AIMS: To investigate the expression of p53 protein in malignant and benign lymphoid tissues. METHODS: Tissue from 42 non-Hodgkin's lymphomas, 10 Hodgkin's lymphomas, three atypical hyperplasias and five benign reactive hyperplasias was studied immunohistochemically for the expression of p53 protein. RESULTS: Of the 42 non-Hodgkin's lymphomas, 13 (31%) were positive for p53 in some of the tumour cells. In two cases the proportion of positive cells was more than 10% and in four cases it was between 1-5%. These six cases consisted of three Burkitt's lymphomas, one immunoblastic lymphoma, one centroblastic diffuse lymphoma and one angioimmunoblastic lymphoma. In seven cases the proportion of p53 positive tumour cells was less than 1%. These cases comprised three centroblastic diffuse, three centroblastic polymorphic diffuse, and one angioimmunoblastic type lymphoma. In three out of 10 (30%) Hodgkin's lymphomas, a proportion of the Reed-Sternberg cells were p53 positive. One of these was a mixed cellular subtype and two nodular sclerosing subtypes. p53 protein was not expressed in the three atypical hyperplasias or the five benign reactive hyperplasias of the lymph nodes. CONCLUSIONS: The presence of p53 positivity in non-Hodgkin's and Hodgkin's lymphomas indicates that mutations of the p53 gene may play a part in the development of these tumours. The concentration of p53 positivity in high grade lymphomas suggests that p53 is involved in the transformation of low grade lymphomas to more aggressive types. Because no p53 positivity was observed in benign lesions of the lymph nodes, positive p53 immunohistochemical staining in a lymphoid lesion suggests malignancy.
AIMS: To investigate the expression of p53 protein in malignant and benign lymphoid tissues. METHODS: Tissue from 42 non-Hodgkin's lymphomas, 10 Hodgkin's lymphomas, three atypical hyperplasias and five benign reactive hyperplasias was studied immunohistochemically for the expression of p53 protein. RESULTS: Of the 42 non-Hodgkin's lymphomas, 13 (31%) were positive for p53 in some of the tumour cells. In two cases the proportion of positive cells was more than 10% and in four cases it was between 1-5%. These six cases consisted of three Burkitt's lymphomas, one immunoblastic lymphoma, one centroblastic diffuse lymphoma and one angioimmunoblastic lymphoma. In seven cases the proportion of p53 positive tumour cells was less than 1%. These cases comprised three centroblastic diffuse, three centroblastic polymorphic diffuse, and one angioimmunoblastic type lymphoma. In three out of 10 (30%) Hodgkin's lymphomas, a proportion of the Reed-Sternberg cells were p53 positive. One of these was a mixed cellular subtype and two nodular sclerosing subtypes. p53 protein was not expressed in the three atypical hyperplasias or the five benign reactive hyperplasias of the lymph nodes. CONCLUSIONS: The presence of p53 positivity in non-Hodgkin's and Hodgkin's lymphomas indicates that mutations of the p53 gene may play a part in the development of these tumours. The concentration of p53 positivity in high grade lymphomas suggests that p53 is involved in the transformation of low grade lymphomas to more aggressive types. Because no p53 positivity was observed in benign lesions of the lymph nodes, positive p53 immunohistochemical staining in a lymphoid lesion suggests malignancy.
Authors: E Feinstein; G Cimino; R P Gale; G Alimena; R Berthier; K Kishi; J Goldman; A Zaccaria; A Berrebi; E Canaani Journal: Proc Natl Acad Sci U S A Date: 1991-07-15 Impact factor: 11.205
Authors: S J Baker; E R Fearon; J M Nigro; S R Hamilton; A C Preisinger; J M Jessup; P vanTuinen; D H Ledbetter; D F Barker; Y Nakamura; R White; B Vogelstein Journal: Science Date: 1989-04-14 Impact factor: 47.728
Authors: I Chiba; T Takahashi; M M Nau; D D'Amico; D T Curiel; T Mitsudomi; D L Buchhagen; D Carbone; S Piantadosi; H Koga Journal: Oncogene Date: 1990-10 Impact factor: 9.867