Johannes Andreas Grib Fibiger

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Johannes Andreas Grib Fibiger
Fibiger won a Nobel Prize in 1926
Fibiger won a Nobel Prize in 1926
Born April 23, 1867
Silkeborg
Died January 30, 1928
Copenhagen
Nationality Danish
Known for cancer
Notable awards 1926 Nobel Prize in Physiology or Medicine

Johannes Andreas Grib Fibiger (April 23, 1867 SilkeborgJanuary 30, 1928 Copenhagen) was a Danish scientist who won the 1926 Nobel Prize in Physiology or Medicine. Fibiger had claimed to find an organism he called Spiroptera carcinoma that caused cancer in mice and rats. He received Nobel prize for this discovery. Later, it was shown that this specific organism was not the primary cause of the tumors. Moreover, Katsusaburo Yamagiwa, only two years later in 1915 has successfully induced squamous cell carcinoma by painting crude coal tar on the inner surface of rabbits' ears. Yamagiwa's work has became the primary basis for this line of research.[1] Because of this, some consider Fibiger's Nobel Prize to be undeserved particularly because Yamagiwa did not receive the prize.[2] But others credit Fibiger with showing that external stimuli can induce cancer and proving the correlation by experimental method. Encycropedia Britanica's guide to Nobel Prizes in cancer research mention Yamagiwa's work as milestone without mentioning Fibiger. [3]

While studying tuberculosis in lab rats, Fibiger found tumors in some of his rats. He discovered that these tumors were associated with parasitic nematode worms that had been living in some cockroaches that the rats had eaten. He thought that these organisms may have been the cause of the cancer. In fact, the rats had been suffering from a vitamin A deficiency and this was the main cause of the tumors. The parasites had merely caused the tissue irritation that drove the damaged cells into cancer; any tissue irritation could have induced the tumors.

Although the specific link between the parasites and cancer was later known to be relatively unimportant, it was discovered later that tissue damage was a cause of cancer. This was an important advance in cancer research.

One of his experiments from 1898 is by some regarded as the first controlled clinical trial.[4]

Fibiger became a medical doctor in 1890 and studied under Robert Koch and Emil Adolf von Behring in Berlin. He received his research doctorate from the University of Copenhagen in 1895 and became a professor there.

  1. ^ Yamagiwa, then Director of the Department of Pathology at Tokyo Im perial University Medical School, had theorized that repetition or continuation of chronic irritation caused precan cerous alterations in previously normal epithelium. If the irritant continued its action, carcinoma could result. These data, publicly presented at a special meeting of the Tokyo Medical Society and reprinted below, focused attention on chemical carcinogenesis. Further more, his experimental method pro vided researchers with a means of pro ducing cancer in the laboratory and an ticipated investigation of specific carci nogenic agents and the precise way in which they acted. Within a decade, Keller and associates extracted a highly potent carcinogenic ‘¿�hydrocarbonfrom coal tar. Dr. Yamagiwa had begun a new era in cancer research.[1]
  2. ^ “Katsusaburo Yamagiwa’s Nobel candidacy: Physiology or medicine in the 1920s” by James R. Bartholomew (25 pp) [7] explores the candidacy of Yamagiwa, who had developed the world’s first efficient method for producing cancer artificially in the laboratory by swabbing coal tar on rabbits’ ears, which had stimulated activity among cancer researchers worldwide. Johannes Fibiger of Denmark, who discovered how to use parasites to cause cancer in rats two years before Yamagiwa’s achievement, received the prize, probably because nominations were often greatly influenced by acquaintanceship, geography, and the marginalization that distance from other centers imposed on the Japanese.[2]
  3. ^ [3]
  4. ^ A. Hrobjartsson, P. C. Gotzsche & C. Gluud (October 1998). "The controlled clinical trial turns 100 years: Fibiger's trial of serum treatment of diphtheria". BMJ 317 (7167): 1243–1245. PMID 9794873. 

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