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In this paper, we investigate whether, and how, audit effectiveness differentiation between Big 6 and non-Big 6 auditors is influenced by a conflict or convergence of reporting incentives faced by corporate managers and external auditors. In so doing, we incorporate into our analysis the possibility that managers self-select both external auditors and discretionary accruals, using the two stage "treatment effects" model. Our results show that only when managers have incentives to prefer income-increasing accrual choices are Big 6 auditors more effective than non-Big 6 auditors in deterring/monitoring opportunistic earnings management. Contrary to conventional wisdom, we find Big 6 auditors are less effective than non -Big 6 auditors when both managers and auditors have incentives to prefer incomedecreasing accrual choices and thus no conflict of reporting incentives exists between the two parties. The above findings are robust to different proxies for opportunistic earnings management and different proxies for the direction of earnings management incentives.Les conclusions de la présente étude corroborent les données expérimentales de Hirst (1994) selon lesquelles les vérificateurs sont, en général, en mesure d'« établir la distinction entre les explications fournies par les clients dont la motivation à gérer le résultat diffère ». Bien que l'expérience de Hirst soit axée sur la sensibilité de l'ensemble des vérificateurs externes aux motivations des cadres à la gestion opportuniste du résultat, les auteurs arrivent à des résultats qui donnent en outre à penser que la capacité des vérificateurs externes de discriminer les différentes motivations de déclaration des cadres peut différer selon qu'il s'agit de vérificateurs des Six Grands ou de vérificateurs d'autres cabinets. Enfin, à la connaissance des auteurs, cette étude est la première dont le plan de recherche incorpore explicitement le facteur de la sélection personnelle ou de l'endogénéité dans l'analyse des choix discrétionnaires de constatations.

von Recklinghausen neurofibromatosis (NF1) is a common hereditary disorder characterized by neural crest-derived tumors, particularly benign neurofibromas whose malignant transformation to neurofibrosarcomas can be fatal. The NF1 gene has been mapped to a small region of chromosome 17q, but neither the nature of the primary defect nor the mechanisms involved in tumor progression are understood. We have tested whether NF1 might be caused by the inactivation of a tumor suppressor gene on 17q, analogous to that on chromosome 22 in NF2, by searching for deletions of chromosome 17 in NF1-derived tumor specimens. Both neurofibrosarcomas from patients with "atypical" NF and 5 of 6 neurofibrosarcomas from NF1 patients displayed loss of alleles for polymorphic DNA markers on chromosome 17. However, the common region of deletion was on 17p and did not include the NF1 region of 17q. Since no loss of markers on chromosome 17 was observed in any of 30 benign tumors from NF1 patients, the 17p deletions seen in neurofibrosarcomas are probably associated with tumor progression and/or malignancy. This region contains a candidate gene for tumor progression, p53, which has recently been implicated in the progression of a broad array of human cancers. In a preliminary search for p53 aberrations by direct sequencing of polymerase chain reaction-amplified DNA from 7 neurofibrosarcomas, 2 tumors that contained point mutations in exon 4 of the p53 gene were found, suggesting a role for this gene in at least some neurofibrosarcomas. Thus the formation of malignant neurofibrosarcomas may result from several independent genetic events including mutation of the NF1 gene, whose mechanism of tumorigenesis remains uncertain, and subsequent loss of a "tumor suppressor" gene on 17p, most likely p53.

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