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Relevant bibliographies by topics / Cloning tyrosine kinase genes

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Academic literature on the topic 'Cloning tyrosine kinase genes'

Author: Grafiati

Published: 4 June 2021

Last updated: 1 February 2022

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Journal articles on the topic "Cloning tyrosine kinase genes"

1

Beeler, J. F., W. J. LaRochelle, M. Chedid, S. R. Tronick, and S. A. Aaronson. "Prokaryotic expression cloning of a novel human tyrosine kinase." Molecular and Cellular Biology 14, no. 2 (February 1994): 982–88. http://dx.doi.org/10.1128/mcb.14.2.982.

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Screening of a human embryonic lung fibroblast cDNA expression library with antiphosphotyrosine antibodies led to isolation of a novel protein kinase. A clone, designated A6, contained a 3-kb cDNA insert with a predicted open reading frame of 350 amino acids. DNA sequence analysis failed to reveal any detectable similarity with previously known genes, and the predicted A6 protein lacked any of the motifs commonly conserved in the catalytic domains of protein kinases. However, the bacterially expressed beta-galactosidase-A6 fusion protein demonstrated both tyrosine and serine phosphorylation in an in vitro kinase assay and phosphorylated exogenous substrates including myelin basic protein specifically on tyrosine residues. The enzyme also displayed biochemical properties analogous to those of other protein tyrosine kinases. The A6 gene was found to be expressed widely at the transcript level in normal tissues and was evolutionarily conserved. Thus, A6 represents a novel tyrosine kinase which is highly divergent from previously described members of this important class of regulatory molecules.

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2

Beeler, J. F., W. J. LaRochelle, M. Chedid, S. R. Tronick, and S. A. Aaronson. "Prokaryotic expression cloning of a novel human tyrosine kinase." Molecular and Cellular Biology 14, no. 2 (February 1994): 982–88. http://dx.doi.org/10.1128/mcb.14.2.982-988.1994.

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Screening of a human embryonic lung fibroblast cDNA expression library with antiphosphotyrosine antibodies led to isolation of a novel protein kinase. A clone, designated A6, contained a 3-kb cDNA insert with a predicted open reading frame of 350 amino acids. DNA sequence analysis failed to reveal any detectable similarity with previously known genes, and the predicted A6 protein lacked any of the motifs commonly conserved in the catalytic domains of protein kinases. However, the bacterially expressed beta-galactosidase-A6 fusion protein demonstrated both tyrosine and serine phosphorylation in an in vitro kinase assay and phosphorylated exogenous substrates including myelin basic protein specifically on tyrosine residues. The enzyme also displayed biochemical properties analogous to those of other protein tyrosine kinases. The A6 gene was found to be expressed widely at the transcript level in normal tissues and was evolutionarily conserved. Thus, A6 represents a novel tyrosine kinase which is highly divergent from previously described members of this important class of regulatory molecules.

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3

Gibson, S., B. Leung, JA Squire, M. Hill, N. Arima, P. Goss, D. Hogg, and GB Mills. "Identification, cloning, and characterization of a novel human T-cell- specific tyrosine kinase located at the hematopoietin complex on chromosome 5q." Blood 82, no. 5 (September 1, 1993): 1561–72. http://dx.doi.org/10.1182/blood.v82.5.1561.1561.

