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Journal of Clinical Oncology, Vol 22, No 2 (January 15), 2004: pp. 381-383 © 2004 American Society of Clinical Oncology. DOI: 10.1200/JCO.2004.99.160
Inflammatory Breast Carcinoma: The Sphinx of Breast Cancer ResearchThe University of Texas M.D. Anderson Cancer Center, Houston, TX To the Editor: We have read with interest the article and the accompanying editorial in the June 15, 2003, issue of the Journal of Clinical Oncology, concerning the differences in biology and prognosis between inflammatory breast cancer (IBC) and noninflammatory locally advanced breast cancer (Non-IBC LABC) [1,2]. Anderson et al [1], using data from the Surveillance, Epidemiology, and End-Results Program, concluded that IBC appears to be a distinct biologic entity because of younger age at diagnosis, poorer tumor grade, and negative estrogen receptor status. The manuscript also indicated that IBC was associated with worse prognosis compared to non-IBC LABC. At the University of Texas M.D. Anderson Cancer Center we have accumulated the largest single-institution experience in the United States in the management of all forms of LABC, including IBC [3]. We welcomed this article that confirms our single institution observations and generates renewed interest for this aggressive form of breast cancer. However, we would like to take this opportunity to address some important diagnostic and therapeutic aspects that will guide the reader in the interpretation of these data and direct future similar investigations. The distinction between classic IBC and non-IBC LABC with secondary inflammatory features is extremely difficult even for the most experienced clinician. To distinguish the two entities it is necessary to document the rapid onset of symptoms and signs based on the classic diagnostic criteria for IBC established by Haagensen [4]. These criteria include diffuse erythema, edema involving more than two-thirds of the breast, peau d'orange, tenderness, induration, warmth, enlargement of the breast, and diffuseness (or absence) of a tumor on palpation. In some cases, the pathological documentation of lymphatic embolization (code EOD 70) is utilized as a contributory but not pathognomonic criterion. The diagnosis of IBC in this series is based entirely on the reporting institution's assessment. Unfortunately, IBC is often misdiagnosed, and the differentiation between primary and secondary IBC is not often made. The cases described as IBC in this series matched the pathologic criteria only in 66% of cases. There is no other information to support the correct distinction of the remaining cases from advanced disease with inflammatory features [5]. The comparison group is represented by a heterogeneous group of conditions, including operable (stage IIIA) and inoperable (stage IIIB) LABC. It is not possible to describe the proportion of patients that belong to the two categories. This appears quite an important, possibly crucial point for the following conclusions. In the analysis of the two groups it is noted that "...IBC were more likely to be axillary lymph-node-negative", and a significant proportion had unknown data on the lymph nodal status. It is obvious that this portends a potentially misleading interpretation of the data considering that probably most of these patients received induction chemotherapy (IC). In fact, the authors suggest that the standard of care of IBC would have been IC followed by surgery, but does not mention that this is also the standard of care for patients with inoperable (stage IIIB) LABC [6], implying that the majority of the cases categorized as non-IBC LABC were most likely operable (stage IIIA) disease. Clearly, the inoperable non-IBC LABC represents the most appropriate comparison group when assessing prognosis. In fact, the use of IC has significantly contributed to change the natural history of locally advanced disease (including IBC), and disparities in diagnostic groups and heterogeneity in systemic and locoregional treatments may, in part, explain the differences in prognosis described between these two groups [3,7-9]. Several other groups have described the clinical, pathologic, and prognostic differences between IBC and non-IBC LABC [10-12]. Others have identified possible biologic markers characteristic of IBC that require validation studies [13,14]. It is our impression that the manuscript from Anderson et al [1] brings a great contribution to the debate, but must be interpreted with caution with regards to some conclusions in consideration of the potential biases not eliminated by the large number of cases. These comments clearly want to support these efforts targeted to better describe the biologic characteristics of IBC from epidemiological data sets. Additionally, we agree on the potential for important epidemiologic and clinical analysis using the data from the Surveillance, Epidemiology, and End-Results Program. Authors' Disclosures of Potential Conflicts of Interest The authors indicated no potential conflicts of interest. REFERENCES
1. Anderson WF, Chu KC, Chang S: Inflammatory breast cancer and noninflammatory locally advanced breast cancer carcinoma: Distinct clinicopathologic entities? J Clin Oncol 21:2254-2259, 2003
2. Harlan LC, Hankey BF: The Surveillance, Epidemiology, and End-Results Program database as a resource for conducting descriptive epidemiologic and clinical studies. J Clin Oncol 21:2232-2233, 2003
3. Cristofanilli M, Byzdar AU, Hortobagyi GN: Update on the management of inflammatory breast cancer. Oncologist 8:141-148, 2003 4. Haagensen C. Diseases of the Breast, Second Edition. Philadelphia, PA: Saunders, 576-584, 1971 5. Piera J, Alonso M, Ojeda M, et al: Locally advanced breast cancer with inflammatory component: A clinical entity with poor prognosis. Radiother Oncol 7:199-204, 1986[Medline] 6. Hortobagyi GN: Progress in systemic chemotherapy of primary breast cancer: An overview. J Natl Cancer Inst Monogr 30:72-79, 2001
7. Kuerer HM, Newman LA, Smith TL, et al: Clinical course of breast cancer patients with complete pathologic primary tumor and axillary lymph node response to doxorubicin-based neoadjuvant chemotherapy. J Clin Oncol 17:460-469, 1999 8. Thoms WW Jr, McNeese MD, Fletcher GH, et al: Multimodality treatment for inflammatory breast cancer. Int J Radiat Oncol Biol Phys 17:739-745, 1989[Medline] 9. Singletary SE, Ames FC, Buzdar AU: Management of inflammatory breast cancer. World J Surg 18:87-92, 1994[CrossRef][Medline] 10. Low JA, Berman AW, Steinberg SM, et al: Long-term follow-up for inflammatory (IBC) and non-inflammatory (NIBC) stage III breast cancer patients treated with combination chemotherapy. Proc Am Soc Clin Oncol 21:63a, 2002 (abstr 251) 11. Aziz SA, Pervez S, Khan S, et al: Case control study of prognostic markers and disease outcome in inflammatory carcinoma breast: A unique clinical experience. Breast J 7:398-404, 2001[CrossRef][Medline] 12. Kleer CG, van Golen KL, Braun T, et al: Persistent E-cadherin expression in inflammatory breast cancer. Mod Pathol 14:458-464, 2001[CrossRef][Medline]
13. Tomlinson JS, Alpaugh ML, Barsky SH: An intact overexpressed E-cadherin/alpha, beta-catenin axis characterizes the lymphovascular emboli of inflammatory breast carcinoma. Cancer Res 61:5231-5241, 2001
14. van Golen KL, Wu ZF, Qiao XT, et al: RhoC GTPase, a novel transforming oncogene for human mammary epithelial cells that partially recapitulates the inflammatory breast cancer phenotype. Cancer Res 60:5832-5838, 2000
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Copyright © 2004 by the American Society of Clinical Oncology, Online ISSN: 1527-7755. Print ISSN: 0732-183X
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