Inflammatory Breast Cancer Management and Biology

Inflammatory breast cancer (IBC) is a rare and highly aggressive form of breast cancer characterised clinically by rapid onset of erythema, oedema and peau d’orange, and pathologically by extensive dermal lymphatic invasion. Multimodal management—encompassing neoadjuvant chemotherapy, surgery and radiotherapy—remains the cornerstone of therapy, with treatment tailored according to hormone receptor and HER2 status. Advances in molecular profiling have revealed that IBC shares many genomic features with non-IBC yet demonstrates distinct biological hallmarks, including strong E-cadherin expression, high angiogenic activity and a propensity for early dissemination. Recent studies have highlighted the role of the tumour microenvironment in driving IBC aggression: reciprocal interactions with mesenchymal stromal cells and macrophages via cytokines such as interleukin-6 activate JAK/STAT3 signalling, promoting invasion and treatment resistance. Concurrently, genomic analyses indicate variable homologous recombination deficiency and reduced intratumour heterogeneity in triple-negative IBC, suggesting exploitable DNA repair vulnerabilities. Together, these insights underpin emerging strategies that combine targeted inhibitors with immunomodulatory and locoregional approaches to improve outcomes in this formidable disease.

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Inflammatory Breast Cancer Management and Biology publication trend

The graph below shows the total number of articles in inflammatory breast cancer management and biology across all publications each year (not limited to Nature Index journals).

Technical terms

Homologous recombination deficiency (HRD): A tumour phenotype reflecting impaired repair of DNA double-strand breaks via the homologous recombination pathway, conferring sensitivity to certain DNA-damaging agents.

Pathologic complete response (pCR): The absence of residual invasive cancer in breast and axillary specimens following neoadjuvant therapy, used as a surrogate marker for improved long-term survival.

JAK/STAT3 signalling: A key cytokine-driven pathway involving Janus kinases and STAT3 transcription factors that promotes tumour cell proliferation, survival and immune suppression.

Intratumour heterogeneity: The coexistence of distinct clonal populations within a single tumour, which can drive therapeutic resistance and impact prognosis.

Actionable genomic alteration (AGA): A somatic DNA change for which there exists a targeted therapy with established or investigational clinical utility.

References

1. Clinical outcomes of de novo metastatic HER2-positive inflammatory breast cancer. npj Breast Cancer (2023).
2. Mutational landscape of inflammatory breast cancer. Journal of Translational Medicine (2024).
3. TBCRC 039: a phase II study of preoperative ruxolitinib with or without paclitaxel for triple-negative inflammatory breast cancer. Breast Cancer Research (2024).
4. Mesenchymal stem cells and macrophages interact through IL-6 to promote inflammatory breast cancer in pre-clinical models. Oncotarget (2016).
5. Inflammatory breast cancer shows angiogenesis with high endothelial proliferation rate and strong E-cadherin expression. British Journal of Cancer (2003).
6. Molecular biology of breast cancer metastasis Inflammatory breast cancer: clinical syndrome and molecular determinants. Breast Cancer Research (2000).