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Results: 1 to 10 of 178

Publication Record


Gene-edited MLE-15 Cells as a Model for the Hermansky-Pudlak Syndromes.
Kook S, Qi A, Wang P, Meng S, Gulleman P, Young LR, Guttentag SH
(2018) Am J Respir Cell Mol Biol 58: 566-574
MeSH Terms: Alveolar Epithelial Cells, Animals, CRISPR-Associated Protein 9, CRISPR-Cas Systems, Cell Line, Clustered Regularly Interspaced Short Palindromic Repeats, Disease Models, Animal, Gene Editing, Genetic Markers, Genetic Predisposition to Disease, Hermanski-Pudlak Syndrome, Humans, Mice, Inbred C57BL, Mice, Transgenic, Mutation, Phenotype
Show Abstract · Added April 1, 2019
Defining the mechanisms of cellular pathogenesis in rare lung diseases such as Hermansky-Pudlak syndrome (HPS) is often complicated by loss of the differentiated phenotype of cultured primary alveolar type 2 (AT2) cells, as well as by a lack of durable cell lines that are faithful to both AT2-cell and rare disease phenotypes. We used CRISPR/Cas9 gene editing to generate a series of HPS-specific mutations in the MLE-15 cell line. The resulting MLE-15/HPS cell lines exhibit preservation of AT2 cellular functions, including formation of lamellar body-like organelles, complete processing of surfactant protein B, and known features of HPS specific to each trafficking complex, including loss of protein targeting to lamellar bodies. MLE-15/HPS1 and MLE-15/HPS2 (with a mutation in Ap3β1) express increased macrophage chemotactic protein-1, a well-described mediator of alveolitis in patients with HPS and in mouse models. We show that MLE-15/HPS9 and pallid AT2 cells (with a mutation in Bloc1s6) also express increased macrophage chemotactic protein-1, suggesting that mice and humans with BLOC-1 mutations may also be susceptible to alveolitis. In addition to providing a flexible platform to examine the role of HPS-specific mutations in trafficking AT2 cells, MLE-15/HPS cell lines provide a durable resource for high-throughput screening and studies of cellular pathophysiology that are likely to accelerate progress toward developing novel therapies for this rare lung disease.
0 Communities
1 Members
0 Resources
16 MeSH Terms
Multiethnic genome-wide meta-analysis of ectopic fat depots identifies loci associated with adipocyte development and differentiation.
Chu AY, Deng X, Fisher VA, Drong A, Zhang Y, Feitosa MF, Liu CT, Weeks O, Choh AC, Duan Q, Dyer TD, Eicher JD, Guo X, Heard-Costa NL, Kacprowski T, Kent JW, Lange LA, Liu X, Lohman K, Lu L, Mahajan A, O'Connell JR, Parihar A, Peralta JM, Smith AV, Zhang Y, Homuth G, Kissebah AH, Kullberg J, Laqua R, Launer LJ, Nauck M, Olivier M, Peyser PA, Terry JG, Wojczynski MK, Yao J, Bielak LF, Blangero J, Borecki IB, Bowden DW, Carr JJ, Czerwinski SA, Ding J, Friedrich N, Gudnason V, Harris TB, Ingelsson E, Johnson AD, Kardia SL, Langefeld CD, Lind L, Liu Y, Mitchell BD, Morris AP, Mosley TH, Rotter JI, Shuldiner AR, Towne B, Völzke H, Wallaschofski H, Wilson JG, Allison M, Lindgren CM, Goessling W, Cupples LA, Steinhauser ML, Fox CS
(2017) Nat Genet 49: 125-130
MeSH Terms: Adipocytes, Animals, Body Fat Distribution, Cell Differentiation, Cohort Studies, Ethnic Groups, Female, Genetic Loci, Genetic Markers, Genetic Predisposition to Disease, Genome-Wide Association Study, Humans, Male, Mice, Mice, Inbred C57BL, Obesity, Phenotype, Polymorphism, Single Nucleotide
Show Abstract · Added September 11, 2017
Variation in body fat distribution contributes to the metabolic sequelae of obesity. The genetic determinants of body fat distribution are poorly understood. The goal of this study was to gain new insights into the underlying genetics of body fat distribution by conducting sample-size-weighted fixed-effects genome-wide association meta-analyses in up to 9,594 women and 8,738 men of European, African, Hispanic and Chinese ancestry, with and without sex stratification, for six traits associated with ectopic fat (hereinafter referred to as ectopic-fat traits). In total, we identified seven new loci associated with ectopic-fat traits (ATXN1, UBE2E2, EBF1, RREB1, GSDMB, GRAMD3 and ENSA; P < 5 × 10; false discovery rate < 1%). Functional analysis of these genes showed that loss of function of either Atxn1 or Ube2e2 in primary mouse adipose progenitor cells impaired adipocyte differentiation, suggesting physiological roles for ATXN1 and UBE2E2 in adipogenesis. Future studies are necessary to further explore the mechanisms by which these genes affect adipocyte biology and how their perturbations contribute to systemic metabolic disease.
