Simon Baker
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drsimonbaker.bsky.social
Simon Baker
@drsimonbaker.bsky.social
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Bladder cell biologist working with normal and cancer human tissue models for Kidney Research UK and @yorkagainstcancer.bsky.social. We study how bladder cancer is initiated by BK polyomavirus-induced APOBEC3 cytosine deaminases.
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drsimonbaker.bsky.social
This work was hosted @biologyatyork.bsky.social, @ybri-uoy.bsky.social and @yorkbioscience.bsky.social. With collaborators at @universityofleeds.bsky.social, @lthtresearchcomms.bsky.social, @leedsth.nhs.uk, University of Texas at San Antonio and the National Cancer Institute at Bethesda.
December 4, 2025 at 7:35 AM
drsimonbaker.bsky.social
The fantastic authors on Bluesky are @sallyjamesyork.bsky.social, @asmasonomics.bsky.social, @karen-hogg.bsky.social, @imartincorena.bsky.social, @starrett.bsky.social
December 4, 2025 at 7:35 AM
drsimonbaker.bsky.social
With thanks to our funders @kidneyresearchuk.org and @yorkagainstcancer.bsky.social for supporting #bladdercancer research which is so often neglected. #cancer #cancerresearch #APOBEC
December 4, 2025 at 7:35 AM
drsimonbaker.bsky.social
These findings suggest a model of bladder carcinogenesis where the urothelial response to BK virus infections drives the initiating APOBEC mutations, but the virus is not required in the arising tumour.
A model for bladder cancer initiation where persistent BK virus infections of the kidney reactivate and shed decoy cells into the urine infecting the urothelium. In late-stage infections, the urothelium isolates and apically extrudes infected cells (marked by expression of the Viral capsid major Protein 1 “VP1”). In the viral extrusion microenvironment, bystander cells express interferon-regulated APOBEC3A, which damages the host genome. This is a hypothesis for how bladder cancers become defined by APOBEC3A/B mutagenesis without any virus present in the final tumour.
December 4, 2025 at 7:35 AM
drsimonbaker.bsky.social
"Transmutagenesis" describes the observation of bystander cells that were negative for viral proteins and proximal to infected neighbours acquiring APOBEC3A mediated potentially cancer initiating mutations.
Flow cytometry was used to sort a population that was high in antiviral APOBEC3 cytidine deaminase expression but had no detectable viral protein expression. Nanorate sequencing (NanoSeq) was then used to capture the APOBEC mutational signature forming in these cells. Could these cells be the progenitors of bladder cancers with APOBEC mutations in their genome but no trace of viruses?
December 4, 2025 at 7:35 AM
drsimonbaker.bsky.social
Chronic (>21 day) BK virus infections of normal human urothelium led to robust inductions of APOBEC3 mutational signatures. APOBEC3A was induced by bystander cells (negative for viral proteins) and in association with apical extrusion of infected cells by interferon signalling.
Histology images showing coordinated apical extrusion of BK virus infected cells by the healthy tissue. APOBEC3 cytidine deaminases were upregulated in bystander cells (without detectable viral proteins) involved in the apical extrusion process.
December 4, 2025 at 7:35 AM
drsimonbaker.bsky.social
Our evidence suggests there could be a route to bladder cancer prevention by stopping/controlling the reactivation of persistent BK virus infections.
Mutograph image showing that mutational signatures characteristic of antiviral APOBECs form in the genomes of urothelial cells when cultures are infected with BK virus.
December 4, 2025 at 7:35 AM