Examining correlation of altmetric score and citation number in dermatology journal articles.

OBJECTIVES: Determine the correlation between Altmetric score and citation number for publications in high-impact dermatology journals and examine the characteristics of these articles. MATERIALS AND METHODS: Four high-impact dermatology journals were examined for the top 10% of articles as ranked by Altmetric score. Spearman's Rank correlation coefficient was performed on log-transformed Altmetric scores and citation numbers. Dimensions and Altmetric were used to determine journal characteristics. RESULTS: Among the 165 articles analyzed, Altmetric score does not correlate with citation number (rs = 0.0047 and ρ = .953) or type of observational study. The highest performing journal articles represented a variety of journal types and topics. CONCLUSIONS: Online attention does not necessarily correspond with dissemination through traditional citation. While Altmetric scores convey much information about online dissemination, both Altmetric scores and citation numbers should be taken into account when evaluating a publication's impact.

Molecular analysis of cyclin D1 modulators PRKN and FBX4 as candidate tumor suppressors in sporadic parathyroid adenomas.

OBJECTIVE: Primary hyperparathyroidism is most often caused by a sporadic single-gland parathyroid adenoma (PTA), a tumor type for which cyclin D1 is the only known and experimentally validated oncoprotein. However, the molecular origins of its frequent overexpression have remained mostly elusive. In this study, we explored a potential tumorigenic mechanism that could increase cyclin D1 stability through a defect in molecules responsible for its degradation. METHODS: We examined two tumor suppressor genes known to modulate cyclin D1 ubiquitination, PRKN and FBXO4 (FBX4), for evidence of classic two-hit tumor suppressor inactivation within a cohort of 82 PTA cases. We examined the cohort for intragenic inactivating and splice site mutations by Sanger sequencing and for locus-associated loss of heterozygosity (LOH) by microsatellite analysis. RESULTS: We identified no evidence of bi-allelic tumor suppressor inactivation of PRKN or FBXO4 via inactivating mutation or splice site perturbation, neither in combination with nor independent of LOH. Among the 82 cases, we encountered previously documented benign single nucleotide polymorphisms (SNPs) in 35 tumors at frequencies similar to those reported in the germlines of the general population. Eight cases exhibited intragenic LOH at the PRKN locus, in some cases extending to cover at least an additional 1.7 Mb of chromosome 6q25-26. FBXO4 was not affected by LOH. CONCLUSION: The absence of evidence for specific bi-allelic inactivation in PRKN and FBXO4 in this sizeable cohort suggests that these genes only rarely, if ever, serve as classic driver tumor suppressors responsible for the growth of PTAs.