The Experts below are selected from a list of 264 Experts worldwide ranked by ideXlab platform
Paul Wordsworth - One of the best experts on this subject based on the ideXlab platform.
-
Evidence of Genetic association between TNFRSF1A encoding the p55 tumour necrosis factor receptor, and ankylosing spondylitis in UK Caucasians.
Clinical and experimental rheumatology, 2012Co-Authors: Tugce Karaderi, J J Pointon, Thomas Wordsworth, David Harvey, L H Appleton, C J Cohen, C Farrar, Alice Harin, Matthew A. Brown, Paul WordsworthAbstract:To replicate the possible Genetic association between ankylosing spondylitis (AS) and TNFRSF1A. TNFRSF1A was re-sequenced in 48 individuals with AS to identify novel polymorphisms. Nine single nucleotide polymorphisms (SNPs) in TNFRSF1A and 5 SNPs in the neighbouring Gene SCNN1A were genotyped in 1604 UK Caucasian individuals with AS and 1019 matched controls. An extended study was implemented using additional genotype data on 8 of these SNPs from 1400 historical controls from the 1958 British Birth Cohort. A meta-analysis of previously published results was also undertaken. One novel variant in intron 6 was identified but no new coding variants. No definite associations were seen in the initial study but in the extended study there were weak associations with rs4149576 (p=0.04) and rs4149577 (p=0.007). In the meta-analysis consistent, somewhat stronger associations were seen with rs4149577 (p=0.002) and rs4149578 (p=0.006). These studies confirm the weak Genetic associations between AS and TNFRSF1A. In view of the previously reported associations of TNFRSF1A with AS, in Caucasians and Chinese, and the biological plausibility of this candidate Gene, Replication of this finding in well powered studies is clearly indicated.
-
evidence of Genetic association between tnfrsf1a encoding the p55 tumour necrosis factor receptor and ankylosing spondylitis in uk caucasians
Clinical and Experimental Rheumatology, 2012Co-Authors: Tugce Karaderi, J J Pointon, Thomas Wordsworth, David Harvey, L H Appleton, C J Cohen, C Farrar, Alice Harin, Matthew A. Brown, Paul WordsworthAbstract:Objectives: To replicate the possible Genetic association between ankylosing spondylitis (AS) and TNFRSF1A. Methods: TNFRSF1A was re-sequenced in 48 individuals with AS to identify novel polymorphisms. Nine single nucleotide polymorphisms (SNPs) in TNFRSF1A and 5 SNPs in the neighbouring Gene SCNN1A were genotyped in 1604 UK Caucasian individuals with AS and 1019 matched controls. An extended study was implemented using additional genotype data on 8 of these SNPs from 1400 historical controls from the 1958 British Birth Cohort. A meta-analysis of previously published results was also undertaken. Results: One novel variant in intron 6 was identified but no new coding variants. No definite associations were seen in the initial study but in the extended study there were weak associations with rs4149576 (p=0.04) and rs4149577 (p=0.007). In the metaanalysis consistent, somewhat stronger associations were seen with rs4149577 (p=0.002) and rs4149578 (p=0.006). Conclusions: These studies confirm the weak Genetic associations between AS and TNFRSF1A. In view of the previously reported associations of TNFRSF1A with AS, in Caucasians and Chinese, and the biological plausibility of this candidate Gene, Replication of this finding in well powered studies is clearly indicated.
Tugce Karaderi - One of the best experts on this subject based on the ideXlab platform.
-
Evidence of Genetic association between TNFRSF1A encoding the p55 tumour necrosis factor receptor, and ankylosing spondylitis in UK Caucasians.
Clinical and experimental rheumatology, 2012Co-Authors: Tugce Karaderi, J J Pointon, Thomas Wordsworth, David Harvey, L H Appleton, C J Cohen, C Farrar, Alice Harin, Matthew A. Brown, Paul WordsworthAbstract:To replicate the possible Genetic association between ankylosing spondylitis (AS) and TNFRSF1A. TNFRSF1A was re-sequenced in 48 individuals with AS to identify novel polymorphisms. Nine single nucleotide polymorphisms (SNPs) in TNFRSF1A and 5 SNPs in the neighbouring Gene SCNN1A were genotyped in 1604 UK Caucasian individuals with AS and 1019 matched controls. An extended study was implemented using additional genotype data on 8 of these SNPs from 1400 historical controls from the 1958 British Birth Cohort. A meta-analysis of previously published results was also undertaken. One novel variant in intron 6 was identified but no new coding variants. No definite associations were seen in the initial study but in the extended study there were weak associations with rs4149576 (p=0.04) and rs4149577 (p=0.007). In the meta-analysis consistent, somewhat stronger associations were seen with rs4149577 (p=0.002) and rs4149578 (p=0.006). These studies confirm the weak Genetic associations between AS and TNFRSF1A. In view of the previously reported associations of TNFRSF1A with AS, in Caucasians and Chinese, and the biological plausibility of this candidate Gene, Replication of this finding in well powered studies is clearly indicated.
