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Academic literature on the topic 'Tyrosine Kinase Inhibitors Targeting'

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Published: 10 December 2022
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Journal articles on the topic "Tyrosine Kinase Inhibitors Targeting"

1

Deininger, Michael. "Targeting Tyrosine Kinase Receptors." Blood 122, no. 21 (November 15, 2013): SCI—25—SCI—25. http://dx.doi.org/10.1182/blood.v122.21.sci-25.sci-25.

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Abstract Protein tyrosine kinases (PTKs) regulate cell growth and other key functions. Constitutive PTK activation by somatic mutations, overexpression, or abnormal upstream signaling is characteristic of many cancers, including hematologic malignancies, providing a rationale for therapeutically targeting PTKs with small molecules. Imatinib, an ATP-competitive inhibitor of BCR-ABL1, the PTK causal to chronic myeloid leukemia (CML), established a paradigm for tyrosine kinase inhibitors (TKIs) as cancer therapeutics. Although a relatively weak inhibitor, imatinib is effective in most patients with chronic phase CML (CML-CP), while responses are transient in blastic phase (CML-BP). Point mutations in the BCR-ABL1 kinase domain have emerged as a major mechanism of drug resistance. The more potent second-generation TKIs – dasatinib, nilotinib, and bosutinib – induce deeper and faster responses and are active against many imatinib-resistant mutants, with the exception of T315I in the gatekeeper position of the catalytic site. This problem was addressed with ponatinib, a third-generation TKI covering all single BCR-ABL1 mutants, including T315I. Ponatinib has excellent clinical activity in CML-CP patients who failed other TKIs, while responses in CML-BP are short-lived. Some patients fail ponatinib due to BCR-ABL1 compound mutations, suggesting even third-generation TKIs cannot completely prevent mutational escape by the disease-initiating kinase. Another unsolved problem is that TKIs fail to efficiently target CML stem cells, leading to recurrence of active leukemia upon discontinuation. Despite these shortcomings, TKIs have completely changed the face of CML. Unfortunately, repeating this success in other hematologic malignancies has been challenging, likely reflecting differences in disease biology as much as suboptimal design of early compounds. CML-CP represents one extreme of the spectrum, where a single genetic lesion is sufficient to produce the phenotype and the hierarchy of hematopoietic differentiation is maintained. The situation is different in acute myeloid leukemia (AML) with activating FLT3 mutations. Not only these AML cases have mutations in other genes, they typically acquire FLT3 mutations late during disease evolution, implying that the disease-initiating clone will be impervious to FLT3 inhibition. Progress has been made through successive development of more potent TKIs with improved pharmacology, leading to quizartinib. It is clear, however, that FLT3 inhibitors cannot be used as single agents if there is a curative intent and the same may be true for JAK2 inhibitors in myelofibrosis. The first approved JAK2 inhibitor, ruxolitinib, dramatically improves symptoms, but has yet to demonstrate a significant impact on the malignant clone and is certainly not curative. It remains to be seen whether this reflects the fact that JAK2 activation is not the disease–initiating event, lack of inhibitor specificity towards the mutant JAK2 kinase, or other undesirable off-target effects that may be overcome with improved drugs. A completely new chapter was opened with ibrutinib, an irreversible inhibitor of Bruton’s tyrosine kinase (BTK), for the treatment of chronic lymphocytic leukemia (CLL). BTK is essential for signal transduction from the B-cell receptor (BCR). No activating mutations in BTK have been identified in lymphoma or CLL, but constitutive BCR signaling is critical to CLL cell survival in the microenvironment. Early studies show excellent clinical activity in patients with advanced CLL, although many responses are incomplete; much like the imatinib responses in late CML-CP. Ibrutinib may have a similarly profound effect upon CLL as imatinib on CML, but perhaps also similar limitations, such as the inability to eradicate residual leukemia; this of course needs to be tested in frontline studies. TKIs have had a significant albeit uneven impact upon treatment paradigms in hematologic malignancies. Future progress will involve optimizing compounds in terms of potency, selectivity, and pharmacokinetics. Allosteric inhibitors may add to the armamentarium. From the target perspective, it is likely that most activated kinase alleles have been discovered and the focus should shift to identification of disease-critical unmutated kinases. Lastly, identifying synthetically lethal inhibitor combinations will be critical to fully exploit the potential of TKI therapy. Disclosures: Deininger: BMS: Consultancy, Membership on an entity’s Board of Directors or advisory committees, Research Funding; ARIAD: Consultancy, Membership on an entity’s Board of Directors or advisory committees; NOVARTIS: Consultancy, Membership on an entity’s Board of Directors or advisory committees, Research Funding; CELGENE: Research Funding; GENZYME: Research Funding; INCYTE: Consultancy, Membership on an entity’s Board of Directors or advisory committees; GILEAD: Research Funding.
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2

Chen, Jin-Shuen, Li-Chien Chang, Shyh-Jer Huang, and Chao-Wen Cheng. "Targeting Spleen Tyrosine Kinase-Bruton’s Tyrosine Kinase Axis for Immunologically Mediated Glomerulonephritis." BioMed Research International 2014 (2014): 1–6. http://dx.doi.org/10.1155/2014/814869.

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The importance of B-cell activation and immune complex-mediated Fc-receptor activation in the pathogenesis of immunologically mediated glomerulonephritis has long been recognized. The two nonreceptor tyrosine kinases, spleen tyrosine kinase (Syk) and Bruton’s tyrosine kinase (Btk), are primarily expressed by hematopoietic cells, and participate in B-cell-receptor- and Fc-receptor-mediated activation. Pharmacological inhibitors of Syk or Btk are undergoing preclinical development and clinical trials for several immune diseases; and Syk inhibitors have been shown to reduce disease activity in rheumatoid arthritis patients. However, the clinical therapeutic efficacies of these inhibitors in glomerulonephritis have not been evaluated. Herein, we review recent studies of Syk and Btk inhibitors in several experimental primary and secondary glomerulonephritis models. These inhibitors suppressed development of glomerular injury, and also ameliorated established kidney disease. Thus, targeting Syk and Btk signaling pathways is a potential therapeutic strategy for glomerulonephritis, and further evaluation is recommended.
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Forster, Michael, Xiaojun Julia Liang, Martin Schröder, Stefan Gerstenecker, Apirat Chaikuad, Stefan Knapp, Stefan Laufer, and Matthias Gehringer. "Discovery of a Novel Class of Covalent Dual Inhibitors Targeting the Protein Kinases BMX and BTK." International Journal of Molecular Sciences 21, no. 23 (December 4, 2020): 9269. http://dx.doi.org/10.3390/ijms21239269.

