1,720,969 research outputs found
Reactive oxygen species mediate N-(4-hydroxyphenyl)retinamide-induced cell death in malignant T cells and are inhibited by the HTLV-I oncoprotein Tax
No full textN-(4-hydroxyphenyl)retinamide (HPR) is a synthetic retinoid that inhibits growth of many human tumor cells, including those resistant to natural retinoids. HPR is an effective chemopreventive agent for prostate, cervix, breast, bladder, skin and lung cancers, and has shown promise for the treatment of neuroblastomas. We have previously shown that HPR inhibits proliferation and induces apoptosis of human T-cell lymphotropic virus type I (HTLV-I)-associated adult T-cell leukemia (ATL) and HTLV-I-negative malignant T cells, whereas no effect is observed on normal lymphocytes. In this report, we identified HPR-induced reactive oxygen species (ROS) generation as the key mediator of cell cycle arrest and apoptosis of malignant T cells. HPR treatment of HTLV-I-negative malignant T cells was associated with a rapid and progressive ROS accumulation. Pre-treatment with the antioxidants vitamin C and dithiothreitol inhibited ROS generation, prevented HPR-induced ceramide accumulation, cell cycle arrest, cytochrome c release, caspase-activation and apoptosis. Therefore, anti-oxidants protected malignant T cells from HPR-induced growth inhibition. The expression of the HTLV-I oncoprotein Tax abrogated HPR-induced ROS accumulation in HTLV-I-infected cells, which explains their lower sensitivity to HPR. Defining the mechanism of free radical induction by HPR may support a potential therapeutic role for this synthetic retinoid in ATL and HTLV-I-negative T-cell lymphomas.Barna G, 2005, ANTICANCER RES, V25, P4179; Bazarbachi A, 2001, VIRUS RES, V78, P79, DOI 10.1016-S0168-1702(01)00286-6; Bazarbachi A, 2004, LANCET ONCOL, V5, P664, DOI 10.1016-S1470-2045(04)01608-0; Boya P, 2003, ONCOGENE, V22, P6220, DOI 10.1038-sj.onc.1206827; Cereseto A, 1996, BLOOD, V88, P1551; Darwiche N, 2005, BIOCHEM J, V392, P231, DOI 10.1042-BJ20050578; Darwiche N, 2001, Hematol J, V2, P127, DOI 10.1038-sj.thj.6200098; Darwiche N, 2004, LEUKEMIA, V18, P607, DOI 10.1038-sj.leu.2403245; Delia D, 1997, CARCINOGENESIS, V18, P943, DOI 10.1093-carcin-18.5.943; DELIA D, 1993, CANCER RES, V53, P6036; DiPietrantonio AM, 2000, CANCER RES, V60, P4331; Hail N, 2001, J BIOL CHEM, V276, P45614, DOI 10.1074-jbc.M106559200; Hail N, 2000, CANCER EPIDEM BIOMAR, V9, P1293; Hatoum A, 2001, CARCINOGENESIS, V22, P1955, DOI 10.1093-carcin-22.12.1955; Jeang KT, 2001, CYTOKINE GROWTH F R, V12, P207, DOI 10.1016-S1359-6101(00)00028-9; Kawakami A, 1999, BLOOD, V94, P3847; Kawata S, 2003, J VIROL, V77, P7291, DOI 10.1128-JVI.77.13.7291-7299.2003; Kfoury Y, 2005, CELL DEATH DIFFER, V12, P871, DOI 10.1038-sj.cdd.4401624; Kharbanda S, 1997, P NATL ACAD SCI USA, V94, P6939, DOI 10.1073-pnas.94.13.6939; Kim DG, 2002, J BIOL CHEM, V277, P38930, DOI 10.1074-jbc.M205941200; Kim HJ, 2006, ONCOGENE, V25, P2785, DOI 10.1038-sj.onc.1209303; Lovat PE, 2004, ANN NY ACAD SCI, V1028, P81, DOI 10.1196-annals.1322.009; Mologni L, 1999, BLOOD, V93, P1045; Oridate N, 1997, J NATL CANCER I, V89, P1191, DOI 10.1093-jnci-89.16.1191; Satoh E, 2005, BIOL PHARM BULL, V28, P941, DOI 10.1248-bpb.28.941; SMITH MR, 1991, J CLIN INVEST, V88, P1038, DOI 10.1172-JCI115364; Sun SY, 1999, MOL PHARMACOL, V55, P403; Suzuki S, 1999, ONCOGENE, V18, P6380, DOI 10.1038-sj.onc.1203024; Ulukaya E, 2003, CELL DEATH DIFFER, V10, P856, DOI 10.1038-sj.cdd.4401242; Wu JM, 2001, APOPTOSIS, V6, P377, DOI 10.1023-A:1011342220621; Yoshida M, 2001, ANNU REV IMMUNOL, V19, P475, DOI 10.1146-annurev.immunol.19.1.47511111
