Experts and Doctors on protein kinase inhibitors in New York, United States

Summary

Locale: New York, United States
Topic: protein kinase inhibitors

Top Publications

  1. He M, Capelletti M, Nafa K, Yun C, Arcila M, Miller V, et al. EGFR exon 19 insertions: a new family of sensitizing EGFR mutations in lung adenocarcinoma. Clin Cancer Res. 2012;18:1790-7 pubmed publisher
    ..While these mutations may be missed through the use of some mutation-specific assays, the addition of PCR product size analysis to multigene assays allows sensitive detection of both exon 19 insertion and deletion mutations. ..
  2. Siegelin M, Borczuk A. Epidermal growth factor receptor mutations in lung adenocarcinoma. Lab Invest. 2014;94:129-37 pubmed publisher
    ..In doing so, we will examine other oncogenic pathways whose status in tumor samples may impact therapeutic responses despite presence of activating EGFR mutations. ..
  3. Mukhopadhyay S, Frias M, Chatterjee A, Yellen P, Foster D. The Enigma of Rapamycin Dosage. Mol Cancer Ther. 2016;15:347-53 pubmed publisher
    ..Rapamycin and PA have opposite effects on mTOR whereby rapamycin destabilizes and PA stabilizes both mTOR complexes. In this review, we discuss the properties of rapamycin dosage in the context of anticancer therapeutics. ..
  4. Kawashima S, Takemoto A, Nurse P, Kapoor T. A chemical biology strategy to analyze rheostat-like protein kinase-dependent regulation. Chem Biol. 2013;20:262-71 pubmed publisher
    ..Our strategy is general and can be used to examine the functions of other molecular rheostats. ..
  5. Martínez Gil L, Alamares Sapuay J, Ramana Reddy M, Goff P, Premkumar Reddy E, Palese P. A small molecule multi-kinase inhibitor reduces influenza A virus replication by restricting viral RNA synthesis. Antiviral Res. 2013;100:29-37 pubmed publisher
    ..In addition, ON108110 also inhibits other viruses including vesicular stomatitis virus and Newcastle disease virus, suggesting that this compound may represent a novel class of antiviral agents. ..
  6. Liu V, White D, Zakowski M, Travis W, Kris M, Ginsberg M, et al. Pulmonary toxicity associated with erlotinib. Chest. 2007;132:1042-4 pubmed
    ..Similar to reports in patients receiving gefitinib, those with pathologic findings of UIP on resected lung specimens or known pulmonary fibrosis may be at particular risk for erlotinib pulmonary toxicity. ..
  7. Peters U, Cherian J, Kim J, Kwok B, Kapoor T. Probing cell-division phenotype space and Polo-like kinase function using small molecules. Nat Chem Biol. 2006;2:618-26 pubmed
    ..Further testing of compounds based on 'privileged scaffolds', such as the DAP scaffold, could lead to new cell-division probes and antimitotic agents. ..
  8. Pratilas C, Solit D. Targeting the mitogen-activated protein kinase pathway: physiological feedback and drug response. Clin Cancer Res. 2010;16:3329-34 pubmed publisher
  9. Elkabets M, Vora S, Juric D, Morse N, Mino Kenudson M, Muranen T, et al. mTORC1 inhibition is required for sensitivity to PI3K p110α inhibitors in PIK3CA-mutant breast cancer. Sci Transl Med. 2013;5:196ra99 pubmed publisher
    ..Our findings suggest that simultaneous administration of mTORC1 inhibitors may enhance the clinical activity of p110α-targeted drugs and delay the appearance of resistance. ..

More Information

Publications206 found, 100 shown here

  1. Pernis A, Ricker E, Weng C, Rozo C, Yi W. Rho Kinases in Autoimmune Diseases. Annu Rev Med. 2016;67:355-74 pubmed publisher
    ..Given the potential promise of the ROCKs as therapeutic targets, we also outline the approaches that could be employed to inhibit the ROCKs in autoimmune disorders. ..
  2. Li W, Miller W. Role of the activation loop tyrosines in regulation of the insulin-like growth factor I receptor-tyrosine kinase. J Biol Chem. 2006;281:23785-91 pubmed
    ..The results demonstrate that Tyr1135 plays a particularly important role in stabilizing the autoinhibited conformation of the activation loop, while Tyr1136 plays the key role in stabilizing the open, activated conformation of IGF1R. ..
  3. Belum V, Fontanilla Patel H, Lacouture M, Rodeck U. Skin toxicity of targeted cancer agents: mechanisms and intervention. Future Oncol. 2013;9:1161-70 pubmed publisher
    ..Emergent insights into the pathomechanisms involved and the use of this knowledge base to alleviate cutaneous adverse events are discussed. ..
  4. Zhao Z, Liu Q, Bliven S, Xie L, Bourne P. Determining Cysteines Available for Covalent Inhibition Across the Human Kinome. J Med Chem. 2017;60:2879-2889 pubmed publisher
    ..This study provides new insights into cysteine reactivity and preference which is important for the prospective development of covalent kinase inhibitors. ..