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The nonreceptor tyrosine TEC kinases are key regulators of the immune system and play a crucial role in the pathogenesis of diverse hematological malignancies. In contrast to the substantial efforts in inhibitor development for Bruton’s tyrosine kinase (BTK), specific inhibitors of the other TEC kinases, including the bone marrow tyrosine kinase on chromosome X (BMX), remain sparse. Here we present a novel class of dual BMX/BTK inhibitors, which were designed from irreversible inhibitors of Janus kinase (JAK) 3 targeting a cysteine located within the solvent-exposed front region of the ATP binding pocket. Structure-guided design exploiting the differences in the gatekeeper residues enabled the achievement of high selectivity over JAK3 and certain other kinases harboring a sterically demanding residue at this position. The most active compounds inhibited BMX and BTK with apparent IC50 values in the single digit nanomolar range or below showing moderate selectivity within the TEC family and potent cellular target engagement. These compounds represent an important first step towards selective chemical probes for the protein kinase BMX.
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Manzo, Lawaly Maman, Moudirat Lawaly, and Lui YU. "Growth Factor Receptor Tyrosine Kinase Inhibitors in Non-small cell lung cancer." Indian Journal of Pharmaceutical and Biological Research 3, no. 02 (June 30, 2015): 81–87. http://dx.doi.org/10.30750/ijpbr.3.2.10.

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Aberrant increased expression and activation of receptor tyrosine kinases occur frequently in human carcinomas. Several small molecules targeting receptor tyrosine kinases, which have crucial roles in the growth factor signaling that promote tumor progression in various malignancies, including non-small cell lung cancer (NSCLC), are currently in clinical development. Therapeutic strategies include inhibition of growth factor tyrosine kinase function. Drugs of this type include those that target the epidermal growth factor receptor tyrosine kinase, those that target vascular endothelial growth factor receptors tyrosine kinase and those that target anaplastic lymphoma receptor tyrosine kinase. In this review we first discuss the role of receptor tyrosine kinases in human malignancies, and focus on discussing the potential use of epidermal growth factor receptor tyrosine kinase inhibitors and the vascular endothelial growth factor receptors tyrosine kinase inhibitors in NSCLC. In addition, we discuss the contribution of growth factor receptor tyrosine kinase inhibitors to the clinically observed resistance, and toxicity.
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Cher, Chae Yin, Cheuk Him Man, Stephen S. Y. Lam, Eric S. K. Ho, Nelson K. L. Ng, Marie-Anne Hospital, Jerome Tamburini, and Anskar Y. H. Leung. "Targeting Polo-like Kinase in Acute Myeloid Leukemia." Blood 124, no. 21 (December 6, 2014): 2234. http://dx.doi.org/10.1182/blood.v124.21.2234.2234.

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Abstract Acute myeloid leukemia (AML) carrying fms-like tyrosine kinase 3 (FLT3)-internal tandem duplication (ITD) is associated with poor prognosis when treated with conventional chemotherapy and allogeneic hematopoietic stem cell transplantation (HSCT). Despite much interest in tyrosine kinase inhibitor (TKI) targeting FLT3 activation, drug resistance is invariable and acquisition of secondary point mutation in the tyrosine kinase domain (TKD) of FLT3 was frequently reported. We have shown that genes encoding cell cycle regulators including polo-like kinase 1 (PLK1), cell division cycle 25 homolog A (CDC25A), cyclin B2 (CCNB2), and cyclin E1 (CCNE1) were up-regulated in sorafenib-resistant primary AML samples. In particular, PLK1, a member of the polo-like kinase family, has been found to express at several checkpoints critical for cell cycle progression. PLK1 inhibitors have recently been exploited for the treatment of both solid organ and haematological cancers. We hypothesized that aberrant cell cycle progression mediated by increased PLK1 expression might confer survival advantage to drug resistant AML cells and be targetable by PLK1 inhibition. In vitro treatment with PLK1 inhibitors volasertib and BI 2536 significantly inhibited the growth of 8 AML cell lines (KG-1, ML2, MOLM-13, MV4-11, Kasumi-1, NB4, THP-1 and OCI-AML3) with IC50 (all in nM) ranging from 48.7 - 98.4 (volasertib) and 35.1 - 81.6 (BI 2536). The growth inhibitory effects of PLK1 inhibition on two FLT3-ITD+ cell lines, MOLM-13 and MV411, correlated with induction of apoptosis and cell cycle arrest at G2/M phase. Moreover, both PLK1 inhibitors significantly suppressed the growth of a sorafenib resistant MOLM-13R cell line and sorafenib naïve MOLM-13N cell line. Introduction of FLT3-ITD alone or FLT3-ITD and TKD double mutations into Ba/F3 cell lines sensitized them to the growth inhibitory effects of PLK1 inhibitors. Primary FLT3-ITD+ AML cells obtained from patients at TKI resistance were shown to be more sensitive to PLK1 inhibitors than those obtained before treatment. The results suggested that the TKI resistant clones could be effectively targeted by PLK1 inhibition, providing an insight to the design of combination treatment with FLT3 inhibitors in FLT3-ITD+ AML. Disclosures No relevant conflicts of interest to declare.
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Grimminger, Friedrich, Ralph T. Schermuly, and Hossein A. Ghofrani. "Targeting non-malignant disorders with tyrosine kinase inhibitors." Nature Reviews Drug Discovery 9, no. 12 (December 2010): 956–70. http://dx.doi.org/10.1038/nrd3297.

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7

Pasquet, Jean-Max, Romain Gioia, Claire Drullion, Valerie Lagarde, Cedric Leroy, Serge Roche, Bruno Cardinaud, and Francois-Xavier Mahon. "Tyrosine Kinase Proteins profiling of Nilotinib Resistant Chronic Myelogenous Leukemia Cells Unravels a Tyrosine Kinase-Mediated Bypass." Blood 114, no. 22 (November 20, 2009): 2175. http://dx.doi.org/10.1182/blood.v114.22.2175.2175.

