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Latest Articles Include:

• Data producers deserve citation credit
  - Nat Genet 41(10):1045 (2009)
  Datasets released to public databases in advance of (or with) research publications should be given digital object identifiers to allow databases and journals to give quantitative citation credit to the data producers and curators.
• Alzheimer's disease beyond APOE
  - Nat Genet 41(10):1047-1048 (2009)
  Two genome-wide association studies together report three new susceptibility loci for late-onset Alzheimer's disease. CLU, PICALM and CR1 may be involved in amyloid- clearance from the brain.
• Interferon-alfa, interferon- and hepatitis C
  - Nat Genet 41(10):1048-1050 (2009)
  Three new studies report genetic variants near IL28B, which encodes interferon-3 (interleukin 28B), are associated with response to treatment of chronic hepatitis C virus infection with interferon-alfa/ribavirin combination therapy. This renews interest in how interferons suppress viremia and could lead to improved clinical decisions for chronic HCV infection treatment based on individual genotype.
• Tcf proteins are deeply rooted in skin
  - Nat Genet 41(10):1050-1051 (2009)
  Adult mammalian tissues are maintained by multipotent stem cells, many of which are highly responsive to soluble Wnt proteins. A new study reports the requirement of two Tcf family members, Tcf3 and Tcf4, in the development and maintenance of epithelial stem cells in skin through Wnt-dependent and -independent processes.
• Research highlights
  - Nat Genet 41(10):1052 (2009)
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• Identification of a new prostate cancer susceptibility locus on chromosome 8q24
  Yeager M Chatterjee N Ciampa J Jacobs KB Gonzalez-Bosquet J Hayes RB Kraft P Wacholder S Orr N Berndt S Yu K Hutchinson A Wang Z Amundadottir L Feigelson HS Thun MJ Diver WR Albanes D Virtamo J Weinstein S Schumacher FR Cancel-Tassin G Cussenot O Valeri A Andriole GL Crawford ED Haiman CA Henderson B Kolonel L Le Marchand L Siddiq A Riboli E Key TJ Kaaks R Isaacs W Isaacs S Wiley KE Gronberg H Wiklund F Stattin P Xu J Zheng SL Sun J Vatten LJ Hveem K Kumle M Tucker M Gerhard DS Hoover RN Fraumeni JF Hunter DJ Thomas G Chanock SJ - Nat Genet 41(10):1055-1057 (2009)
  We report a genome-wide association study in 10,286 cases and 9,135 controls of European ancestry in the Cancer Genetic Markers of Susceptibility (CGEMS) initiative. We identify a new association with prostate cancer risk on chromosome 8q24 (rs620861, P = 1.3 10-10, heterozygote OR = 1.17, 95% CI 1.10–1.24; homozygote OR = 1.33, 95% CI 1.21–1.45). This defines a new locus associated with prostate cancer susceptibility on 8q24.
• Multiple loci on 8q24 associated with prostate cancer susceptibility
  Al Olama AA Kote-Jarai Z Giles GG Guy M Morrison J Severi G Leongamornlert DA Tymrakiewicz M Jhavar S Saunders E Hopper JL Southey MC Muir KR English DR Dearnaley DP Ardern-Jones AT Hall AL O'Brien LT Wilkinson RA Sawyer E Lophatananon A The UK Genetic Prostate Cancer Study Collaborators/British Association of Urological Surgeons' Section of Oncology The UK Prostate testing for cancer and Treatment study (ProtecT Study) Collaborators Horwich A Huddart RA Khoo VS Parker CC Woodhouse CJ Thompson A Christmas T Ogden C Cooper C Donovan JL Hamdy FC Neal DE Eeles RA Easton DF - Nat Genet 41(10):1058-1060 (2009)
  Previous studies have identified multiple loci on 8q24 associated with prostate cancer risk. We performed a comprehensive analysis of SNP associations across 8q24 by genotyping tag SNPs in 5,504 prostate cancer cases and 5,834 controls. We confirmed associations at three previously reported loci and identified additional loci in two other linkage disequilibrium blocks (rs1006908: per-allele OR = 0.87, P = 7.9 10-8; rs620861: OR = 0.90, P = 4.8 10-8). Eight SNPs in five linkage disequilibrium blocks were independently associated with prostate cancer susceptibility.