0 Communities
2 Members
0 Resources
18 MeSH Terms
Multiethnic Exome-Wide Association Study of Subclinical Atherosclerosis.
Natarajan P, Bis JC, Bielak LF, Cox AJ, Dörr M, Feitosa MF, Franceschini N, Guo X, Hwang SJ, Isaacs A, Jhun MA, Kavousi M, Li-Gao R, Lyytikäinen LP, Marioni RE, Schminke U, Stitziel NO, Tada H, van Setten J, Smith AV, Vojinovic D, Yanek LR, Yao J, Yerges-Armstrong LM, Amin N, Baber U, Borecki IB, Carr JJ, Chen YI, Cupples LA, de Jong PA, de Koning H, de Vos BD, Demirkan A, Fuster V, Franco OH, Goodarzi MO, Harris TB, Heckbert SR, Heiss G, Hoffmann U, Hofman A, Išgum I, Jukema JW, Kähönen M, Kardia SL, Kral BG, Launer LJ, Massaro J, Mehran R, Mitchell BD, Mosley TH, de Mutsert R, Newman AB, Nguyen KD, North KE, O'Connell JR, Oudkerk M, Pankow JS, Peloso GM, Post W, Province MA, Raffield LM, Raitakari OT, Reilly DF, Rivadeneira F, Rosendaal F, Sartori S, Taylor KD, Teumer A, Trompet S, Turner ST, Uitterlinden AG, Vaidya D, van der Lugt A, Völker U, Wardlaw JM, Wassel CL, Weiss S, Wojczynski MK, Becker DM, Becker LC, Boerwinkle E, Bowden DW, Deary IJ, Dehghan A, Felix SB, Gudnason V, Lehtimäki T, Mathias R, Mook-Kanamori DO, Psaty BM, Rader DJ, Rotter JI, Wilson JG, van Duijn CM, Völzke H, Kathiresan S, Peyser PA, O'Donnell CJ, CHARGE Consortium
(2016) Circ Cardiovasc Genet 9: 511-520
MeSH Terms: African Continental Ancestry Group, Apolipoprotein B-100, Apolipoprotein E2, Asymptomatic Diseases, Carotid Artery Diseases, Carotid Intima-Media Thickness, Cholesterol, LDL, Computed Tomography Angiography, Coronary Angiography, Coronary Artery Disease, European Continental Ancestry Group, Exome, Gene Frequency, Genetic Markers, Genetic Predisposition to Disease, Genome-Wide Association Study, Humans, Odds Ratio, Oligonucleotide Array Sequence Analysis, Phenotype, Prognosis, Risk Assessment, Risk Factors, Vascular Calcification
Show Abstract · Added September 11, 2017
BACKGROUND - The burden of subclinical atherosclerosis in asymptomatic individuals is heritable and associated with elevated risk of developing clinical coronary heart disease. We sought to identify genetic variants in protein-coding regions associated with subclinical atherosclerosis and the risk of subsequent coronary heart disease.
METHODS AND RESULTS - We studied a total of 25 109 European ancestry and African ancestry participants with coronary artery calcification (CAC) measured by cardiac computed tomography and 52 869 participants with common carotid intima-media thickness measured by ultrasonography within the CHARGE Consortium (Cohorts for Heart and Aging Research in Genomic Epidemiology). Participants were genotyped for 247 870 DNA sequence variants (231 539 in exons) across the genome. A meta-analysis of exome-wide association studies was performed across cohorts for CAC and carotid intima-media thickness. APOB p.Arg3527Gln was associated with 4-fold excess CAC (P=3×10). The APOE ε2 allele (p.Arg176Cys) was associated with both 22.3% reduced CAC (P=1×10) and 1.4% reduced carotid intima-media thickness (P=4×10) in carriers compared with noncarriers. In secondary analyses conditioning on low-density lipoprotein cholesterol concentration, the ε2 protective association with CAC, although attenuated, remained strongly significant. Additionally, the presence of ε2 was associated with reduced risk for coronary heart disease (odds ratio 0.77; P=1×10).
