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Relevant bibliographies by topics / CDK [Cylin dependent kinase]

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Academic literature on the topic 'CDK [Cylin dependent kinase]'

Author: Grafiati

Published: 4 June 2021

Last updated: 17 February 2022

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Journal articles on the topic "CDK [Cylin dependent kinase]"

1

Matsuoka, M., J. Y. Kato, R. P. Fisher, D. O. Morgan, and C. J. Sherr. "Activation of cyclin-dependent kinase 4 (cdk4) by mouse MO15-associated kinase." Molecular and Cellular Biology 14, no. 11 (November 1994): 7265–75. http://dx.doi.org/10.1128/mcb.14.11.7265.

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The assembly of functional holoenzymes composed of regulatory D-type cyclins and cyclin-dependent kinases (cdks) is rate limiting for progression through the G1 phase of the mammalian somatic cell cycle. Complexes between D-type cyclins and their major catalytic subunit, cdk4, are catalytically inactive until cyclin-bound cdk4 undergoes phosphorylation on a single threonyl residue (Thr-172). This step is catalyzed by a cdk-activating kinase (CAK) functionally analogous to the enzyme which phosphorylates cdc2 and cdk2 at Thr-161/160. Here, we demonstrate that the catalytic subunit of mouse cdc2/cdk2 CAK (a 39-kDa protein designated p39MO15) can assemble with a regulatory protein present in either insect or mammalian cells to generate a CAK activity capable of phosphorylating and enzymatically activating both cdk2 and cdk4 in complexes with their respective cyclin partners. A newly identified 37-kDa cyclin-like protein (cyclin H [R. P. Fisher and D. O. Morgan, Cell 78:713-724, 1994]) can assemble with p39MO15 to activate both cyclin A-cdk2 and cyclin D-cdk4 in vitro, implying that CAK is structurally reminiscent of cyclin-cdk complexes themselves. Antisera produced to the p39MO15 subunit can completely deplete mammalian cell lysates of CAK activity for both cyclin A-cdk2 and cyclin D-cdk4, with recovery of activity in the resulting immune complexes. By using an immune complex CAK assay, CAK activity for cyclin A-cdk2 and cyclin D-cdk4 was detected both in quiescent cells and invariantly throughout the cell cycle. Therefore, although it is essential for the enzymatic activation of cyclin-cdk complexes, CAK appears to be neither rate limiting for the emergence of cells from quiescence nor subject to upstream regulatory control by stimulatory mitogens.

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Matsuoka, M., J. Y. Kato, R. P. Fisher, D. O. Morgan, and C. J. Sherr. "Activation of cyclin-dependent kinase 4 (cdk4) by mouse MO15-associated kinase." Molecular and Cellular Biology 14, no. 11 (November 1994): 7265–75. http://dx.doi.org/10.1128/mcb.14.11.7265-7275.1994.

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The assembly of functional holoenzymes composed of regulatory D-type cyclins and cyclin-dependent kinases (cdks) is rate limiting for progression through the G1 phase of the mammalian somatic cell cycle. Complexes between D-type cyclins and their major catalytic subunit, cdk4, are catalytically inactive until cyclin-bound cdk4 undergoes phosphorylation on a single threonyl residue (Thr-172). This step is catalyzed by a cdk-activating kinase (CAK) functionally analogous to the enzyme which phosphorylates cdc2 and cdk2 at Thr-161/160. Here, we demonstrate that the catalytic subunit of mouse cdc2/cdk2 CAK (a 39-kDa protein designated p39MO15) can assemble with a regulatory protein present in either insect or mammalian cells to generate a CAK activity capable of phosphorylating and enzymatically activating both cdk2 and cdk4 in complexes with their respective cyclin partners. A newly identified 37-kDa cyclin-like protein (cyclin H [R. P. Fisher and D. O. Morgan, Cell 78:713-724, 1994]) can assemble with p39MO15 to activate both cyclin A-cdk2 and cyclin D-cdk4 in vitro, implying that CAK is structurally reminiscent of cyclin-cdk complexes themselves. Antisera produced to the p39MO15 subunit can completely deplete mammalian cell lysates of CAK activity for both cyclin A-cdk2 and cyclin D-cdk4, with recovery of activity in the resulting immune complexes. By using an immune complex CAK assay, CAK activity for cyclin A-cdk2 and cyclin D-cdk4 was detected both in quiescent cells and invariantly throughout the cell cycle. Therefore, although it is essential for the enzymatic activation of cyclin-cdk complexes, CAK appears to be neither rate limiting for the emergence of cells from quiescence nor subject to upstream regulatory control by stimulatory mitogens.

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Harper, J. W., S. J. Elledge, K. Keyomarsi, B. Dynlacht, L. H. Tsai, P. Zhang, S. Dobrowolski, C. Bai, L. Connell-Crowley, and E. Swindell. "Inhibition of cyclin-dependent kinases by p21." Molecular Biology of the Cell 6, no. 4 (April 1995): 387–400. http://dx.doi.org/10.1091/mbc.6.4.387.

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p21Cip1 is a cyclin-dependent kinase (Cdk) inhibitor that is transcriptionally activated by p53 in response to DNA damage. We have explored the interaction of p21 with the currently known Cdks. p21 effectively inhibits Cdk2, Cdk3, Cdk4, and Cdk6 kinases (Ki 0.5-15 nM) but is much less effective toward Cdc2/cyclin B (Ki approximately 400 nM) and Cdk5/p35 (Ki > 2 microM), and does not associate with Cdk7/cyclin H. Overexpression of P21 arrests cells in G1. Thus, p21 is not a universal inhibitor of Cdks but displays selectivity for G1/S Cdk/cyclin complexes. Association of p21 with Cdks is greatly enhanced by cyclin binding. This property is shared by the structurally related inhibitor p27, suggesting a common biochemical mechanism for inhibition. With respect to Cdk2 and Cdk4 complexes, p27 shares the inhibitory potency of p21 but has slightly different kinase specificities. In normal diploid fibroblasts, the vast majority of active Cdk2 is associated with p21, but this active kinase can be fully inhibited by addition of exogenous p21. Reconstruction experiments using purified components indicate that multiple molecules of p21 can associate with Cdk/cyclin complexes and inactive complexes contain more than one molecule of p21. Together, these data suggest a model whereby p21 functions as an inhibitory buffer whose levels determine the threshold kinase activity required for cell cycle progression.