  5. Ozawa T, Brennan C, Wang L, Squatrito M, Sasayama T, Nakada M, et al. PDGFRA gene rearrangements are frequent genetic events in PDGFRA-amplified glioblastomas. Genes Dev. 2010;24:2205-18 pubmed publisher
    ..These results suggest the possibility that these PDGFRA mutants behave as oncogenes in this subset of gliomas, and that the prevalence of such rearrangements may have been considerably underestimated. ..
  6. Gao S, Chang Q, Mao N, Daly L, Vogel R, Chan T, et al. JAK2 inhibition sensitizes resistant EGFR-mutant lung adenocarcinoma to tyrosine kinase inhibitors. Sci Signal. 2016;9:ra33 pubmed publisher
    ..Our results reveal a mechanism whereby JAK2 inhibition overcomes acquired resistance to EGFR inhibitors and support the use of combination therapy with JAK and EGFR inhibitors for the treatment of EGFR-dependent NSCLC. ..
  7. Hoffmann H, Palese P, Shaw M. Modulation of influenza virus replication by alteration of sodium ion transport and protein kinase C activity. Antiviral Res. 2008;80:124-34 pubmed publisher
    ..Furthermore, we raise the possibility that compounds that result in increased viral titers may be beneficial for boosting the production of tissue culture-grown influenza vaccines. ..
  8. Kuntz K, O Connell M. The G(2) DNA damage checkpoint: could this ancient regulator be the Achilles heel of cancer?. Cancer Biol Ther. 2009;8:1433-9 pubmed
    ..It will also discuss the present status and future of potential cancer therapies aimed at inactivating this signaling pathway in tumor cells. ..
  9. Koppikar P, Abdel Wahab O, Hedvat C, Marubayashi S, Patel J, Goel A, et al. Efficacy of the JAK2 inhibitor INCB16562 in a murine model of MPLW515L-induced thrombocytosis and myelofibrosis. Blood. 2010;115:2919-27 pubmed publisher
    ..However, we did not observe a decrease in the size of the malignant clone in the bone marrow of treated mice at the end of therapy, which suggests that JAK2 inhibitor therapy, by itself, was not curative in this MPN model. ..
  10. Korets S, Musa F, Curtin J, Blank S, Schneider R. Dual mTORC1/2 inhibition in a preclinical xenograft tumor model of endometrial cancer. Gynecol Oncol. 2014;132:468-73 pubmed publisher
    ..Based on this study, mTORC1/2 kinase inhibitors warrant further investigation as a potential treatment for endometrial cancer. ..
  11. Motzer R, Hutson T, Tomczak P, Michaelson M, Bukowski R, Rixe O, et al. Sunitinib versus interferon alfa in metastatic renal-cell carcinoma. N Engl J Med. 2007;356:115-24 pubmed
    ..gov numbers, NCT00098657 and NCT00083889 [ClinicalTrials.gov]). ..
  12. Poulikakos P, Persaud Y, Janakiraman M, Kong X, Ng C, Moriceau G, et al. RAF inhibitor resistance is mediated by dimerization of aberrantly spliced BRAF(V600E). Nature. 2011;480:387-90 pubmed publisher
  13. Akinleye A, Chen Y, Mukhi N, Song Y, Liu D. Ibrutinib and novel BTK inhibitors in clinical development. J Hematol Oncol. 2013;6:59 pubmed publisher
  14. Yu H, Sima C, Huang J, Solomon S, Rimner A, Paik P, et al. Local therapy with continued EGFR tyrosine kinase inhibitor therapy as a treatment strategy in EGFR-mutant advanced lung cancers that have developed acquired resistance to EGFR tyrosine kinase inhibitors. J Thorac Oncol. 2013;8:346-51 pubmed publisher
    ..Local therapy followed by continued treatment with an EGFR TKI is well tolerated and associated with long PFS and OS. Further study in selected individuals in the context of other systemic options is required. ..
  15. Karoulia Z, Gavathiotis E, Poulikakos P. New perspectives for targeting RAF kinase in human cancer. Nat Rev Cancer. 2017;17:676-691 pubmed publisher
  16. Chen Y, Rodrik V, Foster D. Alternative phospholipase D/mTOR survival signal in human breast cancer cells. Oncogene. 2005;24:672-9 pubmed
    ..The data presented here identify an alternative survival signal that is dependent on PLD and mTOR and is active in a breast cancer cell line where the PI3K survival pathway is not active. ..
  17. Obligado S, Ibraghimov Beskrovnaya O, Zuk A, Meijer L, Nelson P. CDK/GSK-3 inhibitors as therapeutic agents for parenchymal renal diseases. Kidney Int. 2008;73:684-90 pubmed
    ..Novel biomarkers of therapy are aiding the process of drug development. This review will highlight these advancements in renal therapeutics. ..
  18. Chiu C, Puente N, Grandes P, Castillo P. Dopaminergic modulation of endocannabinoid-mediated plasticity at GABAergic synapses in the prefrontal cortex. J Neurosci. 2010;30:7236-48 pubmed publisher
    ..Facilitation of eCB-LTD may be one mechanism by which DA modulates neuronal activity in the PFC and regulates PFC-mediated behavior in vivo. ..
