Recognising Victimhood: Lessons from the International Criminal Court and Mass Claim Programmes for the Compensation Procedure Parallel to the Trial of International Crimes in the Netherlands

In the Netherlands, the Dutch criminal court in The Hague (hereinafter: ‘Netherlands International Crimes Court’ or ‘NIC court’) is assigned to try international crimes, and to provide compensation to victims of such crimes. Whereas it has specific criminal laws at its disposal to try international crimes, it applies ‘regular’ Dutch civil law to assess claims for compensation. Yet compensation for international crimes entails challenges that are quite different from domestic crimes: international crimes are normally committed against a large number of victims, and frequently result in bodily harm. This article argues that the NIC court will most likely rule a large number of claims for compensation inadmissible, as a consequence of which victims cannot benefit from the advantages inherent in the award of compensation within the criminal process. It then explores the adjudicative and reparatory standards that the International Criminal Court and mass claim programmes have applied to simplify both the adjudication of a large number of claims, and the calculation of a large number of instances of bodily damage. It is submitted that adoption by the NIC court of international reparatory standards could facilitate the assessment of a large number of civil claims within the criminal process, without prejudice to the legitimate interests of the defendant for an adequate procedure. However, these standards require the NIC court to strike a new balance between tailor-made compensation and symbolic compensation, and thereby between corrective justice and restorative justice

Antimetastatic gene expression profiles mediated by retinoic acid receptor beta 2 in MDA-MB-435 breast cancer cells

BACKGROUND: The retinoic acid receptor beta 2 (RARβ2) gene modulates proliferation and survival of cultured human breast cancer cells. Previously we showed that ectopic expression of RARβ2 in a mouse xenograft model prevented metastasis, even in the absence of the ligand, all-trans retinoic acid. We investigated both cultured cells and xenograft tumors in order to delineate the gene expression profiles responsible for an antimetastatic phenotype. METHODS: RNA from MDA-MB-435 human breast cancer cells transduced with RARβ2 or empty retroviral vector (LXSN) was analyzed using Agilent Human 1A Oligo microarrays. The one hundred probes with the greatest differential intensity (p < 0.004, jointly) were determined by selecting the top median log ratios from eight-paired microarrays. Validation of differences in expression was done using Northern blot analysis and quantitative RT-PCR (qRT-PCR). We determined expression of selected genes in xenograft tumors. RESULTS: RARβ2 cells exhibit gene profiles with overrepresentation of genes from Xq28 (p = 2 × 10(-8)), a cytogenetic region that contains a large portion of the cancer/testis antigen gene family. Other functions or factors impacted by the presence of exogenous RARβ2 include mediators of the immune response and transcriptional regulatory mechanisms. Thirteen of fifteen (87%) of the genes evaluated in xenograft tumors were consistent with differences we found in the cell cultures (p = 0.007). CONCLUSION: Antimetastatic RARβ2 signalling, direct or indirect, results in an elevation of expression for genes such as tumor-cell antigens (CTAG1 and CTAG2), those involved in innate immune response (e.g., RIG-I/DDX58), and tumor suppressor functions (e.g., TYRP1). Genes whose expression is diminished by RARβ2 signalling include cell adhesion functions (e.g, CD164) nutritional or metabolic processes (e.g., FABP6), and the transcription factor, JUN