The high-risk benign tumor: Evidence from the two-stage skin cancer model and relevance for human cancer
No full textBenign tumors that form following chemical initiation and promotion in the mouse skin can be grouped into two classes. The majority of papillomas do not progress to squamous cell carcinoma (SCC), and these are designated as low-risk or terminally benign papillomas. In contrast, a much smaller group forms the true precursor to the SCC, and these have a significantly higher frequency and rate of malignant conversion than the bulk of low-risk papillomas. In standard two-stage carcinogenesis studies both tumor types are present, but grossly indistinguishable. Here we describe properties and potential origins of high-risk papillomas and discuss the relevance of this model for certain human cancers with defined premalignant states. © 2007 wiley-Liss, Inc.Bernstein SC, 1996, DERMATOL SURG, V22, P243; Brown K, 1998, CURR BIOL, V8, P516, DOI 10.1016-S0960-9822(98)70203-9; BROWN K, 1990, P NATL ACAD SCI USA, V87, P538, DOI 10.1073-pnas.87.2.538; CUI W, 1994, CANCER RES, V54, P5831; Darwiche N, 1996, CANCER RES, V56, P4942; DARWICHE N, 1995, CANCER RES, V55, P2774; DARWICHE N, 2007, IN PRESS ONCOGENE; Fu W, 2003, ARCH DERMATOL, V139, P66, DOI 10.1001-archderm.139.1.66; Germain P, 2006, PHARMACOL REV, V58, P760, DOI 10.1124-pr.58.4.7; Glick A, 1999, P NATL ACAD SCI USA, V96, P14949, DOI 10.1073-pnas.96.26.14949; Glick AB, 1996, CANCER RES, V56, P3645; GLICK AB, 1993, P NATL ACAD SCI USA, V90, P6076, DOI 10.1073-pnas.90.13.6076; GLICK AB, 1994, GENE DEV, V8, P2429, DOI 10.1101-gad.8.20.2429; HENNINGS H, 1985, CARCINOGENESIS, V6, P1607, DOI 10.1093-carcin-6.11.1607; HENNINGS H, 1970, CANCER RES, V30, P312; HENNINGS H, 1990, CANCER RES, V50, P653; KRUSZEWSKI FH, 1987, CANCER RES, V47, P3783; Morris RJ, 2000, J CLIN INVEST, V106, P3, DOI 10.1172-JCI10508; Reibel J, 2003, CRIT REV ORAL BIOL M, V14, P47; ROWE DE, 1992, J AM ACAD DERMATOL, V26, P976, DOI 10.1016-0190-9622(92)70144-5; Schepman KP, 1998, ORAL ONCOL, V34, P270, DOI 10.1016-S1368-8375(98)80007-9; SHUBIK P, 1953, BRIT J CANCER, V7, P342, DOI 10.1038-bjc.1953.32; TENNENBAUM T, 1992, CANCER RES, V52, P2966; Tennenbaum T, 1998, CANCER RES, V58, P1435; TENNENBAUM T, 1993, CANCER RES, V53, P4803; Woodworth CD, 2004, CARCINOGENESIS, V25, P1771, DOI 10.1093-carcin-bgh170; Yuspa SH, 1998, J DERMATOL SCI, V17, P1, DOI 10.1016-S0923-1811(97)00071-611111
Research highlights
No full text[No abstract available]Firestone GL, 2009, EXPERT REV MOL MED, V11, DOI 10.1017-S1462399409001239; Ghantous A, 2010, DRUG DISCOV TODAY, V15, P668, DOI 10.1016-j.drudis.2010.06.002; Scherf U, 2000, NAT GENET, V24, P236, DOI 10.1038-73439; Sertel S, 2010, CHEM-BIOL INTERACT, V185, P42, DOI 10.1016-j.cbi.2010.02.0020
Human T-cell lymphotropic virus type I-transformed T-cells have a partial defect in ceramide synthesis in response to N-(4-hydroxyphenyl)retinamide
