ODERN concepts of cancer immunology originated from the classic observations by Jensen, Loeb, Tyzzer, and Little in the early years of the 20th century of the rejection of transplanted allogeneic tumors and the acceptance of syngeneic tumors. 1 Despite this law of transplantation, there are several clinical examples of the accidental transplantation of a malignant tumor or tumor cells into a healthy recipient. [2][3][4][5] We describe the accidental transplantation of a malignant sarcoma from a patient to a surgeon. Using molecular methods, we showed that the sarcomas in the unrelated patient and surgeon were genetically identical. CASE REPORTA 32-year-old man underwent emergency surgery to remove a malignant fibrous histiocytoma from his abdomen and died shortly thereafter of postoperative complications. During the operation the 53-year-old surgeon injured the palm of his left hand while placing a drain. The lesion was immediately disinfected and dressed. Five months later, the surgeon consulted a hand specialist because of a hard, circumscribed, tumor-like swelling, 3.0 cm (1.2 in.) in diameter, in his left palm at the base of the middle finger, where he had been injured during the operation. An extensive examination, including laboratory tests, did not reveal any signs of immune deficiency. The tumor was completely excised. Histologic examination revealed that it was a malignant fibrous histiocytoma. Two years later, the surgeon's condition was good, and there was no evidence of recurrence or metastasis of the tumor.The pathologist who investigated both the patient's tumor and the surgeon's tumor raised the question whether the tumors were identical.

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T cell clones isolated from class II MHC-disparate MLR combinations, and specific for I-Ak and I-Ek molecules, respectively, are shown to induce acute lethal graft-vs-host disease in unirradiated recipients. Cytolytic and noncytolytic clones are equally efficient in this respect. The lethal disease is dependent on recognition of the stimulatory class II molecules in the host. The clones home to lungs and liver, and become activated in these organs as demonstrated by an in vivo thymidine incorporation assay. After activation, a severe vascular leak syndrome develops causing death of the recipients within 5 d after the injection of 5 x 10(6) to 10(7) cloned cells. The disease develops without the participation of secondary host-derived inflammatory mechanisms, such as mast cell degranulation, complement activation, and the release of prostaglandins, oxygen radicals, or proteolytic enzymes. The results raise the possibility that Th cells can directly influence vascular permeability, and control, thereby, the acute inflammatory reaction of blood vessels.