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Musgrove, Elizabeth A., Alexander Swarbrick, Christine S. L. Lee, Ann L. Cornish, and Robert L. Sutherland. "Mechanisms of Cyclin-Dependent Kinase Inactivation by Progestins." Molecular and Cellular Biology 18, no. 4 (April 1, 1998): 1812–25. http://dx.doi.org/10.1128/mcb.18.4.1812.

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ABSTRACT The steroid hormone progesterone regulates proliferation and differentiation in the mammary gland and uterus by cell cycle phase-specific actions. In breast cancer cells the predominant effect of synthetic progestins is long-term growth inhibition and arrest in G1 phase. Progestin-mediated growth arrest of T-47D breast cancer cells was preceded by inhibition of cyclin D1-Cdk4, cyclin D3-Cdk4, and cyclin E-Cdk2 kinase activities in vitro and reduced phosphorylation of pRB and p107. This was accompanied by decreases in the expression of cyclins D1, D3, and E, decreased abundance of cyclin D1- and cyclin D3-Cdk4 complexes, increased association of the cyclin-dependent kinase (CDK) inhibitor p27 with the remaining Cdk4 complexes, and changes in the molecular masses and compositions of cyclin E complexes. In control cells cyclin E eluted from Superdex 200 as two peaks of ∼120 and ∼200 kDa, with the 120-kDa peak displaying greater cyclin E-associated kinase activity. Following progestin treatment, almost all of the cyclin E was in the 200-kDa, low-activity form, which was associated with the CDK inhibitors p21 and p27; this change preceded the inhibition of cell cycle progression. These data suggest preferential formation of this higher-molecular-weight, CDK inhibitor-bound form and a reduced number of cyclin E-Cdk2 complexes as mechanisms for the decreased cyclin E-associated kinase activity following progestin treatment. Ectopic expression of cyclin D1 in progestin-inhibited cells led to the reappearance of the 120-kDa active form of cyclin E-Cdk2 preceding the resumption of cell cycle progression. Thus, decreased cyclin expression and consequent increased CDK inhibitor association are likely to mediate the decreases in CDK activity accompanying progestin-mediated growth inhibition.

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Endicott, Jane A., and Martin E. M. Noble. "Structural characterization of the cyclin-dependent protein kinase family." Biochemical Society Transactions 41, no. 4 (July 18, 2013): 1008–16. http://dx.doi.org/10.1042/bst20130097.

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Structural studies of members of the CDK (cyclin-dependent protein kinase) family have made a significant contribution to our understanding of the regulation of protein kinases. The structure of monomeric unphosphorylated CDK2 was the first of an inactive protein kinase to be determined and, since then, structures of other members of the CDK family, alone, in complex with regulatory proteins and in differing phosphorylation states, have enhanced our understanding of the molecular mechanisms regulating protein kinase activity. Recently, our knowledge of the structural biology of the CDK family has been extended by determination of structures for members of the transcriptional CDK and CDK-like kinase branches of the extended family. We include these recent structures in the present review and consider them in the light of current models for CDK activation and regulation.

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DINARINA, Ana, Laurent H. PEREZ, Amparo DAVILA, Markus SCHWAB, Tim HUNT, and Angel R. NEBREDA. "Characterization of a new family of cyclin-dependent kinase activators." Biochemical Journal 386, no. 2 (February 22, 2005): 349–55. http://dx.doi.org/10.1042/bj20041779.

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Progression through the cell cycle is regulated by CDKs (cyclin-dependent kinases), which associate with activating partners, named cyclins, to efficiently phosphorylate substrates. We previously reported the identification of RINGO, a Xenopus protein that can activate CDK1 and CDK2 despite lack of sequence similarity to cyclins, which plays a role in the regulation of the meiotic cell cycle in oocytes. In the present study we report the characterization of four mammalian RINGO proteins, which are 53–68% identical with Xenopus RINGO in a central core of about 75 residues. We show that all RINGO family members can bind to and activate CDK1 and CDK2, albeit with different efficiencies, but they do not bind to CDK4 or CDK6. The core RINGO sequences are critical for CDK activation. We also identified key residues in CDK2 that are required for RINGO binding. All RINGO proteins can also bind the CDK inhibitor p27Kip1, but with an inverse efficiency of their ability to bind to CDK1. Our results identify a new family of mammalian proteins that can activate CDKs and therefore potentially function as cell cycle regulators. The ability of RINGO proteins to activate CDK1 and CDK2 suggest also cyclin-independent roles for these kinases.

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Shapiro, Geoffrey I. "Cyclin-Dependent Kinase Pathways As Targets for Cancer Treatment." Journal of Clinical Oncology 24, no. 11 (April 20, 2006): 1770–83. http://dx.doi.org/10.1200/jco.2005.03.7689.

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Cyclin-dependent kinases (cdks) are critical regulators of cell cycle progression and RNA transcription. A variety of genetic and epigenetic events cause universal overactivity of the cell cycle cdks in human cancer, and their inhibition can lead to both cell cycle arrest and apoptosis. However, built-in redundancy may limit the effects of highly selective cdk inhibition. Cdk4/6 inhibition has been shown to induce potent G1 arrest in vitro and tumor regression in vivo; cdk2/1 inhibition has the most potent effects during the S and G2 phases and induces E2F transcription factor–dependent cell death. Modulation of cdk2 and cdk1 activities also affects survival checkpoint responses after exposure to DNA-damaging and microtubule-stabilizing agents. The transcriptional cdks phosphorylate the carboxy-terminal domain of RNA polymerase II, facilitating efficient transcriptional initiation and elongation. Inhibition of these cdks primarily affects the accumulation of transcripts with short half-lives, including those encoding antiapoptosis family members, cell cycle regulators, as well as p53 and nuclear factor-kappa B–responsive gene targets. These effects may account for apoptosis induced by cdk9 inhibitors, especially in malignant hematopoietic cells, and may also potentiate cytotoxicity mediated by disruption of a variety of pathways in many transformed cell types. Current work is focusing on overcoming pharmacokinetic barriers that hindered development of flavopiridol, a pan-cdk inhibitor, as well as assessing novel classes of compounds potently targeting groups of cell cycle cdks (cdk4/6 or cdk2/1) with variable effects on the transcriptional cdks 7 and 9. These efforts will establish whether the strategy of cdk inhibition is able to produce therapeutic benefit in the majority of human tumors.

