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Search Results: 1 - 10 of 5030 matches for " Bruce AJ Ponder "
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Breast Cancer Research: a meeting point as well as a journal
Bruce AJ Ponder
Breast Cancer Research , 1999, DOI: 10.1186/bcr1
Abstract: Like most new developments, translational research grows best at the meeting point of different disciplines. Therefore, it is not only difficult, it demands that the researchers assemble knowledge from other fields and deploy it in systems with which they are less familiar. Thus, the molecular geneticist may need to understand the cell types and lineages in the mammary gland, or the principles of epidemiology, and similarly the cell biologist may become concerned with trials of endocrine therapy and prevention.The aims of Breast Cancer Research, and the justification for another new journal, are to address exactly this need. Guided by 11 Associate Editors with a wide perspective of their specialist fields, and supported by a group of scientists active in the laboratory and the clinic, we will publish original reports in any area of biology or medicine related to breast cancer. We will also commission and publish a range of reviews, commentaries, up to the minute meeting reports and dispatches highlighting the latest developments. We aim to integrate and interpret biologically based research across the whole spectrum relevant to breast cancer, to make it accessible to the breast cancer community, and to keep in view the goal, however distant, of practical application.Breast Cancer Research is no ordinary journal; the technical developments now available through the Internet have made it possible for a new type of publication to emerge with many advantages over the traditional printed format. As a result Breast Cancer Research will be primarily web-based. The Internet not only provides an ideal medium for the rapid publication of research but also a forum for comment and discussion. Our website will provide a gateway to the wide range of information available on the web which we hope will help our subscribers to gain access to new fields and develop their research.In these ways we hope to be not just a journal, but a meeting point for the breast cancer research commun
Breast Cancer Research – the first ten years
Frances Mulvany, Bruce AJ Ponder
Breast Cancer Research , 2008, DOI: 10.1186/bcr1873
Abstract: Breast Cancer Research is committed to open access publication of research articles, and remains the only journal in the breast cancer field dedicated to open access. Open access means research is universally and freely available via the Internet. Authors retain their own copyright, allowing them to grant any third party the right to use, reproduce and disseminate the article. Open access has broad benefits both for scientists and the general public. Anyone with an Internet connection is able to read the research for free without having to rely on access to a library with a subscription. For example, the 2006 paper by Scutt et al. [2] received wide coverage [3] and was instantly available for any interested patients or clinicians – something that is much more difficult for articles published in subscription based journals.Over the last ten years, there have been massive leaps forward in open access publishing. Many more journals now offer open access options, and there is more support for this publishing model within the scientific community. In particular, many funders now advocate open access by making it a condition of funding that a version of the accepted article is made available in a public repository such as PubMed Central. A recent exciting development has been the announcement of the National Institutes of Health (NIH) Public Access Policy [4], which comes into place in April this year.Open access allows our research to be accessible to a vast potential audience, with over 80,000 articles downloaded from our website every month. Indeed, our most highly accessed article from Arpino and colleagues [5] has been downloaded over 35,000 times since publication. Our highly visible research is complemented by educational reviews and timely opinion pieces. The type of articles published has changed over the years, expanding in 2003 to encompass endocrinology [6], and adding new sections such as clinical trial updates [7].Breast Cancer Research has always aimed to m
Extent of differential allelic expression of candidate breast cancer genes is similar in blood and breast
