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Journal articles on the topic 'Tyrosine kinom'

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Published: 4 June 2021

Last updated: 4 February 2022

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1

Bardelli, A. "Mutational Analysis of the Tyrosine Kinome in Colorectal Cancers." Science 300, no. 5621 (2003): 949. http://dx.doi.org/10.1126/science.1082596.

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2

Creeden, Justin F., Khaled Alganem, Ali S. Imami, et al. "Kinome Array Profiling of Patient-Derived Pancreatic Ductal Adenocarcinoma Identifies Differentially Active Protein Tyrosine Kinases." International Journal of Molecular Sciences 21, no. 22 (2020): 8679. http://dx.doi.org/10.3390/ijms21228679.

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Pancreatic cancer remains one of the most difficult malignancies to treat. Minimal improvements in patient outcomes and persistently abysmal patient survival rates underscore the great need for new treatment strategies. Currently, there is intense interest in therapeutic strategies that target tyrosine protein kinases. Here, we employed kinome arrays and bioinformatic pipelines capable of identifying differentially active protein tyrosine kinases in different patient-derived pancreatic ductal adenocarcinoma (PDAC) cell lines and wild-type pancreatic tissue to investigate the unique kinomic net

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3

Loriaux, Marc, Ross Levine, Jeffrey Tyner, et al. "High-Throughput Sequence Analysis of the Tyrosine Kinome in Acute Myeloid Leukemia." Blood 110, no. 11 (2007): 886. http://dx.doi.org/10.1182/blood.v110.11.886.886.

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Abstract Mutations that result in constitutive tyrosine kinase activation occur in a wide spectrum of human malignancies, including acute myeloid leukemia (AML). Although activating mutations in the tyrosine kinases FLT3 and c-KIT occur in a significant proportion of patients with AML, the genomic events responsible for oncogenic signaling in most patients with AML have not been identified. To determine whether other aberrantly activated tyrosine kinases contribute to the pathogenesis of AML, we employed high throughput (HT) DNA sequence analysis to screen the exons encoding domains implicated

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Tyner, Jeffrey W., Denise K. Walters, Stephanie G. Willis, et al. "RNAi screening of the tyrosine kinome identifies therapeutic targets in acute myeloid leukemia." Blood 111, no. 4 (2008): 2238–45. http://dx.doi.org/10.1182/blood-2007-06-097253.

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Despite vast improvements in our understanding of cancer genetics, a large percentage of cancer cases present without knowledge of the causative genetic events. Tyrosine kinases are frequently implicated in the pathogenesis of numerous types of cancer, but identification and validation of tyrosine kinase targets in cancer can be a time-consuming process. We report the establishment of an efficient, functional screening assay using RNAi technology to directly assess and compare the effect of individually targeting each member of the tyrosine kinase family. We demonstrate that siRNA screening ca

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Angus, Steven P., Timothy Stuhlmiller, Noah Sciaky, et al. "TBCRC 036: Window of opportunity clinical trial reveals adaptive kinome reprogramming in single and combination HER2-targeting in breast cancer (BrCa)." Journal of Clinical Oncology 35, no. 15_suppl (2017): 1027. http://dx.doi.org/10.1200/jco.2017.35.15_suppl.1027.

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1027 Background: HER2 targeting is challenging due to heterogeneity in response and resistance. Adaptive kinome reprogramming (AKRP) is a resistance mechanism to kinase-targeted therapy (Rx) in TNBC ( Cancer Discovery2017). We studied AKRP in HER2+ BrCa by comparing transcriptome and kinome profiles before and after Rx with FDA-approved anti-HER2 drugs and combinations: trastuzumab (T), pertuzumab (P), T+P, or T+ lapatinib (T+L). Profiling was by RNA sequencing (RNAseq) and multiplexed inhibitor beads coupled with mass spectrometry (MIB/MS). MIB affinity-purification selectively enriches the f

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6

Ha, Jacqueline R., Peter M. Siegel, and Josie Ursini-Siegel. "The Tyrosine Kinome Dictates Breast Cancer Heterogeneity and Therapeutic Responsiveness." Journal of Cellular Biochemistry 117, no. 9 (2016): 1971–90. http://dx.doi.org/10.1002/jcb.25561.

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7

Tong, Jiefei, Mohamed Helmy, Florence M. G. Cavalli, et al. "Integrated analysis of proteome, phosphotyrosine-proteome, tyrosine-kinome, and tyrosine-phosphatome in acute myeloid leukemia." PROTEOMICS 17, no. 6 (2017): 1600361. http://dx.doi.org/10.1002/pmic.201600361.

