A Novel Gene, CRR9, Which Was Up-Regulated in CDDP-Resistant Ovarian Tumor Cell Line, Was Associated with Apoptosis
02 Feb 2001-Biochemical and Biophysical Research Communications (Academic Press)-Vol. 280, Iss: 4, pp 1148-1154
TL;DR: Transfection assay showed that the CDDP-sensitive strain 2008 with CRR 9 was more sensitive to CDDP, indicating that CRR9 was not associated with theCDDP-resistance, but the CD DP-induced apoptosis.
About: This article is published in Biochemical and Biophysical Research Communications.The article was published on 2001-02-02. It has received 137 citations till now. The article focuses on the topics: Differential display & Northern blot.
Citations
More filters
deCODE genetics1, Radboud University Nijmegen Medical Centre2, University of Iceland3, University of Turin4, Karolinska Institutet5, German Cancer Research Center6, St James's University Hospital7, University of Brescia8, Katholieke Universiteit Leuven9, Maastricht University10, University of Birmingham11, University of Zaragoza12, Northwestern University13, Radboud University Nijmegen14, University of Gothenburg15, Imperial College London16
TL;DR: It is found that rs401681[C] on chromosome 5p15 satisfied the threshold for genome-wide significance and seems to confer protection against cutaneous melanoma, and investigation of the region led to rs2736098[A], which showed stronger association with some cancer types, but neither variant could fully account for the association of the other.
Abstract: The common sequence variants that have recently been associated with cancer risk are particular to a single cancer type or at most two. Following up on our genome-wide scan of basal cell carcinoma, we found that rs401681[C] on chromosome 5p15.33 satisfied our threshold for genome-wide significance (OR = 1.25, P = 3.7 x 10(-12)). We tested rs401681 for association with 16 additional cancer types in over 30,000 cancer cases and 45,000 controls and found association with lung cancer (OR = 1.15, P = 7.2 x 10(-8)) and urinary bladder, prostate and cervix cancer (ORs = 1.07-1.31, all P < 4 x 10(-4)). However, rs401681[C] seems to confer protection against cutaneous melanoma (OR = 0.88, P = 8.0 x 10(-4)). Notably, most of these cancer types have a strong environmental component to their risk. Investigation of the region led us to rs2736098[A], which showed stronger association with some cancer types. However, neither variant could fully account for the association of the other. rs2736098 corresponds to A305A in the telomerase reverse transcriptase (TERT) protein and rs401681 is in an intron of the CLPTM1L gene.
599 citations
Cites background from "A Novel Gene, CRR9, Which Was Up-Re..."
...Expression of CLPTM1L has been shown to sensitize ovarian cancer cells to cisplatin-induced apoptosi...
[...]
International Agency for Research on Cancer1, University of Toronto2, National Institutes of Health3, Charles University in Prague4, Palacký University, Olomouc5, Cancer Care Ontario6, Ontario Institute for Cancer Research7, McGill University8, Women's College, Kolkata9, Norwegian University of Science and Technology10, University of Tromsø11, Uppsala University12, Fred Hutchinson Cancer Research Center13, Pomeranian Medical University14, University of Liverpool15, French Alternative Energies and Atomic Energy Commission16, Council on Education for Public Health17
TL;DR: The susceptibility region contains two genes, TERT and CLPTM1L, suggesting that one or both may have a role in lung cancer etiology, and two uncorrelated disease markers at 5p15.33 are detected.
Abstract: We carried out a genome-wide association study of lung cancer (3,259 cases and 4,159 controls), followed by replication in 2,899 cases and 5,573 controls. Two uncorrelated disease markers at 5p15.33, rs402710 and rs2736100 were detected by the genome-wide data (P - 2 x 10(-7) and P = 4 x 10(-6)) and replicated by the independent study series (P = 7 x 10(-5) and P = 0.016). The susceptibility region contains two genes, TERT and CLPTM1L, suggesting that one or both may have a role in lung cancer etiology.
556 citations
TL;DR: A genome-wide association study of lung cancer comparing 511,919 SNP genotypes in 1,952 cases and 1,438 controls confirmed the most significant association was attained at 15q25.1 and identified two newly associated risk loci mapping to 6p21.33 and 5p15.33.
Abstract: We conducted a genome-wide association (GWA) study of lung cancer comparing 511,919 SNP genotypes in 1,952 cases and 1,438 controls. The most significant association was attained at 15q25.1 (rs8042374; P = 7.75 x 10(-12)), confirming recent observations. Pooling data with two other GWA studies (5,095 cases, 5,200 controls) and with replication in an additional 2,484 cases and 3,036 controls, we identified two newly associated risk loci mapping to 6p21.33 (rs3117582, BAT3-MSH5; P(combined) = 4.97 x 10(-10)) and 5p15.33 (rs401681, CLPTM1L; P(combined) = 7.90 x 10(-9)).
