Breast implant-associated anaplastic large cell lymphoma (BI-ALCL) is a rare T-cell lymphoma that arises around breast implants. Most patients manifest with periprosthetic effusion, whereas a subset of patients develops a tumor mass or lymph node involvement (LNI). The aim of this study is to describe the pathologic features of lymph nodes from patients with BI-ALCL and assess the prognostic impact of LNI. Clinical findings and histopathologic features of lymph nodes were assessed in 70 patients with BI-ALCL. LNI was defined by the histologic demonstration of ALCL in lymph nodes. Fourteen (20%) patients with BI-ALCL had LNI, all lymph nodes involved were regional, the most frequent were axillary (93%). The pattern of involvement was sinusoidal in 13 (92.9%) cases, often associated with perifollicular, interfollicular, and diffuse patterns. Two cases had Hodgkin-like patterns. The 5-year overall survival was 75% for patients with LNI and 97.9% for patients without LNI at presentation (P=0.003). Six of 49 (12.2%) of patients with tumor confined by the capsule had LNI, compared with LNI in 8/21 (38%) patients with tumor beyond the capsule. Most patients with LNI achieved complete remission after various therapeutic approaches. Two of 14 (14.3%) patients with LNI died of disease compared with 0/56 (0%) patients without LNI. Twenty percent of patients with BI-ALCL had LNI by lymphoma, most often in a sinusoidal pattern. We conclude that BI-ALCL beyond capsule is associated with a higher risk of LNI. Involvement of lymph nodes was associated with decreased overall survival. Misdiagnosis as Hodgkin lymphoma is a pitfall.

Little is known about matrix biochemistry and cell differentiation patterns in chondrogenic neoplasms. This is the first description of the focal expression of collagen type X by neoplastic chondrocytes in situ and its incorporation into the extracellular matrix of cartilaginous tumors. This shows that neoplastic chondrocytes have the potential to undergo the full program of cell differentiation, including hypertrophy, comparable to their physiological counterparts in the growth plate. However, only in benign osteochondromas was a zonal expression of type X collagen found similar to that observed in the growth plate, where the cells immediately above the ossification frontier are selectively positive for type X collagen. In enchondromas and chondrosarcomas, the expression was randomly distributed within the tumors. Surprisingly, in less differentiated chondrosarcomas with spindle-shaped cells and non-cartilaginous extracellular matrix, exceptional expression of collagen type X was observed, which indicates potential uncoupling of collagen type X expression from the differentiated chondrocytic phenotype in neoplastic chondrocytes in vivo.

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