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Evaluation of p53 alterations in occult lymph node metastases
Author(s) -
Maruyama Riichiroh,
Sugio Kenji,
Fukuyama Yasuro,
Hamatake Motoharu,
Sakada Takashi,
Saitoh Genkichi,
Sugimachi Keizo
Publication year - 2000
Publication title -
journal of surgical oncology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.201
H-Index - 111
eISSN - 1096-9098
pISSN - 0022-4790
DOI - 10.1002/(sici)1096-9098(200003)73:3<143::aid-jso6>3.0.co;2-b
Subject(s) - medicine , lymph node , occult , lymph , pathology , immunostaining , immunohistochemistry , gene mutation , mediastinal lymph node , mutation , cancer , metastasis , gene , biology , biochemistry , alternative medicine
Background and Objectives This study was designed to evaluate p53 alterations in occult lymph node metastases. Methods We examined 41 patients with stage I non‐small‐cell lung cancer. We investigated p53 gene mutation by polymerase chain reaction and single‐strand conformation polymorphism analysis of exons 5–8, p53 protein accumulation by immunostaining with monoclonal antibody DO‐7, and detection of tumor cells in lymph nodes by immunohistochemistry with monoclonal antibodies to cytokeratin (CK). Results p53 gene mutation was detected in 34% of tumors and nuclear p53 accumulation in 46%. CK‐positive cells in the hilar and mediastinal region lymph nodes were detected in 43.9% of patients and 29.3%, respectively. Of the 14 cases with p53 mutation and the 19 cases with p53 accumulation, 12 and 15 had micrometastases in the hilar or mediastinal lymph nodes, respectively. However, p53 alterations were not significantly associated with occult lymph node metastases. In cases with occult lymph node metastases, the 5‐year survival was 81.9% for the p53 wild‐type group and 45.8% for the p53 mutation group. Conclusions p53 alterations are not correlated with occult lymph node metastases, while p53 gene mutation is considered to be an unfavorable prognostic marker in patients with occult lymph node metastases. J. Surg. Oncol. 2000;73:143–147 . © 2000 Wiley‐Liss, Inc.