Fibiger fed cockroaches carrying the parasite Spiroptera (now called Gongylonema) to rats and observed tumors forming in their stomachs. At that time the cause of cancer was unknown, so linking it to infection was revolutionary. His papers introduced the idea that a parasite could trigger carcinogenesis and shook the medical world. This concept paved the way for later studies on Helicobacter pylori and virus-related cancers. However, later scientists found that many of the tumors were benign growths caused by vitamin-A deficiency, not true cancer. The story shows how science evolves and why verification and reproducibility are vital.

Between 1913 and 1915 Johannes Fibiger infected rats with Gongylonema neoplasticum and reported squamous-cell-like gastric lesions that he interpreted as malignant. He coined the term “Spiroptera carcinoma,” presenting it as direct evidence that a parasite could induce cancer. In the context of flourishing bacteriology, placing cancer research within an infectious-disease framework was highly influential, and the Nobel Committee judged that this discovery opened a new frontier in medicine, awarding him the 1926 prize. Subsequent work in the 1930s, however, showed that vitamin-A deficiency diets and chronic inflammation were major contributors, and truly malignant tumors were rare. Nonetheless, Fibiger’s infectious-etiology viewpoint is regarded as a starting point for today’s research on virus-, bacterium-, and parasite-related cancers.

In a series of 1913 papers, Fibiger dissected rats infected with Gongylonema neoplasticum and, using paraffin sections, described erosive epithelial proliferations that resembled squamous-cell carcinoma with keratin pearls. Tumor incidence rose under high-fat, vitamin-A-deficient diets and decreased when parasite ovaries were removed, leading him to postulate a parasite-derived toxin acting as a tumor promoter. Subsequent models by Cloudman, Bullock, and others concluded that most lesions were hyperplasias or keratinizing ulcers, with bona-fide malignancy rare, yet the etiological scheme anticipated Helicobacter-gastric cancer and HBV-hepatocarcinoma research. Modern reinterpretations frame the system as a multifactorial model in which inflammatory cytokine networks, diminished retinoic acid signaling, and parasite antigens driving a Th2 bias synergistically increase oncogenic risk.