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The William Harvey Research Institute - Faculty of Medicine and Dentistry

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Mitochondrial redox metabolism as a therapeutic target in B cell lymphoma

Code: BC-DTP_2026_08

Title: Mitochondrial redox metabolism as a therapeutic target in B cell lymphoma

Primary Supervisor: Andy Fintch

Email: a.finch@qmul.ac.uk

Institute: Barts Cancer Institute

Secondary Supervisor: John Riches

Email: j.riches@qmul.ac.uk

Institute: Barts Cancer Institute

Lay Summary:

B cell lymphoma accounts for over 4% of all UK cancer diagnoses and the mainstay of treatment is based upon chemotherapy, which carries many side-effects. A significant subset of B cell lymphomas carry mutations in the MYC gene and this drives growth and multiplication of the cancer cells. This excessive drive for growth is accompanied by a high demand for energy and we have found that cells with mutant MYC die when energy supply is limited. Unfortunately, MYC-driven B cell lymphomas often contain high activity of a second gene, called BCL-2. BCL-2 blocks cell death and so B cell lymphomas that have both MYC and BCL-2 (double-hit lymphoma - DHL) are very aggressive and hard to treat because they grow very fast and are resistant to being killed by chemotherapy. This project is focused upon understanding why MYC-active B cells die when energy supply is limited and whether we can restore this cell death in DHL as a novel, effective and safe therapy.

We have discovered that MYC overloads the cellular energy machinery (which uses electrons just like electrical goods) and greatly increases the likelihood of those electrons spilling out and causing damage (akin to an electrical short circuit), resulting in cell death. In this project, we will discover exactly how the electrons leak from the cellular machinery and develop ways to encourage that in B cell lymphomas.

Through this research, we hope to discover new therapies for B cell lymphoma and particularly for the most aggressive DHLs.

Aims:

  1. To discover how MYC activation primes B cell mitochondria to produce ROS and trigger apoptosis.
  2. To discover how electrons exit the mitochondrial ETC under specific metabolic conditions in B cell lymphoma.
  3. To demonstrate the therapeutic potential of targeting mitochondrial redox metabolism in B cell lymphoma through pharmacological and nutrient interventions.
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