As yet, only a few studies (Table 1) focused on the fate of p53AAb in the follow-up of tumor patients. In 1994, Angelopoulou et al.  monitored five patients with ovarian cancer and one with breast cancer and showed that temporal changes of p53AAb correlated with disease progression or regression. The authors concluded that this immunization represents a continous process driven by the tumor and is not a temporally isolated event. In a later report on another breast cancer patient, reappearance of p53AAb was observed two years after initial therapy which predated the clinical diagnosis of a relapse by three months (Lu-bin et al. as cited in ). With 17 initially seropositive head and neck cancer patients, 5/8 recurrences were accompanied by an increase in p53AAb levels ; levels of the three others remained unchanged as in six of nine patients without a relapse. The remaining three patients showed an increase in p53AAb without indications of a recurrence (32 months into follow-up). In gastric cancer, 14/15 patients with preoperative p53AAb remained seropositive after surgery; all patients died within 2-12 months . Remarkably, the only patient who was seronegative after tumor resection was still alive 17 months later. All 14 patients with persisting antibodies were diagnosed with prognosti-cally poor tumor stage III/IV - 30% of the patients from the respective seronegative group, however, survived. For lung cancer patients, it was shown that p53AAb present at the time of carcinoma diagnosis may persist during disease progression . p53AAb levels in one patient with tracheal chondromata increased over a period of 2 years concomitantly with tumor development until clinical lung cancer diagnosis; therapeutical intervention by chemotherapy was paralleled by a sharp decrease in p53AAb . The usefulness of p53AAb in trailing therapy was investigated by a study on 16 seropositive patients with inoperable lung cancer . A substantial decrease in p53AAb during therapy was noted for 12 patients - four had unchanged p53AAb levels or a decrease of less than 50%. Since chemotherapy can eventually lead to (partial) immunosuppression, the authors addressed the questionable specificity of the observed p53AAb drop by simultaneous analyses of HAV antibodies. These antibodies are frequently found in the normal population and were present in all studied cancer patients at the time of diagnosis. Neither total serum immunoglobulins nor HAV antibodies changed significantly during monitoring underlining the specificity of the p53AAb changes in response to cancer treatment. The authors saw a trend toward an asso
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