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Abstract Abstract 2175 Poster Board II-152 Targeting the tyrosine kinase activity of Bcr-Abl is an attractive therapeutic strategy in Chronic Myeloid Leukemia (CML) and in Bcr-Abl positive Acute Lymphoblastic Leukemia. Whereas imatinib, a selective inhibitor of Bcr-Abl tyrosine kinase, is now used in frontline therapy for CML, second generation inhibitors such as nilotinib or dasatinib have been developed for the treatment of imatinib-resistant or –intolerant disease. We have shown that one of the mechanisms of resistance to nilotinib is an increasing expression of the p53/56 Lyn kinase, both at mRNA and protein level in cell lines. This result was confirmed in vivo in nilotinib-resistant CML patients (Mahon et al. Cancer Res., 2008, 68(23):9809-16.). To elucidate Lyn mediated-nilotinib resistance, a phosphoproteomic study was performed by Stable Isotope Labelling with Amino acid in Cell culture (SILAC) which highlights the potential role of downstream tyrosine kinases. Among different candidate proteinsThe Spleen tyrosine kinase Syk and the UFO family receptor tyrosine kinase Axl were the most relevant in the nilotinib resistant cell line as compared to the sensitive counterpart. Syk hyperphosphorylation was confirmed in the nilotinib resistant cell line using western blot at least on tyrosine residues Y323 and Y525/526, two critical tyrosine residues respectively involved in Lyn-mediated Syk phosphorylation and autophosphorylation-associated Syk activation. Lyn interacts with Syk as detected in Syk immunoprecipitates in nilotinib resistant cells. Furthermore, Syk-Lyn interaction is inhibited by dasatinib suggesting the requirement of Lyn kinase activity and Syk phosphorylation. Targeting Syk expression in nilotinib resistant cells by siRNA or tyrosine kinase activity by pharmacological inhibitors leads respectively to a partial (35%) or to a full restoration of nilotinib sensitivity. Moreover, the identification of Axl by SILAC is correlated to a 9 fold increase of its level of expression in the resistant cell line and the inhibition of Axl tyrosine kinase activity decreases proliferation of both nilotinib sensitive and resistant CML cells. All together these results disclose a new pathway for tyrosine kinase inhibitors resistance in CML involving at least the two Lyn downstream tyrosine kinases Syk and Axl. Disclosures: Mahon: Amgen: Honoraria; Novartis Pharma: Consultancy, Honoraria, Research Funding; Alexion: Consultancy, Honoraria.
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Sakle, Nikhil S., Shweta A. More, Sachin A. Dhawale, and Santosh N. Mokale. "Targeting Small Molecule Tyrosine Kinases by Polyphenols: New Move Towards Anti-tumor Drug Discovery." Current Drug Discovery Technologies 17, no. 5 (December 23, 2020): 585–615. http://dx.doi.org/10.2174/1570163816666190808120843.

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Background: Cancer is a complex disease involving genetic and epigenetic alteration that allows cells to escape normal homeostasis. Kinases play a crucial role in signaling pathways that regulate cell functions. Deregulation of kinases leads to a variety of pathological changes, activating cancer cell proliferation and metastases. The molecular mechanism of cancer is complex and the dysregulation of tyrosine kinases like Anaplastic Lymphoma Kinase (ALK), Bcr-Abl (Fusion gene found in patient with Chronic Myelogenous Leukemia (CML), JAK (Janus Activated Kinase), Src Family Kinases (SFKs), ALK (Anaplastic lymphoma Kinase), c-MET (Mesenchymal- Epithelial Transition), EGFR (Epidermal Growth Factor receptor), PDGFR (Platelet-Derived Growth Factor Receptor), RET (Rearranged during Transfection) and VEGFR (Vascular Endothelial Growth Factor Receptor) plays major role in the process of carcinogenesis. Recently, kinase inhibitors have overcome many problems of traditional cancer chemotherapy as they effectively separate out normal, non-cancer cells as well as rapidly multiplying cancer cells. Methods: Electronic databases were searched to explore the small molecule tyrosine kinases by polyphenols with the help of docking study (Glide-7.6 program interfaced with Maestro-v11.3 of Schrödinger 2017) to show the binding energies of polyphenols inhibitor with different tyrosine kinases in order to differentiate between the targets. Results: From the literature survey, it was observed that the number of polyphenols derived from natural sources alters the expression and signaling cascade of tyrosine kinase in various tumor models. Therefore, the development of polyphenols as a tyrosine kinase inhibitor against targeted proteins is regarded as an upcoming trend for chemoprevention. Conclusion: In this review, we have discussed the role of polyphenols as chemoreceptive which will help in future for the development and discovery of novel semisynthetic anticancer agents coupled with polyphenols.
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van der Kuip, Heiko, Lara Wohlbold, Carsten Oetzel, Matthias Schwab, and Walter E. Aulitzky. "Mechanisms of Clinical Resistance to Small Molecule Tyrosine Kinase Inhibitors Targeting Oncogenic Tyrosine Kinases." American Journal of PharmacoGenomics 5, no. 2 (2005): 101–12. http://dx.doi.org/10.2165/00129785-200505020-00003.

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Shojaee, Seyedmehdi, Maike Buchner, Huimin Geng, Bolland Silvia, Phillip Koeffler, and Markus Muschen. "Targeting Inhibitory Phosphatases in Tyrosine Kinase-Driven Leukemias." Blood 118, no. 21 (November 18, 2011): 1382. http://dx.doi.org/10.1182/blood.v118.21.1382.1382.

