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| 1 | Role of Akt signaling in resistance to DNA-targeted therapy显示文摘The Akt signal transduction pathway controls most hallmarks of cancer. Activation of the Akt cascade promotes a malignant phenotype and is also widely implicated in drug resistance. Therefore, the modulation of Akt activity is regarded as an attractive strategy to enhance the efficacy of cancer therapy and irradiation. This pathway consists of phosphatidylinositol 3 kinase(PI3K), mammalian target of rapamycin, and the transforming serine-threonine kinase Akt protein isoforms, also known as protein kinase B. DNA-targeted agents, such as platinum agents, taxanes, and antimetabolites, as well as radiation have had a significant impact on cancer treatment by affecting DNA replication, which is aberrantly activated in malignancies. However, the caveat is that they may also trigger the activation of repairing mechanisms, such as upstream and downstream cascade of Akt survival pathway. Thus, each target can theoretically be inhibited in view of improving the potency of conventional treatment. Akt inhibitors, e.g., MK-2206 and perifosine, or PI3K modulators, e.g., LY294002 and Wortmannin, have shown some promising results in favor of sensitizing the cancer cells to the therapy in vitro and in vivo, which have provided the rationale for incorporation of these novel agents into multimodality treatment of different malignancies. Nevertheless, despite the acceptable safety profile of some of these agents in the clinical studies, with regard to the efficacy, the results are still too preliminary. Hence, we need to wait for the upcoming data from the ongoing trials before utilizing them into the standard care of cancer patients. | Abolfazl Avan Ravi Narayan Elisa Giovannetti Godefridus J Peters | 2016 | World Journal of Clinical Oncology2016，7，5： | 12 |
| 2 | Role of E3 ubiquitin ligases in lung cancer显示文摘E3 ubiquitin ligases are a large family of proteins that catalyze the ubiquitination of many protein substrates for targeted degradation by the 26S proteasome.Therefore,E3 ubiquitin ligases play an essential role in a variety of biological processes including cell cycle regulation,proliferation and apoptosis.E3 ubiquitin ligases are often found overexpressed in human cancers,including lung cancer,and their deregulation has been shown to contribute to cancer development.However,the lack of specific inhibitors in clinical trials is a major issue in targeting E3 ubiquitin ligases with currently only one E3 ubiquitin ligase inhibitor being tested in the clinical setting.In this review,we focus on E3 ubiquitin ligases that have been found deregulated in lung cancer.Furthermore,we discuss the processes in which they are involved and evaluate them as potential anti-cancer targets.By better understanding the mechanisms by which E3 ubiquitin ligases regulate biological processes and their exact role in carcinogenesis,we can improve the development of specific E3 ubiquitin ligase inhibitors and pave the way for novel treatment strategies for cancer patients. | Barbara C Snoek Leonie HAM de Wilt Gerrit Jansen Godefridus J Peters | 2013 | World Journal of Clinical Oncology2013，4，3： | 5 |
| 3 | Efficacy of thioguanine treatment in inflammatory bowel disease: A systematic review显示文摘AIM To critically assess the available literature regarding the efficacy of thioguanine treatment in inflammatory bowel disease(IBD) patients, irrespective of the(hepato-) toxicity profile.METHODS A systematic literature search of the MEDLINE database using Pub Med was performed using the keywords 'thioguanine', '6-TG', 'thioguanine', 'inflammatory bowel disease', 'IBD', 'Crohn's disease', 'Ulcerative colitis' and 'effectiveness' in order to identify relevant articles published in English starting from 2000. Reference lists of the included articles were crosschecked for missing articles. Reviewed manuscripts concerning the effectiveness of thioguanine treatment in IBD were reviewed by the authors and the data were extracted. Data were subsequently analyzed with descriptive statistics. Due to the lack of standardized outcomes, a formal meta-analysis was not performed.RESULTS A total of 11 applicable studies were found that involved the effectiveness of