Search Results (1,954)

The objectives of this paper were to assess the genetic diversity, population structure, genetic differentiation, and phylogenetic relationships among seven duck populations using 14 microsatellite (MS) markers. This paper included 176 individuals representing seven duck populations of Bangladesh: indigenous duck (BLD), Nageswari (NAG), Rupali (RUP), Jinding (JIN), Pekin (PEK), BAU Black and White (BWC), and BAU White (WHC). A total of 133 alleles were observed with a mean of 9.50 alleles per locus. Genetic diversity was evaluated using measures such as allele frequency, observed and expected heterozygosity, and Shannon’s information index with average values of 5.44 ± 0.31, 0.59 ± 0.02, 0.64 ± 0.02, and 1.28 ± 0.05, respectively. Population differentiation and inbreeding analysis (F-statistics) indicated moderate genetic diversity and a slight degree of inbreeding across populations. Analysis of molecular variance indicated that 75% of the total genetic diversity was attributable to the within-population variation, whereas 9% and 16% were attributed to the variation among individuals and population differentiation, respectively. Indigenous duck populations (BLD, NAG, and RUP) had a close genetic relationship with JIN ducks and an intermediate relationship with two crossbreds (BWC and WHC), and the highest genetic distance was observed with PEK ducks. Neighbor-joining phylogenetic analysis revealed that the Bangladeshi indigenous duck populations formed a single cluster, while the two crossbreds (BWC and WHC) and PEK exhibited their distinct genetic identities in separate clusters. Furthermore, structure analysis at K = 2 to 5 confirmed the distinct genetic architecture (ΔK = 4.00) of the studied duck populations. This paper provides important insights into genetic diversity measures and population differentiation that will be helpful in future genetic improvement, conservation initiatives, and the design of appropriate breeding programs. Full article

Background/Objectives: Circulating tumour DNA (ctDNA) assays enable non-invasive assessment of tumour burden and treatment response in oncology. However, quantitative ctDNA outputs (such as variant allele frequency, tumour fraction, and aggregate burden scores) remain difficult to interpret and compare across platforms. This evidence-mapping review evaluates current quantitative reporting approaches in pancreatic ductal adenocarcinoma (PDAC) and examines the potential role of KRAS mutant ctDNA as a biologically grounded reference metric. Methods: A systematic literature search was conducted across PubMed/MEDLINE and Scopus to identify studies reporting quantitative ctDNA metrics in PDAC. Eligible studies included those measuring plasma KRAS mutations and/or reporting variant allele frequency, tumour fraction, or multi-locus aggregate metrics. Additional relevant primary studies identified through broader manual searching of PubMed were assessed against the same prespecified eligibility and classification criteria before inclusion. Data were synthesised narratively, focusing on reporting frameworks, units of measurement, assay characteristics, and the interpretability of quantitative outputs across platforms. Results: Substantial heterogeneity was observed in ctDNA quantification methods and reporting standards. Ratio-based metrics such as variant allele frequency and tumour fraction were commonly used but varied according to assay design, plasma input volume, and background cell-free DNA levels. Few studies reported absolute mutant molecule counts per unit volume. Given that approximately 90–95% of PDACs harbour truncal activating KRAS mutations, plasma KRAS was consistently represented across platforms and demonstrated potential as a shared quantitative anchor. Limited standardisation was noted in distinguishing detectability from quantifiability based on sampling depth and counting statistics. Conclusions: Current ctDNA reporting in PDAC lacks a shared quantitative reference, limiting cross-study comparability. Reporting KRAS mutant molecules per millilitre and adopting an assay-agnostic framework distinguishing detection from quantification may improve interpretability, support harmonisation across platforms, and facilitate cumulative learning in pancreatic cancer ctDNA research. Full article