-
evidence of Genetic association between tnfrsf1a encoding the p55 tumour necrosis factor receptor and ankylosing spondylitis in uk caucasians
Clinical and Experimental Rheumatology, 2012Co-Authors: Tugce Karaderi, J J Pointon, Thomas Wordsworth, David Harvey, L H Appleton, C J Cohen, C Farrar, Alice Harin, Matthew A. Brown, Paul WordsworthAbstract:Objectives: To replicate the possible Genetic association between ankylosing spondylitis (AS) and TNFRSF1A. Methods: TNFRSF1A was re-sequenced in 48 individuals with AS to identify novel polymorphisms. Nine single nucleotide polymorphisms (SNPs) in TNFRSF1A and 5 SNPs in the neighbouring Gene SCNN1A were genotyped in 1604 UK Caucasian individuals with AS and 1019 matched controls. An extended study was implemented using additional genotype data on 8 of these SNPs from 1400 historical controls from the 1958 British Birth Cohort. A meta-analysis of previously published results was also undertaken. Results: One novel variant in intron 6 was identified but no new coding variants. No definite associations were seen in the initial study but in the extended study there were weak associations with rs4149576 (p=0.04) and rs4149577 (p=0.007). In the metaanalysis consistent, somewhat stronger associations were seen with rs4149577 (p=0.002) and rs4149578 (p=0.006). Conclusions: These studies confirm the weak Genetic associations between AS and TNFRSF1A. In view of the previously reported associations of TNFRSF1A with AS, in Caucasians and Chinese, and the biological plausibility of this candidate Gene, Replication of this finding in well powered studies is clearly indicated.
Aliza Amiel - One of the best experts on this subject based on the ideXlab platform.
-
aneuploidy and asynchronous Replication in non alcholic fatty liver disease and cryptogenic cirrhosis
Gene, 2016Co-Authors: Ido Laish, Atya Mannassegree, Ruth Hadary, Fred M Konikoff, Aliza Amiel, Yona KitaycoheAbstract:Abstract Background/aims Non-alcoholic fatty liver disease (NAFLD) and cryptogenic cirrhosis (CC), which is largely a late sequela of NAFLD, are considered pre-neoplastic conditions that might progress to hepatocellular carcinoma. Aneuploidy, telomere aggregates and synchronization of Replication were evaluated as markers of Genetic instability in these patients. Methodology Peripheral blood lymphocytes from 22 patients with NAFLD, 20 patients with CC and 20 age-matched healthy controls were analyzed. To determine random aneuploidy, we used the fluorescence in situ hybridization (FISH) with probes for chromosomes 9 and 18. The rate of aneuploidy was inferred from the fraction of cells revealing one, three or more hybridization signals per cell. Aggregate size was divided into three fusion groups of 2–5, 6–10 and 11–15 telomeres, relative to the size of a single telomere. The Replication pattern was determined by FISH in two pairs of alleles, 15qter and 13qter. Asynchrony was determined by the presence of one single and one set of double dots in the same cell. Results Significantly higher random aneuploidy rate was found in the CC patients than in the control group, and to a lesser degree in NAFLD patients. Telomere aggregates were insignificantly higher in both groups. Only patients with CC showed significantly higher rate of asynchronous Replication with proportionately more cells with two single dots among the normal cells (p Conclusions These results likely reflect changes in Gene Replication and cell cycle progression in these conditions, possibly correlating with their malignant potential.
-
Asynchronous Replication of alleles in genomes carrying a microdeletion.
The Israel Medical Association journal : IMAJ, 2002Co-Authors: Aliza Amiel, Orit Reish, Elena Gaber, Ronit Masterman, Tally Tohami, Moshe D. FejginAbstract:Background: While most allelic pairs of DNA replicate synchronously during the S phase of the cell cycle, some Genes normally replicate asynchronously, i.e., Genes on the X chromosome and imprinted Genes. The Replicationcontrol mechanism is unknown but was shown to be impaired in malignancies and chromosomal trisomies where Replication pattern becomes asynchronous. Objectives: To determine the level of asynchronization in Replication timing of cells from patients with microdeleted genomes. Methods: We applied monocolor fluorescent in situ hybridization with different probes on leukocytes from microdeleted genomes. Results: All samples derived from the microdeleted genomes showed significantly higher levels of an asynchronized pattern compared to normal individuals. Conclusions: Even a "small" Genetic imbalance (microdeletion) can interfere with Gene Replication and cell cycle progression, as previously shown in full trisomies.
