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Academic literature on the topic 'Gene amplificatin'

Author: Grafiati

Published: 4 June 2021

Last updated: 11 February 2022

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Journal articles on the topic "Gene amplificatin"

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Minarikova, Petra, Lucie Benesova, Tereza Halkova, Barbora Belsanova, Inna Tuckova, Frantisek Belina, Ladislav Dusek, Miroslav Zavoral, and Marek Minarik. "Prognostic Importance of Cell Cycle Regulators Cyclin D1 (CCND1) and Cyclin-Dependent Kinase Inhibitor 1B (CDKN1B/p27) in Sporadic Gastric Cancers." Gastroenterology Research and Practice 2016 (2016): 1–8. http://dx.doi.org/10.1155/2016/9408190.

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Background. Gastric cancer is known for a notable variety in the course of the disease. Clinical factors, such as tumor stage, grade, and localization, are key in patient survival. It is expected that molecular factors such as somatic mutations and gene amplifications are also underlying tumor biological behavior and may serve as factors for prognosis estimation.Aim. The purpose of this study was to examine gene amplifications from a panel of genes to uncover potential prognostic marker candidates.Methods. A panel of gene amplifications including 71 genes was tested by multiplex ligation-dependent probe amplification (MLPA) technique in 76 gastric cancer samples from a Caucasian population. The correlation of gene amplification status with patient survival was determined by the Kaplan-Meier method.Results. The amplification of two cell cycle regulators,CCND1andCDKN1B, was identified to have a negative prognostic role. The medial survival of patients with gastric cancer displaying amplification compared to patients without amplification was 192 versus 725 days forCCND1(P=0.0012) and 165 versus 611 days forCDKN1B(P=0.0098).Conclusion. Gene amplifications ofCCND1andCDKN1Bare potential candidates to serve as prognostic markers for the stratification of patients based on the estimate of survival in the management of gastric cancer patients.

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Dorsey, M., C. Peterson, K. Bray, and C. E. Paquin. "Spontaneous amplification of the ADH4 gene in Saccharomyces cerevisiae." Genetics 132, no. 4 (December 1, 1992): 943–50. http://dx.doi.org/10.1093/genetics/132.4.943.

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Abstract Five spontaneous amplifications of the ADH4 gene were identified among 1,894 antimycin A-resistant mutants isolated from a diploid strain after growth at 15 degrees. Four of these amplifications are approximately 40-kb linear extrachromosomal palindromes carrying telomere homologous sequences at each end similar to a previously isolated amplification. ADH4 is located at the extreme left end of chromosome VII, and the extrachromosomal fragments appear to be the fusion of two copies of the end of this chromosome. The fifth amplification is a chromosomal amplification carrying an extra copy of ADH4 on both homologs of chromosome VII. These results suggest that the ADH system can be used to study amplification in Saccharomyces cerevisiae.

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Brochet, Mathieu, Elisabeth Couvé, Mohamed Zouine, Claire Poyart, and Philippe Glaser. "A Naturally Occurring Gene Amplification Leading to Sulfonamide and Trimethoprim Resistance in Streptococcus agalactiae." Journal of Bacteriology 190, no. 2 (November 16, 2007): 672–80. http://dx.doi.org/10.1128/jb.01357-07.

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ABSTRACT Gene amplifications have been detected as a transitory phenomenon in bacterial cultures. They are predicted to contribute to rapid adaptation by simultaneously increasing the expression of genes clustered on the chromosome. However, genome amplifications have rarely been described in natural isolates. Through DNA array analysis, we have identified two Streptococcus agalactiae strains carrying tandem genome amplifications: a fourfold amplification of 13.5 kb and a duplication of 92 kb. Both amplifications were located close to the terminus of replication and originated independently from any long repeated sequence. They probably arose in the human host and showed different stabilities, the 13.5-kb amplification being lost at a frequency of 0.003 per generation and the 92-kb tandem duplication at a frequency of 0.035 per generation. The 13.5-kb tandem amplification carried the five genes required for dihydrofolate biosynthesis and led to both trimethoprim (TMP) and sulfonamide (SU) resistance. Resistance to SU probably resulted from the increased synthesis of dihydropteroate synthase, the target of this antibiotic, whereas the amplification of the whole pathway was responsible for TMP resistance. This revealed a new mechanism of resistance to TMP involving an increased dihydrofolate biosynthesis. This is, to our knowledge, the first reported case of naturally occurring antibiotic resistance resulting from genome amplification in bacteria. The low stability of DNA segment amplifications suggests that their role in antibiotic resistance might have been underestimated.

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Haferlach, Claudia, Vera Grossmann, Melanie Zenger, Alexander Kohlmann, Wolfgang Kern, Susanne Schnittger, and Torsten Haferlach. "Gene Amplifications Are Rare Events in AML and MDS and Are Associated with Complex Karyotype, TP53 Deletions and Very Poor Survival." Blood 118, no. 21 (November 18, 2011): 2524. http://dx.doi.org/10.1182/blood.v118.21.2524.2524.

