vitro against 60 human cancer cell lines in the NCI's (National Cancer Institute, USA) anticancer drug screen. As a result, protodioscin was cytotoxic against most cell lines from leukemia and solid tumors in the NCI's human cancer panel, especially selectively against one leukemia line (MOLT-4), one NSCLC line (A549/ATCC), two colon cancer lines (HCT-116 and SW-620), one CNS cancer line (SNB-75), one melanoma line (LOX IMVI), and one renal cancer line (786 - 0) with GI50 < or = 2.0 microM. In the general view of mean graphs, leukemia, colon cancer and prostate cancer are the most sensitive subpanels, while ovarian cancer is the least sensitive subpanel. Based on an analysis of COMPARE computer program with protodioscin as a seed compound, no compounds in the NCI's anticancer drug screen database have cytotoxicity patterns (mean graphs) similar to those of protodioscin, indicating that a potential novel mechanism of anticancer action is involved.
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PMID:Protodioscin (NSC-698 796): its spectrum of cytotoxicity against sixty human cancer cell lines in an anticancer drug screen panel. 1198 50


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