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| 1 | Inhibition of GSK3B Bypass Drug Resistance of p53-Null Colon Carcinomas by Enabling Necroptosis in Response to Chemotherapy显示文摘 | Emanuela Grassilli Robert Narloch Elena Federzoni Leonarda Ianzano Fabio Pisano Roberto Giovannoni Gabriele Romano Laura Masiero Biagio Eugenio Leone Serena Bonin Marisa Donada Giorgio Stanta Kristian Helin Marialuisa Lavitrano | 2013 | Clinical Cancer Research2013，，14： | 3 |
| 2 | Emerging actionable targets to treat therapyresistant colorectal cancers显示文摘In the last two decades major improvements have been reached in the early diagnosis of colorectal cancer(CRC)and,besides chemotherapy,an ampler choice of therapeutic approaches is now available,including targeted and immunotherapy.Despite that,CRC remains a“big killer”mainly due to the development of resistance to therapies,especially when the disease is diagnosed after it is already metastatic.At the same time,our knowledge of the mechanisms underlying resistance has been rapidly expanding which allows the development of novel therapeutic options in order to overcome it.As far as resistance to chemotherapy is concerned,several contributors have been identified such as:intake/efflux systems upregulation;alterations in the DNA damage response,due to defect in the DNA checkpoint and repair systems;dysregulation of the expression of apoptotic/anti-apoptotic members of the BCL2 family;overexpression of oncogenic kinases;the presence of cancer stem cells;and the composition of the tumoral microenvironment and that of the gut microbiota.Interestingly,several mechanisms are also involved in the resistance to targeted and/or immunotherapy.For example,overexpression and/or hyperactivation and/or amplification of oncogenic kinases can sustain resistance to targeted therapy whereas the composition of the gut microbiota,as well as that of the tumoral niche,and defects in DNA repair systems are crucial for determining the response to immunotherapy.In this review we will make an overview of the main resistance mechanisms identified so far and of the new therapeutic approaches to overcome it. | Emanuela Grassilli Maria Grazia Cerrito | 2022 | Cancer Drug Resistance2022，5，1： | 2 |
| 3 | Cell proliferation and cell death in immumnosenescence显示文摘 | Troiano E Grassilli C | 1992 | Ann NY Acad Sci1992，663，： | 1 |
| 4 | Mitochondrial modificatiorts during rat thyrmcyte atxotosks: a study at the dngte cell level显示文摘 | Cossarizza A Kalashnikovn G Grassilli E | 1994 | Exp Cell Res1994，214，： | 1 |
| 5 | GSK3A is redundant with GSK3B in modulating drug resistance and chemotherapy-induced necroptosis显示文摘 | Grassilli E Ianzano L Bonomo S | 2014 | PLoS One2014，9，10： | 1 |
| 6 | Inhibition of GSK3B bypass drug resistance of p53-null colonc carcinomas by enabling necroptosis in response to chemotherapy显示文摘 | Grassilli E Narloch R Federzoni E | 2013 | Clin Cancer Res2013，19，14： | 1 |
| 7 | Inhibition of GSK3B bypass drug resistance of p53-null colon carcinomas by enabling necroptosis in response to chemotherapy 显示文摘 | Grassilli E Narloch R Federzoni E | 2013 | Clin Cancer Res2013，19，14： | 1 |
| 8 | Autocrine nerve growth factor protects human keratinocytes from apoptosis through its high affinity receptor (TRK) :A role for Bcl-2 显示文摘 | Pincelli C Haake AR Benassi L Grassilli E Maqnoni C Ottani D | 1997 | J Invest Dermatol1997，109，6： | 1 |
| 9 | Cell proliferation and cell death in immumnosenescence显示文摘 | Monti L Troiano E Grassilli C | 1992 | Ann NY Acad Sci1992，663，： | 1 |
| 10 | Vavl modu-lates protein expression during ATRA-indueed maturation of APL-derived promyeloeytes: a proteomie-based analysis 显示文摘 | Bertagnolo V Grassilli S Bavelloni A | 2008 | J Proteome Res2008，7，9： | 1 |
| 11 | Studies of relationship between cell proliferation and cell death显示文摘 | Grassilli E | | 0，，： | 1 |
| 12 | Cell proliferation and cell death in immunosenescence 显示文摘 | Monti D T roiano L Grassilli E | 1992 | Ann N Y Acad Sci1992，663，： | 1 |
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