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Abstract Abstract 1382 Background: Current therapy approaches for tyrosine kinase-driven leukemias including Ph+ ALL and CML are almost entirely focused on the development of more potent tyrosine kinase inhibitors (TKI) with the goal to reduce oncogenic signaling below a minimum threshold that is required for the survival of leukemia cells. Studying regulators of BCR-ABL1 kinase signaling strength, we found that three key inhibitory phosphatases (INPP5D/SHIP1, PTEN and PTPN6/SHP1) are expressed at high levels in Ph+ ALL and CML cells. Both INPP5D and PTEN dephosphorylate phosphatidylinositol-3,4,5-trisphosphate, as 5- and 3-phosphatases, respectively. Thereby, both INPP5D and PTEN negatively regulate PI3K/PI5K- and AKT-mediated activation signals. Like INPP5D, PTPN6 is recruited to ITIM motifs in the cytoplasmic tails of inhibitory surface recepotors and negatively regulates activation signals from tyrosine kinases and activating receptors. Results: We hypothesized that Cre-mediated inducible deletion of INPP5D, PTEN and PTPN6 will result in increased oncogenic signaling downstream of BCR-ABL1 and induce blast crisis-transformation of CML and a more aggressive form of Ph+ALL-like leukemia. Surprisingly, however, genetic deletion of INPP5D, PTEN and PTPN6 resulted in drastic upregulation of reactive oxygen species (ROS), accumulation of Arf, p53 and p21, cellular senescence and subsequent cell death of leukemia cells. The deleterious effects of inducible deletion of INPP5D, PTEN and PTPN6 were comparatively mild in CML and drastic in Ph+ ALL-like leukemia Studying BCR-ABL1-transformed Inpp5dfl/fl Ptenfl/fl and Ptpn6fl/fl leukemia cells in vivo, we observed that induction of Cre-mediated deletion resulted in rapid leukemia regression and “cure” of leukemia transplant recipient mice. Pharmacological targeting inhibitory phosphatases for the treatment of leukemia seems counter intuitive because it represents effectively the opposite of current TKI-based therapies. Small molecule inhibition of Pten using the compound VO-OHpic effectively killed patient-derived leukemia cells carrying the T315I mutant BCR-ABL1. Based on these findings, we propose that pharmacological blockade of inhibitory phosphatases represents a powerful means to induce leukemia cell death owing to excessive oncogene signaling. In this case, oncogenic tyrosine kinase signaling is increased above a maximum tolerable threshold, and leukemia cells die because of excessive oxidative stress. Normal cells lacking the BCR-ABL1 oncogene are spared because they are less dependent on inhibitory signaling molecules to counterbalance. According to our concept, tyrosine kinase-driven leukemia cells can only thrive within a certain “comfort zone” of signal strength. Both attenuation below and exaggeration above this “comfort zone” of signal strength results in cell death. If validated, our approach of phosphatase-inhibition will lead to the discovery and development of multiple new targets for therapy and will significantly broaden currently available treatment options for blast crisis CML and Ph+ ALL. Disclosures: No relevant conflicts of interest to declare.
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Dissertations / Theses on the topic "Tyrosine Kinase Inhibitors Targeting"

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Aljohani, Hashim M. "Targeting Tyrosine Kinase Drug Resistance Mechanisms and Metastatic Pathways in Brain Tumors." University of Cincinnati / OhioLINK, 2020. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1595846160285645.

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Padi, Sathish K. R., Libia A. Luevano, Ningfei An, Ritu Pandey, Neha Singh, Jin H. Song, Jon C. Aster, Xue-Zhong Yu, Shikhar Mehrotra, and Andrew S. Kraft. "Targeting the PIM protein kinases for the treatment of a T-cell acute lymphoblastic leukemia subset." IMPACT JOURNALS LLC, 2017. http://hdl.handle.net/10150/624055.

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New approaches are needed for the treatment of patients with T-cell acute lymphoblastic leukemia (T-ALL) who fail to achieve remission with chemotherapy. Analysis of the effects of pan-PIM protein kinase inhibitors on human T-ALL cell lines demonstrated that the sensitive cell lines expressed higher PIM1 protein kinase levels, whereas T-ALL cell lines with NOTCH mutations tended to have lower levels of PIM1 kinase and were insensitive to these inhibitors. NOTCH-mutant cells selected for resistance to gamma secretase inhibitors developed elevated PIM1 kinase levels and increased sensitivity to PIM inhibitors. Gene profiling using a publically available T-ALL dataset demonstrated overexpression of PIM1 in the majority of early T-cell precursor (ETP)-ALLs and a small subset of non-ETP ALL. While the PIM inhibitors blocked growth, they also stimulated ERK and STAT5 phosphorylation, demonstrating that activation of additional signaling pathways occurs with PIM inhibitor treatment. To block these pathways, Ponatinib, a broadly active tyrosine kinase inhibitor (TKI) used to treat chronic myelogenous leukemia, was added to this PIM-inhibitor regimen. The combination of Ponatinib with a PIM inhibitor resulted in synergistic T-ALL growth inhibition and marked apoptotic cell death. Treatment of mice engrafted with human T-ALL with these two agents significantly decreased the tumor burden and improved the survival of treated mice. This dual therapy has the potential to be developed as a novel approach to treat T-ALL with high PIM expression.
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Zielger, David Women's &amp Children's Health Faculty of Medicine UNSW. "Targeting anti-apoptotic mechanisms in malignant gliomas." Awarded by:University of New South Wales. Women's & Children's Health, 2009. http://handle.unsw.edu.au/1959.4/43713.

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Novel strategies for the treatment of malignant gliomas are urgently needed. They are characterised by an inherent resistance to both chemo- and radiotherapeutics resulting in unrelenting tumour progression. While the exact mechanisms of treatment resistance remain undefined, it is now recognized that multiple components within the apoptotic pathway are heavily dysregulated in glioma cells and that the over-expression of anti-apoptotic proteins in patient samples correlates with inferior patient survival. The Inhibitor of Apoptosis Proteins (lAPs) represent the final molecular blockade preventing cellular apoptosis and have been identified as a potential rational therapeutic target in gliomas. The work described herein was focused on the development of novel therapeutic strategies that target the lAPs in malignant gliomas, that are readily translatable to the clinic, and that have the potential to improve patient outcomes. The first series of studies examined the hypothesis that targeting the lAPs in conjunction with other conventional and targeted therapies would overcome treatment resistance, and enhance anti-tumour activity. The novel, small molecule, lAP inhibitor LBW242 was shown to successfully target the lAPs in glioma cells and inhibit their ability to bind to and inactivate caspases. However when tested as a single agent in vitro, no stand alone anti-glioma activity of LBW242 was demonstrated. A screen of the activity of LBW242 in combination other pro-apoptotic compounds led to the discovery that lAP inhibition applied in combination with receptor tyrosine kinase (RTK) inhibition led to enhanced caspase activation and induction of apoptosis with a subsequent synergistic anti-glioma effect. The most profound effect was demonstrated with the specific combination of PDGFR and lAP inhibition both in vitro and in vivo as well as in primary patient derived glioma tumourspheres. While multiple RTKs have previously been validated as rational therapeutic targets, the clinical failure of RTK inhibitors in glioma patients has to date remained unexplained. The results in this thesis provide a novel explanation for the resistance of glioma cells to these targeted therapies, and more importantly offer a clinically tractable strategy of overcoming that resistance and improving patient outcomes. The second series of studies investigated the mechanism of synergy between lAP and RTK inhibition. The results showed that PDGFR inhibition does not stimulate apoptosis in glioma cells by previously described pathways. A screen of the entire apoptotic pathway revealed that treatment with imatinib modulates the expression of the anti-apoptotic protein NOL3/ARC. The results showed that imatinib treatment leads to down-regulation of NOL3 and that this effect is critical to the synergy between lAP and PDGFR inhibition. Further analysis suggested a critical role for NOL3 in gliomagenesis and treatment resistance NOL3 was found to be highly expressed in malignant gliomas and with expression levels that are inversely correlated with patient outcomes. A role for NOL3 has not previously been described in malignant gliomas. Finally, a series of studies were undertaken that tested the use of LBW242 in combination with the standard-of-care therapies of irradiation and temozolomide. In vitro assays demonstrated that LBW242 enhanced the pro-apoptotic activity of radiotherapy, and clonogenic assays showed that the combination therapy led to a synergistic anti-glioma effect in multiple glioma cell lines. Athymic mice bearing established human malignant glioma tumour xenografts treated with LBW242 plus radiation and temozolomide demonstrated a profound and synergistic suppression of tumour growth. Neurosphere assays revealed that the combination of radiation and LBW242 led to a pro-apoptotic effect in highly resistant glioma stem cells with a corresponding inhibition of tumour growth. The results indicate a potentially powerful strategy to enhance the therapeutic activity of standard-of-care therapies in glioma patients. Collectively, the findings of the studies in this thesis contribute to a better understanding of the mechanisms of treatment resistance in malignant gliomas, and demonstrate that the pro-apoptotic and anti-glioma effects of radiotherapy, chemotherapy and specific targeted therapies can be enhanced by the addition of a novel, small molecule lAP inhibitor. These results are readily translatable to clinical trial, and offer the potential for improved treatment outcomes for glioma patients.
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Mukhtar, Lenah. "Targeting the Mevalonate Pathway Enhances the Efficacy of Epidermal Growth Factor Receptor – Tyrosine Kinase Inhibitors in Head and Neck Squamous Cell Carcinoma." Thesis, Université d'Ottawa / University of Ottawa, 2020. http://hdl.handle.net/10393/40391.

