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| 1 | Medication errors inthe PACU显示文摘 | Hicks RW Becker SC Windle PE | 2007 | J Perianesth Nurs2007，22，6： | 1 |
| 2 | Perfusion measurement in acute pancreatitis using dynamic perfusion MDCT 显示文摘 | Bize PE Platon A Becker CD | 2006 | Am J Roentgenol2006，186，1： | 1 |
| 3 | Medication errors in the PACU显示文摘 | Hicks RW Becker SC Windle PE | 2007 | J Perianesth Nurs2007，22，6： | 1 |
| 4 | A new x-chromosomal muscular dystrophy 显示文摘 | Becker PE Kiener FA | 1955 | Arch Psychiatr Nervenkr Z Gesamte Neurol Psychiatr1955，193，： | 1 |
| 5 | Water potenti gradients for gaps and slopes in a Panamanian tropical moist forest's dry season显示文摘 | Becker P Rabenold PE Idol JR Smith AP | | 0，，： | 1 |
| 6 | Pneumoconiosis in carbon electrode workers显示文摘 | Petsonk EL Storey E Becker PE | 1988 | Occup Med1988，30，11： | 1 |
| 7 | Perfusion measurement in a- cute pancreatitis using dynamic perfusion MDCT显示文摘 | Bize PE Platon A Becker CD | 2006 | AJR2006，186，1： | 1 |
| 8 | Direct and Indirect Use of Energy and Materials in Engineering and Construcon显示文摘 | Pick HJ Becker PE | 1975 | Applied Energy1975，1，1： | 1 |
| 9 | A reappraisal of mouth-to-mouth ventilation during bystander initiated cardiopulmonary resuscitation:a statement for healthcare professionals from the Ventilation Working Group of the Basic Life Support Subcommittees,American Heart Association显示文摘 | Becker LB BergKA Pepe PE | 1997 | Circulation1997，96，： | 1 |
| 10 | Perfusion Measurement in Acute Pancreatitis Using Dynamic Perfusion MDCT显示文摘 | Bize PE Platon A Becker CD | 2006 | AJR2006，186，1： | 1 |
| 11 | A reappraisal of mouth - to mouth ventilation during bystander - initiated cardiopulmonary resuscitation: a statement for healthcare professionals from the Ventilation Working Group of the Basic Life Support Subcommittees, American Heart Association显示文摘 | Becker LB Berg RA Pepe PE | 1997 | Circulation1997，96，： | 1 |
| 12 | Perfusion Measurement in Acute Panereatitis Using Dynamic Perfusion MDCT显示文摘 | Bize PE Platon A Becker CD a al | 2006 | AJR2006，186，1： | 1 |
| 13 | Perfusion measurement in acutepan- crcatitis using dynamic perfusion MDCT显示文摘 | Bize PE Platon D Becker CD | 2006 | AJR Am J Roeatgenol2006，186，1： | 1 |
| 14 | Rescue of p53 functions by in vitro-transcribed mRNA impedes the growth of high-grade serous ovarian cancer显示文摘Background:The cellular tumor protein p53(TP53)is a tumor suppressor gene that is frequently mutated in human cancers.Among various cancer types,the very aggressive high-grade serous ovarian carcinoma(HGSOC)exhibits the high-est prevalence of TP53 mutations,present in>96%of cases.Despite intensive efforts to reactivate p53,no clinical drug has been approved to rescue p53 func-tion.In this study,our primary objective was to administer in vitro-transcribed(IVT)wild-type(WT)p53-mRNA to HGSOC cell lines,primary cells,and ortho-topic mouse models,with the aim of exploring its impact on inhibiting tumor growth and dissemination,both in vitro and in vivo.Methods:To restore the activity of p53,WT p53 was exogenously expressed in HGSOC cell lines using a mammalian vector system.Moreover,IVT WT p53 mRNA was delivered into different HGSOC model systems(primary cells and patient-derived organoids)using liposomes and studied for proliferation,cell cycle progression,apoptosis,colony formation,and chromosomal instabil-ity.Transcriptomic alterations induced by p53 mRNA were analyzed using RNA sequencing in OVCAR-8 and primary HGSOC cells,followed by ingenuity path-way analysis.In vivo effects on tumor growth and metastasis were studied using orthotopic xenografts and metastatic intraperitoneal mouse models.Results:Reactivation of the TP53 tumor suppressor gene was explored in differ-ent HGSOC model systems using newly designed IVT mRNA-based methods.The introduction of WT p53 mRNA triggered dose-dependent apoptosis,cell cycle arrest,and potent long-lasting inhibition of HGSOC cell proliferation.Transcriptome analysis of OVCAR-8 cells upon mRNA-based p53 reactivation revealed significant alterations in gene expression related to p53 signaling,such as apoptosis,cell cycle regulation,and DNA damage.Restoring p53 function concurrently reduces chromosomal instability within the HGSOC cells,under-scoring its crucial contribution in safeguarding genomic integrity by moderating the baseline occurrence of double-strand breaks arising from replication stress.Furthermore,in various mouse models,treatment with p53 mRNA reduced tumor growth and inhibited tumor cell dissemination in the peritoneal cavity in a dose-dependent manner.Conclusions:The IVT mRNA-based reactivation of p53 holds promise as a potential therapeutic strategy for HGSOC,providing valuable insights into the molecular mechanisms underlying p53 function and its relevance in ovarian cancer treatment. | Monika Raab Izabela Kostova Samuel Peña-Llopis Daniela Fietz Monika Kressin Seyed Mohsen Aberoumandi Evelyn Ullrich Sven Becker Mourad Sanhaji Klaus Strebhardt | 2024 | Cancer Communications2024，44，1： | 0 |
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