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Abstract Abstract 2524 Background: Gene amplifications are usually defined as the presence of more than 6 copies of a gene per cell. These supernumerary copies are located either extrachromosomally in double minutes (small acentric chromosome structures) or intrachromosomally in homogeneously staining regions. Such gene amplifications are rare but recurrent phenomenons in AML and MDS. So far, only small case studies have been reported. Aims: 1) to determine the frequency of gene amplifications in a large AML and MDS cohort, 2) to characterize the amplified regions and accompanying abnormalities, 3) to analyze the impact of specific amplifications on outcome. Patients and Methods: Out of 4,248 AML and 3,689 MDS studied by chromosome banding analysis (CBA) we identified 105 AML patients (2.5%) with gene amplifications (80/3,478 (2.3%) de novo AML, 7/478 (1.5%) s-AML, 18/292 (6.2%) t-AML) and 46 (1.2%) MDS. All cases with gene amplification were studied by 24-color FISH in addition to CBA in order to characterize the amplified regions and the accompanying abnormalities in detail. Further, interphase (IP)-FISH was performed with probes for TP73, HOXD cluster, EVI1, CMYC, JAK2, NUP214, MLL, ZNF4, GLTSCR1, ERG, RUNX1, BCR and CLRF, if 24-color FISH suggested amplification of these genes. In a subcohort of 12 patients genomic arrays (Human CGH Whole-Genome Array, NimbleGen, Madison, WI; Genome-Wide Human SNP Array 6.0, Affymetrix, Santa Clara, CA) were performed to characterize the amplified region in more detail. Results: In 28/151 pts (18.5%) the amplification was located in double minutes and in the remaining 123 cases intrachromosomally (81.5%). The following regions were found to be amplified: 1p (n=1, containing TP73), 2q (n=1, containing HOXD cluster), 3q (n=1, containing EVI1), 7p (n=1), 8q (n=29, containing CMYC in 28/29 pts), 9p (n=2, containing JAK2), 9q (n=1, containing NUP214), 11q (n=81, containing MLL in 80/81 cases), 13q (n=2), chromosome 19 (n=10, containing ZNF4 in 5 cases and GLTSCR1 in 2 cases), 21q (n=19, containing ERG in 16 and RUNX1 in 6 cases), 22q (n=2, containing BCR) and Xp (n=1, containing CLRF). In median, 8 accompanying chromosomal aberrations per cases were observed (range 0–21). 124/151 (82.1%) cases had a complex aberrant karyotype, defined as 4 or more abnormalities. However, in 2 cases the double minutes were the sole abnormalities. Gene amplifications were not observed in patients with disease defining aberration like t(8;21), inv(16), t(15;17) or those carrying NPM1 or CEPBA mutations (mutation status available in 89 and 37 patients, respectively). However, 2 cases with t(6;11)(q27;q23)/MLL-AF6 harbored an amplification of CMYC. In 88 cases the copy number status of TP53 was determined by IP-FISH. A TP53 deletion was detected in 49 (55.7%) pts. Interestingly, 14/16 (87.5%) cases with double minutes compared to 35/72 (48.6%) patients with intrachromosomal gene amplifications showed a TP53 deletion (p=0.004). Only 3 chromosomal regions were amplified in double minutes: 8q24/CMYC (n=14), 11q23/MLL (n=12) and 13q (n=2). In 6 cases with 8q amplification, 2 cases with 11q amplification and 4 cases with 21q amplification genomic arrays were performed. While the amplified region was quite homogeneous in cases with 8q amplification and contained in all cases the CMYC gene, amplified regions on 11q and 21q were heterogeneous and amplified regions were interspersed with regions of deletions. Interestingly, MLL and CBL were amplified in all analyzed cases with 11q23 amplification. In all analyzed cases with 21q22 amplification ERG was located within the amplified region while RUNX1 was amplified in 3/4 cases and deleted in the remaining case. In AML, overall survival was short in cases with gene amplification (median OS 11.3 months) and was particularly short in cases accompanied by complex karyotype (6.3 mo vs 18.6 mo in cases with non-complex karyotype, p=0.049). Conclusions: 1) MLL is the most frequently amplified gene in AML and MDS. 2) Gene amplifications occur predominantly in complex aberrant karyotypes. 3) Prognosis is poor in this subset of cases, and even more dismal if these amplifications are accompanied by complex karyotype. 4) The association of gene amplifications, complex karyotypes and TP53 deletions suggests that the unfavorable prognosis is due to chromosome instability facilitating the occurrence of additional genetic aberrations triggering resistance to chemotherapy. Disclosures: Haferlach: MLL Munich Leukemia Laboratory: Employment, Equity Ownership. Grossmann:MLL Munich Leukemia Laboratory: Employment. Zenger:MLL Munich Leukemia Laboratory: Employment. Kohlmann:MLL Munich Leukemia Laboratory: Employment. Kern:MLL Munich Leukemia Laboratory: Employment, Equity Ownership. Schnittger:MLL Munich Leukemia Laboratory: Employment, Equity Ownership. Haferlach:MLL Munich Leukemia Laboratory: Employment, Equity Ownership.

