It is suggested that ID2, EBV-LMP1 and P16(INK4A) could play an important role in the evolution of classical Hodgkin lymphoma, and be considered as potential adjunct markers to identify HRS cells in diagnosis.
Effects of adenovirus-mediated expression of p27Kip1, p21Waf1 and p16INK4A in cell lines derived from t(2;5) anaplastic large cell lymphoma and Hodgkin's disease.
The p16 and p15 promoter regions were studied using methylation-specific polymerase chain reaction in 53 CD30 non-Hodgkin's lymphomas (25 anaplastic large-cell, 13 peripheral T cell, and 15 anaplastic diffuse large B cell) and 26 Hodgkin's lymphomas, with the aim of comparing the methylation status of these tumor suppressor genes in anaplastic large-cell lymphomas and other related entities. p16 and p15 methylation was detected, respectively, in 28% and 60% of CD30 non-Hodgkin's lymphomas and in 38% and 42% of Hodgkin's neoplasms.
Nucleolar p14(ARF) overexpression in Reed-Sternberg cells in Hodgkin's lymphoma: absence of p14(ARF)/Hdm2 complexes is associated with expression of alternatively spliced Hdm2 transcripts.
To determine whether inactivation of this gene is implicated in the development of Hodgkin's disease, we immunostained 40 cases with a monoclonal antibody for the p16 protein.
p16(INK4a) gene inactivation by deletions, mutations, and hypermethylation is associated with transformed and aggressive variants of non-Hodgkin's lymphomas.
While loss of RB function was a rare event in human lymphomagenesis, p16 was absent in some 25% of high-grade non-Hodgkin's lymphomas; diffuse large cell lymphomas were the primary target of tumor suppressor gene inactivation.
Detection of single and associated lesions of the Bcl-1, Bcl-2, Bcl-6, c-myc, p53 and p16 genes in B-cell non-Hodgkin's lymphomas: value of molecular analysis for a better assignment of the histologic subtype.
We present an allelotype analysis of 35 cases of non-Hodgkin lymphomas and normal pairs using four microsatellite markers that flank the region occupied by the CDKN2 gene locus at 9p21.
The CDKN2 gene is also inactivated in some patients with non-Hodgkin's lymphomas, adult T-cell leukemias, and lymphoid blastic crisis of chronic myelogenous leukemias.
We identified the homozygous deletion of P15 and P16 genes in 13 tumors from 12 patients, all belonging to diffuse large-cell histology; 10 had this diagnosis made on presentation, 1 had transformed from small lymphocytic lymphoma, and 1 had transformed from Hodgkin's disease.
To determine if CDKN2 or another closely related gene on 9p is the target of 9p deletions in ALL and other hematologic malignancies, we analyzed 20 primary patient samples (13 ALL, 2 acute myeloid leukemias [AML], and 5 non-Hodgkin's lymphomas [NHL]) with 9p rearrangements using Southern blot analysis, fluorescence in situ hybridization (FISH), and single-strand conformation polymorphism (SSCP) for alterations of CDKN2.