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8

Tyner, Jeffrey W., Marc Loriaux, Stephanie G. Willis, et al. "RNAi Screening of the Tyrosine Kinome Identifies Therapeutic Targets in Leukemia Patients." Blood 112, no. 11 (2008): 758. http://dx.doi.org/10.1182/blood.v112.11.758.758.

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Abstract A large percentage of cancer cases present without knowledge of the causative genetic events. Tyrosine kinases are frequently implicated in the pathogenesis of cancer, but identification of specific tyrosine kinases as cancer targets has been a slow process. In the near future, whole-genome sequencing will enable vast amounts of sequence data to be collected, however clinical application of this information will require a detailed understanding of the functional consequences of each sequence change. Here, we present an RNAi-assisted protein target identification (RAPID) assay by which

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9

Tyner, Jeffrey W., Stephanie Willis, Michael W. N. Deininger, and Brian J. Druker. "RNAi Functional Screening of the Tyrosine Kinome Identifies Therapeutic Targets in Acute Myeloid Leukemia Patients." Blood 110, no. 11 (2007): 208. http://dx.doi.org/10.1182/blood.v110.11.208.208.

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Abstract A large percentage of cancer cases present without knowledge of the causative genetic events. Tyrosine kinases are frequently implicated in the pathogenesis of cancer, but identification of specific tyrosine kinases as cancer targets has been a slow process. Tyrosine kinases are thought to play a causative role in acute myeloid leukemia (AML), based in part on the high percentage of cases with phosphorylation of STAT5—a marker for activity of tyrosine kinase signaling. However, known abnormalities in tyrosine kinases in AML are restricted to internal tandem duplications of FLT3 or gen

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10

Loriaux, Marc M., Ross L. Levine, Jeffrey W. Tyner, et al. "High-throughput sequence analysis of the tyrosine kinome in acute myeloid leukemia." Blood 111, no. 9 (2008): 4788–96. http://dx.doi.org/10.1182/blood-2007-07-101394.

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Abstract To determine whether aberrantly activated tyrosine kinases other than FLT3 and c-KIT contribute to acute myeloid leukemia (AML) pathogenesis, we used high-throughput (HT) DNA sequence ana-lysis to screen exons encoding the activation loop and juxtamembrane domains of 85 tyrosine kinase genes in 188 AML patients without FLT3 or c-KIT mutations. The screen identified 30 nonsynonymous sequence variations in 22 different kinases not previously reported in single-nucleotide polymorphism (SNP) databases. These included a novel FLT3 activating allele and a previously described activating mut

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11

Johnson, Gary L., Keith D. Amos, James S. Duncan, et al. "Kinome reprogramming response to MEK inhibition: A window-of-opportunity trial in triple-negative breast cancer (TNBC)." Journal of Clinical Oncology 31, no. 15_suppl (2013): 512. http://dx.doi.org/10.1200/jco.2013.31.15_suppl.512.

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512 Background: Targeted therapy (Rx) in TNBC is challenging due to heterogeneity and cancer cell kinome “reprogramming” in response to targeted kinase inhibitors (Cell 149:307, 2012). In preclinical TNBC models specific kinases (e.g., DDR1/2, PDGFRbeta, VEGFR2, AXL) are activated in response to MEK inhibition. Our studies define unique kinome reprogramming in basal-like (BBC) versus claudin-low (CL). This study compared kinome profiles of TNBC pre- and post- MEK1/2 inhibition with GSK1120212 (trametinib, T) using multiplexed inhibitor beads coupled with mass spectrometry (MIB/MS). Methods: El

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12

Loh, Mignon L., Jinghui Zhang, Richard C. Harvey, et al. "Tyrosine kinome sequencing of pediatric acute lymphoblastic leukemia: a report from the Children's Oncology Group TARGET Project." Blood 121, no. 3 (2013): 485–88. http://dx.doi.org/10.1182/blood-2012-04-422691.

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Abstract One recently identified subtype of pediatric B-precursor acute lymphoblastic leukemia (ALL) has been termed BCR-ABL1–like or Ph-like because of similarity of the gene expression profile to BCR-ABL1 positive ALL suggesting the presence of lesions activating tyrosine kinases, frequent alteration of IKZF1, and poor outcome. Prior studies demonstrated that approximately half of these patients had genomic lesions leading to CRLF2 overexpression, with half of such cases harboring somatic mutations in the Janus kinases JAK1 and JAK2. To determine whether mutations in other tyrosine kinases m

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13

Prickett, Todd D., Neena S. Agrawal, Xiaomu Wei, et al. "Analysis of the tyrosine kinome in melanoma reveals recurrent mutations in ERBB4." Nature Genetics 41, no. 10 (2009): 1127–32. http://dx.doi.org/10.1038/ng.438.