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Tang, Yidan, Baiyang Lu, Zhentong Zhu, and Bingling Li. "Establishment of a universal and rational gene detection strategy through three-way junction-based remote transduction." Chemical Science 9, no. 3 (2018): 760–69. http://dx.doi.org/10.1039/c7sc03190d.

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Matsui, Atsuka, Tatsuya Ihara, Hiraku Suda, Hirofumi Mikami, and Kentaro Semba. "Gene amplification: mechanisms and involvement in cancer." BioMolecular Concepts 4, no. 6 (December 1, 2013): 567–82. http://dx.doi.org/10.1515/bmc-2013-0026.

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AbstractGene amplification was recognized as a physiological process during the development of Drosophila melanogaster. Intriguingly, mammalian cells use this mechanism to overexpress particular genes for survival under stress, such as during exposure to cytotoxic drugs. One well-known example is the amplification of the dihydrofolate reductase gene observed in methotrexate-resistant cells. Four models have been proposed for the generation of amplifications: extrareplication and recombination, the breakage-fusion-bridge cycle, double rolling-circle replication, and replication fork stalling and template switching. Gene amplification is a typical genetic alteration in cancer, and historically many oncogenes have been identified in the amplified regions. In this regard, novel cancer-associated genes may remain to be identified in the amplified regions. Recent comprehensive approaches have further revealed that co-amplified genes also contribute to tumorigenesis in concert with known oncogenes in the same amplicons. Considering that cancer develops through the alteration of multiple genes, gene amplification is an effective acceleration machinery to promote tumorigenesis. Identification of cancer-associated genes could provide novel and effective therapeutic targets.

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Vleugel, Marije M., Reinhard Bos, Horst Buerger, Petra van der Groep, Outi R. Saramäki, Tapio Visakorpi, Elsken van der Wall, and Paul J. van Diest. "No Amplifications of Hypoxia-Inducible Factor-1α Gene in Invasive Breast Cancer: A Tissue Microarray Study." Analytical Cellular Pathology 26, no. 5-6 (January 1, 2004): 347–51. http://dx.doi.org/10.1155/2004/532413.

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Objective: Hypoxia Inducible Factor‐1 (HIF‐1) is an important transcription factor that stimulates tumour growth and metastases via several pathways, including angiogenesis and altered metabolism. Activation of HIF‐1 depends on the levels of its α‐subunit, which increase during hypoxia. Recent studies showed that the HIF‐1α gene was amplified in prostate cancer, leading to overexpression of HIF‐1α at normoxia. The aim of this study was to evaluate the presence of HIF‐1α gene amplifications in invasive breast cancer as an explanation for HIF‐1α protein overexpression. Methods: Protein and gene expression of HIF‐1α were analyzed on a tissue microarray of 94 breast cancers by immunohistochemistry and fluorescent in situ hybridization (FISH), respectively. Results: Overexpression of HIF‐1α protein was found in 58/94 (62%) of patients. No amplifications of the HIF‐1α gene were detected. Conclusion: Increased protein levels of HIF‐1α are not associated with amplification of the HIF‐1α gene in human breast cancer. Therefore, other mechanisms than gene amplification must be responsible for HIF‐α overexpression at normoxia.

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Saito, I., R. Groves, E. Giulotto, M. Rolfe, and G. R. Stark. "Evolution and stability of chromosomal DNA coamplified with the CAD gene." Molecular and Cellular Biology 9, no. 6 (June 1989): 2445–52. http://dx.doi.org/10.1128/mcb.9.6.2445.

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We have compared clones of Syrian hamster cells selected for the first amplification of the CAD gene with clones selected for further amplification. The large domain amplified initially was not reamplified as an intact unit. Instead, subregions were reamplified preferentially, and parts of the initial array were often lost. These events reduced the average amount of coamplified DNA accompanying each copy of the selected gene. The degree of amplification was small in the first step (about three extra copies of CAD per cell), but second-step amplifications to a high copy number (up to 60 extra copies per cell) occurred frequently. After several separate steps of amplification, highly condensed arrays that brought many CAD genes close together were formed. In striking contrast to the stability of these highly amplified arrays, the low-copy chromosomal arrays formed early were quite unstable and were often lost completely within 1 or 2 months of growth without selection. The results suggest that different mechanisms may be involved in the first step of amplification and in the later evolution of an already amplified array.

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Saito, I., R. Groves, E. Giulotto, M. Rolfe, and G. R. Stark. "Evolution and stability of chromosomal DNA coamplified with the CAD gene." Molecular and Cellular Biology 9, no. 6 (June 1989): 2445–52. http://dx.doi.org/10.1128/mcb.9.6.2445-2452.1989.

