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| 1 | Circulating endothelial and progenitor cells:Evidence from acute and long-term exercise effects显示文摘Circulating bone-marrow-derived cells,named endothelial progenitor cells(EPCs),are capable of maintaining,generating,and replacing terminally differentiated cells within their own specific tissue as a consequence of physiological cell turnover or tissue damage due to injury.Endothelium maintenance and restoration of normal endothelial cell function is guaranteed by a complex physiological procedure in which EPCs play a significant role.Decreased number of peripheral blood EPCs has been associated with endothelial dysfunction and high cardiovascular risk.In this review,we initially report current knowledge with regard to the role of EPCs in healthy subjects and the clinical value of EPCs in different disease populations such as arterial hypertension,obstructive sleep-apnea syndrome,obesity,diabetes mellitus,peripheral arterial disease,coronary artery disease,pulmonary hypertension,and heart failure.Recent studies have introduced the novel concept that physical activity,either performed as a single exercise session or performed as part of an exercise training program,results in a significant increase of circulating EPCs.In the second part of this review we provide preliminary evidence from recent studies investigating the effects of acute and long-term exercise in healthy subjects and athletes as well as in disease populations. | Matina Koutroumpi Stavros Dimopoulos Katherini Psarra Theodoros Kyprianou Serafim Nanas | 2012 | World Journal of Cardiology2012，4，12： | 18 |
| 2 | 在 colorectal 癌症的地岬发信号小径,变化和他们的角色显示文摘 Two of the main cellular pathways in which the RAS protein operates are the mitogen-activated protein kinases (MAPK) and phosphoinositide-3 kinase (PI3K) pathways. In a normal cell, these are important in controlling several functions, such as cell growth and survival. It becomes self-evident that these events will be disrupted in a malignant cell with a deregulated MAPK or PI3K pathway. Mutations in genes involved in these pathways and interacting with RAS, as well as RAS itself will be discussed. The second part of this review concentrates on how crucial RAS signaling is in colorectal cancer progression, with references to treatment response and prognosis when RAS or other related mutations are present. | Kypros Zenonos Katy Kyprianou | 2013 | World Journal of Gastrointestinal Oncology2013，5，5： | 8 |
| 3 | Prostate tumor neuroendocrine differentiation via EMT: The road less traveled显示文摘The long-standing challenge in the treatment of prostate cancer is to overcome therapeutic resistance during progression to lethal disease.Aberrant transforming-growth factor-b(TGF-b)signaling accelerates prostate tumor progression in a transgenic mouse model via effects on epithelial-mesenchymal transition(EMT),and neuroendocrine differentiation driving tumor progression to castration-resistant prostate cancer(CRPC).Neuroendocrine prostate cancer(NEPC)is highly aggressive exhibiting reactivation of developmental programs associated with EMT induction and stem cell-like characteristics.The androgen receptor(AR)is a critical driver of tumor progression as well as therapeutic response in patients with metastatic CRPC.The signaling interactions between the TGF-β mechanistic network and AR axis impact the EMT phenotypic conversions,and perturbation of epithelial homeostasis via EMT renders a critical venue for epithelial derived tumors to become invasive,acquire the neuroendocrine phenotype,and rapidly metastasize.Combinations of microtubule targeting taxane chemotherapy and androgen/AR targeting therapies have survival benefits in CRPC patients,but therapeutic resistance invariability develops,leading to mortality.Compelling evidence from our group recently demonstrated that chemotherapy(cabazitaxel,second line taxane chemotherapy),or TGF-β receptor signaling targeted therapy,caused reversion of EMT to mesenchymal-epithelial transition and tumor re-differentiation,in in vitro and in vivo prostate cancer models.In this review,we discuss the functional contribution of EMT dynamic changes to the development of the neuroendocrine phenotypedthe newly characterized pathological feature of prostate tumors in the context of the tumor microenvironment-navigated cell lineage changes and the role of this neuroendocrine phenotype in metastatic progression and therapeutic resistance. | Haley Dicken Patrick J.Hensley Natasha Kyprianou | 2019 | Asian Journal of Urology2019，6，1： | 3 |