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14

Tyner, J. W., M. M. Loriaux, H. Erickson, et al. "High-throughput mutational screen of the tyrosine kinome in chronic myelomonocytic leukemia." Leukemia 23, no. 2 (2008): 406–9. http://dx.doi.org/10.1038/leu.2008.187.

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15

Elst, Arja ter, Maikel P. Peppelenbosch, Sander H. Diks, et al. "Kinome Profiling in Acute Myeloid Leukemia as a New Approach for Target Discovery." Blood 112, no. 11 (2008): 1201. http://dx.doi.org/10.1182/blood.v112.11.1201.1201.

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Abstract Acute myeloid leukemia (AML) is a heterogeneous disease, characterized by a multitude of genetic events. Activating mutations in receptor tyrosine kinases have been identified in 50% of AML primary blasts, and deregulation of one or more signal transduction pathways including the JAK/STAT, RAS/Raf/MEK/ERK, and PI3K/AKT pathways is common (Kornblau et al., 2006). High-throughput procedures which generate comprehensive descriptions of cellular signaling without a priori assumptions in each sample, would enable us to directly assess a broader range of targets for future treatment strateg

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16

Bozulic, L., P. J. Morin, T. Hunter, and B. A. Hemmings. "Meeting Report: Targeting the Kinome--20 Years of Tyrosine Kinase Inhibitor Research in Basel." Science's STKE 2007, no. 374 (2007): pe8. http://dx.doi.org/10.1126/stke.3742007pe8.

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17

Vyse, Simon, Howard Desmond, and Paul H. Huang. "Advances in mass spectrometry based strategies to study receptor tyrosine kinases." IUCrJ 4, no. 2 (2017): 119–30. http://dx.doi.org/10.1107/s2052252516020546.

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Receptor tyrosine kinases (RTKs) are key transmembrane environmental sensors that are capable of transmitting extracellular information into phenotypic responses, including cell proliferation, survival and metabolism. Advances in mass spectrometry (MS)-based phosphoproteomics have been instrumental in providing the foundations of much of our current understanding of RTK signalling networks and activation dynamics. Furthermore, new insights relating to the deregulation of RTKs in disease, for instance receptor co-activation and kinome reprogramming, have largely been identified using phosphopro

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18

Logie, Emilie, Chandra S. Chirumamilla, Claudina Perez-Novo, et al. "Covalent Cysteine Targeting of Bruton’s Tyrosine Kinase (BTK) Family by Withaferin-A Reduces Survival of Glucocorticoid-Resistant Multiple Myeloma MM1 Cells." Cancers 13, no. 7 (2021): 1618. http://dx.doi.org/10.3390/cancers13071618.

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Multiple myeloma (MM) is a hematological malignancy characterized by plasma cells’ uncontrolled growth. The major barrier in treating MM is the occurrence of primary and acquired therapy resistance to anticancer drugs. Often, this therapy resistance is associated with constitutive hyperactivation of tyrosine kinase signaling. Novel covalent kinase inhibitors, such as the clinically approved BTK inhibitor ibrutinib (IBR) and the preclinical phytochemical withaferin A (WA), have, therefore, gained pharmaceutical interest. Remarkably, WA is more effective than IBR in killing BTK-overexpressing gl

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19

Claudio, Jaime O., Razi Khaja, Lihua Zhuang, et al. "Sequencing the Multiple Myeloma Kinome: Absence of Mutation in Known Malignancy-Associated Kinases." Blood 104, no. 11 (2004): 783. http://dx.doi.org/10.1182/blood.v104.11.783.783.

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Abstract In approximately 50% of Multiple Myeloma (MM), translocation of non random genes into the IgH locus is believed to be the seminal event in the pathogenesis of the disease. Another 50% of cases are hyperdiploid and trisomic to certain autosomes, but do not harbor any translocation and thus are believed to have genetic alterations in unidentified loci. These observations, together with the finding of somatic mutations in FGFR3, N- and K-RAS, MYC, TP53 and CDKN2C/p18INK4C during the later stages of MM indicate that defective signaling pathways likely play a role in the progression of thi

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20

Krayem, Mohamad, Philippe Aftimos, Ahmad Najem, et al. "Kinome Profiling to Predict Sensitivity to MAPK Inhibition in Melanoma and to Provide New Insights into Intrinsic and Acquired Mechanism of Resistance." Cancers 12, no. 2 (2020): 512. http://dx.doi.org/10.3390/cancers12020512.