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Abstract Signal transduction through the T-cell receptor and cytokine receptors on the surface of T lymphocytes occurs largely via tyrosine phosphorylation of intracellular substrates. Because neither the T-cell receptor nor cytokine receptors contain intrinsic kinase domains, signal transduction is thought to occur via association of these receptors with intracellular protein tyrosine kinases. Although several members of the SRC and SYK families of tyrosine kinases have been implicated in signal transduction in lymphocytes, it seems likely that additional tyrosine kinases involved in signal transduction remain to be identified. To identify unique T-cell tyrosine kinases, we used polymerase chain reaction-based cloning with degenerate oligonucleotides directed at highly conserved motifs of tyrosine kinase domains. We have cloned the complete cDNA for a unique human tyrosine kinase that is expressed mainly in T lymphocytes (EMT) and natural killer (NK) cells. The cDNA of EMT predicts an open reading frame of 1866 bp encoding a protein with a predicted size of 72 Kd, which is in keeping with its size on Western blotting. A single 6.2-kb EMT mRNA and 72-Kd protein were detected in T lymphocytes and NK-like cell lines, but were not detected in other cell lineages. EMT contains both SH2 and SH3 domains, as do many other intracellular kinases. EMT does not contain the N-terminal myristylation site or the negative regulatory tyrosine phosphorylation site in its carboxyterminus that are found in the SRC family of tyrosine kinases. EMT is related to the B-cell progenitor kinase (BPK), which has recently been implicated in X-linked hypogammaglobulinemia, to the TECI mammalian kinase, which has been implicated in liver neoplasia, to the more widely expressed TECII mammalian kinase, and to the Drosophila melanogaster Dsrc28 kinase. Sequence comparison suggests that EMT is likely the human homologue of a recently identified murine interleukin-2 (IL-2)-inducible T cell kinase (ITK). However, unlike ITK, EMT message and protein levels do not vary markedly on stimulation of human IL-2-responsive T cells with IL-2. Taken together, it seems that EMT is a member of a new family of intracellular kinases that includes BPK, TECI, and TECII. EMT was localized to chromosome 5q31–32, a region that contains the genes for several growth factors and receptors as well as early activation genes, particularly those involved in the hematopoietic system. Furthermore, the 5q31–32 region is implicated in the genesis of the 5q- syndrome associated with myelodysplasia and development of leukemia.(ABSTRACT TRUNCATED AT 400 WORDS)

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4

Gibson, S., B. Leung, JA Squire, M. Hill, N. Arima, P. Goss, D. Hogg, and GB Mills. "Identification, cloning, and characterization of a novel human T-cell- specific tyrosine kinase located at the hematopoietin complex on chromosome 5q." Blood 82, no. 5 (September 1, 1993): 1561–72. http://dx.doi.org/10.1182/blood.v82.5.1561.bloodjournal8251561.

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Signal transduction through the T-cell receptor and cytokine receptors on the surface of T lymphocytes occurs largely via tyrosine phosphorylation of intracellular substrates. Because neither the T-cell receptor nor cytokine receptors contain intrinsic kinase domains, signal transduction is thought to occur via association of these receptors with intracellular protein tyrosine kinases. Although several members of the SRC and SYK families of tyrosine kinases have been implicated in signal transduction in lymphocytes, it seems likely that additional tyrosine kinases involved in signal transduction remain to be identified. To identify unique T-cell tyrosine kinases, we used polymerase chain reaction-based cloning with degenerate oligonucleotides directed at highly conserved motifs of tyrosine kinase domains. We have cloned the complete cDNA for a unique human tyrosine kinase that is expressed mainly in T lymphocytes (EMT) and natural killer (NK) cells. The cDNA of EMT predicts an open reading frame of 1866 bp encoding a protein with a predicted size of 72 Kd, which is in keeping with its size on Western blotting. A single 6.2-kb EMT mRNA and 72-Kd protein were detected in T lymphocytes and NK-like cell lines, but were not detected in other cell lineages. EMT contains both SH2 and SH3 domains, as do many other intracellular kinases. EMT does not contain the N-terminal myristylation site or the negative regulatory tyrosine phosphorylation site in its carboxyterminus that are found in the SRC family of tyrosine kinases. EMT is related to the B-cell progenitor kinase (BPK), which has recently been implicated in X-linked hypogammaglobulinemia, to the TECI mammalian kinase, which has been implicated in liver neoplasia, to the more widely expressed TECII mammalian kinase, and to the Drosophila melanogaster Dsrc28 kinase. Sequence comparison suggests that EMT is likely the human homologue of a recently identified murine interleukin-2 (IL-2)-inducible T cell kinase (ITK). However, unlike ITK, EMT message and protein levels do not vary markedly on stimulation of human IL-2-responsive T cells with IL-2. Taken together, it seems that EMT is a member of a new family of intracellular kinases that includes BPK, TECI, and TECII. EMT was localized to chromosome 5q31–32, a region that contains the genes for several growth factors and receptors as well as early activation genes, particularly those involved in the hematopoietic system. Furthermore, the 5q31–32 region is implicated in the genesis of the 5q- syndrome associated with myelodysplasia and development of leukemia.(ABSTRACT TRUNCATED AT 400 WORDS)

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5

Neale, Jennifer C. C., Thomas P. Kenny, and M. Eric Gershwin. "Cloning and Sequencing of Protein Kinase cDNA from Harbor Seal (Phoca vitulina) Lymphocytes." Clinical and Developmental Immunology 11, no. 2 (2004): 157–63. http://dx.doi.org/10.1080/10446670410001722195.