CONCLUSIONS - Exome-wide association meta-analysis demonstrates that protein-coding variants in APOB and APOE associate with subclinical atherosclerosis. APOE ε2 represents the first significant association for multiple subclinical atherosclerosis traits across multiple ethnicities, as well as clinical coronary heart disease.
© 2016 American Heart Association, Inc.
0 Communities
1 Members
0 Resources
24 MeSH Terms
Defining a Contemporary Ischemic Heart Disease Genetic Risk Profile Using Historical Data.
Mosley JD, van Driest SL, Wells QS, Shaffer CM, Edwards TL, Bastarache L, McCarty CA, Thompson W, Chute CG, Jarvik GP, Crosslin DR, Larson EB, Kullo IJ, Pacheco JA, Peissig PL, Brilliant MH, Linneman JG, Denny JC, Roden DM
(2016) Circ Cardiovasc Genet 9: 521-530
MeSH Terms: Aged, Aged, 80 and over, Atherosclerosis, Blood Pressure, Case-Control Studies, Chi-Square Distribution, Cross-Sectional Studies, Diabetes Mellitus, Type 2, Electronic Health Records, Female, Genetic Markers, Genetic Predisposition to Disease, Genome-Wide Association Study, Humans, Hypertension, Incidence, Linear Models, Lipids, Male, Middle Aged, Molecular Epidemiology, Myocardial Ischemia, Phenotype, Polymorphism, Single Nucleotide, Prevalence, Prognosis, Proportional Hazards Models, Risk Assessment, Risk Factors, Time Factors, United States
Show Abstract · Added April 6, 2017
BACKGROUND - Continued reductions in morbidity and mortality attributable to ischemic heart disease (IHD) require an understanding of the changing epidemiology of this disease. We hypothesized that we could use genetic correlations, which quantify the shared genetic architectures of phenotype pairs and extant risk factors from a historical prospective study to define the risk profile of a contemporary IHD phenotype.
METHODS AND RESULTS - We used 37 phenotypes measured in the ARIC study (Atherosclerosis Risk in Communities; n=7716, European ancestry subjects) and clinical diagnoses from an electronic health record (EHR) data set (n=19 093). All subjects had genome-wide single-nucleotide polymorphism genotyping. We measured pairwise genetic correlations (rG) between the ARIC and EHR phenotypes using linear mixed models. The genetic correlation estimates between the ARIC risk factors and the EHR IHD were modestly linearly correlated with hazards ratio estimates for incident IHD in ARIC (Pearson correlation [r]=0.62), indicating that the 2 IHD phenotypes had differing risk profiles. For comparison, this correlation was 0.80 when comparing EHR and ARIC type 2 diabetes mellitus phenotypes. The EHR IHD phenotype was most strongly correlated with ARIC metabolic phenotypes, including total:high-density lipoprotein cholesterol ratio (rG=-0.44, P=0.005), high-density lipoprotein (rG=-0.48, P=0.005), systolic blood pressure (rG=0.44, P=0.02), and triglycerides (rG=0.38, P=0.02). EHR phenotypes related to type 2 diabetes mellitus, atherosclerotic, and hypertensive diseases were also genetically correlated with these ARIC risk factors.
CONCLUSIONS - The EHR IHD risk profile differed from ARIC and indicates that treatment and prevention efforts in this population should target hypertensive and metabolic disease.
© 2016 American Heart Association, Inc.
0 Communities
5 Members
0 Resources
31 MeSH Terms
Genetic resilience to amyloid related cognitive decline.
