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Article ; Online: Rapid and reversible suppression of ALT by DAXX in osteosarcoma cells.

Yost, Kathryn E / Clatterbuck Soper, Sarah F / Walker, Robert L / Pineda, Marbin A / Zhu, Yuelin J / Ester, Corbin D / Showman, Soyeon / Roschke, Anna V / Waterfall, Joshua J / Meltzer, Paul S

Scientific reports

2019 Volume 9, Issue 1, Page(s) 4544

Abstract: Many tumors maintain chromosome-ends through a telomerase-independent, DNA-templated mechanism called alternative lengthening of telomeres (ALT). While ALT occurs in only a subset of tumors, it is strongly associated with mutations in the genes ATRX and ... ...

Abstract	Many tumors maintain chromosome-ends through a telomerase-independent, DNA-templated mechanism called alternative lengthening of telomeres (ALT). While ALT occurs in only a subset of tumors, it is strongly associated with mutations in the genes ATRX and DAXX, which encode components of an H3.3 histone chaperone complex. The role of ATRX and DAXX mutations in potentiating the mechanism of ALT remains incompletely understood. Here we characterize an osteosarcoma cell line, G292, with wild-type ATRX but a unique chromosome translocation resulting in loss of DAXX function. While ATRX and DAXX form a complex in G292, this complex fails to localize to nuclear PML bodies. We demonstrate that introduction of wild type DAXX suppresses the ALT phenotype and restores the localization of ATRX/DAXX to PML bodies. Using an inducible system, we show that ALT-associated PML bodies are disrupted rapidly following DAXX induction and that ALT is again restored following withdrawal of DAXX.
MeSH term(s)	Bone Neoplasms/genetics ; Bone Neoplasms/pathology ; Co-Repressor Proteins/genetics ; Humans ; Molecular Chaperones/genetics ; Mutation ; Osteosarcoma/genetics ; Osteosarcoma/pathology ; Phenotype ; Telomerase/genetics ; Telomerase/metabolism ; Telomere Homeostasis ; Tumor Cells, Cultured
Chemical Substances	Co-Repressor Proteins ; DAXX protein, human ; Molecular Chaperones ; TERT protein, human (EC 2.7.7.49) ; Telomerase (EC 2.7.7.49)
Language	English
Publishing date	2019-03-14
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Intramural
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-019-41058-8
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Author Correction: Interaction between the microbiome and TP53 in human lung cancer.

Greathouse, K Leigh / White, James R / Vargas, Ashely J / Bliskovsky, Valery V / Beck, Jessica A / von Muhlinen, Natalia / Polley, Eric C / Bowman, Elise D / Khan, Mohammed A / Robles, Ana I / Cooks, Tomer / Ryan, Bríd M / Padgett, Noah / Dzutsev, Amiran H / Trinchieri, Giorgio / Pineda, Marbin A / Bilke, Sven / Meltzer, Paul S / Hokenstad, Alexis N /

Stickrod, Tricia M / Walther-Antonio, Marina R / Earl, Joshua P / Mell, Joshua C / Krol, Jaroslaw E / Balashov, Sergey V / Bhat, Archana S / Ehrlich, Garth D / Valm, Alex / Deming, Clayton / Conlan, Sean / Oh, Julia / Segre, Julie A / Harris, Curtis C

Genome biology

2020 Volume 21, Issue 1, Page(s) 41

Abstract: Following publication of the original paper [1], the authors submitted a new Additional file 5 to replace the one containing formatting issues. The updated Additional file 5 is published in this correction. ...

Abstract	Following publication of the original paper [1], the authors submitted a new Additional file 5 to replace the one containing formatting issues. The updated Additional file 5 is published in this correction.
Language	English
Publishing date	2020-02-20
Publishing country	England
Document type	Published Erratum
ZDB-ID	2040529-7
ISSN	1474-760X ; 1474-760X
ISSN (online)	1474-760X
ISSN	1474-760X
DOI	10.1186/s13059-020-01961-0
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Article: Author Correction: Interaction between the microbiome and TP53 in human lung cancer

Greathouse, K. Leigh / White, James R / Vargas, Ashely J / Bliskovsky, Valery V / Beck, Jessica A / von Muhlinen, Natalia / Polley, Eric C / Bowman, Elise D / Khan, Mohammed A / Robles, Ana I / Cooks, Tomer / Ryan, Bríd M / Padgett, Noah / Dzutsev, Amiran H / Trinchieri, Giorgio / Pineda, Marbin A / Bilke, Sven / Meltzer, Paul S / Hokenstad, Alexis N /

Genome biology. 2020 Dec., v. 21, no. 1

2020

Abstract	Following publication of the original paper [1], the authors submitted a new Additional file 5 to replace the one containing formatting issues. The updated Additional file 5 is published in this correction.
Language	English
Dates of publication	2020-12
Size	p. 41.
Publishing place	BioMed Central
Document type	Article
Note	Published Erratum
ZDB-ID	2040529-7
ISSN	1474-760X ; 1465-6906
ISSN (online)	1474-760X
ISSN	1465-6906
DOI	10.1186/s13059-020-01961-0
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Article ; Online: Interaction between the microbiome and TP53 in human lung cancer.