Background/Objectives: Myeloid neoplasms (MNs) with SF3B1 mutations define a distinct entity associated with a favorable prognosis. However, not all MN patients harboring SF3B1 mutations meet the diagnostic criteria for this entity, and different mutation types may be associated with distinct clinical outcomes. We aimed to evaluate the impact of variant allele frequency (VAF) and SF3B1 mutation type across hematopoietic lineages to improve patient stratification. Methods: VAF and the distribution of the p.K700E hotspot compared with other SF3B1 variants were evaluated using paired sequencing data from bone marrow (myeloid) and CD3⁺ (non-myeloid) samples from 23 MN patients with SF3B1 mutations to assess their association with clinical outcomes. Results: Overall, 47.8% of SF3B1 mutations detected in myeloid samples (VAF 42.4%) were also identified in the lymphoid lineage (VAF 17.8%). SF3B1 VAF in CD3⁺ samples correlated with worse prognosis markers. No differences were observed in overall co-mutation burden; however, only myeloid-restricted SF3B1 mutations appeared to represent initiating events. p.K700E mutations (n = 12) were restricted to the myeloid lineage, whereas non-p.K700E mutations (n = 11) were predominantly detected in both myeloid and lymphoid lineages, suggesting multilineage involvement. Conclusions: Distinct mutational patterns and clonal progression mechanisms were observed for different SF3B1 mutation types and depending on the affected hematopoietic lineage. Our findings suggest that the SF3B1 VAF across different lineages may refine patient stratification beyond mutation type alone. Full article

Background/Objectives: Bud sports (somatic mutations) offer a quick way to develop new bougainvillea varieties by altering specific traits while keeping the desirable genetic background of the original cultivar. However, we still lack a comprehensive understanding of their genomic architecture and the molecular mechanisms behind their formation. This study aimed to characterize the population genomic characteristics of bud sports derived from the commercial variety Bougainvillea × buttiana ‘Miss Manila’. Methods: We employed genotyping by sequencing (GBS) on 39 accessions, including 27 bud sports and 12 conventional varieties. Population genomic analyses, such as principal component analysis (PCA), phylogenetic reconstruction, ADMIXTURE, and diversity statistics (π, He, Tajima’s D), were performed on 64,810 high-quality SNPs. Genome-wide scans for differentiation (FST) and selective sweeps (XP-CLR) were also conducted. Results: Bud sports showed significantly lower genetic diversity (π and He) than conventional varieties, which matches their clonal origin. PCA, phylogenetic, and ADMIXTURE analyses (optimal K = 4) revealed clear genetic differentiation and distinct population structures between the two groups. The bud sport population possessed fewer private alleles and a less negative Tajima’s D value. Genomic scans identified regions under selection in bud sports, with functional annotation pointed to genes involved in ubiquitin-mediated proteolysis and RNA transport. Notably, Bou_119143 (UDP-rhamnose rhamnosyltransferase 1) showed a high mutation frequency specifically in bud sports. Conclusions: We provide the first population-genomic evidence that bud sports of ‘Miss Manila’ are genetically distinct clonal lineages, shaped by somatic mutation and selection. These findings support bud sports as efficient sources for germplasm innovation. The identified genomic regions and candidate genes lay a foundation for future marker-assisted selection and molecular breeding in bougainvillea. Full article

Background/Objectives: Growing evidence suggests that disruption of circadian rhythms contributes to the pathogenesis of inflammation and inflammatory bowel disease; however, clinical data linking circadian gene variants to ulcerative colitis remain limited. In this study, we aimed to investigate associations between key circadian rhythm gene polymorphisms and clinical and treatment-related characteristics in ulcerative colitis. Methods: A total of 107 patients with ulcerative colitis and 80 healthy controls were included in this single-center cross-sectional study. The BMAL1 rs7950226, CLOCK rs1801260, and CRY1 rs2287161 polymorphisms were analyzed using the polymerase chain reaction–restriction fragment length polymorphism (PCR-RFLP) method. Genotype and allele frequency distributions were compared between patients and controls, and associations with clinical characteristics were evaluated within the ulcerative colitis cohort. Results: Genotype distributions of BMAL1 rs7950226 and CLOCK rs1801260 were similar between patients with ulcerative colitis and healthy controls; however, the G allele of BMAL1 was more frequent in patients (p = 0.028). Within the ulcerative colitis cohort, CLOCK rs1801260 genotypes were significantly associated with inflammatory and treatment-related characteristics, with the CC genotype linked to higher C-reactive protein levels (p = 0.021) and the TT genotype associated with increased azathioprine use (p = 0.006). Conclusions: These findings suggest a potential association between circadian rhythm gene variants and clinical features of ulcerative colitis, particularly in relation to inflammatory activity and treatment requirements, and provide preliminary clinical insight that warrants further investigation in larger and longitudinal studies. Full article

