Altered serum AFP levels have been observed concurrent with aberrant growth manifestation in some birth defects (increased in open neural tube defects, and omphalocele and decreased in Down syndrome) and a subset of endodermal-derived malignancies, most frequently hepatoblastoma (HB), hepatocellular carcinoma (HCC), and germ cell tumors (GCTs), some esophageal and pancreatic carcinomas, and also some benign conditions, particularly those associated with liver damage and regeneration. In normal fetuses, AFP binds the hormone estradiol. AFP is found in monomeric as well as in dimeric and trimeric forms, and binds copper, nickel, fatty acids, and bilirubin. A major mammalian oncofetal protein, AFP is a member of the albuminoid gene superfamily, which consists of AFP, serum albumin, vitamin D-binding protein, and alpha-albumin (afamin) on chromosome 4. Characterized as a glycoprotein that is normally produced during gestation by the yolk sac and the liver during fetal life, AFP is highly elevated in the circulation of newborns, and concentration decreases (half-life, 5 days) to 10–20 μg/L during the first 12 months of infant life. īergstrand and Czar first identified α-fetoprotein (AFP) in human fetuses in 1956. In general, elevated levels of these biomarkers have been implicated as playing an important role in different types of cancer, and some play a significant role as prognostic indicators. Tumor markers can be measured in the blood, cerebrospinal fluid, or serous effusions. Traditional cancer biomarkers are biologically measured substances that are expressed by malignant tissues, or generated by the host in response to the tumor and aid the clinician in diagnosis, staging, assessing response to treatment, and detecting disease recurrence. The accurate diagnosis of pediatric solid tumors and the timely recognition of disease recurrence involve the combination of clinical suspicion, imaging techniques, tissue biopsy, and serum tumor markers.
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