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H. Miles Prince, Ricky Johnstone, Commentary on: Biomarkers Provide Clues to Early Events in the Pathogenesis of Breast Implant-Associated Anaplastic Large Cell Lymphoma, Aesthetic Surgery Journal, Volume 36, Issue 7, July/August 2016, Pages 782–783, https://doi.org/10.1093/asj/sjw065
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Breast implant-associated anaplastic large cell lymphoma (BIA-ALCL) is a rare form of T-cell non-Hodgkin lymphoma (NHL) and is being increasingly recognized as a complication of breast implants.1 There has now been close to 200 cases reported in the literature although the actual number of cases is likely to be higher; in the United States alone, the FDA have received 258 medical device reports which include confirmed and unconfirmed reports. The true incidence is likely underestimated due to both lack of awareness of this condition (and hence not submitting seroma fluid for detailed pathological analysis) and under-reporting. Collaborative efforts are underway to determine the true incidence, the relative risk, and etiological factors that may predispose to this lymphoma. For a recent perspective from the FDA, we refer the reader to their website.2
For the non-oncologist, it is important to gain a perspective where this disease fits into other types of lymphoma. Firstly, this is the one of the least common forms of lymphoma involving the breast; 90% are actually B-cell lymphomas comprising the subtypes of marginal zone lymphoma, follicular lymphoma, and diffuse large B-cell lymphoma. Only 9% of breast lymphoma are of T-cell type. T-cell NHL is a rare type of NHL in itself and peripheral T-cell lymphoma (PTCL) is the most common subtype − of which anaplastic large cell lymphoma (ALCL) makes up approximately 15% of all PTCL. The classic type of ALCL is typically a systemic disease which pathologically contains anaplastic appearing large cells that almost universally express the CD30 antigen on their surface. Systemic ALCL is further subcategorized according to the expression or absence of the ALK protein; ALK-expressing lymphomas have a superior outcome over ALK-negative lesions. Another important type of ALCL is the cutaneous type; this lesion is considered part of a spectrum of cutaneous lymphoproliferative disorders (LPD) that express CD30 and range from the indolent relapsing/regressing lesions of lymphomatoid papulosis (LyP) to the potentially more aggressive primary cutaneous ALCL (pcALCL). The latter, although at the aggressive end of the cutaneous CD30+ LPD spectrum, has a much better outcome over its systemic counterparts. Of note, the pcALCL lesions (like BIA-ALCL) virtually never express the ALK protein.