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Protein kinases (PKs) play critical roles in signal transduction and activation of lymphocytes. The identification of PK genes provides a tool for understanding mechanisms of immunotoxic xenobiotics. As part of a larger study investigating persistent organic pollutants in the harbor seal and their possible immunomodulatory actions, we sequenced harbor seal cDNA fragments encoding PKs. The procedure, using degenerate primers based on conserved motifs of human protein tyrosine kinases (PTKs), successfully amplified nine phocid PK gene fragments with high homology to human and rodent orthologs. We identified eight PTKs and one dual (serine/threonine and tyrosine) kinase. Among these were several PKs important in early signaling events through the B- and T-cell receptors (FYN, LYN, ITK and SYK) and a MAP kinase involved in downstream signal transduction. V-FGR, RET and DDR2 were also expressed. Sequential activation of protein kinases ultimately induces gene transcription leading to the proliferation and differentiation of lymphocytes critical to adaptive immunity. PKs are potential targets of bioactive xenobiotics, including persistent organic pollutants of the marine environment; characterization of these molecules in the harbor seal provides a foundation for further research illuminating mechanisms of action of contaminants speculated to contribute to large-scale die-offs of marine mammals via immunosuppression.

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6

Iwama, A., K. Okano, T. Sudo, Y. Matsuda, and T. Suda. "Molecular cloning of a novel receptor tyrosine kinase gene, STK, derived from enriched hematopoietic stem cells." Blood 83, no. 11 (June 1, 1994): 3160–69. http://dx.doi.org/10.1182/blood.v83.11.3160.3160.

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Abstract To identify the novel receptor tyrosine kinases (RTKs) critical to the proliferation of hematopoietic stem cells, we performed polymerase chain reaction-based cloning from highly purified murine hematopoietic stem cells. Lineage marker-negative, c-KIT-positive, and Ly6A/E- or Sca- 1-positive (Lin-c-KIT+Sca-1+) cells were sorted by a fluorescence- activated cell sorter. Two sets of degenerate oligonucleotide primers were directed to the conserved sequences of the catalytic domain, and were used to amplify cDNAs that encode protein tyrosine kinases (PTKs). One hundred cDNA clones were sequenced and 8 RTKs were identified, as well as 12 non-RTKs and 2 serine/threonine kinases. Sixteen cDNAs were identical to the known kinase genes (PKC beta, JAK-1, JAK-2, TYK-2, HCK, FGR, FYN, BLK, c-FES, FER, c-ABL, c-KIT, FLK-1, FLK-2, IGF1R, and ECK). Six novel cDNA sequences (stk series) were identified. However, three of them turned out to be BPK, RYK, and TEK. The remaining three showed high homology to S6 kinase II, JAK-2, and v-SEA/c-MET, respectively. Characterization of full-length cDNA sequence of the v- SEA/cMET-related gene showed that this was a novel RTK gene and we named this gene STK (stem cell-derived tyrosine kinase). We identified two distinct forms of STK cDNA; the short one encoded a putative truncated protein that lacked most of the extracellular domain. STK was expressed at various stages of hematopoietic cells, including stem cells, but we could not detect any apparent expression in other adult tissues. The expression of the truncated form of mRNA was more predominant than that of the complete form. STK was assigned by fluorescent in situ hybridization to the R-positive F1 band of chromosome 9, the same region to which hepatic growth factor-like protein has been assigned. Characterization of these PTKs, including STK, will be helpful to elucidate the molecular mechanism of the growth regulation of hematopoietic stem cells.