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Chen, J., P. Saha, S. Kornbluth, B. D. Dynlacht, and A. Dutta. "Cyclin-binding motifs are essential for the function of p21CIP1." Molecular and Cellular Biology 16, no. 9 (September 1996): 4673–82. http://dx.doi.org/10.1128/mcb.16.9.4673.

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The cyclin-dependent kinase (Cdk) inhibitor p21 is induced by the tumor suppressor p53 and is required for the G1-S block in cells with DNA damage. We report that there are two copies of a cyclin-binding motif in p21, Cy1 and Cy2, which interact with the cyclins independently of Cdk2. The cyclin-binding motifs of p21 are required for optimum inhibition of cyclin-Cdk kinases in vitro and for growth suppression in vivo. Peptides containing only the Cy1 or Cy2 motif partially inhibit cyclin-Cdk kinase activity in vitro and DNA replication in Xenopus egg extracts. A monoclonal antibody which recognizes the Cy1 site of p21 specifically disrupts the association of p21 with cyclin E-Cdk2 and with cyclin D1-Cdk4 in cell extracts. Taken together, these observations suggest that the cyclin-binding motif of p21 is important for kinase inhibition and for formation of p21-cyclin-Cdk complexes in the cell. Finally, we show that the cyclin-Cdk complex is partially active if associated with only the cyclin-binding motif of p21, providing an explanation for how p21 is found associated with active cyclin-Cdk complexes in vivo. The Cy sequences may be general motifs used by Cdk inhibitors or substrates to interact with the cyclin in a cyclin-Cdk complex.

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Gitig, Diana M., and Andrew Koff. "Cdk Pathway: Cyclin-Dependent Kinases and Cyclin-Dependent Kinase Inhibitors." Molecular Biotechnology 19, no. 2 (2001): 179–88. http://dx.doi.org/10.1385/mb:19:2:179.

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Susanti, Ni Made Pitri, and Daryono Hadi Tjahjono. "Cyclin-Dependent Kinase 4 and 6 Inhibitors in Cell Cycle Dysregulation for Breast Cancer Treatment." Molecules 26, no. 15 (July 24, 2021): 4462. http://dx.doi.org/10.3390/molecules26154462.

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In cell development, the cell cycle is crucial, and the cycle progression’s main controllers are endogenous CDK inhibitors, cyclin-dependent kinases (CDKs), and cyclins. In response to the mitogenic signal, cyclin D is produced and retinoblastoma protein (Rb) is phosphorylated due to activated CDK4/CDK6. This causes various proteins required in the cell cycle progression to be generated. In addition, complexes of CDK1-cyclin A/B, CDK2-cyclin E/A, and CDK4/CDK6-cyclin D are required in each phase of this progression. Cell cycle dysregulation has the ability to lead to cancer. Based on its role in the cell cycle, CDK has become a natural target of anticancer therapy. Therefore, understanding the CDK structures and the complex formed with the drug, helps to foster the development of CDK inhibitors. This development starts from non-selective CDK inhibitors to selective CDK4/CDK6 inhibitors, and these have been applied in clinical cancer treatment. However, these inhibitors currently require further development for various hematologic malignancies and solid tumors, based on the results demonstrated. In drug development, the main strategy is primarily to prevent and asphyxiate drug resistance, thus a determination of specific biomarkers is required to increase the therapy’s effectiveness as well as patient selection suitability in order to avoid therapy failure. This review is expected to serve as a reference for early and advanced-stage researchers in designing new molecules or repurposing existing molecules as CDK4/CDK6 inhibitors to treat breast cancer.

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Dissertations / Theses on the topic "CDK [Cylin dependent kinase]"

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Even, Yasmine. "Caractéristiques et fonctions d'une Cdk-like, CDC2L5." Paris 6, 2005. http://www.theses.fr/2005PA066136.

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Birot, Adrien. "Regulation of fission yeast cohesin by the Cyclin Dependent Kinase PeF1." Thesis, Bordeaux, 2016. http://www.theses.fr/2016BORD0386/document.

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Le complexe cohésine est un complexe protéique en forme d'anneau composé de quatre sous-unités essentielles très conservées: Smc1, Smc3, Rad21 et Scc3. Par sa capacité à encercler les molécules d’ADN, les cohésines participent à de nombreux processus cellulaires tels que la ségrégation des chromosomes, la signalisation et la réparation des dommages à l’ADN, la régulation de la transcription et l'organisation du génome. Pour assurer ces différentes fonctions biologiques les cohésines doivent être finement régulées à la fois dans le temps et l’espace. Ces régulations reposent en partie sur le contrôle de leur association à la chromatine (capture de l’ADN). Cela nécessite l'action d'un «facteur de chargement » composé de deux protéines conservées et essentielles, Mis4 et Ssl3 chez la levure S. pombe. Comment ce complexe régule la capture de l’ADN par l’anneau de cohésine dans l'espace et le temps demeure à ce jour très mal compris. Afin d’identifier des régulateurs de l’association des cohésines à la chromatine, nous avons réalisé un crible génétique visant à rechercher des suppresseurs de la mutation thermosensible mis4-367. Ce crible a conduit à l’identification de la Cyclin-Dependent Kinase Pef1 qui agit comme un régulateur négatif de la cohésion des chromatides soeurs en contrôlant vraisemblablement négativement l’association des cohésines à la chromatine. De forts arguments expérimentaux indiquent que Pef1 exerce sa fonction en régulant directement la phosphorylation de la sous-unité Rad21 du complexe cohésine. De façon intéressante, via un autre crible génétique, nous avons identifié la phosphatase Pph3/Psy2 qui joue un rôle dans l’établissement de la cohésion des chromatides soeurs en contrôlant la déphosphorylation de Rad21.Ensemble, ces données suggèrent que le contrôle de l’état de phosphorylation de la sous-unité Rad21 du complexe cohésine joue un rôle central dans le processus de cohésion chez la levure S. Pombe
Cohesin is a highly conserved ring-shaped protein complex made of four essential subunits: Psm1, Psm3, Rad21 and Psc3. By its ability to capture DNA molecules within its ring-like structure, cohesion plays a key role in many cellular processes such as chromosome segregation, DNA damage signalling and repair, transcriptional gene regulation and nuclear organization. To ensure all of its biological functions, cohesin must be tightly regulated in space and time. This regulation relies in part on the control of cohesin binding to chromatin (DNA capture). Cohesin recruitment to chromatin requires the action of a “loading complex” made of two conserved and essential proteins named Mis4 and Ssl3 in the fission yeast. How this complex regulates where and when DNA capture by the cohesin ring must occur remains poorly understood. To identify regulators of cohesin binding to chromatin we have performed a genetic screen for suppressors of the thermosensitive mutation mis4-367. This genetic screen has led to the identification of the cyclin-dependent-kinase Pef1 that acts as a negative regulator of sister chromatids cohesion may be bynegatively controlling cohesin binding to chromatin. Strong experimental evidences indicate that Pef1 exerts its function at least in part by directly phosphorylating the Rad21 subunit of the cohesin complex. Interestingly, a genetic screen made in parallel identified the Pph3/Psy2 phosphatase as implicated in the establishment of sister chromatid cohesion by regulating Rad21 dephosphorylation. Strikingly, the control of Rad21 phosphorylation status appears central to the cohesion process in the fission yeast S. pombe

