Commentary
See article on page 259
Genes means pancreatitis
| The first 150 words of the full text of this article appear below. |
Identifying the molecular mechanisms responsible for acute and chronic pancreatitis in humans is one of the most difficult problems in modern science. Major obstacles include the inaccessibility of the human pancreas to observation, the unpredictability of disease onset, the non-specific nature of abdominal pain early in the course of acute pancreatitis, an inability to biopsy the pancreas safely, difficulty in distinguishing initiating events from the concomitant inflammatory response, and the obvious problems of investigating a tissue that self-destructs during the disease process. Even fundamental questions as to whether pancreatitis begins in the acinar cell or through pathology related to the pancreatic ducts continue to be debated.1 2 Animal models also fail to provide critical insights, partly because of the artificial methods used to induce pancreatitis.3-5
The discovery of the mutations in the cationic trypsinogen gene
responsible for hereditary forms of pancreatitis in American and
European kindreds6 7
provided tremendous insights into the
Relevant Article
- Mutations in exons 2 and 3 of the cationic trypsinogen gene in Japanese families with hereditary pancreatitis
- I Nishimori, M Kamakura, K Fujikawa-Adachi, M Morita, S Onishi, K Yokoyama, I Makino, H Ishida, M Yamamoto, S Watanabe, and M Ogawa
Gut 1999 44: 259-263.[Abstract] [Full Text] [PDF]
This article has been cited by other articles:
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Lerch, M. M., Neoptolemos, J. P.
(1999). RESPONSE: Re: Maternal Inheritance Pattern of Hereditary Pancreatitis in Patients With Pancreatic Carcinoma. JNCI J Natl Cancer Inst
91: 1590a-1591a
[Full Text] -
WHITCOMB, D C
(1999). Hereditary pancreatitis: new insights into acute and chronic pancreatitis. Gut
45: 317-322
[Full Text]
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