  19. Peterson S, Li Y, Wu Baer F, Chait B, Baer R, Yan H, et al. Activation of DSB processing requires phosphorylation of CtIP by ATR. Mol Cell. 2013;49:657-67 pubmed publisher
    ..Chromatin binding by modified CtIP precedes extensive resection and full checkpoint activation...
  20. Cohen S, Koenig A, Wang L, Kwok K, Mebus C, Riese R, et al. Efficacy and safety of tofacitinib in US and non-US rheumatoid arthritis patients: pooled analyses of phase II and III. Clin Exp Rheumatol. 2016;34:32-6 pubmed
    ..Incidence rates for adverse events of special interest were similar between the US and ROW PII/PIII populations. Patients in the US achieved similar efficacy and safety with tofacitinib 5 and 10 mg BID compared with patients in ROW. ..
  21. Heidary N, Naik H, Burgin S. Chemotherapeutic agents and the skin: An update. J Am Acad Dermatol. 2008;58:545-70 pubmed publisher
    ..In addition, they should be able to formulate appropriate management strategies for these reactions. ..
  22. Leboeuf R, Baumgartner J, Benezra M, Malaguarnera R, Solit D, Pratilas C, et al. BRAFV600E mutation is associated with preferential sensitivity to mitogen-activated protein kinase kinase inhibition in thyroid cancer cell lines. J Clin Endocrinol Metab. 2008;93:2194-201 pubmed publisher
  23. Rodrik Outmezguine V, Chandarlapaty S, Pagano N, Poulikakos P, Scaltriti M, Moskatel E, et al. mTOR kinase inhibition causes feedback-dependent biphasic regulation of AKT signaling. Cancer Discov. 2011;1:248-59 pubmed publisher
    ..The addition of RTK inhibitors can prevent this reactivation of AKT signaling and cause profound cell death and tumor regression in vivo, highlighting the possible need for combinatorial approaches to block feedback-regulated pathways. ..
  24. Winthrop K, Curtis J, Lindsey S, Tanaka Y, Yamaoka K, Valdez H, et al. Herpes Zoster and Tofacitinib: Clinical Outcomes and the Risk of Concomitant Therapy. Arthritis Rheumatol. 2017;69:1960-1968 pubmed publisher
    ..Patients receiving treatment with tofacitinib and GCs appear to have a greater risk of developing HZ compared with patients receiving tofacitinib monotherapy without GCs. ..
  25. Bachow S, Lamanna N. Evolving Strategies for the Treatment of Chronic Lymphocytic Leukemia in the Upfront Setting. Curr Hematol Malig Rep. 2016;11:61-70 pubmed publisher
    ..Here, we review standard upfront therapies and new agents and combinations that are on the horizon for CLL. ..
  26. Wang Y, Zhou X, Oberoi K, Phelps R, COUWENHOVEN R, Sun M, et al. p38 Inhibition ameliorates skin and skull abnormalities in Fgfr2 Beare-Stevenson mice. J Clin Invest. 2012;122:2153-64 pubmed publisher
    ..The demonstration of a pathogenic role for p38 activation may lead to the development of therapeutic strategies for BSS and related conditions, such as acanthosis nigricans or craniosynostosis. ..
  27. Ambrosini G, Seelman S, Qin L, Schwartz G. The cyclin-dependent kinase inhibitor flavopiridol potentiates the effects of topoisomerase I poisons by suppressing Rad51 expression in a p53-dependent manner. Cancer Res. 2008;68:2312-20 pubmed publisher
    ..In conclusion, after DNA damage by Topo I poisons, flavopiridol targets homologous recombination through a p53-dependent down-regulation of Rad51, resulting in enhancement of apoptosis. ..
  28. Llovet J, Bruix J. Molecular targeted therapies in hepatocellular carcinoma. Hepatology. 2008;48:1312-27 pubmed publisher
    ..Ultimately, a molecular classification of HCC based on genome-wide investigations and identification of patient subclasses according to drug responsiveness will lead to a more personalized medicine. ..
  29. Benezra M, Hambardzumyan D, Penate Medina O, Veach D, Pillarsetty N, Smith Jones P, et al. Fluorine-labeled dasatinib nanoformulations as targeted molecular imaging probes in a PDGFB-driven murine glioblastoma model. Neoplasia. 2012;14:1132-43 pubmed
    ..18)F-SKI249380 is a PDGFR-selective tracer, which demonstrates improved delivery to PDGFB-driven high-grade gliomas and facilitates treatment planning when coupled with nanoformulations and quantitative PET imaging approaches. ..
  30. Reddy M, Akula B, Jatiani S, Vasquez Del Carpio R, Billa V, Mallireddigari M, et al. Discovery of 2-(1H-indol-5-ylamino)-6-(2,4-difluorophenylsulfonyl)-8-methylpyrido[2,3-d]pyrimidin-7(8H)-one (7ao) as a potent selective inhibitor of Polo like kinase 2 (PLK2). Bioorg Med Chem. 2016;24:521-44 pubmed publisher
    ..Here, we describe the synthesis, structure activity relationship, in vitro kinase specificity and biological activity of the lead compound, 7ao. ..
