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Siang-Boon Koh

Researcher at Harvard University

Publications -  21
Citations -  439

Siang-Boon Koh is an academic researcher from Harvard University. The author has contributed to research in topics: Medicine & Cancer research. The author has an hindex of 8, co-authored 17 publications receiving 293 citations. Previous affiliations of Siang-Boon Koh include University of Cambridge & National University of Singapore.

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An automated fitting procedure and software for dose-response curves with multiphasic features

TL;DR: A robust approach to fit dose-response curves with various degrees of complexity is provided, which, together with the provided software implementation, should enable a wide audience to easily process their own data.
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The ATR Inhibitor AZD6738 Synergizes with Gemcitabine In Vitro and In Vivo to Induce Pancreatic Ductal Adenocarcinoma Regression

TL;DR: AZD6738 in combination with gemcitabine merits evaluation in a clinical trial in patients with PDAC, and the combination induced regression of a subgroup of KPC autochthonous tumors, which generally do not respond well to conventional chemotherapy.
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CHK1 Inhibition Synergizes with Gemcitabine Initially by Destabilizing the DNA Replication Apparatus

TL;DR: A systematic definition of how pancreatic cancer cells harboring mutant p53 respond to this combination therapy is reported, by combining mathematical models with large-scale quantitative biologic analyses of single cells and cell populations to suggest a "foot-in-the-door" mechanism for drug synergy.
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A quantitative FastFUCCI assay defines cell cycle dynamics at a single-cell level.

TL;DR: The utility of the FastFUCCI assay for quantifying spatiotemporal dynamics and its potential in preclinical drug development is demonstrated and evidence that targeting the DNA replication origin activity sensitised cells to paclitaxel is found.
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Mechanistic Distinctions between CHK1 and WEE1 Inhibition Guide the Scheduling of Triple Therapy with Gemcitabine.

TL;DR: This work provides quantitative insights into the mechanisms of DDRi chemosensitization, leading to the rational development of a tolerable multitherapeutic regimen.