Hohman TJ, Dumitrescu L, Cox NJ, Jefferson AL, Alzheimer’s Neuroimaging Initiative
(2017) Brain Imaging Behav 11: 401-409
MeSH Terms: Adaptation, Psychological, Aged, Amyloidogenic Proteins, Cognitive Dysfunction, Cognitive Reserve, Female, Genetic Markers, Genetic Predisposition to Disease, Humans, Incidence, Male, Nerve Tissue Proteins, Prevalence, Risk Factors, United States
Show Abstract · Added April 10, 2018
Preclinical Alzheimer's disease (AD) is characterized by amyloid deposition in the absence of overt clinical impairment. There is substantial heterogeneity in the long-term clinical outcomes among amyloid positive individuals, yet limited work has focused on identifying molecular factors driving resilience from amyloid-related cognitive impairment. We apply a recently developed predicted gene expression analysis (PrediXcan) to identify genes that modify the association between baseline amyloid deposition and longitudinal cognitive changes. Participants free of clinical AD (n = 631) were selected from the AD Neuroimaging Initiative (ADNI) who had a baseline positron emission tomography measure of amyloid deposition (quantified as a standard uptake value ratio), longitudinal neuropsychological data, and genetic data. PrediXcan was used to impute gene expression levels across 15 heart and brain tissues. Mixed effect regression models assessed the interaction between predicted gene expression levels and amyloid deposition on longitudinal cognitive outcomes. The predicted gene expression levels for two genes in the coronary artery (CNTLN, PROK1) and two genes in the atrial appendage (PRSS50, PROK1) interacted with amyloid deposition on episodic memory performance. The predicted gene expression levels for two additional genes (TMC4 in the basal ganglia and HMBS in the aorta) interacted with amyloid deposition on executive function performance. Post-hoc analyses provide additional validation of the HMBS and PROK1 effects across two independent subsets of ADNI using two additional metrics of amyloid deposition. These results highlight a subset of unique candidate genes of resilience and provide evidence that cell-cycle regulation, angiogenesis, and heme biosynthesis likely play a role in AD progression.
0 Communities
2 Members
0 Resources
MeSH Terms
Reconstructing the Backbone of the Saccharomycotina Yeast Phylogeny Using Genome-Scale Data.
Shen XX, Zhou X, Kominek J, Kurtzman CP, Hittinger CT, Rokas A
(2016) G3 (Bethesda) 6: 3927-3939
MeSH Terms: Ascomycota, Computational Biology, Genetic Markers, Genome, Fungal, Genomics, Phylogeny, Workflow
Show Abstract · Added April 6, 2017
Understanding the phylogenetic relationships among the yeasts of the subphylum Saccharomycotina is a prerequisite for understanding the evolution of their metabolisms and ecological lifestyles. In the last two decades, the use of rDNA and multilocus data sets has greatly advanced our understanding of the yeast phylogeny, but many deep relationships remain unsupported. In contrast, phylogenomic analyses have involved relatively few taxa and lineages that were often selected with limited considerations for covering the breadth of yeast biodiversity. Here we used genome sequence data from 86 publicly available yeast genomes representing nine of the 11 known major lineages and 10 nonyeast fungal outgroups to generate a 1233-gene, 96-taxon data matrix. Species phylogenies reconstructed using two different methods (concatenation and coalescence) and two data matrices (amino acids or the first two codon positions) yielded identical and highly supported relationships between the nine major lineages. Aside from the lineage comprised by the family Pichiaceae, all other lineages were monophyletic. Most interrelationships among yeast species were robust across the two methods and data matrices. However, eight of the 93 internodes conflicted between analyses or data sets, including the placements of: the clade defined by species that have reassigned the CUG codon to encode serine, instead of leucine; the clade defined by a whole genome duplication; and the species Ascoidea rubescens These phylogenomic analyses provide a robust roadmap for future comparative work across the yeast subphylum in the disciplines of taxonomy, molecular genetics, evolutionary biology, ecology, and biotechnology. To further this end, we have also provided a BLAST server to query the 86 Saccharomycotina genomes, which can be found at http://y1000plus.org/blast.
Copyright © 2016 Shen et al.
0 Communities
1 Members
0 Resources
7 MeSH Terms
Prenatal Diagnosis of Alveolar Capillary Dysplasia with Misalignment of Pulmonary Veins.
Prothro SL, Plosa E, Markham M, Szafranski P, Stankiewicz P, Killen SA
(2016) J Pediatr 170: 317-8
MeSH Terms: Adult, Chorionic Villi Sampling, Fatal Outcome, Female, Forkhead Transcription Factors, Gene Deletion, Genetic Markers, Humans, Persistent Fetal Circulation Syndrome, Pregnancy, Pulmonary Alveoli, Pulmonary Veins
Show Abstract · Added March 18, 2020
Alveolar capillary dysplasia with misalignment of pulmonary veins (ACDMPV) is a rare, lethal cause of neonatal respiratory failure and persistent pulmonary hypertension. We present a presumptive prenatal diagnosis of ACDMPV based on chorionic villus sampling of a FOXF1 mutation in a fetus with extra-pulmonary anomalies often associated with ACDMPV.