  31. Regales L, Balak M, Gong Y, Politi K, Sawai A, Le C, et al. Development of new mouse lung tumor models expressing EGFR T790M mutants associated with clinical resistance to kinase inhibitors. PLoS ONE. 2007;2:e810 pubmed
    ..The models should also be useful for developing improved therapies for patients with lung cancers harboring EGFR(T790M) alone or in conjunction with drug-sensitive EGFR kinase domain mutations. ..
  32. Gordon J, Udeh U, Doobay K, Magro C, Wildman H, Davids M, et al. Imatinib mesylate (Gleevec™) in the treatment of diffuse cutaneous systemic sclerosis: results of a 24-month open label, extension phase, single-centre trial. Clin Exp Rheumatol. 2014;32:S-189-93 pubmed
    ..002). This study demonstrates long-term safety and tolerability of imatinib in a substantial proportion of patients with dcSSc. This is important in evaluating the relevance of this therapy in a chronic disease such as SSc. ..
  33. Eng J, Woo K, Sima C, Plodkowski A, Hellmann M, Chaft J, et al. Impact of Concurrent PIK3CA Mutations on Response to EGFR Tyrosine Kinase Inhibition in EGFR-Mutant Lung Cancers and on Prognosis in Oncogene-Driven Lung Adenocarcinomas. J Thorac Oncol. 2015;10:1713-9 pubmed publisher
    ..There was no evidence that clinical benefit from EGFR TKI monotherapy is affected by a concurrent PIK3CA mutation in EGFR-mutant lung cancers. ..
  34. Xiong Y, Hannon G, Zhang H, Casso D, Kobayashi R, Beach D. p21 is a universal inhibitor of cyclin kinases. Nature. 1993;366:701-4 pubmed
    ..Furthermore, overexpression of p21 inhibits the proliferation of mammalian cells. Our results indicate that p21 may be a universal inhibitor of cyclin kinases. ..
  35. Kubo T, Piperdi S, Rosenblum J, Antonescu C, Chen W, Kim H, et al. Platelet-derived growth factor receptor as a prognostic marker and a therapeutic target for imatinib mesylate therapy in osteosarcoma. Cancer. 2008;112:2119-29 pubmed publisher
  36. Malumbres M, Perez de Castro I, Santos J, Perez Olle R, Fernandez Piqueras J, Pellicer A. An AC-repeat adjacent to mouse Cdkn2B allows the detection of specific allelic losses in the p15INK4b and p16INK4a tumor suppressor genes. Mamm Genome. 1998;9:183-5 pubmed
    ..Since the allelic losses can be detected by a simple PCR amplification, this AC-repetitive sequence is specially useful as a genetic marker for these Cdkn2 genes and specifically for the p15INK4b cell cycle inhibitor. ..
  37. Lacouture M, Schadendorf D, Chu C, Uttenreuther Fischer M, Stammberger U, O BRIEN D, et al. Dermatologic adverse events associated with afatinib: an oral ErbB family blocker. Expert Rev Anticancer Ther. 2013;13:721-8 pubmed publisher
    ..This article summarizes current data on the dermatologic AEs associated with afatinib treatment across the clinical trial program, and provides strategies for their effective management. ..
  38. Gocher A, Azabdaftari G, Euscher L, Dai S, Karacosta L, Franke T, et al. Akt activation by Ca2+/calmodulin-dependent protein kinase kinase 2 (CaMKK2) in ovarian cancer cells. J Biol Chem. 2017;292:14188-14204 pubmed publisher
    ..CaMKK2 knockdown potentiated the effects of the chemotherapeutic drugs carboplatin and PX-866 to reduce proliferation and survival of OVCa cells. ..
  39. Bick M, Lamour V, Rajashankar K, Gordiyenko Y, Robinson C, Darst S. How to switch off a histidine kinase: crystal structure of Geobacillus stearothermophilus KinB with the inhibitor Sda. J Mol Biol. 2009;386:163-77 pubmed publisher
  40. Vivanco I, Rohle D, Versele M, Iwanami A, Kuga D, Oldrini B, et al. The phosphatase and tensin homolog regulates epidermal growth factor receptor (EGFR) inhibitor response by targeting EGFR for degradation. Proc Natl Acad Sci U S A. 2010;107:6459-64 pubmed publisher
    ..Our study identifies a critical role for PTEN in EGFR signal termination and suggests that more potent EGFR inhibition should overcome resistance caused by PI3K pathway activation. ..
  41. Yu H, Arcila M, Rekhtman N, Sima C, Zakowski M, Pao W, et al. Analysis of tumor specimens at the time of acquired resistance to EGFR-TKI therapy in 155 patients with EGFR-mutant lung cancers. Clin Cancer Res. 2013;19:2240-7 pubmed publisher
    ..More comprehensive methods to characterize molecular alterations in this setting are needed to improve our understanding of acquired resistance to EGFR-TKIs. ..
