CytopathologyVolume 21, Issue 4 p. 273-275 Diagnosis of alveolar rhabdomyosarcoma in effusion cytology: a diagnostic pitfall S. A. Thiryayi, S. A. Thiryayi Manchester Cytology CentreSearch for more papers by this authorD. N. Rana, D. N. Rana Manchester Cytology CentreSearch for more papers by this authorJ. Roulson, J. Roulson Department of HistopathologySearch for more papers by this authorP. Crosbie, P. Crosbie Department of Respiratory Medicine, Manchester Royal InfirmarySearch for more papers by this authorM. Woodhead, M. Woodhead Department of Respiratory Medicine, Manchester Royal InfirmarySearch for more papers by this authorB. P. Eyden, B. P. Eyden Department of Histopathology, Christie NHS Foundation Trust, Manchester, UKSearch for more papers by this authorP. S. Hasleton, P. S. Hasleton Department of HistopathologySearch for more papers by this author S. A. Thiryayi, S. A. Thiryayi Manchester Cytology CentreSearch for more papers by this authorD. N. Rana, D. N. Rana Manchester Cytology CentreSearch for more papers by this authorJ. Roulson, J. Roulson Department of HistopathologySearch for more papers by this authorP. Crosbie, P. Crosbie Department of Respiratory Medicine, Manchester Royal InfirmarySearch for more papers by this authorM. Woodhead, M. Woodhead Department of Respiratory Medicine, Manchester Royal InfirmarySearch for more papers by this authorB. P. Eyden, B. P. Eyden Department of Histopathology, Christie NHS Foundation Trust, Manchester, UKSearch for more papers by this authorP. S. Hasleton, P. S. Hasleton Department of HistopathologySearch for more papers by this author First published: 07 July 2010 https://doi.org/10.1111/j.1365-2303.2009.00700.xCitations: 11 Sakinah A. Thiryayi, Manchester Cytology Centre, Manchester Royal Infirmary, Oxford Road, Manchester M13 9WL, UKTel.: +44 161 276 5111; Fax: +44 161 276 5149;E-mail: sakinah.a.t@hotmail.co.uk Read the full textAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat Citing Literature Volume21, Issue4August 2010Pages 273-275 RelatedInformation

Prostate cancer (CaP) cells preferentially metastasise to the bone marrow, a microenvironment that plays a substantial role in the sustenance and progression of the CaP tumour. Here we use a combination of FTIR microspectroscopy and histological stains to increase molecular specificity and probe the biochemistry of metastatic CaP cells in bone marrow tissue derived from a limited source of paraffin-embedded biopsies of different patients. This provides distinction between the following dominant metabolic processes driving the proliferation of the metastatic cells in each of these biopsies: glycerophospholipid synthesis from triacylglyceride, available from surrounding adipocytes, in specimen 1, through significantly high (p ≤ 0.05) carbohydrate (8.23 ± 1.44 cm−1), phosphate (6.13 ± 1.5 cm−1) and lipid hydrocarbon (24.14 ± 5.9 cm−1) signals compared with the organ-confined CaP control (OC CaP), together with vacuolation of cell cytoplasm; glycolipid synthesis in specimen 2, through significantly high (p ≤ 0.05) carbohydrate (5.51 ± 0.04 cm−1) and high lipid hydrocarbon (17.91 ± 2.3 cm−1) compared with OC CaP, together with positive diastase-digested periodic acid Schiff staining in the majority of metastatic CaP cells; glycolysis in specimen 3, though significantly high (p ≤ 0.05) carbohydrate (8.86 ± 1.78 cm−1) and significantly lower (p ≤ 0.05) lipid hydrocarbon (11.67 ± 0.4 cm−1) than OC CaP, together with negative diastase-digested periodic acid Schiff staining in the majority of metastatic CaP cells. Detailed understanding of the biochemistry underpinning the proliferation of tumour cells at metastatic sites may help towards refining chemotherapeutic treatment.

The autopsy is in decline, despite the fact that accurate mortality statistics remain essential for public health and health service planning. The falling autopsy rate combined with the Coroners Review and Human Tissue Act have contributed to this decline, and to a falling use of autopsy histology, with potential impact on clinical audit and mortality statistics. At a time when the need for reform and improvement in the death certification process is so prominent, we felt it important to assess the value of the autopsy and autopsy histology. We carried out a meta‐analysis of discrepancies between clinical and autopsy diagnoses and the contribution of autopsy histology. There has been little improvement in the overall rate of discrepancies between the 1960s and the present. At least a third of death certificates are likely to be incorrect and 50% of autopsies produce findings unsuspected before death. In addition, the cases which give rise to discrepancies cannot be identified prior to autopsy. Over 20% of clinically unexpected autopsy findings, including 5% of major findings, can be correctly diagnosed only by histological examination. Although the autopsy and particularly autopsy histology are being undermined, they are still the most accurate method of determining the cause of death and auditing accuracy of clinical diagnosis, diagnostic tests and death certification.