Asbestos Cancer Update 2008

Department of Ophthalmology, Chungnam National University Hospital, #640 Daesa-dong, Jung-gu, Daejeon 301-721, Korea. kcs61@cnu.ac.kr

BACKGROUND/AIMS: Helicobacter pylori is well known to be responsible for gastric mucosa-associated lymphoid tissue (MALT) lymphoma. This study evaluates whether H pylori is also responsible for conjunctival MALT lymphoma and which strain of H pylori is associated with conjunctival MALT lymphoma. METHODS: Fifteen cases of conjunctival MALT lymphoma were investigated. Eight biopsies of normal conjunctiva were also investigated as controls. The specimens were investigated for the presence of H pylori DNA with polymerase chain reaction (PCR) using 16S rDNA primer. When the PCR using 16S rDNA was positive for H pylori, the specimens were analysed for the virulent gene with PCR using vacA s1/2 primer and vacA m1/2 primer. RESULTS: H pylori DNA was identified in all 15 specimens of conjunctival MALT lymphomas and none of the controls. Of these 15 H pylori positive lymphoma specimens, the vacA s1 and vacA m2 alleles were detected in two, and only vacA s1 allele was detected in 11. CONCLUSIONS: H pylori is thought to play a role in the pathogenesis of conjunctival MALT lymphoma, and H pylori with vacA s1 allele appears to be a virulent strain for conjunctival MALT lymphoma.

Share This

Departments of Surgical and Gastroenterological Sciences, Padua University, Padua, Italy. fabio.farinati@unipd.it

Gastric carcinogenesis is a complex, multistep and multifactorial event, characterized by progressive cyto-histological dedifferentiation, in which the role of Helicobacter pylori infection has been established. Among the pathways relevant to gastric carcinogenesis and correlated with H. pylori infection, it has been demonstrated that the production of reactive oxygen species, with damage to the DNA, may be quite important. Oxidative damage, alone and/or in combination with exogenous and endogenous factors, induces several molecular changes. The assumption is that, in precancerous lesions, these molecular changes belong to the same biological spectrum as their invasive counterpart. The molecular profile of these preneoplastic lesions is heterogeneous, however, and there are still no molecular markers enabling the distinction between atypical hyperplastic lesions and low-grade noninvasive neoplasia (NiN) or between high-grade NiN and early invasive neoplasia. Indeed, within the spectrum of morphological changes characterizing this multistep evolution, dysplasia (NiN) is the lesion coming closest to the development of invasive adenocarcinoma. Several of the genetic and epigenetic alterations reported in gastric precancerous lesions affect DNA repair system genes, tumor suppressor genes, oncogenes, cell cycle regulators, growth factors, and adhesion molecules. Although we await reliable molecular markers, it is best to monitor patients harboring NiN closely with endoscopy and extensive bioptic sampling, and to eradicate any H. pylori to prevent the accumulation of oxidative DNA damage and its consequent progression. The growing body of evidence of the regression of precancerous changes and the high prevalence of superficial gastric carcinoma demonstrated in long-term follow-up studies on NiN make this approach mandatory.

Share This