Outliving Cancer The Incidence Turnover at Old Age in Both 在老年的发病率不够用周转癌中.pptVIP

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Outliving Cancer The Incidence Turnover at Old Age in Both 在老年的发病率不够用周转癌中.ppt

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Outliving Cancer The Incidence Turnover at Old Age in Both 在老年的发病率不够用周转癌中

Age Specific Cancer Incidence for Two Major Historical Models, Compared to SEER Data and Beta-Senescence Model Beta Fit to SEER DataAge-specific incidence per 100,000 (Ries et al 2000) Beta Fit to SEER DataAge-specific incidence per 100,000 (Ries et al 2000) Beta Fit to SEER DataAge-specific incidence per 100,000 (Ries et al 2000) Beta Fit to SEER DataAge-specific incidence per 100,000 (Ries et al 2000) Beta Fit to SEER DataAge-specific incidence per 100,000 (Ries et al 2000) Age-Specific Incidence Normalized to the Peak Value for Each Cancer. All Male Sites Except Childhood Cancers (Hodgkins, Thyroid, Testes). Estimated Lifespan Probability of Cancer: Area Under the Curve Is the Turnover Present in Mice?Mice Data Sources Need undosed controls data for full natural lifetime (~3 years). Need sufficient numbers for statistical significance in cancer incidence trends. NTP data is limited due to 2-year “lifetime”, except rare dietary restricted studies to 1100 days. ED01 data (courtesy R. Kodell) of 2-AAF included 24,000 single strain female mice, uniform conditions, and allowed to live to 1001 days. Age-specific mortality is appropriate measure for comparison to human incidence results ED01 Control Mice Age-Specific Mortality With Beta Function Fit. ED01 Control Mice Age-Specific Mortality With Beta Function Fit. Cell Replicative Senescence As Possible Biological Cause of the Turnover Cell Replicative Senescence: Cells Retaining Proliferative Ability Decrease With Number of Cell Divisions. Cell Replicative Senescence: Increase in Age Decreases the Number of Cells With Replicative Capacity. Cell Replicative Senescence: Beta-Senescence Model Search for Senescence Interventions to Test the Model: Altered longevity, modeled as to = b-1Altered cancer, modeled as I(t) = (at)k-1(1-bt) Mice with altered p53 (gene which is well known to influence senescence): set lifetime to = b-1, then calculate cancer. Mice with long-term dosing of melatonin (kno