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We have compared clones of Syrian hamster cells selected for the first amplification of the CAD gene with clones selected for further amplification. The large domain amplified initially was not reamplified as an intact unit. Instead, subregions were reamplified preferentially, and parts of the initial array were often lost. These events reduced the average amount of coamplified DNA accompanying each copy of the selected gene. The degree of amplification was small in the first step (about three extra copies of CAD per cell), but second-step amplifications to a high copy number (up to 60 extra copies per cell) occurred frequently. After several separate steps of amplification, highly condensed arrays that brought many CAD genes close together were formed. In striking contrast to the stability of these highly amplified arrays, the low-copy chromosomal arrays formed early were quite unstable and were often lost completely within 1 or 2 months of growth without selection. The results suggest that different mechanisms may be involved in the first step of amplification and in the later evolution of an already amplified array.

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Moelans, Cathy B., Hanneke N. Monsuur, Johannes H. de Pinth, Remco D. Radersma, Roel A. de Weger, and Paul J. van Diest. "ESR1 Amplification is Rare in Breast Cancer and is Associated with High Grade and High Proliferation: A Multiplex Ligation-Dependent Probe Amplification Study." Analytical Cellular Pathology 33, no. 1 (2010): 13–18. http://dx.doi.org/10.1155/2010/619180.

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Background: Expression of estrogen receptor alpha (ERα) is predictive for endocrine therapy response and an important prognostic factor in breast cancer. Overexpression of ERα can be caused by estrogen receptor 1 (ESR1) gene amplification and was originally reported to be a frequent event associated with a significantly longer survival for ER-positive women treated with adjuvant tamoxifen monotherapy, which was however questioned by subsequent studies.Methods: This study aimed to reanalyze the frequency of ESR1 amplification by multiplex ligation-dependent probe amplification (MLPA) and fluorescence in situ hybridisation (FISH), and to assess clinicopathologic correlations. MLPA was performed in a group of 135 breast cancer patients, and gains/amplifications were subjected to FISH.Results: True ESR1 amplification by MLPA was rare (2%) and only 6% more patients showed a modest gain of ESR1. All MLPA-detected ESR1 amplifications and nearly all ESR1 gains were also FISH amplified and gained, but not all FISH amplifications/gains were MLPA amplified/gained, leading to an overall concordance of only 60% between both techniques. All 3 MLPA and FISH ESR1 amplified cases had high ERα expression, but there was no obvious correlation between ESR1 gain and ER status by IHC. ESR1 gains/amplifications were not associated with HER2 gain/amplification, but seemed to be associated with older age. Surprisingly, ESR1 gain/amplification was not associated with low grade as reported previously, but correlated with high grade and high proliferation. Furthermore, ESR1 gain/amplification by MLPA was not associated with nodal status or tumor size (pT status).Conclusion: ESR1 amplification as detected by MLPA is rare in breast cancer, and seems to be associated with high ERα expression, high age, high grade and high proliferation. This study confirms previous studies that showed differences in the ESR1 amplification frequencies detected by different techniques.

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Dissertations / Theses on the topic "Gene amplificatin"

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George, Rani Elizabeth. "Gene co-amplification with MYCN in neuroblastoma." Thesis, University of Newcastle Upon Tyne, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.363879.

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Santarius, Thomas. "Analysis of gene amplification in human cancer." Thesis, University of Cambridge, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.611463.

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Scott, Deborah Karen. "Identification and characterisation of genes co-amplified with the MYCN oncogene in neuroblastoma." Thesis, University of Newcastle Upon Tyne, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.268359.

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McArthur, James G. "Genetic elements which increase the frequency of gene amplification." Thesis, McGill University, 1989. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=74313.

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Members of the HSAG family of mammalian genomic elements were subcloned into the pSV2-DHFR expression vector and shown to encourage vector amplification in cis when transfected into a variety of cell lines. The interaction of multiple positive acting elements was required for this effect, with the native configuration of these elements in HSAG-1 producing the greatest effect. These positive acting elements; purine-pyrimidine tracts, Alu-like repetitive elements, stem-loop structures, and A+T rich sequences, have been previously associated with "hotspots" for recombination. Analysis of the structure of amplified vector sequences in MTX resistant pSV2-DHFR-HSAG-1 transfectants showed that these cells possessed a greater number of novel-joints indicating that HSAG elements may stimulate local recombination. Other experiments demonstrating an interaction between vector and HSAG sequences support this conclusion. We suggest that the stimulation of local recombination events by HSAG elements during vector amplification produces novel joints which then encourage further amplification.

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Heard, Edith. "Analysis of a gene amplification event in rat cells." Thesis, Imperial College London, 1990. http://hdl.handle.net/10044/1/46336.

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Banér, Johan. "Genetic analyses using rolling circle or PCR amplified padlock probes /." Uppsala : Acta Universitatis Upsaliensis : Univ.-bibl. [distributör], 2003. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-3339.

