Assessing Implicit Theories in Sexual Offending Using Indirect Measures: Feasibility, Reliability, and Incremental Validity.

This study assessed psychometric qualities of indirect measures assessing Implicit Theories (ITs) of sexual offending: Implicit Association Task (IAT), Implicit Relational Assessment Procedure (IRAP), and Relational Responding Task (RRT). For comparison reasons, aggressive behavior was also assessed. In a male sample from the general population ( = 109), we assessed each measure's (a) feasibility (mean latency, error rate, passing criteria), (b) internal consistency, (c) convergent and discriminant validity, and (d) incremental and predictive validity.

Factor Structure and Construct Validity of the Levenson Self-Report Psychopathy Scale (LSRP): A Replication and Extension in Dutch Nonclinical Participants.

The Levenson Self-Report Psychopathy (LSRP) scale is widely used to assess psychopathic traits in noninstitutionalized samples. Recent studies suggest that a three-factor structure measuring Egocentricity, Callousness, and Antisocial factors outperformed the original two-factor structure of the LSRP. This study replicated and extended these findings by examining the factor structure and construct validity of a Dutch version of the LSRP in a community sample ( = 856, subsamples ranging between 140 and 572 participants).

PTD4-apoptin induces Bcl-2-insensitive apoptosis in human cervical carcinoma in vitro and in vivo.

Worldwide, cervix carcinoma is among the most dangerous cancer types, and novel therapies are under development. Cancer treatments are often hampered because of lack of specificity. The chicken anemia virus-derived apoptin induces apoptosis selectively in tumor cells and leaves normal cells unharmed.

Exploration of the (Interrater) Reliability and Latent Factor Structure of the Alcohol Use Disorders Identification Test (AUDIT) and the Drug Use Disorders Identification Test (DUDIT) in a Sample of Dutch Probationers.

Background: The use of brief, reliable, valid, and practical measures of substance use is critical for conducting individual (risk and need) assessments in probation practice. In this exploratory study, the basic psychometric properties of the Alcohol Use Disorders Identification Test (AUDIT) and the Drug Use Disorders Identification Test (DUDIT) are evaluated.

Methods: The instruments were administered as an oral interview instead of a self-report questionnaire.

Apoptin towards safe and efficient anticancer therapies.

The chicken anemia virus derived protein apoptin harbors cancer-selective cell killing characteristics, essentially based on phosphorylation-mediated nuclear transfer in cancer cells and efficient cytoplasmic degradation in normal cells. Here, we describe a growing set of preclinical experiments underlying the promises of the anti-cancer potential of apoptin. Various non-replicative oncolytic viral vector systems have revealed the safety and efficacy of apoptin.

Mitotic catastrophe triggered in human cancer cells by the viral protein apoptin.

Mitotic catastrophe is an oncosuppressive mechanism that senses mitotic failure leading to cell death or senescence. As such, it protects against aneuploidy and genetic instability, and its induction in cancer cells by exogenous agents is currently seen as a promising therapeutic end point. Apoptin, a small protein from Chicken Anemia Virus (CAV), is known for its ability to selectively induce cell death in human tumor cells.

Proteasomal insensitivity of apoptin in tumor cells.

The small viral protein apoptin is capable of inducing apoptosis selectively in human tumor cells. In normal cells apoptin localizes in the cytoplasm where it forms aggregates, becomes epitope-shielded and eventually degraded. By inhibiting the proteasome activity with the chemical inhibitors bortezomib and Ada-Ahx(3)L(3)VS apoptin levels can be stabilized in normal cells similar to the tumor suppressor p53 protein.

PP2A inactivation is a crucial step in triggering apoptin-induced tumor-selective cell killing.

Apoptin (apoptosis-inducing protein) harbors tumor-selective characteristics making it a potential safe and effective anticancer agent. Apoptin becomes phosphorylated and induces apoptosis in a large panel of human tumor but not normal cells. Here, we used an in vitro oncogenic transformation assay to explore minimal cellular factors required for the activation of apoptin.

Development and application of an in vitro apoptin kinase assay.

Apoptin, a protein derived from chicken anemia virus (CAV), induces apoptosis selectively in human tumor cells as compared with normal cells. This activity depends on phosphorylation and relocation of apoptin to the nucleus of cancer cells. Here, we describe an in vitro kinase assay that allows the biochemical characterization of apoptin kinase activity in tumor cells.

Stem-loop structures can effectively substitute for an RNA pseudoknot in -1 ribosomal frameshifting.

-1 Programmed ribosomal frameshifting (PRF) in synthesizing the gag-pro precursor polyprotein of Simian retrovirus type-1 (SRV-1) is stimulated by a classical H-type pseudoknot which forms an extended triple helix involving base-base and base-sugar interactions between loop and stem nucleotides. Recently, we showed that mutation of bases involved in triple helix formation affected frameshifting, again emphasizing the role of the triple helix in -1 PRF. Here, we investigated the efficiency of hairpins of similar base pair composition as the SRV-1 gag-pro pseudoknot.

PTD4-apoptin protein and dacarbazine show a synergistic antitumor effect on B16-F1 melanoma in vitro and in vivo.

PTD4-apoptin protein enters cells and harbors tumor-selective cell death activity. Dacarbazine is the mainstay of treatment for malignant melanoma. In this study, we investigated the cytotoxic effect of PTD4-apoptin protein and/or dacarbazine in mouse B16-F1 and human A875 and SK-MEL-5 melanoma cells in vitro and by means of a mouse B16-F1 melanoma model in vivo.