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Northen, Julian S. "Design of novel pyrimido[5,4-d]pyrimidine cyclin dependent kinase (cdk) inhibitors." Thesis, University of Newcastle Upon Tyne, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.391320.

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Parsons, Rachel. "The design and synthesis of pyrimidine based cyclin-dependent kinase (CDK) inhibitors." Thesis, University of Newcastle Upon Tyne, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.408491.

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Bonnet, Christine. "Un motif sur la cycline B nécessaire à l'activation de CDK1 chez la levure ?" Paris 6, 2002. http://www.theses.fr/2002PA066509.

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Nafati, Mehdi. "Caractérisation fonctionnelle des inhibiteurs de Cyclin-Dependent Kinase (CDK) dans le fruit de tomate (Solanum lycopersicum)." Thesis, Bordeaux 2, 2010. http://www.theses.fr/2010BOR21712/document.

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Au sein de l’unité mixte de recherche 619 de l’Institut National de Recherche Agronomique, le groupe « Organogénèse du Fruit et Endoréduplication » étudie les acteurs moléculaires prenant part au contrôle du cycle cellulaire dans le fruit de tomate. L’objet de la présente thèse est l’étude de l’inhibiteur du cycle cellulaire Kip-Related Protein, et son rôle durant le développement du fruit. Identification de motifs protéiques fonctionnels chez l’Inhibiteur de Kinase Cycline-Dependent SlKRP1 chez Solanum lycopersicum : Leur rôle dans les interactions avec des partenaires du cycle cellulaire Les Kip-related proteins (KRPs) jouent un rôle majeur dans la régulation du cycle cellulaire. Il a été montré qu’ils inhibent les complexes CDK/Cyclin et ainsi bloquent la progression du cycle cellulaire. Malgré leur manque d’homologie avec leurs homologues animaux au delà de leur motif de liaison CDK/Cyclin, localisé à l’extrémité C-terminal de la protéine dans les séquences de plante, des études antérieurs ont montré la présence de motifs conservés spécifiques aux plantes chez certaines KRPs. Nous n’avons cependant que peu d’information concernant leur fonction. Nous montrons ici que les KRPs sont distribués en deux sous groupes phylogénétiques, et que chaque sous-groupe dispose de courts motifs spécifiques conservés. Les KRPs du sous-groupe 1 disposent ainsi de six motifs conservés entre eux. Utilisant SlKRP1, qui appartient au sous-groupe 1, nous avons identifié des motifs responsables de la localisation de la protéine et de ses interactions protéine-protéine. Nous montrons que le motif 2 est responsable de l’interaction avec CSN5, une sous-unité du complexe signalosome, et que le motif 5 a un effet redondant avec le motif 3 pour ce qui est de la localisation sub-cellulaire de la protéine. Nous montrons de plus que SlKRP1 est capable de guider SlCDKA1 et SlCycD3;1 vers le noyau, et ce même en l’absence du motif de liaison CDK/Cycline précédemment référencé. Ce nouveau site d’interaction est probablement localisé dans la partie centrale de la séquence de SlKRP1. Ces résultats apportent de nouveaux indices quant au rôle de la partie encore méconnue de cette protéine. La surexpression de SlKRP1 dans le mésocarpe de tomate détruit la proportionnalité entre endoréduplication et taille cellulaire Le fruit est un organe spécialisé résultant du développement de l’ovaire après pollinisation et fertilisation, et qui offre un environnement adéquat pour la maturation des graines et leur dispersion. De part leur importance en nutrition humaine et leur importance économique, les espèces à fruit charnu ont été le sujet d’étude développementales principalement orientée vers la formation de l’ovaire, la mise à fruit et la maturation du fruit. La phase de croissance du fruit a été beaucoup moins étudiée, bien que la division cellulaire et la croissance cellulaire prenant place durant cette période soient cruciales à la détermination de la taille finale du fruit, ainsi que de sa masse et sa forme. Le développement du mésocarpe du fruit de tomate se déroule par la succession d’une phase de division cellulaire suivie d’une phase d’expansion cellulaire associée à l’endoréduplication, menant à la formation de cellules géantes (jusqu’à 0,5mm) avec des niveaux de ploïdie pouvant atteindre 256C. Bien qu’une relation évidente entre endoréduplication et croissance cellulaire ait été montrée par de nombreux exemples chez les plantes, le rôle exact de l’endoréduplication n’a toujours pas été élucidé, étant donné que la plupart des expériences induisant une modification du niveau d’endoréduplication dans la plante affectaient aussi la division cellulaire. Nous avons étudié la cinétique du dévelopement du mésocarpe de tomate au niveau morphologique et cytologique et avons étudié l’effet de la diminution du niveau d’endoréduplication sur le dévelopement du fruit en sur-exprimant l’inhibiteur du cycle cellulaire Kip-Related Protein 1 (SlKRP1) spécifiquement dans les cellules en croissance du mésocarpe de tomate. Nous montrons une proportionnalité directe entre endoréduplication et taille cellulaire durant le développement normal du fruit, ce qui nous a permis de construire un modèle de développement du mésocarpe définissant l’épaisseur du péricarpe en ne prenant en compte que le nombre de divisions cellulaires et le nombre de tours d’endoréduplication. De façon surprenante, les mésocarpes de tomate affectés dans leur niveau d’endoréduplication par la sur-expression de SlKRP1 ne sont pas affectés au niveau de la taille des cellules ou du fruit, ni dans leur contenu métabolique. Nos résultats démontrent pour la première fois qu’alors que le niveau de ploïdie est étroitement lié avec la taille des cellules et du fruit, l’endoréduplication n’est pas responsable de la croissance cellulaire du mésocarpe de tomate