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Wong, Ka-lun, and 王嘉倫. "Development of loop-mediated isothermal amplification assay for rapid diagnosis of tuberculosis." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2013. http://hdl.handle.net/10722/193531.

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Tuberculosis (TB), a severe disease caused by Mycobacteria tuberculosis (MTb), remains a globally severe health problem. In modern days, emergence of drug resistant TB is a new threat to public health since it can lead to treatment failure, increased transmission of TB to other hosts and further development of drug resistant complications. The traditional diagnostic method for TB by Acid Fast Bacilli (AFB) smear and Löwenstein–Jensen medium (LJ) culture are poor in sensitivity and time consuming respectively. There is a need for rapid diagnosis and identification of MTb. Nucleic acid amplification like PCR and real-time PCR are options for rapid diagnosis. However, such techniques require sophisticated technique and complex equipment. The high cost would constitute a barrier for countries with a high demand but only limited resources. Loop-mediated isothermal amplification (LAMP) assay is a novel technique, proven by many studies as to its high sensitivity and highly specificity to MTb. Most importantly, LAMP assay is economical and affordable by developing countries. The first objective of this study was to evaluate the analytical sensitivity and specificity of LAMP assay. The specificity of LAMP assay was determined by performing LAMP assay on 19 clinical isolates, which had already been identified previously. The clinical isolates included 14 mycobacteria tuberculosis complex (MTb), and five mycobacteria other than tuberculosis (MOTT) strains that were positive for AFB smear and LJ culture but negative for IS6110 single-tube nested real time PCR. The specificity was 100%. The analytical sensitivity as well as the limit of detection (LOD) were determined by testing on a duplicate set of serial DNA dilution, where each duplicate consisted of dilution of 100,000, 10,000, 1000, 300, 100, 10 and 1 colony forming unit/milliliter (CFU/ml). The LOD of LAMP assay was about 3 CFU per reaction. The second objective of this study evaluated the diagnostic performance of LAMP assay against AFB culture and IS6110 single tube nested real time PCR for identification of MTb in 200 respiratory specimens from 123 patients. All the specimens have already been tested for IS6110 single tube nested real time PCR, and culture results and AFB smears results have been obtained for all the specimens. Sensitivity, specificity, positive predictive value (PPV) and negative predictive value (NPV) of three diagnostic methods (AFB smear microscopy, LAMP assay amplification and IS6110 single-tube nested real time PCR) were calculated with 95% confidence interval using LJ culture as gold standard. The LAMP assay had a sensitivity of 80%, specificity of 92.6%, PPV of 60% and NPV of 97.1%. However, MTb might fail to grow on the LJ culture medium for various reasons, for instance, MTb might already be dead after antibiotic treatment of the patient, or there might be poor laboratory practices during the processing of the specimens. Since the LJ culture method could produce false negatives in the situations described above, an alternative to the LJ culture method, ‘Hybrid Method’ was used as the gold standard. Under this method, a specimen was regarded as positive if the LJ culture result was positive. On the other hand, if a specimen generated a negative result using the LJ culture method, the results from the LAMP assay and IS6110 nested real time PCR would be considered, i.e., if both the LAMP assay and IS6110 nested real time PCR gave positive results while the results of LJ culture were negative, the specimen was referred to be positive in this case. In other words, a specimen would be regarded as negative if and only if the LJ culture result was negative and at least one of the LAMP assay or IS6110 was negative at the same time. Along the same line, the sensitivity, specificity, PPV and NPV of the three diagnostic methods (AFB smear microscopy, LAMP assay amplification and IS6110 single-tube nested real time PCR) were calculated with 95% confidence interval against the Hybrid Method. After resolution, the LAMP assay had a sensitivity of 87.0%, specificity of 100%, PPV of 100% and NPV of 97.1%. Our results showed that the LAMP assay has a great potential to be a new TB diagnostic test, especially in developing countries, with its lot of advantages like ease of use, cheap and fast. The LAMP assay in the study showed a high specificity, however, the sensitivity has to be improved before application in clinical use. For comparison of clinical performance, IS6110 single tube nested real time PCR had a higher sensitivity than that of LAMP assay (100% vs 80% using culture as gold standard; 100% vs 87% using ‘Hybrid Method’ as gold standard). However, LAMP assay had a higher specificity than that of IS6110 single tube nested real time PCR (92.6% vs 90.7% using culture as gold standard; 100% vs 98% using ‘Hybrid Method’ as gold standard). LAMP had been proven to be a potential and powerful tool in clinical diagnosis of MTb. Further improvement on its sensitivity is required to enable its extensive use in the clinic in the future.
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Pandita, Ajay. "Molecular cytogenetic analysis and gene amplification in rhabdomyosarcoma and neuroblastoma." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2000. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape4/PQDD_0028/NQ49926.pdf.

