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Susumu Kobayashi

Researcher at Beth Israel Deaconess Medical Center

Publications -  648
Citations -  23408

Susumu Kobayashi is an academic researcher from Beth Israel Deaconess Medical Center. The author has contributed to research in topics: Total synthesis & Epidermal growth factor receptor. The author has an hindex of 62, co-authored 629 publications receiving 21514 citations. Previous affiliations of Susumu Kobayashi include Chiba University & University of Tokyo.

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Clinical benefits of steroid therapy on surgical stress in patients with esophageal cancer

TL;DR: Perioperative steroid therapy was safe and effective for the inhibition of inflammatory mediators and the improvement of the postoperative clinical course of patients with esophageal cancer.
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Creation of novel chiral synthons with enzymes and applications to natural product synthesis. 15. Efficient introduction of chiral centers into cyclohexane ring

TL;DR: The chiral half-ester obtained by asymmetric hydrolysis of the symmetric diester 1 with pig liver esterase has been shown to be a versatile synthon for various chiral cyclohexane derivatives.
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Biological functions of a novel lipid mediator, cyclic phosphatidic acid

TL;DR: A novel bioactive lipid that was isolated originally from myxoamoebae of a true slime mold, Physarum polycephalum, and has now been detected in a wide range of organisms from slime molds to humans is focused on.
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Dual ALK and EGFR inhibition targets a mechanism of acquired resistance to the tyrosine kinase inhibitor crizotinib in ALK rearranged lung cancer.

TL;DR: Activation of EGFR as a mechanism of resistance to crizotinib in preclinical models of ALK translocated NSCLC is identified, and the use of AlK plus EGFR TKIs could be explored for this important cohort of NSCLCs.
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β-catenin contributes to lung tumor development induced by EGFR mutations

TL;DR: It is shown that β-Catenin is essential for development of EGFR-mutated lung cancers and that targeting the β-catenin pathway may provide novel strategies to prevent lung cancer development or overcome resistance to EGFR TKIs.