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7

Iwama, A., K. Okano, T. Sudo, Y. Matsuda, and T. Suda. "Molecular cloning of a novel receptor tyrosine kinase gene, STK, derived from enriched hematopoietic stem cells." Blood 83, no. 11 (June 1, 1994): 3160–69. http://dx.doi.org/10.1182/blood.v83.11.3160.bloodjournal83113160.

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To identify the novel receptor tyrosine kinases (RTKs) critical to the proliferation of hematopoietic stem cells, we performed polymerase chain reaction-based cloning from highly purified murine hematopoietic stem cells. Lineage marker-negative, c-KIT-positive, and Ly6A/E- or Sca- 1-positive (Lin-c-KIT+Sca-1+) cells were sorted by a fluorescence- activated cell sorter. Two sets of degenerate oligonucleotide primers were directed to the conserved sequences of the catalytic domain, and were used to amplify cDNAs that encode protein tyrosine kinases (PTKs). One hundred cDNA clones were sequenced and 8 RTKs were identified, as well as 12 non-RTKs and 2 serine/threonine kinases. Sixteen cDNAs were identical to the known kinase genes (PKC beta, JAK-1, JAK-2, TYK-2, HCK, FGR, FYN, BLK, c-FES, FER, c-ABL, c-KIT, FLK-1, FLK-2, IGF1R, and ECK). Six novel cDNA sequences (stk series) were identified. However, three of them turned out to be BPK, RYK, and TEK. The remaining three showed high homology to S6 kinase II, JAK-2, and v-SEA/c-MET, respectively. Characterization of full-length cDNA sequence of the v- SEA/cMET-related gene showed that this was a novel RTK gene and we named this gene STK (stem cell-derived tyrosine kinase). We identified two distinct forms of STK cDNA; the short one encoded a putative truncated protein that lacked most of the extracellular domain. STK was expressed at various stages of hematopoietic cells, including stem cells, but we could not detect any apparent expression in other adult tissues. The expression of the truncated form of mRNA was more predominant than that of the complete form. STK was assigned by fluorescent in situ hybridization to the R-positive F1 band of chromosome 9, the same region to which hepatic growth factor-like protein has been assigned. Characterization of these PTKs, including STK, will be helpful to elucidate the molecular mechanism of the growth regulation of hematopoietic stem cells.

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8

Guasch, Géraldine, Cornel Popovici, Francine Mugneret, Max Chaffanet, Pierre Pontarotti, Daniel Birnbaum, and Marie-Josèphe Pébusque. "Endogenous retroviral sequence is fused to FGFR1 kinase in the 8p12 stem-cell myeloproliferative disorder with t(8;19)(p12;q13.3)." Blood 101, no. 1 (January 1, 2003): 286–88. http://dx.doi.org/10.1182/blood-2002-02-0577.

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Abstract FGFR1, a transmembrane receptor tyrosine kinase for fibroblast growth factors, is constitutively activated by chromosomal translocations in an atypical stem-cell myeloproliferative disorder. The FGFR1 tyrosine domain is fused to dimerization domains encoded by 4 alternative genes: FOP at 6q27, CEP110 at 9q33,FIM/ZNF198 at 13q12, and BCR at 22q11. In this study, we report the molecular cloning of the t(8;19)(p12;q13.3), the fifth translocation associated with this syndrome. Reverse transcriptase–polymerase chain reaction (RT-PCR) analysis and fluorescence in situ hybridization (FISH) demonstrated that the translocation resulted in a long terminal repeat of human endogenous retrovirus gene (HERV-K)/fibroblast growth factor receptor 1 (FGFR1) fusion transcript that incorporated 5′ sequences from HERV-K fused in frame to 3′ FGFR1 sequences encoding the kinase domain. RT-PCR detected only 1 of the 2 possible fusion transcripts,HERV-K/FGFR1.

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9

Guasch, Géraldine, Gary J. Mack, Cornel Popovici, Nicole Dastugue, Daniel Birnbaum, Jérome B. Rattner, and Marie-Josèphe Pébusque. "FGFR1 is fused to the centrosome-associated proteinCEP110 in the 8p12 stem cell myeloproliferative disorder with t(8;9)(p12;q33)." Blood 95, no. 5 (March 1, 2000): 1788–96. http://dx.doi.org/10.1182/blood.v95.5.1788.005k15_1788_1796.