533 citations
Mayo Clinic1, National Institutes of Health2, Harvard University3, Science Applications International Corporation4, New York University5, Utrecht University6, University of Toronto7, University of Minnesota8, Mercy Medical Center (Baltimore, Maryland)9, University of California, San Francisco10, American Cancer Society11, Johns Hopkins University12, Fred Hutchinson Cancer Research Center13, University of Texas MD Anderson Cancer Center14, Yale University15, Vanderbilt University16, University of Paris-Sud17, German Cancer Research Center18, Veterans Health Administration19, Umeå University20, Georgetown University21, Memorial Sloan Kettering Cancer Center22, University of Pittsburgh23, Imperial College London24, French Institute of Health and Medical Research25, Academy of Athens26, Kaiser Permanente27, National Institute for Health and Welfare28, University at Buffalo29, Group Health Cooperative30
TL;DR: This paper conducted a genome-wide association study of pancreatic cancer in 3,851 affected individuals (cases) and 3,934 unaffected controls drawn from 12 prospective cohort studies and 8 case-control studies and identified eight SNPs that map to three loci on chromosomes 13q22.1, 1q32.1 and 5p15.33.
Abstract: We conducted a genome-wide association study of pancreatic cancer in 3,851 affected individuals (cases) and 3,934 unaffected controls drawn from 12 prospective cohort studies and 8 case-control studies. Based on a logistic regression model for genotype trend effect that was adjusted for study, age, sex, self-described ancestry and five principal components, we identified eight SNPs that map to three loci on chromosomes 13q22.1, 1q32.1 and 5p15.33. Two correlated SNPs, rs9543325 (P = 3.27 x 10(-11), per-allele odds ratio (OR) 1.26, 95% CI 1.18-1.35) and rs9564966 (P = 5.86 x 10(-8), per-allele OR 1.21, 95% CI 1.13-1.30), map to a nongenic region on chromosome 13q22.1. Five SNPs on 1q32.1 map to NR5A2, and the strongest signal was at rs3790844 (P = 2.45 x 10(-10), per-allele OR 0.77, 95% CI 0.71-0.84). A single SNP, rs401681 (P = 3.66 x 10(-7), per-allele OR 1.19, 95% CI 1.11-1.27), maps to the CLPTM1L-TERT locus on 5p15.33, which is associated with multiple cancers. Our study has identified common susceptibility loci for pancreatic cancer that warrant follow-up studies.
509 citations
Mayo Clinic1, National Institutes of Health2, Harvard University3, Science Applications International Corporation4, New York University5, Utrecht University6, University of Toronto7, University of Minnesota8, Mercy Medical Center (Baltimore, Maryland)9, University of California, San Francisco10, American Cancer Society11, Johns Hopkins University12, Fred Hutchinson Cancer Research Center13, University of Texas MD Anderson Cancer Center14, Yale University15, Vanderbilt University16, University of Paris-Sud17, German Cancer Research Center18, Veterans Health Administration19, Umeå University20, Georgetown University21, Memorial Sloan Kettering Cancer Center22, University of Pittsburgh23, Imperial College London24, French Institute of Health and Medical Research25, Academy of Athens26, Kaiser Permanente27, National Institute for Health and Welfare28, University at Buffalo29, Group Health Cooperative30
TL;DR: This study has identified common susceptibility loci for pancreatic cancer that warrant follow-up studies and identified eight SNPs that map to three loci on chromosomes 13q22.1, 1q32.1 and 5p15.1 that are associated with multiple cancers.
Abstract: We conducted a genome-wide association study of pancreatic cancer in 3,851 affected individuals (cases) and 3,934 unaffected controls drawn from 12 prospective cohort studies and 8 case-control studies. Based on a logistic regression model for genotype trend effect that was adjusted for study, age, sex, self-described ancestry and five principal components, we identified eight SNPs that map to three loci on chromosomes 13q22.1, 1q32.1 and 5p15.33. Two correlated SNPs, rs9543325 (P = 3.27 x 10(-11), per-allele odds ratio (OR) 1.26, 95% CI 1.18-1.35) and rs9564966 (P = 5.86 x 10(-8), per-allele OR 1.21, 95% CI 1.13-1.30), map to a nongenic region on chromosome 13q22.1. Five SNPs on 1q32.1 map to NR5A2, and the strongest signal was at rs3790844 (P = 2.45 x 10(-10), per-allele OR 0.77, 95% CI 0.71-0.84). A single SNP, rs401681 (P = 3.66 x 10(-7), per-allele OR 1.19, 95% CI 1.11-1.27), maps to the CLPTM1L-TERT locus on 5p15.33, which is associated with multiple cancers. Our study has identified common susceptibility loci for pancreatic cancer that warrant follow-up studies.
494 citations
References
More filters
Mark Raymond Adams1, Susan E. Celniker2, Robert A. Holt1, Cheryl A. Evans1 +191 more•Institutions (23)
TL;DR: The nucleotide sequence of nearly all of the approximately 120-megabase euchromatic portion of the Drosophila genome is determined using a whole-genome shotgun sequencing strategy supported by extensive clone-based sequence and a high-quality bacterial artificial chromosome physical map.