-
The influence of cytoGenetic aberrations on Gene Replication in chronic lymphocytic leukemia patients.
Cancer genetics and cytogenetics, 2001Co-Authors: Aliza Amiel, Elena Gaber, Avishay Elis, Svetlana Sherker, Y. Manor, Moshe D. FejginAbstract:Abstract Chronic lymphocytic leukemia (CLL) is the most common leukemia in humans, with the major cytoGenetic aberrations of trisomy 12 and deletion of 13q14. This study examined the influence of these aberrations on General Gene Replication. The study group included three subgroups: (1) 15 CLL patients, (2) 4 CLL patients with trisomy 12, (3) 3 CLL patients with deletions in 13q14. Five healthy individuals served as a control group. Monocolor fluorescence in situ hybridization (FISH) with probes for c-myc , HER -2/ neu , and p53 was applied to lymphocyte nuclei for the evaluation of Replication timing. Asynchronous Replication (SD) rate was significantly higher in all CLL patients ( P P P
-
Replication pattern in cancer asynchronous Replication in multiple myeloma and in monoclonal gammopathy
Cancer Genetics and Cytogenetics, 1999Co-Authors: Aliza Amiel, Elena Gabe, Moshe D Fejgi, I Kirgne, Y Mano, Michael LishneAbstract:In this study we evaluated the Replication pattern and cell-cycle dynamics of cells from patients considered to have a premalignant condition (monoclonal gammopathy, or MGUS) and patients with multiple myeloma (MM), as well as healthy controls. We applied the fluorescence in situ hybridization (FISH) technique with the TP53, RB-1 and 21q22 loci on the patient's cells. Asynchrony was determined by the presence of one single and one set of double dots in the same cell. The rate of asynchronic Replication was significantly higher in the cells from MM patients, with intermediate value in the cells from MGUS, while the lowest rate was in cells from controls. We suggest that these results may reflect the changes in Gene Replication and cell-cycle progression that occur in premalignant and malignant cells.
-
asynchronous Replication of p53 and 21q22 loci in chronic lymphocytic leukemia
Human Genetics, 1997Co-Authors: Aliza Amiel, Tali Litmanovich, Elena Gabe, Michael Lishne, Lydia Avivi, Moshe D FejgiAbstract:In this study, in order to evaluate the Replication pattern and the cell cycle dynamics of normal and malignant cells from patients with chronic lymphocytic leukemia, we applied the FISH technique with the p53 Gene. Asynchrony was determined by the presence of one single and one set of double dots in the same cell. The rate of asynchronous Replication was significantly higher in malignant cells than in normal cells (a mean of 28 vs 13, respectively, P = 0.023). There were proportionately more cells with two single dots among the normal cells (P = 0.0047). These results probably reflect the changes in Gene Replication and cell cycle progression that occur in malignant cells.
L H Appleton - One of the best experts on this subject based on the ideXlab platform.
-
Evidence of Genetic association between TNFRSF1A encoding the p55 tumour necrosis factor receptor, and ankylosing spondylitis in UK Caucasians.
Clinical and experimental rheumatology, 2012Co-Authors: Tugce Karaderi, J J Pointon, Thomas Wordsworth, David Harvey, L H Appleton, C J Cohen, C Farrar, Alice Harin, Matthew A. Brown, Paul WordsworthAbstract:To replicate the possible Genetic association between ankylosing spondylitis (AS) and TNFRSF1A. TNFRSF1A was re-sequenced in 48 individuals with AS to identify novel polymorphisms. Nine single nucleotide polymorphisms (SNPs) in TNFRSF1A and 5 SNPs in the neighbouring Gene SCNN1A were genotyped in 1604 UK Caucasian individuals with AS and 1019 matched controls. An extended study was implemented using additional genotype data on 8 of these SNPs from 1400 historical controls from the 1958 British Birth Cohort. A meta-analysis of previously published results was also undertaken. One novel variant in intron 6 was identified but no new coding variants. No definite associations were seen in the initial study but in the extended study there were weak associations with rs4149576 (p=0.04) and rs4149577 (p=0.007). In the meta-analysis consistent, somewhat stronger associations were seen with rs4149577 (p=0.002) and rs4149578 (p=0.006). These studies confirm the weak Genetic associations between AS and TNFRSF1A. In view of the previously reported associations of TNFRSF1A with AS, in Caucasians and Chinese, and the biological plausibility of this candidate Gene, Replication of this finding in well powered studies is clearly indicated.