thioguanine therapy in IBD. Eight studies were conducted in a prospectivemanner, in the remaining three studies, data was collected retrospectively. In total, 353 IBD-patients(225 patients with Crohn's disease, 119 with ulcerative colitis and nine with unclassified IBD) with prior azathioprine/mercaptopurine resistance and/or intolerance(n = 321) or de novo thioguanine administration(n = 32) were included for analysis, of which 228(65%) had clinical improvement on thioguanine therapy, based on standard IBD questionnaires, biochemical parameters or global physician assessments. Short-term results were based on 268 treatment years(median follow-up 9 mo, range 3-22 mo) with a median daily dose of 20 mg(range 10-80 mg). Discontinuation, mostly due to adverse events, was reported in 72 patients(20%). CONCLUSION The efficacy of thioguanine therapy in IBD patients intolerant to conventional thiopurine therapy is observed in 65%, with short term adverse events in 20% of patients. | Berrie Meijer Chris JJ Mulder Godefridus J Peters Adriaan A van Bodegraven Nanne KH de Boer | 2016 | World Journal of Gastroenterology2016，22，40： | 5 |
| 4 | FOLFIRINOX and translational studies: Towards personalized therapy in pancreatic cancer显示文摘Pancreatic cancer is an extremely aggressive disease; although progress has been made in the last few years, the prognosis of these patients remains dismal. FOLFIRINOX is now considered a standard treatment in first-line setting, since it demonstrated an improved overall and progression-free survival vs gemcitabine alone. However, the enthusiasm over the benefit of this three-drug regimen is tempered by the associated increased toxicity profile, and many efforts have been made to improve the feasibility of this schedule. After a more recent phase Ⅲ trial showing an improved outcome over gemcitabine, the combination of gemcitabine/nab-paclitaxel emerged as another standard first-line treatment. However, this treatment is also associated with more side effects. In addition, despite initial promising data on the predictive role of SPARClevels, recent studies showed that these levels are not associated with nab-paclitaxel efficacy. The choice to use this treatment over FOLFIRINOX is therefore a topic of debate, also because no validated biomarkers to guide FOLFIRINOX treatment are available. In the era of actionable mutations and target agents it would be desirable to identify molecular factors or biomarkers to predict response to therapy in order to maximize the efficacy of treatment and avoid useless toxic effects for non-responding patients. However, until today the milestone of treatment for pancreatic cancer remains chemotherapy combinations, without predictive or monitoring tools existing to optimize therapy. This review analyzes the state-of-the-art treatments, promises and limitations of targeted therapies, ongoing trials and future perspectives, including potential role of microR NAs as predictive biomarkers. | Chiara Caparello Laura L Meijer Ingrid Garajova Alfredo Falcone Tessa Y Le Large Niccola Funel Geert Kazemier Godefridus J Peters Enrico Vasile Elisa Giovannetti | 2016 | World Journal of Gastroenterology2016，22，31： | 4 |
| 5 | How to overcome ATP-binding cassette drug efflux transporter-mediated drug resistance?显示文摘P-glycoprotein(ABCB1),multidrug resistance protein-1(ABCC1)and breast cancer resistance protein(ABCG2)belong to the ATP-binding cassette(ABC)superfamily of proteins that play an important physiological role in protection of the body from toxic xenobiotics and endogenous metabolites.Beyond this,these transporters determine the toxicity profile of many drugs,and confer multidrug resistance(MDR)in cancer cells associated with a poor treatment outcome of cancer patients.It has long been hypothesized that inhibition of ABC drug efflux transporters will increase drug accumulation and thereby overcome MDR,but until now no approved inhibitor of these transporters is available in the clinic.In this review we present molecular strategies to overcome this type of drug resistance and discuss for each of these strategies their promising value or indicate underlying reasons for their limited success. | Adrian C.Jaramillo Farah Al Saig Jacqueline Cloos Gerrit Jansen Godefridus J.Peters | 2018 | Cancer Drug Resistance2018，1，1： | 3 |