• Personalized copy number and segmental duplication maps using next-generation sequencing
  - Nat Genet 41(10):1061-1067 (2009)
  Despite their importance in gene innovation and phenotypic variation, duplicated regions have remained largely intractable owing to difficulties in accurately resolving their structure, copy number and sequence content. We present an algorithm (mrFAST) to comprehensively map next-generation sequence reads, which allows for the prediction of absolute copy-number variation of duplicated segments and genes. We examine three human genomes and experimentally validate genome-wide copy number differences. We estimate that, on average, 73–87 genes vary in copy number between any two individuals and find that these genic differences overwhelmingly correspond to segmental duplications (odds ratio = 135; P < 2.2 10-16). Our method can distinguish between different copies of highly identical genes, providing a more accurate assessment of gene content and insight into functional constraint without the limitations of array-based technology.
• Tcf3 and Tcf4 are essential for long-term homeostasis of skin epithelia
  - Nat Genet 41(10):1068-1075 (2009)
  Single-layered embryonic skin either stratifies to form epidermis or responds to Wnt signaling (stabilized -catenin) to form hair follicles. Postnatally, stem cells continue to differentially use Wnt signaling in long-term tissue homeostasis. We have discovered that embryonic progenitor cells and postnatal hair follicle stem cells coexpress Tcf3 and Tcf4, which can act as transcriptional activators or repressors. Using loss-of-function studies and transcriptional analyses, we uncovered consequences to the absence of Tcf3 and Tcf4 in skin that only partially overlap with those caused by -catenin deficiency. We established roles for Tcf3 and Tcf4 in long-term maintenance and wound repair of both epidermis and hair follicles, suggesting that Tcf proteins have both Wnt-dependent and Wnt-independent roles in lineage determination.
• Polyhomeotic has a tumor suppressor activity mediated by repression of Notch signaling
  - Nat Genet 41(10):1076-1082 (2009)
  Polycomb Group (PcG) proteins silence critical developmental genes and modulate cell proliferation. Using the Drosophila melanogaster eye as a model system, we show that cells with mutations in the gene locus (ph) that encodes the PcG protein Polyhomeotic (PH) overproliferate and lose both the ability to differentiate and their normal polarity. They invade the neighboring tissues and, when combined with an activated form of the Ras proto-oncogene, they trigger the formation of metastases. PcG proteins bind to multiple genes in the Notch pathway and control their transcription as well as Notch signaling. The massive cell-autonomous overproliferation of ph mutant cell clones can be rescued by ectopic expression of a dominant negative form of Notch or by RNA interference (RNAi)-mediated repression of Notch. Conversely, overexpression of ph induces a small-eye phenotype that is rescued by activation of Notch signaling. These data show that ph is a tumor suppressor locus th! at controls cellular proliferation by silencing multiple Notch signaling components.
• Genome-wide association study identifies 19p13.3 (UNC13A) and 9p21.2 as susceptibility loci for sporadic amyotrophic lateral sclerosis
  - Nat Genet 41(10):1083-1087 (2009)
  We conducted a genome-wide association study among 2,323 individuals with sporadic amyotrophic lateral sclerosis (ALS) and 9,013 control subjects and evaluated all SNPs with P < 1.0 10-4 in a second, independent cohort of 2,532 affected individuals and 5,940 controls. Analysis of the genome-wide data revealed genome-wide significance for one SNP, rs12608932, with P = 1.30 10-9. This SNP showed robust replication in the second cohort (P = 1.86 10-6), and a combined analysis over the two stages yielded P = 2.53 10-14. The rs12608932 SNP is located at 19p13.3 and maps to a haplotype block within the boundaries of UNC13A, which regulates the release of neurotransmitters such as glutamate at neuromuscular synapses. Follow-up of additional SNPs showed genome-wide significance for two further SNPs (rs2814707, with P = 7.45 10-9, and rs3849942, with P = 1.01 10-8) in the combined analysis of both stages. These SNPs are located at chromosome 9p21.2, in a linkage region fo! r familial ALS with frontotemporal dementia found previously in several large pedigrees.
• Genome-wide association study identifies variants at CLU and PICALM associated with Alzheimer's disease
  - Nat Genet 41(10):1088-1093 (2009)
  We undertook a two-stage genome-wide association study (GWAS) of Alzheimer's disease (AD) involving over 16,000 individuals, the most powerful AD GWAS to date. In stage 1 (3,941 cases and 7,848 controls), we replicated the established association with the apolipoprotein E (APOE) locus (most significant SNP, rs2075650, P = 1.8 10-157) and observed genome-wide significant association with SNPs at two loci not previously associated with the disease: at the CLU (also known as APOJ) gene (rs11136000, P = 1.4 10-9) and 5' to the PICALM gene (rs3851179, P = 1.9 10-8). These associations were replicated in stage 2 (2,023 cases and 2,340 controls), producing compelling evidence for association with Alzheimer's disease in the combined dataset (rs11136000, P = 8.5 10-10, odds ratio = 0.86; rs3851179, P = 1.3 10-9, odds ratio = 0.86).