-
evidence of Genetic association between tnfrsf1a encoding the p55 tumour necrosis factor receptor and ankylosing spondylitis in uk caucasians
Clinical and Experimental Rheumatology, 2012Co-Authors: Tugce Karaderi, J J Pointon, Thomas Wordsworth, David Harvey, L H Appleton, C J Cohen, C Farrar, Alice Harin, Matthew A. Brown, Paul WordsworthAbstract:Objectives: To replicate the possible Genetic association between ankylosing spondylitis (AS) and TNFRSF1A. Methods: TNFRSF1A was re-sequenced in 48 individuals with AS to identify novel polymorphisms. Nine single nucleotide polymorphisms (SNPs) in TNFRSF1A and 5 SNPs in the neighbouring Gene SCNN1A were genotyped in 1604 UK Caucasian individuals with AS and 1019 matched controls. An extended study was implemented using additional genotype data on 8 of these SNPs from 1400 historical controls from the 1958 British Birth Cohort. A meta-analysis of previously published results was also undertaken. Results: One novel variant in intron 6 was identified but no new coding variants. No definite associations were seen in the initial study but in the extended study there were weak associations with rs4149576 (p=0.04) and rs4149577 (p=0.007). In the metaanalysis consistent, somewhat stronger associations were seen with rs4149577 (p=0.002) and rs4149578 (p=0.006). Conclusions: These studies confirm the weak Genetic associations between AS and TNFRSF1A. In view of the previously reported associations of TNFRSF1A with AS, in Caucasians and Chinese, and the biological plausibility of this candidate Gene, Replication of this finding in well powered studies is clearly indicated.
David Harvey - One of the best experts on this subject based on the ideXlab platform.
-
Evidence of Genetic association between TNFRSF1A encoding the p55 tumour necrosis factor receptor, and ankylosing spondylitis in UK Caucasians.
Clinical and experimental rheumatology, 2012Co-Authors: Tugce Karaderi, J J Pointon, Thomas Wordsworth, David Harvey, L H Appleton, C J Cohen, C Farrar, Alice Harin, Matthew A. Brown, Paul WordsworthAbstract:To replicate the possible Genetic association between ankylosing spondylitis (AS) and TNFRSF1A. TNFRSF1A was re-sequenced in 48 individuals with AS to identify novel polymorphisms. Nine single nucleotide polymorphisms (SNPs) in TNFRSF1A and 5 SNPs in the neighbouring Gene SCNN1A were genotyped in 1604 UK Caucasian individuals with AS and 1019 matched controls. An extended study was implemented using additional genotype data on 8 of these SNPs from 1400 historical controls from the 1958 British Birth Cohort. A meta-analysis of previously published results was also undertaken. One novel variant in intron 6 was identified but no new coding variants. No definite associations were seen in the initial study but in the extended study there were weak associations with rs4149576 (p=0.04) and rs4149577 (p=0.007). In the meta-analysis consistent, somewhat stronger associations were seen with rs4149577 (p=0.002) and rs4149578 (p=0.006). These studies confirm the weak Genetic associations between AS and TNFRSF1A. In view of the previously reported associations of TNFRSF1A with AS, in Caucasians and Chinese, and the biological plausibility of this candidate Gene, Replication of this finding in well powered studies is clearly indicated.
-
evidence of Genetic association between tnfrsf1a encoding the p55 tumour necrosis factor receptor and ankylosing spondylitis in uk caucasians
Clinical and Experimental Rheumatology, 2012Co-Authors: Tugce Karaderi, J J Pointon, Thomas Wordsworth, David Harvey, L H Appleton, C J Cohen, C Farrar, Alice Harin, Matthew A. Brown, Paul WordsworthAbstract:Objectives: To replicate the possible Genetic association between ankylosing spondylitis (AS) and TNFRSF1A. Methods: TNFRSF1A was re-sequenced in 48 individuals with AS to identify novel polymorphisms. Nine single nucleotide polymorphisms (SNPs) in TNFRSF1A and 5 SNPs in the neighbouring Gene SCNN1A were genotyped in 1604 UK Caucasian individuals with AS and 1019 matched controls. An extended study was implemented using additional genotype data on 8 of these SNPs from 1400 historical controls from the 1958 British Birth Cohort. A meta-analysis of previously published results was also undertaken. Results: One novel variant in intron 6 was identified but no new coding variants. No definite associations were seen in the initial study but in the extended study there were weak associations with rs4149576 (p=0.04) and rs4149577 (p=0.007). In the metaanalysis consistent, somewhat stronger associations were seen with rs4149577 (p=0.002) and rs4149578 (p=0.006). Conclusions: These studies confirm the weak Genetic associations between AS and TNFRSF1A. In view of the previously reported associations of TNFRSF1A with AS, in Caucasians and Chinese, and the biological plausibility of this candidate Gene, Replication of this finding in well powered studies is clearly indicated.