Year Three Appendix

Total Page:16

File Type:pdf, Size:1020Kb

Year Three Appendix PHYSICAL SCIENCES-ONCOLOGY CENTER PROGRAM Appendix Fall 2012 Appendix 1 2 Physical Sciences-Oncology Center Program Table of Contents 1. Publications ...............................................................................................................................................................................1 2. Patents Disclosures/Applications ............................................................................................................................................31 3. Clinical Samples and Trials ......................................................................................................................................................35 4. Additional Center Highlights ...................................................................................................................................................41 5. Pilot Projects .............................................................................................................................................................................71 6. Trans-Network Projects ............................................................................................................................................................77 7. Young Investigator Trans-Network ...........................................................................................................................................81 8. PS-OC Cores ..............................................................................................................................................................................85 9. PS-OC Outreach Programs ........................................................................................................................................................89 10. PS-OC Courses ........................................................................................................................................................................101 11. Trainee Exchanges ..................................................................................................................................................................105 12. Trainee Transitions .................................................................................................................................................................109 13. PS-OC Investigator Interactions with the Media ..................................................................................................................115 14. PS-OC Investigator Conferences and Seminars ....................................................................................................................121 15. OPSO Staff Invited Presentations ...........................................................................................................................................159 16. OPSO Staff Symposium and Workshops ................................................................................................................................165 17. PS-OC Investigator Meeting Agendas ....................................................................................................................................169 17.1 First Annual Principal Investigator Meeting ................................................................................................................171 17.2 Second Annual Principal Investigator Meeting ...........................................................................................................183 17.3 Third Annual Principal Investigator Meeting ..............................................................................................................195 17.4 Joint Meeting of Junior Investigators .........................................................................................................................207 18. Science Technology Policy Institute Memos ..........................................................................................................................209 19. Extended Scientific Report emplateT .....................................................................................................................................223 20. Survey Questions ....................................................................................................................................................................243 21. Survey Results ........................................................................................................................................................................345 Appendix i ii Physical Sciences-Oncology Center Program 1. Publications Appendix 1 2 Physical Sciences-Oncology Center Program 1. PS-OC Peer-Reviewed Publications 1. Abaci, H.E., Devendra, R., Smith, Q., Gerecht, S. & Drazer, G. Design and development of microbioreactors for long- term cell culture in controlled oxygen microenvironments. Biomed Microdevices 14, 145-152 (2012). 