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The hallmark of the 8p12 stem cell myeloproliferative disorder (MPD) is the disruption of the FGFR1 gene, which encodes a tyrosine kinase receptor for members of the fibroblast growth factor family.FGFR1 can be fused to at least 3 partner genes at chromosomal regions 6q27, 9q33, or 13q12. We report here the cloning of the t(8;9)(p12;q33) and the detection of a novel fusion betweenFGFR1 and the CEP110 gene, which codes for a novel centrosome-associated protein with a unique cell-cycle distribution. CEP110 is widely expressed at various levels in different tissues and is predicted to encode a 994-amino acid coiled-coil protein with 4 consensus leucine zippers [L-X(6)-L-X(6)-L-X(6)-L]. Both reciprocal fusion transcripts are expressed in the patient's cells. The CEP110-FGFR1 fusion protein encodes an aberrant tyrosine kinase of circa 150-kd, which retains most of CEP110 with the leucine zipper motifs and the catalytic domain of FGFR1. Transient expression studies show that the CEP110-FGFR1 protein has a constitutive kinase activity and is located within the cell cytoplasm.

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10

Benini, Stefano, Lorenzo Caputi, and Michele Cianci. "Cloning, purification, crystallization and 1.57 Å resolution X-ray data analysis of AmsI, the tyrosine phosphatase controlling amylovoran biosynthesis in the plant pathogenErwinia amylovora." Acta Crystallographica Section F Structural Biology Communications 70, no. 12 (November 28, 2014): 1693–96. http://dx.doi.org/10.1107/s2053230x14024947.

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The Gram-negative bacteriumErwinia amylovorais a destructive pathogen of plants belonging to the Rosaceae family. Amongst its pathogenicity factors,E. amylovoraproduces the exopolysaccharide amylovoran, which contributes to the occlusion of plant vessels, causing wilting of shoots and eventually resulting in plant death. Amylovoran biosynthesis requires the presence of 12 genes (fromamsA toamsL) clustered in theamsregion of theE. amylovoragenome. They mostly encode glycosyl transferases (AmsG, AmsB, AmsD, AmsE, AmsJ and AmsK), proteins involved in amylovoran translocation and assembly (AmsH, AmsL and AmsC), and also a tyrosine kinase (AmsA) and a tyrosine phosphatase (AmsI), which are both involved in the regulation of amylovoran biosynthesis. The low-molecular-weight protein tyrosine phosphatase AmsI was overexpressed as a His6-tagged protein inEscherichia coli, purified and crystallized. X-ray diffraction data were collected to a maximum resolution of 1.57 Å in space groupP3121.

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Dissertations / Theses on the topic "Cloning tyrosine kinase genes"

1

Jones, P. F. "Cloning and expression of tyrosine kinase genes." Thesis, University of Oxford, 1987. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.382626.

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Suen, Ki-Ling. "Cloning of protein kinase genes from a carrot cDNA library." Diss., Georgia Institute of Technology, 1991. http://hdl.handle.net/1853/25431.

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Schweighoffer, Edina. "The role of Syk protein tyrosine kinase in B cell development and function." Thesis, Open University, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.250493.

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Coffer, Paul James. "The identification, cloning and characterisation of novel mammalian protein-serine kinase genes." Thesis, Open University, 1991. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.293298.

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Moncrieff, Colin Lindsay. "Cloning and characterisation of a novel DMPK-related gene : CDC42BPB." Thesis, University of Glasgow, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.323439.

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Chen, Yi-Jun Grace. "Cloning and expression of three protein kinase genes of Colletotrichum gloeosporioides f. sp. malvae." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp03/MQ40402.pdf.

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Pylayeva, Yuliya. "Role of focal adhesion kinase in mammary gland tumorigenesis /." Access full-text from WCMC, 2008. http://proquest.umi.com/pqdweb?did=1528351831&sid=1&Fmt=2&clientId=8424&RQT=309&VName=PQD.

