Correction: Applying Personal Genetic Data to Injury Risk Assessment in Athletes.

[This corrects the article DOI: 10.1371/journal.pone.0122676.]

Applying Personal Genetic Data to Injury Risk Assessment in Athletes

<div><p>Recent studies have identified genetic markers associated with risk for certain sports-related injuries and performance-related conditions, with the hope that these markers could be used by individual athletes to personalize their training and diet regimens. We found that we could greatly expand the knowledge base of sports genetic information by using published data originally found in health and disease studies. For example, the results from large genome-wide association studies for low bone mineral density in elderly women can be re-purposed for low bone mineral density in young endurance athletes. In total, we found 124 single-nucleotide polymorphisms associated with: anterior cruciate ligament tear, Achilles tendon injury, low bone mineral density and stress fracture, osteoarthritis, vitamin/mineral deficiencies, and sickle cell trait. Of these single nucleotide polymorphisms, 91% have not previously been used in sports genetics.</p><p>We conducted a pilot program on fourteen triathletes using this expanded knowledge base of genetic variants associated with sports injury. These athletes were genotyped and educated about how their individual genetic make-up affected their personal risk profile during an hour-long personal consultation. Overall, participants were favorable of the program, found it informative, and most acted upon their genetic results.</p><p>This pilot program shows that recent genetic research provides valuable information to help reduce sports injuries and to optimize nutrition. There are many genetic studies for health and disease that can be mined to provide useful information to athletes about their individual risk for relevant injuries.</p></div

Example Summary of an Athlete's Genetic Profile.

<p>Each athlete was given information related to the categories tested. The summary page gives four color-coded risk levels for each trait: decreased risk (green), average (black), slightly increased risk (yellow), or increased risk (red). Further information, including background information, injury mechanism, genetic basis, and prevention strategies was accessible by clicking on the category in the side menu.</p

Relevance of Selected Injuries and Conditions to Athletes.

<p>Relevance of Selected Injuries and Conditions to Athletes.</p

Areas of Interest for Genetic Markers.

<p>Six sports related categories were tested in athletes that relate to different injuries or attributes in different locations of the human body. For each category we list the number of associated single nucleotide polymorphisms (SNPs) that we reported on as well as the overall effect size, based on odds ratios or β-coefficients, for having a genetic risk in that category.</p

Summary of Athlete Cohort.

<p>Note: Numbers listed are the mean from all athletes in the cohort and numbers in brackets are the min-max range for those characteristics.</p><p>*: Varsity status is defined as whether or not the athlete participated on an NCAA Div 1, II, or III Varsity level team (swimming, cross-country, track-and-field, crew) for at least 1 year prior to being on the Stanford Triathlon Team.</p><p>**: Self-reported average training hours per week during the collegiate season from Sept 1^st, 2012 to May 1^st, 2013. Training was periodized, includes off days plus rest weeks, includes structured team plus individual workouts, and is not limited by discipline.</p><p>***: Injury status is defined as any athlete who was limited in their training, could not participate in team workouts, or was unable to race for at least one day due to a diagnosed injury from Sept 1^st to Aug 31^st of each season.</p><p>Summary of Athlete Cohort.</p

Summary of Findings from the Genetic Literature Review.

<p>*: Effect size estimates are based on odds ratios reported for published SNPs associated with each category. Odds ratios of 1.0–1.3 are small effects, 1.3–2.0 are medium effects, and greater than 2.0 are large effectsVarsity status is defined as whether or not the athlete participated on an NCAA Div 1, II, or III Varsity level team (swimming, cross-country, track-and-field, crew) for at least 1 year prior to being on the Stanford Triathlon Team.</p><p>**: Level of evidence based on criteria for assessment of cumulative evidence of genetic associations from Ioannidis et al 2008 [<a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0122676#pone.0122676.ref014" target="_blank">14</a>].</p><p>Summary of Findings from the Genetic Literature Review.</p

Chemokine Ligand 5 (CCL5) and chemokine receptor (CCR5) genetic variants and prostate cancer risk among men of African Descent: a case-control study

<p>Abstract</p> <p>Background</p> <p>Chemokine and chemokine receptors play an essential role in tumorigenesis. Although chemokine-associated single nucleotide polymorphisms (SNPs) are associated with various cancers, their impact on prostate cancer (PCA) among men of African descent is unknown. Consequently, this study evaluated 43 chemokine-associated SNPs in relation to PCA risk. We hypothesized inheritance of variant chemokine-associated alleles may lead to alterations in PCA susceptibility, presumably due to variations in antitumor immune responses.</p> <p>Methods</p> <p>Sequence variants were evaluated in germ-line DNA samples from 814 African-American and Jamaican men (279 PCA cases and 535 controls) using Illumina’s Goldengate genotyping system.</p> <p>Results</p> <p>Inheritance of <it>CCL5</it> rs2107538 (AA, GA+AA) and rs3817655 (AA, AG, AG+AA) genotypes were linked with a 34-48% reduction in PCA risk. Additionally, the recessive and dominant models for <it>CCR5</it> rs1799988 and <it>CCR7</it> rs3136685 were associated with a 1.52-1.73 fold increase in PCA risk. Upon stratification, only <it>CCL5</it> rs3817655 and <it>CCR7</it> rs3136685 remained significant for the Jamaican and U.S. subgroups, respectively.</p> <p>Conclusions</p> <p>In summary, <it>CCL5</it> (rs2107538, rs3817655) and <it>CCR5</it> (rs1799988) sequence variants significantly modified PCA susceptibility among men of African descent, even after adjusting for age and multiple comparisons. Our findings are only suggestive and require further evaluation and validation in relation to prostate cancer risk and ultimately disease progression, biochemical/disease recurrence and mortality in larger high-risk subgroups. Such efforts will help to identify genetic markers capable of explaining disproportionately high prostate cancer incidence, mortality, and morbidity rates among men of African descent.</p