Ana-Teresa Maia, Inmaculada Spiteri, Alvin JX Lee, Martin O'Reilly, Linda Jones, Carlos Caldas, Bruce AJ Ponder
Breast Cancer Research , 2009, DOI: 10.1186/bcr2458
Abstract: We measured differential allelic expression of 12 candidate genes possibly related to breast cancer susceptibility (BRCA1, BRCA2, C1qA, CCND3, EMSY, GPX1, GPX4, MLH3, MTHFR, NBS1, TP53 and TRXR2) in breast tissue (n = 40) and fresh blood (n = 170) of healthy individuals and EBV-transformed lymphoblastoid cells (n = 19). Differential allelic expression ratios were determined by Taqman assay. Ratio distributions were compared using t-test and Wilcoxon rank sum test, for mean ratios and variances respectively.We show that differential allelic expression is common among these 12 candidate genes and is comparable between breast and blood (fresh and transformed lymphoblasts) in a significant proportion of them. We found that eight out of nine genes with DAE in breast and fresh blood were comparable, as were 10 out of 11 genes between breast and transformed lymphoblasts.Our findings support the use of differential allelic expression in blood as a surrogate for breast tissue in future studies on predisposition to breast cancer.Approximately 70% of the genetic risk associated with breast cancer is still unaccounted for and it is predicted that the remainder of susceptibility loci will include common, low-effect variants that most likely have regulatory effects. Recent genome-wide association studies (GWAS) have identified variants that account for an additional 5.9% of the genetic risk [1-5]. These variants are mostly associated with intronic and intergenic regions, with the most significant variant regulating the level of gene expression of FGFR2 [6]. However, as most of the identified risk loci have small effects, very large numbers of patients will have to be examined to identify further risk variants. An alternative approach for the identification of regulatory risk variants could be to use differences in allelic gene expression in heterozygotes as a quantitative phenotype [7-9].Preferential expression from one allele is a common feature of the human genome (up to 60% of
Differential gene expression in the murine gastric fundus lacking interstitial cells of Cajal
Yataro Daigo, Ichiro Takayama, Bruce AJ Ponder, Carlos Caldas, Sean M Ward, Kenton M Sanders, Masayuki A Fujino
BMC Gastroenterology , 2003, DOI: 10.1186/1471-230x-3-14
Abstract: The gene expression profile of the gastric fundus of wild type and W/WV mice was assayed by murine microarray analysis displaying a total of 8734 elements. Queried genes from the microarray analysis were confirmed by semi-quantitative reverse transcription-polymerase chain reaction.Twenty-one genes were differentially expressed in wild type and W/WV mice. Eleven transcripts had 2.0–2.5 fold higher mRNA expression in W/WV gastric fundus when compared to wild type tissues. Ten transcripts had 2.1–3.9 fold lower expression in W/WV mutants in comparison with wild type animals. None of these genes have ever been implicated in any bowel motility function.These data provides evidence that several important genes have significantly changed in the murine fundus of W/WV mutants that lack intramuscular interstitial cells of Cajal and have reduced enteric motor neurotransmission.Interstitial cells of Cajal (ICC) are gastrointestinal (GI) pacemaker cells and intermediaries in enteric motor neurotransmission in the GI tract [1,2]. ICC express KIT/c-kit and depend on signalling via the gene product protein, KIT, a receptor tyrosine kinase which is essential for development and maintenance of the ICC phenotype [3]. Mutations in the white-spotting locus (i.e. W/WV) result in reduced KIT expression. These mutant animals develop few ICC at the level of the myenteric plexus (IC-MY) in the small intestine and the reduced ICC numbers is associated with a loss of slow wave activity. Intramuscular ICC (IC-IM) located in the stomach, lower esophageal and pyloric sphincters are absent in W/WV mutant animals [4]. Reduced numbers of ICC have also been reported in several GI motility disorders, such as chronic intestinal pseudo-obstruction [5,6], infantile hypertrophic pyloric stenosis [7-9], Hirschsprung's disease [10-12], slow-transit constipation and certain forms of gastroparesis [13,14].The association between motility disorders and loss of specific populations of ICC suggests that a more
Differential gene expression profile in the small intestines of mice lacking pacemaker interstitial cells of Cajal
