@article{smith_waddell_dean_anandan_gurney_kabnick_little_mcdonald_mohan_marenda_et al._2021, title={Course-based undergraduate research experiences are a viable approach to increase access to research experiences in biology}, volume={6}, ISSN={0021-9266 2157-6009}, url={http://dx.doi.org/10.1080/00219266.2021.1933135}, DOI={10.1080/00219266.2021.1933135}, abstractNote={ABSTRACT Course-based undergraduate research experiences (CUREs) have been described as a mechanism to allow more undergraduates to engage in research experiences. To understand whether CUREs are viable to scale-up undergraduate access to research experiences, it is essential to carefully evaluate whether CUREs promote comparable self-reported outcomes for students and are less resource intensive than undergraduate research internships. In comparing student outcomes from four distinct CUREs to outcomes from students engaged in a summer research programme in the biology department at one institution, we found that students in both experiences self-report comparable gains on all items studied using the Undergraduate Research Student Self-Assessment tool. CURE students report similar levels of satisfaction with aspects of research experiences, such as amount of time spent conducting research and working with a mentor, compared with students engaged in the summer research programme. The CUREs studied here are less resource intensive than the summer research programme, and still led to comparable self-reported outcomes. These courses increased the number of biology undergraduates able to engage in research experiences, suggesting that CUREs are a viable option to expand access to research experiences that promote expected learning outcomes in a more efficient way.}, journal={Journal of Biological Education}, publisher={Informa UK Limited}, author={Smith, Kevin P.W. and Waddell, Edward A. and Dean, Annette N. and Anandan, Shivanthi and Gurney, Susan and Kabnick, Karen and Little, Joy and McDonald, Matthew and Mohan, Jaya and Marenda, Daniel R. and et al.}, year={2021}, month={Jun}, pages={1–15} }
 @article{madden_lahue_gordy_little_nichols_calvert_dunn_smukowski heil_2021, title={Sugar‐seeking insects as a source of diverse bread‐making yeasts with enhanced attributes}, volume={39}, ISSN={0749-503X 1097-0061}, url={http://dx.doi.org/10.1002/yea.3676}, DOI={10.1002/yea.3676}, abstractNote={AbstractInsects represent a particularly interesting habitat in which to search for novel yeasts of value to industry. Insect‐associated yeasts have the potential to have traits relevant to modern food and beverage production due to insect–yeast interactions, with such traits including diverse carbohydrate metabolisms, high sugar tolerance, and general stress tolerance. Here, we consider the potential value of insect‐associated yeasts in the specific context of baking. We isolated 63 yeast strains from 13 species of hymenoptera from the United States, representing 37 yeast species from 14 genera. Screening for the ability to ferment maltose, a sugar important for bread production, resulted in the identification of 13 strains of Candida, Lachancea, and Pichia species. We assessed their ability to leaven dough. All strains produced baked loaves comparable to a commercial baking strain of Saccharomyces cerevisiae. The same 13 strains were also grown under various sugar and salt conditions relevant to osmotic challenges experienced in the manufacturing processes and the production of sweet dough. We show that many of these yeast strains, most notably strains of Lachancea species, grow at a similar or higher rate and population size as commercial baker's yeast. We additionally assessed the comparative phenotypes and genetics of insect‐associated S. cerevisiae strains unable to ferment maltose and identified baking‐relevant traits, including variations in the HOG1 signaling pathway and diverse carbohydrate metabolisms. Our results suggest that non‐conventional yeasts have high potential for baking and, more generally, showcase the success of bioprospecting in insects for identifying yeasts relevant for industrial uses.}, number={1-2}, journal={Yeast}, publisher={Wiley}, author={Madden, Anne A. and Lahue, Caitlin and Gordy, Claire L. and Little, Joy L. and Nichols, Lauren M. and Calvert, Martha D. and Dunn, Robert R. and Smukowski Heil, Caiti}, year={2021}, month={Nov}, pages={108–127} }
 @article{apellido_balchander_erlich_gocal_gocal_haile_kang_koduri_natrajan_parikh_et al._2019, title={Complete Genome Sequences of 12 B1 Cluster Mycobacteriophages, Gareth, JangoPhett, Kailash, MichaelPhcott, PhenghisKhan, Phleuron, Phergie, PhrankReynolds, PhrodoBaggins, Phunky, Vaticameos, and Virapocalypse}, volume={8}, ISBN={2576-098X}, ISSN={2576-098X}, url={http://dx.doi.org/10.1128/MRA.01387-18}, DOI={10.1128/MRA.01387-18}, abstractNote={
            Twelve B1 cluster mycobacteriophages were isolated from soil samples collected in Philadelphia, PA, USA, using
            Mycobacterium smegmatis
            mc
            2
            155 as a host, and were sequenced. The genome sequences range in size from 66,887 bp to 68,953 bp in length and have between 99 and 105 putative protein-coding genes.