Background/Objectives: Hearing impairment is a highly prevalent sensory disorder resulting from a variety of causes. A high proportion of autosomal recessive non-syndromic hearing impairment is linked to the GJB2 (OMIM 121011) gene which encodes for a gap junction protein, connexin-26. Alterations of genes that encode for connexins can lead to changes in cell ion content and cause hearing impairment. Methods: GJB2 gene polymorphisms (c.71G>A, p.Trp24*rs104894396; c.457G>A, p.Val153Ile, rs111033186; c.380G>A, p.Arg127His, rs111033196; c.109G>A, p.Val37Ile, rs72474224; and c.269T>C, p.Leu90Pro, rs80338945) were analyzed in the Roma population of Croatia. Loci were genotyped using the KASP method. Results: Altered alleles were detected on the loci c.71G>A, c.457G>A and c.380G>A and statistically significant differences in allele frequencies were noticed. Furthermore, in comparison to worldwide populations, the Roma population also shows statistically significant difference in allele frequency of these loci. Conclusions: This study reveals marked genetic differentiation among Croatian Roma particularly with respect to the c.71G>A variant. Characterizing such population-specific mutational heterogeneity is crucial for the accurate prevention, diagnosis, and clinical management of autosomal recessive nonsyndromic hearing loss. Full article

Background/Objectives: Multiple epiphyseal dysplasia (MED) is a clinically and genetically heterogeneous group of disorders characterized by a waddling gait, joint pain, and early-onset osteoarthritis. The aim of this study was to compare the genetic characteristics and long-term clinical follow-up findings of 22 patients with MED from 17 unrelated families. Methods: Molecular diagnosis was performed using clinical exome analysis and exome sequencing. Seventeen children were followed for a median of 5.5 years. Results: Eighteen disease-related variants were identified: 47% in COMP, 11.8% each in COL9A2 and COL9A3 in a monoallelic state, 17.6% in SLC26A2, and 11.8% each in MATN3 and CANT1 in a biallelic state. Some COMP mutations previously identified in pseudoachondroplasia, an allelic disorder of MED1, were shown in our study to exhibit a typical MED1 or intermediate phenotype. In contrast, it was confirmed that certain mutations in SLC26A2 lead to MED4 phenotype. Furthermore, it has been observed that biallelic variants in MATN3 may be associated with the MED5 phenotype. In patients with MED2 and MED3, the knee joint is affected, while in other types, the hip joint is predominantly affected. In 15 children followed until ages 11–18, height decreased slightly as they grew older but remained normal or at the lower limit, and slow progression was observed in the waddling gait and joint pain, except in the intermediate form. Conclusions: This study reveals the frequency of disease-related variants, including seven novel ones, in genes leading to MED1–5 and 7 phenotypes, and expands the spectrum of genetic and clinical phenotypes. Full article

Most glaucoma genetic data derive from European and East Asian cohorts, leaving high-consanguinity Middle Eastern populations under-characterized. This review synthesizes 33 Saudi-specific genetic studies (2014–2024, >9000 participants) to define a population-level glaucoma genetic architecture that diverges substantially from global models and carries direct precision medicine implications. Three findings distinguish the Saudi landscape. First, CYP1B1 functions as the dominant causal gene across both primary congenital glaucoma (PCG) and juvenile-onset open-angle glaucoma (JOAG), accounting for 76–86% of cases, with two founder alleles, p.G61E (penetrance 87.7%) and p.R469W (penetrance 93%), driving severe, early-onset phenotypes. Critically, MYOC and LTBP2, the primary JOAG genes in other populations, carry no pathogenic variants in Saudi cohorts, rendering standard multi-ethnic gene panels inadequate for this population. Second, adult-onset glaucoma follows a distinct polygenic architecture where APOE ε2 confers a near five-fold risk for primary angle-closure glaucoma (OR = 4.82), an effect absent or inconsistent in global datasets, and NOS3 variants associate with primary open-angle glaucoma specifically in men, a sex-stratified signal unreported outside Saudi cohorts. The MTHFR T/T genotype, common in European and Asian POAG patients, is entirely absent locally, indicating population-specific allelic distributions that alter folate-metabolism-related optic nerve susceptibility. Third, ACVR1 rs12997 associates across POAG, PACG, and pseudoexfoliation glaucoma (PXG), positioning BMP/TGF-β signaling as a shared mechanistic pathway spanning multiple subtypes. These findings argue for Saudi-specific genetic panels, CYP1B1-centered cascade testing in consanguineous families, and polygenic risk models incorporating local allele frequencies rather than globally derived weights. Full article