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Epidermal growth factor receptor (EGFR) is highly expressed in head and neck squamous cell carcinoma (HNSCC) and non-small cell lung cancer (NSCLC) and is a key regulator of tumor cell growth and survival. Erlotinib, also known as tarceva, (a first-generation) and afatinib, also known as giotrif, (a second-generation) are tyrosine kinase inhibitors (TKIs) of EGFR. These TKIs are recognized therapeutic agents in these tumor types, as they inhibit EGFR signaling but show limited activity as single agents. Novel strategies will likely require EGFR-TKIs combination with an agent(s) that will enhance their therapeutic efficacy. Recently, we have demonstrated that combining statins, inhibitors of the mevalonate pathway, with erlotinib enhanced EGFR inhibition and induced synergistic cytotoxicity through the activation of cellular integrated stress response pathway (ISR) regulated by the induction of activating transcription factor 3 (ATF3). In our Phase I clinical trial, combining rosuvastatin with erlotinib, while demonstrating clinical activity, this treatment also showed statin-induced myopathies likely the result of diminished ubiquinone levels, which limited their utilization. Therefore, alternative strategies are warranted. Targeting geranylgeranyl diphosphate (GGPP) synthesis or its incorporation, a downstream mevalonate metabolite, represents such an approach with the potential to circumvent statin-associated toxicities but retain the efficacy in combination with EGFR inhibitors. In this project, we evaluated the effect of the combination of geranylgeranyl transferase-I inhibitor (GGTI-298) with the EGFR inhibitor, tarceva, (aim 1) and a GGPP synthase inhibitor, digeranyl bisphosphonate (DGBP), with the EGFR inhibitor, afatinib, (aim 2). For aim 1, we demonstrated that GGTI-298 treatment induced ATF3 expression in SCC9 and SCC25 cells and in a cohort of ex-vivo tumor tissues. Furthermore, GGTI-298 and tarceva induced synergistic cytotoxicity in SCC cells that was dependent on ATF3 expression, as ATF3 deficient murine embryonic fibroblasts (ATF3-/- MEFs) displayed attenuated cytotoxicity in response to GGTI-298 alone and in combination with tarceva. Similarly, SCC9 sub-lines that were selected as resistant to GGTI-298 through prolonged exposure to this agent also failed to demonstrate synergy with treatment of GGTI-298 in combination with tarceva. For aim 2, we demonstrated that the specific GGPP synthase inhibitor, DGBP, induced cytotoxicity in SCC cells. We further demonstrated this specificity as specific shRNA targeting of GGPP synthase as well as the inhibitor DGBP significantly enhanced the cytotoxic activity of the EGFR-TKI afatinib in SCC cells. DGBP as well as afatinib treatments induced ATF3 expression in SCC cells in vitro and in a cohort of ex-vivo tumor tissues. Co-administration of the downstream metabolite GGPP inhibits the induction of ATF3 and the cytotoxic and apoptotic effects associated with DGBP treatment. Furthermore, the synergistic cytotoxicity induced by the combination of DGBP and afatinib in SCC cells was also dependent on the expression of ATF3 through the induction of cellular stress response pathways. Taken together, these results suggest the potential clinical utility of combining downstream mevalonate inhibitors (GGTI-298 or DGBP) with EGFR inhibitors in HNSCC patients as a novel and more refined combination therapeutic approach.
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Hamilton, Julie Anne. "Targeting epithelial-to-mesenchymal transition (EMT) in feline oral squamous cell carcinoma (FOSCC)." Thesis, University of Edinburgh, 2018. http://hdl.handle.net/1842/31357.