Genome biology

2018 Volume 19, Issue 1, Page(s) 123

Abstract: Background: Lung cancer is the leading cancer diagnosis worldwide and the number one cause of cancer deaths. Exposure to cigarette smoke, the primary risk factor in lung cancer, reduces epithelial barrier integrity and increases susceptibility to ... ...

Abstract	Background: Lung cancer is the leading cancer diagnosis worldwide and the number one cause of cancer deaths. Exposure to cigarette smoke, the primary risk factor in lung cancer, reduces epithelial barrier integrity and increases susceptibility to infections. Herein, we hypothesize that somatic mutations together with cigarette smoke generate a dysbiotic microbiota that is associated with lung carcinogenesis. Using lung tissue from 33 controls and 143 cancer cases, we conduct 16S ribosomal RNA (rRNA) bacterial gene sequencing, with RNA-sequencing data from lung cancer cases in The Cancer Genome Atlas serving as the validation cohort. Results: Overall, we demonstrate a lower alpha diversity in normal lung as compared to non-tumor adjacent or tumor tissue. In squamous cell carcinoma specifically, a separate group of taxa are identified, in which Acidovorax is enriched in smokers. Acidovorax temporans is identified within tumor sections by fluorescent in situ hybridization and confirmed by two separate 16S rRNA strategies. Further, these taxa, including Acidovorax, exhibit higher abundance among the subset of squamous cell carcinoma cases with TP53 mutations, an association not seen in adenocarcinomas. Conclusions: The results of this comprehensive study show both microbiome-gene and microbiome-exposure interactions in squamous cell carcinoma lung cancer tissue. Specifically, tumors harboring TP53 mutations, which can impair epithelial function, have a unique bacterial consortium that is higher in relative abundance in smoking-associated tumors of this type. Given the significant need for clinical diagnostic tools in lung cancer, this study may provide novel biomarkers for early detection.
MeSH term(s)	Adult ; Aged ; Biodiversity ; Comamonadaceae/classification ; Comamonadaceae/physiology ; Female ; Humans ; Lung Neoplasms/genetics ; Lung Neoplasms/microbiology ; Male ; Microbiota/genetics ; Middle Aged ; Mutation/genetics ; Neoplasms, Squamous Cell/genetics ; Neoplasms, Squamous Cell/microbiology ; Proteobacteria/metabolism ; Reproducibility of Results ; Smokers ; Tumor Suppressor Protein p53/genetics ; Tumor Suppressor Protein p53/metabolism
Chemical Substances	Tumor Suppressor Protein p53
Language	English
Publishing date	2018-08-24
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2040529-7
ISSN	1474-760X ; 1474-760X
ISSN (online)	1474-760X
ISSN	1474-760X
DOI	10.1186/s13059-018-1501-6
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Article: Papillary thyroid cancer and polymorphic variants in TSHR- and RET-related genes: a nested case-control study within a cohort of U.S. radiologic technologists.

Lönn, Stefan / Bhatti, Parveen / Alexander, Bruce H / Pineda, Marbin A / Doody, Michele M / Struewing, Jeffery P / Sigurdson, Alice J

Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology

2007 Volume 16, Issue 1, Page(s) 174–177

Abstract: Several variants in the TSHR and RET signaling pathways genes have been reported to be related to cancer risk. We hypothesized that polymorphic variants in these genes are associated with the risk of papillary thyroid cancer. A nested case-control study ... ...