          }, number={8}, journal={Microbiology Resource Announcements}, publisher={American Society for Microbiology}, author={Apellido, Kristofer A. and Balchander, Divya and Erlich, Matthew C. and Gocal, Jakub K. and Gocal, Wiktoria A. and Haile, Selam and Kang, Annette K. and Koduri, Sravya and Natrajan, Maanasa and Parikh, Ayush A. and et al.}, editor={Dennehy, John J.Editor}, year={2019}, month={Feb} }
 @article{pradhan_nako_tran_aluri_anandarajan_betini_bhatt_chengalvala_cox_delvadia_et al._2018, title={Complete Genome Sequence of Cluster J Mycobacteriophage Superphikiman}, volume={6}, ISSN={2169-8287}, url={http://dx.doi.org/10.1128/genomeA.01538-17}, DOI={10.1128/genomeA.01538-17}, abstractNote={ABSTRACT
          Mycobacteriophage Superphikiman is a cluster J bacteriophage which was isolated from soil collected in Philadelphia, PA. Superphikiman has a 109,799-bp genome with 239 predicted genes, including 2 tRNA genes.}, number={5}, journal={Genome Announcements}, publisher={American Society for Microbiology}, author={Pradhan, Pratik and Nako, Sprikena and Tran, Trinh and Aluri, Lavanya S. and Anandarajan, Dharman and Betini, Niteesha and Bhatt, Shivangi D. and Chengalvala, Swetha and Cox, Nicole E. and Delvadia, Bela P. and et al.}, year={2018}, month={Feb} }
 @article{hanauer_graham_betancur_bobrownicki_cresawn_garlena_jacobs-sera_kaufmann_pope_russell_et al._2017, title={An inclusive Research Education Community (iREC): Impact of the SEA-PHAGES program on research outcomes and student learning}, volume={114}, ISSN={0027-8424 1091-6490}, url={http://dx.doi.org/10.1073/pnas.1718188115}, DOI={10.1073/pnas.1718188115}, abstractNote={Significance
          The Science Education Alliance–Phage Hunters Advancing Genomics and Evolutionary Science program is an inclusive Research Education Community with centralized programmatic and scientific support, in which broad student engagement in authentic science is linked to increased accessibility to research experiences for students; increased persistence of these students in science, technology, engineering, and mathematics; and increased scientific productivity for students and faculty alike.}, number={51}, journal={Proceedings of the National Academy of Sciences}, publisher={Proceedings of the National Academy of Sciences}, author={Hanauer, David I. and Graham, Mark J. and Betancur, Laura and Bobrownicki, Aiyana and Cresawn, Steven G. and Garlena, Rebecca A. and Jacobs-Sera, Deborah and Kaufmann, Nancy and Pope, Welkin H. and Russell, Daniel A. and et al.}, year={2017}, month={Dec}, pages={13531–13536} }
 @article{little_serzhanova_izumchenko_egleston_parise_klein-szanto_loudon_shubina_seo_kurokawa_et al._2014, title={A requirement for Nedd9 in luminal progenitor cells prior to mammary tumorigenesis in MMTV-HER2/ErbB2 mice}, volume={33}, ISSN={0950-9232 1476-5594}, url={http://dx.doi.org/10.1038/onc.2012.607}, DOI={10.1038/onc.2012.607}, abstractNote={Overexpression of the NEDD9/HEF1/Cas-L scaffolding protein is frequent, and drives invasion and metastasis in breast, head and neck, colorectal, melanoma, lung and other types of cancer. We have examined the consequences of genetic ablation of Nedd9 in the MMTV-HER2/ERBB2/neu mouse mammary tumor model. Unexpectedly, we found that only a limited effect on metastasis in MMTV-neu;Nedd9−/− mice compared with MMTV-neu;Nedd9+/+ mice, but instead a dramatic reduction in tumor incidence (18 versus 80%), and a significantly increased latency until tumor appearance. Orthotopic reinjection and tail-vein injection of cells arising from tumors, coupled with in vivo analysis, indicated tumors arising in MMTV-neu;Nedd9−/− mice had undergone mutational selection that overcame the initial requirement for Nedd9. To better understand the defects in early tumor growth, we compared mammary progenitor cell pools from MMTV-neu;Nedd9−/− versus MMTV-neu;Nedd9+/+ mice. The MMTV-neu;Nedd9−/− genotype selectively reduced both the number and colony-forming potential of mammary luminal epithelial progenitor cells, while not affecting basal epithelial progenitors. MMTV-neu;Nedd9−/− mammospheres had striking defects in morphology and cell