Purpose: The aim of this study is to identify highly cited articles and examine trends and characteristics in research on periacetabular osteotomy. Materials and Methods: The 50 most highly cited articles on periacetabular osteotomy research were identified using Scopus. Data regarding article demographics and publication were collected from each article and an analysis was performed. Results: The mean citation count was 125±37. The article with the highest total citation count (796), five-year citation count (327), and five-year citation density (65/year) was reported by Reinhold Ganz. The five-year citation density showed strong correlation with total citation density (r=0.930, P<0.001). Reinhold Ganz, the most productive author, was listed on 13 articles in the cohort with 455 weighted citation points. Conclusion This study provides a collection of articles examining periacetabular osteotomies and demonstrates that citation count can be regarded as an acceptable measure of the contemporary academic influence of an article.

Distal biceps rupture is a relatively uncommon injury that can significantly affect quality of life. Early complications following biceps tendon repair are not well described in the literature. This study utilizes a national surgical database to determine the incidence of and predictors for short-term complications following distal biceps tendon repair. Methods: The American College of Surgeons’ National Surgical Quality Improvement Program database was used to identify patients undergoing distal biceps repair between January 1, 2011, and December 31, 2017. Patient demographic variables of sex, age, body mass index, American Society of Anesthesiologists class, functional status, and several comorbidities were collected for each patient, along with 30-day postoperative complications. Binary logistic regression was used to calculate risk ratios for these complications using patient predictor variables. Results: Early postoperative surgical complications (0.5%)—which were mostly infections (0.4%)—and medical complications (0.3%) were rare. A readmission risk factor was diabetes (risk ratio [RR], 4.238; 95% confidence interval [CI], 1.180–15.218). Non-home discharge risk factors were smoking (RR, 3.006; 95% CI, 1.123–8.044) and ≥60 years of age (RR, 4.150; 95% CI, 1.611– 10.686). Maleness was protective for medical complications (RR, 0.024; 95% CI, 0.005–0.126). Surgical complication risk factors were obese class II (RR, 4.120; 95% CI, 1.123–15.120), chronic obstructive pulmonary disease (COPD; RR, 21.981; 95% CI, 3.719–129.924), and inpatient surgery (RR, 8.606; 95% CI, 2.266–32.689). Conclusions: Complication rates after distal biceps repair are low. Various patient demographics, medical comorbidities, and surgical factors were all predictive of short-term complications.

Purpose: The purpose of this study was to determine if somatic mutations are associated with clinical and pathologic outcomes in patients with borderline resectable pancreatic cancer (BRPC) or locally advanced pancreatic cancer (LAPC) who were treated with neoadjuvant chemotherapy and stereotactic body radiotherapy (SBRT). Materials and Methods: Patients treated with neoadjuvant chemotherapy and SBRT followed by surgical resection from August 2016 to January 2019 and who underwent next generation sequencing of their primary tumor were included in the study. Next-generation sequencing was performed either in-house with a Solid Tumor Panel or with FoundationOne CDx. Univariate (UVA) and multivariable analyses (MVA) were performed to determine associations between somatic mutations and pathologic and clinical outcomes. Results: Thirty-five patients were included in the study. Chemotherapy consisted of modified FOLFIRINOX, gemcitabine and nab-paclitaxel, or gemcitabine and capecitabine. Patients were treated with SBRT in 33 Gy in 5 fractions. On UVA and MVA, tumors with KRAS G12V mutation demonstrated better pathologic tumor regression grade (TRG) to neoadjuvant therapy when compared to tumors with other KRAS mutations (odds ratio = 0.087; 95% confidence interval [CI], 0.009–0.860; p = 0.036). On UVA and MVA, mutations in NOTCH1/2 were associated with worse overall survival (hazard ratio [HR] = 4.15; 95% CI, 1.57–10.95; p = 0.004) and progression-free survival (HR = 3.61; 95% CI, 1.41–9.28; p = 0.008). On UVA, only mutations in NOTCH1/2 were associated with inferior distant metastasis-free survival (HR = 3.38; 95% CI, 1.25–9.16; p = 0.017). Conclusion In BRPC and LAPC, the KRAS G12V mutation was associated with better TRG following chemotherapy and SBRT. Additionally, NOTCH1/2 mutations were associated with worse overall survival, distant metastasis-free survival, and progression-free survival.