Abstract	Several variants in the TSHR and RET signaling pathways genes have been reported to be related to cancer risk. We hypothesized that polymorphic variants in these genes are associated with the risk of papillary thyroid cancer. A nested case-control study was conducted within the U.S. Radiologic Technologists cohort. Eligible validated papillary thyroid cancer cases (n = 167) and frequency-matched (by sex and birth year) controls (n = 491) donated blood for analysis. There were no statistically significant associations between papillary thyroid cancer and 10 selected polymorphic variants in analyses of men and women combined. A borderline significant increasing risk was found for RET G691S (P(trend) = 0.05) and was especially pronounced among young women. For women under 38 years (the median age at diagnosis), the odds ratios were 2.1 (95% confidence interval, 1.2-3.7) for those heterozygous for the RET G691S polymorphism and 3.7 (95% confidence interval, 1.1-11.8) for those who were homozygous (P(trend) = 0.001). Our data provide limited evidence that TSHR- and RET-related genes are related to papillary thyroid cancer risk.
MeSH term(s)	Adult ; Aged ; Carcinoma, Papillary/blood ; Carcinoma, Papillary/genetics ; Case-Control Studies ; Female ; Humans ; Male ; Middle Aged ; Polymorphism, Genetic ; Proto-Oncogene Proteins c-ret/blood ; Proto-Oncogene Proteins c-ret/genetics ; Receptors, Thyrotropin/blood ; Receptors, Thyrotropin/genetics ; Thyroid Neoplasms/blood ; Thyroid Neoplasms/genetics
Chemical Substances	Receptors, Thyrotropin ; Proto-Oncogene Proteins c-ret (EC 2.7.10.1) ; RET protein, human (EC 2.7.10.1)
Language	English
Publishing date	2007-01
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, N.I.H., Intramural
ZDB-ID	1153420-5
ISSN	1055-9965
ISSN	1055-9965
DOI	10.1158/1055-9965.EPI-06-0665
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Article: Interaction between the microbiome and TP53 in human lung cancer [Erratum: Dec. 2020, v.21(1), p.41]

Genome biology. 2018 Dec., v. 19, no. 1

2018

Abstract: BACKGROUND: Lung cancer is the leading cancer diagnosis worldwide and the number one cause of cancer deaths. Exposure to cigarette smoke, the primary risk factor in lung cancer, reduces epithelial barrier integrity and increases susceptibility to ... ...

Abstract	BACKGROUND: Lung cancer is the leading cancer diagnosis worldwide and the number one cause of cancer deaths. Exposure to cigarette smoke, the primary risk factor in lung cancer, reduces epithelial barrier integrity and increases susceptibility to infections. Herein, we hypothesize that somatic mutations together with cigarette smoke generate a dysbiotic microbiota that is associated with lung carcinogenesis. Using lung tissue from 33 controls and 143 cancer cases, we conduct 16S ribosomal RNA (rRNA) bacterial gene sequencing, with RNA-sequencing data from lung cancer cases in The Cancer Genome Atlas serving as the validation cohort. RESULTS: Overall, we demonstrate a lower alpha diversity in normal lung as compared to non-tumor adjacent or tumor tissue. In squamous cell carcinoma specifically, a separate group of taxa are identified, in which Acidovorax is enriched in smokers. Acidovorax temporans is identified within tumor sections by fluorescent in situ hybridization and confirmed by two separate 16S rRNA strategies. Further, these taxa, including Acidovorax, exhibit higher abundance among the subset of squamous cell carcinoma cases with TP53 mutations, an association not seen in adenocarcinomas. CONCLUSIONS: The results of this comprehensive study show both microbiome-gene and microbiome-exposure interactions in squamous cell carcinoma lung cancer tissue. Specifically, tumors harboring TP53 mutations, which can impair epithelial function, have a unique bacterial consortium that is higher in relative abundance in smoking-associated tumors of this type. Given the significant need for clinical diagnostic tools in lung cancer, this study may provide novel biomarkers for early detection.
Keywords	Acidovorax ; adenocarcinoma ; biomarkers ; carcinogenesis ; diagnostic techniques ; epithelium ; fluorescence in situ hybridization ; genome ; humans ; lung neoplasms ; lungs ; microbiome ; microorganisms ; ribosomal RNA ; risk factors ; sequence analysis ; somatic mutation ; species diversity ; squamous cell carcinoma
Language	English
Dates of publication	2018-12
Size	p. 123.
Publishing place	BioMed Central
Document type	Article
ZDB-ID	2040529-7
ISSN	1474-760X ; 1465-6906
ISSN (online)	1474-760X
ISSN	1465-6906
DOI	10.1186/s13059-018-1501-6
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Article ; Online: Expression and mutational status of c-kit in thymic epithelial tumors.

Petrini, Iacopo / Zucali, Paolo A / Lee, Hye Seung / Pineda, Marbin A / Meltzer, Paul S / Walter-Rodriguez, Beatriz / Roncalli, Massimo / Santoro, Armando / Wang, Yisong / Giaccone, Giuseppe

Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer

2010 Volume 5, Issue 9, Page(s) 1447–1453

Abstract: Background: Overexpression of c-kit, a tyrosine kinase receptor protein encoded by the protooncogene kit, has been previously reported in thymic epithelial tumors and in other neoplasms such as gastrointestinal stromal tumors, myeloproliferative ... ...