2. Balzer, E.M. & Konstantopoulos, K. Intercellular adhesion: Mechanisms for growth and metastasis of epithelial cancers. Wiley Interdisciplinary Reviews-Systems Biology and Medicine 4, 171-181 (2012). 3. Barrett, L.E., et al. Self-renewal does not predict tumor growth potential in mouse models of high-grade glioma. Cancer Cell 21, 11-24 (2012). 4. Basanta, D., Gatenby, R.A. & Anderson, A.R.A. Exploiting evolution to treat drug resistance: Combination therapy and the double bind. Molecular Pharmaceutics 9, 914-921 (2012). 5. Basanta, D., et al. Investigating prostate cancer tumour-stroma interactions: Clinical and biological insights from an evolutionary game. Br J Cancer 106, 174-181 (2012). 6. Battistini, F., Hunter, C.A., Moore, I.K. & Widom, J. Structure-based identification of new high-affinity nucleosome binding sequences. Journal of Molecular Biology 420, 8-16 (2012). 7. Bergethon, K., et al. Ros1 rearrangements define a unique molecular class of lung cancers.J Clin Oncol 30, 863-870 (2012). 8. Bryan, A.K., Engler, A., Gulati, A. & Manalis, S.R. Continuous and long-term volume measurements with a commercial coulter counter. PLoS One 7, 17 (2012). 9. Carbonaro, M., Escuin, D., O’Brate, A., Thadani-Mulero, M. & Giannakakou, P. Microtubules regulate hypoxia- inducible factor-1 alpha protein trafficking and activity implications for taxane therapy.Journal of Biological Chemistry 287, 11859-11869 (2012). 10. Carey, S.P., Kraning-Rush, C.M., Williams, R.M. & Reinhart-King, C.A. Biophysical control of invasive tumor cell behavior by extracellular matrix microarchitecture. Biomaterials 33, 4157-4165 (2012). 11. Charest, J.M., Califano, J.P., Carey, S.P. & Reinhart-King, C.A. Fabrication of substrates with defined mechanical properties and topographical features for the study of cell migration. Macromol Biosci 12, 12-20 (2012). 12. Chen, S.H., Dallas, M.R., Balzer, E.M. & Konstantopoulos, K. Mucin 16 is a functional selectin ligand on pancreatic cancer cells. Faseb Journal 26, 1349-1359 (2012). 13. Cheng, Y.K., et al. A mathematical methodology for determining the temporal order of pathway alterations arising during gliomagenesis. PLoS Comput Biol 8, 5 (2012). 14. Chmielecki, J., et al. Egfr-mutant lung adenocarcinomas treated first-line with the novel egfr inhibitor, xl647, can subsequently retain moderate sensitivity to erlotinib. Journal of Thoracic Oncology 7, 434-442 (2012). 15. Cho, E.H., et al. Characterization of circulating tumor cell aggregates identified in patients with epithelial tumors. Phys Biol 9, 3 (2012). 16. Ciriello, G., Cerami, E., Sander, C. & Schultz, N. Mutual exclusivity analysis identifies oncogenic network modules. Genome Res 22, 398-406 (2012). 17. Damani, S., et al. Characterization of circulating endothelial cells in acute myocardial infarction. Sci Transl Med 4(2012). 18. Fraley, S.I., Feng, Y., Giri, A., Longmore, G.D. & Wirtz, D. Dimensional and temporal controls of three-dimensional cell migration by zyxin and binding partners. Nat Commun 3(2012). Appendix 3 19. Galban, S., et al. Dw-mri as a biomarker to compare therapeutic outcomes in radiotherapy regimens incorporating temozolomide or gemcitabine in glioblastoma. PLoS One 7, 20 (2012). 20. Gao, D., et al. Myeloid progenitor cells in the premetastatic lung promote metastases by inducing mesenchymal to epithelial transition. Cancer Res 72, 1384-1394 (2012). 21. Gibson, D.S., et al. Biomarkers in rheumatology, now and in the future. Rheumatology 51, 423-433 (2012). 22. Govern, C.C., Yang, M. & Chakraborty, A.K. Identifying dynamical bottlenecks of stochastic transitions in biochemical networks. Phys Rev Lett 108, 30 (2012). 23. Gu, S., et al. Applying a patient-specific bio-mathematical model of glioma growth to develop virtual [18f]-fmiso-pet images. Math Med Biol 29, 31-48 (2012). 24. Guo, W., et al. Slug and sox9 cooperatively determine the mammary stem cell state. Cell 148, 1015-1028 (2012). 25. Haeno, H., et al. Computational modeling of pancreatic cancer reveals kinetics of metastasis suggesting optimum treatment strategies. Cell 148, 362-375 (2012). 26. Hielscher, A.C., Qiu, C. & Gerecht, S. Breast cancer cell-derived matrix supports vascular morphogenesis. Am J Physiol Cell Physiol 302, 25 (2012). 27. Hughes, A.D., et al. Microtube device for selectin-mediated capture of viable circulating tumor cells from blood. Clin Chem 58, 846-853 (2012). 28. Huynh, K.A., McCaffery, J.M. & Chen, K.L. Heteroaggregation of multiwalled carbon nanotubes and hematite nanoparticles: Rates and mechanisms. Environ Sci Technol 46, 5912-5920 (2012).
