Abstract

Tumour associated alkaline phosphatase related to the placental isozyme was first described in a patient with small cell cancer of the lung by Fishman et al. [l] and named Regan isozyme. This finding had a significant impact on the future work in oncodevelopmental biology and later on, the Nagao [2] and Kasahara isozymes [3] were discovered in sera from patients with cancer. Recently, it has become clear that trace amounts of placental-like alkaline phosphatases are normally found in several tissues such as testis [4], non-malignant endocervix [5], lung and thymus [6]. The expression of isozymes related to the placental alkaline phosphatases during malignancy may be the result of an enhanced eutopic expression of a gene already transcribed and translated in the tissue of the origin [7]. The appearance of significantly elevated levels of placental-like alkaline phosphatases in healthy nonpregnant individuals is a strong indicator of an underlying malignancy, but also smoking causes a slight increase which may interfere with the clinical evaluation of placental-like alkaline phosphatase as a tumour marker. The increased serum levels of placental-like alkaline phosphatase as well as the elevated levels of CEA in smokers comparing with healthy controls indicate that this phosphatase isozyme is, in fact, derived from the lung tissue [8]. The normal lung may thus express eutopically trace amounts of this phosphatase isozyme, an expression which is enhanced by smoking. The clinical use of PLAP and the PLAP-like isozyme as diagnostic tools is not so widespread as markers like CPA, a-fetoprotein and others, because the frequency of elevated serum samples of phosphatase isozymes is low. The incidence of raised serum levels of placental and placental-like alkaline phos-

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