title: Emerging Roles of SPINK1 in Cancer.
abstract: BACKGROUND
  Tumor-associated trypsin inhibitor (TATI) was originally isolated from the urine of a patient with ovarian cancer. It was later shown to be produced by many other tumors and several normal tissues. It had earlier been isolated from the pancreas and was hence called pancreatic secretory trypsin inhibitor (PSTI). It belongs to a family of protease inhibitors presently called serine peptidase inhibitor Kazal type (SPINK). In the SPINK family TATI/PSTI is SPINK1, which is the name used in this review.
  
  
  BACKGROUND
  In addition to being a protease inhibitor, SPINK1 also acts as an acute-phase reactant and a growth factor. Furthermore, it has been shown to modulate apoptosis. Overexpression of SPINK1 predicts an unfavorable outcome in several cancers and determination of SPINK1 in serum can be used to identify patients at increased risk of aggressive disease. Thus serum SPINK1 can be used as a prognostic tumor marker. Because SPINK1 acts as a growth factor and an inhibitor of apoptosis in some cancers, it has also been suggested that it can be a therapeutic target in cancer. However, because SPINK1 is the major physiological inhibitor of trypsin, inhibition of SPINK1 may increase the risk of pancreatitis.
  
  
  CONCLUSIONS
  Taking into account the many functions of SPINK1, assessing the role of SPINK1 in cancer has several potentially important clinical applications ranging from a biomarker to a potential new target for cancer therapy.
authors.affiliation: Department of Clinical Chemistry, University of Helsinki, Finland.
authors.forename: Kati
authors.initials: K
authors.lastname: Räsänen
authors.affiliation: Department of Clinical Chemistry, University of Helsinki, Finland, Laboratory Division (HUSLAB), Helsinki University Central Hospital, Helsinki, Finland.
authors.forename: Outi
authors.initials: O
authors.lastname: Itkonen
authors.affiliation: Department of Clinical Chemistry, University of Helsinki, Finland.
authors.forename: Hannu
authors.initials: H
authors.lastname: Koistinen
authors.affiliation: Department of Clinical Chemistry, University of Helsinki, Finland, Laboratory Division (HUSLAB), Helsinki University Central Hospital, Helsinki, Finland. ulf-hakan.stenman@helsinki.fi.
authors.forename: Ulf-Håkan
authors.initials: UH
authors.lastname: Stenman
mesh_terms: D001943:Breast Neoplasms / Q000235:genetics / Q000503:physiopathology; D002352:Carrier Proteins / Q000235:genetics* / Q000378:metabolism*; D005260:Female; D006801:Humans; D008297:Male; D009369:Neoplasms / Q000235:genetics* / Q000503:physiopathology*; D010051:Ovarian Neoplasms / Q000235:genetics / Q000503:physiopathology; D010190:Pancreatic Neoplasms / Q000235:genetics / Q000503:physiopathology; D011471:Prostatic Neoplasms / Q000235:genetics / Q000503:physiopathology; D014359:Trypsin Inhibitor, Kazal Pancreatic
chemical_list: D002352:Carrier Proteins; C486642:SPINK1 protein, human; D014359:Trypsin Inhibitor, Kazal Pancreatic