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Mitogen-activated protein kinase (MAPK) inhibition with the combination of BRAF (Rapidly Accelerated Fibrosarcoma) and MEK (Mitogen-activated protein kinase kinase) inhibitors has become the standard of first-line therapy of metastatic melanoma harbouring BRAF V600 mutations. However, about half of the patients present with primary resistance while the remaining develop secondary resistance under prolonged treatment. Thus, there is a need for predictive biomarkers for sensitivity and/or resistance to further refine the patient population likely to benefit from MAPK inhibitors. In this study, w

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Mi, Tian, Zhengqi Wang, and Kevin Bunting. "The Cooperative Relationship between STAT5 and Reactive Oxygen Species in Leukemia: Mechanism and Therapeutic Potential." Cancers 10, no. 10 (2018): 359. http://dx.doi.org/10.3390/cancers10100359.

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Reactive oxygen species (ROS) are now recognized as important second messengers with roles in many aspects of signaling during leukemogenesis. They serve as critical cell signaling molecules that regulate the activity of various enzymes including tyrosine phosphatases. ROS can induce inactivation of tyrosine phosphatases, which counteract the effects of tyrosine kinases. ROS increase phosphorylation of many proteins including signal transducer and activator of transcription-5 (STAT5) via Janus kinases (JAKs). STAT5 is aberrantly activated through phosphorylation in many types of cancer and thi

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22

Smithberger, Erin, Abigail Shelton, Madison Butler, et al. "CSIG-10. GENOTYPE – KINOME GUIDED DEVELOPMENT OF PRECISION EGFR-TARGETED THERAPEUTICS FOR GLIOBLASTOMA." Neuro-Oncology 22, Supplement_2 (2020): ii29. http://dx.doi.org/10.1093/neuonc/noaa215.122.

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Abstract Glioblastoma (GBM) is an aggressive primary brain tumor with poor survival and limited treatment options. However, it is an attractive candidate for precision therapeutic approaches due to the frequency of amplification and/or activating mutations in the epidermal growth factor receptor (EGFR) gene and the availability of several brain penetrant second- and third-generation EGFR tyrosine kinase inhibitors (TKI). We used comprehensive molecular profiling of a panel of genetically engineered mouse astrocyte models to examine whether mutational profiles, particularly EGFR and PTEN status

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23

Chang, Long-Sheng, Janet L. Oblinger, Abbi E. Smith, et al. "Brigatinib causes tumor shrinkage in both NF2-deficient meningioma and schwannoma through inhibition of multiple tyrosine kinases but not ALK." PLOS ONE 16, no. 7 (2021): e0252048. http://dx.doi.org/10.1371/journal.pone.0252048.

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Neurofibromatosis Type 2 (NF2) is an autosomal dominant genetic syndrome caused by mutations in the NF2 tumor suppressor gene resulting in multiple schwannomas and meningiomas. There are no FDA approved therapies for these tumors and their relentless progression results in high rates of morbidity and mortality. Through a combination of high throughput screens, preclinical in vivo modeling, and evaluation of the kinome en masse, we identified actionable drug targets and efficacious experimental therapeutics for the treatment of NF2 related schwannomas and meningiomas. These efforts identified b

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24

Pucelik, Barbara, Agata Barzowska, Janusz M. Dąbrowski та Anna Czarna. "Diabetic Kinome Inhibitors—A New Opportunity for β-Cells Restoration". International Journal of Molecular Sciences 22, № 16 (2021): 9083. http://dx.doi.org/10.3390/ijms22169083.

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Diabetes, and several diseases related to diabetes, including cancer, cardiovascular diseases and neurological disorders, represent one of the major ongoing threats to human life, becoming a true pandemic of the 21st century. Current treatment strategies for diabetes mainly involve promoting β-cell differentiation, and one of the most widely studied targets for β-cell regeneration is DYRK1A kinase, a member of the DYRK family. DYRK1A has been characterized as a key regulator of cell growth, differentiation, and signal transduction in various organisms, while further roles and substrates are th

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Grey, William, Rakhee Chauhan, Manuel Garcia-Albornoz, Hector Huerga Encabo, Neil McDonald та Dominique Bonnet. "Activation of the Receptor Tyrosine Kinase (RET) By GDNF/GFRα1 Improves Cord Blood-Derived HSC in Vitro expansion and In Vivo engraftment". Blood 134, Supplement_1 (2019): 1924. http://dx.doi.org/10.1182/blood-2019-121331.

