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Background: To the authors' knowledge, the frequency and clinical impact of errors in the anatomic pathology diagnosis of cancer have been poorly characterized to date., Methods: The authors examined errors in patients who underwent anatomic pathology tests to determine the presence or absence of cancer or precancerous lesions in four hospitals. They analyzed 1 year of retrospective errors detected through a standardized cytologic-histologic correlation process (in which patient same-site cytologic and histologic specimens were compared). Medical record reviews were performed to determine patient outcomes. The authors also measured the institutional frequency, cause (i.e., pathologist interpretation or sampling), and clinical impact of diagnostic cancer errors., Results: The frequency of errors in cancer diagnosis was found to be dependent on the institution (P < 0.001) and ranged from 1.79-9.42% and from 4.87-11.8% of all correlated gynecologic and nongynecologic cases, respectively. A statistically significant association was found between institution and error cause (P < 0.001); the cause of errors resulting from pathologic misinterpretation ranged from 5.0-50.7% (the remainder were due to clinical sampling). A statistically significant association was found between institution and assignment of the clinical impact of error (P < 0.001); the aggregated data demonstrated that for gynecologic and nongynecologic errors, 45% and 39%, respectively, were associated with harm. The pairwise kappa statistic for interobserver agreement on cause of error ranged from 0.118-0.737., Conclusions: Errors in cancer diagnosis are reported to occur in up to 11.8% of all reviewed cytologic-histologic specimen pairs. To the authors' knowledge, little agreement exists regarding whether pathology errors are secondary to misinterpretation or poor clinical sampling of tissues and whether pathology errors result in serious harm., (Copyright 2005 American Cancer Society)

From 1973 to 1982, 189 patients were treated at the Dartmouth-Hitchcock Medical Center for Stage C or D prostatic carcinoma. In eight of these cases (4.2%), there was clinical or pathological evidence for intracranial metastases. The condition of subdural neoplastic spread, not from contiguous bone, was identified in five cases, two of which were suspected before death. Four of these five patients were thrombocytopenic or pancytopenic at the time of the diagnosis. Intraparenchymal brain metastases were identified in six cases. Cerebellar, temporal bone, cavernous sinus, and splenium infiltration by tumor were unusual findings in individual cases. The results of chest x-rays and respiratory status were poor predictors of lung metastases in four of five patients on whom autopsies were performed. This article describes the spectrum of radiographic and pathologic findings of intracranial prostatic carcinoma, and suggests that the likely mechanism of brain metastasis in these cases is by the dural veins and Virchow-Robin spaces.