Wonderful, I already started reading!!
Posts by Kamila Naxerova
Tumor promotion through the lens of evolution
This review grew out of many long conversations, shared ideas, and lively discussions
It has been a real pleasure to think together with Allan, Paul, Eve, and Abel about how tumours develop and how carcinogens shape cancer risk
rdcu.be/fdC2J
Excited to share our latest work in Nature. Applying single-molecule and single-cell DNA sequencing methods, we uncover an extraordinary landscape of somatic mutations in immune checkpoint genes in autoimmune B cells, suggesting that somatic mutations may be key to autoimmunity [1/n] rdcu.be/fdqbr
Did you catch our news during #MarkSymposium?
We’re accepting applications for our 2026 Emerging Leader Awards, now offering $1 million over 4 years & open to investigators worldwide!
Submit your LOI by April 30: themarkfoundation.org/emerging-lea...
#ResearchFunding
Sweet!!!
Of course there could be additional biological factors like virally mediated HSC death (hypothetical) that would really affect CH emergence but I guess that is for the hematologists to find out :)
Agree with you! I think all it would take is to “translate” the infection into number of excess divisions, and then you can immediately get the increase in clone size with the standard model. So all you need is the increase in division per time unit multiplied by time (infection duration).
If you mean mathematical models, we have done both neutral evolution and positive selection under a variety of conditions (Heyde 2021 and also McAlpine 2022). I am sure there is lots of room for improvement but generally hematopoiesis is easy to model because we have most relevant parameters
Same here! We are doing a lot of that with various methods, none is perfect but together they give a good picture. Happy to chat anytime!
This is from Hormaechea-Agulla 2021. You have to measure proliferation increase at the HSC level because that is where the clone expansion happens. Obviously harder to do in humans but we hav done it for atherosclerosis and it's substantial. Hope this helps :)
The precise increase would depend on a lot of factors, including the severity of the infection, personal genetic and lifestyle factors etc. But generally chronic elevation would be worse. Some useful quantifications exist in the mouse, will link below.
From the point of view of somatic evolutionary theory, the mechanism is simple: more infections -> more hematopoietic activity -> more stem cell divisions -> faster clone expansion. Holds for all self-renewing tissues and all proliferative stimuli.
The conference is quickly filling up! Don't wait to sign up. We also received some funding and can offer fellowships to graduate students and postdocs. Won't cover the whole cost but will certainly make it much easier!
📢 Postdoc position available in my lab
We study mutagenesis, population genetics, and Mendelian genomics—linking the origins of mutations to their biological and disease consequences.
Details about research directions:
labs.utsouthwestern.edu/seplyarskiy-...
Please reach out if interested.
🚨 New paper from our lab just published in Nature🚨
www.nature.com/articles/s41...
Discover how 🌱 tumour formation is shaped by tissue context from the very beginning. Cancer is not driven by genetics alone
✨Fantastic team led by Greta Skrupskelyte, Eduardo Rojo, @hariajith.bsky.social
Check out this important advance in mitochondrial 🧬 lineage tracing by @gaoteng.bsky.social and @wengchen.bsky.social from our group, in collaboration with @jswlab.bsky.social 👇👇
Please come join us - so excited for this conference!
David Cheek's Seminar
IICD welcomes next David Cheek from @harvard.edu on Feb. 11 at 2 PM, as part of our seminar series. Dr. Cheek will discuss causation in cancer genomes. Register: cancerdynamics.columbia.edu/events/iicd-...
cc: @harvardmed.bsky.social @naxerova.bsky.social
📢 Announcing The Mark Foundation 2026 Emerging Leader Award winners! 📢
We are committing $3.75 million to 5 visionary early-career scientists poised to lead the next generation of oncology breakthroughs. We can't wait to see their impact!
themarkfoundation.org/2026/01/2026...
The abstract deadline for Mutations in Time and Space 2026 closes in 3 weeks time. Sign up here: coursesandconferences.wellcomeconnectingscience.org/event/mutati...
As well as thrilling science, the programme includes dinner at the beautiful King's College in Cambridge.
@eventswcs.bsky.social
Happy new year/paper!
A new tech (scG2P) maps genotype (DNA) to phenotype (RNA) in single cells, bringing together the worldviews of genetic & transcriptional heterogeneity. With scG2P we define how mosaicism drivers increase clonal fitness in the aging esophagus
aacrjournals.org/cancerdiscov...
Somatic and germline mutational processes across the tree of life www.biorxiv.org/content/10.64898/2025.12...
My age was 75, Bach being the common denominator
How sad. Time for a Rahbari sperm testing company! 🥰
Very cool!
@kevinmonahan.bsky.social & I have an open clinical #PhD position between @stmarkshospital.bsky.social and @icr.ac.uk If you're interested in the biology of pre-cancer in the bowel & want to translate biology for cancer prevention this one could be for you... funded by the brilliant #40tude
Come to Germany and do a PhD with DKFZ. You'll be supported by an international community doing amazing science in a fantastic place.
I joined the DKTK from the UK 3 months ago and couldn't be happier with how easy it has been fitting in. The quality of work here is phenomenal and you should apply!
New @natgenet.nature.com paper from the brilliant @eszterlakatos.bsky.social presents evidence that chromatin alterations disrupt antigen presentation & neoantigens in colorectal cancer. Also that immune escape is part of the "Big Bang", at the outset of CRC growth. www.nature.com/articles/s41...
The exciting next instalment of Mutations in Time and Space... Open for registration now