Summary: | Bacground/Aim. Mucosa-associated lymphoid tissue (MALT) lymphoma accounts for
5-17% non-Hodgkin lymphomas (NHL). The molecular pathogenesis of MALT
lymphomas is not well-established. The aim of this study was to evaluate
immunohistochemically determined nuclear coexpression of BCL10 and NF-kappaB
(NF-κB) in tumor cells of gastric MALT lymphoma and its impact on the
patogenesis and outcome of the disease. Methods. Medical records of 35
patients with newly diagnosed gastric MALT lymphoma were analyzed and biopsy
specimens were immunostained for BCL10 and NF-kB expression (p65 subunit).
Results. The median age of 35 patients diagnosed with gastric MALT lymphoma
was 63.5 years (male/female = 21/14). Symptoms were present in 23/35 (65.7%)
patients with the weight loss as the most common symptom. Gastric MALT
lymphomas were usually localized in the stomach corpus and corpus and antrum
(45.7% and 31.2%, respectively). H. pylori infection was confirmed in 20 out
of 30 (66.7%) patients. Treatment options were as follows: immunochemotherapy
in 10 (28.5%) patients, surgery in 9 (25.8%) patients, combined surgery and
chemotherapy in 14 (40%) patients and supportive measures in 2 (5.7%)
patients. Complete remission was achieved in 13 (37.1%) patients and partial
remission in two (5.7%) patients. Sixteen (45.7%) patients had disease
progression (p < 0.001). Cytoplasmatic expression of BCL10 in tumor cells was
detected in 19 (54.3%) specimens. Nuclear expression was detected in no
specimen. Cytoplasmic expression of NF-κB was present in 22 (65.7%)
specimens, but nuclear expression was not detected in any specimens.
Conclusion. Nuclear expressions (activation) of NF-κB p65 subunit and BCL10
were not detected in specimens of gastric MALT lymphoma. The correlation of
nuclear coexpression of BCL10 and NF-κB in gastric MALT lymphoma was not
established. These results indicate that other mechanisms and signal pathways
are active in lymphogenesis of gastric MALT lymphoma, as that apoptotic
inhibition is not the main, nor the only mechanism in tumorogenesis.
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