No full textTreatment with the synthetic retinoid HPR [N-(4-hydroxyphenyl)-retinamide] causes growth arrest and apoptosis in HTLV-I (human T-cell lymphotropic virus type-I)-positive and HTLV-I-negative malignant T-cells [8]. It was observed that HPR-mediated growth inhibition was associated with ceramide accumulation only in HTLV-I-negative cells. The aim of the present study was to investigate the mechanism by which HPR differentially regulates ceramide metabolism in HTLV-I-negative and HTLV-I-positive malignant T-cells. Clinically achievable concentrations of HPR caused early dose-dependent increases in ceramide levels only in HTLV-I-negative cells and preceded HPR-induced growth suppression. HPR induced de novo synthesis of ceramide in HTLV-I-negative, but not in HTLV-I-positive, cells. Blocking ceramide glucosylation in HTLV-I-positive cells, which leads to accumulation of endogenous ceramide, rendered these cells more sensitive to HPR. Exogenous cell-permeant ceramides that function partially by generating endogenous ceramide induced growth suppression in all tested malignant lymphocytes, were consistently found to be less effective in HTLV-I-positive cells confirming their defect in de novo ceramide synthesis. Owing to its multipotent activities, the HTLV-I-encoded Tax protein was suspected to inhibit ceramide synthesis. Tax-transfected Molt-4 and HELA cells were less sensitive to HPR and C6-ceramide mediated growth inhibition respectively and produced lower levels of endogenous ceramide. Together, these results indicate that HTLV-I-positive cells are defective in de novo synthesis of ceramide and that therapeutic modalities that bypass this defect are more likely to be successful. © 2005 Biochemical Society.Andrieu-Abadie N, 2001, FREE RADICAL BIO MED, V31, P717, DOI 10.1016-S0891-5849(01)00655-4; Batra S, 2004, CANCER RES, V64, P5415, DOI 10.1158-0008-5472.CAN-04-0377; Bielawska A, 2001, ANAL BIOCHEM, V298, P141, DOI 10.1006-abio.2001.5342; BIELAWSKA A, 1993, J BIOL CHEM, V268, P26226; BLIGH EG, 1959, CAN J BIOCHEM PHYS, V37, P911; Cai ZZ, 1997, J BIOL CHEM, V272, P6918; Chen YR, 1999, MOL PHARMACOL, V56, P1271; Chmura SJ, 1997, CANCER RES, V57, P4340; Chmura SJ, 1997, CANCER RES, V57, P1270; CIFONE MG, 1994, J EXP MED, V180, P1547, DOI 10.1084-jem.180.4.1547; Darwiche N, 2001, Hematol J, V2, P127, DOI 10.1038-sj.thj.6200098; Darwiche N, 2004, LEUKEMIA, V18, P607, DOI 10.1038-sj.leu.2403245; Dbaibo GS, 1998, J CLIN INVEST, V102, P329, DOI 10.1172-JCI1180; DBAIBO GS, 1995, P NATL ACAD SCI USA, V92, P1347, DOI 10.1073-pnas.92.5.1347; DELIA D, 1993, CANCER RES, V53, P6036; DiPietrantonio AM, 1998, INT J CANCER, V78, P53, DOI 10.1002-(SICI)1097-0215(19980925)78:153::AID-IJC103.0.CO;2-6; Erdreich-Epstein A, 2002, J BIOL CHEM, V277, P49531, DOI 10.1074-jbc.M209962200; GarciaRuiz C, 1997, J BIOL CHEM, V272, P11369; Gatza ML, 2003, ONCOGENE, V22, P5141, DOI 10.1038-sj.onc.1206549; Gulbins E, 2003, PHARMACOL RES, V47, P393, DOI 10.1016-S1043-6618(03)00052-5; Hannun YA, 2000, TRENDS CELL BIOL, V10, P73, DOI 10.1016-S0962-8924(99)01694-3; Hannun YA, 1996, SCIENCE, V274, P1855, DOI 10.1126-science.274.5294.1855; KALEMKERIAN GP, 1995, J NATL CANCER I, V87, P1674, DOI 10.1093-jnci-87.22.1674; Lavie Y, 1997, J BIOL CHEM, V272, P1682; Lee TK, 1998, TAIWAN J MATH, V2, P457; MATHIAS S, 1993, SCIENCE, V259, P519, DOI 10.1126-science.8424175; Maurer BJ, 2000, J NATL CANCER I, V92, P1897, DOI 10.1093-jnci-92.23.1897; Maurer BJ, 1999, J NATL CANCER I, V91, P1138, DOI 10.1093-jnci-91.13.1138; Michael JM, 1997, CANCER RES, V57, P3600; Nicholson