INTRODUCTION: We evaluated the immunohistochemical expression of p53, Ki67, CD30, and CD117 and correlated it with histological features and presence of clinical metastasis at diagnosis of testicular seminomas. MATERIALS AND METHODS: A retrospective study of 62 patients was performed in patients with pure seminoma. The retroperitoneum was staged with computed tomography scan and the thorax with simple x-rays and/or computed tomography scan. Pathologists were unaware of the clinical stage of the patients. Manual microarrays were created from a tissue representative of tumor. The expression of p53, Ki67, CD30, and CD117 was evaluated as negative, any degree of expression, and expression in more than 50% of neoplastic cells. Univariate and multivariate analysis were performed. RESULTS: Sixty-two cases were analyzed: 43 cases were in clinical stage I (69.4%), 17 were in clinical stage II (27.4%), and 2 were in clinical stage III (3.2%). Fifty-six cases expressed CD117 (90%), 42 p53 (68%), 8 CD30 (13%), and all cases Ki67. There were no differences in p53, Ki67, CD30, and CD117 expression between testicular seminoma with and without clinical metastasis at diagnosis, regardless of the magnitude of expression. Neither of them found positive association between these marker expressions and morphologic risk factors such as tumor size greater than 6 cm and rete testis invasion. CONCLUSIONS: This study shows that expression of p53, Ki67, and CD30 and loss of CD117 expression fail to predict the presence of clinical metastasis at diagnosis of testicular seminoma and do not correlate with other histopathological risk factors in clinical stage I patients.
INTRODUCTION: We evaluated the immunohistochemical expression of p53, Ki67, CD30, and CD117 and correlated it with histological features and presence of clinical metastasis at diagnosis of testicular seminomas. MATERIALS AND METHODS: A retrospective study of 62 patients was performed in patients with pure seminoma. The retroperitoneum was staged with computed tomography scan and the thorax with simple x-rays and/or computed tomography scan. Pathologists were unaware of the clinical stage of the patients. Manual microarrays were created from a tissue representative of tumor. The expression of p53, Ki67, CD30, and CD117 was evaluated as negative, any degree of expression, and expression in more than 50% of neoplastic cells. Univariate and multivariate analysis were performed. RESULTS: Sixty-two cases were analyzed: 43 cases were in clinical stage I (69.4%), 17 were in clinical stage II (27.4%), and 2 were in clinical stage III (3.2%). Fifty-six cases expressed CD117 (90%), 42 p53 (68%), 8 CD30 (13%), and all cases Ki67. There were no differences in p53, Ki67, CD30, and CD117 expression between testicular seminoma with and without clinical metastasis at diagnosis, regardless of the magnitude of expression. Neither of them found positive association between these marker expressions and morphologic risk factors such as tumor size greater than 6 cm and rete testis invasion. CONCLUSIONS: This study shows that expression of p53, Ki67, and CD30 and loss of CD117 expression fail to predict the presence of clinical metastasis at diagnosis of testicular seminoma and do not correlate with other histopathological risk factors in clinical stage I patients.
Authors: Beatriz Chaves Lourenço; Catarina Guimarães-Teixeira; Bianca C T Flores; Vera Miranda-Gonçalves; Rita Guimarães; Mariana Cantante; Paula Lopes; Isaac Braga; Joaquina Maurício; Carmen Jerónimo; Rui Henrique; João Lobo Journal: Life (Basel) Date: 2022-02-10