Background: Heart failure (HF) is a complex disease and one of the major causes of morbidity and mortality in the world. Increased B-type natriuretic peptide (BNP) levels have been associated with HF. The NPPB:rs198389 (c.-381T > C) promoter polymorphism has been found to modulate BNP levels. Aim: To investigate possible associations among the NPPB:rs198389 polymorphism, N-terminal pro-BNP (NT-proBNP) concentrations, and phenotypic features in Polish patients with HF. Methods: The study group comprised 250 patients with HF. Genomic DNA was extracted from blood, and genotyping was performed using PCR-RFLP. Results: There were no significant differences in the distributions of NPPB genotypes or alleles between HF females and HF males. Except for body height, there were no significant differences in phenotypic features among HF patients regarding NPPB:rs198389 genotypes. There were also no significant differences in the distributions of either NPPB:rs198389 genotypes or alleles across NT-proBNP concentration terciles. However, age, left-ventricular-mass index, C-reactive-protein levels, serum-creatinine concentrations, and the incidence of myocardial infarction, left ventricular hypertrophy, or reduced ejection fraction (EF) were significantly lower in patients from the lower tercile (LT) than in patients from the middle and/or upper terciles. EF and the frequency of preserved EF in LT patients were significantly higher than those from other terciles. Conclusions: Our results did not confirm associations between NPPB:rs198389 and NT-proBNP serum concentrations or clinical phenotypes in Polish patients with HF. Full article

Inflammatory joint diseases, including osteoarthritis, are multifactorial disorders in which dysregulated innate immune signaling and non-coding RNA (ncRNA)-mediated regulation of gene expression play essential roles. MicroRNA-155 (miR-155), its host gene MIR155HG, and Toll-like receptor 4 (TLR4) form a tightly linked inflammatory signaling axis, yet their combined genetic variability in chronic joint inflammation remains insufficiently characterized. The aim of this study was to investigate genetic variants in MIR155HG exon 3, mature miR-155, and TLR4 exon 3 and assess their potential synergistic role in chronic inflammatory joint disease. A case–control study was conducted with 100 cases (50 osteoarthritis patients and 50 matched healthy controls). Genomic DNA was analysed using polymerase chain reaction (PCR) and Sanger sequencing. Variant alleles and genotypes were identified, and their allele frequencies and genotypes were calculated using Mutation Surveyor. Detected variants were compared with public databases, and in silico tools were used to estimate the structural impact of TLR4 missense mutations. Sixteen heterozygous variants were identified in MIR155HG exon 3, most of them novel and population-specific. Interestingly, the highest variant frequencies for MIR155HG exon 3 were observed at positions 12448G>GC and 12481T>TA (both 64.3%), followed by 12442T>TC (57.1%). Additionally, two novel variants were detected in the miR-155 gene (chr21:29,694,314 G>A and chr21:29,646,351 T>C), each present at an allele frequency of 7.1% and absent from current external variant databases. Moreover, two rare TLR4 exon-3 variants were identified; a synonymous variant, c.147C>A (Pro49Pro; rs375037549), and a missense mutation, c.148G>A (Asp50Asn; rs776561489). Notably, in silico analyses and molecular dynamic simulations indicated that the Asp50Asn (D50N) substitution destabilizes the TLR4 protein. Conclusion: Concurrent variants in MIR155HG, miR-155, and TLR4 suggest a convergent regulatory molecular axis that may contribute to disease susceptibility and inflammatory progression. Full article