| 6 | Better to be alone than in bad company:The antagonistic effect of cisplatin and crizotinib combination therapy in non-small cell lung cancer显示文摘AIM To investigate the potential benefit of combining the cMET inhibitor crizotinib and cisplatin we performed in vitro combination studies.METHODS We tested three different treatment schemes in four non-small cell lung cancer(NSCLC) cell lines with a different cMET/epidermal growth factor receptor genetic background by means of the sulforhodamine B assay and performed analysis with Calcusyn.RESULTS All treatment schemes showed an antagonistic effect in all cell lines,independent of the cMET status.Despite their different genetic backgrounds,all cell lines(EBC-1,HCC827,H1975 and LUDLU-1) showed antagonistic combination indexes ranging from 1.3-2.7.These results were independent of the treatment schedule.CONCLUSION These results discourage further efforts to combine cMET inhibition with cisplatin chemotherapy in NSCLC. | Nele Van Der Steen Christophe Deben Vanessa Deschoolmeester An Wouters Filip Lardon Christian Rolfo Paul Germonpré Elisa Giovannetti Godefridus J Peters Patrick Pauwels | 2016 | World Journal of Clinical Oncology2016，7，6： | 2 |
| 7 | Cancer drug resistance: a new perspective显示文摘INTRODUCTION Cancer drug resistance has been and unfortunately still is a major problem in cancer therapy.Almost any therapy(except surgery)that is being used in the treatment of cancer can result in resistance.Unfortunately there is a large group of patients that will either not respond to the applied therapy(intrinsic resistance)or will become resistant during therapy(acquired resistance).Sometimes patients can become resistant to one specific drug and remain sensitive to other drugs(one-drug resistance);another group of patients may become resistant to one drug and will be resistant to other unrelated drugs as well(multiple drug resistance,MDR). | Godefridus J.Peters | 2018 | Cancer Drug Resistance2018，1，1： | 2 |
| 8 | Protective autophagy by thymidine causes resistance to rapamycin in colorectal cancer cells in vitro显示文摘Aim:Thynidine phosphorylase(TP)acts as a proangiogenic growth factor which may regulate mammalian Target of Rapamycin(mTOR).We investigated whether the TP substrate thymidine and overexpression of TP affected mTOR signaling by comparing Colo320(TP deficient)cells and its TP-transfected variant(Colo320TP1).Methods:Drug resistance was assessed with the sulforhodamine B assay,protein expression with Western blotting,cell cycle distribution and cell death with Fluorescence-activated cell sorting analysis,and autophagy with immunofluorescence.Results:Colo320 and Colo320TP1 cells had comparable levels of sensitivity to the mTOR inhibitor rapamycin.Thymidine treatment led to 13-and 50-fold resistance to rapamycin in Colo320 and Colo320TP1 cells,respectively.In Colo320TP1 cells,the thymidine phosphorylase inhibitor(TPI)reversed the thymidine induced resistance to rapamycin,but not in Colo320 cells,indicating a role for TP in the protection.Thymidine increased p70/S6k-phosphorylation(downstream of mTOR)in Colo320TP1,but it was not affected in Colo320.As a mechanism behind resistance,we studied the levels of autophagy and found that,in Colo320TP1 cells,autophagy was highly induced by thymidine-rapamycin,which was decreased by TPI.In addition,the autophagy inhibitor 3-methyl-adenine completely inhibited autophagy and its protection.Conclusion:Rapamycin resistance in TP-expressing cancer cells may therefore be related to thymidine-mediated autophagy activation. | I.V.Bijnsdorp Godefridus J.Peters | 2021 | Cancer Drug Resistance2021，4，3： | 2 |
| 9 | Simulation as decision tool for capacity planning显示文摘 | Siebren Droothuis Godefridus G van' Merode Arie Hasman | 2001 | Computer Methods and Programs in Biomedicine2001，，66： | 1 |
| 10 | Simulation as decision tool for capacity planning显示文摘 | Siebren Droothuis Godefridus G van Merode Arie Hasman | 2001 | Computer Methods and Programs in Biomedicine2001，，66： | 1 |
| 11 | Intracellular Trafficking of MDR Transporters and Relevance of SNPs 显示文摘 | LETIZIA PORCELLI CLARA LEMOS GODEFRIDUS J | 2009 | Current Topics in Medicinal Chem- istry2009，9，： | 1 |