  42. Cheng S, Ma J, Guo A, Lu P, Leonard J, Coleman M, et al. BTK inhibition targets in vivo CLL proliferation through its effects on B-cell receptor signaling activity. Leukemia. 2014;28:649-57 pubmed publisher
    ..Our findings suggest that the cell proliferation is one of the essential properties of CLL. Blocking cell proliferation via inhibition of BTK-mediated signaling may contribute to clinical responses in ibrutinib-treated patients. ..
  43. Smolen J, Landewe R, Bijlsma J, Burmester G, Chatzidionysiou K, Dougados M, et al. EULAR recommendations for the management of rheumatoid arthritis with synthetic and biological disease-modifying antirheumatic drugs: 2016 update. Ann Rheum Dis. 2017;76:960-977 pubmed publisher
  44. Pedranzini L, Dechow T, Berishaj M, Comenzo R, Zhou P, Azare J, et al. Pyridone 6, a pan-Janus-activated kinase inhibitor, induces growth inhibition of multiple myeloma cells. Cancer Res. 2006;66:9714-21 pubmed
    ..Thus, P6 is a more sensitive and specific inhibitor of JAK-STAT3 activity compared with AG490 and potently inhibited the growth of primary myeloma cells and myeloma-derived cell lines grown on BMSCs. ..
  45. Landau H, McNeely S, Nair J, Comenzo R, Asai T, Friedman H, et al. The checkpoint kinase inhibitor AZD7762 potentiates chemotherapy-induced apoptosis of p53-mutated multiple myeloma cells. Mol Cancer Ther. 2012;11:1781-8 pubmed publisher
    ..These data provide a rationale for testing these combinations in patients with relapsed and/or refractory multiple myeloma. ..
  46. Gomes E, Papa L, Hao T, Rockwell P. The VEGFR2 and PKA pathways converge at MEK/ERK1/2 to promote survival in serum deprived neuronal cells. Mol Cell Biochem. 2007;305:179-90 pubmed
    ..Taken together, these findings suggested that PKA and VEGFR2 converge at the MEK/ERK1/2 pathway to protect serum starved neuronal cells from a caspase-dependent cell death. ..
  47. Ramalingam S, Jänne P, Mok T, O Byrne K, Boyer M, Von Pawel J, et al. Dacomitinib versus erlotinib in patients with advanced-stage, previously treated non-small-cell lung cancer (ARCHER 1009): a randomised, double-blind, phase 3 trial. Lancet Oncol. 2014;15:1369-78 pubmed publisher
    ..Further study of irreversible EGFR inhibitors should be restricted to patients with activating EGFR mutations. Pfizer. ..
  48. Tu S, Chi A, Lim S, Cui G, Dubeykovskaya Z, Ai W, et al. Gastrin regulates the TFF2 promoter through gastrin-responsive cis-acting elements and multiple signaling pathways. Am J Physiol Gastrointest Liver Physiol. 2007;292:G1726-37 pubmed
    ..Regulation of TFF2 by gastrin may play a role in the maintenance and repair of the gastrointestinal mucosa. ..
  49. Song Z, Lu P, Furman R, Leonard J, Martin P, Tyrell L, et al. Activities of SYK and PLCgamma2 predict apoptotic response of CLL cells to SRC tyrosine kinase inhibitor dasatinib. Clin Cancer Res. 2010;16:587-99 pubmed publisher
    ..The study further implicates that SYK might serve as a more effective therapeutic target in CLL treatment. ..
  50. Novosyadlyy R, Kurshan N, Lann D, Vijayakumar A, Yakar S, LeRoith D. Insulin-like growth factor-I protects cells from ER stress-induced apoptosis via enhancement of the adaptive capacity of endoplasmic reticulum. Cell Death Differ. 2008;15:1304-17 pubmed publisher
  51. Dasgupta B, Muller W. Endothelial Src kinase regulates membrane recycling from the lateral border recycling compartment during leukocyte transendothelial migration. Eur J Immunol. 2008;38:3499-507 pubmed publisher
  52. Poulikakos P, Zhang C, Bollag G, Shokat K, Rosen N. RAF inhibitors transactivate RAF dimers and ERK signalling in cells with wild-type BRAF. Nature. 2010;464:427-30 pubmed publisher
    ..In agreement with this prediction, RAF inhibitors do not inhibit ERK signalling in cells that coexpress BRAF(V600E) and mutant RAS. ..
  53. Miller V, Riely G, Zakowski M, Li A, Patel J, Heelan R, et al. Molecular characteristics of bronchioloalveolar carcinoma and adenocarcinoma, bronchioloalveolar carcinoma subtype, predict response to erlotinib. J Clin Oncol. 2008;26:1472-8 pubmed publisher
    ..These data suggest that histologic subtype and molecular characteristics should be reported in clinical trials in NSCLC using EGFR-directed therapy. ..
  54. Lecanda J, Ganapathy V, D Aquino Ardalan C, Evans B, Cadacio C, Ayala A, et al. TGFbeta prevents proteasomal degradation of the cyclin-dependent kinase inhibitor p27kip1 for cell cycle arrest. Cell Cycle. 2009;8:742-56 pubmed
    ..The TGFbeta/p27 axis might provide novel therapeutic targets for cancer. ..
