Browsing by Subject "Survival"
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Item Smoking cessation and survival among people diagnosed with non-metastatic cancer(BioMed Central Ltd., 2020-08-05) Barnett, Tracey E.; Lu, Yan; Gehr, Aaron W.; Ghabach, Bassam; Ojha, Rohit P.BACKGROUND: We aimed to estimate the effects of smoking cessation on survival among people diagnosed with cancer. METHODS: We used data from a Comprehensive Community Cancer Program that is part of a large urban safety-net hospital system. Eligible patients were diagnosed with primary invasive solid tumors between 2013 and 2015, and were current smokers at time of diagnosis. Our exposure of interest was initiation of smoking cessation within 6 months of cancer diagnosis. We estimated inverse probability weighted restricted mean survival time (RMST) differences and risk ratio (RR) for all cause 3-year mortality. RESULTS: Our study population comprised 369 patients, of whom 42% were aged < 55 years, 59% were male, 44% were racial/ethnic minorities, and 59% were uninsured. The 3-year RMST was 1.8 (95% CL: - 1.5, 5.1) months longer for individuals who initiated smoking cessation within 6 months of cancer diagnosis. The point estimate for risk of 3-year mortality was lower for initiation of smoking cessation within 6 months of diagnosis compared with no initiation within 6 months (RR = 0.72, 95% CL: 0.37, 1.4). CONCLUSIONS: Our point estimates suggest longer 3-year survival, but the results are compatible with 1.5 month shorter or 5.1 longer 3-year overall survival after smoking cessation within 6 months of cancer diagnosis. Future studies with larger sample sizes that test the comparative effectiveness of different smoking cessation strategies are needed for more detailed evidence to inform decision-making about the effect of smoking cessation on survival among cancer patients. IMPLICATIONS FOR CANCER SURVIVORS: The benefits of smoking cessation after cancer diagnosis may include longer survival, but the magnitude of benefit is unclear.Item Tip110 is required for embryonic stem cell survival and embryonic development(2016-08-01) Whitmill, Amanda J.; Johnny J. He; Geoffrey Guttmann; Khalid TimaniHIV-1 Tat-interacting protein of 110 kDa, Tip110, has roles in tumor antigen presentation, pre-mRNA splicing, transcription of viral and host genes, and protein degradation. Tip110 is also known to be up-regulated in a variety of cancers and to regulate and/or interact with a variety of transcription factors, oncogenes, and pluripotency factors. As such, Tip110 has been shown to effect pluripotency, proliferation, apoptosis, and the cell cycle when knocked down in vitro. However, the function of Tip110 in embryonic development remains largely uncharacterized. One early study has shown that loss of a Tip110 ortholog leads to embryonic lethality in zebrafish. Our studies have shown that transgenic mouse embryos lacking expression of a functional Tip110 protein die several days post-implantation in vivo. In the present study, we determined how Tip110 knockout affects mouse embryonic development and investigated the underlying molecular mechanisms. We found that Tip110 loss did not impair embryo growth from the zygote to the blastocyst stage nor did it impair the blastocysts ability to implant into the uterine lining in vivo. Extended culture of blastocysts in vitro revealed that Tip110 loss impaired both blastocyst outgrowth formation and derivation of mouse embryonic stem cells from blastocysts. In vivo embryos could survive until the post-implantation stage where they eventually perished. The premature death of these embryos was characterized by a clear retardation in embryonic development resulting in underdeveloped or more commonly, completely resorbed mouse embryos around 8.5 or 9.5 days post coitum. Microarray analysis of Tip110-/- cells derived from mouse blastocysts revealed that Tip110 loss favored differentiation but not self-renewal, pluripotency, or cell cycling through a complex regulatory network of stem cell factors. Tip110-/- cells also had perturbations in many other signaling and cellular processes including mRNA processing and proteasome degradation. Taken together, these findings document for the first time the lethal effects of complete loss of Tip110 on mammalian embryonic development and suggest that Tip110 is an important regulator of not only embryonic development but also stem cell factors.