@article{meals_roy_medvedev_wallace_neviaser_o'brien_2016, title={Identifying the Risk of Swallowing-Related Pulmonary Complications in Older Patients With Hip Fracture}, volume={39}, ISSN={["1938-2367"]}, DOI={10.3928/01477447-20151222-07}, abstractNote={
            To identify and potentially modify the risk of pulmonary complications in a group of older patients with hip fracture, the authors obtained speech and language pathology consultations for these patients. Then they performed a retrospective chart review of all patients 65 years and older who were admitted to their institution between June 2011 and July 2013 with acute hip fracture, were treated surgically, and had a speech and language pathology evaluation in the immediate perioperative period. The authors identified 52 patients who met the study criteria. According to the American Society of Anesthesiologists (ASA) classification system, at the time of surgery, 1 patient (2%) was classified as ASA I, 12 patients (23%) were ASA II, 26 (50%) were ASA III, and 12 (23%) were ASA IV. Based on a speech and language pathology evaluation, 22 patients (42%) were diagnosed with dysphagia. Statistical analysis showed that ASA III status and ASA IV status were meaningful predictors of dysphagia and that dysphagia itself was a strong risk factor for pulmonary aspiration, pneumonia, and aspiration pneumonitis. Evaluation by a speech and language pathologist, particularly of patients classified as ASA III or ASA IV, may be an efficient means of averting pulmonary morbidity that is common in older patients with hip fracture. [
            Orthopedics.
            2016; 39(1):e93–e97.]
          }, number={1}, journal={ORTHOPEDICS}, author={Meals, Clifton and Roy, Siddharth and Medvedev, Gleb and Wallace, Matthew and Neviaser, Robert J. and O'Brien, Joseph}, year={2016}, pages={E93–E97} }
 @article{poorman_borst_moroff_roy_labelle_motsinger-reif_breen_2015, title={Comparative cytogenetic characterization of primary canine melanocytic lesions using array CGH and fluorescence in situ hybridization}, volume={23}, ISSN={["1573-6849"]}, DOI={10.1007/s10577-014-9444-6}, abstractNote={Melanocytic lesions originating from the oral mucosa or cutaneous epithelium are common in the general dog population, with up to 100,000 diagnoses each year in the USA. Oral melanoma is the most frequent canine neoplasm of the oral cavity, exhibiting a highly aggressive course. Cutaneous melanocytomas occur frequently, but rarely develop into a malignant form. Despite the differential prognosis, it has been assumed that subtypes of melanocytic lesions represent the same disease. To address the relative paucity of information about their genomic status, molecular cytogenetic analysis was performed on the three recognized subtypes of canine melanocytic lesions. Using array comparative genomic hybridization (aCGH) analysis, highly aberrant distinct copy number status across the tumor genome for both of the malignant melanoma subtypes was revealed. The most frequent aberrations included gain of dog chromosome (CFA) 13 and 17 and loss of CFA 22. Melanocytomas possessed fewer genome wide aberrations, yet showed a recurrent gain of CFA 20q15.3–17. A distinctive copy number profile, evident only in oral melanomas, displayed a sigmoidal pattern of copy number loss followed immediately by a gain, around CFA 30q14. Moreover, when assessed by fluorescence in situ hybridization (FISH), copy number aberrations of targeted genes, such as gain of c-MYC (80 % of cases) and loss of CDKN2A (68 % of cases), were observed. This study suggests that in concordance with what is known for human melanomas, canine melanomas of the oral mucosa and cutaneous epithelium are discrete and initiated by different molecular pathways.}, number={2}, journal={CHROMOSOME RESEARCH}, author={Poorman, Kelsey and Borst, Luke and Moroff, Scott and Roy, Siddharth and Labelle, Philippe and Motsinger-Reif, Alison and Breen, Matthew}, year={2015}, month={Jun}, pages={171–186} }
 @article{hertz_roy_jack_motsinger-reif_drobish_clark_carey_dees_mcleod_2014, title={Genetic heterogeneity beyond CYP2C8*3 does not explain differential sensitivity to paclitaxel-induced neuropathy}, volume={145}, ISSN={["1573-7217"]}, DOI={10.1007/s10549-014-2910-1}, abstractNote={The development of paclitaxel-induced peripheral neuropathy (PIPN) is influenced by drug exposure and patient genetics. The purpose of this analysis was to expand on a previous reported association of CYP2C8*3 and PIPN risk by investigating additional polymorphisms in CYP2C8 and in hundreds of other genes potentially relevant to paclitaxel pharmacokinetics. Clinical data was collected prospectively in an observational registry of newly diagnosed breast cancer patients. Patients treated with paclitaxel-containing regimens were genotyped using the Affymetrix DMET™ Plus chip. Patients who carried the CYP2C8*2, *3, or *4 variant were collapsed into a low-metabolizer CYP2C8 phenotype for association with PIPN. Separately, all SNPs that surpassed quality control were assessed individually and as a composite of genetic ancestry for associations with PIPN. 412 paclitaxel-treated patients and 564 genetic markers were included in the analysis. The risk of PIPN was significantly greater in the CYP2C8 low-metabolizer group (HR = 1.722, p = 0.018); however, the influences of the *2 and *4 SNPs were not independently significant (*2: p = 0.847, *4: p = 0.408). One intronic SNP in ABCG1 (rs492338) surpassed the exploratory significance threshold for an association with PIPN in the Caucasian cohort (p = 0.0008) but not in the non-Caucasian replication group (p = 0.54). Substantial genetic variability was observed within self-reported racial groups but this genetic variability was not associated with risk of grade 2+ PIPN. The pharmacogenetic heterogeneity within a cohort of breast cancer patients is dramatic, though we did not find evidence that this heterogeneity directly influences the risk of PIPN beyond the contribution of CYP2C8*3.}, number={1}, journal={BREAST CANCER RESEARCH AND TREATMENT}, author={Hertz, Daniel L. and Roy, Siddharth and Jack, John and Motsinger-Reif, Alison A. and Drobish, Amy and Clark, L. Scott and Carey, Lisa A. and Dees, E. Claire and McLeod, Howard L.}, year={2014}, month={May}, pages={245–254} }