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Squamous cell carcinoma of the head and neck (HNSCC) is an extremely common and devastating disease with a bleak prognosis. Despite intensive research, survival rates have not improved over the past 30 years principally due to untreatable recurrent/metastasising disease. Feline oral squamous cell carcinoma (FOSCC) is an equally common disease in cats with an even less favourable prognosis than humans. Human and feline squamous cell carcinomas share similar etiopathogenesis, molecular markers, tumour biology and treatment thus making FOSCC an excellent model for HNSCC. Epithelial to mesenchymal transition (EMT), under the direction microRNAs (miRNAs/mirs) could be a key driver in oncogenic transformation and chemoresistance. The aim of this study was to induce resistance to characterise the EMT/resistance phenotype and to investigate whether common miRNA-mediated pathways are present in HNSCC and FOSCC that drive this phenomenon. We used epidermal growth factor (EGFR)-inhibitor gefitinib to induce resistance in HNSCC and FOSCC and investigated the associated EMT-related molecular changes. In vitro and in vivo invasive and migratory properties of both species were explored to determine whether resistance and/or EMT status conferred a functional advantage. We determined the miRNA expression pattern during acquisition of resistance to gefitinib in both species by next generation sequencing and screened candidate miRNAs as potential therapeutics. We found that gefitinib-resistance produced a previously unrecognised biphasic response that consisted of two distinct phenotypes, a highly invasive mesenchymal phenotype during early resistance, and a more epithelial phenotype associated with established resistance. The biphasic nature of this transition may prove critical in establishing effective therapeutic targets and the timing of treatment to overcome resistance or in preventing local invasion or metastatic spread of squamous cell carcinoma. We found that the major anti-apoptotic PI3K/AKT pathway was activated in transitioning and resistant cells of both species as demonstrated upregulation of AKT, pAKT and c-FLIP together with inactivation of PTEN by phosphorylation. This indicates that avoidance of apoptosis may be a major pathway in resistance that could be targeted therapeutically. We showed that three miRNAs were differentially expressed in both gefitinib-resistant human and feline cell lines: miR-107 was downregulated, and miR-551b and miR-574 were upregulated. These microRNAs provide potential therapeutic targets in the fight against drug resistance in head and neck cancer although much further research needs to be conducted to elucidate the complex network of interactions that may be affected by targeting these powerful regulatory molecules.
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Fujita, Haruyuki. "The tyrosine kinase inhibitor dasatinib suppresses cytokine production by plasmacytoid dendritic cells by targeting endosomal transport of CpG DNA." Kyoto University, 2013. http://hdl.handle.net/2433/174784.

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Katsoulas, Athanasia. "Design and mechanism of action of novel agents termed "combi-molecules" engineered for tandem targeting for Bcr-abl expressing leukemia cells." Thesis, McGill University, 2007. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=111884.

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Bcr-abl expression being associated with anti-apoptotic signaling and expression of DNA repair enzymes, we surmised that single molecules capable of blocking abl tyrosine kinase (TK) function and damaging DNA should lead to compounds with potency superior to that of GleevecRTM. To this end, we designed novel agents termed "combi-molecules" programmed to not only behave as bcr-abl inhibitors on their own, but also to further degrade to another inhibitor and a DNA damaging species. The released inhibitor was designed to sustain bcr-abl inhibition following degradation of the combi-molecule and the DNA damaging species to activate pathways leading to apoptosis. To model this strategy termed "combi-targeting", we synthesized ZRCM5 (a monoalkyltriazene) that showed antiproliferative activity superior to that of the classical DNA damaging agent TemodalRTM, but not to that of Gleevec RTM. This result was imputed to the rather weak bcr-abl inhibitory activity of ZRCM5 and its strong DNA damaging property. Another prototype designed to contain an aniline mustard moiety (AK04) was a strong bcr-abl inhibitor but a poor DNA alkylating agent. Its cytotoxic activity was again stronger than that of the clinical alkylating agent chlorambucil but inferior to that of GleevecRTM. Further chemical studies directed at structural modification of the benzamide moiety led to the synthesis of ZRF1 with strong potency against bcr-abl TK and strong DNA damaging property. This novel optimized combi-molecule showed a 1.6-3-fold greater potency than GleevecRTM against bcr-abl expressing cells. Further investigation with ZRF1, showed that its cytotoxic potency was dependent on the p53 wild-type status of the cells. In cells expressing wild-type p53, p21 transactivation was associated with cell cycle arrest and that of Bax with apoptosis. In addition to, the pro-apoptotic effect of bcr-abl inhibition, these multiple mechanisms of action may synergistically enhance the cytotoxic potency of ZRF1 in p53 wild-type cells. The study conclusively demonstrated that p53 is a major determinant for the cytotoxic advantage of the novel combi-molecular approach in chronic myelogenous leukemia (CML), a disease in which 70-85% of all cases express wild-type p53.
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Lai, Damian. "Targeting tyrosine kinase inhibitor-insensitive chronic myeloid leukemia stem/progenitor cells by effective inhibition of a novel PP2A-AHI-1-BCR-ABL-JAK2-complex." Thesis, University of British Columbia, 2015. http://hdl.handle.net/2429/54591.

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Imatinib Mesylate (IM) and other tyrosine kinase inhibitors (TKIs) have had a major impact on treatment of early phase Chronic Myeloid Leukemia (CML) patients. However, TKI monotherapies are not curative and initial and acquired resistance remain challenges. Particularly, CML stem cells are less responsive to TKIs and are a critical target population for TKI resistance. Thus, improved treatments targeting key elements active in CML stem cells are needed. One candidate is Abelson helper integration site-1 (AHI-1), an oncogene that is highly upregulated in CML stem cells and interacts with multiple kinases, including BCR-ABL and JAK2. AHI-1-mediated complexes regulate TKI response/resistance of CML stem/progenitor cells, indicating that AHI-1 is a new therapeutic target in CML. By screening the Prestwick Chemical Library, a specific growth inhibitory compound that potentially targets AHI-1 was identified: Cantharidin (CAN), an inhibitor of protein phosphatase 2A (PP2A). CAN is toxic however, so two new PP2A inhibitors, LB100 and LB102, were identified for this study. These new inhibitors specifically inhibit PP2A activity and suppress growth of CML cell lines. Importantly, these new PP2A inhibitors selectively target CML stem/progenitor cells while sparing healthy stem/progenitor cells. When combined with TKIs there is significant further suppression of growth in cell lines and in CD34+ treatment-naïve IM-nonresponder cells. Furthermore, this combination effect was determined to be synergistic. Cell cycle analysis showed that treatment with PP2A inhibitors alone induced a shift from G1 to G2/M phase. Confocal microscopy confirmed that the G2/M arrest led to mitotic catastrophe. However a similar shift in cell population was observed after combination with IM, suggesting that the G2/M phase arrest is solely due to PP2A inhibition. Mechanistically, the PP2A-PR55α subunit was identified as a new AHI-1 interacting protein. Western blot analysis showed that, compared to single agents, the combination treatment greatly suppresses protein expression of AHI-1, BCR-ABL, JAK2, STAT5, AKT, β-catenin, P-38 and JNK. The combination treatment also affected PP2A and BCR-ABL-mediated β-catenin dephosphorylation/phosphorylation. These results indicate that simultaneously targeting both BCR-ABL and PP2A activities in CML stem/progenitor cells may provide a novel treatment option for CML patients, through destabilization of the protein-protein interactions mediated by AHI-1.
Medicine, Faculty of
Medicine, Department of
Experimental Medicine, Division of
Graduate
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Sørum, Christopher. "Synthesis of new tyrosine kinase inhibitors." Thesis, Norges teknisk-naturvitenskapelige universitet, Institutt for kjemi, 2009. http://urn.kb.se/resolve?urn=urn:nbn:no:ntnu:diva-6863.