Within the Joint Research Unit 619 of the National Institute of Agronomic Research (INRA), the group "Organogenesis of the Fruit and endoreduplication" examines the molecular players involved in cell cycle control in tomato fruit. The purpose of this thesis is the study of the cell cycle inhibitor Kip-Related Protein and its role during fruit development. Identification of protein motifs in the functional inhibitor of Cyclin-Dependent Kinase in Solanum lycopersicum SlKRP1: Their role in interactions with partners in the cell cycle The Kip-related proteins (KRPs) play a major role in the regulation of cell cycle. It has been shown to inhibit the CDK / Cyclin and thus block cell cycle progression. Despite their lack of homology with their counterparts in animals beyond their binding motif CDK / Cyclin, located at the C-terminal protein sequences in the plant, previous studies have shown the presence of conserved motifs plant specific in some KRPs, but there is little information about their function. We show here that the KRPs are distributed into two phylogenetic groups, and that each subgroup has specific short conserved motifs. The KRPs from subgroup 1 have six conserved motifs. Using SlKRP1, which belongs to subgroup 1, we have identified the motifs responsible for the localization of the protein and protein-protein interactions. We demonstrate that the pattern 2 is responsible for the interaction with CSN5, a subunit of the signalosome complex, and that the motif 5 is redundant with motif 3 with respect to the sub-cellular localization of the protein. We also show that SlKRP1 is capable of guiding SlCDKA1 and SlCycD3; 1 to the nucleus, even in the absence of CDK / cyclin binding motif previously referenced. This new site of interaction is probably located in the central part of the sequence of SlKRP1. These results provide new clues about the role of the little-known part of this protein. Overexpression of SlKRP1 in tomato mesocarp disrupts the proportionality between endoreduplication and cell size The fruit is a specialized organ which results from the ovary after pollination and fertilization, and provides a suitable environment for seed maturation and dispersal. Because of their importance in human nutrition and economic importance, fleshy fruit species have been the subject of study mainly focused on the developmental formation of the ovary, fruit set and fruit ripening. The stage of fruit growth has been much less studied, although cell division and cell growth taking place during this period are crucial to determining the final size of the fruit, as well as its mass and shape. The development of tomato fruit mesocarp occurs by the estate of a phase of cell division followed by a phase of cell expansion associated with endoreduplication, leading to the formation of giant cells (up to 0.5 mm) with ploidy levels of up to 256C. Although a clear relationship between endoreduplication and cell growth has been shown by many examples in plants, the exact role of endoreduplication has still not been elucidated, since most of the experiments leading to a change in the level of endoreduplication in plants also affected cell division. We studied the kinetics of the development of tomato mesocarp morphologically and cytologically and studied the effect of the reduced level of endoreduplication in the development of the fruit over-expressing the cell cycle inhibitor Kip-Related Protein 1 (SlKRP1) specifically in the growing cells of the tomato mesocarp. We show a direct proportionality between endoreduplication and cell size during normal development of the fruit, which allowed us to build a model for development of mesocarp defining the thickness of the pericarp by taking into account the number of cell divisions and the number of rounds of endoreduplication. Surprisingly, the tomato mesocarps affected in their level of endoreduplication by over-expression of SlKRP1 are not affected in terms of cell size and fruit, or on their metabolic content. Our results demonstrate for the first time that while the level of ploidy is closely linked with cell size and fruit, endoreduplication is not responsible for the cell growth of tomato mesocarp

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Handschick, Katja [Verfasser]. "Cyclin-dependent kinase (CDK) 6: ein molekularer Schalter zwischen dem Zellzyklus und der inflammatorischen Genregulation / Katja Handschick." Gießen : Universitätsbibliothek, 2014. http://d-nb.info/106858968X/34.

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Riley, Nicola Amy. "Cyclin-dependent kinase (CDK) inhibitor drugs induce apoptosis in human neutrophils through regulation of critical survival proteins." Thesis, University of Edinburgh, 2012. http://hdl.handle.net/1842/8171.