Yataro Daigo, Ichiro Takayama, Bruce AJ Ponder, Carlos Caldas, Sean M Ward, Kenton M Sanders, Masayuki A Fujino
BMC Gastroenterology , 2003, DOI: 10.1186/1471-230x-3-17
Abstract: By using the same method we isolated additional candidate genes that were specifically down- or up-regulated in W/WV mice. Novel transcripts were designated as DDWMEST.We isolated seven candidates that were specifically down- or up-regulated in W/WV mice. Two novel transcripts, DDWMEST 1 and -91 were increased in both fed and fasted W/WV mice. Expression of another five genes was suppressed in W/WV mice: ARG2 (Arginase II), ONZIN (encoding leukemia inhibitory factor regulated protein), and three novel transcripts: DDWMEST62, -84, and -100. Together with the previous report, we identified fifteen differentially expressed genes in total in the small intestines of W/WV mice. Eight of these genes were reduced in the jejunums of W/WV mice compared to age matched wild type mice, whereas the other seven genes showed an increase in expression. Differential expression was the same in fasted and fed animals, suggesting that the differences were independent of the dietetic state of the animal.Several known and novel genes are differentially expressed in the small intestines of W/WV mice. Differential gene comparison might contribute to our understanding of motility disorders associated with the loss of the interstitial cells of Cajal.Interstitial cells of Cajal (ICC) are pacemakers [1-3] and mediators of enteric motor neuro-transmission [4,5]. KIT, a receptor tyrosine kinase, is essential for the development and maintenance of the ICC phenotype [6,7]. Animals with reduced KIT expression (e.g the W/WV mutant mouse) develop few ICC at the level of the myenteric plexus (IC-MY) in the small intestine [2,3], and lose intramuscular ICC (IC-IM) in the stomach [4]. The loss of IC-MY is associated with a loss of electrical slow waves in the small intestine. Loss of IC-IM is associated with the disruption of enteric neuro-transmission in the gut [4].Absolute or relative loss of ICC has been reported in many gastrointestinal (GI) motility disorders [8-12]. The association between disease
Common ERBB2 polymorphisms and risk of breast cancer in a white British population: a case–control study
Patrick R Benusiglio, Fabienne Lesueur, Craig Luccarini, Donald M Conroy, Mitul Shah, Douglas F Easton, Nick E Day, Alison M Dunning, Paul D Pharoah, Bruce AJ Ponder
Breast Cancer Research , 2005, DOI: 10.1186/bcr982
Abstract: We aimed to determine if common polymorphisms (frequency ≥ 5%) in ERBB2 were associated with breast cancer risk in a white British population. Five single-nucleotide polymorphisms (SNPs) were selected for study: SNP 1 near the promoter, SNP 2 in intron 1, SNP 3 in intron 4, SNP 4 in exon 17 (I655V), and SNP 5 in exon 27 (A1170P). We tested their association with breast cancer in a large case–control study (n = 2192 cases and 2257 controls).There were no differences in genotype frequencies between cases and controls for any of the SNPs examined. To investigate the possibility that a common polymorphism not included in our study might be involved in breast cancer predisposition, we also constructed multilocus haplotypes. Our set of SNPs generated all existing (n = 6) common haplotypes and no differences were seen in haplotype frequencies between cases and controls (P = 0.44).In our population, common ERBB2 polymorphisms are not involved in predisposition to breast cancer.Breast cancer is the most common cause of cancer in women in the United Kingdom and is, after lung cancer, the most common cause of cancer death (Office for National Statistics). Positive family history is a well-established risk factor for the disease: the risk to first-degree relatives of a breast cancer case is about twice the population risk [1]. Most of the excess familial risk associated with breast cancer is likely to be genetic in origin [2,3]. However, only about a third of this risk is accounted for by known genes, the most important being BRCA1 and BRCA2, while the remainder might be explained by a combination of weakly predisposing alleles [2-4]. A gene thought to be involved in low-level susceptibility to breast cancer is ERBB2 (HER2). This gene is located on chromosome 17q12–q21, spans 38 kilobases, and comprises 27 coding exons. It is a member of the ERBB family, a family of protein tyrosine kinases involved in cell division, migration, adhesion, differentiation, and apoptosis and consi
BRCA1 and BRCA2 mutations in a population-based study of male breast cancer