Background: Parkinson’s disease (PD) is clinically heterogeneous, yet the genetic architecture underlying this heterogeneity remains incompletely understood. We examined the genetic correlates of four complementary PD subtyping frameworks: the clinical motor subtype (tremor-dominant [TD] vs. postural instability/gait difficulty [PIGD]), alpha-synuclein seed amplification assay status (SAA+ vs. SAA−), the pathological subtype (brain-first vs. body-first, based on the presence of REM sleep behavior disorder), and the data-driven subtype (diffuse malignant [DM] vs. mild-motor predominant [MMP] vs. intermediate [IM]). Methods: We analyzed 1390 PD patients from the Parkinson’s Progression Markers Initiative (PPMI) with genotypes available for seven PD-associated genes (LRRK2, GBA1, SNCA, PRKN, PINK1, PARK7, VPS35), including specific variant resolutions (LRRK2 G2019S, R1441G/C/H; GBA1 N409S, severe variants; SNCAA53T), and APOE (ε2/ε3/ε4 alleles). Genetic variant frequencies were compared across subtypes using chi-square or Fisher’s exact tests with the Benjamini–Hochberg false discovery rate (FDR) correction. Effect sizes were quantified using Cramér’s V. multivariable logistic regression estimated adjusted odds ratios with Wald-based 95% confidence intervals. Results: Among genotyped PD patients, LRRK2 carriers constituted 13.7% (190/1390; 170 G2019S, 18 R1441G/C/H), GBA1 8.6% (119/1390; 96 N409S, 23 severe), and SNCA 2.0% (28/1390; all A53T). APOE ε4 carriers comprised 23.4% (323/1380). SAA-negative patients were markedly enriched for LRRK2 variants (37.1% vs. 10.2%, p = 3.7 × 10⁻¹⁹, q < 0.001, V = 0.25), specifically G2019S (28.5% vs. 9.6%, p = 4.9 × 10⁻¹¹, q < 0.001) and R1441G/C/H (7.9% vs. 0.5%, p = 2.7 × 10⁻¹², q < 0.001). Body-first PD was enriched for GBA1 carriers (12.3% vs. 6.7%, p = 0.004, q = 0.021) and had less LRRK2 carriers (7.9% vs. 15.0%, p = 0.002, q = 0.013). The DM subtype had the highest GBA1 frequency (14.0% vs. MMP 5.9%, p < 0.001, q = 0.003). After FDR correction, 10 out of 48 univariate tests remained significant. Clinical subtypes (TD vs. PIGD) showed only nominal LRRK2 differences that did not survive FDR correction. The APOE genotype did not differ across any framework. Conclusions: PD subtypes defined by alpha-synuclein pathology (SAA), pathological onset pattern (brain-first/body-first), and data-driven classification (DM/MMP/IM) show distinct genetic profiles that survive multiple comparison correction. LRRK2 variants strongly associate with SAA negativity (V = 0.25); GBA1 variants associate with the severe body-first onset and the diffuse malignant subtype. Full article

Peripheral artery disease (PAD) is a global health burden affecting over 200 million individuals and is frequently complicated by limb-threatening ischemia, leading to major amputations. Despite known clinical risk factors, the genetic basis underlying amputation risk in PAD remains poorly defined. In this study, we performed a multi-pronged genome-wide association study (GWAS) to identify genetic variants associated with lower extremity amputation in patients with PAD, using data from the All of Us Research Program. Two analytical strategies were employed: a targeted GWAS using ClinVar variants on the full cohort and a comprehensive genome-wide association study using Allele Count/Allele Frequency (ACAF) data on a balanced subset of the cohort. The ClinVar analysis of 118,871 variants in 7558 PAD patients (405 with amputation, 7153 without) identified 3 suggestive associations with a genomic inflation factor of 1.046. The ACAF analysis of 7,784,837 quality-controlled variants in 804 balanced samples (399 cases, 405 controls) yielded 35 suggestive associations (p < 1 × 10⁻⁵) with a genomic inflation factor of 1.017. No variants achieved suggestive significance in both analyses. These findings highlight candidate loci for further validation and may inform future development of risk prediction tools and targeted interventions to reduce limb loss in PAD. All associations are exploratory and require independent replication. Full article