polarity. All of these defects were seen predominantly in the context of the HER2/neu oncogene, and were not associated with randomization of the plane of mitotic division, but rather with depressed expression the cell attachment protein FAK, accompanied by increased sensitivity to small molecule inhibitors of FAK and SRC. Surprisingly, in spite of these significant differences, only minimal changes were observed in the gene expression profile of Nedd9−/− mice, indicating critical Nedd9-dependent differences in cell growth properties were mediated via post-transcriptional regulation of cell signaling. Coupled with emerging data indicating a role for NEDD9 in progenitor cell populations during the morphogenesis of other tissues, these results indicate a functional requirement for NEDD9 in the growth of mammary cancer progenitor cells.}, number={4}, journal={Oncogene}, publisher={Springer Science and Business Media LLC}, author={Little, J L and Serzhanova, V and Izumchenko, E and Egleston, B L and Parise, E and Klein-Szanto, A J and Loudon, G and Shubina, M and Seo, S and Kurokawa, M and et al.}, year={2014}, month={Jan}, pages={411–420} }
 @article{seeger-nukpezah_little_serzhanova_golemis_2013, title={Cilia and cilia-associated proteins in cancer}, volume={10}, ISSN={1740-6765}, url={http://dx.doi.org/10.1016/j.ddmec.2013.03.004}, DOI={10.1016/j.ddmec.2013.03.004}, abstractNote={The primary cilium is a well-established target in the pathogenesis of numerous developmental and chronic disorders, and more recently is attracting interest as a structure relevant to cancer. Here we discuss mechanisms by which changes in cilia can contribute to the formation and growth of tumors. We emphasize the cancer-relevance of cilia-dependent signaling pathways and proteins, including mTOR, VHL, TSC, WNT, Aurora-A, NEDD9 and Hedgehog, and highlight the emerging role of ciliary dysfunction in renal cell carcinoma, medulloblastoma and breast cancer.}, number={3-4}, journal={Drug Discovery Today: Disease Mechanisms}, publisher={Elsevier BV}, author={Seeger-Nukpezah, Tamina and Little, Joy L. and Serzhanova, Victoria and Golemis, Erica A.}, year={2013}, month={Dec}, pages={e135–e142} }
 @inbook{little_golemis_2013, place={New York}, title={NEDD9}, ISBN={9781461466130}, url={http://dx.doi.org/10.1007/978-1-4614-6613-0_44-2}, DOI={10.1007/978-1-4614-6613-0_44-2}, booktitle={Cancer Therapeutic Targets}, publisher={Springer}, author={Little, Joy and Golemis, Erica}, editor={Marshall, John L.Editor}, year={2013} }
 @article{tikhmyanova_little_golemis_2009, title={CAS proteins in normal and pathological cell growth control}, volume={67}, ISSN={1420-682X 1420-9071}, url={http://dx.doi.org/10.1007/s00018-009-0213-1}, DOI={10.1007/s00018-009-0213-1}, abstractNote={Proteins of the CAS (Crk-associated substrate) family (BCAR1/p130Cas, NEDD9/HEF1/Cas-L, EFS/SIN and CASS4/HEPL) are integral players in normal and pathological cell biology. CAS proteins act as scaffolds to regulate protein complexes controlling migration and chemotaxis, apoptosis, cell cycle, and differentiation, and have more recently been linked to a role in progenitor cell function. Reflecting these complex functions, over-expression of CAS proteins has now been strongly linked to poor prognosis and increased metastasis in cancer, as well as resistance to first-line chemotherapeutics in multiple tumor types including breast and lung cancers, glioblastoma, and melanoma. Further, CAS proteins have also been linked to additional pathological conditions including inflammatory disorders, Alzheimer's and Parkinson's disease, as well as developmental defects. This review will explore the roles of the CAS proteins in normal and pathological states in the context of the many mechanistic insights into CAS protein function that have emerged in the past decade.}, number={7}, journal={Cellular and Molecular Life Sciences}, publisher={Springer Science and Business Media LLC}, author={Tikhmyanova, Nadezhda and Little, Joy L. and Golemis, Erica A.}, year={2009}, month={Nov}, pages={1025–1048} }