KM, 1999, BRIT J CANCER, V81, P423, DOI 10.1038-sj.bjc.6690711; O'Donnell PH, 2002, LEUKEMIA, V16, P902, DOI 10.1038-sj-leu-2402485; Ogretmen B, 2002, J BIOL CHEM, V277, P12960, DOI 10.1074-jbc.M110699200; Ogretmen B, 2001, J BIOL CHEM, V276, P32506, DOI 10.1074-jbc.M101350200; OKAZAKI T, 1990, J BIOL CHEM, V265, P15823; Oridate N, 1997, J NATL CANCER I, V89, P1191, DOI 10.1093-jnci-89.16.1191; Perry DK, 2000, ANN NY ACAD SCI, V905, P91; Pettus BJ, 2002, BBA-MOL CELL BIOL L, V1585, P114, DOI 10.1016-S1388-1981(02)00331-1; Pettus BJ, 2003, FASEB J, V17, P1411, DOI 10.1096-fj.02-1038com; Pise-Masison CA, 2001, J BIOL CHEM, V276, P200; Pise-Masison CA, 2000, MOL CELL BIOL, V20, P3377, DOI 10.1128-MCB.20.10.3377-3386.2000; RADIN NS, 1994, MOL CHEM NEUROPATHOL, V21, P111, DOI 10.1007-BF02815346; Reynolds CP, 2004, CANCER LETT, V206, P169, DOI 10.1016-j.canlet.2003.08.034; RIEBELING C, 2003, J BIOL CHEM, V279, P43452; Ruvolo PP, 2003, PHARMACOL RES, V47, P383, DOI 10.1016-S1043-6618(03)00050-1; Spinedi A, 1998, CELL DEATH DIFFER, V5, P785, DOI 10.1038-sj.cdd.4400428; TEPPER CG, 1995, P NATL ACAD SCI USA, V92, P8443, DOI 10.1073-pnas.92.18.8443; Wang HT, 2003, UROLOGY, V61, P1047, DOI 10.1016-S0090-4295(02)02511-6; Wang HT, 2001, CANCER RES, V61, P5102; Wu JM, 2001, APOPTOSIS, V6, P377, DOI 10.1023-A:1011342220621; Zhao S, 2004, J CELL PHYSIOL, V199, P47, DOI 10.1002-jcp.1045356
Going Beyond Counting First Authors in Author Co-citation Analysis
Full text linkThe present study examines one of the fundamental aspects of author co-citation analysis (ACA) - the way co-citation
counts are defined. Co-citation counting provides the data on which all subsequent statistical analyses and mappings
are based, and we compare ACA results based on two different types of co-citation counting - the traditional type that
only counts the first one among a cited work's authors on the one hand and a non-traditional type that takes into
account the first 5 authors of a cited work on the other hand. Results indicate that the picture produced through this non-traditional author co-citation counting contains more coherent author groups and is therefore considerably clearer. However, this picture represents fewer specialties in the research field being studied than that produced through the traditional first-author co-citation counting when the same number of top-ranked authors is selected and analyzed. Reasons for these effects are discussed
Stage-Specific Effect of N-(4-Hydroxyphenyl)Retinamide on Cell Growth in Squamous Cell Carcinogenesis
No full textSquamous cell carcinoma (SCC) is the most prevalent form of epithelial cancer. SCC results when normal epithelial cells undergo multiple neoplastic changes that culminate in the evolution of an invasive cancer. Retinoids are commonly used as chemopreventive and treatment agents in skin cancer; however, SCC progression is accompanied by a gradual loss of retinoid responsiveness. The synthetic retinoid N-(4-hydroxyphenyl)retinamide (HPR) has shown promising anti-neoplastic activity in a variety of tumor cells, including those that are resistant to all-trans retinoic acid (t-RA). We investigated the effect of HPR on growth and apoptosis of squamous cells at different stages of carcinogenesis. We then determined if retinoic acid receptor (RAR) overexpression affected the outcome of HPR treatment. To model SCC