Integrative genomics identifies LMO1 as a neuroblastoma oncogene
GWAS identifies oncogene A genome-wide association study (GWAS) has shown that single nucleotide variants within the LMO1 locus are associated with inherited susceptibility to neuroblastoma, a childhood cancer of the sympathetic nervous system. LMO1 encodes a transcriptional regulator previously lin...
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| Published in | Nature (London) Vol. 469; no. 7329; pp. 216 - 220 |
|---|---|
| Main Authors | , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
London
Nature Publishing Group UK
13.01.2011
Nature Publishing Group |
| Subjects | |
| Online Access | Get full text |
| ISSN | 0028-0836 1476-4687 1476-4687 |
| DOI | 10.1038/nature09609 |
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| Abstract | GWAS identifies oncogene
A genome-wide association study (GWAS) has shown that single nucleotide variants within the
LMO1
locus are associated with inherited susceptibility to neuroblastoma, a childhood cancer of the sympathetic nervous system.
LMO1
encodes a transcriptional regulator previously linked to cancers. Acquired structural variation in the same locus is common in patients with neuroblastoma, suggesting that loci identified through GWAS approaches might also be prone to somatic alterations that influence tumour progression. Such studies could help to identify potential therapy targets and/or biomarkers of cancer aggressiveness.
Here, single nucleotide variants within the
LMO1
locus are shown to be associated with inherited susceptibility to neuroblastoma, a childhood cancer of the sympathetic nervous system. Acquired structural variation in the same locus was also frequently found in neuroblastoma patients, leading to the suggestion that loci identified through genome-wide association studies might be also prone to somatic alterations and therefore identify potential therapy targets and/or biomarkers of tumour aggressiveness.
Neuroblastoma is a childhood cancer of the sympathetic nervous system that accounts for approximately 10% of all paediatric oncology deaths
1
,
2
. To identify genetic risk factors for neuroblastoma, we performed a genome-wide association study (GWAS) on 2,251 patients and 6,097 control subjects of European ancestry from four case series. Here we report a significant association within LIM domain only 1 (
LMO1
) at 11p15.4 (rs110419, combined
P
= 5.2 × 10
−16
, odds ratio of risk allele = 1.34 (95% confidence interval 1.25–1.44)). The signal was enriched in the subset of patients with the most aggressive form of the disease.
LMO1
encodes a cysteine-rich transcriptional regulator, and its paralogues (
LMO2
,
LMO3
and
LMO4
) have each been previously implicated in cancer. In parallel, we analysed genome-wide DNA copy number alterations in 701 primary tumours. We found that the
LMO1
locus was aberrant in 12.4% through a duplication event, and that this event was associated with more advanced disease (
P
< 0.0001) and survival (
P
= 0.041). The germline single nucleotide polymorphism (SNP) risk alleles and somatic copy number gains were associated with increased
LMO1
expression in neuroblastoma cell lines and primary tumours, consistent with a gain-of-function role in tumorigenesis. Short hairpin RNA (shRNA)-mediated depletion of
LMO1
inhibited growth of neuroblastoma cells with high
LMO1
expression, whereas forced expression of
LMO1
in neuroblastoma cells with low
LMO1
expression enhanced proliferation. These data show that common polymorphisms at the
LMO1
locus are strongly associated with susceptibility to developing neuroblastoma, but also may influence the likelihood of further somatic alterations at this locus, leading to malignant progression. |
|---|---|
