Selected Articles from This Issue

The risk for colorectal cancer and colon polyps, the precursors to colorectal cancer, varies between people for largely unclear reasons, one of which is field cancerization. The evidence for field cancerization in the colon has been modest to date. In this study, Yu and colleagues carried out studies using methylated EVL as a marker for field cancerization in the colon and a possible risk biomarker for colon polyps. The authors found mEVL associated with a 3X increased risk for colon polyps. Results provide more support for colon field cancerization and suggest mEVL may be a novel risk marker for colorectal cancer and therapeutic target for colorectal cancer chemoprevention.

Human papillomavirus (HPV) cell entry through host cell surface receptors could correlate with infectivity and may play a role in cervical precancer progression. It has been shown that heparan sulfate proteoglycans (HSPG), specifically the syndecan and glypican gene families are required on the cell surface for HPV infection. However, the role of genetic variants in these receptors with cervical precancer is not well documented. Analyzing data from the MACS/WIHS Combined Cohort Study, Mukherjee and colleagues reported that variants in SDC2, SDC3, ITGA6 and GPC5 were associated with increased odds of cervical precancer, both CIN3+ and HSIL, in African American women.

The higher incidence of non–Hodgkin lymphomas (NHL) in males is not well understood but may involve reactive oxygen species (ROS). Using untargeted adductomics of human serum albumin (HSA) from incident NHL cases and controls, this study by Grigoryan, Imani, and colleagues discovered ROS adducts that discriminated for NHL incidence between sexes. Adduct clusters dominated by HSA-Cys34 oxidation products implicated redox biology in the etiology of NHL, and differential clustering highlighted sex-related differences in pathways and effects of diet and alcohol consumption. Intriguingly, an adduct from enteric microbial metabolism was more abundant in male cases than controls, thereby implicating systemic inflammation induced by gut-microbial translocation as a risk factor for NHL.

This study by Edwards and colleagues establishes predictive validity of the sex and racial/ethnic identity specific urinary cotinine and Total Nicotine Equivalents-2 (TNE-2) cut-points (from Wave 1, 2014) on estimating tobacco use (Wave 4, 2017) from the PATH Study. The predictive validity of the W1 cut-points to classify exclusive cigarette and polytobacco cigarette use at W4 was high, >90% sensitivity and specificity, except among polytobacco Hispanic smokers. The W1 cut-points remain valid for biochemical verification of self-reported tobacco use in W4. They can be used in clinical and epidemiological studies to reduce misclassification of cigarette smoking, a leading cause of cancer-related morbidity and mortality.