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Coren, Grant Robert. "Methotrexate resistance and gene amplification in choriocarcinoma cells in vitro." Thesis, Imperial College London, 1991. http://hdl.handle.net/10044/1/46728.

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Amaral, Lizabeth Pereira. "Developmentally interesting cytokines upregulated during human stem cell amplification in vitro." Link to electronic thesis, 2002. http://www.wpi.edu/Pubs/ETD/Available/etd-0422102-170335.

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Books on the topic "Gene amplificatin"

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Ruth, Laura. Gene amplification technologies: End users, marketers, and markets. New York: Kalorama Information, 2002.

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PCR primer design. New York: Humana Press, 2015.

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Kuncio, Gerald S. Selected abstracts on translocation and amplification of oncogenes. Bethesda, MD: U.S. Dept. of Health and Human Services, Public Health Service, National Institutes of Health, International Cancer Research Data Bank, National Cancer Institute, 1987.

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United States International Trade Commission. Certain gene amplification thermal cyclers and subassemblies thereof from the United Kingdom: Determination of the Commission in investigation no. 731-TA-485 (preliminary) under the Tariff Act of 1930, together with the information obtained in the investigation. Washington, DC: U.S. International Trade Commission, 1990.

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United States International Trade Commission. Certain gene amplification thermal cyclers and subassemblies thereof from the United Kingdom: Determination of the Commission in investigation no. 731-TA-485 (preliminary) under the Tariff Act of 1930, together with the information obtained in the investigation. Washington, DC: U.S. International Trade Commission, 1990.

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Lauerman, Lloyd Herman. Nucleic acid amplification assays for diagnosis of animal diseases. [Madison, Wis.]: American Association of Veterinary Laboratory Diagnosticians, 1998.

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Rousseau, André. Cyclin D1 gene amplification and protein overexpression in dysplastic oral mucosa and oral cancer. [Toronto: Faculty of Dentistry, University of Toronto], 2000.

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Bagasra, Omar. In Situ PCR techniques. New York: Wiley-Liss, 1997.

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Billia, Filio. Analysis of differential gene expression in a complex differentiating hierarchy by global amplification of cDNA from single hemopoietic precursors. Ottawa: National Library of Canada = Bibliothèque nationale du Canada, 1997.

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1943-, Erlich Henry A., ed. PCR technology: Principles and applications for DNA amplification. New York: Oxford University Press, 1994.

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Book chapters on the topic "Gene amplificatin"

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Gooch, Jan W. "Gene Amplification." In Encyclopedic Dictionary of Polymers, 895. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-1-4419-6247-8_13812.

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Peck, Stewart B., Carol C. Mapes, Netta Dorchin, John B. Heppner, Eileen A. Buss, Gustavo Moya-Raygoza, Marjorie A. Hoy, et al. "Gene Amplification." In Encyclopedia of Entomology, 1587. Dordrecht: Springer Netherlands, 2008. http://dx.doi.org/10.1007/978-1-4020-6359-6_1043.

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Kriegler, Michael. "Selection and Amplification." In Gene Transfer and Expression, 103–13. London: Palgrave Macmillan UK, 1990. http://dx.doi.org/10.1007/978-1-349-11891-5_6.

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Peccoud, Jean, and Christine Jacob. "Statistical Estimations of PCR Amplification Rates." In Gene Quantification, 111–28. Boston, MA: Birkhäuser Boston, 1998. http://dx.doi.org/10.1007/978-1-4612-4164-5_7.

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Miller, Orlando J., and Eeva Therman. "DNA and Gene Amplification." In Human Chromosomes, 369–83. New York, NY: Springer New York, 2001. http://dx.doi.org/10.1007/978-1-4613-0139-4_25.

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Palacios, Rafael, Susana Brom, Guillermo Dávila, Margarita Flores, Ma Lourdes Girard, David Romero, and Tomasz Stepkowski. "Gene Amplification in Rhizobium." In New Horizons in Nitrogen Fixation, 581–85. Dordrecht: Springer Netherlands, 1993. http://dx.doi.org/10.1007/978-94-017-2416-6_52.

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Kim, Chungyeul, Yongkuk Song, and Soonmyung Paik. "Assays for Gene Amplification." In Biomarkers in Breast Cancer, 65–77. Totowa, NJ: Humana Press, 2006. http://dx.doi.org/10.1385/1-59259-915-x:065.

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Wahl, G. M., S. Carroll, P. Gaudray, J. Meinkoth, and J. Ruiz. "Applications of Gene Transfer in the Analysis of Gene Amplification." In Gene Transfer, 289–323. Boston, MA: Springer US, 1986. http://dx.doi.org/10.1007/978-1-4684-5167-2_11.

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Gonzales, Frank, and Sherrol H. McDonough. "Application of Transcription-Mediated Amplification to Quantification of Gene Sequences." In Gene Quantification, 189–201. Boston, MA: Birkhäuser Boston, 1998. http://dx.doi.org/10.1007/978-1-4612-4164-5_11.

