Bunsyo Shiotani

[Bunsyo Shiotani @BunShiotani]

A new paper from B-Lab is out in Nat Commun!
We discovered that ATR-regulated PrimPol switches between fork slowing and repriming to help cells tolerate oncogenic KRAS-induced replication stress, promoting survival while limiting error-prone DNA synthesis. https://t.co/YfFTxuKSHV

[Bunsyo Shiotani @BunShiotani]

New PAPER alert! Led by Yano, our latest study shows how PARPi-induced heterochromatin amplifies replication stress and ATRi sensitivity, revealing a new strategy to target SMARCA4-deficient tumors.
Link→https://t.co/sJqLS7zgLr

[Bunsyo Shiotani @BunShiotani]

Happy to share a new review from our lab: Tolerance of Oncogene-Induced Replication Stress: A Fuel for Genomic Instability
https://t.co/f0gT9glu9m

[Bunsyo Shiotani @BunShiotani]

Good news! My work "Emerging strategies for cancer therapy by ATR inhibitors" has received over 3,000 views since publication! Read it here https://t.co/tKt5pQOSyw #ViewsMilestone

[国立がん研究センター研究所 NCCRI Japan Official Account @NccriOfficial]

【研究成果】ゲノムストレス応答学ユニットの五十嵐太一（北里大学連携大学院生）らの研究が @NatureComms に掲載されました。正常細胞が発がん初期においてKRAS変異に応答し、生存のために危機回避的に複製を行う結果、ゲノム異常を獲得するメカニズムを解明しました。https://t.co/127oxx26Wr

[国立が���研究センター研究所 NCCRI Japan Official Account @NccriOfficial]

[Research] The paper from Lab of Genome Stress Signaling (Shiotani lab) is now online, revealing a crucial role of ATR-PrimPol in enabling precancerous cells to survive KRAS-induced replication stress and expand clonally with genomic instability. https://t.co/127oxx26Wr