malignant progression, we used a panel of murine keratinocytes representing different stages of squamous cell carcinogenesis. This panel consisted of primary keratinocytes, SP1 and 308 papilloma cell lines, the PAM-212 squamous carcinoma cell line, and the spindle 17 cell line. With the exception of the primary keratinocytes, all cells were unresponsive to t-RA treatment. Pharmacological concentrations of HPR were non-cytotoxic to all keratinocytes tested and HPR sensitivity was stage-dependent, with the papilloma cell lines being the most sensitive, and the spindle cells being the most resistant. Overexpression of RARγ in SP1 papilloma cells enhanced growth suppression and apoptosis induction by HPR. HPR-induced growth suppression was accompanied by a simultaneous block in the G1 phase of the cell cycle in RAR-transduced and control SP1 cells and differential regulation of cell cycle and apoptotic mediators. © 2004 Wiley-Liss, Inc.ASUMENDI A, 2002, BRIT J CANCER, V12, P1951; BOISE LH, 1993, CELL, V74, P597, DOI 10.1016-0092-8674(93)90508-N; Bruno S, 2002, CARCINOGENESIS, V23, P447, DOI 10.1093-carcin-23.3.447; Chambon P, 1996, FASEB J, V10, P940; Chan LNL, 1997, LEUKEMIA LYMPHOMA, V25, P271; Clifford JL, 1999, CANCER RES, V59, P14; COSTA A, 1994, CANCER RES, V54, pS2032; D'Ambrosio SM, 2000, ANTICANCER RES, V20, P2273; DARWICHE N, 1995, CANCER RES, V55, P2774; DELIA D, 1993, CANCER RES, V53, P6036; Denning MF, 1998, J BIOL CHEM, V273, P29995, DOI 10.1074-jbc.273.45.29995; deThe H, 1996, FASEB J, V10, P955; Di Cunto F, 1998, SCIENCE, V280, P1069, DOI 10.1126-science.280.5366.1069; DiPietrantonio AM, 2000, CANCER RES, V60, P4331; DiPietrantonio AM, 1998, INT J CANCER, V78, P53, DOI 10.1002-(SICI)1097-0215(19980925)78:153::AID-IJC103.0.CO;2-6; Faderl S, 2003, LEUKEMIA RES, V27, P259, DOI 10.1016-S0145-2126(02)00162-5; Fanjul AN, 1996, J BIOL CHEM, V271, P22441; Fisher GJ, 1996, NATURE, V379, P335, DOI 10.1038-379335a0; FISHER GJ, 1994, J BIOL CHEM, V269, P20629; Follen M, 2001, CLIN CANCER RES, V7, P3356; FORMELLI F, 1993, J CLIN ONCOL, V11, P2036; Formelli F, 1996, FASEB J, V10, P1014; FORMELLI F, 2000, VITAMIN A RETINOIDS, P241; GANDER RJ, 1978, CHEM ABSTR 89892, V88; Goyette P, 2000, J BIOL CHEM, V275, P16497, DOI 10.1074-jbc.M909382199; GREENHALGH DA, 1990, P NATL ACAD SCI USA, V87, P643, DOI 10.1073-pnas.87.2.643; GRIFFITHS CEM, 1994, ARCH DERMATOL RES, V287, P53, DOI 10.1007-BF00370719; Hatoum A, 2001, CARCINOGENESIS, V22, P1955, DOI 10.1093-carcin-22.12.1955; HENNINGS H, 1980, CELL, V19, P245, DOI 10.1016-0092-8674(80)90406-7; HONG WK, 1990, NEW ENGL J MED, V323, P795, DOI 10.1056-NEJM199009203231205; Langenfeld J, 1997, P NATL ACAD SCI USA, V94, P12070, DOI 10.1073-pnas.94.22.12070; LEVINE N, 1998, J AM ACAD DERMATOL S, V39, P62; LOTAN R, 1995, J NATL CANCER I, V87, P1655, DOI 10.1093-jnci-87.22.1655; Maurer BJ, 1999, J NATL CANCER I, V91, P1138, DOI 10.1093-jnci-91.13.1138; Moon TE, 1997, CANCER EPIDEM BIOMAR, V6, P949; ODONNELL PH, 2002, LEUKEMIA, V5, P902; Oridate N, 1997, J NATL CANCER I, V89, P1191, DOI 10.1093-jnci-89.16.1191; Pergolizzi R, 1999, INT J CANCER, V81, P829; PONZONI M, 1995, CANCER RES, V55, P853; SANI BP, 1995, CARCINOGENESIS, V16, P2531, DOI 10.1093-carcin-16.10.2531; Spinella MJ, 1999, J BIOL CHEM, V274, P22013, DOI 10.1074-jbc.274.31.22013; STRICKLAND JE, 1988, CANCER RES, V48, P165; Sun SY, 1999, MOL