 @article{izumchenko_singh_plotnikova_tikhmyanova_little_serebriiskii_seo_kurokawa_egleston_klein-szanto_et al._2009, title={NEDD9 Promotes Oncogenic Signaling in Mammary Tumor Development}, volume={69}, ISSN={0008-5472 1538-7445}, url={http://dx.doi.org/10.1158/0008-5472.can-09-0795}, DOI={10.1158/0008-5472.can-09-0795}, abstractNote={Abstract
               In the past 3 years, altered expression of the HEF1/CAS-L/NEDD9 scaffolding protein has emerged as contributing to cancer metastasis in multiple cancer types. However, whereas some studies have identified elevated NEDD9 expression as prometastatic, other work has suggested a negative role in tumor progression. We here show that the Nedd9-null genetic background significantly limits mammary tumor initiation in the MMTV-polyoma virus middle T genetic model. Action of NEDD9 is tumor cell intrinsic, with immune cell infiltration, stroma, and angiogenesis unaffected. The majority of the late-appearing mammary tumors of MMTV-polyoma virus middle T;Nedd9−/− mice are characterized by depressed activation of proteins including AKT, Src, FAK, and extracellular signal-regulated kinase, emphasizing an important role of NEDD9 as a scaffolding protein for these prooncogenic proteins. Analysis of cells derived from primary Nedd9+/+ and Nedd9−/− tumors showed persistently reduced FAK activation, attachment, and migration, consistent with a role for NEDD9 activation of FAK in promoting tumor aggressiveness. This study provides the first in vivo evidence of a role for NEDD9 in breast cancer progression and suggests that NEDD9 expression may provide a biomarker for tumor aggressiveness. [Cancer Res 2009;69(18):7198–206]}, number={18}, journal={Cancer Research}, publisher={American Association for Cancer Research (AACR)}, author={Izumchenko, Eugene and Singh, Mahendra K. and Plotnikova, Olga V. and Tikhmyanova, Nadezhda and Little, Joy L. and Serebriiskii, Ilya G. and Seo, Sachiko and Kurokawa, Mineo and Egleston, Brian L. and Klein-Szanto, Andres and et al.}, year={2009}, month={Sep}, pages={7198–7206} }
 @article{little_wheeler_koumenis_kridel_2008, title={Disruption of crosstalk between the fatty acid synthesis and proteasome pathways enhances unfolded protein response signaling and cell death}, volume={7}, ISSN={1535-7163 1538-8514}, url={http://dx.doi.org/10.1158/1535-7163.mct-08-0558}, DOI={10.1158/1535-7163.mct-08-0558}, abstractNote={Abstract
               Fatty acid synthase (FASN) is the terminal enzyme responsible for fatty acid synthesis and is up-regulated in tumors of various origins to facilitate their growth and progression. Because of several reports linking the FASN and proteasome pathways, we asked whether FASN inhibitors could combine with bortezomib, the Food and Drug Administration-approved proteasome inhibitor, to amplify cell death. Indeed, bortezomib treatment augmented suboptimal FASN inhibitor concentrations to reduce clonogenic survival, which was paralleled by an increase in apoptotic markers. Interestingly, FASN inhibitors induced accumulation of ubiquinated proteins and enhanced the effects of bortezomib treatment. In turn, bortezomib increased fatty acid synthesis, suggesting crosstalk between the pathways. We hypothesized that cell death resulting from crosstalk perturbation was mediated by increased unfolded protein response (UPR) signaling. Indeed, disruption of crosstalk activated and saturated the adaptation arm of UPR signaling, including eIF2α phosphorylation, activating transcription factor 4 expression, and X-box-binding protein 1 splicing. Furthermore, although single agents did not activate the alarm phase of the UPR, crosstalk interruption resulted in activated c-Jun NH2-terminal kinase and C/EBP homologous protein-dependent cell death. Combined, the data support the concept that the UPR balance between adaptive to stress signaling can be exploited to mediate increased cell death and suggests novel applications of FASN inhibitors for clinical use. [Mol Cancer Ther 2008;7(12):3816–24]}, number={12}, journal={Molecular Cancer Therapeutics}, publisher={American Association for Cancer Research (AACR)}, author={Little, Joy L. and Wheeler, Frances B. and Koumenis, Constantinos and Kridel, Steven J.}, year={2008}, month={Dec}, pages={3816–3824} }
