Error rates in reporting prostatic core biopsies.

AIMS: To evaluate the false-negative and false-positive error rates both in a screening and a non-screening population. METHODS AND RESULTS: A total of 4192 prostatic biopsies were reported in a 6-year period by 15 consultant histopathologists, two of whom had an interest in uropathology and were deemed to be specialists (J.O. and C.S.). All biopsies were reviewed prior to the multidisciplinary team (MDT) meeting. The overall false-negative rate was 1.7% (screening 2.1%, non-screening 1.5%). The overall false-positive rate was 0.5% (screening 0.9%, non-screening 0.4%). These error rates varied among pathologists, with the false-negative rate ranging from 0% to 9.3%, and the false-positive rate ranging from 0% to 3.8%. CONCLUSION: The false-negative rate was three times greater than the false-positive rate, showing that detection of significant pathology is far greater in the negative biopsies. More errors occurred in the screening population than in the non-screening population. The consultants making the most errors were non-specialists, but the specialists also made false-negative errors, suggesting that just using specialist reporting alone would not have eradicated errors.

Errors in prostate core biopsy diagnosis in an era of specialisation and double reporting.

AIM: To examine the effects of specialist reporting on error rates in prostate core biopsy diagnosis. METHOD: Biopsies were reported by eight specialist uropathologists over 3 years. New cancer diagnoses were double-reported and all biopsies were reviewed for the multidisciplinary team (MDT) meeting. Diagnostic alterations were recorded in supplementary reports and error rates were compared with a decade previously. RESULTS: 2600 biopsies were reported. 64.1% contained adenocarcinoma, a 19.7% increase. The false-positive error rate had reduced from 0.4% to 0.06%. The false-negative error rate had increased from 1.5% to 1.8%, but represented fewer absolute errors due to increased cancer incidence. CONCLUSIONS: Specialisation and double-reporting have reduced false-positive errors. MDT review of negative cores continues to identify a very low number of false-negative errors. Our data represents a 'gold standard' for prostate biopsy diagnostic error rates. Increased use of MRI-targeted biopsies may alter error rates and their future clinical significance.

Ketamine cystitis as a mimic of carcinoma in situ.

AIMS: To describe the histopathological features of a series of patients with ketamine-related cystitis. METHODS AND RESULTS: Seventeen patients with ketamine-related cystitis, who had undergone biopsy, were identified and reviewed. Twelve showed ulceration with significant urothelial atypia. In 10 of these, immunohistochemistry was performed; 9/10 had high p53 immunoreactivity and 7/10 had moderate to high levels of Ki67 reactivity, but all were negative for cytokeratin 20. CONCLUSIONS: Ketamine can lead to reactive urothelial changes that can mimic carcinoma in situ, but the long-term cancer risk remains unknown.

Contemporary prostate biopsy reporting: insights from a survey of clinicians' use of pathology data.

AIM: To determine how clinicians use data in contemporary prostate biopsy reports. METHODS: A survey was circulated to members of the British Association of Urological Surgeons and the British Uro-oncology Group. RESULTS: Responses were received from 114 respondents (88 urologists, 26 oncologists). Ninety-seven (94%) use the number of positive cores from each side and 43 (42%) use the % number of positive cores. When determining the number and percentage of positive cores, 72 (71%) would not differentiate between targeted and non-targeted samples. If multiple Gleason Scores (GS) were included in a report, 77 (78%) would use the worst GS even if present in a core with very little tumour, 12% would use the global GS and 10% the GS in the core most involved by tumour. Fifty-five (55%) either never or rarely used perineural invasion for patient management. CONCLUSIONS: The number of positive cores is an important parameter for patient management but may be difficult to determine in the laboratory due to core fragmentation so the biopsy taker must indicate the number of biopsies obtained. Multiple biopsies taken from a single site are often interpreted by clinicians as separate cores when determining the number of positive cores so pathologists should also report the number of sites positive. Clinicians have a non-uniform approach to the interpretation of multiple GS in prostate biopsy reports so we recommend that pathologists also include a single 'bottom-line' GS for each case to direct the clinician's treatment decision.

Death certification: do consultant pathologists do it better?

The completion of the medical certificate of cause of death is required for registration of a death, and this data helps plan healthcare services for the country. Many audits have shown them to be inaccurately completed by junior doctors, but the authors examined whether advice from consultant pathologists could improve this. Using the Office for National Statistics guidelines, the authors found that only 56% of the certificates were appropriately completed. The planned introduction of medical examiners to England and Wales is aimed at improving this situation, but consultant pathologists will still issue causes of death following postmortems, and it would seem prudent to train pathologists as well.

Competition amongst Eph receptors regulates contact inhibition of locomotion and invasiveness in prostate cancer cells.

Metastatic cancer cells typically fail to halt migration on contact with non-cancer cells. This invasiveness is in contrast to normal mesenchymal cells that retract on contact with another cell. Why cancer cells are defective in contact inhibition of locomotion is not understood. Here, we analyse the dynamics of prostate cancer cell lines co-cultured with fibroblasts, and demonstrate that a combinatorial code of Eph receptor activation dictates whether cell migration will be contact inhibited. The unimpeded migration of metastatic PC-3 cells towards fibroblasts is dependent on activation of EphB3 and EphB4 by ephrin-B2, which we show activates Cdc42 and cell migration. Knockdown of EphB3 and EphB4 restores contact inhibition of locomotion to PC-3 cells. Conversely, homotypic collisions between two cancer cells results in contact inhibition of locomotion, mediated by EphA-Rho-Rho kinase (ROCK) signalling. Thus, the migration of cancer cells can switch from restrained to invasive, depending on the Eph-receptor profile of the cancer cell and the reciprocal ephrin ligands expressed by neighbouring cells.

Lichenoid and granulomatous stomatitis: an entity or a non-specific inflammatory process?

BACKGROUND: The presence of lichenoid or granulomatous inflammation in an oral mucosal biopsy usually suggests a distinct range of diagnostic possibilities. However, the presence of both patterns of inflammation in the same biopsy is uncommon. METHODS: A clinico-pathological study of six patients. RESULTS: All the patients in this study presented with similar mucosal lesions of the upper lip. Microscopically the lesions were characterized by the presence of lichenoid inflammation with concomitant granulomatous inflammation. The lesions were persistent and refractory to treatment with steroid medications, but remained localized and did not appear to herald the onset of systemic inflammatory or neoplastic disease. CONCLUSION: We propose the designation 'lichenoid and granulomatous stomatitis' for the cases described in this study. The clinico-pathological features of a subset of these cases suggest an unusual drug eruption.