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Allogeneic hematopoietic stem cell (HSC) transplantation is the gold standard therapy for numerous hematological disorders, but limitations exist in HSC number available per donor and our relative inability to successfully expand transplantable HSCs in vitro. In recent years, promising new molecules have been discovered, which are able to expand HSCs in vitro and improve transplantation in vivo in immunodeficient mouse models and non-human primates (e.g. SR1 and UM171). Here we demonstrate that acute activation of the receptor tyrosine kinase, RET, by its key ligand and co-receptor (GDNF/GFRα1

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Cho, Nancy L., Chi-Iou Lin, Jinyan Du, et al. "Global tyrosine kinome profiling of human thyroid tumors identifies Src as a promising target for invasive cancers." Biochemical and Biophysical Research Communications 421, no. 3 (2012): 508–13. http://dx.doi.org/10.1016/j.bbrc.2012.04.034.

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27

Shelton, Abigail, Erin Smithberger, Madison Butler, et al. "DDRE-24. ACQUIRED RESISTANCE TO TARGETED INHIBITORS IN EGFR-DRIVEN GLIOBLASTOMA: IDENTIFICATION OF DUAL KINASE TARGETS." Neuro-Oncology 22, Supplement_2 (2020): ii66. http://dx.doi.org/10.1093/neuonc/noaa215.269.

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Abstract Glioblastoma (GBM) is a devastating primary brain tumor with 5-year survival &lt; 5%. CDKN2A deletion (~60%) and EGFR amplification (55–60%) mutations frequently co-occur in these tumors. EGFR is an attractive therapeutic target due to its mutational frequency and availability of multiple brain-penetrant tyrosine kinase inhibitors (TKI). Several EGFR TKI have failed clinically, due in part to acquired resistance. To mechanistically examine this type of resistance, we used genetically engineered mouse astrocytes harboring Cdkn2a deletion and EGFRvIII, a common (35%) activating muta

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Ninio, Nissani, Meirson, et al. "Hepatitis C Virus Enhances the Invasiveness of Hepatocellular Carcinoma via EGFR-Mediated Invadopodia Formation and Activation." Cells 8, no. 11 (2019): 1395. http://dx.doi.org/10.3390/cells8111395.

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Hepatocellular carcinoma (HCC) represents the fifth most common cancer worldwide and the third cause of cancer-related mortality. Hepatitis C virus (HCV) is the leading cause of chronic hepatitis, which often results in liver fibrosis, cirrhosis, and eventually HCC. HCV is the most common risk factor for HCC in western countries and leads to a more aggressive and invasive disease with poorer patient survival rates. However, the mechanism by which the virus induces the metastatic spread of HCC tumor cells through the regulation of invadopodia, the key features of invasive cancer, is still unkno

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29

Zhao, Xiaohong, Huijuan Jiang, Michelle Wang, et al. "Targeting Kinome Reprogramming for Overcoming Ibrutinib-Resistance (IR) in Mantle Cell Lymphoma (MCL)." Blood 132, Supplement 1 (2018): 2651. http://dx.doi.org/10.1182/blood-2018-99-116756.

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Abstract Mantle cell lymphoma (MCL) is an aggressive and incurable B-cell malignancy. Prognosis remains poor due to emergence of drug resistance and MCL progression. Ibrutinib is a novel B-cell receptor (BCR) downstream bruton's tyrosine kinase (BTK) inhibitor with high response rates reported in MCL patients. The initial success of ibrutinib is likely attributed to attenuation of BCR-dependent lymphoma-tumor microenvironment (TME) interactions. Moreover, despite the dramatic responses to ibrutinib, ibrutinib resistance (IR) inevitably develops. Remarkably, once patients relapse after ibrutini

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Druillennec, Sabine, Coralie Dorard, and Alain Eychène. "Alternative Splicing in Oncogenic Kinases: From Physiological Functions to Cancer." Journal of Nucleic Acids 2012 (2012): 1–14. http://dx.doi.org/10.1155/2012/639062.

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Among the 518 protein kinases encoded by the human kinome, several of them act as oncoproteins in human cancers. Like other eukaryotic genes, oncogenes encoding protein kinases are frequently subjected to alternative splicing in coding as well as noncoding sequences. In the present paper, we will illustrate how alternative splicing can significantly impact on the physiological functions of oncogenic protein kinases, as demonstrated by mouse genetic model studies. This includes examples of membrane-bound tyrosine kinases receptors (FGFR2, Ret, TrkB, ErbB4, and VEGFR) as well as cytosolic protei

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Kampen, Kim R., Arja ter Elst, Sander H. Diks, et al. "Insights in Dynamic Kinome Reprogramming As a Consequence of MEK Inhibition in MLL-Rearranged AML." Blood 120, no. 21 (2012): 2338. http://dx.doi.org/10.1182/blood.v120.21.2338.2338.