 @misc{little_kridel_2008, title={Fatty Acid Synthase Activity in Tumor Cells}, ISBN={9781402088308 9781402088315}, ISSN={0306-0225}, url={http://dx.doi.org/10.1007/978-1-4020-8831-5_7}, DOI={10.1007/978-1-4020-8831-5_7}, abstractNote={While normal tissues are tightly regulated by nutrition and a carefully balanced system of glycolysis and fatty acid synthesis, tumor cells are under significant evolutionary pressure to bypass many of the checks and balances afforded normally. Cancer cells have high energy expenditure from heightened proliferation and metabolism and often show increased lipogenesis. Fatty acid synthase (FASN), the enzyme responsible for catalyzing the ultimate steps of fatty acid synthesis in cells, is expressed at high levels in tumor cells and is mostly absent in corresponding normal cells. Because of the unique expression profile of FASN, there is considerable interest not only in understanding its contribution to tumor cell growth and proliferation, but also in developing inhibitors that target FASN specifically as an anti-tumor modality. Pharmacological blockade of FASN activity has identified a pleiotropic role for FASN in mediating aspects of proliferation, growth and survival. As a result, a clearer understanding of the role of FASN in tumor cells has been developed.}, journal={Subcellular Biochemistry}, publisher={Springer Netherlands}, author={Little, Joy L. and Kridel, Steven J.}, year={2008}, month={Aug}, pages={169–194} }
 @article{little_wheeler_fels_koumenis_kridel_2007, title={Inhibition of Fatty Acid Synthase Induces Endoplasmic Reticulum Stress in Tumor Cells}, volume={67}, ISSN={0008-5472 1538-7445}, url={http://dx.doi.org/10.1158/0008-5472.can-06-1794}, DOI={10.1158/0008-5472.can-06-1794}, abstractNote={Abstract
               Fatty acid synthase (FAS), the cellular enzyme that synthesizes palmitate, is expressed at high levels in tumor cells and is vital for their survival. Through the synthesis of palmitate, FAS primarily drives the synthesis of phospholipids in tumor cells. In this study, we tested the hypothesis that the FAS inhibitors induce endoplasmic reticulum (ER) stress in tumor cells. Treatment of tumor cells with FAS inhibitors induces robust PERK-dependent phosphorylation of the translation initiation factor eIF2α and concomitant inhibition of protein synthesis. PERK-deficient transformed mouse embryonic fibroblasts and HT-29 colon carcinoma cells that express a dominant negative PERK (ΔC-PERK) are hypersensitive to FAS inhibitor–induced cell death. Pharmacologic inhibition of FAS also induces the processing of X-box binding protein-1, indicating that the IRE1 arm of the ER stress response is activated when FAS is inhibited. Induction of ER stress is further confirmed by the increased expression of the ER stress–regulated genes CHOP, ATF4, and GRP78. FAS inhibitor–induced ER stress is activated prior to the detection of caspase 3 and PARP cleavage, primary indicators of cell death, whereas orlistat-induced cell death is rescued by coincubation with the global translation inhibitor cycloheximide. Lastly, FAS inhibitors cooperate with the ER stress inducer thapsigargin to enhance tumor cell killing. These results provide the first evidence that FAS inhibitors induce ER stress and establish an important mechanistic link between FAS activity and ER function. [Cancer Res 2007;67(3):1262–9]}, number={3}, journal={Cancer Research}, publisher={American Association for Cancer Research (AACR)}, author={Little, Joy L. and Wheeler, Frances B. and Fels, Diane R. and Koumenis, Constantinos and Kridel, Steven J.}, year={2007}, month={Feb}, pages={1262–1269} }