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Humphreys-Pereira, Danny A., Taeho Kim, and Joong-Ki Park. "Characterization of nematode mitochondrial genomes." In Techniques for work with plant and soil nematodes, 250–64. Wallingford: CABI, 2021. http://dx.doi.org/10.1079/9781786391759.0250.

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Abstract This chapter presents procedures on polymerase chain reaction (PCR) amplification, protocols for PCR, cloning and sequencing, and mitochondrial genome annotation and gene identification for the characterization of nematodes.

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Conference papers on the topic "Gene amplificatin"

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Stoicescu, Ramona, Razvan-Alexandru Stoicescu, Codrin Gheorghe, Adina Honcea, and Iulian Bratu. "CONSIDERATIONS ON SARS-COV-2 DIAGNOSIS IN THE LABORATORY OF UNIVERSITY EMERGENCY CLINICAL HOSPITAL OF CONSTANTA." In GEOLINKS Conference Proceedings. Saima Consult Ltd, 2021. http://dx.doi.org/10.32008/geolinks2021/b1/v3/07.

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Coronaviruses are members of the Coronaviridae family. They are enveloped, non-segmented, positive-sense, single-stranded RNA viruses. Their genome size is about 30 kilobases (kb) which consist, at the 5’ end, of non-structural open reading frames (ORFs: ORF1a, ORF 1b) which code for 16 non structural proteins, and at the 3’ end the genes which code for four structural proteins including membrane (M), envelope (E), spike (S), and nucleocapsid (N) proteins. Due to the rapid spread of COVID-19, a reliable detection method is needed for patient diagnosis especially in the early stages of the disease. WHO has recommended nucleic acid amplification tests such as real-time reverse transcription-polymerase chain reaction (RT-PCR). The assay detects three SARS-CoV-2 RNA targets: the envelope (E) gene, the nucleocapsid (N) gene and a region of the open reading frame (ORF1) of the RNA-dependent RNA polymerase (RdRp) gene from SARS-CoV-2 virus isolate Wuhan-Hu-1. Our study was made in the first 3 months of the year 2021 using the real-time RT PCR results obtained in the Cellular Biology ward of the University Emergency Clinical Hospital. In our lab we are testing the inpatients from the hospital wards (Neurology, Pediatrics, Surgery, Internal medicine, ICU, Cardiology, etc.); we are also testing the outpatients from Dialysis and Oncology, 2 days prior to their therapy; we also test the health care personnel. The number of tests we performed was: in January 1456, with 399 positive results (27.4%), 33 deaths; in February 1273 tests, 221 positive (17.36%), 16 deaths; in March 1471 tests, 373 positive (25.36%), 37 deceased.

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Jinhe Wang and Nan Zhang. "Process control of gene amplification instrument." In 2008 3rd IEEE Conference on Industrial Electronics and Applications (ICIEA). IEEE, 2008. http://dx.doi.org/10.1109/iciea.2008.4582801.

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Wang, Jinhe. "Thermal Gradient Instrument for Gene Amplification." In 2008 2nd International Conference on Bioinformatics and Biomedical Engineering. IEEE, 2008. http://dx.doi.org/10.1109/icbbe.2008.697.

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Okada, Masaya, Takuya Kubo, Kanako Masumoto, and Shigeki Iwanaga. "Super resolution imaging of HER2 gene amplification." In SPIE BiOS, edited by Jörg Enderlein, Ingo Gregor, Zygmunt K. Gryczynski, Rainer Erdmann, and Felix Koberling. SPIE, 2016. http://dx.doi.org/10.1117/12.2213918.

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Jinhe Wang. "The analysis and design of gene amplification system." In 2008 Chinese Control and Decision Conference (CCDC). IEEE, 2008. http://dx.doi.org/10.1109/ccdc.2008.4598144.

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Daly, John, and Mark Davies. "A Quantitative Free Convection DNA Amplifier." In ASME/JSME 2007 Thermal Engineering Heat Transfer Summer Conference collocated with the ASME 2007 InterPACK Conference. ASMEDC, 2007. http://dx.doi.org/10.1115/ht2007-32381.

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The Polymerase Chain Reaction (PCR) has been used extensively to amplify targeted nucleic acids for many applications in molecular biology and, increasingly, in medical diagnostics. Outlined in this paper is a PCR device which takes account of the advantages offered by free convection. The design is, in it fundamental format a time-wise isothermal well-based thermocycler. A temperature gradient induced across the well causes convection forces to circulate the sample through the required temperatures necessary for amplification. Quantitative amplification is demonstrated with real time measurements of SYBR Green I fluorescence within the free convective DNA amplifier. Amplification of an 86-bp fragment of the pGEM®-T vector (Promega) is performed in a 25μl volume in eight minutes. A 10-fold dilution series and methods for calculating effective cycle times are presented. Also detailed within this paper are PIV and thermal imaging results of the free convection cavity. This device presents an opportunity for the development of a practical and inexpensive gene-expression measurement system.