| AbstractList | Neuroblastoma is a childhood cancer of the sympathetic nervous system that accounts for approximately 10% of all paediatric oncology deaths. To identify genetic risk factors for neuroblastoma, we performed a genome-wide association study (GWAS) on 2,251 patients and 6,097 control subjects of European ancestry from four case series. Here we report a significant association within LIM domain only 1 (LMO1) at 11p15.4 (rs110419, combined P = 5.2 × 10(-16), odds ratio of risk allele = 1.34 (95% confidence interval 1.25-1.44)). The signal was enriched in the subset of patients with the most aggressive form of the disease. LMO1 encodes a cysteine-rich transcriptional regulator, and its paralogues (LMO2, LMO3 and LMO4) have each been previously implicated in cancer. In parallel, we analysed genome-wide DNA copy number alterations in 701 primary tumours. We found that the LMO1 locus was aberrant in 12.4% through a duplication event, and that this event was associated with more advanced disease (P < 0.0001) and survival (P = 0.041). The germline single nucleotide polymorphism (SNP) risk alleles and somatic copy number gains were associated with increased LMO1 expression in neuroblastoma cell lines and primary tumours, consistent with a gain-of-function role in tumorigenesis. Short hairpin RNA (shRNA)-mediated depletion of LMO1 inhibited growth of neuroblastoma cells with high LMO1 expression, whereas forced expression of LMO1 in neuroblastoma cells with low LMO1 expression enhanced proliferation. These data show that common polymorphisms at the LMO1 locus are strongly associated with susceptibility to developing neuroblastoma, but also may influence the likelihood of further somatic alterations at this locus, leading to malignant progression. Neuroblastoma is a childhood cancer of the sympathetic nervous system that accounts for approximately 10% of all paediatric oncology deaths (1,2). To identify genetic risk factors for neuroblastoma, we performed a genome-wide association study (GWAS) on 2,251 patients and 6,097 control subjects of European ancestry from four case series. Here we report a significant association within LIM domain only 1 (LMO1) at 11p15.4 (rs110419, combined P= 5.2 X [10.sup-16], odds ratio of risk allele = 1.34 (95% confidence interval 1.25-1.44)). The signal was enriched in the subset ofpatients with the most aggressive form of the disease. LMO1 encodes a cysteine-rich transcriptional regulator, and its paralogues (LMO2, LMO3 and LMO4) have each been previously implicated in cancer. In parallel, we analysed genome-wide DNA copy number alterations in 701 primary tumours. We found that the LMO1 locus was aberrant in 12.4% through a duplication event, and that this event was associated with more advanced disease (P < 0.0001) and survival (P = 0.041). The germline single nucleotide polymorphism (SNP) risk alleles and somatic copy number gains were associated with increased LMO1expression in neuroblastoma cell lines and primary tumours, consistent with a gain-of-function role in tumorigenesis. Short hairpin RNA (shRNA)-mediated depletion of LMO1 inhibited growth of neuroblastoma cells with high LMO1 expression, whereas forced expression of LMO1 in neuroblastoma cells with low LMO1expression enhanced proliferation. These data show that common polymorphisms at the LMO1 locus are strongly associated with susceptibility to developing neuroblastoma, but also may influence the likelihood of further somatic alterations at this locus, leading to malignant progression. Neuroblastoma is a childhood cancer of the sympathetic nervous system that accounts for approximately 10% of all paediatric oncology deaths 1 , 2 . To identify genetic risk factors for neuroblastoma, we performed a genome-wide association study (GWAS) on 2,251 patients and 6,097 control subjects of European ancestry from four case series. Here we report a significant association within LIM domain only 1 ( LMO1 ) at 11p15.4 (rs110419, combined P = 5.2 × 10 −16 , odds ratio of risk allele = 1.34 (95% confidence interval 1.25–1.44)). The signal was enriched in the subset of patients with the most aggressive form of the disease. LMO1 encodes a cysteine-rich transcriptional regulator, and its paralogues ( LMO2 , LMO3 and LMO4 ) have each been previously implicated in cancer. In parallel, we analysed genome-wide DNA copy number alterations in 701 primary tumours. We found that the LMO1 locus was aberrant in 12.4% through a duplication event, and that this event was associated with more advanced disease ( P < 0.0001) and survival ( P = 0.041). The germline single nucleotide polymorphism (SNP) risk alleles and somatic copy number gains were associated with increased LMO1 expression in neuroblastoma cell lines and primary tumours, consistent with a gain-of-function role in tumorigenesis. Short