Biweekly administration of cetuximab in Japanese patients with recurrent or metastatic head and neck cancer

Tanaka, Nobukazu; Enokida, Tomohiro; Fujisawa, Takao; Okano, Susumu; Wada, Akihisa; Sato, Masanobu; Tanaka, Hideki; Takeshita, Naohiro; Tahara, Makoto

doi:10.1007/s10147-022-02226-5

Cited by 3 publications

(2 citation statements)

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“…Overexpression of EGFR has been detected in more than 27.9% of OSCC cases and is associated with lymph node metastasis 4 . Based on the molecular pathogenesis, the strategies to directly inhibit EGFR activity with small chemicals (e.g., gefitinib) and with biopharmaceuticals (e.g., cetuximab) should have worked as promising molecular‐targeted therapies paired with other chemotherapeutics and radiation therapy in cancer treatment 5–10 . In fact, cetuximab monotherapy and/or combined therapies often bring favorable responses toward patients 11–15 .…”

Section: Introductionmentioning

confidence: 99%

“… 4 Based on the molecular pathogenesis, the strategies to directly inhibit EGFR activity with small chemicals (e.g., gefitinib) and with biopharmaceuticals (e.g., cetuximab) should have worked as promising molecular‐targeted therapies paired with other chemotherapeutics and radiation therapy in cancer treatment. 5 , 6 , 7 , 8 , 9 , 10 In fact, cetuximab monotherapy and/or combined therapies often bring favorable responses toward patients. 11 , 12 , 13 , 14 , 15 However, the prognosis is still relatively unfavorable, with the 5‐year overall survival estimated to be less than 50% in OSCC.…”

Section: Introductionmentioning

confidence: 99%

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Inhibition of VEGFR2 and EGFR signaling cooperatively suppresses the proliferation of oral squamous cell carcinoma

et al. 2023

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BackgroundEpidermal growth factor receptor (EGFR) is frequently overexpressed in oral squamous cell carcinoma (OSCC), and EGFR‐targeting therapeutics have been widely employed to treat patients with a variety of carcinomas including OSCC. Here, we aimed to investigate alternative signaling for OSCC survival under the disruption of EGFR signaling.MethodsOSCC cell lines, namely HSC‐3 and SAS, were utilized to investigate how EGFR disruption affects cell proliferation. Gene set enrichment analysis was performed to examine how EGFR disruption affects oncogenic signaling in OSCC cells. Disruption of KDR gene was performed using CRISPR/Cas9 techniques. A VEGFR inhibitor, vatalanib was used to research the impact of VEGFR inhibition on OSCC survival.ResultsEGFR disruption significantly decreased the proliferation and oncogenic signaling including Myc and PI3K‐Akt, in OSCC cells. Chemical library screening assays revealed that VEGFR inhibitors continued to inhibit the proliferation of EGFR‐deficient OSCC cells. In addition, CRISPR‐mediated disruption of KDR/VEGFR2 retarded OSCC cell proliferation. Furthermore, combined erlotinib–vatalanib treatment exhibited a more potent anti‐proliferative effect on OSCC cells, compared to either monotherapy. The combined therapy effectively suppressed the phosphorylation levels of Akt but not p44/42.ConclusionVEGFR‐mediated signaling would be an alternative signaling pathway for the survival of OSCC cells under the disruption of EGFR signaling. These results highlight the clinical application of VEGFR inhibitors in the development of multi‐molecular‐targeted therapeutics against OSCC.

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Section: Introductionmentioning

confidence: 99%