Copyright © 2016 Elsevier Inc. All rights reserved.
0 Communities
1 Members
0 Resources
MeSH Terms
Transcriptomic Analysis of Chronic Hepatitis B and C and Liver Cancer Reveals MicroRNA-Mediated Control of Cholesterol Synthesis Programs.
Selitsky SR, Dinh TA, Toth CL, Kurtz CL, Honda M, Struck BR, Kaneko S, Vickers KC, Lemon SM, Sethupathy P
(2015) mBio 6: e01500-15
MeSH Terms: Carcinoma, Hepatocellular, Cholesterol, Gene Expression Profiling, Gene Expression Regulation, Genetic Markers, Hepatitis B, Chronic, Hepatitis C, Chronic, High-Throughput Nucleotide Sequencing, Humans, Liver, Liver Neoplasms, MicroRNAs
Show Abstract · Added April 25, 2016
UNLABELLED - Chronic hepatitis B (CHB), chronic hepatitis C (CHC), and associated hepatocellular carcinoma (HCC) are characterized by cholesterol imbalance and dyslipidemia; however, the key regulatory drivers of these phenotypes are incompletely understood. Using gene expression microarrays and high-throughput sequencing of small RNAs, we performed integrative analysis of microRNA (miRNA) and gene expression in nonmalignant and matched cancer tissue samples from human subjects with CHB or CHC and HCC. We also carried out follow-up functional studies of specific miRNAs in a cell-based system. These studies led to four major findings. First, pathways affecting cholesterol homeostasis were among the most significantly overrepresented among genes dysregulated in chronic viral hepatitis and especially in tumor tissue. Second, for each disease state, specific miRNA signatures that included miRNAs not previously associated with chronic viral hepatitis, such as miR-1307 in CHC, were identified. Notably, a few miRNAs, including miR-27 and miR-224, were components of the miRNA signatures of all four disease states: CHB, CHC, CHB-associated HCC, and CHC-associated HCC. Third, using a statistical simulation method (miRHub) applied to the gene expression data, we identified candidate master miRNA regulators of pathways controlling cholesterol homeostasis in chronic viral hepatitis and HCC, including miR-21, miR-27, and miR-33. Last, we validated in human hepatoma cells that both miR-21 and miR-27 significantly repress cholesterol synthesis and that miR-27 does so in part through regulation of the gene that codes for the rate-limiting enzyme 3-hydroxy-3-methyl-glutaryl-coenzyme A (HMG-CoA) reductase (HMGCR).
IMPORTANCE - Hepatitis B virus (HBV) and hepatitis C virus (HCV) are phylogenetically unrelated hepatotropic viruses that persistently infect hundreds of millions of people world-wide, often leading to chronic liver disease and hepatocellular carcinoma (HCC). Chronic hepatitis B (CHB), chronic hepatitis C (CHC), and associated HCC often lead to cholesterol imbalance and dyslipidemia. However, the regulatory mechanisms underlying the dysregulation of lipid pathways in these disease states are incompletely understood. MicroRNAs (miRNAs) have emerged as critical modulators of lipid homeostasis. Here we use a blend of genomic, molecular, and biochemical strategies to identify key miRNAs that drive the lipid phenotypes of chronic viral hepatitis and HCC. These findings provide a panoramic view of the miRNA landscape in chronic viral hepatitis, which could contribute to the development of novel and more-effective miRNA-based therapeutic strategies.
Copyright © 2015 Selitsky et al.
0 Communities
1 Members
0 Resources
12 MeSH Terms
Fine-scale mapping of the 4q24 locus identifies two independent loci associated with breast cancer risk.