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Prata, Rodrigo Ferreira. "Papel do Tyrosine receptor Kinase B (TrkB) na regulação de genes do metabolismo hepático de colesterol e triglicerídeos." reponame:Repositório Institucional da UFABC, 2012.

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9

Summy, Justin Matthew. "Functional domain contributions to signaling specificity between the non-receptor tyrosine kinases c-src and c-yes." Morgantown, W. Va. : [West Virginia University Libraries], 2001. http://etd.wvu.edu/templates/showETD.cfm?recnum=2239.

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Thesis (Ph. D.)--West Virginia University, 2001.
Title from document title page. Document formatted into pages; contains vi, 195 p. : ill. (some col.). Vita. Includes abstract. Includes bibliographical references (p. 182-190).

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10

AGNES, FRANCOIS. "Etude de la structure des genes codant les recepteurs tyrosine kinase avec des domaines de type immunoglobuline : un modele d'evolution moleculaire." Paris 6, 1995. http://www.theses.fr/1995PA066005.

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Les recepteurs tyrosine kinase (rtk) possedant cinq, trois et sept domaines de type immunoglobuline dans leur region extracytoplasmique se repartissent respectivement dans les sous-classes iii, iv et v. Les genes humains qui codent les recepteurs des sous-classes iii et v sont groupes en paire ou en triplet sur trois chromosomes. Les genes kit et fms (rtkiii) ont une structure exon/intron identique dans la partie codant la region intracellulaire et similaire dans la partie codant la region extracellulaire ; ce sont deux genes homologues qui derivent probablement d'un ancetre commun. Sur la base de ces resultats et de la localisation en tandem des genes rtkiii, un modele d'evolution par duplication en cis et en trans concernant les genes de la sous-classe iii a ete postule. La structure exon/intron des genes flt3 et pdgfra (rtkiii) a ete determinee dans la partie codant la region intracellulaire. La comparaison de la structure de ces deux genes avec celle des genes kit et fms permet de confirmer le modele d'evolution par duplication en cis et en trans specifique des genes rtk de sous-classe iii. Elle montre que la structure exon/intron observee est une caracteristique des genes de la sous-classe iii. La structure genomique des genes flt4 (sous-classe v) et fgfr4 (sous-classe iv) a aussi ete determinee. Dans la partie codant la region intracellulaire, la comparaison de la structure de ces genes avec celle des genes de la sous-classe iii montre que les genes des sous-classes iii et v ont la meme structure exon/intron et que celle ci est similaire a celle des genes de la sous-classe iv. Ces resultats permettent d'elargir le modele d'evolution par duplications en cis et en trans aux genes de la sous-classe v et de proposer un origine ancestrale commune pour les genes des trois sous-classes. Dans la partie codant la region extracellulaire, la comparaison des genes des trois sous-classes montre qu'au sein de chaque sous-classe, la structure exon/intron est identique et que les genes appartenant aux sous-classes iii et v ont une structure similaire. Les analogies de structure mises en evidence entre des genes des trois sous-classes indiquent que l'ancetre commun etait probablement un gene codant un recepteur a trois domaines de type immunoglobuline. Sur la base de la conservation de la position d'un certain nombre d'introns, nous postulons que le gene ancestral etait deja partiellement morcele, qu'il contenait des exons plus grand et quelques introns, que les duplications ont concerne des genes entiers et que plusieurs introns se sont inseres, apres les duplications geniques, a des sites differents suivant les sous-classes

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Books on the topic "Cloning tyrosine kinase genes"

1

Mustelin, Tomas. Src family tyrosine kinases in leukocytes. Austin: R.G. Landes, 1994.

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Zhao, Genshi. Biosynthesis of phenylalanine and tyrosine in pseudomonas aeruginosa and zymomonas mobilis: Molecular cloning of the genes encoding cyclohexadienyl dehydratase and cyclohexadienyl dehydrogenase, and characterization of the gene products. 1991.

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3

Eisen, Tim. The patient with renal cell cancer. Edited by Giuseppe Remuzzi. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0172.