• Genome-wide association study identifies variants at CLU and CR1 associated with Alzheimer's disease
  - Nat Genet 41(10):1094-1099 (2009)
  The gene encoding apolipoprotein E (APOE) on chromosome 19 is the only confirmed susceptibility locus for late-onset Alzheimer's disease. To identify other risk loci, we conducted a large genome-wide association study of 2,032 individuals from France with Alzheimer's disease (cases) and 5,328 controls. Markers outside APOE with suggestive evidence of association (P < 10-5) were examined in collections from Belgium, Finland, Italy and Spain totaling 3,978 Alzheimer's disease cases and 3,297 controls. Two loci gave replicated evidence of association: one within CLU (also called APOJ), encoding clusterin or apolipoprotein J, on chromosome 8 (rs11136000, OR = 0.86, 95% CI 0.81–0.90, P = 7.5 10-9 for combined data) and the other within CR1, encoding the complement component (3b/4b) receptor 1, on chromosome 1 (rs6656401, OR = 1.21, 95% CI 1.14–1.29, P = 3.7 10-9 for combined data). Previous biological studies support roles of CLU and CR1 in the clearance of amyloid (! A) peptide, the principal constituent of amyloid plaques, which are one of the major brain lesions of individuals with Alzheimer's disease.
• IL28B is associated with response to chronic hepatitis C interferon- and ribavirin therapy
  - Nat Genet 41(10):1100-1104 (2009)
  Hepatitis C virus (HCV) infects 3% of the world's population. Treatment of chronic HCV consists of a combination of PEGylated interferon- (PEG-IFN-) and ribavirin (RBV). To identify genetic variants associated with HCV treatment response, we conducted a genome-wide association study of sustained virological response (SVR) to PEG-IFN-/RBV combination therapy in 293 Australian individuals with genotype 1 chronic hepatitis C, with validation in an independent replication cohort consisting of 555 individuals. We report an association to SVR within the gene region encoding interleukin 28B (IL28B, also called IFN3; rs8099917 combined P = 9.25 10-9, OR = 1.98, 95% CI = 1.57–2.52). IL28B contributes to viral resistance and is known to be upregulated by interferons and by RNA virus infection. These data suggest that host genetics may be useful for the prediction of drug response, and they also support the investigation of the role of IL28B in the treatment of HCV and in othe! r diseases treated with IFN-.
• Genome-wide association of IL28B with response to pegylated interferon- and ribavirin therapy for chronic hepatitis C
  - Nat Genet 41(10):1105-1109 (2009)
  The recommended treatment for patients with chronic hepatitis C, pegylated interferon- (PEG-IFN-) plus ribavirin (RBV), does not provide sustained virologic response (SVR) in all patients. We report a genome-wide association study (GWAS) to null virological response (NVR) in the treatment of patients with hepatitis C virus (HCV) genotype 1 within a Japanese population. We found two SNPs near the gene IL28B on chromosome 19 to be strongly associated with NVR (rs12980275, P = 1.93 10-13, and rs8099917, 3.11 10-15). We replicated these associations in an independent cohort (combined P values, 2.84 10-27 (OR = 17.7; 95% CI = 10.0–31.3) and 2.68 10-32 (OR = 27.1; 95% CI = 14.6–50.3), respectively). Compared to NVR, these SNPs were also associated with SVR (rs12980275, P = 3.99 10-24, and rs8099917, P = 1.11 10-27). In further fine mapping of the region, seven SNPs (rs8105790, rs11881222, rs8103142, rs28416813, rs4803219, rs8099917 and rs7248668) located in the IL2! 8B region showed the most significant associations (P = 5.52 10-28–2.68 10-32; OR = 22.3–27.1). Real-time quantitative PCR assays in peripheral blood mononuclear cells showed lower IL28B expression levels in individuals carrying the minor alleles (P = 0.015).