| 12 | Prognostic factors in gemcitabine–cisplatin polychemotherapy regimens in pancreatic cancer: XPD‐Lys751Gln polymorphism strikes back显示文摘 | Amir Avan Paola Pacetti Michele Reni Michele Milella Enrico Vasile Andrea Mambrini Vanja Vaccaro Sara Caponi Stefano Cereda Godefridus J. Peters Maurizio Cantore Elisa Giovannetti | 2013 | Int. J. Cancer2013，，4： | 1 |
| 13 | Association between DNA-repair polymorphisms and survival in pancreatic cancer patients treated with combination chemotherapy显示文摘 | Elisa Giovannetti Paola Pacetti Michele Reni Leticia G Leon Andrea Mambrini Enrico Vasile Michele Ghidini Niccola Funel Matteo Lucchesi Stefano Cereda Godefridus J Peters Maurizio Cantore | 2011 | Pharmacogenomics2011，，12： | 1 |
| 14 | Crizotinib Inhibits Metabolic Inactivation of Gemcitabine in c-Met–driven Pancreatic Carcinoma显示文摘 | Amir Avan Viola Caretti Niccola Funel Elena Galvani Mina Maftouh Richard J. Honeywell Tonny Lagerweij Olaf Van Tellingen Daniela Campani Dieter Fuchs Henk M. Verheul Gerrit-Jan Schuurhuis Ugo Boggi Godefridus J. Peters Thomas Würdinger Elisa Giovannetti | 2013 | Cancer Research2013，，22： | 1 |
| 15 | Enterprise resource planning for hospitals 显示文摘 | Godefridus G van Merode Siebren Groothuis | 2004 | International Journal of Medi- cal Informatics2004，，73： | 1 |
| 16 | Simu- lation as decision tool for capacity planning 显示文摘 | Siebren Groothuis Godefridus G van Merode Arie Hasman | 2001 | Computer Methods and Programs in Biomedicine2001，66，5： | 1 |
| 17 | Gemcitabine chemoresistance in pancreatic cancer: Molecular mechanisms and potential solutions显示文摘 | Roland Andersson Ursula Aho Bo I. Nilsson Godefridus J. Peters Mar?al Pastor-Anglada Wenche Rasch Marit L. Sandvold | 2009 | Scandinavian Journal of Gastroenterology2009，，7： | 1 |
| 18 | Tyrosine kinase inhibitors:Multi-targeted or single-targeted?显示文摘Since in most tumors multiple signaling pathways are involved,many of the inhibitors in clinical development are designed to affect a wide range of targeted kinases.The most important tyrosine kinase families in the development of tyrosine kinase inhibitors are the ABL,SCR,platelet derived growth factor,vascular endothelial growth factor receptor and epidermal growth factor receptor families.Both multi-kinase inhibitors and singlekinase inhibitors have advantages and disadvantages,which are related to potential resistance mechanisms,pharmacokinetics,selectivity and tumor environment.In different malignancies various tyrosine kinases are mutated or overexpressed and several resistance mechanisms exist.Pharmacokinetics is influenced by interindividual differences and differs for two single targeted inhibitors or between patients treated by the same tyrosine kinase inhibitor.Different tyrosine kinase inhibitors have various mechanisms to achieve selectivity,while differences in gene expression exist between tumor and stromal cells.Considering these aspects,one type of inhibitor can generally not be preferred above the other,but will depend on the specific genetic constitution of the patient and the tumor,allowing personalized therapy.The most effective way of cancer treatment by using tyrosine kinase inhibitors is to consider each patient/tumor individually and to determine the strategy that specifically targets the consequences of altered(epi)genetics of the tumor.This strategy might result in treatment by a single multi kinase inhibitor for one patient,but in treatment by a couple of single kinase inhibitors for other patients. | Fleur Broekman Elisa Giovannetti Godefridus J Peters | 2011 | World Journal of Clinical Oncology2011，2，2： | 1 |
| 19 | Detection of an alternatively spliced form of deoxycytidine kinase mRNA in the 2′-2′-difluorodeoxycytidine (gemcitabine)-resistant human ovarian cancer cell line AG6000显示文摘 | Ashraf Said Al-Madhoun Clasina L van der Wilt Willem J.P Loves Jose M Padron Staffan Eriksson Iannis Talianidis Godefridus J Peters | 2004 | Biochemical Pharmacology2004，，4： | 1 |
| 20 | Sensitivity to ionizing radiation and chemotherapeutic agents in gemcitabine-resistant human tumor cell lines显示文摘 | Chris van Bree Natasja Castro Kreder Willem J.P Loves Nicolaas A.P Franken Godefridus J Peters Jaap Haveman | 2002 | International Journal of Radiation Oncology, Biology, Physics2002，，1： | 1 |
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