#MathOnco Issue 112: cancer microenvironment, cell motility, micromet resistance, angiogenesis construction, and heteregeneity.
This week in
Math Oncology
Apr. 23, 2020 ~ Issue 112
From the editor
Hello!
While many of us are undoubtedly stuck at home during days of self-isolation, that hasn't stopped the continuous avalanche of math oncology news! This is probably the fullest edition yet (13 manuscripts!).
This week in math oncology brought us articles on the cancer microenvironment, cell motility, micromet resistance, angiogenesis construction, and several studies on heteregeneity.
Please Enjoy!
-Jeffrey West
#MathOnco Publications
Integrating genetic and non‐genetic drivers of somatic evolution during carcinogenesis: the biplane model
Authors: Robert A. Gatenby, Stanislav Avdieiev, Kenneth Y. Tsai, Joel S. Brown
Intratumor Heterogeneity: The Rosetta Stone of Therapy Resistance
Authors: Andriy Marusyk, Michalina Janiszewska, Kornelia Polyak
How heterogeneity drives tumour growth: a computational study
Authors: Hector Gomez
Review: Mathematical Modeling of Prostate Cancer and Clinical Application
Authors: Tin Phan, Sharon M. Crook, Alan H. Bryce, Carlo C. Maley, Eric J. Kostelich, Yang Kuang
Why is cancer not more common? A changing microenvironment may help to explain why, and suggests strategies for anti-cancer therapy
Authors: Xiaowei Jiang, Ian P. M. Tomlinson
The Human Tumor Atlas Network: Charting Tumor Transitions across Space and Time at Single-Cell Resolution
Authors: Orit Rozenblatt-Rosen, Aviv Regev, Philipp Oberdoerffer, Tal Nawy, ..., Sudhir Srivastava, Kai Tan, Robert B. West, Elizabeth H. Williams
Cancer cell lines show high heritability for motility but not generation time
Authors: Anastasia V. Wass, George Butler, Tiffany B. Taylor, Philip R. Dash, Louise J. Johnson
Drug-Induced Resistance in Micrometastases: Analysis of Spatio-Temporal Cell Lineages
Authors: Judith Pérez-Velázquez, Katarzyna A. Rejniak
A pharmacodynamic model of clinical synergy in multiple myeloma
Authors: Praneeth Sudalagunta, Maria C. Silva, Rafael R. Canevarolo, Raghunandan Reddy Alugubelli, ..., Rachid Baz, Mark B. Meads, Kenneth H. Shain, Ariosto S. Silva
Angiogenic Networks in Tumors— Insights via Mathematical Modeling
Authors: Mohsen Dorraki, Anahita Fouladzadeh, Andrew Allison, Claudine S. Bonder, Derek Abbott
#MathOnco Preprints
Rapid Assessment of T-Cell Receptor Specificity of the Immune Repertoire
Authors: Xingcheng Lin, Jason T. George, Nicholas P. Schafer, Cecilia Clementi, José N. Onuchic, Herbert Levine
Invasion of homogeneous and polyploid populations in nutrient-limiting environments
Authors: Gregory J. Kimmel, Mark Dane, Laura Heiser, Philipp M. Altrock, Noemi Andor
NFATc acts as a non-canonical phenotypic stability factor for a hybrid epithelial/mesenchymal phenotype
Authors: Ayalur Raghu Subbalakshmi, Deepali Kundnani, Kuheli Biswas, Anandamohan Ghosh, Samir Hanash, Satyendra C Tripathi, Mohit Kumar Jolly
A spatial game to simulate evolutionary treatments
The Mathematical Oncology Blog
Alex Bakos: "In cancer, intratumor heterogeneity is crucial to tumor evolution, as the more diverse a tumor is, the better it’s able to adapt to different situations. Cancer cells consist of many different genotypes and phenotypes that can lead each other to be quite different from one another and understanding this intra-tumor diversity and the different traits that emerge from this diversity is key to understanding how tumors evolve1. In the context of drug resistance, it’s been seen that the majority of a tumor before a drug is first applied is phenotypically vulnerable to the drug, but there exists a small population of tolerant cells, also called persistors, who are not fully resistant to the drug, but merely able to survive the treatment. These tolerant cells are seen as a precursor to the existence of full on treatment-resistance in a tumor. Additionally, it’s been seen experimentally that stromal cells can dramatically reduce the ability of a drug to kill tumor cells that might otherwise be vulnerable to the treatment.'"
#MathOnco - Book of the month
The Book of Why:
The New Science of Cause and Effect
Judea Pearl: "Correlation is not causation. This mantra, chanted by scientists for more than a century, has led to a virtual prohibition on causal talk. Today, that taboo is dead. The causal revolution, instigated by Judea Pearl and his colleagues, has cut through a century of confusion and established causality--the study of cause and effect--on a firm scientific basis. His work explains how we can know easy things, like whether it was rain or a sprinkler that made a sidewalk wet; and how to answer hard questions, like whether a drug cured an illness. Pearl's work enables us to know not just whether one thing causes another: it lets us explore the world that is and the worlds that could have been."
Jobs
Computational Approaches to Breast Cancer Evolution - Postdoc (Marc Ryser)
Postdoctoral Fellow in Mathematical Oncology (Russell Rockne)
Pre-leukemic Dynamics – MSc or PhD Studentship (Morgan Craig)
Quantitative Systems Pharmacology (QSP) Modeler - Cell Therapy (Dean Bottino)
Math/statistical models of stem cell lineage dynamics and cancer genomics - Postdoc (Adam MacLean)
Postdoctoral Research Position in Computational Oncology (Tom Yankeelov)
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