FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2156688939> ?p ?o ?g. }

• W2156688939 endingPage "2" @default.
• W2156688939 startingPage "1" @default.
• W2156688939 abstract "A better understanding of key regulatory pathways perturbed in cancers has led to the development of a molecularly targeted therapeutic approach. As a result, new generations of compounds aimed at inhibiting specific pathways that play prominent roles in urological cancers have been developed and continue to evolve. The possibility of being able to perform molecular profiling in tumors would, at least in theory, provide the clinician with information needed to manage a personalized therapeutic regimen according to an individual patient's needs. While this modality is already being implemented in other cancer fields, personalized medicine for patients suffering from advanced lower urogenital tumors is still in the developmental phase. This impetus has prompted a concerted effort from investigators in the fields of basic, translational, and clinical research to develop and implement a tailored treatment approach. In this issue, we present a collection of seven articles that contribute to our knowledge of personalized medicine for urological cancers.Androgen deprivation therapy (ADT) for advanced prostate cancer is one of the earliest forms of targeted therapy and has remained the choice of treatment by physicians. Unfortunately, most patients will eventually become non-responsive to ADT and succumb to the disease. Since its inception, knowledge for the understanding of androgen receptor (AR) signaling and mechanisms driving the resistance to ADT has been significantly improved. As a result, a new generation of therapeutic agents has been developed. The paper by X. Hou and T. W. Flaig gives a historical account of ADT for metastatic prostate cancer and summarizes current advancements in hormonal therapies using newly developed agents such as MDV3100, TOK-001, and TAK-700. The association between insulin and androgens in prostate cancer progression is detailed by J. H. Gunter et al. In this review, the authors describe the inverse relationship between insulin and testosterone levels and the metabolic crosstalk between the two signaling axes. The authors discuss the effects of ADT-induced hyperinsulinaemia and describe the direct effects of insulin on prostate tumor cells and its clinical implications. The 5 α-reductase inhibitors represent an important family of enzymes that mediate the conversion of testosterone to the more potent dihydrotestosterone (DHT). Consequently, several compounds have been developed to inhibit the activity of the enzymes to prevent and treat a number of diseases. The paper by F. Azzouni et al. goes into great detail to describe the basic biochemical properties and functions of the 5 α-reductase isozyme family and its clinical significance with regards to prostate cancer prevention and treatment.Gene inactivation of PTEN is a common occurrence in prostate cancers and is associated to metastatic potential, androgen independence, and poor prognosis. The review by M. A. De Velasco and H. Uemura chronicles the evolution of the PTEN-deficient genetically engineered mouse (GEM) and the cooperation between PTEN and other genetic alterations that contribute to tumor progression. The authors also describe the usefulness of GEM models for biomarker and drug discovery. Also in this issue, two reviews delve into the progress towards personalized medicine for muscle invasive and metastatic bladder cancer. J. S. Chang et al. review potential molecular biomarkers currently under investigation and discuss their future. In the second paper A. Kawashima et al. review the excision repair cross-complementing group 1 (ERCC1) gene and its role in tumor development and therapeutic resistance to cytotoxic DNA-damaging chemotherapy and ionizing radiation. Finally, in the original paper by R. Nagarajan et al. the authors use the apparent diffusion coefficient, derived from diffusion-weighted (DWI) imaging, to identify higher-grade prostate cancer lesions. Although the data is preliminary, the authors' findings reveal a potential for the use of DWI imaging to differentiate those patients with high-grade lesions." @default.
• W2156688939 created "2016-06-24" @default.
• W2156688939 creator A5058934672 @default.
• W2156688939 creator A5060302039 @default.
• W2156688939 creator A5078445671 @default.
• W2156688939 creator A5089480920 @default.
• W2156688939 date "2012-01-01" @default.
• W2156688939 modified "2023-09-26" @default.
• W2156688939 title "Personalized Cancer Therapy for Urological Cancers: From Bench to Bedside and Back" @default.
• W2156688939 cites W1550300650 @default.
• W2156688939 cites W1568417506 @default.
• W2156688939 cites W169007637 @default.