| 4 | Mechanisms navigating the TGF-βpathway in prostate cancer显示文摘Few pharmacotherapies are currently available to treat castration resistant prostate cancer(CRPC),with low impact on patient survival.Transforming growth factor-b(TGF-b)is a multi-functional peptide with opposite roles in prostate tumorigenesis as an inhibitor in normal growth and early stage disease and a promoter in advanced prostate cancer.Dysregulated TGF-b signaling leads to a cascade of events contributing to oncogenesis,including upregulated proliferation,decreased apoptosis,epithelial-to-mesenchymal transition(EMT)and evasion of immune surveillance.TGF-b signaling pathway presents an appropriate venue for establishing a therapeutic targeting platform in CRPC.Exploitation of TGF-b effectors and their cross talk with the androgen axis pathway will provide new insights into mechanisms of resistance of the current antiandrogen therapeutic strategies and lead to generation of new effective treatment modalities for CRPC.Points of functional convergence of TGF-b with key oncogenic pathways,including mitogen-activated protein kinase(MAPK)and androgen receptor(AR),are discussed as navigated within the EMT landscape in the tumor microenvironment.In this context the emerging anti-TGF-b pharmacotherapies for prostate cancer treatment are considered.Targeting the functional cross-talk between the TGF-b signaling effectors with the androgen axis supports the development of novel therapeutic strategies for treating CRPC with high specificity and efficacy in a personalized-medicine approach. | Zheng Cao Natasha Kyprianou | 2015 | Asian Journal of Urology2015，2，1： | 3 |
| 5 | Caspase control: protagonists of cancer cell apoptosis 显示文摘 | Fiandalo M Kyprianou N | 2012 | Exp Oncol2012，34，： | 1 |
| 6 | Pricing Israeli options: a pathwise approach 显示文摘 | KUHN C KYPRIANOU A E SCHMK K V | 2007 | Probability and Stochastic Processes2007，79，1： | 1 |
| 7 | Anoikis and survival connections in the tumor microenvironment: is there a role in prostate cancer metastasis? 显示文摘 | Rennebeck G Martelli M Kyprianou N | 2005 | Cancer Res2005，65，11： | 1 |
| 8 | Epithelial mesenchymal transition (EMT)in prostate growth and tumor progression 显示文摘 | Grant CM Kyprianou N | 2013 | Transl Androl Urol2013，2，3： | 1 |
| 9 | Doxazosin and terazosin suppress prostate growth by inducing apoptosis:clinical significance显示文摘 | Kyprianou N | 2003 | J Urol2003，169，4： | 1 |
| 10 | Transforming growth factor beta and prostate cancer显示文摘 | Zhu B Kyprianou N | 2005 | Cancer Treat Res2005，126，1： | 1 |
| 11 | Apoptotic versus proliferative activities in human benign prostatic hyperplasia显示文摘 | Kyprianou N Tu H Jacobs SC | 1996 | Hum Pathol1996，27，： | 1 |
| 12 | MASPIN sensitizesprostate cancer cells to doxazosin-induced apoptosis显示文摘 | Tahmatzopoulos A Sheng S Kyprianou N | 2005 | Oncogene2005，24，34： | 1 |
| 13 | Caspase control:protagonists ofcancer cell apoptosis显示文摘 | Fiandalo MV Kyprianou N | 2012 | Exp Oncol2012，34，3： | 1 |
| 14 | Doxazosin and terazosin suppress p rostate growth by inducing apoptosis:clinical significance显示文摘 | Kyprianou N | 2003 | J Urol2003，169，： | 1 |
| 15 | Radiation-induced apoptosis:predictive and therapeutic significance in radiotherapy of prostate cancer (review)显示文摘 | Szostak M J Kyprianou N | 2000 | Oncol Rep2000，7，4： | 1 |
| 16 | Radiation-induced apoptosis:predictive and therapeutic significance in radiotherapy of prostate cancer (review)显示文摘 | Szostak M J Kyprianou N | 2000 | Oncol Rep2000，7，4： | 1 |
| 17 | Apoptotic versus proliferative activities in human benign prostatic hyperplasia显示文摘 | Tu H Jacobs SC | 1996 | Hum Pathol1996，27，7： | 1 |
| 18 | Suppression of human prostate cancer cell growth by a1-adre-noceptor antagonist doxazosin and terazosin via induction of apoptosis显示文摘 | Kyprianou N Benning C | 2000 | Cancer Res2000，60，16： | 1 |
| 19 | Apoptic versus proliferative activ-ities in human benign prostatic hyperplasia 显示文摘 | Kyprianou N Tu H Jacobs SC | 1996 | Hum Pathol1996，17，： | 1 |
| 20 | Apoptotic versus prolifer- ative activities in human benign prostatic hyperplasia显示文摘 | Kyprianou N Tu H Jacobs SC | 1996 | Hum Patholy1996，27，7： | 1 |
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