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Renal cancer is the commonest malignancy of the kidney and worldwide, accounts for between 2% and 3% of the total cancer burden. The mainstay of curative treatment remains surgery. There have been significant advances in surgical technique, the most important ones being nephron-sparing surgery and laparoscopic nephrectomy. The medical treatment of advanced renal cell cancer has only improved markedly in the last decade with the development of antiangiogenic tyrosine-kinase inhibitors, inhibitors of mammalian target of rapamycin, and a diminished role for immunotherapy.Tyrosine-kinase inhibitor therapy results in reduction of tumour volume in around three-quarters of patients and doubles progression-free survival, but treatment is not curative. The management of side effects in patients on maintenance tyrosine-kinase inhibitors has improved in the last 3 years, although still presents difficulties which have to be actively considered.The molecular biology of renal cell carcinoma is better understood than for the majority of solid tumours. The commonest form of renal cancer, clear-cell carcinoma of the kidney, is strongly associated with mutations in the von Hippel–Lindau gene and more recently with chromatin-remodelling genes such as PBRM1. These genetic abnormalities lead to a loss of control of angiogenesis and uncontrolled proliferation of tumour cells. There is a very wide spectrum of tumour behaviour from the extremely indolent to the terribly aggressive. It is not currently known what accounts for this disparity in tumour behaviour.A number of outstanding questions are being addressed in scientific and clinical studies such as a clearer understanding of prognostic and predictive molecular biomarkers, the role of adjuvant therapy, the role of surgery in the presence of metastatic disease, how best to use our existing agents, and investigation of novel targets and therapeutic agents, especially novel immunotherapies.

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Book chapters on the topic "Cloning tyrosine kinase genes"

1

Druker, Brian J., Sayuri Ohno, Elisabeth Buchdunger, Shu Tamura, Jürg Zimmermann, and Nicholas B. Lydon. "Selective Killing of BCR-ABL Positive Cells with a Specific Inhibitor of the ABL Tyrosine Kinase." In Cancer Genes, 255–67. Boston, MA: Springer US, 1996. http://dx.doi.org/10.1007/978-1-4615-5895-8_16.

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Ma, Leyuan, Justine Roderick, Michelle A. Kelliher, and Michael R. Green. "High-Throughput Screening of Tyrosine Kinase Inhibitor Resistant Genes in CML." In Methods in Molecular Biology, 159–73. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4939-4011-0_14.

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Kasahara, Masanori, Camilo Canel, E. Churchill McKinney, and Martin F. Flajnik. "Molecular Cloning of Nurse Shark cDNAs with High Sequence Similarity to Nucleoside Diphosphate Kinase Genes." In Molecular Evolution of the Major Histocompatibility Complex, 491–99. Berlin, Heidelberg: Springer Berlin Heidelberg, 1991. http://dx.doi.org/10.1007/978-3-642-84622-9_40.

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Schmeichel, C. J., S. T. Satek, and S. A. Weitzman. "Restriction Polymorphisms in Tyrosine Kinase Genes in Cells Transformed by Reactive Oxidants: Evidence for Concerted Methylation Changes in a Family of Genes." In Eicosanoids and Other Bioactive Lipids in Cancer, Inflammation and Radiation Injury, 475–78. Boston, MA: Springer US, 1993. http://dx.doi.org/10.1007/978-1-4615-3520-1_94.

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Padmavathi, Ganesan, Krishan Kumar Thakur, Anand Anip, Devivasha Bordoloi, and Ajaikumar B. Kunnumakkara. "The Receptor Tyrosine Kinase ALK — Its Fusion Partners and Their Implication in Various Cancers." In Fusion Genes and Cancer, 81–109. WORLD SCIENTIFIC, 2017. http://dx.doi.org/10.1142/9789813200944_0004.

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6

Fwilks, Andrew. "[45] Cloning members of protein-tyrosine kinase family using polymerase chain reaction." In Methods in Enzymology, 533–46. Elsevier, 1991. http://dx.doi.org/10.1016/0076-6879(91)00169-w.

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Kraus, M. H., and S. A. Aaronson. "[46] Detection and isolation of novel protein-tyrosine kinase genes employing reduced stringency hybridization." In Methods in Enzymology, 546–56. Elsevier, 1991. http://dx.doi.org/10.1016/0076-6879(91)00170-2.