hairpin RNA (shRNA)-mediated depletion of LMO1 inhibited growth of neuroblastoma cells with high LMO1 expression, whereas forced expression of LMO1 in neuroblastoma cells with low LMO1 expression enhanced proliferation. These data show that common polymorphisms at the LMO1 locus are strongly associated with susceptibility to developing neuroblastoma, but also may influence the likelihood of further somatic alterations at this locus, leading to malignant progression. GWAS identifies oncogene A genome-wide association study (GWAS) has shown that single nucleotide variants within the LMO1 locus are associated with inherited susceptibility to neuroblastoma, a childhood cancer of the sympathetic nervous system. LMO1 encodes a transcriptional regulator previously linked to cancers. Acquired structural variation in the same locus is common in patients with neuroblastoma, suggesting that loci identified through GWAS approaches might also be prone to somatic alterations that influence tumour progression. Such studies could help to identify potential therapy targets and/or biomarkers of cancer aggressiveness. Here, single nucleotide variants within the LMO1 locus are shown to be associated with inherited susceptibility to neuroblastoma, a childhood cancer of the sympathetic nervous system. Acquired structural variation in the same locus was also frequently found in neuroblastoma patients, leading to the suggestion that loci identified through genome-wide association studies might be also prone to somatic alterations and therefore identify potential therapy targets and/or biomarkers of tumour aggressiveness. Neuroblastoma is a childhood cancer of the sympathetic nervous system that accounts for approximately 10% of all paediatric oncology deaths 1 , 2 . To identify genetic risk factors for neuroblastoma, we performed a genome-wide association study (GWAS) on 2,251 patients and 6,097 control subjects of European ancestry from four case series. Here we report a significant association within LIM domain only 1 ( LMO1 ) at 11p15.4 (rs110419, combined P = 5.2 × 10 −16 , odds ratio of risk allele = 1.34 (95% confidence interval 1.25–1.44)). The signal was enriched in the subset of patients with the most aggressive form of the disease. LMO1 encodes a cysteine-rich transcriptional regulator, and its paralogues ( LMO2 , LMO3 and LMO4 ) have each been previously implicated in cancer. In parallel, we analysed genome-wide DNA copy number alterations in 701 primary tumours. We found that the LMO1 locus was aberrant in 12.4% through a duplication event, and that this event was associated with more advanced disease ( P < 0.0001) and survival ( P = 0.041). The germline single nucleotide polymorphism (SNP) risk alleles and somatic copy number gains were associated with increased LMO1 expression in neuroblastoma cell lines and primary tumours, consistent with a gain-of-function role in tumorigenesis. Short hairpin RNA (shRNA)-mediated depletion of LMO1 inhibited growth of neuroblastoma cells with high LMO1 expression, whereas forced expression of LMO1 in neuroblastoma cells with low LMO1 expression enhanced proliferation. These data show that common polymorphisms at the LMO1 locus are strongly associated with susceptibility to developing neuroblastoma, but also may influence the likelihood of further somatic alterations at this locus, leading to malignant progression. Neuroblastoma is a childhood cancer of the sympathetic nervous system that accounts for approximately10%of all paediatric oncology deaths. To identify genetic risk factors for neuroblastoma, we performed a genome-wide association study (GWAS) on 2,251 patients and 6,097 control subjects of European ancestry from four case series. Here we report a significant association within LIM domain only 1 (LMO1) at 11p15.4 (rs110419, combined P = 5.2 × 10^sup -16^, odds ratio of risk allele = 1.34 (95% confidence interval 1.25-1.44)). The signal was enriched in the subset of patients with the most aggressive form of the disease. LMO1 encodes a cysteine-rich transcriptional regulator, and its paralogues (LMO2, LMO3 and LMO4) have each been previously implicated in cancer. In parallel, we analysed genome-wide DNA copy number alterations in 701 primary tumours. We found that the LMO1 locus was aberrant in 