Abstract

Inflammatory breast cancer (IBC) is both the least frequent and the most severe form of epithelial breast cancer. The diagnosis is based on clinical inflammatory signs and is reinforced by pathological findings. Significant progress has been made in the management of IBC in the past 20 years. Yet survival among IBC patients is still only one-half that among patients with non-IBC. Identification of the molecular determinants of IBC would probably lead to more specific treatments and to improved survival. In the present article we review recent advances in the molecular pathogenesis of IBC. A more comprehensive view will probably be obtained by pan-genomic analysis of human IBC samples, and by functional in vitro and in vivo assays. These approaches may offer better patient outcome in the near future.

Highlights

  • Inflammatory breast cancer (IBC) is diagnosed on the basis of signs of rapid progression, such as localized or generalized breast induration, redness and edema [1]

  • Most patients have palpable In a series of 80 IBC samples, ERBB2 assessed using invaded axillary lymph nodes, and up to 30% have distant Southern blotting was amplified in 41% of cases, metastases at diagnosis [1]

  • There is disagreement over whether breast cancer with 96 IBC tumors were amplified for ERBB2, compared with secondary inflammatory signs qualifies as IBC

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Summary

Introduction

Inflammatory breast cancer (IBC) is diagnosed on the basis of signs of rapid progression, such as localized or generalized breast induration, redness and edema [1]. The prognosis remains poor, with a 3-year survival rate of only about 40%, compared with 85% among patients with non-IBC [2,3]. These survival data have hardly improved in the past 5 years [3,7]. The small size of diagnostic samples may have hindered past molecular studies Because of their similar treatment, IBC is rarely studied separately from other forms of locally advanced breast cancer (LABC), despite differences in age-specific incidence rates, clinical presentation, histology, hormone receptor status and, prognosis [8,9,10,11]. The present review will focus on clinicopathological and biological knowledge of IBC

Clinicopathological data
The rapid onset of inflammatory signs and the very high
Other genes involved in IBC
Findings
Conclusions
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