Guo X, Long J, Zeng C, Michailidou K, Ghoussaini M, Bolla MK, Wang Q, Milne RL, Shu XO, Cai Q, Beesley J, Kar SP, Andrulis IL, Anton-Culver H, Arndt V, Beckmann MW, Beeghly-Fadiel A, Benitez J, Blot W, Bogdanova N, Bojesen SE, Brauch H, Brenner H, Brinton L, Broeks A, Brüning T, Burwinkel B, Cai H, Canisius S, Chang-Claude J, Choi JY, Couch FJ, Cox A, Cross SS, Czene K, Darabi H, Devilee P, Droit A, Dörk T, Fasching PA, Fletcher O, Flyger H, Fostira F, Gaborieau V, García-Closas M, Giles GG, Grip M, Guénel P, Haiman CA, Hamann U, Hartman M, Hollestelle A, Hopper JL, Hsiung CN, Ito H, Jakubowska A, Johnson N, Kabisch M, Kang D, Khan S, Knight JA, Kosma VM, Lambrechts D, Le Marchand L, Li J, Lindblom A, Lophatananon A, Lubinski J, Mannermaa A, Manoukian S, Margolin S, Marme F, Matsuo K, McLean CA, Meindl A, Muir K, Neuhausen SL, Nevanlinna H, Nord S, Olson JE, Orr N, Peterlongo P, Putti TC, Rudolph A, Sangrajrang S, Sawyer EJ, Schmidt MK, Schmutzler RK, Shen CY, Shi J, Shrubsole MJ, Southey MC, Swerdlow A, Teo SH, Thienpont B, Toland AE, Tollenaar RA, Tomlinson IP, Truong T, Tseng CC, van den Ouweland A, Wen W, Winqvist R, Wu A, Yip CH, Zamora MP, Zheng Y, Hall P, Pharoah PD, Simard J, Chenevix-Trench G, kConFab Investigators, Dunning AM, Easton DF, Zheng W
(2015) Cancer Epidemiol Biomarkers Prev 24: 1680-91
MeSH Terms: Breast Neoplasms, Case-Control Studies, Chromosome Mapping, Chromosomes, Human, Pair 4, Female, Genetic Loci, Genetic Markers, Genetic Predisposition to Disease, Genome-Wide Association Study, Humans, Logistic Models, Polymorphism, Single Nucleotide, Risk Factors
Show Abstract · Added September 28, 2015
BACKGROUND - A recent association study identified a common variant (rs9790517) at 4q24 to be associated with breast cancer risk. Independent association signals and potential functional variants in this locus have not been explored.
METHODS - We conducted a fine-mapping analysis in 55,540 breast cancer cases and 51,168 controls from the Breast Cancer Association Consortium.
RESULTS - Conditional analyses identified two independent association signals among women of European ancestry, represented by rs9790517 [conditional P = 2.51 × 10(-4); OR, 1.04; 95% confidence interval (CI), 1.02-1.07] and rs77928427 (P = 1.86 × 10(-4); OR, 1.04; 95% CI, 1.02-1.07). Functional annotation using data from the Encyclopedia of DNA Elements (ENCODE) project revealed two putative functional variants, rs62331150 and rs73838678 in linkage disequilibrium (LD) with rs9790517 (r(2) ≥ 0.90) residing in the active promoter or enhancer, respectively, of the nearest gene, TET2. Both variants are located in DNase I hypersensitivity and transcription factor-binding sites. Using data from both The Cancer Genome Atlas (TCGA) and Molecular Taxonomy of Breast Cancer International Consortium (METABRIC), we showed that rs62331150 was associated with level of expression of TET2 in breast normal and tumor tissue.
CONCLUSION - Our study identified two independent association signals at 4q24 in relation to breast cancer risk and suggested that observed association in this locus may be mediated through the regulation of TET2.
IMPACT - Fine-mapping study with large sample size warranted for identification of independent loci for breast cancer risk.
©2015 American Association for Cancer Research.
0 Communities
4 Members
0 Resources
13 MeSH Terms
TRIzol and Alu qPCR-based quantification of metastatic seeding within the skeleton.
Preston Campbell J, Mulcrone P, Masood SK, Karolak M, Merkel A, Hebron K, Zijlstra A, Sterling J, Elefteriou F
(2015) Sci Rep 5: 12635
MeSH Terms: Alu Elements, Animals, Biomarkers, Tumor, Bone Neoplasms, Cell Line, Tumor, DNA, Neoplasm, Gene Expression Profiling, Genetic Markers, Guanidines, Mice, Mice, Nude, Phenols, RNA, Neoplasm, Real-Time Polymerase Chain Reaction, Reproducibility of Results, Sensitivity and Specificity
Show Abstract · Added September 14, 2016
Current methods for detecting disseminated tumor cells in the skeleton are limited by expense and technical complexity. We describe a simple and inexpensive method to quantify, with single cell sensitivity, human metastatic cancer in the mouse skeleton, concurrently with host gene expression, using TRIzol-based DNA/RNA extraction and Alu sequence qPCR amplification. This approach enables precise quantification of tumor cells and corresponding host gene expression during metastatic colonization in xenograft models.
1 Communities
3 Members
0 Resources
16 MeSH Terms