12.4% through a duplication event, and that this event was associated with more advanced disease (P < 0.0001) and survival (P = 0.041).The germline single nucleotide polymorphism (SNP) risk alleles and somatic copy number gains were associated with increased LMO1 expression in neuroblastoma cell lines and primary tumours, consistent with a gain-of-function role in tumorigenesis. Short hairpin RNA (shRNA)-mediated depletion of LMO1 inhibited growth of neuroblastoma cells with high LMO1 expression, whereas forced expression ofLMO1 in neuroblastoma cells with low LMO1 expression enhanced proliferation. These data show that common polymorphisms at the LMO1 locus are strongly associated with susceptibility to developing neuroblastoma, but also may influence the likelihood of further somatic alterations at this locus, leading to malignant progression. [PUBLICATION ABSTRACT] Neuroblastoma is a childhood cancer of the sympathetic nervous system that accounts for approximately 10% of all paediatric oncology deaths. To identify genetic risk factors for neuroblastoma, we performed a genome-wide association study (GWAS) on 2,251 patients and 6,097 control subjects of European ancestry from four case series. Here we report a significant association within LIM domain only 1 (LMO1) at 11p15.4 (rs110419, combined P = 5.2 × 10(-16), odds ratio of risk allele = 1.34 (95% confidence interval 1.25-1.44)). The signal was enriched in the subset of patients with the most aggressive form of the disease. LMO1 encodes a cysteine-rich transcriptional regulator, and its paralogues (LMO2, LMO3 and LMO4) have each been previously implicated in cancer. In parallel, we analysed genome-wide DNA copy number alterations in 701 primary tumours. We found that the LMO1 locus was aberrant in 12.4% through a duplication event, and that this event was associated with more advanced disease (P < 0.0001) and survival (P = 0.041). The germline single nucleotide polymorphism (SNP) risk alleles and somatic copy number gains were associated with increased LMO1 expression in neuroblastoma cell lines and primary tumours, consistent with a gain-of-function role in tumorigenesis. Short hairpin RNA (shRNA)-mediated depletion of LMO1 inhibited growth of neuroblastoma cells with high LMO1 expression, whereas forced expression of LMO1 in neuroblastoma cells with low LMO1 expression enhanced proliferation. These data show that common polymorphisms at the LMO1 locus are strongly associated with susceptibility to developing neuroblastoma, but also may influence the likelihood of further somatic alterations at this locus, leading to malignant progression.Neuroblastoma is a childhood cancer of the sympathetic nervous system that accounts for approximately 10% of all paediatric oncology deaths. To identify genetic risk factors for neuroblastoma, we performed a genome-wide association study (GWAS) on 2,251 patients and 6,097 control subjects of European ancestry from four case series. Here we report a significant association within LIM domain only 1 (LMO1) at 11p15.4 (rs110419, combined P = 5.2 × 10(-16), odds ratio of risk allele = 1.34 (95% confidence interval 1.25-1.44)). The signal was enriched in the subset of patients with the most aggressive form of the disease. LMO1 encodes a cysteine-rich transcriptional regulator, and its paralogues (LMO2, LMO3 and LMO4) have each been previously implicated in cancer. In parallel, we analysed genome-wide DNA copy number alterations in 701 primary tumours. We found that the LMO1 locus was aberrant in 12.4% through a duplication event, and that this event was associated with more advanced disease (P < 0.0001) and survival (P = 0.041). The germline single nucleotide polymorphism (SNP) risk alleles and somatic copy number gains were associated with increased LMO1 expression in neuroblastoma cell lines and primary tumours, consistent with a gain-of-function role in tumorigenesis. Short hairpin RNA (shRNA)-mediated depletion of LMO1 inhibited growth of neuroblastoma cells with high LMO1 expression, whereas forced expression of LMO1 in neuroblastoma cells with low LMO1 expression enhanced proliferation. These data show that common polymorphisms at the LMO1 locus are strongly associated with susceptibility to developing neuroblastoma, but also may influence the likelihood of further somatic alterations at this locus, leading to malignant progression. |