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Abstract Abstract 2338 Cancer arises when somatic cells are able to escape the restraints that normally withhold them from unlimited expansion. Cancer progression is thought to be the net result of signaling through various protein-kinase mediated networks driving cell proliferation and survival. The kinome networks can be affected by numerous factors; including acquired or selected mutations as well as environmental cross talk. Additionally, the loss of phosphatases could be a causative factor for activation of multiple tyrosine kinases as well (Cell. 2011 Mar 4;144(5):703–18). Deregulated ki

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Verkhivker, G. M. "Exploring sequence-structure relationships in the tyrosine kinome space: functional classification of the binding specificity mechanisms for cancer therapeutics." Bioinformatics 23, no. 15 (2007): 1919–26. http://dx.doi.org/10.1093/bioinformatics/btm277.

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Murrow, Lyndsay M., Sireesha V. Garimella, Tamara L. Jones, Natasha J. Caplen, and Stanley Lipkowitz. "Identification of WEE1 as a potential molecular target in cancer cells by RNAi screening of the human tyrosine kinome." Breast Cancer Research and Treatment 122, no. 2 (2009): 347–57. http://dx.doi.org/10.1007/s10549-009-0571-2.

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Brown, Jennifer R., Ross Levine, Elke Raderschall, Christina Thompson, D. Gary Gilliland, and Arnold S. Freedman. "Systematic Genomic Screen for Tyrosine Kinase Mutations in CLL." Blood 110, no. 11 (2007): 2069. http://dx.doi.org/10.1182/blood.v110.11.2069.2069.

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Abstract Genomic screens have identified activating somatic mutations in tyrosine kinases in a spectrum of acute and chronic hematologic malignancies. These mutations lead to increased cellular proliferation and/or impairment of apoptosis. Chronic lymphocytic leukemia is a common chronic leukemia of adults that is thought to result at least in part from failure of apoptosis. Recent data suggest that CLL cell turnover is higher than previously thought and may correlate with disease progression, suggesting that somatic mutations that activate signal transduction may contribute to CLL pathogenesi

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Cheng, Peng, Emma Phillips, Sung-Hak Kim, et al. "Kinome-wide shRNA Screen Identifies the Receptor Tyrosine Kinase AXL as a Key Regulator for Mesenchymal Glioblastoma Stem-like Cells." Stem Cell Reports 4, no. 5 (2015): 899–913. http://dx.doi.org/10.1016/j.stemcr.2015.03.005.

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Sergeys, Jurgen, Inge Van Hove, Tjing-Tjing Hu, et al. "The retinal tyrosine kinome of diabetic Akimba mice highlights potential for specific Src family kinase inhibition in retinal vascular disease." Experimental Eye Research 197 (August 2020): 108108. http://dx.doi.org/10.1016/j.exer.2020.108108.

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Qiu, Yuran, Xiaolan Yin, Xinyi Li, et al. "Untangling Dual-Targeting Therapeutic Mechanism of Epidermal Growth Factor Receptor (EGFR) Based on Reversed Allosteric Communication." Pharmaceutics 13, no. 5 (2021): 747. http://dx.doi.org/10.3390/pharmaceutics13050747.

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Dual-targeting therapeutics by coadministration of allosteric and orthosteric drugs is drawing increased attention as a revolutionary strategy for overcoming the drug-resistance problems. It was further observed that the occupation of orthosteric sites by therapeutics agents has the potential to enhance allosteric ligand binding, which leads to improved potency of allosteric drugs. Epidermal growth factor receptor (EGFR), as one of the most critical anti-cancer targets belonging to the receptor tyrosine kinase family, represents a quintessential example. It was revealed that osimertinib, an AT

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Tyner, Jeffrey W., Luke Fletcher, Wayne Yang, et al. "Development of a Small-Molecule Inhibitor Screen to Rapidly Identify Key Signaling Pathways in Leukemogenesis." Blood 114, no. 22 (2009): 708. http://dx.doi.org/10.1182/blood.v114.22.708.708.

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Abstract Abstract 708 Aberrantly activated tyrosine kinases and their associated signaling pathways are critical to leukemogenesis and primary acute myeloid leukemia (AML) cell viability. While aberrant kinase activation has been confirmed in a significant percentage of AML, constitutive phosphorylation of STAT5, a marker of tyrosine kinase activation, is present in the majority of AML samples indicating that as yet unidentified tyrosine kinases can be aberrantly activated and contribute to leukemogenesis. Efforts to identify activating tyrosine kinase mutations using high-throughput sequencin

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Pflug, Alexander, Marianne Schimpl, J. Willem M. Nissink, et al. "A-loop interactions in Mer tyrosine kinase give rise to inhibitors with two-step mechanism and long residence time of binding." Biochemical Journal 477, no. 22 (2020): 4443–52. http://dx.doi.org/10.1042/bcj20200735.

