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Publication Listing for the MeSH term DEATH. Found 6 abstracts

Barrero CA, Perez-Leal O, Aksoy M, Moncada C, Ji R, Lopez Y, Mallilankaraman K, Madesh M, Criner GJ, Kelsen SG, Merali S. Histone 3.3 Participates in a Self-Sustaining Cascade of Apoptosis That Contributes to the Progression of Chronic Obstructive Pulmonary Disease. Am J Respir Crit Care Med. 2013 Sep;188(6):673-83.   PMCID: PMC3826185
Zhang HB, Rosenberg S, Coffey FJ, He YW, Manser T, Hardy RR, Zhang JK. A Role for cFLIP in B Cell Proliferation and Stress MAPK Regulation. Journal of Immunology. 2009 Jan;182(1):207-15.   PMCID: PMC 2720129
Mellert H, Sykes SM, Murphy ME, McMahon SB. The ARF/oncogene pathway activates p53 acetylation within the DNA binding domain. Cell cycle (Georgetown, Tex). 2007 Jun;6(11):1304-6.
Tolcher AW, Mita M, Meropol NJ, von Mehren M, Patnaik A, Padavic K, Hill M, Mays T, McCoy T, Fox NL, Halpern W, Corey A, Cohen RB. Phase I pharmacokinetic and biologic correlative study of mapatumumab, a fully human monoclonal antibody with agonist activity to tumor necrosis factor-related apoptosis-inducing ligand receptor-1. Journal of Clinical Oncology. 2007 Apr;25(11):1390-5.
Valicenti RK, DeSilvio M, Hanks GE, Porter A, Brereton H, Rosenthal SA, Shipley WU, Sandler HM, Haile RW, Thomas DC, McGuire V, Felberg A, John EM, Milne RL, Hopper JL, Jenkins MA, Levine AJ, Daly MM, Buys SS, Senie RT, Andrulis IL, Knight JA, Godwin AK, Southey M, McCredie MR, Giles GG, Andrews L, Tucker K, Miron A, Apicella C, Tesoriero A, Bane A, Pike MC, Whittemore AS. Posttreatment prostatic-specific antigen doubling time as a surrogate endpoint for prostate cancer-specific survival: An analysis of radiation therapy oncology group protocol 92-02 BRCA1 and BRCA2 mutation carriers, oral contraceptive use, and breast cancer before age 50. INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS LA English DT Article DE prostate cancer; prostate-specific antigen doubling time; mortality; surrogate endpoint. 2006 Oct;15(10):1863-70.
Eves EM, Xiong W, Bellacosa A, Kennedy SG, Tsichlis PN, Rosner MR, Hay N. Akt, a target of phosphatidylinositol 3-kinase, inhibits apoptosis in a differentiating neuronal cell line. Molecular and Cellular Biology. 1998 Apr;18(4):2143-52.
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MeSH cloud from publications including the MeSH term DEATH

DEATH ACTIVATION acetylation DOMAIN PROTEIN RECEPTOR NERVE GROWTH-FACTOR PC12 ARF LOCUS the risk of dying requirements for a surrogate endpoint of CSS Thus surrogate endpoint PCR PHOSPHOINOSITIDE 3-KINASE Respiratory System FADD but did not meet all of Prentice's significantly associated with CSS NF-KAPPA-B NONCARRIERS PREDICT the randomized treatment SIGNAL-TRANSDUCTION SYMPATHETIC NEURONS TP53 RISK DECOY RECEPTORS cytotoxicity independent of randomized treatment in this cohort The endpoints were PROTOONCOGENE BCL-2 V-AKT significant predictors of CSS (P-Cox < 0001) After adjusting for T MYC hMOF OVARIAN-CANCER RISK AB (Purpose:) under bar We evaluated whether posttreatment ARF TUMOR-SUPPRESSOR K120 Gleason score and PSA stage-all of Prentice's requirements were not ENDOPLASMIC-RETICULUM STRESS (Methods and Materials: ) under bar We analyzed posttreatment PSA WOMEN on Radiation Therapy Oncology Group Protocol 92-02 From June 1992 to time to PSADT (assuming first-order kinetics for a minimum of 3 rising REGISTRY HGS-ETR1 or in combination with 24 65-70 Gy of radiation therapy (n = 761) PSADT < 6 months (pc < 0001) 0002)-PSADT < 9 months (P-Cox < indicating that the effect of PSADT on CSS was not independent of met of prostate cancer is not fully explained by PSADT (c) 2006 Elsevier and PSADT < 12 months (P-Cox < 0001) but not for PSADT < 3 0001) p53 randomized treatment was a significant predictor for CSS (p(Cox) = GENE months of adjuvant androgen deprivation (n = 753) Using an adjusted P53-DEPENDENT APOPTOSIS RADICAL PROSTATECTOMY men were randomized to neoadjuvant androgen deprivation and April 1995 Inc prostatic-specific antigen doubling time (PSADT) was predictive of MUTATIONS prostate cancer mortality by testing the Prentice requirements for a CHROMATIN FLICE-INHIBITORY PROTEIN p19ARF MDM2 (Results: ) under bar After a median follow-up time of 59 years PSA measurements) and cancer-specific survival (CSS) SIGNALING PATHWAYS FAILURE OXIDATIVE INJURY MORTALITY chronic obstructive pulmonary disease MEDIATORS INK4A CASPASE-8 CDKN2A LUNG INFLAMMATION ASTHMA FAS-MEDIATED APOPTOSIS 514 men with localized prostate cancer measurements in a cohort of 1 Critical Care Medicine apoptosis proteomics CANCER-CELLS RECURRENCE COPD (T2c-4 and PSA level < 150 ng UNFOLDED PROTEIN RESPONSE we tested if PSADT was prognostic and Cox proportional hazards model (Conclusions) under bar Prostatic specific antigen doubling time is CELLS PROTEIN-KINASE-C EXTRACELLULAR (P-Cox = 04) The significant posttreatment PSADTs were also EPIDEMIOLOGY histone H33 HISTONES C-FLIP TIP60 HISTORY GROWTH treated and monitored prospectively mL)
Last updated on Friday, January 03, 2020