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During the second quarter of 2018, the company incurred $273.3 million of tax expense, despite earning $41.7 million of income before taxes, as a result of the non-deductible acquired in-process research and development charges totaling $1,558 billion related to the acquisitions of ARMO Biosciences and AurKa Pharma.
United States-based Eli Lilly and Company has agreed to acquire AurKa Pharma, a Canada-based cancer drug developer, from TVM Capital Life Science, it was reported yesterday.
AurKa Pharma is a company established by investment advisory and fund managers group TVM Capital Life Science to develop oncology compound AK-01, an Aurora kinase A inhibitor that was originally discovered at Lilly.
Gene Full name Description Degree MAPK14 Mitogen-activated Down 68 protein kinase 14 ESR1 Estrogen receptor 1 Up 54 PTEN Phosphatase and Down 52 tensin homolog MTOR Mechanistic target Up 40 of rapamycin ATM ATM serine/threonine Up 35 kinase ICAM1 Intercellular Down 33 adhesion molecule 1 CD40 CD40 molecule Up 32 AURKA Aurora kinase A Down 31 PRKDC Protein kinase, DNA-activated, Down 29 catalytic polypeptide TK2 Thymidine kinase 2, Up 29 mitochondrial Degree was used for describing the importance of protein nodes in network.
It was found that expression of TP53 (HR 1.9, p = 31 x [10.sup.-7]) was associated with worse overall survival (OS) for glioma patients, as well as TOP2A (HR 4.4, p = 0), CDK1 (HR 4.8, p = 0), CCNB1 (HR 5.9, p = 0), CDC20 (HR 5.2, p = 0), CCNA2 (HR 5.1, p = 0), NDC80 (HR 5.8, p = 0), AURKA (HR 5.3, p = 0), BIRC5 (HR 5, p = 0), CCNB2 (HR 5.4, p = 0), KIF11 (HR 2.3, p = 15 x [10.sup.-10]), and MAD2L1 (HR 4.4, p = 0), while expression of PHLPP2 (HR 0.41, p = 1.3x [10.sup.-11]), DLG4 (HR 0.59, p = 35 x [10.sup.-5]), and MYC (HR 0.58, p = 2.1 x [10.sup.-5]) was associated with better overall survival (OS) for glioma patients (Figure 3).
The genes ESR, MUC1, AURKA, RAD51, TOP2A, ADAM17, SCGB2A2, KRT19, and EPCAM were expressed in most of the ONR samples.
Investigations on future therapies are under progress and possible targets include survivin [55, 56] and the AURKA (Aurora Kinase A) and NOTCH1 (Notch Homologue 1) oncogenic pathways [57]; modulation of gene expression with hypomethylating agents [58], immunoconjugates of anti-CD56 monoclonal antibodies [59], and inhibitors of tubule polymerization [42] are other possibilities.
Likewise, S315 of protein TP53 (P04637) can be catalyzed by AURKA, CDK1, CDK2, and so on [27, 28].
Corsini et al., "HIF-1 is involved in the negative regulation of AURKA expression in breast cancer cell lines under hypoxic conditions," Breast Cancer Research and Treatment, vol.
Drug Target Phase n Population [greater than or Erlotinib EGFR II 24 equal to] 18 y Refractory C-Raf [greater than or Sorafenib B-RafVEGFR2 II 12 equal to] 18 y C-Kit PDGFR Refractory Imatinib C-Kit PDGFR [greater than or VEGFR II 7 equal to] 10 y Refractory Dasatinib C-Kit SRC II 14 [greater than or equal to] 13 y Refractory Alisertib AURKA II 10 [greater than or equal to] 18 y Refractory Bevacizumab/ Angiogenesis/mTOR II -- [greater than or RAD001 equal to] 18 y Refractory Ganetespib/ Hsp90 I/II -- [greater than or Sirolimus mTOR equal to] 16 y Refractory Drug Outcome Results Ref.
Jin, "MicroRNA-1243p affects proliferation, migration and apoptosis of bladder cancer cells through targeting AURKA," Cancer Biomarkers, vol.