Professional background

Dr Mark Linch is a consultant medical oncologist specialising in the treatment of prostate and bladder cancer, and honorary senior lecturer at University College London (UCL) Cancer Institute where he leads the uro-oncology biology group.

Dr Linch is currently principal Investigator or co-investigator in numerous clinical trials in prostate, bladder and penile cancer, both early and late phase, meaning that most patients at UCLH will have the opportunity to be involved in cutting edge therapeutic research.

Dr Linch leads on a number of studies involving in depth profiling of patients’ cancers, looking for genetic, protein and immune cell changes that are associated with cancer.

Through this work, Dr Linch hopes to be able to match individual patients with effective therapies, incorporate immunotherapy into routine clinical practice for urological malignancies and help develop novel therapies.

Research interests

Dr Linch was awarded a Cancer Research UK (CRUK) Fellowship in 2007 to study for a PhD at the London Research Institute/Francis Crick Institute and then continued post-doctoral research at the LRI while completing his oncology training at the Royal Marsden Hospital (RMH).

In 2012 he was appointed consultant medical oncologist and clinician scientist at the RMH before his recruitment to UCLH in June 2014.

His research programme is funded by the NIHR/BRC, CRUK and Prostate Cancer Foundation and focuses on the genomic and proteomic heterogeneity of prostate and bladder cancer and characterisation of the immune landscape of these cancers. His laboratory and clinical activities have combined to help identify biomarkers that guide the drug discovery process and have led to a patent and over 20 peer-reviewed papers, including lead author papers in Science Signaling, Biochemical Journal and Carcinogenesis.

Publications

Linch M, Sanz-Garcia M, Rosse C, Riou P, Peel N, Madsen C, Sahai E, Downward J, Khwaja A, Dillon C, Roffey J, Cameron A, Parker PJ. Regulation of polarized morphogenesis by protein kinase C iota in oncogenic epithelial spheroids. Carcinogenesis. 2014 Feb;35(2):396-406.

Rossé C, Lagoutte E, Irondelle M, Monteiro P, Sengmanivong L, Paul-Gilloteaux P, Linch M, Bièche I, Parker P, Chavrier P. Breast tumor cell invasion requires regulation of late endosome-to-plasma membrane trafficking of MT1-MMP by aPKC. Proc Natl Acad Sci U S A. 2014 May 6;111(18):E1872-9.

Linch M, Sanz-Garcia M, Soriano E, Zhang Y, Riou P, Rosse C, Cameron A, Knowles P, Purkiss A, Kjaer S, McDonald NQ, Parker PJ. A cancer-associated mutation in atypical protein kinase C iota occurs in a substrate-specific recruitment motif. Science signaling 2013;6:ra82.

Linch M*, Kjaer S*, Purkiss A, Kostelecky B, Knowles PP, Rosse C, Riou P, Soudy C, Kaye S, Patel B, Soriano E, Murray-Rust J, et al. Adenosine-binding motif mimicry and cellular effects of a thieno[2,3-d]pyrimidine-based chemical inhibitor of atypical protein kinase C isozymes. The Biochemical journal 2013;451:329-42. *Joint 1st Authors

Linch M, Miah A, Thway K, Judson IR, Benson C. Systemic treatment of soft tissue sarcoma: current gold standard and novel therapies. Nat Rev Clin Oncol. 2014 Apr;11(4):187-202.