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The activation loop (A-loop) plays a key role in regulating the catalytic activity of protein kinases. Phosphorylation in this region enhances the phosphoryl transfer rate of the kinase domain and increases its affinity for ATP. Furthermore, the A-loop possesses autoinhibitory functions in some kinases, where it collapses onto the protein surface and blocks substrate binding when unphosphorylated. Due to its flexible nature, the A-loop is usually disordered and untraceable in kinase domain crystal structures. The resulting lack of structural information is regrettable as it impedes the design

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Kiflemariam, Sara, Viktor Ljungström, Fredrik Pontén, and Tobias Sjöblom. "Tumor Vessel Up-Regulation of INSR Revealed by Single-Cell Expression Analysis of the Tyrosine Kinome and Phosphatome in Human Cancers." American Journal of Pathology 185, no. 6 (2015): 1600–1609. http://dx.doi.org/10.1016/j.ajpath.2015.02.019.

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Boyanova, Desislava, Santosh Nilla, Ingvild Birschmann, Thomas Dandekar, and Marcus Dittrich. "PlateletWeb: a systems biologic analysis of signaling networks in human platelets." Blood 119, no. 3 (2012): e22-e34. http://dx.doi.org/10.1182/blood-2011-10-387308.

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Abstract Understanding the cellular mechanisms of platelet activation and their pharmacologic modulation is of major interest for basic and clinical research. Here we introduce a comprehensive human platelet repository (PlateletWeb) for systems biologic analysis of platelets in the functional context of integrated networks. Functional, drug, and pathway associations provide a first systemic insight into various aspects of platelet functionality and pharmacologic regulation. Detailed manual curation of recent platelet proteome and transcriptome studies yielded more than 5000 platelet proteins.

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Mehta, Amitkumar N., Christopher Willey, Michael Crowley, et al. "Integrated comprehensive high-throughput kinomics profiling and whole exome sequencing of penile squamous cell cancer (PSCC)." Journal of Clinical Oncology 32, no. 4_suppl (2014): 383. http://dx.doi.org/10.1200/jco.2014.32.4_suppl.383.

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383 Background: Molecular drivers in penile squamous cell cancer (PSCC), an orphan malignancy, remain unclear. The Cancer Genome Atlas (TCGA) is not studying PSCC and the Catalogue of Somatic Mutations in Cancer (COSMIC) investigators have reported only targeted analyses of PSCC. We report the first integrated analyses of comprehensive kinomics and whole exome sequencing (seq) in tumors from patients (pts) with PSCC . Methods: We performed integrated functional kinomics profiling and comprehensive exome-seq of two frozen tissue samples from men with PSCC with a matched normal tissue procured f

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Mehta, Amitkumar N., Christopher Douglas Willey, Joshua Anderson, et al. "Comprehensive kinase profiling to classify clear cell (cc)-renal cell carcinoma (RCC)." Journal of Clinical Oncology 32, no. 4_suppl (2014): 409. http://dx.doi.org/10.1200/jco.2014.32.4_suppl.409.

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409 Background: Comprehensive high throughput functional kinase activity in localized cc-RCC tumors may assist in devising a classification system and help identify potential therapeutic targets. Methods: Patients (pts) with localized tumors undergoing surgery with minimum follow-up of 18 months underwent kinomics of fresh frozen cc-RCC tumors and matched normal renal tissue using the PamStation12 high-content phospho-peptide substrate microarray system (PamGene). The protein tyrosine kinome (PTK) and serine/threonine kinome (STK) PamChips were used to measure global kinase activity. Advanced

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Shelton, Abigail, Erin Smithberger, Madison Butler, et al. "DRES-07. DEFINING THE MECHANISMS OF ACQUIRED RESISTANCE TO TYROSINE KINASE INHIBITORS IN EGFR-DRIVEN GLIOBLASTOMAS USING INTEGRATED KINOME AND TRANSCRIPTOME PROFILING." Neuro-Oncology 20, suppl_6 (2018): vi77. http://dx.doi.org/10.1093/neuonc/noy148.314.

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Tyner, Jeffrey W., Heidi Erickson, Stephen Oh, et al. "Small-Molecule Inhibitor Screen Rapidly Identifies Key Signaling Pathways in Leukemogenesis." Blood 112, no. 11 (2008): 2519. http://dx.doi.org/10.1182/blood.v112.11.2519.2519.