Purpose: To investigate the role of pre- and post-stereotactic body radiation therapy (SBRT) neutrophil-to-lymphocyte ratio (NLR) in patients with localized pancreatic cancer treated with anti-PD-1 (programmed cell death protein-1) antibody and SBRT. Materials and Methods: This was a retrospective review of 68 patients with borderline resectable or locally advanced pancreatic cancer treated with anti-PD-1 antibody and SBRT after multi-agent chemotherapy. Immunotherapy was administered with 5-fraction SBRT in the neoadjuvant, concurrent, or adjuvant/maintenance setting. Clinical outcomes included overall survival (OS), local progression-free survival, distant metastasis-free survival, and progression-free survival. Median pre- and post-SBRT peripheral blood markers were compared with the Mann-Whitney U test. Univariate and multivariable analyses (UVA and MVA) were performed to identify variables associated with clinical outcomes. Linear regression was performed to determine correlations between variables and peripheral blood markers. Results: A total of 68 patients were included in the study. The percent change between median pre- and post-SBRT absolute lymphocyte count (ALC), absolute neutrophil count, and NLR were -36.0% (p < 0.001), -5.6% (p = 0.190), and +35.7% (p = 0.003), respectively. Median OS after SBRT was 22.4 months. On UVA, pre-SBRT CA19-9 (hazard ratio [HR] = 1.001; 95% confidence interval [CI], 1.000–1.001; p = 0.031), post-SBRT ALC (HR = 0.33; 95% CI, 0.11–0.91; p = 0.031), and post-SBRT NLR (HR = 1.13; 95% CI, 1.04–1.22; p = 0.009) were associated with OS. On MVA, induction chemotherapy duration (HR = 0.75; 95% CI, 0.57–0.99; p = 0.048) and post-SBRT NLR (HR = 1.14; 95% CI, 1.04–1.23; p = 0.002) predicted for OS. Patients with post-SBRT NLR ≥3.2 had a median OS of 15.6 months versus 27.6 months in patients with post-SBRT NLR <3.2 (p = 0.009). On MVA linear regression, log10CTV had a negative correlation with post-SBRT ALC (regression coefficient = -0.314; 95% CI, -0.626 to -0.003; p = 0.048). Conclusion Elevated NLR after SBRT is primarily due to depletion of lymphocytes and associated with worse survival outcomes in localized pancreatic cancer treated with anti-PD-1 antibody. Larger CTVs were associated with decreased post-SBRT ALC.

There is evidence that a substantial part of genetic predisposition to prostate cancer (PCa) may be due to lower penetrance genes which are found by genome-wide association studies. We have recently conducted such a study and seven new regions of the genome linked to PCa risk have been identified. Three of these loci contain candidate susceptibility genes: MSMB, LMTK2 and KLK2/3. The MSMB and KLK2/3 genes may be useful for PCa screening, and the LMTK2 gene might provide a potential therapeutic target. Together with results from other groups, there are now 23 germline genetic variants which have been reported. These results have the potential to be developed into a genetic test. However, we consider that marketing of tests to the public is premature, as PCa risk can not be evaluated fully at this stage and the appropriate screening protocols need to be developed. Follow-up validation studies, as well as studies to explore the psychological implications of genetic profile testing, will be vital prior to roll out into healthcare.
Genetic Predisposition to Disease ; genetics ; Genetic Testing ; Humans ; Kallikreins ; genetics ; Male ; Membrane Proteins ; genetics ; Prostatic Neoplasms ; diagnosis ; genetics ; Prostatic Secretory Proteins ; genetics ; Protein-Serine-Threonine Kinases ; genetics ; Risk Factors