Victoria M Basham, Julian M Lipscombe, Joanna M Ward, Simon A Gayther, Bruce AJ Ponder, Douglas F Easton, Paul DP Pharoah
Breast Cancer Research , 2001, DOI: 10.1186/bcr419
Abstract: We have carried out a population-based study of 94 MBC cases collected in the UK. We screened genomic DNA for mutations in BRCA1 and BRCA2 and used family history data from these cases to calculate the risk of breast cancer to female relatives of MBC cases. We also estimated the contribution of BRCA1 and BRCA2 to this risk.Nineteen cases (20%) reported a first-degree relative with breast cancer, of whom seven also had an affected second-degree relative. The breast cancer risk in female first-degree relatives was 2.4 times (95% confidence interval [CI] = 1.4–4.0) the risk in the general population. No BRCA1 mutation carriers were identified and five cases were found to carry a mutation in BRCA2. Allowing for a mutation detection sensitivity frequency of 70%, the carrier frequency for BRCA2 mutations was 8% (95% CI = 3–19). All the mutation carriers had a family history of breast, ovarian, prostate or pancreatic cancer. However, BRCA2 accounted for only 15% of the excess familial risk of breast cancer in female first-degree relatives.These data suggest that other genes that confer an increased risk for both female and male breast cancer have yet to be found.Male breast cancer (MBC) is a rare disease and little is known about its aetiology. However, female first-degree relatives of MBC cases are at increased risk of breast cancer [1,2,3,4,5,6], which suggests that there is an inherited component to the disease. Several genes that are associated with a high lifetime risk of breast cancer in women have been identified during the past decade. One of these, BRCA2, has also been shown to confer a significant risk of breast cancer in men, and a recent study found the risk of breast cancer in male BRCA2 mutation carriers from multiple case breast/ovarian cancer families to be 80-fold higher than in the general population [7]. This equates to a 7% risk of breast cancer by age 80. The prevalence of BRCA2 mutations in MBC cases unselected for family history has been estimated in
Common variation in EMSY and risk of breast and ovarian cancer: a case-control study using HapMap tagging SNPs
Patrick R Benusiglio, Fabienne Lesueur, Craig Luccarini, Joan McIntosh, Robert N Luben, Paula Smith, Alison Dunning, Douglas F Easton, Bruce AJ Ponder, Paul D Pharoah
BMC Cancer , 2005, DOI: 10.1186/1471-2407-5-81
Abstract: We used a genetic association study design to determine if common genetic variation (frequency ≥ 5%) in EMSY was associated with breast or ovarian cancer risk in the British population. Haplotype tagging single-nucleotide polymorphisms (htSNPs) were selected from the HapMap database and genotyped using Taqman? in two large study sets of white British women (n [breast set] = 2343 cases and 2284 controls, n [ovarian set] = 864 cases and 864 controls). HapMap data might be insufficient to tag genetic variation in EMSY comprehensively. We therefore screened the gene promoter and coding sequences with denaturing high performance liquid chromatography in order to identify additional SNPs that are most likely to be functional.HapMap data on 22 SNPs show that 4 htSNPs tag 4 common haplotypes: rs2282611 (5'up t>g), rs4245443 (IVS7 g>a), rs2513511 (IVS16 a>g), rs2155220 (3'down c>t). We observed no association between any of the genotypes or associated haplotypes and breast or ovarian cancer risk. Seventeen out of the 18 remaining HapMap polymorphisms (94%) were well tagged by the 4 selected htSNPs (r2s > 0.8). Genotype frequencies for two further SNPs identified by screening and located near exon-intron boundaries, rs2508740 (IVS9 a>g) and rs11600501 (IVS10 c>t), were also similar in cases and controls. In order to simulate unidentified SNPs, we performed the leave-one-out cross-validation procedure on the HapMap data; over 95% of the common genetic variation was well represented by tagging polymorphisms. We are therefore likely to have tagged any common, functional variants present in our population.We found no association between common genetic variation in EMSY and risk of breast or ovarian cancer in two large study sets of white British women.Breast and ovarian cancer are two of the most common causes of cancer in women in the United Kingdom (Office for National Statistics). Together, they account for about a third of all new cancer cases and a quarter of cancer deaths.
