Abstract: P16/INK4A is tumor suppressor protein that plays a critical role in cell cycle regulation. Loss of P16 protein expression has been implicated in pathogenesis of many cancers, including lymphoma. Therefore, we sought to investigate if loss of P16 protein expression is associated with lymphoma and/or any specific lymphoma subtypes (Hodgkin-s lymphoma (HL) and nonHodgkin-s lymphoma (NHL)). Fifty-five lymphoma cases consisted of 30 cases of HL and 25 cases of NHL, with an age range of 3 to 78 years, were examined for loss of P16 by immunohistochemical technique using a specific antibody reacting against P16. In total, P16 loss was seen in 33% of all lymphoma cases. P16 loss was identified in 47.7% of HL cases. In contrast, only 16% of NHL showed loss of P16. Loss of P16 was seen in 67% of HL patients with 50 years of age or older, whereas P16 loss was found in only 42% of HL patients with less than 50 years of age. P16 loss in HL is somewhat higher in male (55%) than in female (30%). In subtypes of HL, P16 loss was found exclusively in all cases of lymphocyte depletion, lymphocyte predominance and unclassified cases, whereas P16 loss was seen in 39% of mixed cellularity and 29% of nodular sclerosis cases. In low grade NHL patients, P16 loss was seen in approximately one-third of cases, whereas no or very rare of P16 loss was found in intermediate and high grade cases. P16 loss did not show any correlation with age or gender of NHL patients. In conclusion, the high rate of P16 loss seen in our study suggests that loss of P16 expression plays a critical role in the pathogenesis of lymphoma, particularly with HL.
Abstract: The aim of this study was to estimate the frequency of
EBV infection in Hodgkin's lymphoma (HL) and non-Hodgkin's
lymphoma (NHL) occurring in Jordanian patients. A total of 55
patients with lymphoma were examined in this study. Of 55 patients,
30 and 25 were diagnosed as HL and NHL, respectively. The four
HL subtypes were observed with the majority of the cases exhibited
the mixed cellularity (MC) subtype followed by the nodular sclerosis
(NS). The high grade was found to be the commonest subtype of
NHL in our sample, followed by the low grade. The presence of EBV
virus was detected by immunostating for expression of latent
membrane protein-1 (LMP-1). The frequency of LMP-1 expression
occurred more frequent in patients with HL (60.0%) than in patients
with NHL (32.0%). The frequency of LMP-1 expression was also
higher in patients with MC subtype (61.11%) than those patients with
NS (28.57%). No age or gender difference in occurrence of EBV
infection was observed among patient with HL. By contrast, the
prevalence of EBV infection in NHL patients aged below 50 was
lower (16.66%) than in NHL patients aged 50 or above (46.15%). In
addition, EBV infection was more frequent in females with NHL
(38.46%) than in male with NHL (25%). In NHL cases, the
frequency of EBV infection in intermediate grade (60.0%) was high
when compared with frequency of low (25%) or high grades (25%).
In conclusion, analysis of LMP-1 expression indicates an important
role for this viral oncogene in the pathogenesis of EBV-associated
malignant lymphomas. These data also support the previous findings
that people with EBV may develop lymphoma and that efforts to
maintain low lymphoma should be considered for people with EBV
infection.