  55. Yazici Y, Regens A. Promising new treatments for rheumatoid arthritis - the kinase inhibitors. Bull NYU Hosp Jt Dis. 2011;69:233-7 pubmed
    ..This paper will review some of the relevant published data for these agents and discuss where they may be placed in our treatment options for RA. ..
  56. Hu W, Sung T, Jessen B, Thibault S, Finkelstein M, Khan N, et al. Mechanistic Investigation of Bone Marrow Suppression Associated with Palbociclib and its Differentiation from Cytotoxic Chemotherapies. Clin Cancer Res. 2016;22:2000-8 pubmed publisher
    ..These results shed light on the mechanism and support risk management of palbociclib-induced bone marrow toxicity in the clinic. ..
  57. Baselga J, Morales S, Awada A, Blum J, Tan A, Ewertz M, et al. A phase II study of combined ridaforolimus and dalotuzumab compared with exemestane in patients with estrogen receptor-positive breast cancer. Breast Cancer Res Treat. 2017;163:535-544 pubmed publisher
    ..Therefore, the combination is not being further pursued. ..
  58. Agaram N, Laquaglia M, Ustun B, Guo T, Wong G, Socci N, et al. Molecular characterization of pediatric gastrointestinal stromal tumors. Clin Cancer Res. 2008;14:3204-15 pubmed publisher
    ..In vitro drug screening showed that second-generation kinase inhibitors may provide greater clinical benefit in pediatric GIST. ..
  59. Bachleitner Hofmann T, Sun M, Chen C, Liska D, Zeng Z, Viale A, et al. Antitumor activity of SNX-2112, a synthetic heat shock protein-90 inhibitor, in MET-amplified tumor cells with or without resistance to selective MET Inhibition. Clin Cancer Res. 2011;17:122-33 pubmed publisher
    ..Our study provides evidence for the efficacy of HSP-90 inhibition in MET-amplified cancer cells, particularly when MET kinase inhibitor resistance has emerged. ..
  60. Wu J, Zhu A. Targeting insulin-like growth factor axis in hepatocellular carcinoma. J Hematol Oncol. 2011;4:30 pubmed publisher
    ..IGF axis is increasingly recognized as one of the most relevant pathways in HCC and agents targeting this axis can potentially play an important role in the treatment of HCC. ..
  61. Janjigian Y, Viola Villegas N, Holland J, Divilov V, Carlin S, Gomes Dagama E, et al. Monitoring afatinib treatment in HER2-positive gastric cancer with 18F-FDG and 89Zr-trastuzumab PET. J Nucl Med. 2013;54:936-43 pubmed publisher
    ..Afatinib demonstrated antitumor activity in HER2-positive gastric cancer in vivo. (89)Zr-trastuzumab PET specifically delineated HER2-positive gastric cancer and can be used to measure the pharmacodynamic effects of afatinib. ..
  62. Ausoni S, Boscolo Rizzo P, Singh B, da Mosto M, Spinato G, Tirelli G, et al. Targeting cellular and molecular drivers of head and neck squamous cell carcinoma: current options and emerging perspectives. Cancer Metastasis Rev. 2016;35:413-26 pubmed publisher
  63. Ho A, Musi E, Ambrosini G, Nair J, Deraje Vasudeva S, de Stanchina E, et al. Impact of combined mTOR and MEK inhibition in uveal melanoma is driven by tumor genotype. PLoS ONE. 2012;7:e40439 pubmed publisher
    ..These results suggest that the clinical efficacy of combined MEK and mTOR kinase inhibition will be determined by tumor genotype, and that BRAF mutant malignancies will be particularly susceptible to this strategy. ..
  64. Juric D, Krop I, Ramanathan R, Wilson T, Ware J, Sanabria Bohorquez S, et al. Phase I Dose-Escalation Study of Taselisib, an Oral PI3K Inhibitor, in Patients with Advanced Solid Tumors. Cancer Discov. 2017;7:704-715 pubmed publisher
    ..i>Cancer Discov; 7(7); 704-15. ©2017 AACR.See related commentary by Rodon and Tabernero, p. 666This article is highlighted in the In This Issue feature, p. 653. ..
  65. Chmielecki J, Foo J, Oxnard G, Hutchinson K, Ohashi K, Somwar R, et al. Optimization of dosing for EGFR-mutant non-small cell lung cancer with evolutionary cancer modeling. Sci Transl Med. 2011;3:90ra59 pubmed publisher
    ..This modeling predicted alternative therapeutic strategies that could prolong the clinical benefit of TKIs against EGFR-mutant NSCLCs by delaying the development of resistance. ..
  66. Bruix J, Takayama T, Mazzaferro V, Chau G, Yang J, Kudo M, et al. Adjuvant sorafenib for hepatocellular carcinoma after resection or ablation (STORM): a phase 3, randomised, double-blind, placebo-controlled trial. Lancet Oncol. 2015;16:1344-54 pubmed publisher
    ..Our data indicate that sorafenib is not an effective intervention in the adjuvant setting for hepatocellular carcinoma following resection or ablation. ..