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Abstract Aberrantly activated tyrosine kinases and their associated signaling pathways are critical to leukemogenesis and primary acute myeloid leukemia (AML) cell viability. While aberrant kinase activation has been confirmed in a significant percentage of AML, constitutive phosphorylation of STAT5, a marker of tyrosine kinase activation, is present in the majority of AML samples indicating that as yet unidentified tyrosine kinases can be aberrantly activated and contribute to leukemogenesis. Efforts to identify activating tyrosine kinase mutations using high-throughput sequencing have identi

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Zuchman, Rina, Roni Koren, and Benjamin A. Horwitz. "Developmental Roles of the Hog1 Protein Phosphatases of the Maize Pathogen Cochliobolus heterostrophus." Journal of Fungi 7, no. 2 (2021): 83. http://dx.doi.org/10.3390/jof7020083.

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Protein phosphorylation cascades are universal in cell signaling. While kinome diversity allows specific phosphorylation events, relatively few phosphatases dephosphorylate key signaling proteins. Fungal mitogen activated protein kinases (MAPK), in contrast to their mammalian counterparts, often show detectable basal phosphorylation levels. Dephosphorylation, therefore, could act as a signal. In Cochliobolus heterostrophus, the Dothideomycete causing Southern corn leaf blight, ferulic acid (FA)—an abundant phenolic found in plant host cell walls—acts as a signal to rapidly dephosphorylate the

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Zhang, Jinghui, Charles Mullighan, Richard Harvey, et al. "Lack of Somatic Sequence Mutations In Protein Tyrosine Kinase Genes Other Than the JAK Kinase Family In High Risk B-Precursor Childhood Acute Lymphoblastic Leukemia (ALL): A Report From the Children's Oncology Group (COG) High-Risk (HR) ALL TARGET Project." Blood 116, no. 21 (2010): 2752. http://dx.doi.org/10.1182/blood.v116.21.2752.2752.

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Abstract Abstract 2752 Introduction: We recently identified a poor prognostic subgroup of pediatric BCR-ABL1 negative ALL patients characterized by deletion of IKZF1 (encoding the lymphoid transcription factor IKAROS) and a gene expression signature similar to BCR-ABL1 positive ALL, raising the possibility of activated tyrosine kinase signaling within this leukemia subtype. Targeted sequencing revealed activating sequence mutations in the Janus tyrosine kinases (JAK1 (N=3), JAK2 (N=17) and JAK3 (N=1)) in 21 of 187 (11.2%) BCR-ABL1 negative, high-risk pediatric ALL cases. All 21 cases with JAK

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Wang, Michelle, Xiaohong Zhao, Huijuan Jiang, et al. "CDK9 As a New Therapeutic Vulnerability for Ibrutinib Resistance Mantle Cell Lymphoma (MCL)." Blood 136, Supplement 1 (2020): 34–35. http://dx.doi.org/10.1182/blood-2020-141386.

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MCL is an aggressive B-cell lymphoma with poor prognosis due to emergence of drug resistant populations and lymphoma progression. Ibrutinib is a bruton's tyrosine kinase (BTK) inhibitor that was shown to have high response rates in MCL patients. However, as the use of this drug continues to grow in MCL and other B-cell lymphomas, emergence of resistance and fatal progression are of increasing clinical concern. Currently the mechanisms driving IR are poorly understood and no recurrent driver mutations have been identified in MCL. We have modeled acquired resistance to ibrutinib and implemented

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Verkhivker, Gennady M. "Computational proteomics of biomolecular interactions in the sequence and structure space of the tyrosine kinome: Deciphering the molecular basis of the kinase inhibitors selectivity." Proteins: Structure, Function, and Bioinformatics 66, no. 4 (2006): 912–29. http://dx.doi.org/10.1002/prot.21287.

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Arnaldez, Fernanda Irene, Choh L. Yeung, Carly J. Smith, Natasha Caplen, and Lee J. Helman. "Identification of TNK2 as a critical kinase in rhabdomyosarcoma through a loss of function shRNA screen." Journal of Clinical Oncology 30, no. 15_suppl (2012): 9511. http://dx.doi.org/10.1200/jco.2012.30.15_suppl.9511.

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9511 Background: Rhabdomyosarcoma is the most common pediatric soft tissue sarcoma. Embryonal rhabdomyosarcomas (ERMS) are characterized by 11p15 LOH while alveolar rhabdomyosarcomas harbor a translocation between PAX3 or PAX7 and FOXO1. Relapsed or metastatic disease has a 5-year survival rate of 25%. Methods: We sought to identify critical genes for rhabdomyosarcoma cell growth and survival. We performed a loss-of-function shRNA screen where a library of 15,000 shRNAs was introduced in RH30 (ARMS) and RD (ERMS) cells engineered to express the bacterial tetracycline repressor in a tet-on syst

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