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Neutrophil apoptosis is an important process contributing to the resolution of inflammation. This is because it allows the neutrophil membrane to remain intact preventing it’s potentially histotoxic contents from being released into the extra-cellular milieu, a process that can contribute to the exacerbation of many inflammatory disorders such as rheumatoid arthritis. When considering the life-span of a neutrophil and how it can be augmented by various inflammatory mediators to allow it to carry out its essential protective role in the body’s innate immune defences it is also important to consider how to terminate this process when the inflammatory insult has been dealt with or when the system goes awry. It is this information that we believe may hold the key to developing novel anti-inflammatory therapies. Through exploitation of the mechanisms controlling neutrophil apoptosis, it may be possible to selectively target these cells to enter apoptosis, and therefore help aid the process of resolution, especially if used in conjunction with treatments that up-regulate phagocytosis of apoptotic cells. This is important given that the main treatment for disorders of the inflammatory response are glucocorticoids, which whilst proven to be a powerful treatment for eosinophil based diseases such as asthma where they increase eosinophil apoptosis in conjunction with enhancing phagocytic clearance of apoptotic cells, glucocorticoids have been found to have the converse affect on neutrophils, actually serving to prolong their life-span potentially exacerbating the condition. Furthermore, it has been previously shown that the transcription factor nuclear factor kappa B (NF-κB) plays a pivotal role in neutrophil apoptosis, becoming activated by inflammatory agents such as lipopolysaccharide (LPS) and tumour necrosis factor-alpha (TNF-α). NF-κB activation results in the transcription of many pro-inflammatory agents and anti-apoptotic proteins such as X-linked inhibitor of apoptosis (X-IAP) increasing the life-span of the neutrophil. Interestingly, it has also been demonstrated that key neutrophil survival proteins such as myeloid cell leukemia-1 (Mcl-1) are not directly regulated by NF-κB activation. Therefore it is because of the aforementioned reasons that I have chosen to investigate further neutrophil apoptosis including the role played by NF-κB. Thus, I have investigated the hypothesis that NF-κB-dependent and independent survival proteins critically regulate the rates of neutrophil apoptosis and that newly identified pro-apoptotic agents such as the cyclin-dependent kinase (CDK) inhibitor, R-roscovitine interferes with the expression of such survival proteins. It has been previously found by myself and others in our laboratory during the course of this thesis that cyclin dependent kinase inhibitor (CDKi) drugs such as R-roscovitine are powerful novel anti-inflammatory agents with the ability to up-regulate rates of neutrophil apoptosis in vitro and influence the resolution of neutrophilic inflammation in vivo. Whilst the exact mechanism of CDK inhibitor drugs on neutrophil apoptosis remains elusive, work shown in this thesis demonstrates that R-roscovitine has the ability to over-ride powerful anti-apoptotic signals from pro-inflammatory agents such as granulocyte-macrophage colony stimulating factor (GM-CSF) and LPS causing the neutrophils to enter apoptosis. Furthermore, it has been found that R-roscovitine causes a decrease in levels of the antiapoptotic protein Mcl-1 in as little as 2h and that it prevents the maintenance / protective effect that GM-CSF has on the Mcl-1 protein levels. In addition R-roscovitine may also reduce levels of the NF-κB regulated protein X-IAP. The effect of R-roscovitine on X-IAP was investigated further using an X-IAP HIV-tat construct, though results from this remain inconclusive. This is because although the X-IAP construct appeared to be extending neutrophil longevity, it was discovered that LPS contamination of the construct had occurred which could therefore pose an alternative explanation for the increase in neutrophil life-span. As X-IAP, TNF-α and LPS are all regulated by NF-κB and given that NF-κB is already known to be a key player in neutrophil biology, the effects of R-roscovitine on this important transcription factor were investigated. It was discovered that R-roscovitine does not directly activate NF-κB, since this CDK inhibitor drug does not cause degradation and loss of the cytoplasmic inhibitor of NF-κB, IκBα. This lack of NF-κB activation was confirmed since R-roscovitine did not mobilize the NF-κB subunit, p65, from the cytoplasm to the nucleus. Furthermore, R-roscovitine (unlike the NF-κB inhibitor gliotoxin) does not interfere with the ability of LPS or TNF-α to activate NF-κB. Therefore by R-roscovitine to induce apoptosis, although this does not rule out the involvement of NF-κB at a later stage. When considering a reagent for possible use as a novel anti-inflammatory agent I think it is important to assess what effects it has on the activation state of the neutrophil. Therefore the effects of R-roscovitine on the activation markers CD62L, CD11b and shape change were assessed. It was found that R-roscovitine alone did not cause any significant neutrophil activation as measured using the parameters stated above. Importantly, it was also found that R-roscovitine did not interfere with the activation states induced by the inflammatory mediators GM-CSF, LPS, TNF-α or leukotriene B4 (LTB4). Another important consideration is the effect of R-roscovitine on the removal of apoptotic cells by macrophage phagocytosis. Results demonstrated that pre-treatment of macrophages with R-roscovitine did not augment their uptake of apoptotic neutrophils. In addition Rroscovitine did not detrimentally affect the increase in phagocytosis that results from macrophage treatment with the synthetic glucocorticoid dexamethasone. The data presented in this thesis suggest that CDK inhibitor drugs such as R-roscovitine are novel powerful pro-apoptotic agents for neutrophils with the ability to over-ride antiapoptotic signals from multiple pro-inflammatory mediators. It has been discovered that Rroscovitine causes a reduction in one of the neutrophil’s most prominent anti-apoptotic proteins (Mcl-1) whilst not altering the activation state of the neutrophil and furthermore it does not interfere with the uptake of apoptotic neutrophils by macrophages or result in any alteration to the increase in phagocytosis caused by treatment with dexamethasone. In conclusion, CDK inhibitor drugs such as R-roscovitine have the potential to be promising candidates for novel anti-inflammatory agents with the ability to selectively target neutrophil apoptosis whilst not interfering with steroid induced up-regulation of phagocytosis, therefore allowing a two pronged attack to help treat neutrophil based inflammatory disorders.

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Weitensteiner, Sabine. "Cyclin-dependent kinase 5 in endothelial cell migration: Elucidating regulatory mechanisms upstream of Cdk5 and evaluating novel Cdk inhibitors as anti-angiogenic drugs." Diss., lmu, 2011. http://nbn-resolving.de/urn:nbn:de:bvb:19-136480.

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Gloulou, Olfa. "Identification de nouvelles structures inhibitrices de kinases : conception synthèse et évaluation biologique." Thesis, Paris 5, 2013. http://www.theses.fr/2013PA05P637/document.