  67. Wendel H, de Stanchina E, Fridman J, Malina A, Ray S, Kogan S, et al. Survival signalling by Akt and eIF4E in oncogenesis and cancer therapy. Nature. 2004;428:332-7 pubmed
  68. Bean J, Brennan C, Shih J, Riely G, Viale A, Wang L, et al. MET amplification occurs with or without T790M mutations in EGFR mutant lung tumors with acquired resistance to gefitinib or erlotinib. Proc Natl Acad Sci U S A. 2007;104:20932-7 pubmed
    ..Taken together, these data suggest that MET amplification occurs independently of EGFR(T790M) mutations and that MET may be a clinically relevant therapeutic target for some patients with acquired resistance to gefitinib or erlotinib. ..
  69. Sawai A, Chandarlapaty S, Greulich H, Gonen M, Ye Q, Arteaga C, et al. Inhibition of Hsp90 down-regulates mutant epidermal growth factor receptor (EGFR) expression and sensitizes EGFR mutant tumors to paclitaxel. Cancer Res. 2008;68:589-96 pubmed publisher
  70. Ang C, O Reilly E, Abou Alfa G. Targeted agents and systemic therapy in hepatocellular carcinoma. Recent Results Cancer Res. 2013;190:225-46 pubmed publisher
    ..Several pathways are now implicated in hepatocarcinogenesis and agents that target these pathways continue to be developed. ..
  71. Bachleitner Hofmann T, Sun M, Chen C, Tang L, Song L, Zeng Z, et al. HER kinase activation confers resistance to MET tyrosine kinase inhibition in MET oncogene-addicted gastric cancer cells. Mol Cancer Ther. 2008;7:3499-508 pubmed publisher
  72. Zhao Z, Xie L, Bourne P. Insights into the binding mode of MEK type-III inhibitors. A step towards discovering and designing allosteric kinase inhibitors across the human kinome. PLoS ONE. 2017;12:e0179936 pubmed publisher
    ..Subsequently, we screened and predicted allosteric binding sites across the human kinome, suggesting other kinases as potential targets suitable for type-III inhibitors. ..
  73. Rybin V, Guo J, Steinberg S. Protein kinase D1 autophosphorylation via distinct mechanisms at Ser744/Ser748 and Ser916. J Biol Chem. 2009;284:2332-43 pubmed publisher
    ..Rather, autophosphorylation at Ser916 is required for subsequent autophosphorylation at Ser748. Finally, this study exposes a novel role for Ser916 and/or Ser748 autophosphorylation to terminate the cellular PKD1 signaling response. ..
  74. Cai J, Hong Y, Weng C, Tan C, Imperato McGinley J, Zhu Y. Androgen stimulates endothelial cell proliferation via an androgen receptor/VEGF/cyclin A-mediated mechanism. Am J Physiol Heart Circ Physiol. 2011;300:H1210-21 pubmed publisher
  75. Hewing N, Weskamp G, Vermaat J, Farage E, Glomski K, Swendeman S, et al. Intravitreal injection of TIMP3 or the EGFR inhibitor erlotinib offers protection from oxygen-induced retinopathy in mice. Invest Ophthalmol Vis Sci. 2013;54:864-70 pubmed publisher
  76. Wang L, Ko C, Meyers E, Pedroja B, Pelaez N, Bernstein A. Concentration-dependent effects of transforming growth factor ?1 on corneal wound healing. Mol Vis. 2011;17:2835-46 pubmed
    ..Together, our data demonstrate that low concentrations of TGF?1 promote p38MAPK activation that is a key to HCF migration, suggesting that a low concentration of TGF? may be useful in treating non-healing corneal wounds. ..
  77. Krepler C, Xiao M, Sproesser K, Brafford P, Shannan B, Beqiri M, et al. Personalized Preclinical Trials in BRAF Inhibitor-Resistant Patient-Derived Xenograft Models Identify Second-Line Combination Therapies. Clin Cancer Res. 2016;22:1592-602 pubmed publisher
    ..These studies provide evidence for biomarker development to appropriately select personalized therapies of patients and avoid treatment failures. See related commentary by Hartsough and Aplin, p. 1550. ..
  78. Dickler M, Cobleigh M, Miller K, Klein P, Winer E. Efficacy and safety of erlotinib in patients with locally advanced or metastatic breast cancer. Breast Cancer Res Treat. 2009;115:115-21 pubmed publisher
    ..Erlotinib had minimal activity in unselected previously treated women with advanced breast cancer. Predictive factors are needed to identify breast cancer patients who may derive benefit from erlotinib treatment. ..
  79. Yuan A, Kurtz S, Barysauskas C, Pilotte A, Wagner A, Treister N. Oral adverse events in cancer patients treated with VEGFR-directed multitargeted tyrosine kinase inhibitors. Oral Oncol. 2015;51:1026-1033 pubmed publisher
    ..Oral dysesthesia is more commonly associated with VR-TKIs than with bevacizumab or imatinib. Management is largely empirical and requires further investigation. ..