Stimulation of ribosomal frameshifting by antisense LNA.

Programmed ribosomal frameshifting is a translational recoding mechanism commonly used by RNA viruses to express two or more proteins from a single mRNA at a fixed ratio. An essential element in this process is the presence of an RNA secondary structure, such as a pseudoknot or a hairpin, located downstream of the slippery sequence. Here, we have tested the efficiency of RNA oligonucleotides annealing downstream of the slippery sequence to induce frameshifting in vitro.

Anticancer genes: inducers of tumour-specific cell death signalling.

Recent studies have revealed a new class of genes encoding proteins with specific anticancer activity. Upon ectopic expression, these factors cause cell death specifically in tumour cells by apoptosis, autophagy or mitotic catastrophe, yet normal cells are spared. Some of these genes or their encoded proteins are in clinical development and show promising results, and their signalling pathways are currently under intense investigation.

Apoptin enhances radiation-induced cell death in poorly responding head and neck squamous cell carcinoma cells.

Treatment of head and neck cancers is still rather poor and worldwide new treatment options are sought. Sensitizing radioresistant tumours by combining irradiation with other therapeutics to induce apoptosis are widely investigated. We examined whether chicken anaemia virus-derived apoptin protein would have a beneficial effect on irradiation of radiosensitive SCC61 and radioresistant SQD9 human head and neck squamous carcinoma cell lines.

Proteins selectively killing tumor cells.

All human cells have a genetic program that upon activation will cause cell death, named apoptosis. Cancer cells can grow due to unbalances in proliferation, cell cycle regulation and their apoptosis machinery: genomic mutations resulting in non-functional pro-apoptosis proteins or over-expression of anti-apoptosis proteins form the basis of tumor formation. Surprisingly, lessons learned from viruses show that cancer cannot be regarded simply as the opposite of apoptosis.

A mouse model for oral squamous cell carcinoma.

Despite recent advances, the prognosis of oral squamous cell carcinoma is still poor. Therapeutic options such as radiotherapy, chemotherapy, surgery and the novel treatment option gene therapy are being investigated in animal models. Diverse models have been studied to induce oral squamous cell carcinomas.

PTD4-apoptin protein therapy inhibits tumor growth in vivo.

Apoptin protein harbors tumor-selective cell death activity, which makes it a potential anticancer therapy candidate. This study reports an apoptin therapy approach based on protein transduction domain 4 (PTD4)-mediated transduction of recombinant apoptin protein. In vitro, the PTD4-apoptin fusion protein is located in the nucleus and induces cell death in, e.

Apoptosis-inducing proteins in chicken anemia virus and TT virus.

Torque teno viruses (TTVs) share several genomic similarities with the chicken anemia virus (CAV). CAV encodes the protein apoptin that specifically induces apoptosis in (human) tumor cells. Functional studies reveal that apoptin induces apoptosis in a very broad range of (human) tumor cells.

Apoptin induces apoptosis in an oral cancer mouse model.

Apoptin, a chicken anemia virus-derived protein, induces apoptosis in various tumor cell lines and xenografted tumors. Its apoptotic activity is not hampered by tumor-suppressor p53 mutations or overexpression of anti-apoptosis proteins Bcl-2 or Bcl-x(L). We report for the first time the effects of apoptin expression in primary oral tumors, induced by the carcinogen 4-Nitroquinoline- 1-oxide in immunocompetent mice.

Viral elements sense tumorigenic processes: approaching selective cancer therapy.

Viruses can produce viral oncoproteins that drive multiple genetic alterations as the consequence of neoplastic transformation. Viral proteins encoded by onco-related viruses such as polyomavirus SV40 or Epstein-Barr virus are involved in cellular processes resulting in imbalance between proliferation and cell death, knowledge of which continues to be crucial for combating cancer. On the other hand, viruses also generate viral components that, from a cold viral protein, can become a tumor-selective killer by sensing cellular tumorigenic hallmarks.

Apoptin: therapeutic potential of an early sensor of carcinogenic transformation.

The avian virus-derived protein apoptin induces p53-independent apoptosis in a tumor-specific way. Apoptin acts as a multimeric complex and forms superstructures upon binding to DNA. In tumor cells, apoptin is phosphorylated and mainly nuclear, whereas in normal cells it is unphosphorylated, cytoplasmic, and becomes readily neutralized.

Additive cytotoxic effect of apoptin and chemotherapeutic agents paclitaxel and etoposide on human tumour cells.

Gene therapy experiments in animal models have shown that apoptin expression results in tumour regression without any significant side effects. Therefore, apoptin is regarded as a potential anticancer drug for clinical applications. In this study, we analysed whether chemotherapeutic agents combined with apoptin treatment could result in enhanced cytotoxicity in human tumour cell cultures.

Apoptin-induced apoptosis: potential for antitumor therapy.

Cytotoxic anticancer agents often exert their effect by inducing apoptosis. Many tumors, however, are resistant to chemotherapy. This is due to lack of expression of certain genes essential in mediating the apoptotic signal, such as p53, or to over-expression of apoptosis inhibitors, such as bcl-2 or bcr-abl.

Inhibition of hepatocarcinoma by systemic delivery of Apoptin gene via the hepatic asialoglycoprotein receptor.

Specificity is a prerequisite for systemic gene therapy of hepatocarcinoma. In vitro, the tumor-specific viral death effector Apoptin selectively induces apoptosis in malignant hepatic cells. Intratumoral treatment of xenografted subcutaneous hepatomas with Apoptin results in tumor regression.