Conclusions

What can be generalized about the value of p53 serology and its usefullness with respect to the p53 status in cancer patients? While mutational analysis and im-munohistochemistry (IHC) require tumor specimens which may be scarce and depend on rather time-consuming and laborious techniques, p53AAb are more readily analyzed. Additionally, p53AAb evaluation may be the only available approach during monitoring. It should be emphasized that p53AAb represent a more global approach in the assessment of p53 alterations. IHC and gene analysis, on the other hand, can produce a wealth of information but are local analyses relying on tumor sampling. This is particularly tricky when the neoplasm is heterogenous or highly conta minated with normal cells. Furthermore, the precise relationship between p53 mutations and immunohisto-logic protein detection remains controversial. It should be cautioned against the assumption that p53 accumulation is always associated with a gene mutation [92]. Not at least technical factors influence IHC results and their interpretation [93-96]. Moreover, since epigenetic phenomena may account for a significant proportion of the IHC-positive tumors, p53 mutational analysis is not always the best approach. The obvious disadvantage of p53AAb as an acceptable tumor marker—its low sensitivity [27]—is alleviated by the expectation that it may turn out to be quantitatively useful during follow-up with some patient subgroups, particularly if established tumor markers like alpha-fetoprotein or CEA and/or clinical surveillance remain noninformative.

Previous to our results, p53AAb did not surface during monitoring of preoperatively seronegative cancer patients [28,34,88,90], This observation led to the assumption that each patient may have an inherent capacity to develop an anti-p53 humoral response linked to the site of a p53 mutation or MHC class [88], We like to build on an interpretation given by Zalcman et al. [88] for p53AAb-positive lung cancer patients who developed nonimmunogenic metastases. If that seronegative relapse was due to a tumoral clone retaining its virulent potential but without any p53 mutation, than it is also feasible that a previously seronegative tumor sheds subclone cells, possibly with a lately acquired p53 mutation, that grow into metastases with p53 immunogenic potential.

p53AAb in patients with AID or potentially oncogenic viral infections by HTLV-1 or HCV could open new vistas for research. With more reports on p53AAb predating a clinical diagnosis of cancer, screening for p53AAb of clearly defined groups with hereditary cancer risk or habituary/occupational exposure to hazardous substances may be well advised. Future studies with larger numbers of monitored patients have to establish the validity of the observed association between p53AAb levels and disease status. The magnitude of p53AAb levels could turn out to be generally informative in the interpretation of a cancer-specific p53 humoral response and its differentiation from a weaker reaction as in patients with AID. We hope that the evaluation of the anti-p53 humoral response during follow-up will become another helpful tool in effective patient care.

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