  80. Barr P, Brown J, Hillmen P, O Brien S, Barrientos J, Reddy N, et al. Impact of ibrutinib dose adherence on therapeutic efficacy in patients with previously treated CLL/SLL. Blood. 2017;129:2612-2615 pubmed publisher
    ..The trial was registered at www.clinicaltrials.gov as #NCT01578707. ..
  81. Serrano M, Hannon G, Beach D. A new regulatory motif in cell-cycle control causing specific inhibition of cyclin D/CDK4. Nature. 1993;366:704-7 pubmed
    ..p16 seems to act in a regulatory feedback circuit with CDK4, D-type cyclins and retinoblastoma protein. ..
  82. Knight Z, Lin H, Shokat K. Targeting the cancer kinome through polypharmacology. Nat Rev Cancer. 2010;10:130-7 pubmed publisher
    ..If it is necessary to inhibit multiple kinases, how do we choose which ones? In this Opinion article, we discuss some of the strategies that are currently being used to identify new therapeutic combinations of kinase targets. ..
  83. Shan Y, Eastwood M, Zhang X, Kim E, Arkhipov A, Dror R, et al. Oncogenic mutations counteract intrinsic disorder in the EGFR kinase and promote receptor dimerization. Cell. 2012;149:860-70 pubmed publisher
    ..We also find that phosphorylation of EGFR kinase domain at Tyr845 may suppress the intrinsic disorder, suggesting a molecular mechanism for autonomous EGFR signaling. ..
  84. Diamond E, Durham B, Haroche J, Yao Z, Ma J, Parikh S, et al. Diverse and Targetable Kinase Alterations Drive Histiocytic Neoplasms. Cancer Discov. 2016;6:154-65 pubmed publisher
    ..Refractory patients with MAP2K1- and ARAF-mutant histiocytoses had clinical responses to MEK inhibition and sorafenib, respectively, highlighting the importance of comprehensive genomic analysis of these disorders. ..
  85. Scaltriti M, Elkabets M, Baselga J. Molecular Pathways: AXL, a Membrane Receptor Mediator of Resistance to Therapy. Clin Cancer Res. 2016;22:1313-7 pubmed publisher
    ..The use of AXL inhibitors should be considered in the clinic. ..
  86. Cai W, He J, Zhu L, Chen X, Striker G, Vlassara H. AGE-receptor-1 counteracts cellular oxidant stress induced by AGEs via negative regulation of p66shc-dependent FKHRL1 phosphorylation. Am J Physiol Cell Physiol. 2008;294:C145-52 pubmed
    ..This represents a key mechanism by which AGER1 maintains cellular resistance against OS. Thus the decrease of AGER1 noted in aging and diabetes may further enhance OS and reduce innate antioxidant defenses. ..
  87. Jian J, Pelle E, Yang Q, Pernodet N, Maes D, Huang X. Iron sensitizes keratinocytes and fibroblasts to UVA-mediated matrix metalloproteinase-1 through TNF-? and ERK activation. Exp Dermatol. 2011;20:249-54 pubmed publisher
    ..We conclude that in addition to oestrogen deficiency, increased iron as a result of menopause could be a novel risk factor by sensitizing postmenopausal skin to solar irradiation. ..
  88. Cho S, Cosenza S, Pallela V, Panda G, Reddy M, Reddy E, et al. Determination of the glucuronide metabolite of ON 013100, a benzylstyrylsulfone antineoplastic drug, in colon cancer cells using LC/MS/MS. J Pharm Biomed Anal. 2013;75:138-44 pubmed publisher
    ..41 ?g/ml (0 h) to 0.06 ?g/ml (9 h). The corresponding concentrations of the intact drug in the drug-sensitive cells were from 2.88 ?g/ml to 0.94 ?g/ml. ..
  89. Vivanco I, Mellinghoff I. Epidermal growth factor receptor inhibitors in oncology. Curr Opin Oncol. 2010;22:573-8 pubmed publisher
    ..More complete inhibition of EGFR in tumor cells and more focused clinical drug development remain important goals toward further success with this class of anticancer agents. ..
  90. Soong G, Martin F, Chun J, Cohen T, Ahn D, Prince A. Staphylococcus aureus protein A mediates invasion across airway epithelial cells through activation of RhoA GTPase signaling and proteolytic activity. J Biol Chem. 2011;286:35891-8 pubmed publisher
    ..In vivo, blocking calpain activity impeded bacterial invasion into the lung parenchyma. Thus, S. aureus exploits multiple receptors available on the airway mucosal surface to facilitate invasion across epithelial barriers. ..
  91. Marron T, Martinez Gallo M, Yu J, Cunningham Rundles C. Toll-like receptor 4-, 7-, and 8-activated myeloid cells from patients with X-linked agammaglobulinemia produce enhanced inflammatory cytokines. J Allergy Clin Immunol. 2012;129:184-90.e1-4 pubmed publisher
  92. Georghiou G, Kleiner R, Pulkoski Gross M, Liu D, Seeliger M. Highly specific, bisubstrate-competitive Src inhibitors from DNA-templated macrocycles. Nat Chem Biol. 2012;8:366-74 pubmed publisher