This week in MathOnco 293
Reinforcement learning, systems biology, treatment holidays, spatial patterns, and more.
“This week in Mathematical Oncology” — Apr 25, 2024
> mathematical-oncology.org
From the editor:
This week’s edition of the Math Onco newsletter has papers on topics such as reinforcement learning, systems biology, treatment holidays, spatial patterns, and more.
The cover art this week is from a recent blog post. Will you consider writing a blog post this year? Learn more about the process here.
Thanks,
Jeffrey West
jeffrey.west@moffitt.org
Tumor phylogeography reveals block-shaped spatial heterogeneity and the mode of evolution in Hepatocellular Carcinoma
Xiaodong Liu, Ke Zhang, Neslihan A. Kaya, Zhe Jia, Dafei Wu, Tingting Chen, Zhiyuan Liu, Sinan Zhu, Axel M. Hillmer, Torsten Wuestefeld, Jin Liu, Yun Shen Chan, Zheng Hu, Liang Ma, Li Jiang & Weiwei ZhaiTranscriptome free energy can serve as a dynamic patient-specific biomarker in acute myeloid leukemia
Lisa Uechi, Swetha Vasudevan, Daniela Vilenski, Sergio Branciamore, David Frankhouser, Denis O’Meally, Soheil Meshinchi, Guido Marcucci, Ya-Huei Kuo, Russell Rockne & Nataly Kravchenko-BalashaReinforcement learning informs optimal treatment strategies to limit antibiotic resistance
Davis T. Weaver, Eshan S. King, Jeff Maltas, and Jacob G. ScottBridging systems biology and tissue engineering: Unleashing the full potential of complex 3D in vitro tissue models of disease
Jose L. Cadavid, Nancy T. Li, Alison P. McGuiganInterplay of mutations, alternate mechanisms, and treatment breaks in leukaemia: Understanding and implications studied with stochastic models
H. Jonathan G. Lindström, Astrid S. de Wijn, Ran Friedman
The dynamic fitness landscape of ageing haematopoiesis through clonal competition
Nathaniel Vincent Mon Père, Francesco Terenzi, Benjamin WernerPattern formation along signaling gradients driven by active droplet behaviour of cell groups
Hugh Z Ford, Giulia L Celora, Elizabeth R Westbrook, Mohit P Dalwadi, Benjamin J Walker, Hella Baumann, Cornelis J. Weijer, Philip Pearce, Jonathan R ChubbA three-node Turing gene circuit forms periodic spatial patterns in bacteria
J Tica, M Oliver Huidobro, T Zhu, GKA Wachter, RH Pazuki, E Tonello, H Siebert, MPH Stumpf, RG Endres, M IsalanOxygen, Angiogenesis, Cancer and Immune Interplay in Breast Tumor Micro-Environment: A Computational Investigation
Navid Mohammad Mirzaei, Panayotis G. Kevrekidis, Leili ShahriyariDrug-loaded nanoparticles for cancer therapy: a high-throughput multicellular agent-based modeling study
Yafei Wang, Elmar Bucher, Heber Rocha, Vikram Jadhao, John Metzcar, Randy Heiland, Hermann B. Frieboes, Paul MacklinMathematical analysis of a model-constrained inverse problem for the reconstruction of early states of prostate cancer growth
Elena Beretta, Cecilia Cavaterra, Matteo Fornoni, Guillermo Lorenzo, Elisabetta Rocca
Developmental hematopoietic stem cell fate decisions explain clonal dynamics over lifetime
The Mathematical Oncology Blog
Jesse Kreger, Adam MacLean - April 11, 2024
The newsletter now has a dedicated homepage where we post the cover artwork for each issue. We encourage submissions that coincide with the release of a recent paper from your group. This week’s artwork:
Based on the preprint: Developmental hematopoietic stem cell variation explains clonal hematopoiesis later in life in BioRxiv. See also the related blog post.
Artist: Nightcafe - Jesse Kreger (@jessemkreger), Adam MacLean (@adamlmaclean)
Caption: Clonal expansion of blood stem cells (clonal hematopoiesis or CH) is a hallmark of aging. Blood cancers can develop from such clonal expansions. However, CH without any clinical implications is observed in a large fraction of the aging population. Why is CH pervasive in healthy individuals? What are the origins of CH? These questions are of importance not only to understand the blood system and associated disease risks, but also to shed light on the evolution of somatic variants throughout a human life. In our preprint, we provide an answer to the origins of clonal hematopoiesis. We show that a model comprised of stem cell clones arising during development and evolving throughout life under weak selection is fully consistent with the data, and gives rise to CH as we grow old.
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