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Doepfner, Kathrin T. "Targeting receptor tyrosine kinase signaling in acute myeloid leukemia /." Zürich, 2008. http://opac.nebis.ch/cgi-bin/showAbstract.pl?sys=000253043.

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Books on the topic "Tyrosine Kinase Inhibitors Targeting"

1

Matthews, David J. Targeting protein kinases for cancer therapy. Hoboken, N.J: John Wiley & Sons, 2009.

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E, Gerritsen Mary, ed. Targeting protein kinases for cancer therapy. Hoboken, N.J: John Wiley & Sons, 2010.

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Focosi, Daniele, ed. Resistance to Tyrosine Kinase Inhibitors. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-46091-8.

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Phosphoinositide 3-kinase in health and disease. Heidelberg: Springer Verlag, 2010.

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Rommel, Christian. Phosphoinositide 3-kinase in Health and Disease: Volume 2. Berlin, Heidelberg: Springer-Verlag Berlin Heidelberg, 2011.

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Müller, Gerhard, and Bert Klebl. Protein kinases as drug targets. Weinheim: Wiley-VCH, 2011.

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Fleischmann, Roy. Signalling pathway inhibitors. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0081.

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Oral, small-molecule signalling pathway inhibitors, including ones that inhibit the JAK and SyK pathways, are currently in development for the treatment of rheumatoid arthritis (RA). Tofacitinib is an orally administered small-molecule inhibitor that targets the intracellular Janus kinase 3 and 1 (JAK1/3) molecules to a greater extent than JAK2 while baricitinib (formerly INCB028050) predominantly inhibits JAK1/2. Many of the proinflammatory cytokines implicated in the pathogenesis of RA utilize cell signalling that involves the JAK-STAT pathways and therefore inhibition of JAK-STAT signalling, by targeting multiple RA-associated cytokine pathways, has the potential to simultaneously reduce inflammation, cellular activation, and proliferation of key immune cells. Fostamatinib disodium is an orally available inhibitor of spleen tyrosine kinase (SyK), which is a cytoplasmic tyrosine kinase that is an important mediator of immunoreceptor signalling in mast cells, macrophages, neutrophils, and B cells. Interruption of SyK signalling may interrupt production of tumour necrosis factor (TNF) and metalloproteinase and therefore affect RA disease activity. Tofacitinib has been investigated in multiple phase 2 and phase 3 trials which have investigated its efficacy (clinical, functional, and radiographic) and safety in patients who have failed disease-modifying anti-inflammatory drugs (DMARDs) as monotherapy or in combination with DMARDs, compared to an inhibitor of tumour necrosis factor alpha (TNFα‎) and in patients who have failed TNFα‎ inhibitors. The efficacy of fostamatinib and baricitinib has been investigated in phase 2 trials; both are in large phase 3 clinical programmes. Each of these medications has demonstrated efficacy; their safety profile has been shown to be different from each other and from currently approved biological agents. This chapter discusses what is currently known and understood about their efficacy and safety.
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Focosi, Daniele. Resistance to Tyrosine Kinase Inhibitors. Springer International Publishing AG, 2018.

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Focosi, Daniele. Resistance to Tyrosine Kinase Inhibitors. Springer, 2016.

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Focosi, Daniele. Resistance to Tyrosine Kinase Inhibitors. Springer, 2016.

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Book chapters on the topic "Tyrosine Kinase Inhibitors Targeting"

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Khan, Muzammil Muhammad, Deepika Sarvepalli, Mamoon Ur Rashid, Hammad Zafar, Muhammad Shayan Khan, Effa Zahid, Akash Khetpal, et al. "Gastric Cancer: Role of Phytochemicals and Tyrosine Kinase Inhibitors." In Phytochemicals Targeting Tumor Microenvironment in Gastrointestinal Cancers, 189–208. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-48405-7_9.

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Carboni, Joan M., Mark Wittman, and Fei Huang. "Targeting Insulin-Like Growth Factor Receptor 1 (IGF-1R) and Insulin Receptor Signaling by Tyrosine Kinase Inhibitors in Cancer." In Insulin-like Growth Factors and Cancer, 215–29. Boston, MA: Springer US, 2011. http://dx.doi.org/10.1007/978-1-4614-0598-6_11.

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Cakar, Burcu, and Erdem Göker. "Tyrosine Kinase Inhibitors." In Breast Disease, 617–31. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-26012-9_36.

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Cakar, Burcu, and Erdem Göker. "Tyrosine Kinase Inhibitors." In Breast Disease, 529–39. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-16792-9_35.

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Duhé, Roy J. "Tyrosine Kinase Inhibitors." In Encyclopedia of Cancer, 1–3. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-642-27841-9_6080-2.

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Duhé, Roy J. "Tyrosine Kinase Inhibitors." In Encyclopedia of Cancer, 4705–7. Berlin, Heidelberg: Springer Berlin Heidelberg, 2017. http://dx.doi.org/10.1007/978-3-662-46875-3_6080.

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Duhé, Roy J. "Tyrosine Kinase Inhibitors." In Encyclopedia of Cancer, 3822–24. Berlin, Heidelberg: Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-16483-5_6080.

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Abad, Cybele Lara R., and Raymund R. Razonable. "Tyrosine-Kinase Inhibitors." In Infectious Complications in Biologic and Targeted Therapies, 273–92. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-031-11363-5_15.

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Latham, Antony M., Jayakanth Kankanala, and Sreenivasan Ponnambalam. "Receptor Tyrosine Kinase Inhibitors." In Encyclopedia of Cancer, 1–7. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-642-27841-9_7196-1.

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Latham, Antony M., Jayakanth Kankanala, and Sreenivasan Ponnambalam. "Receptor Tyrosine Kinase Inhibitors." In Encyclopedia of Cancer, 3940–46. Berlin, Heidelberg: Springer Berlin Heidelberg, 2016. http://dx.doi.org/10.1007/978-3-662-46875-3_7196.