| Audience | Academic |
| Author | Winter, Cynthia Attiyeh, Edward F. Diskin, Sharon J. Sasaki, Hiroki Hakonarson, Hakon Glaberson, Wendy Devoto, Marcella Hou, Cuiping Chiavacci, Rosetta Kim, Cecilia Glessner, Joseph Le Nguyen Schnepp, Robert W. Zhang, Haitao Bosse, Kristopher Jagannathan, Jayanti Grant, Struan F. A. Diamond, Maura Iolascon, Achille London, Wendy B. Frackelton, Edward Li, Hongzhe McGrady, Patrick W. Wang, Qun Capasso, Mario Rahman, Nazneen Maris, John M. Saeki, Norihisa Mosse, Yael P. Wang, Kai Mayes, Patrick A. Cole, Kristina A. Garris, Maria |
| AuthorAffiliation | 7 CEINGE Biotecnologie Avanzate, Naples 80145, Italy 6 Division of Human Genetics, Children’s Hospital of Philadelphia, Philadelphia, Pennsylvania, 19104, USA 8 Department of Experimental Medicine, University La Sapienza, Rome 00185, Italy 5 Department of Pediatrics, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania, 19104, USA 2 Division of Oncology and Center for Childhood Cancer Research, Children’s Hospital of Philadelphia, Philadelphia, Pennsylvania 19104, USA 12 Section of Cancer Genetics, Institute of Cancer Research, Sutton, Surrey SM2 5NG, UK 4 Genetics Division, National Cancer Center Research Institute, Tokyo 104-0045, Japan 1 The Center for Applied Genomics, Children’s Hospital of Philadelphia, Philadelphia, Pennsylvania 19104, USA 10 Dana-Farber Children’s Hospital Cancer Center and Children’s Oncology Group, Boston, Massachusetts, 02115, USA 9 Department of Statistics, University of Florida and Children’s Oncology Group, Gainesville, Florida, 32603 USA 11 De |
| AuthorAffiliation_xml | – name: 11 Department of Biochemistry and Medical Biotechnology, University of Naples Federico II, Naples 80131 Italy – name: 8 Department of Experimental Medicine, University La Sapienza, Rome 00185, Italy – name: 4 Genetics Division, National Cancer Center Research Institute, Tokyo 104-0045, Japan – name: 3 Department of Biostatistics and Epidemiology, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania, 19104, USA – name: 6 Division of Human Genetics, Children’s Hospital of Philadelphia, Philadelphia, Pennsylvania, 19104, USA – name: 10 Dana-Farber Children’s Hospital Cancer Center and Children’s Oncology Group, Boston, Massachusetts, 02115, USA – name: 1 The Center for Applied Genomics, Children’s Hospital of Philadelphia, Philadelphia, Pennsylvania 19104, USA – name: 2 Division of Oncology and Center for Childhood Cancer Research, Children’s Hospital of Philadelphia, Philadelphia, Pennsylvania 19104, USA – name: 9 Department of Statistics, University of Florida and Children’s Oncology Group, Gainesville, Florida, 32603 USA – name: 12 Section of Cancer Genetics, Institute of Cancer Research, Sutton, Surrey SM2 5NG, UK – name: 5 Department of Pediatrics, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania, 19104, USA – name: 7 CEINGE Biotecnologie Avanzate, Naples 80145, Italy |
| Author_xml | – sequence: 1 givenname: Kai surname: Wang fullname: Wang, Kai organization: The Center for Applied Genomics, Children’s Hospital of Philadelphia, Present address: Zilkha Neurogenetic Institute, Department of Psychiatry and Preventive Medicine, University of Southern California, Los Angeles, California 90089, USA – sequence: 2 givenname: Sharon J. surname: Diskin fullname: Diskin, Sharon J. organization: Division of Oncology and Center for Childhood Cancer Research, Children’s Hospital of Philadelphia – sequence: 3 givenname: Haitao surname: Zhang fullname: Zhang, Haitao organization: The Center for Applied Genomics, Children’s Hospital of Philadelphia – sequence: 4 givenname: Edward F. surname: Attiyeh fullname: Attiyeh, Edward F. organization: Division of Oncology and Center for Childhood Cancer Research, Children’s Hospital of Philadelphia – sequence: 5 givenname: Cynthia surname: Winter fullname: Winter, Cynthia organization: Division of Oncology and Center for Childhood Cancer Research, Children’s Hospital of Philadelphia – sequence: 6 givenname: Cuiping surname: Hou fullname: Hou, Cuiping organization: The Center for Applied Genomics, Children’s Hospital of Philadelphia – sequence: 7 givenname: Robert W. surname: Schnepp fullname: Schnepp, Robert W. organization: Division of Oncology and Center for Childhood Cancer Research, Children’s Hospital of Philadelphia – sequence: 8 givenname: Maura surname: Diamond fullname: Diamond, Maura organization: Division of Oncology and Center for Childhood Cancer Research, Children’s Hospital of Philadelphia – sequence: 9 givenname: Kristopher surname: Bosse fullname: Bosse, Kristopher organization: Division of Oncology and Center for Childhood Cancer Research, Children’s Hospital of Philadelphia – sequence: 10 givenname: Patrick A. surname: Mayes fullname: Mayes, Patrick A. organization: Division of Oncology and Center for Childhood Cancer Research, Children’s Hospital of Philadelphia – sequence: 11 givenname: Joseph surname: Glessner fullname: Glessner, Joseph organization: The Center for Applied Genomics, Children’s Hospital of Philadelphia – sequence: 12 givenname: Cecilia surname: Kim fullname: Kim, Cecilia organization: The Center for Applied Genomics, Children’s Hospital of Philadelphia – sequence: 13 givenname: Edward surname: Frackelton fullname: Frackelton, Edward organization: The Center for Applied Genomics, Children’s Hospital of Philadelphia – sequence: 14 givenname: Maria surname: Garris fullname: Garris, Maria organization: Division of Oncology and Center for Childhood Cancer Research, Children’s Hospital of Philadelphia – sequence: 15 givenname: Qun surname: Wang fullname: Wang, Qun organization: Division of Oncology and Center for Childhood Cancer Research, Children’s Hospital of Philadelphia – sequence: 16 givenname: Wendy surname: Glaberson fullname: Glaberson, Wendy organization: The Center for Applied Genomics, Children’s Hospital of Philadelphia – sequence: 17 givenname: Rosetta surname: Chiavacci fullname: Chiavacci, Rosetta organization: The Center for Applied Genomics, Children’s Hospital of Philadelphia – sequence: 18 surname: Le Nguyen fullname: Le Nguyen organization: Division of Oncology and Center for Childhood Cancer Research, Children’s Hospital of Philadelphia, Department of Biostatistics and Epidemiology, University of Pennsylvania School of Medicine, Department of Pediatrics, University of Pennsylvania School of Medicine – sequence: 19 givenname: Jayanti surname: Jagannathan fullname: Jagannathan, Jayanti organization: Division of Oncology and Center for Childhood Cancer Research, Children’s Hospital of Philadelphia – sequence: 20 givenname: Norihisa surname: Saeki fullname: Saeki, Norihisa organization: Genetics Division, National Cancer Center Research Institute – sequence: 21 givenname: Hiroki surname: Sasaki fullname: Sasaki, Hiroki organization: Genetics Division, National Cancer Center Research Institute – sequence: 22 givenname: Struan F. A. surname: Grant fullname: Grant, Struan F. A. organization: The Center for Applied Genomics, Children’s Hospital of Philadelphia, Department of Pediatrics, University of Pennsylvania School of Medicine, Division of Human Genetics, Children’s Hospital of Philadelphia – sequence: 23 givenname: Achille surname: Iolascon fullname: Iolascon, Achille organization: CEINGE Biotecnologie Avanzate, Department of Biochemistry and Medical Biotechnology, University of Naples Federico II – sequence: 24 givenname: Yael P. surname: Mosse fullname: Mosse, Yael P. organization: Division of Oncology and Center for Childhood Cancer Research, Children’s Hospital of Philadelphia, Department of Pediatrics, University of Pennsylvania School of Medicine – sequence: 25 givenname: Kristina A. surname: Cole fullname: Cole, Kristina A. organization: Division of Oncology and Center for Childhood Cancer Research, Children’s Hospital of Philadelphia, Department of Pediatrics, University of Pennsylvania School of Medicine – sequence: 26 givenname: Hongzhe surname: Li fullname: Li, Hongzhe organization: Department of Biostatistics and Epidemiology, University of Pennsylvania School of Medicine – sequence: 27 givenname: Marcella surname: Devoto fullname: Devoto, Marcella organization: Department of Biostatistics and Epidemiology, University of Pennsylvania School of Medicine, Department of Pediatrics, University of Pennsylvania School of Medicine, Division of Human Genetics, Children’s Hospital of Philadelphia, Department of Experimental Medicine, University La Sapienza – sequence: 28 givenname: Patrick