Tumor morphology and phenotypic evolution driven by selective pressure from the microenvironment.
By A. Anderson, Alissa M. Weaver, Peter T. Cummings, V. Quaranta. Cell, 2006
772 citations recorded by the source corpus.
Subfields: Cell Biology, Modeling and Simulation, Oncology
View Paper: https://www.semanticscholar.org/paper/922e06f2467d93cf0401400b04ac02e5b2d42927
How researchers see this paper
The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.
In Cell Biology
- Steven M. Wise
- Philip K. Maini
- Hermann B. Frieboes
- Nicola Bellomo
- Vittorio Cristini
- John S. Lowengrub
- Zena Werb
- M. Egeblad
In Modeling and Simulation
- Steven M. Wise
- Philip K. Maini
- Hermann B. Frieboes
- Nicola Bellomo
- Vittorio Cristini
- John S. Lowengrub
- Michael Winkler
In Oncology
- M. Egeblad
- E. Nakasone
- Zena Werb
- Carlo C. Maley
- Steven M. Wise
- Bert Vogelstein
- M. Greaves
- Hermann B. Frieboes
Citations in the corpus
- The tumor microenvironment. (2012, background): “On the contrary, “mild conditions” characterized by a homogenous ECM leads to no clonal dominance and a tumor with smooth, noninvasive margins [53].”
- On the foundations of cancer modelling: Selected topics, speculations, and perspectives (2008, methodology): “Furthermore, recent work by Anderson et al.16 utilises a hybrid discrete model incorporating cell-adhesion, cellmigration and phenotypic mutations, and suggests invasive “fingering” is driven by environmental heterogeneity.”
- Extracellular matrix structure. (2016, background): “Transport of drug molecules through interstitial tissue is depend on convection and diffusion [354].”
- CLONAL EVOLUTION IN CANCER (2012, background): “Mathematical modelling shows cancer-clone evolutionary selection for more robust or malignant phenotypes is less likely in more stable or homogeneous micro-environment”
- Three-dimensional multispecies nonlinear tumor growth--I Model and numerical method. (2008, methodology): “…cellular automaton and agent based models (e.g., see the works of Alarcon et al., 2003; Jiang et al., 2005; Anderson, 2005; Abbott et al., 2006; Anderson et al., 2006; Lee and Rieger, 2006; Bauer et al., 2007; Gerlee and Anderson, 2007a, b; Bartha and Rieger, 2006), single-phase continuum…”
- A spatial model predicts that dispersal and cell turnover limit intratumour heterogeneity (2015, methodology): “Many models of spatially expanding tumours were proposed in the past [13,14,15,16,17,18,21,45,46,47,48], but they either assume very few [13,15,45,47,49,50,51] or no new mutations at all [14,19,20,46,52,53], or one- or two-dimensional growth [14,15,16,17,54,55].”
- Tumors as organs: complex tissues that interface with the entire organism (2010, positive): “Thus, mathematical modeling may facilitate the prediction of malignant behavior based on knowledge of the tissue context (Anderson et al., 2006; Shields et al., 2007; Smallbone et al., 2007).”