PHARMACOL, V55, P403; Sun SY, 2000, CANCER RES, V60, P7149; Ulukaya E, 1999, CANCER TREAT REV, V25, P229, DOI 10.1053-ctrv.1999.0127; Veronesi U, 1999, J NATL CANCER I, V91, P1847, DOI 10.1093-jnci-91.21.1847; VOLLBERG TM, 1992, MOL ENDOCRINOL, V6, P667; WEINBERG WC, 1995, ONCOGENE, V10, P2271; Wu JM, 2001, APOPTOSIS, V6, P377, DOI 10.1023-A:1011342220621; Xu XC, 2001, CANCER RES, V61, P4306; YUSPA SH, 1981, NATURE, V293, P72, DOI 10.1038-293072a0; YUSPA SH, 1989, J CELL BIOL, V109, P1207, DOI 10.1083-jcb.109.3.1207; Zou CP, 1998, CLIN CANCER RES, V4, P1345; Zusi FC, 2002, DRUG DISCOV TODAY, V7, P1165, DOI 10.1016-S1359-6446(02)02526-688
Variations on the Author
Full text link“Variations on the Author” discusses two of Eduardo Coutinho’s recent films (Um Dia na Vida, from 2010, and Últimas Conversas, posthumously released in 2015) and their contribution to the general question of documentary authorship. The director’s filmography is characterized by a consistent yet self-effacing form of authorial self-inscription: Coutinho often features as an interviewer that rather than express opinions propels discourses; an interviewer that is good at listening. This mode of self-inscription characterizes him as an author who is not expressive but who is nonetheless markedly present on the screen. In Um Dia na Vida, however, Coutinho is completely absent form the image, while Últimas Conversas, on the contrary, includes a confessional prologue that moves the director from the margins to the center of his films. This article examines the ways in which these works stand out in the filmography of a director who offers new insights into the notion of cinematic authorship
Appropriate Similarity Measures for Author Cocitation Analysis
Full text linkWe provide a number of new insights into the methodological discussion about author cocitation analysis. We first argue that the use of the Pearson correlation for measuring the similarity between authors’ cocitation profiles is not very satisfactory. We then discuss what kind of similarity measures may be used as an alternative to the Pearson correlation. We consider three similarity measures in particular. One is the well-known cosine. The other two similarity measures have not been used before in the bibliometric literature. Finally, we show by means of an example that our findings have a high practical relevance.information science;Pearson correlation;cosine;similarity measure;author cocitation analysis
Parthenolide: From plant shoots to cancer roots
No full textParthenolide (PTL), a sesquiterpene lactone (SL) originally purified from the shoots of feverfew (Tanacetum parthenium), has shown potent anticancer and anti-inflammatory activities. It is currently being tested in cancer clinical trials. Structure-activity relationship (SAR) studies of parthenolide revealed key chemical properties required for biological activities and epigenetic mechanisms, and led to the derivatization of an orally bioavailable analog, dimethylamino-parthenolide (DMAPT). Parthenolide is the first small molecule found to be selective against cancer stem cells (CSC), which it achieves by targeting specific signaling pathways and killing cancer from its roots. In this review, we highlight the exciting journey of parthenolide, from plant shoots to cancer roots. © 2013 Elsevier Ltd. 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