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Mitsue Kurasawa

Researcher at Chugai Pharmaceutical Co.

Publications -  28
Citations -  528

Mitsue Kurasawa is an academic researcher from Chugai Pharmaceutical Co.. The author has contributed to research in topics: Bevacizumab & Cancer. The author has an hindex of 10, co-authored 24 publications receiving 427 citations.

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Pertuzumab in Combination with Trastuzumab Shows Significantly Enhanced Antitumor Activity in HER2-Positive Human Gastric Cancer Xenograft Models

TL;DR: The clinical benefit of combination therapy with pertuzumab and trastuzumAB for patients with HER2-positive gastric cancers is suggested, through the potentiation of cell growth inhibition, apoptosis activity, cell killing activity by ADCC, and antiangiogenic activity.
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Bevacizumab improves the delivery and efficacy of paclitaxel.

TL;DR: Results suggest that the synergistic antitumor activity of paclitaxel and bevacizumab in combination may be a result of the increase in pac litaxel concentration in tumor resulting from the downregulation of vascular permeability when co-administered with bevaccizumAB.
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Bevacizumab counteracts VEGF-dependent resistance to erlotinib in an EGFR-mutated NSCLC xenograft model

TL;DR: The erlotinib plus bevacizumab combination demonstrated promising efficacy in the B901L xenograft model of EGFR Mut+ NSCLC and elucidated the mode of action of this combination.
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Topoisomerase I inhibitor, irinotecan, depletes regulatory T cells and up-regulates MHC class I and PD-L1 expression, resulting in a supra-additive antitumor effect when combined with anti-PD-L1 antibodies.

TL;DR: Results indicate that irinotecan may enhance the effect of T cell activation caused by anti-PD-L1 treatment by reducing Tregs and augmenting MHC class I–mediated tumor antigen presentation, and concurrent upregulation of PD-L 1 expression can be blocked by the anti- PD- L1 antibody.
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Impact of bevacizumab in combination with erlotinib on EGFR‐mutated non–small cell lung cancer xenograft models with T790M mutation or MET amplification

TL;DR: Adding BEV to ERL did not enhance antitumor activity in primarily ERL‐resistant tumors with T790M mutation; however, BEV+ERL enhanced antitumors activity in T790m mutation‐ or MET amplification‐positive tumors as long as their growth remained significantly suppressed by ERL.