• W2156688939 cites W1729580440 @default.
• W2156688939 cites W184985603 @default.
• W2156688939 cites W1955462222 @default.
• W2156688939 cites W1965373507 @default.
• W2156688939 cites W1967517340 @default.
• W2156688939 cites W1969051501 @default.
• W2156688939 cites W1973315585 @default.
• W2156688939 cites W1976529462 @default.
• W2156688939 cites W1981215159 @default.
• W2156688939 cites W1981318616 @default.
• W2156688939 cites W1981804745 @default.
• W2156688939 cites W1983648619 @default.
• W2156688939 cites W1985481419 @default.
• W2156688939 cites W1985950314 @default.
• W2156688939 cites W1992103956 @default.
• W2156688939 cites W1993984692 @default.
• W2156688939 cites W1994052047 @default.
• W2156688939 cites W1999663083 @default.
• W2156688939 cites W1999912122 @default.
• W2156688939 cites W2002295835 @default.
• W2156688939 cites W2002327466 @default.
• W2156688939 cites W2002865604 @default.
• W2156688939 cites W2003631076 @default.
• W2156688939 cites W2004718750 @default.
• W2156688939 cites W2005939603 @default.
• W2156688939 cites W2008338524 @default.
• W2156688939 cites W2011330675 @default.
• W2156688939 cites W2013968185 @default.
• W2156688939 cites W2015142872 @default.
• W2156688939 cites W2015384505 @default.
• W2156688939 cites W2016594281 @default.
• W2156688939 cites W2019269074 @default.
• W2156688939 cites W2019408938 @default.
• W2156688939 cites W2020105514 @default.
• W2156688939 cites W2021424019 @default.
• W2156688939 cites W2023481449 @default.
• W2156688939 cites W2027134354 @default.
• W2156688939 cites W2027619565 @default.
• W2156688939 cites W2028896857 @default.
• W2156688939 cites W2029877275 @default.
• W2156688939 cites W2033935668 @default.
• W2156688939 cites W2037947860 @default.
• W2156688939 cites W2038437205 @default.
• W2156688939 cites W2040556993 @default.
• W2156688939 cites W2044346962 @default.
• W2156688939 cites W2049695002 @default.
• W2156688939 cites W2052483270 @default.
• W2156688939 cites W2057853521 @default.
• W2156688939 cites W2058448589 @default.
• W2156688939 cites W2060872788 @default.
• W2156688939 cites W2060903877 @default.
• W2156688939 cites W2063024925 @default.
• W2156688939 cites W2065855960 @default.
• W2156688939 cites W2069228387 @default.
• W2156688939 cites W2070991971 @default.
• W2156688939 cites W2071065069 @default.
• W2156688939 cites W2071231934 @default.
• W2156688939 cites W2072353766 @default.
• W2156688939 cites W2073230702 @default.
• W2156688939 cites W2074497307 @default.
• W2156688939 cites W2077301757 @default.
• W2156688939 cites W2078134150 @default.
• W2156688939 cites W2078400569 @default.
• W2156688939 cites W2081251422 @default.
• W2156688939 cites W2081662746 @default.
• W2156688939 cites W2087613535 @default.
• W2156688939 cites W2087823616 @default.
• W2156688939 cites W2089688362 @default.
• W2156688939 cites W2091379839 @default.
• W2156688939 cites W2091863065 @default.
• W2156688939 cites W2094642217 @default.
• W2156688939 cites W2096573752 @default.
• W2156688939 cites W2100220714 @default.
• W2156688939 cites W2100751052 @default.
• W2156688939 cites W2101326112 @default.
• W2156688939 cites W2101995865 @default.
• W2156688939 cites W2102846176 @default.
• W2156688939 cites W2102855165 @default.
• W2156688939 cites W2106925611 @default.
• W2156688939 cites W2108511792 @default.
• W2156688939 cites W2108703423 @default.
• W2156688939 cites W2110155536 @default.
• W2156688939 cites W2111663279 @default.
• W2156688939 cites W2111963490 @default.
• W2156688939 cites W2113156769 @default.
• W2156688939 cites W2113745250 @default.

• next