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Copland, Mhairi, and Tessa L. Holyoake. "Chronic myeloid leukaemia." In Oxford Textbook of Medicine, edited by Chris Hatton and Deborah Hay, 5213–27. Oxford University Press, 2020. http://dx.doi.org/10.1093/med/9780198746690.003.0516.

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Abstract:

Chronic myeloid leukaemia (CML) has a worldwide incidence of 1 to 2 per 100 000 of the population. Most cases are caused by translocation of the distal end of chromosome 9 on to chromosome 22 which leads to the creation of a fusion protein expressed from the fusion gene formed by juxtaposition of parts of the BCR and ABL1 genes. The resulting oncoprotein is a constitutive tyrosine kinase and appears to operate as an initiator for the development of the leukaemia. Clinical features—many patients are asymptomatic at diagnosis, which is made following a routine blood test. Others present with signs and symptoms including fatigue, sweats, fever, weight loss, haemorrhagic manifestations, and abdominal discomfort (due to splenomegaly). Diagnosis—this is typically made by the examination of a peripheral blood film and the demonstration of the Ph chromosome by conventional cytogenetics in a bone marrow aspirate or peripheral blood sample. Polymerase chain reaction analysis of peripheral blood confirms the presence of a BCR-ABL1 transcript and characterizes the BCR-ABL1 junction. Treatment—the original TKI, imatinib, has had a very significant impact on the first-line management of patients with CML. It induces durable complete cytogenetic responses in the majority of patients and prolongs overall survival substantially. Second- and third-generation TKIs show enhanced potency against BCR-ABL1 activity and are licensed within Europe for first-line (dasatinib, nilotinib) or second-line or subsequent (dasatinib, nilotinib, bosutinib, ponatinib) use in CML. Patients with suboptimal responses to first-line treatment can be offered a different second-line TKI; or a third-line TKI, such as ponatinib; or allogeneic stem cell transplantation—for patients less than 65 years of age and with a suitable donor.

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Conference papers on the topic "Cloning tyrosine kinase genes"

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Little, Suzie, Alexa Jury, Dorine Bax, Lawrence Doey, Safa Al-Sarraj, Juliane Jurgensmeier, and Chris Jones. "Abstract 1140: Intratumoral mutual exclusivity of dual amplified receptor tyrosine kinase genes in glioblastoma." 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.am2012-1140.

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Nakata, Asuka, Mai Yamauchi, Rui Yamaguchi, Takashi Kohno, Masao Nagasaki, Teppei Shimamura, Seiya Imoto, et al. "Abstract LB-99: EGF receptor tyrosine kinase defines critical prognostic genes of stage IA lung adenocarcinoma." 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-lb-99.

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Ryu, Hwani, Jie-young Song, Sang-Gu Hwang, and Jiyeon Ahn. "Abstract 287: A novel class III receptor tyrosine kinase inhibitor synergizes with olaparib by inhibition of DNA repair-related genes in non-small cell lung cancer cells." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-287.

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Ryu, Hwani, Jie-young Song, Sang-Gu Hwang, and Jiyeon Ahn. "Abstract 287: A novel class III receptor tyrosine kinase inhibitor synergizes with olaparib by inhibition of DNA repair-related genes in non-small cell lung cancer cells." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-287.

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Tetsu, Osamu, Janyaporn Phuchareon, Annie Chou, Darren P. Cox, David W. Eisele, and Richard CK Jordan. "Abstract 351: Mutations of genes in the c-Kit receptor tyrosine kinase signaling pathway are inactive in adenoid cystic carcinoma of the salivary glands: Implications for c-Kit targeted therapy." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-351.

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Reports on the topic "Cloning tyrosine kinase genes"

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Weier, Heinz-Ulrich. Expression Profiling of Tyrosine Kinase Genes. Fort Belvoir, VA: Defense Technical Information Center, August 2003. http://dx.doi.org/10.21236/ada423672.

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Weier, Heinz U. Expression Profiling of Tyrosine Kinase Genes. Fort Belvoir, VA: Defense Technical Information Center, August 2000. http://dx.doi.org/10.21236/ada391061.

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