• Genetic variant near IRS1 is associated with type 2 diabetes, insulin resistance and hyperinsulinemia
  - Nat Genet 41(10):1110-1115 (2009)
  Genome-wide association studies have identified common variants that only partially explain the genetic risk for type 2 diabetes (T2D). Using genome-wide association data from 1,376 French individuals, we identified 16,360 SNPs nominally associated with T2D and studied these SNPs in an independent sample of 4,977 French individuals. We then selected the 28 best hits for replication in 7,698 Danish subjects and identified 4 SNPs showing strong association with T2D, one of which (rs2943641, P = 9.3 10-12, OR = 1.19) was located adjacent to the insulin receptor substrate 1 gene (IRS1). Unlike previously reported T2D risk loci, which predominantly associate with impaired beta cell function, the C allele of rs2943641 was associated with insulin resistance and hyperinsulinemia in 14,358 French, Danish and Finnish participants from population-based cohorts; this allele was also associated with reduced basal levels of IRS1 protein and decreased insulin induction of IRS1-assoc! iated phosphatidylinositol-3-OH kinase activity in human skeletal muscle biopsies.
• Identification of seven new prostate cancer susceptibility loci through a genome-wide association study
  Eeles RA Kote-Jarai Z Al Olama AA Giles GG Guy M Severi G Muir K Hopper JL Henderson BE Haiman CA Schleutker J Hamdy FC Neal DE Donovan JL Stanford JL Ostrander EA Ingles SA John EM Thibodeau SN Schaid D Park JY Spurdle A Clements J Dickinson JL Maier C Vogel W Dörk T Rebbeck TR Cooney KA Cannon-Albright L Chappuis PO Hutter P Zeegers M Kaneva R Zhang HW Lu YJ Foulkes WD English DR Leongamornlert DA Tymrakiewicz M Morrison J Ardern-Jones AT Hall AL O'Brien LT Wilkinson RA Saunders EJ Page EC Sawyer EJ Edwards SM Dearnaley DP Horwich A Huddart RA Khoo VS Parker CC Van As N Woodhouse CJ Thompson A Christmas T Ogden C Cooper CS Southey MC Lophatananon A Liu JF Kolonel LN Le Marchand L Wahlfors T Tammela TL Auvinen A Lewis SJ Cox A Fitzgerald LM Koopmeiners JS Karyadi DM Kwon EM Stern MC Corral R Joshi AD Shahabi A McDonnell SK Sellers TA Pow-Sang J Chambers S Aitken J Gardiner RA Batra J Kedda MA Lose F Polanowski A Patterson B Serth J Meyer A Luedeke M Stefflova K Ray AM Lange EM Farnham J Khan H Slavov C Mitkova A Cao G The UK Genetic Prostate Cancer Study Collaborators/British Association of Urological Surgeons' Section of Oncology The UK ProtecT Study Collaborators The PRACTICAL Consortium Easton DF - Nat Genet 41(10):1116-1121 (2009)
  Prostate cancer (PrCa) is the most frequently diagnosed cancer in males in developed countries. To identify common PrCa susceptibility alleles, we previously conducted a genome-wide association study in which 541,129 SNPs were genotyped in 1,854 PrCa cases with clinically detected disease and in 1,894 controls. We have now extended the study to evaluate promising associations in a second stage in which we genotyped 43,671 SNPs in 3,650 PrCa cases and 3,940 controls and in a third stage involving an additional 16,229 cases and 14,821 controls from 21 studies. In addition to replicating previous associations, we identified seven new prostate cancer susceptibility loci on chromosomes 2, 4, 8, 11 and 22 (with P = 1.6 10-8 to P = 2.7 10-33).
• Genome-wide association and replication studies identify four variants associated with prostate cancer susceptibility
  Gudmundsson J Sulem P Gudbjartsson DF Blondal T Gylfason A Agnarsson BA Benediktsdottir KR Magnusdottir DN Orlygsdottir G Jakobsdottir M Stacey SN Sigurdsson A Wahlfors T Tammela T Breyer JP McReynolds KM Bradley KM Saez B Godino J Navarrete S Fuertes F Murillo L Polo E Aben KK van Oort IM Suarez BK Helfand BT Kan D Zanon C Frigge ML Kristjansson K Gulcher JR Einarsson GV Jonsson E Catalona WJ Mayordomo JI Kiemeney LA Smith JR Schleutker J Barkardottir RB Kong A Thorsteinsdottir U Rafnar T Stefansson K - Nat Genet 41(10):1122-1126 (2009)
  We report a prostate cancer genome-wide association follow-on study. We discovered four variants associated with susceptibility to prostate cancer in several European populations: rs10934853[A] (OR = 1.12, P = 2.9 10-10) on 3q21.3; two moderately correlated (r2 = 0.07) variants, rs16902094[G] (OR = 1.21, P = 6.2 10-15) and rs445114[T] (OR = 1.14, P = 4.7 10-10), on 8q24.21; and rs8102476[C] (OR = 1.12, P = 1.6 10-11) on 19q13.2. We also refined a previous association signal on 11q13 with the SNP rs11228565[A] (OR = 1.23, P = 6.7 10-12). In a multivariate analysis using 22 prostate cancer risk variants typed in the Icelandic population, we estimated that carriers in the top 1.3% of the risk distribution are at a 2.5 times greater risk of developing the disease than members of the general population.