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Cette thèse a pour objectif l’identification de nouveaux inhibiteurs de kinase et plus particulièrement de kinases dépendantes de cyclines (CDKs). Des inhibiteurs de CDKs sont en essais cliniques depuis une dizaine d’année. Un faisceau d’informations récentes montre que cette nouvelle classe pharmacologique pourrait prochainement occuper une place prépondérante dans la thérapie antitumorale. L’introduction de cette thèse décrit les principaux inhibiteurs de CDKs en se focalisant sur ceux dont le développement clinique est en cours et sur les structures les plus récemment divulguées (2009 à 2013). Trois molécules avancées en études cliniques s’avèrent intéressantes et s’approchent de la mise sur le marché : la Roscovitine (phase clinique IIb), le Dinaciclib (phase clinique III) et le Palbociclib (phase clinique III). D’un point de vue expérimental, cette thèse se décompose en deux parties principales. La première modulation a consisté à rechercher des nouveaux groupements qui pourraient sur des squelettes déjà connus comme les purines apporter un avantage en ce qui concerne l’activité des produits. Les structures cristallines des complexes inhibiteur-enzymes et notamment celles de Roscovitine-CDK2 et CR8-CDK2 ont guidé la conception des nouvelles molécules. C’est ainsi que sur les structures biaryliques déjà connues, un groupement phénol a été greffé sur l’un des cycles conduisant ainsi à de nouveaux inhibiteurs de kinases. Ces molécules sont plus puissantes que les produits non hydroxylés. L’augmentation de l’activité est particulièrement sensible au niveau de la kinase CDK2 qui est impliquée notamment dans régulation du cycle cellulaire. La seconde partie du travail porte sur la recherche de structures isostères des purines. Ainsi, le squelette thieno[3,2-d]pyrimidines a été développé de novo. Deux types d’intermédiaires produits ont été préparés afin de permettre la diversification des structures. En premier temps la voie de synthèse via l’intermédiaire thiométhyle a été conduite, néanmois cette voie présente certaines limites. Le deuxième intermédiaire trihalogéné a permi d’optimiser la préparation des molécules thieno[3,2-d]pyrimidines. Les évaluations des produits préparés ne sont pas totalement terminées. Ces molécules sont moins puissantes que les purines sur les CDKs mais agissent au niveau d’autres kinases
In the introduction, the main functions of cyclin dependent kinases are detailed. Whenever it was possible the link with pathologies where these kinases are overexpressed is presented. This is followed by the description of the inhibitors which are actually undergoing clinical testing. Most of these clinical studies are targeting cancer and leukemia. Impressive clinical results have been disclosed for Dinaciclib, Palbociclib and Roscovitine. The synthesis of two series of compounds is then envisioned. The first series of products are purine derivatives bearing a hydroxybiarylmethyl group on the 6 position of the purine scaffold. Two approaches were compared in the synthesis of the hydroxylbiarylmethylamino group. In both approaches the key step was the orthoformylation of phenols using magnesium chloride as catalyst. The prepared compounds were evaluated against kinases and a tumor cell line. They were found more potent than homologous products without hydroxyls. The second families of products are thieno[3,2-d]pyrimidines. A new general route to these products based on the preparation of 7-bromo-2,4-dichloro-thieno[3,2-d]pyrimidine which can allow the synthesis of a large diversity of trisubstituted derivatives

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Books on the topic "CDK [Cylin dependent kinase]"

1

Orzáez, Mar, Mónica Sancho Medina, and Enrique Pérez-Payá, eds. Cyclin-Dependent Kinase (CDK) Inhibitors. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4939-2926-9.

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Vogt, Peter K., and Steven I. Reed, eds. Cyclin Dependent Kinase (CDK) Inhibitors. Berlin, Heidelberg: Springer Berlin Heidelberg, 1998. http://dx.doi.org/10.1007/978-3-642-71941-7.

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Ip, Nancy Y., and Li-Huei Tsai, eds. Cyclin Dependent Kinase 5 (Cdk5). Boston, MA: Springer US, 2008. http://dx.doi.org/10.1007/978-0-387-78887-6.

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Kaldis, Philipp. The CDK-Activating Kinase (CAK). Springer, 2003.

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Philipp, Kaldis, ed. The CDK-activating kinase (CAK). Georgetown, Tex., U.S.A: Landes Bioscience/Eurekah.com, 2002.

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Vogt, P. K. Cyclin Dependent Kinase (cdk) Inhibitors (Current Topics in Microbiology & Immunology). Edited by P. K. Vogt. SPRINGER-VERLAG, 1998.

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Cyclin Dependent Kinase 5 Cdk5. Springer, 2008.

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B, Kastan M., and Imperial Cancer Research Fund (Great Britain), eds. Checkpoint controls and cancer. Plainview, NY: Cold Spring Harbor Laboratory Press, 1997.

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Book chapters on the topic "CDK [Cylin dependent kinase]"

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Pirincci Ercan, Deniz, and Frank Uhlmann. "Analysis of Cell Cycle Progression in the Budding Yeast S. cerevisiae." In Methods in Molecular Biology, 265–76. New York, NY: Springer US, 2021. http://dx.doi.org/10.1007/978-1-0716-1538-6_19.

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AbstractThe cell cycle is an ordered series of events by which cells grow and divide to give rise to two daughter cells. In eukaryotes, cyclin–cyclin-dependent kinase (cyclin–Cdk) complexes act as master regulators of the cell division cycle by phosphorylating numerous substrates. Their activity and expression profiles are regulated in time. The budding yeast S. cerevisiae was one of the pioneering model organisms to study the cell cycle. Its genetic amenability continues to make it a favorite model to decipher the principles of how changes in cyclin-Cdk activity translate into the intricate sequence of substrate phosphorylation events that govern the cell cycle. In this chapter, we introduce robust and straightforward methods to analyze cell cycle progression in S. cerevisiae. These techniques can be utilized to describe cell cycle events and to address the effects of perturbations on accurate and timely cell cycle progression.

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Wei, Fan-Yan, and Kazuhito Tomizawa. "Cdk5 in Presynapses." In Cyclin Dependent Kinase 5 (Cdk5), 25–33. Boston, MA: Springer US, 2008. http://dx.doi.org/10.1007/978-0-387-78887-6_3.

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Dudits, Dénes, Mátyás Cserháti, Pál Miskolczi, Attila Fehér, Ferhan Ayaydin, and Gábor V. Horváth. "Use of Alfalfa In Vitro Cultures in Studies on Regulation of Cyclin-Dependent Kinase (CDK) Functions." In Biotechnology and Sustainable Agriculture 2006 and Beyond, 149–52. Dordrecht: Springer Netherlands, 2007. http://dx.doi.org/10.1007/978-1-4020-6635-1_20.

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Ohshima, Toshio. "Cdk5/p35 Regulates Neuronal Migration." In Cyclin Dependent Kinase 5 (Cdk5), 1–8. Boston, MA: Springer US, 2008. http://dx.doi.org/10.1007/978-0-387-78887-6_1.

