A profile of mycosis fungoides

between t(11;18)(q21;q21) of gastric MALT lymphomas and CagA strains of H pylori. Furthermore, they show that t(11;18)(q21; q21)-positive MZLs of MALT in other sites do occur, however, in a nonrandom fashion (ie, 38% and 24% in the lung and stomach, respectively, versus 1% in the salivary gland). Ye et al’s proposal that the missing link might be chromosomal damage caused by oxidative stress induced by coinfiltrating neutrophils is intriguing. All the more so since this hypothesis is supported by data from Rollinson and colleagues (page 1007). Fascinatingly, using a completely different line of argument, these authors arrive at the very same conclusion. They show that, in their series of gastric MZLs, the glutathione S-transferase GST T1 null genotype and the Interleukin-1 RN2/2 genotype, but not the GST M1 null genotype or Interleukin-1 RN1/1 genotype, are associated with gastric MZLs. Thus, interindividual variations in inflammatory responses and differences in antioxidative capacity may be the genetic background on which H pylori can eventually exert its oncogenic potential. At this stage, it is certainly very important to investigate whether this interindividual variation of inflammatory response might even lead to a specific genetically defined subset of MZLs. —Thomas F. E. Barth and Peter Möller University of Ulm, Germany