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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
 
 
 
 

Excretion of a tumor-associated trypsin inhibitor (TATI) in urine of patients with gynecological malignancy.

In earlier studies we reported the finding of a tumor-associated peptide that also occurred at high concentrations in early amniotic fluid. Determination of the N-terminal sequence of this peptide revealed that it is closely related or identical to the pancreatic secretory trypsin inhibitor. Therefore, the peptide is called tumor-associated trypsin inhibitor (TATI). The concentration of TATI was determined by radioimmunoassay in the urine of 148 patients with various forms of gynecologic malignancy and in a reference population consisting of 98 patients with non-malignant gynecologic disease, and also in 40 patients with severe infections or inflammatory disease. In the reference population, the median urinary concentration of TATI was 22 micrograms/g creatinine and the central 95% reference interval was 7-50 micrograms/g creatinine. Elevated urinary levels were observed in 53% of all patients with gynecologic cancer, in 63% of those with active disease and 26% of those in clinical remission. The highest urinary TATI level (11,000 micrograms/g creatinine) was over 200 times the upper limit of the reference range. Patients with cervical cancer had the highest frequency of elevated values. Increased excretion of TATI was also observed in patients with severe bronchopulmonary infections and pancreatitis. Although increased excretion of TATI is not cancer-specific, the distinction by elevated levels of TATI between malignant and nonmalignant gynecologic disease is better than by most other putative tumor markers, and the increased excretion of TATI in patients with active disease can be important for the understanding of tumor biology.[1]

References

  1. Excretion of a tumor-associated trypsin inhibitor (TATI) in urine of patients with gynecological malignancy. Huhtala, M.L., Kahanpää, K., Seppälä, M., Halila, H., Stenman, U.H. Int. J. Cancer (1983) [Pubmed]
 
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