 @article{zhao_kridel_thorburn_kooshki_little_hebbar_robbins_2006, title={Fatty acid synthase: a novel target for antiglioma therapy}, volume={95}, ISSN={0007-0920 1532-1827}, url={http://dx.doi.org/10.1038/sj.bjc.6603350}, DOI={10.1038/sj.bjc.6603350}, abstractNote={High levels of fatty acid synthase (FAS) expression have been observed in several cancers, including breast, prostate, colon and lung carcinoma, compared with their respective normal tissue. We present data that show high levels of FAS protein in human and rat glioma cell lines and human glioma tissue samples, as compared to normal rat astrocytes and normal human brain. Incubating glioma cells with the FAS inhibitor cerulenin decreased endogenous fatty acid synthesis by approximately 50%. Cell cycle analysis demonstrated a time- and dose-dependent increase in S-phase cell arrest following cerulenin treatment for 24 h. Further, treatment with cerulenin resulted in time- and dose-dependent decreases in glioma cell viability, as well as reduced clonogenic survival. Increased apoptotic cell death and PARP cleavage were observed in U251 and SNB-19 cells treated with cerulenin, which was independent of the death receptor pathway. Overexpressing Bcl-2 inhibited cerulenin-mediated cell death. In contrast, primary rat astrocytes appeared unaffected. Finally, RNAi-mediated knockdown of FAS leading to reduced FAS enzymatic activity was associated with decreased glioma cell viability. These findings suggest that FAS might be a novel target for antiglioma therapy.}, number={7}, journal={British Journal of Cancer}, publisher={Springer Science and Business Media LLC}, author={Zhao, W and Kridel, S and Thorburn, A and Kooshki, M and Little, J and Hebbar, S and Robbins, M}, year={2006}, month={Sep}, pages={869–878} }
 @article{floyd_farnsworth_kock_mizesko_little_dance_everitt_tichelaar_whitsett_miller_2005, title={Conditional expression of the mutant Ki- rasG12C allele results in formation of benign lung adenomas: development of a novel mouse lung tumor model}, volume={26}, ISSN={1460-2180 0143-3334}, url={http://dx.doi.org/10.1093/carcin/bgi190}, DOI={10.1093/carcin/bgi190}, abstractNote={To determine the effects of expression of mutant Ki-ras on lung tumorigenesis, we developed a bitransgenic mouse model that expresses the human Ki-ras(G12C) allele in alveolar type II and/or Clara cells in a tetracycline-inducible, lung-specific manner. Expression of Ki-ras(G12C) caused multiple, small lung tumors over a 12-month time period. Although tumor multiplicity increased upon continued Ki-ras expression, most lung lesions were hyperplasias or well-differentiated adenomas. This is in contrast to the more severe phenotypes observed in other transgenic mouse models in which different mutant Ki-ras alleles were expressed in the lung. Expression of Ki-ras(G12C) was associated with a 2-fold increase in the activation of the Ras and Ral signaling pathways and increased phosphorylation of Ras downstream effectors, including Erk, p90 ribosomal S6 kinase, ribosomal S6 protein, p38 and MAPKAPK-2. In contrast, expression of the transgene had no effect on the activation of the JNK and Akt signaling pathways. Withdrawal of doxycycline for 1 month resulted in almost a complete absence of proliferative pulmonary lesions, suggesting tumor regression in the absence of Ki-ras expression. Mutant Ki-ras(G12C) expression was sufficient for initial lung tumor transformation, required for maintenance of tumor phenotype, and induced transformation of lung epithelial cells by the activation of multiple effector pathways. These results describe a novel mouse lung tumor model demonstrating benign tumor development in the absence of tumor progression, which will provide a new tool for understanding the early stages of lung tumor pathogenesis.}, number={12}, journal={Carcinogenesis}, publisher={Oxford University Press (OUP)}, author={Floyd, Heather S. and Farnsworth, Charles L. and Kock, Nancy D. and Mizesko, Melissa C. and Little, Joy L. and Dance, Stephanie T. and Everitt, Jeff and Tichelaar, Jay and Whitsett, Jeffrey A. and Miller, Mark Steven}, year={2005}, month={Jul}, pages={2196–2206} }
 @article{xu_turner_little_bleecker_meyers_2002, title={Positive results in association studies are associated with departure from Hardy-Weinberg equilibrium: hint for genotyping error?}, volume={111}, ISSN={0340-6717}, url={http://dx.doi.org/10.1007/s00439-002-0819-y}, DOI={10.1007/s00439-002-0819-y}, number={6}, journal={Human Genetics}, publisher={Springer Science and Business Media LLC}, author={Xu, Jianfeng and Turner, Aubrey and Little, Joy and Bleecker, Eugene and Meyers, Deborah}, year={2002}, month={Dec}, pages={573–574} }