• Analysis of the tyrosine kinome in melanoma reveals recurrent mutations in ERBB4
  - Nat Genet 41(10):1127-1132 (2009)
  Tyrosine phosphorylation is important in signaling pathways underlying tumorigenesis. We performed a mutational analysis of the protein tyrosine kinase (PTK) gene family in cutaneous metastatic melanoma. We identified 30 somatic mutations affecting the kinase domains of 19 PTKs and subsequently evaluated the entire coding regions of the genes encoding these 19 PTKs for somatic mutations in 79 melanoma samples. We found ERBB4 mutations in 19% of individuals with melanoma and found mutations in two other kinases (FLT1 and PTK2B) in 10% of individuals with melanomas. We examined seven missense mutations in the most commonly altered PTK gene, ERBB4, and found that they resulted in increased kinase activity and transformation ability. Melanoma cells expressing mutant ERBB4 had reduced cell growth after shRNA-mediated knockdown of ERBB4 or treatment with the ERBB inhibitor lapatinib. These studies could lead to personalized therapeutics specifically targeting the kinases tha! t are mutationally altered in individual melanomas.
• In vivo RNAi screening identifies regulators of actin dynamics as key determinants of lymphoma progression
  - Nat Genet 41(10):1133-1137 (2009)
  Mouse models have markedly improved our understanding of cancer development and tumor biology. However, these models have shown limited efficacy as tractable systems for unbiased genetic experimentation. Here, we report the adaptation of loss-of-function screening to mouse models of cancer. Specifically, we have been able to introduce a library of shRNAs into individual mice using transplantable E-myc lymphoma cells. This approach has allowed us to screen nearly 1,000 genetic alterations in the context of a single tumor-bearing mouse. These experiments have identified a central role for regulators of actin dynamics and cell motility in lymphoma cell homeostasis in vivo. Validation experiments confirmed that these proteins represent bona fide lymphoma drug targets. Additionally, suppression of two of these targets, Rac2 and twinfilin, potentiated the action of the front-line chemotherapeutic vincristine, suggesting a critical relationship between cell motility and tumor! relapse in hematopoietic malignancies.
• p53 deletion impairs clearance of chromosomal-instable stem cells in aging telomere-dysfunctional mice
  - Nat Genet 41(10):1138-1143 (2009)
  Telomere dysfunction limits the proliferative capacity of human cells and induces organismal aging by activation of p53 and p21 (refs. 1, 2, 3, 4, 5, 6). Although deletion of p21 elongates the lifespan of telomere-dysfunctional mice2, a direct analysis of p53 in telomere-related aging has been hampered by early tumor formation in p53 knockout mice6. Here we analyzed the functional consequences of conditional p53 deletion7. Intestinal deletion of p53 shortened the lifespan of telomere-dysfunctional mice without inducing tumor formation. In contrast to p21 deletion, the deletion of p53 impaired the depletion of chromosomal-instable intestinal stem cells in aging telomere-dysfunctional mice. These instable stem cells contributed to epithelial regeneration leading to an accumulation of chromosomal instability, increased apoptosis, altered epithelial cell differentiation and premature intestinal failure. Together, these results provide the first experimental evidence for an! organ system in which p53-dependent mechanisms prevent tissue destruction in response to telomere dysfunction by depleting genetically instable stem cells.
