PMC:13921 / 17874-19511 JSONTXT

{"target":"https://pubannotation.org/docs/sourcedb/PMC/sourceid/13921","sourcedb":"PMC","sourceid":"13921","source_url":"http://www.ncbi.nlm.nih.gov/pmc/13921","text":"Anti-p53 levels were independent of changes in tumour status\nAs a working hypothesis we proposed that levels of autoantibodies to p53 would reflect tumour behaviour. Thus, for those patients who were positive for p53 autoantibodies at diagnosis, we reasoned that surgical removal of primary tumour might result in reduced p53 autoantibody levels. Should these levels then show a secondary increase associated with relapsed disease, then increasing levels of p53 autoantibodies might act as a biochemical marker of tumour progression. For those patients who were negative for p53 autoantibodies, then, development of recurrent disease may be associated with changes in p53 expression within the metastatic tumour, leading to a switch to an autoantibody-positive status.\nWe found that the presence or absence of p53 autoantibodies was not predictive for presence or absence of recurrent disease. There was an equivalent incidence of active disease at the time of sampling in the autoantibody-negative and autoantibody-positive groups, these being 25.2% and 28.7%, respectively.\nWe found that humoral immune activity against p53 appeared to be relatively restricted to a subgroup of patients in whom, once an autoantibody response had been generated, antibody was likely to persist regardless of tumour behaviour. Thus, antibody-positive patients without clinical recurrence remained antibody positive throughout the follow-up period. Conversely, where no detectable p53 autoantibody was present at the time of primary diagnosis, these patients remained similarly negative for antibody irrespective of subsequent disease activity (Table 3).","divisions":[{"label":"Title","span":{"begin":0,"end":60}}],"tracks":[]}