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- Veen, Violaine C., et al.
(författare)
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Cross-ethnic generalizability of the three-factor model of psychopathy : the youth psychopathic traits inventory in an incarcerated sample of native Dutch and Moroccan immigrant boys
- 2011
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Ingår i: International Journal of Law and Psychiatry. - : Pergamon Press. - 0160-2527 .- 1873-6386. ; 34:2, s. 127-130
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: Previous research provides support for the existence of the psychopathy construct in youths. However, studies regarding the psychometric properties of psychopathy measures with ethnic minority youths are lacking.METHODS: In the present study, the three-factor structure of the Youth Psychopathic Traits Inventory (YPI) was examined for both native Dutch youth (N=158) and an ethnic minority group, Moroccans (N=141), in an incarcerated adolescent population in the Netherlands.RESULTS: Our results showed that the three-factor structure of the YPI is comparable across an ethnic majority and an ethnic minority group in an incarcerated sample in the Netherlands. Moreover, associations between psychopathic traits and mental health problems were similar for both ethnic groups.CONCLUSION: The results support the cross-ethnic generalizability of the three-factor model of psychopathy as measured through the Youth Psychopathic Traits Inventory.
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| 2. |
- Smit, Marjon A., et al.
(författare)
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ROCK1 is a potential combinatorial drug target for BRAF mutant melanoma
- 2014
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Ingår i: Molecular Systems Biology. - : EMBO. - 1744-4292 .- 1744-4292. ; 10:12
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Tidskriftsartikel (refereegranskat)abstract
- Treatment of BRAF mutant melanomas with specific BRAF inhibitors leads to tumor remission. However, most patients eventually relapse due to drug resistance. Therefore, we designed an integrated strategy using (phospho)proteomic and functional genomic platforms to identify drug targets whose inhibition sensitizes melanoma cells to BRAF inhibition. We found many proteins to be induced upon PLX4720 (BRAF inhibitor) treatment that are known to be involved in BRAF inhibitor resistance, including FOXD3 and ErbB3. Several proteins were down-regulated, including Rnd3, a negative regulator of ROCK1 kinase. For our genomic approach, we performed two parallel shRNA screens using a kinome library to identify genes whose inhibition sensitizes to BRAF or ERK inhibitor treatment. By integrating our functional genomic and (phospho)proteomic data, we identified ROCK1 as a potential drug target for BRAF mutant melanoma. ROCK1 silencing increased melanoma cell elimination when combined with BRAF or ERK inhibitor treatment. Translating this to a preclinical setting, a ROCK inhibitor showed augmented melanoma cell death upon BRAF or ERK inhibition in vitro. These data merit exploration of ROCK1 as a target in combination with current BRAF mutant melanoma therapies.
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