Background: Athletic performance is a multifactorial construct influenced by physiological, biomechanical, and psychological determinants. In recent years, genetic factors have been increasingly recognized as contributors to inter-individual variability in performance. In particular, polymorphisms in genes involved in neurobiological pathways have been associated with cognitive processes relevant to sport performance. However, the distribution of cognition-related genetic variants in elite athletes has not been systematically synthesized. Methods: This meta-analysis aimed to examine the distribution of selected candidate gene polymorphisms previously associated with cognition-related traits in elite athletes compared to control populations. A systematic literature search identified 17 eligible case–control studies investigating allele distributions of COMT rs4680, BDNF rs6265, DRD2 rs1800497, OPRM1 rs1799971, and HTR1A rs6295. Pooled analyses were performed using a fixed-effect model, and odds ratios (ORs) with 95% confidence intervals (CIs) were calculated. Results: Elite athletes demonstrated a significantly higher frequency of the G allele of COMT rs4680 (OR = 1.11; 95% CI: 1.02–1.21; p = 0.013) and the G allele of BDNF rs6265 (OR = 1.40; 95% CI: 1.10–1.77; p = 0.005) compared to controls. No significant differences were observed for HTR1A rs6295, DRD2 rs1800497, or OPRM1 rs1799971 polymorphisms (p > 0.05). Conclusions: This meta-analysis indicates that certain genetic variants previously associated with cognition-related traits, particularly COMT rs4680 and BDNF rs6265, are more frequently observed in elite athletes. These findings suggest a potential association between cognition-related genetic pathways and elite athletic status. However, as the present analysis is based on genetic distribution rather than direct cognitive assessments, the results should be interpreted within the context of association rather than causation. Full article

Chronic inflammation contributes to bladder cancer (BC) development and progression through dysregulated cytokine signaling and tumor–immune interactions. This case–control study investigated associations between IL6 rs1800795, TNF rs1800629, CCL2 rs1024611, and VEGFA rs699947 polymorphisms, circulating cytokine levels, clinicopathological characteristics, and autonomic nervous system balance assessed by heart rate variability (HRV) in 73 BC patients and 88 controls. Genotyping was performed using PCR–RFLP, serum cytokine levels were measured by ELISA, and associations were evaluated using logistic, linear regression, and survival analyses. No significant associations with BC risk were observed for IL6, TNF, or VEGFA variants. However, the CCL2 rs1024611 GG genotype was associated with increased BC risk (recessive model: OR = 5.82, p = 0.026). Stratified analyses showed a lower frequency of the IL6 rs1800795 C allele and TNF rs1800629 GA genotype in high-grade and muscle-invasive tumors, suggesting potential associations with reduced tumor aggressiveness. No polymorphism was associated with serum cytokine levels or disease-free survival. In BC patients, the TNF rs1800629 A allele was associated with higher parasympathetic-related HRV indices and lower sympathetic parameters, whereas no such associations were observed in controls. These findings indicate that genetic variation within inflammatory pathways may contribute to BC susceptibility and tumor phenotype and may also modulate neuroimmune interactions. Full article

The insulin-like growth factor 1 (IGF-1) gene plays a key role in growth and production traits in livestock. Limited information is available regarding its genetic polymorphisms in Saudi camel breeds. This study aimed to investigate genetic variation in the IGF-1 gene among Saudi camel breeds to provide baseline genetic information for future association studies. A total of 176 camels representing six Saudi breeds were sampled. DNA was extracted and Polymerase chain reaction (PCR) amplification and Sanger sequencing were applied to detect IGF-1 polymorphisms. Genotype and allele frequencies were calculated across breeds, and statistical comparisons were performed based on proportional distributions to account for unequal sample sizes. Two single-nucleotide polymorphisms (SNPs) were identified: c.365G>A in exon 3 and c.435C>T in exon 5. The exon 3 variant resulted in a missense mutation (p. Arg122His) but was detected in heterozygous form in only one camel, and subsequent screening of 109 additional samples confirmed its rarity. The exon 5 variant was synonymous in isoform X1 and located in the 3′ untranslated region of isoform X2. Sequencing of 176 camels revealed that c.435C>T was highly polymorphic across the examined breeds. Significant differences in genotype frequencies were observed within and among breeds (p < 0.001). The CT genotype predominated in Waddah (60%), Shageh (48%), and Sofor (60%), significantly exceeding CC and TT frequencies (p < 0.001). In Majaheem and Saheli, CT (47%) and TT (45%) were nearly equal and both significantly higher than CC (p < 0.001). Shaele exhibited a distinct pattern, with TT being most frequent (57%), significantly higher than CC (7%, p < 0.001) and CT (36%, p < 0.01). These findings indicate directional selection favoring the C allele in the Waddah and Shageh breeds, whereas the T allele is favored in the remaining breeds. This study provides the first baseline characterization of IGF-1 polymorphisms among Saudi camel breeds. Although no phenotypic associations were assessed, the results offer a foundation for future research examining relationships between IGF-1 variants and economically important traits. Full article