[Homozygous deletion and methylation of p16 and p15 gene in acute leukemia].
OBJECTIVE
To investigate the frequency of p16 and p15 gene inactivation in acute leukemia and to evaluate its clinical significance.


METHODS
Fifty-six patients with newly diagnosed acute leukemia was studied. PCR technique was used to detect homozygous deletion of p16 and p15 gene, restriction enzyme-PCR technique was used to detect gene methylation, and TdT-mediated dUTP-digoxygenin end-labeling (TUNEL) technique was used to detect cell apoptosis.


RESULTS
p16 and/or p15 gene inactivation was detected in 33 of the 56 patients, including 23/38 (60.5%) of the ALL patients (T-ALL 12/16, B-ALL 11/22) and 10/18 (55.5%) of the ANLL patients. For All patients, methylation was the major pathway of p16 and p15 gene inactivation. Patients with p16 and/or p15 gene inactivation had a delayed apoptosis, a poor response to chemotherapy, a lower remission rate and a shortened remission duration.


CONCLUSIONS
The inactivation of p16 and p15 gene plays a key role in the pathogenesis of acute leukemia.
Chen
W
W
Beijing Red-cross Chaoyang Hospital, Capital University of Medical Sciences, Beijing 100020.
Zhang
W
W
Zhu
J
J
D017209:Apoptosis; D018797:Cell Cycle Proteins; D050762:Cyclin-Dependent Kinase Inhibitor p15; D019941:Cyclin-Dependent Kinase Inhibitor p16 / Q000235:genetics*; D019175:DNA Methylation; D017353:Gene Deletion; D006720:Homozygote; D006801:Humans; D015470:Leukemia, Myeloid, Acute / Q000235:genetics* / Q000473:pathology; D054198:Precursor Cell Lymphoblastic Leukemia-Lymphoma / Q000235:genetics* / Q000473:pathology; D014157:Transcription Factors / Q000235:genetics*; D025521:Tumor Suppressor Proteins
C493966:CDKN2B protein, human; D018797:Cell Cycle Proteins; D050762:Cyclin-Dependent Kinase Inhibitor p15; D019941:Cyclin-Dependent Kinase Inhibitor p16; D014157:Transcription Factors; D025521:Tumor Suppressor Proteins