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BackgroundRecent reports have indicated that vascularized lymph node transfer (VLNT) may improve the impaired immunity in lymphedema but there has been no report concerning anti‐cancer immunity. In the early tumor immune response, dendritic cells (DCs) participate in tumor recognition and antigen presentation in local lymphatics. Here, we investigated the impact of VLNT on DC dynamics against cancer in mouse models.MethodsForty‐seven 8‐week‐old C57BL/6 N male mice were divided into three surgical groups: a VLNT model in which a vascularized inguinal lymph node (LN) flap was transferred into the ipsilateral fossa after a popliteal LN was removed; a LN dissection (LND) model in which the popliteal LN was dissected; and a control model in which a skin incision was made at the popliteal fossa and an ipsilateral inguinal LN was removed. Postoperative lymphatic flows were observed by indocyanine green lymphography and B16‐F10‐luc2 mouse melanoma were implanted into the ipsilateral footpad. The proportion of DCs in the transplanted nodes was measured by CD11c immunohistochemistry using digital imaging analysis 4 days after cancer implantation. Metastases to the lungs and LNs were quantitatively evaluated by luciferase assay 4 weeks after cancer implantation.ResultsAfter VLNT, lymphatic reconnection was observed in 59.2% of mice. The proportion of DCs was significantly higher in the VLNT group with lymphatic reconnection (8.6% ± 1.0%) than in the naïve LN (4.3% ± 0.4%) (p < .001). The tumor burden of lung metastases was significantly less in the VLNT group with lymphatic reconnection compared with the LND group (p = .049).ConclusionsMetastasis decreased in mice with reconnected lymphatics after VLNT. A possible explanation was that lymphatic restoration may have contributed to the tumor immune response by allowing DC migration to LNs.

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Malignant melanoma (MM), a well-known skin cancer with a poor prognosis, has various clinical manifestations, but vesiculobullous lesions have seldom been reported. We report a case of MM forming amelanotic vesicles at the site of an in-transit metastasis, and we also review the published reports on vesiculobullous MM. Our patient was an 87-year-old man with a history of a treated plantar MM 2 years previously, who had recurrence of the MM and development of an in-transit metastasis in his lower leg. Histopathological findings revealed vesicles caused by infiltration of the tumour. A review of the English literature revealed nine cases with various clinical presentations of the vesicles or blisters. For patients with MM with vesiculobullous lesions, an accurate medical history and examination of biopsies are of primary importance for management.