Common variants in the ATM, BRCA1, BRCA2, CHEK2 and TP53 cancer susceptibility genes are unlikely to increase breast cancer risk
Caroline Baynes, Catherine S Healey, Karen A Pooley, Serena Scollen, Robert N Luben, Deborah J Thompson, Paul DP Pharoah, Douglas F Easton, Bruce AJ Ponder, Alison M Dunning, the SEARCH breast cancer study
Breast Cancer Research , 2007, DOI: 10.1186/bcr1669
Abstract: We have attempted a comprehensive, single nucleotide polymorphism (SNP)- and haplotype-tagging association study on each of these five genes in up to 4,474 breast cancer cases from the British, East Anglian SEARCH study and 4,560 controls from the EPIC-Norfolk study, using a two-stage study design. Nine tag SNPs were genotyped in ATM, together with five in BRCA1, sixteen in BRCA2, ten in CHEK2 and five in TP53, with the aim of tagging all other known, common variants. SNPs generating the common amino acid substitutions were specifically forced into the tagging set for each gene.No significant breast cancer associations were detected with any individual or combination of tag SNPs.It is unlikely that there are any other common variants in these genes conferring measurably increased risks of breast cancer in our study population.Four of the genes which lie in the DNA damage-recognition and repair pathway, ATM, BRCA1, BRCA2 and TP53, have mutations that are recognised to increase breast cancer susceptibility with moderate to high penetrance. Such mutations are very rare, and most probably of recent origin. A fifth gene, CHEK2, in the same pathway, has a deletion (1100delC) that reaches polymorphic frequencies (>0.01) in some European countries and doubles the risk of breast cancer in female carriers [1]. Together these mutations account for only a small proportion (2% to 5%) of all breast cancer incidences [2,3]. Breast cancer is, however, a common disease and genetic epidemiological data suggest that there is a low-penetrance genetic contribution to most cases [4,5]. It is likely that at least a part of breast cancer aetiology will fit the common disease-common variant hypothesis, which states that patients with a common, complex disease are likely to share some common, low-penetrance alleles that increase their susceptibility to that disease. This raises the question of whether such common, polymorphic susceptibility alleles exist within these five genes in addition t
Minichromosome Maintenance Protein 7 is a potential therapeutic target in human cancer and a novel prognostic marker of non-small cell lung cancer
Gouji Toyokawa, Ken Masuda, Yataro Daigo, Hyun-Soo Cho, Masanori Yoshimatsu, Masashi Takawa, Shinya Hayami, Kazuhiro Maejima, Makoto Chino, Helen I Field, David E Neal, Eiju Tsuchiya, Bruce AJ Ponder, Yoshihiko Maehara, Yusuke Nakamura, Ryuji Hamamoto
Molecular Cancer , 2011, DOI: 10.1186/1476-4598-10-65
Abstract: Immunohistochemical analysis showed that MCM7 was positively stained in 196 of 331 non-small cell lung cancer (NSCLC), 21 of 29 bladder tumor and 25 of 70 liver tumor cases whereas no significant staining was observed in various normal tissues. We also found an elevated expression of MCM7 to be associated with poor prognosis for patients with NSCLC (P = 0.0055). qRT-PCR revealed a higher expression of MCM7 in clinical bladder cancer tissues than in corresponding non-neoplastic tissues (P < 0.0001), and we confirmed that a wide range of cancers also overexpressed MCM7 by cDNA microarray analysis. Suppression of MCM7 using specific siRNAs inhibited incorporation of BrdU in lung and bladder cancer cells overexpressing MCM7, and suppressed the growth of those cells more efficiently than that of normal cell strains expressing lower levels of MCM7.Since MCM7 expression was generally low in a number of normal tissues we examined, MCM7 has the characteristics of an ideal candidate for molecular targeted cancer therapy in various tumors and also as a good prognostic biomarker for NSCLC patients.The emergence of effective cancer chemotherapy is one of the major medical advances of late years [1]. Adjuvant chemotherapy for lung, breast or colon cancer can augment the survival benefit afforded by surgical management [2-4]. Even in patients with advanced solid tumors or recurrences following surgery, chemotherapy can offer lengthened survival of worthwhile quality. In those patients, however, the therapeutic index is narrow: responses are usually partial, often disappointingly brief and unpredictable [5]. In addition, many antitumor agents have also been troubled with issues of sometimes unexpected side effects. These circumstances accentuate the limitation of cytotoxic chemotherapy. Therefore, it remains essential to discover novel therapeutic targets to extend the capability of cancer chemotherapy.DNA replication in eukaryotic cells is a highly regulated process that ensures t
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