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Conference papers on the topic "Tyrosine Kinase Inhibitors Targeting"

1

Shelton, Abby, Erin Smithberger, Madison Butler, Alex Flores, Ryan Bash, Steve Angus, Noah Sciaky, et al. "Abstract 331: Dynamic kinome targeting reveals kinases involved in acquired resistance to tyrosine kinase inhibitors in EGFR-driven glioblastomas." 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.am2019-331.

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Shelton, Abby, Erin Smithberger, Madison Butler, Alex Flores, Ryan Bash, Steve Angus, Noah Sciaky, et al. "Abstract 331: Dynamic kinome targeting reveals kinases involved in acquired resistance to tyrosine kinase inhibitors in EGFR-driven glioblastomas." 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.sabcs18-331.

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Bushman, Destinee, Jared J. Bearss, Venkataswamy Sorna, Hariprasad Vankayalapati, Sunil Sharma, Fenghuang Zhan, and David Bearss. "Abstract 2161: Targeting Bruton's tyrosine kinase (BTK) in multiple myeloma with novel BTK inhibitors." 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.am2013-2161.

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Nakazawa, Youya, Satoshi Kawano, Junji Matsui, Yasuhiro Funahashi, Osamu Tohyama, Hiroki Muto, Takayuki Nakagawa, and Tomohiro Matsushima. "Abstract 2980: Maximizing the efficacy of anti-angiogenesis cancer therapy: A multi-targeting strategy by tyrosine kinase inhibitors." 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.am2014-2980.

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Adelaiye-Ogala, Remi M., Sreenivasulu Chintala, Ashley Orillion, May Elbanna, Ben Elzey, Nur Damayanti, Kiersten M. Miles, et al. "Abstract 4170: Targeting androgen receptor overcomes resistance to tyrosine kinase inhibitors in advanced clear cell renal cell carcinoma." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-4170.

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Pan, Bin, Xiangmin Wang, Kailin Xu, and Takayuki Ikezoe. "Abstract 5892: miR-217 sensitizes chronic myelogenous leukemia cells to tyrosine kinase inhibitors by targeting pro-oncogenic anterior gradient 2." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-5892.

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Njatcha, Christian, Mariya Farooqui, Jennifer R. Grandis, and Jill M. Siegfried. "Abstract 4101: Targeting the EGFR/STAT3 axis in NSCLC with resistance to EGFR tyrosine kinase inhibitors using an oligonucleotide-based decoy." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-4101.

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Setiady, Yulius Y., Ling Dong, Anna Skaletskaya, Jan Pinkas, Robert J. Lutz, John M. Lambert, and Thomas Chittenden. "Abstract 4513: IMGN289, an EGFR-targeting antibody-drug conjugate, is effective against tumor cells that are resistant to EGFR tyrosine kinase inhibitors." 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.am2014-4513.

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Paolo, Daniela D., Laura Emionite, George Liu, Michele Cilli, Annarita D. Fiore, Chiara Brignole, Chris Liang, et al. "Abstract 2622: New therapeutic strategies in neuroblastoma: combined targeting of a novel tyrosine kinase inhibitor and liposomal siRNAs againstALK." 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.am2014-2622.

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Rai, Kammei, Nagio Takigawa, Sachio Ito, Katsuyuki Kiura, Tateji Yasuda, Kenji Shimizu, and Mitsune Tanimoto. "Abstract 1158: Multiple molecular targeting effects by miR-7 in EGFR tyrosine kinase inhibitor-resistant lung cancer xenograft models." 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.am2011-1158.

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Reports on the topic "Tyrosine Kinase Inhibitors Targeting"

1

Miller, Tod. Peptide-Bassed Inhibitors of Neu Tyrosine Kinase. Fort Belvoir, VA: Defense Technical Information Center, June 1999. http://dx.doi.org/10.21236/ada375133.

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Miller, W. T. Peptide-Based Inhibitors of Neu Tyrosine Kinase. Fort Belvoir, VA: Defense Technical Information Center, December 2000. http://dx.doi.org/10.21236/ada392289.

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Rosen, Neal. Development of Targeted Ansamycins as Novel Antiestrogens and Tyrosine Kinase Inhibitors. Fort Belvoir, VA: Defense Technical Information Center, September 1998. http://dx.doi.org/10.21236/ada369205.

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Rosen, Neal. Development of Targeted Ansamycins as Noval Antiestrogens and Tyrosine Kinase Inhibitors. Fort Belvoir, VA: Defense Technical Information Center, September 2000. http://dx.doi.org/10.21236/ada413599.

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Drake, Justin, and Owen Witte. Identification and Targeting of Tyrosine Kinase Activity in Prostate Cancer Initiation, Progression, and Metastasis. Fort Belvoir, VA: Defense Technical Information Center, October 2012. http://dx.doi.org/10.21236/ada575949.

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Drake, Justin, and Owen Witte. Identification and Targeting of Tyrosine Kinase Activity in Prostate Cancer Initiation, Progression, and Metastasis. Fort Belvoir, VA: Defense Technical Information Center, December 2013. http://dx.doi.org/10.21236/ada595692.

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Balk, Steven P. Identification and Targeting of Upstream Tyrosine Kinases Mediating PI3 Kinase Activation in PTEN Deficient Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, June 2010. http://dx.doi.org/10.21236/ada535588.

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Balk, Steven P. Identification and Targeting of Upstream Tyrosine Kinases Mediating PI3 Kinase Activation in PTEN-Deficient Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, June 2009. http://dx.doi.org/10.21236/ada510490.

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Balk, Steven P. Identification and Targeting of Upstream Tyrosine Kinases Mediating PI3 Kinase Activation in PTEN Deficient Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, June 2011. http://dx.doi.org/10.21236/ada550805.

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Tinker, Anna V., Neesha C. Dhani, Prafull Ghatage, Deanna McLeod, Vanessa Samouëlian, Stephen A. Welch, and Alon D. Altman. Immune Checkpoint Inhibitors in Pretreated Metastatic Endometrial Cancer. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, January 2023. http://dx.doi.org/10.37766/inplasy2023.1.0038.

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Review question / Objective: Efficacy and safety of immune checkpoint inhibitors alone or in combination with tyrosine kinase inhibitors in patients with pretreated advanced, persistent, or recurrent metastatic endometrial cancer. Condition being studied: Advanced, persistent, or recurrent metastatic endometrial cancer. Study designs to be included: Non-randomized studies of monotherapy in populations selected for relevant biomarkers such as MMR, microsatellite stability, and PD-L1 expression status and randomized trials of ICI combinations in unselected patients.
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