William Coley, a young surgeon at New York Memorial Hospital, was traumatized by the loss of his first patient to bone cancer in 1891. He was unable to save this young patient and she succumbed to her Sarcoma within 3 months of surgery. He searched the hospital archive to learn more about Sarcoma and discovered the case of a patient with a large sarcoma who had undergone five unsuccessful surgeries over a 3 year period. This case had been determined to be hopeless. After the last of these operations, the patient became very ill from an erysipelas infection.
Coley was astonished to read that after the fever broke and the patient had recovered, the tumour had vanished. Seven years later, the patient was still alive and well. Coley concluded that whatever had caused the fever must also have destroyed the cancer. Coley searched for and found this patient still in excellent health. Coley reasoned that if a chance infection could make tumours vanish, then a purposefully induced infection could do the same.
The hypothesis was tested by infecting his next 10 patients with Streptococcus pyogenes to cause Erysipelas. Some of the patients were difficult to infect, some died, and some had a strong reaction and their disease regressed. Coley switched to deactivated S. pyogenes to avoid the mortality observed with the live strain. Afterxperimentation with various formulations, a combination of S pyogenes and Serratia marcescens was decided upon and became known as Coley’s Toxin.
The preferred method of delivery was injection of the toxin directly into the primary tumour or metastases in increasing doses to avoid immune tolerance. Fever response in the patient was essential to imitate a naturally occurring infection and the body’s natural response. Though Coley met with success, this therapy was abandoned as chemotherapy became more popular.
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Peptides of tetraspanin oncoprotein CD151 trigger active immunity against primary tumour and experimental lung metastasis