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Härter Martin Koch-Gromus Uwe 《Bundesgesundheitsblatt, Gesundheitsforschung, Gesundheitsschutz》2022,65(3):267-269
Bundesgesundheitsblatt - Gesundheitsforschung - Gesundheitsschutz - 相似文献
3.
Matthias Knefel PhD Elisabeth L. Zeilinger PhD Simone Lubowitzki PhD Katharina Krammer MSc Matthias Unseld MD Rupert Bartsch MD Thorsten Fuereder MD Ulrich Jäger MD Barbara Kiesewetter MD Maria Krauth MD Markus Raderer MD Philipp B. Staber MD Peter Valent MD Alexander Gaiger MD 《Cancer》2023,129(21):3466-3475
Background
Survival in cancer patients is associated with a multitude of biological, social, and psychological factors. Although it is well established that all these factors add to overall mortality, it is not well understood how the predictive power of these parameters changes in a comprehensive model and over time.Methods
Patients who attended the authors’ outpatient clinic were invited to participate. The authors followed 5180 mixed cancer patients (51.1% female; mean age, 59.1 years [SD = 13.8]) for up to 16 years and analyzed biological (age, sex, cancer site, anemia), psychological (anxiety, depression), and social variables (marital status, education, employment status) potentially predicting overall survival in a Cox proportional hazards model.Results
The median survival time for the entire sample was 4.3 years (95% confidence interval, 4.0–4.7). The overall survival probabilities for 1 and 10 years were 76.8% and 38.0%, respectively. Following an empirical approach, the authors split the time interval into five periods: acute, subacute, short-term, medium-term, and long-term. A complex pattern of variables predicted overall survival differently in the five periods. Biological parameters were important throughout most of the time, social parameters were either time-independent predictors or tended to be more important in the longer term. Of the psychological parameters, only depression was a significant predictor and lost its predictive power in the long-term.Conclusions
The findings of this study allow the development of comprehensive patient-specific models of risk and resilience factors addressing biopsychosocial needs of cancer patients, paving the way for a personalized treatment plan that goes beyond biomedical cancer care. 相似文献4.
5.
Gordon K. B. Saburov V. O. Koryakin S. N. Gulidov I. A. Fatkhudinov T. Kh. Arutyunyan I. V. Kaprin A. D. Solov’ev A. N. 《Bulletin of experimental biology and medicine》2022,173(2):281-285
Bulletin of Experimental Biology and Medicine - Fast neutron therapy, which previously has demonstrated effective results, but along with a large number of complications, can again be considered a... 相似文献
6.
Zyuz’kov G. N. Zhdanov V. V. Miroshnichenko L. A. Polyakova T. Yu. Stavrova L. A. Simanina E. V. Minakova M. Yu. Agafonov V. I. Churin A. A. 《Bulletin of experimental biology and medicine》2022,173(5):615-619
Bulletin of Experimental Biology and Medicine - The psychopharmacological effects of a stimulator of functions of progenitor cells of the nervous tissue STAT3 inhibitor (STAT3 Inhibitor XIV, LLL12)... 相似文献
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Yevdulov O. V. Yevdulov D. V. Isabekova T. I. Aminov G. I. Aminova I. Yu. 《Biomedical engineering》2022,56(2):146-150
Biomedical Engineering - A mathematical model of a thermoelectric device for the treatment of whitlow by local hypothermia is discussed. The model is based on a solution of the heat conduction task... 相似文献
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Md Maksudul Alam Janmaris Marin Fermin Patrick T. Spiller Chaning Burnett Xiaohua Rong Tara Moore-Medlin Caden O. Maxwell Alok R. Khandelwal Cherie-Ann O. Nathan 《Molecular carcinogenesis》2022,61(1):33-44
TP53 is the most frequently mutated gene in head and neck squamous cell carcinoma (HNSCC). Patients with HPV-negative TP53 mutant HNSCC have the worst prognosis, necessitating additional agents for treatment. Since mutant p53 causes sustained activation of the PI3K/AKT/mTOR signaling pathway, we investigated the effect of rapalogs RAD001 and CCI-779 on HPV-negative mutTP53 HNSCC cell lines and xenografts. Rapalogs significantly reduced cell viability and colony formation. Interestingly, rapalogs-induced autophagy with no effect on apoptosis. Pretreatment with autophagy inhibitors, 3-methyladenine (3-MA) and ULK-101 rescued the cell viability by inhibiting rapalog-induced autophagy, suggesting that both RAD001 and CCI-779 induce non-apoptotic autophagy-dependent cell death (ADCD). Moreover, rapalogs upregulated the levels of ULK1 and pULK1 S555 with concomitant downregulation of the mTORC1 pathway. However, pretreatment of cells with rapalogs prevented the ULK-101-mediated inhibition of ULK1 to sustained autophagy, suggesting that rapalogs induce ADCD through the activation of ULK1. To further translate our in vitro studies, we investigated the effect of RAD001 in HPV-negative mutTP53 (HN31 and FaDu) tumor cell xenograft model in nude mice. Mice treated with RAD001 exhibited a significant tumor volume reduction without induction of apoptosis, and with a concomitant increase in autophagy. Further, treatment with RAD001 was associated with a considerable increase in pULK1 S555 and ULK1 levels through the inhibition of mTORC1. 3-MA reversed the effect of RAD001 on FaDu tumor growth suggesting that RAD001 promotes ACDC in HPV-negative mutTP53 xenograft. This is the first report demonstrating that rapalogs promote non-apoptotic ADCD in HPV-negative mutTP53 HNSCC via the ULK1 pathway. Further studies are required to establish the promising role of rapalogs in preventing the regrowth of HPV-negative mutTP53 HNSCC. 相似文献