Abstract	Background: Overexpression of c-kit, a tyrosine kinase receptor protein encoded by the protooncogene kit, has been previously reported in thymic epithelial tumors and in other neoplasms such as gastrointestinal stromal tumors, myeloproliferative disorders, melanoma, and seminoma. Mutations in the kit gene have been related to response to imatinib in gastrointestinal stromal tumor and one case report of thymic carcinoma. We studied expression of c-kit in a large retrospective series of thymic epithelial malignancies and sequenced the whole gene in a subset of patients. Methods: Thymic epithelial tumors from 120 patients (13 thymic carcinomas and 107 thymomas) were examined. Immunohistochemical staining with an antic-kit polyclonal antibody was performed on a tissue microarray. Mutation analyses of exons 1 to 20 were conducted by direct DNA sequencing of polymerase chain reaction products in eight thymic carcinomas, five thymomas, and one thymic carcinoma cell line. Results: The percentage of c-kit positive cells was significantly higher in thymic carcinoma (46%) than in thymoma (4%). Decreased disease-related survival and progression-free survival were observed in c-kit positive tumors. No mutations were detected. Conclusion: c-kit expression is strongly but not exclusively related to thymic carcinoma histotype, and it is of prognostic value. Mutations are very rare.
MeSH term(s)	Biomarkers, Tumor/genetics ; Biomarkers, Tumor/metabolism ; DNA, Neoplasm/genetics ; Exons/genetics ; Female ; Humans ; Immunoenzyme Techniques ; Male ; Middle Aged ; Mutation/genetics ; Neoplasm Staging ; Polymerase Chain Reaction ; Prognosis ; Proto-Oncogene Proteins c-kit/genetics ; Proto-Oncogene Proteins c-kit/metabolism ; Retrospective Studies ; Survival Rate ; Thymoma/genetics ; Thymoma/metabolism ; Thymoma/pathology ; Thymus Neoplasms/genetics ; Thymus Neoplasms/metabolism ; Thymus Neoplasms/pathology ; Tissue Array Analysis
Chemical Substances	Biomarkers, Tumor ; DNA, Neoplasm ; Proto-Oncogene Proteins c-kit (EC 2.7.10.1)
Language	English
Publishing date	2010-07-22
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Intramural
ZDB-ID	2432037-7
ISSN	1556-1380 ; 1556-0864
ISSN (online)	1556-1380
ISSN	1556-0864
DOI	10.1097/JTO.0b013e3181e96e30
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Article ; Online: The BRCA1 Ashkenazi founder mutations occur on common haplotypes and are not highly correlated with anonymous single nucleotide polymorphisms likely to be used in genome-wide case-control association studies

Zhang Jinghui / Ellis Nathan A / Offit Kenneth / Greene Mark H / Fonseca Libia R / Rowe William H / Pineda Marbin A / Pereira Lutécia / Collins Andrew / Struewing Jeffery P

BMC Genetics, Vol 8, Iss 1, p

2007 Volume 68

Abstract: Abstract Background We studied linkage disequilibrium (LD) patterns at the BRCA1 locus, a susceptibility gene for breast and ovarian cancer, using a dense set of 114 single nucleotide polymorphisms in 5 population groups. We focused on Ashkenazi Jews in ... ...

Abstract	Abstract Background We studied linkage disequilibrium (LD) patterns at the BRCA1 locus, a susceptibility gene for breast and ovarian cancer, using a dense set of 114 single nucleotide polymorphisms in 5 population groups. We focused on Ashkenazi Jews in whom there are known founder mutations, to address the question of whether we would have been able to identify the 185delAG mutation in a case-control association study (should one have been done) using anonymous genetic markers. This mutation is present in approximately 1% of the general Ashkenazi population and 4% of Ashkenazi breast cancer cases. We evaluated LD using pairwise and haplotype-based methods, and assessed correlation of SNPs with the founder mutations using Pearson's correlation coefficient. Results BRCA1 is characterized by very high linkage disequilibrium in all populations spanning several hundred kilobases. Overall, haplotype blocks and pair-wise LD bins were highly correlated, with lower LD in African versus non-African populations. The 185delAG and 5382insC founder mutations occur on the two most common haplotypes among Ashkenazim. Because these mutations are rare, even though they are in strong LD with many other SNPs in the region as measured by D-prime, there were no strong associations when assessed by Pearson's correlation coefficient, r (maximum of 0.04 for the 185delAG). Conclusion Since the required sample size is related to the inverse of r , this suggests that it would have been difficult to map BRCA1 in an Ashkenazi case-unrelated control association study using anonymous markers that were linked to the founder mutations.
Keywords	Genetics ; QH426-470 ; Biology (General) ; QH301-705.5 ; Science ; Q ; DOAJ:Genetics ; DOAJ:Biology ; DOAJ:Biology and Life Sciences
Subject code	616
Language	English
Publishing date	2007-10-01T00:00:00Z
Publisher	BioMed Central
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article: CHEK2:1100delC and female breast cancer in the United States.

