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CdC7 inhibition impairs neuroendocrine transformation in lung and prostate tumors through MYC degradation

Signal Transduction and Targeted Therapy 2024年第8期9卷 3519-3532页

作者： Alvaro Quintanal-Villalonga Kenta Kawasaki Esther Redin Fathema Uddin Swanand Rakhade Vidushi durani Amin Sabet Moniquetta Shafer Wouter R.Karthaus Samir Zaidi Yingqian A.Zhan Parvathy Manoj Harsha Sridhar dennis Kinyua Hong Zhong Barbara P.Mello Metamia Ciampricotti Umesh K.Bhanot Irina Linkov Juan Qiu Radhika A.Patel Colm Morrsey Sanjoy Mehta Jesse Barnes Michael C.Haffner nichlas d.socci Richard P.Koche Elisa de Stanchina Sonia Molina-Pinelo Sohrab Salehi Helena A.Yu Joseph M.Chan Charles M.Rudin department of Medicine Thoracic Oncology ServiceMemorial Sloan Kettering Cancer CenterNew YorkNYUSA Cancer Biology and Genetics Program Sloan Kettering InstituteMemorial Sloan Kettering Cancer CenterNew YorkNYUSA Vagelos College of Physicians and Surgeons Columbia UniversityNew YorkNYUSA Weill Cornell Graduate School of Medical Sciences Weill Cornell MedicineNew YorkNYUA Human Oncology and Pathogenesis Program Memorial Sloan Kettering Cancer CenterNew YorkNYUSA Center for Epigenetics Research Memorial Sloan Kettering Cancer CenterNew YorkNYUSA Pathology Core Facilty Department of Pathology and Laboratory MedicineMSKCCNew YorkNYUSA Antitumor Assessment Core Memorial Sloan Kettering Cancer CenterNew YorkNYUSA divisionsof Human Biology and Clinical Research Fred Hutchinon Cancer CenterSeattleWAUSA deparmentof Urology University of WashingtonSeattleWAUSA Gene Editing&Screening Core Facility Memorial Sloan Kettering Cancer Center New YorkNYUSA department of Laboratory Medicine and Pathology University of WashingtonSeattleWAUSA Bioinfomatics CoreFacility Memorial Soan Kettering Cancer CenterNew YorkNYUSA Institute of Biomedicine of Seille(Bis) HURCSCUniversidad de SevillaSevilleSpain Computational Oncology Department of Epidemiology and BiostatisticsMemorial Sloan Kettering Cancer CenterNew YorkNYUSA Well Cornell Medical College New York NYUSA Present address:Swiss Institute for Experimental Cancer Research(ISREC) School of Life SciencesEPFLLausanneSwitzerland

Neuroendocrine(NE)transformation is a mechanism of resistance to targeted therapy in lung and prostate adenocarcinomas leading to poor *** to date,even if patients at high risk of transformation can be identified by the occurrence of Tumor Protein P53(TP53)and Retinoblastoma Transcriptional Corepressor 1(RB1)mutations in their tumors,no therapeutic strategies are available to prevent or delay histological *** of the cell cycle kinase Cell division Cycle 7(CdC7)occurred in tumors during the initial steps of NE transformation,already after TP53/RB1 co-inactivation,leading to induced sensitivity to the CdC7 inhibitor ***7 inhibition suppressed NE transdifferentiation and extended response to targeted therapy in in vivo models of NE transformation by inducing the proteasome-mediated degradation of the MYC Proto-Oncogen(MYC),implicated in stemness and histological *** overexpression of a degradation-resistant MYC isoform reestablished the NE transformation phenotype observed on targeted therapy,even in the presence of ***7 inhibition also markedly extended response to standard cytotoxics(cisplatin,irinotecan)in lung and prostate small cell carcinoma *** results nominate CdC7 inhibition as a therapeutic strategy to constrain lineage plasticity,as well as to effectively treat NE tumors de novo or after *** simurosertib clinical efficacy trials are ongoing,this concept could be readily translated for patients at risk oftransformation.

关键词： tumors markedly transformation

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Role of nutritional ketosis in the improvement of metabolic parameters following bariatric surgery

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World Journal of diabetes 2022年第1期13卷 54-64页

作者： Fioralba Pindozzi Carlo socci Massimiliano Bissolati Monica Marchi Elisabetta devecchi Alessandro Saibene Caterina Conte Unitàdi Chirurgia Generale Provinciale Ospedale del DeltaLagosanto(FE)44023Italy Transplant and Metabolic/Bariatric Surgery Unit IRCCS Ospedale San RaffaeleMilan 20132Italy department of General Medicine Diabetes and EndocrinologyIRCCS Ospedale San RaffaeleMilan 20132Italy department of Human Sciences and Promotion of the Quality of Life San Raffaele Open UniversityRome 00166Italy department of Endocrinology Nutrition and Metabolic DiseasesIRCCS MultiMedicaMilan 20099Italy

BACKGROUNd Ketone bodies(KB)might act as potential metabolic modulators besides serving as energy *** metabolic surgery(BMS)offers a unique opportunity to study nutritional ketosis,as acute postoperative caloric restriction leads to increased lipolysis and circulating free fatty *** To characterize the relationship between KB production,weight loss(WL)and metabolic changes following *** For this retrospective study we enrolled male and female subjects aged 18-65 years who underwent BMS at a single *** on demographics,anthropometrics,body composition,laboratory values and urinary KB were *** Thirty-nine patients had data available for analyses[74.4%women,mean age 46.5±9.0 years,median body mass index 41.0(38.5;45.4)kg/m^(2),fat mass 45.2%±6.2%,23.1%had diabetes,43.6%arterial hypertension and 74.4%liver steatosis].At 46.0±13.6 d post-surgery,subjects had lost 12.0%±3.6%of pre-operative ***-nine percent developed *** with nutritional ketosis were significantly younger[42.9(37.6;50.7)years vs 51.9(48.3;59.9)years,P=0.018],and had significantly lower fasting glucose[89.5(82.5;96.3)mg/dL vs 96.0(91.0;105.3)mg/dL,P=0.025]and triglyceride levels[108.0(84.5;152.5)mg/dL vs 152.0(124.0;186.0)mg/dL,P=0.045]vs those with *** 6 mo,percent WL was greater in those with postoperative ketosis(-27.5%±5.1%vs 23.8%±4.3%,P=0.035).Urinary KBs correlated with percent WL at 6 and 12 *** metabolic changes were *** Our data support the hypothesis that subjects with worse metabolic status have reduced ketogenic capacity and,thereby,exhibit a lower WL following BMS.

关键词： Obesity Ketone bodies Bariatric surgery Weight loss Glucose metabolism Lipid metabolism

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