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Fleming, Paul, and Tara Dalton. "One-Step Reverse-Transcription PCR on a High-Throughput Micro-Fluidic Device." In ASME 2009 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2009. http://dx.doi.org/10.1115/sbc2009-206623.

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One step reverse-transcription polymerase chain reaction (RT-PCR) assays are an attractive option for further automating gene detection assays. One-step assays can reduce hands–on-time and the risk of sample crossover and contamination. The one-step chemistries are showing increasing use in virus detection and have been reported, in some cases, to be more appropriate than their two-step counterparts [1, 2]. Previous work presented by the Stokes Institute research group outlined a micro fluidic based continuous flow instrument which performed high throughput qPCR in nanolitre sized droplets [3]. This instrument had advantages over commercially available instruments in that it could process far more than the traditional 96 or 384 reaction setup in a single run and the reaction volume was reduced from 20–50 μl down to 30–100 nl sized droplets. Combining one-step chemistry with the technology offered by the devices being developed would lead to a high-throughput RNA-to-signal system capable of reverse transcribing and performing PCR on thousands of nanolitre sized reactions every day. It is envisaged that this technology will also lead to gene expression from single cells contained in nanolitre sized droplets. In this paper, a study was conducted in which an extra thermal region, manufactured from aluminium, was added to the existing continuous flow instruments. This region was maintained at a temperature suitable for reverse transcription, which was 48°C for the one-step kit tested. The thermal region was also a suitable length to maintain the sample at the required temperature for 15 minutes. Using a commercially available one step RT-PCR kit (TaqMan® RNA-to-CT™ 1-Step Kit, 4392653), the device was evaluated for its potential to perform one-step RT-PCR in continuously flowing nanolitre sized droplets. Electrophoresis gels were initially used in assessing specific amplification before an end-point detection method was utilized. RNA was extracted from the leukemic REH cell line with the housekeeping gene, glyceraldehyde-3-phosphate-dehydrogenase (GAPDH) as the gene of interest. To investigate the possibility of further reducing sample preparation and facilitating further automation, amplification from cell lysates without nucleic acid extraction was carried out on the device. Cell lysates were prepared using the cell lysis buffer from the TaqMan® Gene Expression Cells-to-CT™ Kit (Cat #AM1728). It was found that the device was successful in one-step RT-PCR from extracted RNA samples and samples from cell lysates without nucleic acid extraction.

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Matsumoto, Kazuko, Tokuzo Arao, Tetsuya Hamaguchi, Yasuhiro Shimada, Ken Kato, Ichiro Oda, Hirokazu Taniguchi, et al. "Abstract 5: Frequency of FGFR2 gene amplification in gastric cancer." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-5.

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Park, Ji Soo, Jae-Seok Lee, Hyo Sup Shim, Hye Ryun Kim, Sun Min Lim, Joo Hang Kim, and Byoung Chul Cho. "Abstract 4728: FGFR1 gene amplification in small cell lung cancer." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-4728.

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Li, Kelly, Devin Do, Patricia Hegerich, Bruno Ping, David Keys, Nivedita Majumdar, Stephen Jackson, Francisco Cifuentes, and Caifu Chen. "Abstract 1521: Quantitation of HER2 gene amplification using digital PCR." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-1521.

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Reports on the topic "Gene amplificatin"

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Gerbi, Susan A., Alexander Brodsky, and Ben Raphael. Hormonal Involvement in Breast Cancer Gene Amplification. Fort Belvoir, VA: Defense Technical Information Center, October 2008. http://dx.doi.org/10.21236/ada501716.

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Gerbi, Susan A., Alexander Brodsky, and Ben Raphael. Hormonal Involvement in Breast Cancer Gene Amplification. Fort Belvoir, VA: Defense Technical Information Center, October 2010. http://dx.doi.org/10.21236/ada541789.

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Zephyr, Yvelande, and Susan Walsh. Exploring Genetic Variation in a Caffeine Amplification Gene. Genetics Society of America Peer-Reviewed Education Portal (GSA PREP), March 2015. http://dx.doi.org/10.1534/gsaprep.2015.001.

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Sheen, Joon-Ho. A Gene Amplification Phenotype in c-Myc-Induced Mammary Tumors Cells. Fort Belvoir, VA: Defense Technical Information Center, July 2001. http://dx.doi.org/10.21236/ada396567.

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Sheen, Joon-Ho. A Gene Amplification Phenotype in c-Myc-Induced Mammary Tumors Cells. Fort Belvoir, VA: Defense Technical Information Center, July 2000. http://dx.doi.org/10.21236/ada390716.

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Terai, Kenta. How Alterations in the Cdt1 Expression Leads to Gene Amplification in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, July 2009. http://dx.doi.org/10.21236/ada514046.

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Terai, Kenta. How Alterations in the Cdt1 Expression Lead to Gene Amplification in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, July 2011. http://dx.doi.org/10.21236/ada549648.

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