Pattern of p16 and pRb Expression in Acute Leukemia

Lee, Jeong Rim; Lee, Ju Hee; Suh, Jin Tae; Lee, Wu In; Lee, Hee Jue

Abstract

BACKGROUND: There have been evidences that inactivation of tumor supressor genes such as p16 and pRb develops human malignancies. p16 inhibits the cyclin D/cyclin-dependant kinase 4 complex which phosphorylates pRb, thus negatively regulating cell cycle progression. Rb gene inactivation has been observed in various tumor and reported to be reciprocally correlated with p16 expression. The purpose of this study is to evaluate aberrant expression of p16 and pRb in acute leukemia by immunohistochemial stain in clot or biopsy section of the bone marrow.
METHODS
For detection of p16 and pRb, immunohistochemical staining with anti-human mouse monoclonal antibodies to p16 and pRb were done on 62 bone marrow paraffin sections from leukemic patients. In acute lymphoblastic leukemia (ALL), immunophenotyping was performed with indirect immunofluorescent assay and clinical parameters were analyzed depending on status of p16 expression.
RESULTS
In 28 cases (45%), abnormal expression of p16 or pRb were observed. Twenty three of those cases (37%) showed aberrancy only in one protein, in which case, staining intensity was generally more stronger than that of normal expression in both proteins. The proportion of abnormal p16 expression was 30% and 15%, and that of pRb was 30% and 36% in ALL and in acute myelocytic leukemia, respectively. There was no significant clinical correlation between aberrancy of p16 and clinical parameters of acute leukemia.
CONCLUSION
Our results suggest that loss of the p16 and pRb function may contribute to pathogenesis of acute leukemia. Further study is needed in more cases of acute leukemia to evaluate clinical significance of p16 or pRb aberrancy, particularly in ALL.