W. surname: McGrady fullname: McGrady, Patrick W. organization: Department of Statistics, University of Florida and Children’s Oncology Group – sequence: 29 givenname: Wendy B. surname: London fullname: London, Wendy B. organization: Dana-Farber Children’s Hospital Cancer Center and Children’s Oncology Group – sequence: 30 givenname: Mario surname: Capasso fullname: Capasso, Mario organization: CEINGE Biotecnologie Avanzate, Department of Biochemistry and Medical Biotechnology, University of Naples Federico II – sequence: 31 givenname: Nazneen surname: Rahman fullname: Rahman, Nazneen organization: Section of Cancer Genetics, Institute of Cancer Research – sequence: 32 givenname: Hakon surname: Hakonarson fullname: Hakonarson, Hakon email: hakonarson@chop.edu organization: The Center for Applied Genomics, Children’s Hospital of Philadelphia, Department of Pediatrics, University of Pennsylvania School of Medicine, Division of Human Genetics, Children’s Hospital of Philadelphia – sequence: 33 givenname: John M. surname: Maris fullname: Maris, John M. email: maris@chop.edu organization: Division of Oncology and Center for Childhood Cancer Research, Children’s Hospital of Philadelphia, Department of Pediatrics, University of Pennsylvania School of Medicine |
| BackLink | http://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=23711242$$DView record in Pascal Francis https://www.ncbi.nlm.nih.gov/pubmed/21124317$$D View this record in MEDLINE/PubMed |
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| CODEN | NATUAS |
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| Notes | ObjectType-Article-2 SourceType-Scholarly Journals-1 ObjectType-Feature-1 content type line 14 ObjectType-Article-1 ObjectType-Feature-2 content type line 23 These authors contributed equally to this work. Present address: Zilkha Neurogenetic Institute, Department of Psychiatry and Preventive Medicine, University of Southern California, Los Angeles, California 90089, USA. |
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| Snippet | GWAS identifies oncogene
A genome-wide association study (GWAS) has shown that single nucleotide variants within the
LMO1
locus are associated with inherited... Neuroblastoma is a childhood cancer of the sympathetic nervous system that accounts for approximately 10% of all paediatric oncology deaths. To identify... Neuroblastoma is a childhood cancer of the sympathetic nervous system that accounts for approximately 10% of all paediatric oncology deaths (1,2). To identify... Neuroblastoma is a childhood cancer of the sympathetic nervous system that accounts for approximately10%of all paediatric oncology deaths. To identify genetic... Neuroblastoma is a childhood cancer of the sympathetic nervous system that accounts for approximately 10% of all paediatric oncology deaths 1 , 2 . To identify... |
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| SubjectTerms | 631/208/727/2000 631/378/1689/1690 631/67/395 Alleles Biological and medical sciences Biomarkers Cell Line, Tumor Cell physiology Cell Proliferation Cell transformation and carcinogenesis. Action of oncogenes and antioncogenes Children & youth Chromosomes, Human, Pair 11 - genetics Disease Progression DNA Copy Number Variations - genetics DNA-Binding Proteins - genetics Europe - ethnology Fundamental and applied biological sciences. Psychology Gene Duplication - genetics Gene Expression Regulation, Neoplastic - genetics Gene loci Gene therapy Genetic aspects Genetic Predisposition to Disease - genetics Genetics Genetics of eukaryotes. Biological and molecular evolution Genome, Human - genetics Genome-Wide Association Study Genomics Genotype Genotype & phenotype Health risk assessment Human Humanities and Social Sciences Humans Identification and classification Kinases letter LIM Domain Proteins Molecular and cellular biology multidisciplinary Neuroblastoma Neuroblastoma - genetics Neuroblastoma - pathology Odds Ratio Oncogenes Oncogenes - genetics Phenotype Polymorphism, Single Nucleotide - genetics Population genetics, reproduction patterns Risk factors Science Science (multidisciplinary) Survival Rate Transcription Factors - genetics |
| Title | Integrative genomics identifies LMO1 as a neuroblastoma oncogene |
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