Highlights of This Issue

β-microseminoprotein (β-MSP), prostate-specific antigen (PSA), and kallikrein 2 (hK2) are three major secretory products of the prostate. The gene, MSMB, that encodes β-MSP contains a single nucleotide polymorphism (SNP) associated with prostate cancer risk (rs10993994). In this study, Xu and colleagues examined the role of genetic variation at MSMB in determining natural levels of prostate secretions in healthy young men. They report that rs10993994 is significantly correlated with levels of blood and semen β-MSP, free and total PSA, and semen levels of hK2. In addition, the authors uncovered associations between additional SNPs at MSMB with blood and semen β-MSP and semen PSA levels. This work demonstrates that common genetic variation at MSMB controls physiological levels of prostate-secreted proteins and encourages further exploration of this susceptibility locus.

A timely review by Jemal and colleagues describes the changing global patterns of cancer incidence and mortality for select common cancer sites using data compiled by the International Agency for Research on Cancer (IARC). These data represent a wealth of important global cancer trends; for example, the rates for lung and colon cancers in some economically transitioning countries have already surpassed those in the United States. In addition, developing countries continue to be disproportionately affected by cancers related to infectious agents. Importantly, these data reflect the alarming effects of unhealthy lifestyle changes (tobacco use, high calorie diets, and physical inactivity) on the cancer burden in less developed and economically transitioning countries.

Although marketed to tobacco users as potential reduced exposure products (PREP), there is little information about the toxicant exposures for electronic cigarette users. To address this, Vansickel and colleagues evaluated plasma nicotine and carbon monoxide (CO) levels as well as heart rate and subjective measurements in study participants smoking either electronic cigarettes, sham cigarettes, or their own brand. As expected, own brand smokers had significantly increased plasma nicotine and CO concentrations and heart rates within the first five minutes, while electronic and sham cigarette smokers did not. Surprisingly, both own brand and electronic cigarette smokers had significantly decreased tobacco abstinence symptom ratings and increased product acceptability ratings. These encouraging findings illustrate how clinical laboratory methods can be used to understand the acute effects of these and other PREPs for tobacco users.

There is overwhelming evidence for the association between H. pylori and noncardia gastric adenocarcinoma. In addition, H. pylori can induce gastric atrophy, which increases gastric cancer risk. Despite this, it remains unclear if H. pylori is associated with ESCC. To explore these relationships, Cook and colleagues performed a nested casecontrol study within the prospective Alpha-Tocopherol, Beta-Carotene Cancer Prevention (ATBC) Study to assess H. pylori status and gastric atrophy status. As expected, gastric atrophy was associated with ESCC, but there was no evidence for an association between H. pylori and ESCC. These results may suggest that gastric atrophy has a different histogenesis in ESCC, independent of H. pylori. Further studies are warranted to validate these results and help unlock the relationship between gastric atrophy and ESCC.