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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
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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
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Paulmurugan Ramasamy Malhotra Meenakshi Massoud Zahra T. Massoud Tarik F. 《Journal of molecular medicine (Berlin, Germany)》2022,100(7):1093-1093
Journal of Molecular Medicine - 相似文献
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Lina Jansen Lars Schwettmann Christian Behr Andrea Eberle Bernd Holleczek Christina Justenhoven Hiltraud Kajüter Kirsi Manz Frederik Peters Ron Pritzkuleit Andrea Schmidt-Pokrzywniak Eunice Sirri Fabian Tetzlaff Sven Voigtländer Volker Arndt 《International journal of cancer. Journal international du cancer》2023,153(10):1784-1796
Age-standardized cancer incidence has decreased over the last years for many cancer sites in developed countries. Whether these trends led to narrowing or widening socioeconomic inequalities in cancer incidence is unknown. Using cancer registry data covering 48 million inhabitants in Germany, the ecological association between age-standardized total and site specific (colorectal, lung, prostate and breast) cancer incidence in 2007 to 2018 and a deprivation index on district level (aggregated to quintiles) was investigated. Incidence in the most and least deprived districts were compared using Poisson models. Average annual percentage changes (AAPCs) and differences in AAPCs between deprivation quintiles were assessed using Joinpoint regression analyses. Age-standardized incidence decreased strongly between 2007 and 2018 for total cancer and all cancer sites (except female lung cancer), irrespective of the level of deprivation. However, differences in the magnitude of trends across deprivation quintiles resulted in increasing inequalities over time for total cancer, colorectal and lung cancer. For total cancer, the incidence rate ratio between the most and least deprived quintile increased from 1.07 (95% confidence interval: 1.01-1.12) to 1.23 (1.12-1.32) in men and from 1.07 (1.01-1.13) to 1.20 (1.14-1.26) in women. Largest inequalities were observed for lung cancer with 82% (men) and 88% (women) higher incidence in the most vs the least deprived regions in 2018. The observed increase in inequalities in cancer incidence is in alignment with trends in inequalities in risk factor prevalence and partly utilization of screening. Intervention programs targeted at socioeconomically deprived and urban regions are highly needed. 相似文献