• Tissue regenerative delays and synthetic lethality in adult mice after combined deletion of Atr and Trp53
  - Nat Genet 41(10):1144-1149 (2009)
  Trp53 loss of function has previously been shown to rescue tissue maintenance and developmental defects resulting from DNA damage or DNA-repair gene mutations1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12. Here, we report that p53 deficiency severely exacerbates tissue degeneration caused by mosaic deletion of the essential genome maintenance regulator Atr. Combined loss of Atr and p53 (Trp53-/-AtrmKO) led to severe defects in hair follicle regeneration, localized inflammation (Mac1+Gr1+ infiltrates), accelerated deterioration of the intestinal epithelium and synthetic lethality in adult mice. Tissue degeneration in Trp53-/-AtrmKO mice was characterized by the accumulation of cells maintaining high levels of DNA damage. Moreover, the elevated frequency of these damaged cells in both progenitor and downstream compartments in Trp53-/-AtrmKO skin coincided with delayed compensatory tissue renewal from residual ATR-expressing cells. Together, our results indicate that the combined ! loss of Atr and Trp53 in adult mice leads to the accumulation of highly damaged cells, which, consequently, impose a barrier to regeneration from undamaged progenitors.
• A tumor suppressor activity of Drosophila Polycomb genes mediated by JAK-STAT signaling
  - Nat Genet 41(10):1150-1155 (2009)
  A prevailing paradigm posits that Polycomb Group (PcG) proteins maintain stem cell identity by repressing differentiation genes, and abundant evidence points to an oncogenic role for PcG proteins in human cancer1, 2. Here we show using Drosophila melanogaster that a conventional PcG complex can also have a potent tumor suppressor activity. Mutations in any core PRC1 component cause pronounced hyperproliferation of eye imaginal tissue, accompanied by deregulation of epithelial architecture. The mitogenic JAK-STAT pathway is strongly and specifically activated in mutant tissue; activation is driven by transcriptional upregulation of Unpaired (Upd, also known as Outstretched, Os) family ligands. We show here that upd genes are direct targets of PcG-mediated repression in imaginal discs. Ectopic JAK-STAT activity is sufficient to induce overproliferation, whereas reduction of JAK-STAT activity suppresses the PRC1 mutant tumor phenotype. These findings show that PcG protein! s can restrict growth directly by silencing mitogenic signaling pathways, shedding light on an epigenetic mechanism underlying tumor suppression.
• Corrigendum: Genetic variation in the prostate stem cell antigen gene PSCA confers susceptibility to urinary bladder cancer
  - Nat Genet 41(10):1156 (2009)
  Introduction Nat. Genet. 41, 991–995 (2009); published online 2 August; corrected online 23 August 2009 ADVERTISEMENT In the version of this article initially published online, Simonetta Guarrera and Silvia Polidoro were inadvertently omitted from the author list, and an affiliation was omitted for Paolo Vineis. These errors have been corrected in all versions of this article.
• Erratum: Elucidating the role of 8q24 in colorectal cancer
  - Nat Genet 41(10):1156 (2009)
  Introduction Nat. Genet. 41, 868–869 (2009); published online 29 July; corrected after print 27 August 2009 ADVERTISEMENT In the version of this article initially published, there were two errors in the author contact information. The authors are at Scripps Genomic Medicine, Scripps Translational Science Institute and the Scripps Research Institute, La Jolla, California, USA; e-mail: e-mail: kfrazer@scripps.edu or e-mail: kafrazer@ucsd.edu. These errors have been corrected in the HTML and PDF versions of the article.
• Erratum: Genetic variant near IRS1 is associated with type 2 diabetes, insulin resistance and hyperinsulinemia
  - Nat Genet 41(10):1156 (2009)
  Introduction Nat. Genet. 41, 1110–1115; published online 6 September; corrected online 13 September 2009 ADVERTISEMENT In the version of this article initially published online, there were errors in the e-mail addresses of two of the corresponding authors. The correct e-mail address for Robert Sladek is e-mail: robert.sladek@mcgill.ca; the correct e-mail address for Philippe Froguel is e-mail: philippe.froguel@good.ibl.fr. These errors have been corrected for all versions of this article.
• Erratum: Genome-wide association study identifies variants at CLU and PICALM associated with Alzheimer's disease
  - Nat Genet 41(10):1156 (2009)
  Introduction Nat. Genet. 41, 1088–1093 (2009); published online 6 September; corrected after print 28 September 2009 ADVERTISEMENT In the version of this article initially published, the name of the first author of reference 12 was stated incorrectly in the reference list. The correct reference is: "Lambert, J.-C. et al. Genome-wide association study identifies variants at CLU and CR1 associated with Alzheimer's disease. Nat. Genet. advance online publication, doi:10.1038/ng.439 (6 September 2009)." The error has been corrected in the HTML and PDF versions of the article.