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Wen, Yi, Haung Yu, and Karen Duff. "Cdk5 and Neuregulin-1 Signaling." In Cyclin Dependent Kinase 5 (Cdk5), 139–44. Boston, MA: Springer US, 2008. http://dx.doi.org/10.1007/978-0-387-78887-6_10.

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Musacchio, Andrea. "The Structural Bases of CDK5 Activity." In Cyclin Dependent Kinase 5 (Cdk5), 191–210. Boston, MA: Springer US, 2008. http://dx.doi.org/10.1007/978-0-387-78887-6_14.

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Meuer, Katrin, Mathias Bähr, and Jochen H. Weishaupt. "CDK5 and Mitochondrial Cell Death Pathways." In Cyclin Dependent Kinase 5 (Cdk5), 91–106. Boston, MA: Springer US, 2008. http://dx.doi.org/10.1007/978-0-387-78887-6_7.

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Bark, Christina, Marjan Rupnik, Marko Jevsek, Slavena A. Mandic, and Per-Olof Berggren. "Cyclin-Dependent Kinase 5 and Insulin Secretion." In Cyclin Dependent Kinase 5 (Cdk5), 145–58. Boston, MA: Springer US, 2008. http://dx.doi.org/10.1007/978-0-387-78887-6_11.

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Ng, Gary Kar Ho, Lisheng He, and Robert Z. Qi. "Protein–Protein Interactions Involving the N-Terminus of p35." In Cyclin Dependent Kinase 5 (Cdk5), 159–70. Boston, MA: Springer US, 2008. http://dx.doi.org/10.1007/978-0-387-78887-6_12.

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Hisanaga, Shin-ichi, and Koichi Ishiguro. "The Kinase Activity of Cdk5 and Its Regulation." In Cyclin Dependent Kinase 5 (Cdk5), 171–90. Boston, MA: Springer US, 2008. http://dx.doi.org/10.1007/978-0-387-78887-6_13.

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Conference papers on the topic "CDK [Cylin dependent kinase]"

1

Ottaviani, Silvia, Sean Delaney, Hetal Patel, Manikandan Periyasamy, Alexander Bondke, Brian Slafer, Richard Starkey, et al. "Abstract 700: Gene expression profiling of cyclin-dependent kinase (CDK) inhibition in cancer cells." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-700.

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Moussa, Rayan Saleh, Zaklina Kovacevic, Daohai Zhang, Aritee Rosemary Siafakas, and Des R. Richardson. "Abstract A67: Mechanisms involved in regulating the expression of the cyclin-dependent kinase (cdk) inhibitor, p21, by intracellular iron levels." In Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics--Nov 12-16, 2011; San Francisco, CA. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1535-7163.targ-11-a67.

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Rugo, Hope S., Sanjeev Balu, Yunfeng Li, Guifang Chen, Xin Li, Stuart Turner, and Roxana Sin. "Abstract PS10-09: Real-world analysis of concomitant medication use with potential drug-drug interactions (DDI) in patients with metastatic breast cancer (MBC) treated with cylin dependent kinase (CDK) 4/6 inhibitors." In Abstracts: 2020 San Antonio Breast Cancer Virtual Symposium; December 8-11, 2020; San Antonio, Texas. American Association for Cancer Research, 2021. http://dx.doi.org/10.1158/1538-7445.sabcs20-ps10-09.

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Lim, Pei Li, John SW Low, Gerhard Siemeister, Boon Cher Goh, and Wen-son Hsieh. "Abstract 3098: The effects of a pan-cyclin dependent kinase (CDK) inhibitor and its combination with cisplatin in nasopharyngeal carcinoma (NPC)." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-3098.

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Qi, Li, Chunxiao Xu, Kristopher Sarosiek, Azra Ligon, Scott Rodig, Kwok-Kin Wong, Anthony Letai, and Geoffrey I. Shapiro. "Abstract 2016: A subset of small cell lung cancer (SCLC) cell lines is Mcl-1-dependent and responds to cyclin-dependent kinase (cdk)9 inhibitionin vitroandin vivo." 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.am2012-2016.

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Mita, Monica, Anil A. Joy, Alain Mita, Kamalesh Sankhala, Jennifer Moseley, Da Zhang, Paul Statkevich, et al. "Abstract 4718: A randomized phase 2 study of the cyclin-dependent kinase (CDK) inhibitor dinaciclib (SCH 727965) in patients with advanced breast cancer." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-4718.

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Qi, Li, Chunxiao Xu, Kristopher A. Sarosiek, Azra H. Ligon, Scott J. Rodig, Kwok-Kin Wong, Anthony G. Letai, and Geoffrey I. Shapiro. "Abstract LB-22: A subset of small cell lung cancer (SCLC) cell lines is Mcl-1-dependent and responds to cyclin-dependent kinase (cdk)9 inhibition in vitro and in vivo." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-lb-22.

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Qi, Li, and Geoffrey I. Shapiro. "Abstract 575: A subset of small cell lung cancer (SCLC) cell lines are Mcl-1-dependent and undergo apoptosis in response to Flavopiridol-mediated inhibition of cyclin-dependent kinase (cdk) 9." 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.am10-575.

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Warren, Stephen L., John Nemunaitis, Joe Stephenson, Benoit Samson, Anil A. Joy, Da Zhang, Paul Statkevich, et al. "Abstract 2242: A randomized phase 2 study of the cyclin-dependent kinase (CDK) inhibitor Dinaciclib (SCH 727965) in patients with non-small cell lung cancer (NSCLC)." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-2242.

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De Angelis, C., A. Nardone, ML Cataldo, J. Veeraraghavan, X. Fu, M. Giuliano, L. Malorni, R. Jeselsohn, KC Osborne, and R. Schiff. "Abstract P4-03-05: AP-1 as a potential mediator of resistance to the cyclin-dependent kinase (CDK) 4/6-inhibitor palbociclib in ER-positive endocrine-resistant breast cancer." In Abstracts: 2017 San Antonio Breast Cancer Symposium; December 5-9, 2017; San Antonio, Texas. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.sabcs17-p4-03-05.

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