Breast cancer pathology

Breast cancer pathology

Pathology (October 2005) 37(5), pp. 339–340 EDITORIAL Breast cancer pathology C. SOON LEE Department of Anatomical Pathology, Royal Prince Alfred Ho...

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Pathology (October 2005) 37(5), pp. 339–340

EDITORIAL

Breast cancer pathology C. SOON LEE Department of Anatomical Pathology, Royal Prince Alfred Hospital, Camperdown; and Department of Pathology, University of Sydney, New South Wales, Australia

In recent times, the treatment of breast cancer has been significantly improved due to major advances in our knowledge of its tumour biology. This has included a better understanding of risk factors for breast cancer development, the molecular mechanisms underpinning breast cancer pathogenesis and the histopathology of precursor lesions. Elucidation of cell signalling pathways such as the Wnt pathway1 has improved our understanding of the stromal epithelial interaction in some types of breast cancers. Recent clarification of the concept of flat epithelial atypia has contributed further to our understanding of the early development of ductal carcinoma in situ (DCIS) and the progression model of breast carcinogenesis.2 Several new genes and molecules have been found to be important in breast carcinogenesis and some appear to be important in predicting prognosis in breast cancer.3–8 All of these major advances in our knowledge of mechanisms involved in tumour progression have assisted us in the identification of potential prognostic markers in patients with breast cancer.9 In addition, there is an indication that expression microarray analysis may be important for patient-specific profiling and individualised treatment of breast cancer patients.10 Despite these recent advances, accurate histopathological diagnosis of breast cancer and assessment of various important factors that predict prognosis and guide further management remain critical for patients. This is essential not only for the multidisciplinary management of breast cancer patients but because it underpins many of the aspects of breast cancer basic scientific research. Consequently, the quantity and complexity of detail required in pathology reports of breast cancer have increased significantly in recent times. It is probably not coincidental that this has occurred following the introduction of mammographic screening programs over the years. The purpose of the exercise is to record any information that is potentially relevant in determining the patient’s prognosis and most appropriate management. Details of histological subtype, tumour size, tumour grade, presence of lymphovascular invasion, clearance margins, axillary lymph node status, hormone receptor and c-erbB-2 receptor status are now expected in any pathology report of breast cancer. The need for improvement in the detail of reporting has been previously highlighted in a number of large surveys in Australia.11–13 Some of these studies have suggested that the use of synoptic formatted pathology reports may improve the quality of pathology reports.11–13 In this issue of Pathology, Harvey and

colleagues have examined the impact of these recommendations on the quality of recording of important parameters in pathology breast cancer reports; the changes in pathology reporting from 1989 to 1999; and the changes in prognostic factors for breast cancer following the introduction of mammographic screening programs in 1989.14 They found that there had been significant improvements in the quality of pathology reporting and in the recording of important prognostic variables during this time period.14 The paper also highlighted differences in the reporting of DCIS between Australian States where information on this variable, such as its size, is documented less frequently.15 The benefit of synoptic reporting in facilitating more complete recording of data in the pathology report also extends to more rapid and simple transfer of this information to clinical and research databases. However, as Harvey and colleagues aptly conclude, it is unwise to exploit information from such databases without input from pathologists who have expertise in breast pathology as the histopathological complexity of many of these cases can result in misinterpretation of data. This applies equally to many other areas of medicine where cooperation between clinicians and pathologists is critical to the multidisciplinary management of patients.16 Address for correspondence: Professor C. S. Lee, Department of Anatomical Pathology, Royal Prince Alfred Hospital, Missenden Road, Camperdown, NSW 2050, Australia. E-mail: [email protected]. gov.au

References 1. Karim RZ, Tse GMK, Putti TC, Scolyer RA, Lee CS. The significance of the Wnt pathway in the pathology of human cancers. Pathology 2004; 36: 120–8. 2. Ho BCS, Tan PH. Flat epithelial atypia: concepts and controversies of an intraductal lesion of the breast. Pathology 2005; 37: 105–11. 3. Son BH, Chois JS, Lee JH. Prognostic values of KAI1 and surviving expression in an infiltrating ductal carcinoma of the breast. Pathology 2005; 37: 131–6. 4. Mestdagt M, Polette M, Buttice G, et al. Transactivation of MCP1/CCL2 by beta-catenin/TCF-4 in human breast cancer cells. Int J Cancer 2005; Jul 7: (Epub ahead of print). 5. Emberley ED, Niu Y, Curtis L, et al. The S100A7-c-Jun activation domain binding protein 1 pathway enhances prosurvival pathways in breast cancer. Cancer Res 2005; 65: 5696–702. 6. Venter DJ, Ramus SJ, Hammet FM, et al. Complex CGH alterations on chromosome arm 8p at candidate tumor suppressor gene loci in breast cancer cell lines. Cancer Genet Cytogenet 2005; 160: 134–40. 7. Basu A, Rowan BG. Genes related to estrogen action in reproduction and breast cancer. Front Biosci 2005; 10: 2346–72. 8. Rae JM, Johnson MD, Scheys JO, Cordero KE, Larios JM, Lippman ME. GREB1 is a critical regulator of hormone dependent breast cancer growth. Breast Cancer Res Treat 2005; 92: 141–9.

ISSN 0031-3025 printed/ISSN 1465-3931 # 2005 Royal College of Pathologists of Australasia DOI: 10.1080/00313020500254602

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9. Lerwill MF. Current practical applications of diagnostic immunohistochemistry in breast pathology. Am J Surg Pathol 2004; 28: 1076–91. 10. Murphy N, Millar E, Lee CS. Gene expression profiling in breast cancer: towards individualising patient management. Pathology 2005; 37: 271–7. 11. Harvey JM, Sterrett GF, Parsons RW, et al. Breast cancer in Western Australia in 1989: IV. Summary of histopathological assessment in 655 cases. Pathology 1995; 27: 12–7. 12. Bilous M, McCredie M, Porter L. Adequacy of histopathology reports for breast cancer in New South Wales. Pathology 1995; 27: 306–11. 13. Kricker A, Armstrong B, Smith C, et al. An audit of breast cancer pathology reporting in Australia in 1995. Br J Cancer 1999; 80: 563–8.

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14. Harvey JM, Sterrett GF, McEvoy S, et al. Pathology reporting of breast cancer: trends in 1989–1999, following the introduction of mammographic screening in Western Australia. Pathology 2005; 37: 341–6. 15. Provenzano E, Hopper JL, Giles GG, Marr G, Venter DJ, Armes JE. Histological markers that predict clinical recurrence in ductal carcinoma in situ of the breast: an Australian population-based study. Pathology 2004; 36: 221–9. 16. Thompson JF, Scolyer RA. Cooperation between surgical oncologists and pathologists: a key element of multidisciplinary care for patients with cancer. Pathology 2004; 36: 496–503.