GLORIA

GEOMAR Library Ocean Research Information Access

X

Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
Filter
  • Wiley  (3)
  • Hara, Naofumi  (3)
  • Kubo, Toshio  (3)
  • 1
    Online Resource
    Online Resource
    VEGFR2 blockade augments the effects of tyrosine kinase inhibitors by inhibiting angiogenesis and oncogenic signaling in oncogene‐driven non‐small‐cell lung cancers
    Wiley ; 2021
    In:  Cancer Science Vol. 112, No. 5 ( 2021-05), p. 1853-1864
    Details
    In: Cancer Science, Wiley, Vol. 112, No. 5 ( 2021-05), p. 1853-1864
    Abstract: Molecular agents targeting the epidermal growth factor receptor ( EGFR )‐, anaplastic lymphoma kinase ( ALK )‐ or c‐ ros oncogene 1 ( ROS1 ) alterations have revolutionized the treatment of oncogene‐driven non‐small‐cell lung cancer (NSCLC). However, the emergence of acquired resistance remains a significant challenge, limiting the wider clinical success of these molecular targeted therapies. In this study, we investigated the efficacy of various molecular targeted agents, including erlotinib, alectinib, and crizotinib, combined with anti‐vascular endothelial growth factor receptor (VEGFR) 2 therapy. The combination of VEGFR2 blockade with molecular targeted agents enhanced the anti‐tumor effects of these agents in xenograft mouse models of EGFR‐ , ALK‐ , or ROS1 ‐altered NSCLC. The numbers of CD31‐positive blood vessels were significantly lower in the tumors of mice treated with an anti‐VEGFR2 antibody combined with molecular targeted agents compared with in those of mice treated with molecular targeted agents alone, implying the antiangiogenic effects of VEGFR2 blockade. Additionally, the combination therapies exerted more potent antiproliferative effects in vitro in EGFR‐ , ALK‐ , or ROS1 ‐altered NSCLC cells, implying that VEGFR2 inhibition also has direct anti‐tumor effects on cancer cells. Furthermore, VEGFR2 expression was induced following exposure to molecular targeted agents, implying the importance of VEGFR2 signaling in NSCLC patients undergoing molecular targeted therapy. In conclusion, VEGFR2 inhibition enhanced the anti‐tumor effects of molecular targeted agents in various oncogene‐driven NSCLC models, not only by inhibiting tumor angiogenesis but also by exerting direct antiproliferative effects on cancer cells. Hence, combination therapy with anti‐VEGFR2 antibodies and molecular targeted agents could serve as a promising treatment strategy for oncogene‐driven NSCLC.
    Type of Medium: Online Resource
    ISSN: 1347-9032 , 1349-7006
    URL: Issue
    URL: Article
    DOI: 10.1111/cas.v112.5
    DOI: 10.1111/cas.14801
    Language: English
    Publisher: Wiley
    Publication Date: 2021
    detail.hit.zdb_id: 2115647-5
    detail.hit.zdb_id: 2111204-6
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
  • 2
    Online Resource
    Online Resource
    Randomized study comparing mannitol with furosemide for the prevention of cisplatin‐induced renal toxicity in non‐small cell lung cancer: The OLCSG1406 trial
    Wiley ; 2021
    In:  Asia-Pacific Journal of Clinical Oncology Vol. 17, No. 1 ( 2021-02), p. 101-108
    Details
    In: Asia-Pacific Journal of Clinical Oncology, Wiley, Vol. 17, No. 1 ( 2021-02), p. 101-108
    Abstract: Evidence is lacking on the best standard method for forced diuresis to prevent cisplatin‐induced nephrotoxicity. We compared the cisplatin‐induced nephrotoxicity prevention effect of furosemide or mannitol in patients with advanced non‐small cell lung cancer. Methods Patients with advanced non‐small cell lung cancer suitable to receive cisplatin‐containing regimen were randomly assigned to receive furosemide or mannitol with appropriate hydration. The primary endpoint was the proportion of ≥ grade 1 serum creatinine elevation in the first cycle. Results The trial was terminated early with 44 (22 per arm) of the planned 66 patients because of slow accrual. Patients’ characteristics were well balanced with median baseline creatinine clearance of 98.0 and 95.1 mL/min in the furosemide and mannitol arms, respectively. In the first cycle, two (9%) and four (18%) patients developed grade 1 creatinine elevation ( P  = .66), respectively, despite no ≥ grade 2 toxicity. The median times to develop the worst creatinine score were 10 and 8 days, respectively. For all cycles, median times to recover to grade 0 were 56 and 20 days, respectively. The furosemide arm was characterized by relatively high urine output after cisplatin administration (900 vs 550 mL/h), low frequency of unplanned additional hydration (14% vs 32%), and high incidence of hyponatremia (18% and 5%) compared with the mannitol arm. Both arms showed similar progression‐free survival and overall survival. Conclusion The preventive effect of the two forced diuretics on cisplatin‐induced nephrotoxicity was not significantly different. However, the two diuretics have some distinct types of clinical presentations.
    Type of Medium: Online Resource
    ISSN: 1743-7555 , 1743-7563
    URL: Issue
    URL: Article
    DOI: 10.1111/ajco.v17.1
    DOI: 10.1111/ajco.13423
    Language: English
    Publisher: Wiley
    Publication Date: 2021
    detail.hit.zdb_id: 2187409-8
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
  • 3
    Online Resource
    Online Resource
    Efficacy of gilteritinib in comparison with alectinib for the treatment of ALK ‐rearranged non‐small cell lung cancer
    Wiley ; 2023
    In:  Cancer Science
    Details
    In: Cancer Science, Wiley
    Abstract: Gilteritinib is a multitarget tyrosine kinase inhibitor (TKI), approved for the treatment of FLT3‐mutant acute myeloid leukemia, with a broad range of activity against several tyrosine kinases including anaplastic lymphoma kinase (ALK). This study investigated the efficacy of gilteritinib against ALK ‐rearranged non‐small cell lung cancers (NSCLC). To this end, we assessed the effects of gilteritinib on cell proliferation, apoptosis, and acquired resistance responses in several ALK ‐rearranged NSCLC cell lines and mouse xenograft tumor models and compared its efficacy to alectinib, a standard ALK inhibitor. Gilteritinib was significantly more potent than alectinib, as it inhibited cell proliferation at a lower dose, with complete attenuation of growth observed in several ALK ‐rearranged NSCLC cell lines and no development of drug tolerance. Immunoblotting showed that gilteritinib strongly suppressed phosphorylated ALK and its downstream effectors, as well as mesenchymal–epithelial transition factor (MET) signaling. By comparison, MET signaling was enhanced in alectinib‐treated cells. Furthermore, gilteritinib was found to more effectively abolish growth of ALK ‐rearranged NSCLC xenograft tumors, many of which completely receded. Interleukin‐15 (IL‐15) mRNA levels were elevated in gilteritinib‐treated cells, together with a concomitant increase in the infiltration of tumors by natural killer (NK) cells, as assessed by immunohistochemistry. This suggests that IL‐15 production along with NK cell infiltration may constitute components of the gilteritinib‐mediated antitumor responses in ALK ‐rearranged NSCLCs. In conclusion, gilteritinib demonstrated significantly improved antitumor efficacy compared with alectinib against ALK ‐rearranged NSCLC cells, which can warrant its candidacy for use in anticancer regimens, after further examination in clinical trial settings.
    Type of Medium: Online Resource
    ISSN: 1347-9032 , 1349-7006
    URL: Article
    DOI: 10.1111/cas.15958
    Language: English
    Publisher: Wiley
    Publication Date: 2023
    detail.hit.zdb_id: 2115647-5
    detail.hit.zdb_id: 2111204-6
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...