Abstract: The fly Drosophila melanogaster is one of the most intensively studied organisms in biology and serves as a model system for the investigation of many developmental and cellular processes common to higher eukaryotes, including humans. We have determined the nucleotide sequence of nearly all of the approximately 120-megabase euchromatic portion of the Drosophila genome using a whole-genome shotgun sequencing strategy supported by extensive clone-based sequence and a high-quality bacterial artificial chromosome physical map. Efforts are under way to close the remaining gaps; however, the sequence is of sufficient accuracy and contiguity to be declared substantially complete and to support an initial analysis of genome structure and preliminary gene annotation and interpretation. The genome encodes approximately 13,600 genes, somewhat fewer than the smaller Caenorhabditis elegans genome, but with comparable functional diversity.
6,180 citations
TL;DR: Bcl-2 and related cytoplasmic proteins are key regulators of apoptosis, the cell suicide program critical for development, tissue homeostasis, and protection against pathogens.
Abstract: Bcl-2 and related cytoplasmic proteins are key regulators of apoptosis, the cell suicide program critical for development, tissue homeostasis, and protection against pathogens. Those most similar to Bcl-2 promote cell survival by inhibiting adapters needed for activation of the proteases (caspases) that dismantle the cell. More distant relatives instead promote apoptosis, apparently through mechanisms that include displacing the adapters from the pro-survival proteins. Thus, for many but not all apoptotic signals, the balance between these competing activities determines cell fate. Bcl-2 family members are essential for maintenance of major organ systems, and mutations affecting them are implicated in cancer.
5,380 citations
TL;DR: A method to separate and clone individual messenger RNAs (mRNAs) by means of the polymerase chain reaction using a set of oligonucleotide primers, one being anchored to the polyadenylate tail of a subset of mRNAs, the other being short and arbitrary in sequence so that it anneals at different positions relative to the first primer.
Abstract: Effective methods are needed to identify and isolate those genes that are differentially expressed in various cells or under altered conditions. This report describes a method to separate and clone individual messenger RNAs (mRNAs) by means of the polymerase chain reaction. The key element is to use a set of oligonucleotide primers, one being anchored to the polyadenylate tail of a subset of mRNAs, the other being short and arbitrary in sequence so that it anneals at different positions relative to the first primer. The mRNA subpopulations defined by these primer pairs were amplified after reverse transcription and resolved on a DNA sequencing gel. When multiple primer sets were used, reproducible patterns of amplified complementary DNA fragments were obtained that showed strong dependence on sequence specificity of either primer.
5,254 citations
Journal Article•
TL;DR: To determine whether the loss of DNA mismatch repair itself contributes to cisplatin resistance, studies were carried out in isogenic pairs of cell lines proficient or defective in this function.
Abstract: Selection of cells for resistance to cisplatin, a well-recognized mutagen, could result in mutations in genes involved in DNA mismatch repair and thereby to resistance to DNA-alkylating agents. Parental cells of the human ovarian adenocarcinoma cell line 2008 expressed hMLH1 when analyzed with immunoblot. One subline selected for resistance to cisplatin (2008/A) expressed no hMLH1, whereas another (2008/C13*5.25) expressed parental levels. Microsatellite instability was readily demonstrated in 2008/A cells but not in 2008 and in 2008/C13*5.25 cells. In addition, the 2008/A cells were 2-fold resistant to methyl-nitro-nitrosoguanidine and had a 65-fold elevated mutation rate at the HPRT locus as compared to 2008 cells, both of which are consistent with the loss of DNA mismatch repair in these cells. To determine whether the loss of DNA mismatch repair itself contributes to cisplatin resistance, studies were carried out in isogenic pairs of cell lines proficient or defective in this function. HCT116, a human colon cancer cell line deficient in hMLH1 function, was 2-fold resistant to cisplatin when compared to a subline complemented with chromosome 3 and expressing hMLH1. Similarly, the human endometrial cancer cell line HEC59, which expresses no hMSH2, was 2-fold resistant to cisplatin when compared to a subline complemented with chromosome 2 that expresses hMSH2. Therefore, the selection of cells for resistance to cisplatin can result in the loss of DNA mismatch repair, and loss of DNA mismatch repair in turn contributes to resistance to cisplatin.
520 citations
Journal Article•
TL;DR: The cDNA of a new ATP binding cassette superfamily that was specifically enhanced in a cisplatin-resistant human head and neck cancer KB cell line was isolated and a human clone homologous to rat canalicular multispecific organic anion transporter (cMOAT) was found and designated human cMOAT.
Abstract: By targeting the ATP binding conserved domain in three ATP binding cassette superfamily proteins (P-glycoprotein, multidrug resistance protein, and cystic fibrosis transmembrane regulator), we isolated the cDNA of a new ATP binding cassette superfamily that was specifically enhanced in a cisplatin-resistant human head and neck cancer KB cell line. A human clone homologous to rat canalicular multispecific organic anion transporter (cMOAT) was found and designated human cMOAT. Fluorescence in situ hybridization demonstrated the chromosomal locus of the gene on chromosome 10q24. The human cMOAT cDNA hybridized a 6.5-kb mRNA that was expressed 4- to 6-fold higher by three cisplatin-resistant cell lines derived from various human tumors exhibiting decreased drug accumulation. Human cMOAT may function as a cellular cisplatin transporter.
467 citations