Yuki Ishii

 

Yuki Ishii – Research Manager

As Research Manager, I support the research led by Professor Clare Lloyd, which focuses on the mechanisms of inflammation, tissue repair, and remodelling in chronic lung disease. I contribute to the coordination and delivery of research projects within the group, support the development of new experimental approaches, and assist with grant applications and manuscript preparation. I work closely with research staff and play an active role in supervising and mentoring undergraduate and postgraduate students, as well as supporting teaching and training within the lab. I also help facilitate collaborations and organise lab activities.

I obtained my PhD in Japan, where I studied regulators of growth and differentiation in leukemia. I then moved to New York for postdoctoral training at Icahn School of Medicine at Mount Sinai, focusing on the development of novel combination therapies for breast cancer. Following this, I relocated to San Diego and worked as a Project Scientist at UC San Diego, investigating mechanisms of resistance to tyrosine kinase inhibitors in chronic myeloid leukemic. I later joined the Ludwig Institute for Cancer Research as a Research Associate, where I worked on developing compounds targeting synthetic lethal vulnerabilities in breast and ovarian cancers. After moving to London, I joined UCL’s Respiratory Department as a Senior Research Fellow, contributing to projects on mesothelioma, lung regeneration, and lung cancer before joining the Lloyd Lab in 2026.

y.ishii@imperial.ac.uk

Publications (selected)

  • Ishii.Y, Orr.JC, El Mdawar.M, Bairros de Pilger.DR, Pearce.DR, Lazarus.KA, et al. Compound screening in primary human airway basal cells identifies Wnt pathway activators as potential pro-regenerative therapies. J. Cell Science (2025)
  • Ishii.Y, Kolluri.KK, Pennycuick.A, Zhang.X, Nigro.E, Alrifai.D, et al. BAP1 and YY1 regulate expression of death receptors in malignant pleural mesothelioma. J.Biol.Chem (2021)
  • Guo.E#, Ishii.Y#, Mueller.J, Srivatsan.A, Gahman.T, Putnam.CD, Wang.JY, Kolodner.RD. FEN1 endonuclease as a therapeutic target for human cancers with defects in homologous recombination. PNAS (2020)
  • Kolluri.KK#, Alifrangis.C#, Kumar.N#, Ishii.Y#, Price.S, Michaut.M, et al. Loss of functional BAP1 augments sensitivity to TRAIL in cancer cells. Elife (2018)
  • Ishii.Y, Nhiayi. MK, Tse. E, Cheng. J, Massimino. M, Durden. DL, et al. Knockout serum replacement promotes cell survival by preventing BIM from inducing mitochondrial cytochrome c release. PLOS ONE (2015)
  • Ishii.Y, Papa. L, Bahadur U, Yue Z, Aguirre-Ghiso J, Shioda T, et al.   Bortezomib enhances the efficacy of fulvestrant by amplifying the aggregation of the estrogen receptor, which leads to a proapoptotic unfolded protein response. Clin. Cancer Res (2011)
  • Ishii.Y, Waxman.S, Germain.D. Tamoxifen stimulates the growth of cyclin D1 overexpressing breast cancer cells by promoting the activation of STAT3. Cancer Res (2008)
  • Ishii.Y, Pirkmaier.A, Alvarez.JV, Frank.DA, Kaselman.I, et al. Cyclin D1 overexpression and response to Bortezomib treatment in a breast cancer model. JNCI (2006).
  • Ishii.Y, Kasukabe.T, Honma.Y.  Induction of CCAAT/enhancer binding protein-delta by cytokinins, but not by retinoic acid, during granulocytic differentiation of human myeloid leukemia cells. Bri. J. Haematol (2005)
  • Ishii.Y, Hori.Y, Sakai.S, Honma.Y.  Control of differentiation and apoptosis human myeloid leukemia cells by cytokinin and cytokinin nucleosides, plant redifferentiation-inducing hormones. Cell Growth Differ (2002)

 #These authors contributed equally.