Mateus Pereira, Lutécia H / Sigurdson, Alice J / Doody, Michele M / Pineda, Marbin A / Alexander, Bruce H / Greene, Mark H / Struewing, Jeffery P

International journal of cancer

2004 Volume 112, Issue 3, Page(s) 541–543

MeSH term(s)	Breast Neoplasms/genetics ; Checkpoint Kinase 2 ; Female ; Frameshift Mutation ; Genes, BRCA1 ; Genes, BRCA2 ; Genes, Tumor Suppressor ; Genetic Predisposition to Disease ; Genetic Variation ; Humans ; Male ; Middle Aged ; Protein-Serine-Threonine Kinases/genetics ; United States
Chemical Substances	Checkpoint Kinase 2 (EC 2.7.1.11) ; CHEK2 protein, human (EC 2.7.11.1) ; Protein-Serine-Threonine Kinases (EC 2.7.11.1)
Language	English
Publishing date	2004-11-10
Publishing country	United States
Document type	Letter
ZDB-ID	218257-9
ISSN	1097-0215 ; 0020-7136
ISSN (online)	1097-0215
ISSN	0020-7136
DOI	10.1002/ijc.20439
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Article ; Online: The BRCA1 Ashkenazi founder mutations occur on common haplotypes and are not highly correlated with anonymous single nucleotide polymorphisms likely to be used in genome-wide case-control association studies.

Pereira, Lutécia H Mateus / Pineda, Marbin A / Rowe, William H / Fonseca, Libia R / Greene, Mark H / Offit, Kenneth / Ellis, Nathan A / Zhang, Jinghui / Collins, Andrew / Struewing, Jeffery P

BMC genetics

2007 Volume 8, Page(s) 68

Abstract: Background: We studied linkage disequilibrium (LD) patterns at the BRCA1 locus, a susceptibility gene for breast and ovarian cancer, using a dense set of 114 single nucleotide polymorphisms in 5 population groups. We focused on Ashkenazi Jews in whom ... ...

Abstract	Background: We studied linkage disequilibrium (LD) patterns at the BRCA1 locus, a susceptibility gene for breast and ovarian cancer, using a dense set of 114 single nucleotide polymorphisms in 5 population groups. We focused on Ashkenazi Jews in whom there are known founder mutations, to address the question of whether we would have been able to identify the 185delAG mutation in a case-control association study (should one have been done) using anonymous genetic markers. This mutation is present in approximately 1% of the general Ashkenazi population and 4% of Ashkenazi breast cancer cases. We evaluated LD using pairwise and haplotype-based methods, and assessed correlation of SNPs with the founder mutations using Pearson's correlation coefficient. Results: BRCA1 is characterized by very high linkage disequilibrium in all populations spanning several hundred kilobases. Overall, haplotype blocks and pair-wise LD bins were highly correlated, with lower LD in African versus non-African populations. The 185delAG and 5382insC founder mutations occur on the two most common haplotypes among Ashkenazim. Because these mutations are rare, even though they are in strong LD with many other SNPs in the region as measured by D-prime, there were no strong associations when assessed by Pearson's correlation coefficient, r (maximum of 0.04 for the 185delAG). Conclusion: Since the required sample size is related to the inverse of r, this suggests that it would have been difficult to map BRCA1 in an Ashkenazi case-unrelated control association study using anonymous markers that were linked to the founder mutations.
MeSH term(s)	Breast Neoplasms/ethnology ; Breast Neoplasms/genetics ; Case-Control Studies ; Female ; Founder Effect ; Genes, BRCA1 ; Genetic Predisposition to Disease ; Genome, Human ; Haplotypes ; Humans ; Jews/genetics ; Linkage Disequilibrium ; Ovarian Neoplasms/ethnology ; Ovarian Neoplasms/genetics ; Polymorphism, Single Nucleotide ; Sequence Deletion
Language	English
Publishing date	2007-10-04
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, N.I.H., Intramural
ZDB-ID	2041497-3
ISSN	1471-2156 ; 1471-2156
ISSN (online)	1471-2156
ISSN	1471-2156
DOI	10.1186/1471-2156-8-68
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