Recommended publications
  • The Impact of Tumor Stromal Architecture on Therapy Response and Clinical Progression
    bioRxiv preprint doi: https://doi.org/10.1101/451047; this version posted October 24, 2018. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under aCC-BY-NC 4.0 International license. The impact of tumor stromal architecture on therapy response and clinical progression Philipp M. Altrock*,1, Nara Yoon*,2, Joshua A. Bull*,3, Hao Wu4, Javier Ruiz-Ramírez 5, Daria Miroshnychenko1, Gregory J. Kimmel1, Eunjung Kim1, Robert J. Vander Velde1, Katarzyna Rejniak1, Brandon J. Manley1, Fabian Spill*,6, Andriy Marusyk*,1 Abstract— Advances in molecular oncology research complicated by the fact that stroma is spatially complex and culminated in the development of targeted therapies that act on heterogeneous and dynamically changing during disease defined molecular targets either on tumor cells directly (such as progression and therapy response. This lack of attention to inhibitors of oncogenic kinases), or indirectly by targeting the tumor stroma is also fully applicable to clinical diagnostics and tumor microenvironment (such as anti-angiogenesis drugs). decision-making in clear cell renal cell carcinoma (ccRCC), an These therapies can induce strong clinical responses, when aggressive epithelial malignancy. Despite availability of properly matched to patients. Unfortunately, most targeted targeted therapy directed against neoplastic cells directly therapies ultimately fail as tumors evolve resistance. Tumors (mTOR inhibitors) or indirectly (anti-angiogenic agents), late consist not only of neoplastic cells, but also of stroma, whereby stage ccRCC remains incurable7,8. The different stages of this “stroma” is the umbrella term for non-tumor cells and disease show distinct stromal architectures (Figure 1).
    [Show full text]
  • Program Update: Year Three
    PHYSICAL SCIENCES-ONCOLOGY CENTER PROGRAM Program Update: Year Three Fall 2012 Table of Contents 1. Executive Summary .................................................................................................................................................................1 2. Physical Sciences-Oncology Program Organization ...............................................................................................................5 2.1. Introduction ..................................................................................................................................................................7 2.2. Office of Physical Sciences-Oncology Mission ............................................................................................................7 2.3. Program History ...........................................................................................................................................................8 2.3.1 Overview of Spring 2008 Think Tank Meetings ................................................................................................8 2.3.2 Program Development and Funding History ...................................................................................................10 2.4. Strategic Approach and Objectives ...........................................................................................................................11 2.4.1 A Focus on Addressing “Big Questions” in Oncology ....................................................................................11
    [Show full text]
  • Microenvironment Influences Cancer Cell Mechanics from Tumor Growth
    Microenvironment Influences Cancer Cell Mechanics from Tumor Growth 5 to Metastasis Deepraj Ghosh and Michelle R. Dawson Abstract cell motility can easily be combined with anal- The microenvironment in a solid tumor in- ysis of critical cell fate processes, including cludes a multitude of cell types, matrix pro- adhesion, proliferation, and drug resistance, teins, and growth factors that profoundly in- to determine how changes in mechanics con- fluence cancer cell mechanics by providing tribute to cancer progression. This biophysical both physical and chemical stimulation. This approach can be used to systematically inves- tumor microenvironment, which is both dy- tigate the parameters in the tumor that control namic and heterogeneous in nature, plays a cancer cell interactions with the stroma and to critical role in cancer progression from the identify specific conditions that induce tumor- growth of the primary tumor to the develop- promoting behavior, along with strategies for ment of metastatic and drug-resistant tumors. inhibiting these conditions to treat cancer. In- This chapter provides an overview of the bio- creased understanding of the underlying bio- physical tools used to study cancer cell me- physical mechanisms that drive cancer pro- chanics and mechanical changes in the tumor gression may provide insight into novel thera- microenvironment at different stages of cancer peutic approaches in the fight against cancer. progression, including growth of the primary tumor, local invasion, and metastasis. Quan- titative single cell biophysical analysis of in- Keywords tracellular mechanics, cell traction forces, and Cell mechanics · Deformation · Microrheology · Traction force · Epithelial to D. Ghosh mesenchymal transition (EMT) · Motility · Department of Molecular Pharmacology, Physiology, and Adhesion · Metastasis Biotechnology, Brown University, Providence, RI, USA M.
    [Show full text]
  • 3D Models of Angiogenesis
    ID: XX-XXXX; -19-0026 1 1 E Zucchelli et al. 3D angiogenesis models 1:1 H135–H143 MINI REVIEW New artery of knowledge: 3D models of angiogenesis Eleonora Zucchelli1, Qasim A Majid1 and Gabor Foldes1,2 1National Heart and Lung Institute, Imperial College London, London, UK 2Heart and Vascular Center, Semmelweis University, Budapest, Hungary Correspondence should be addressed to G Foldes: [email protected] Abstract Angiogenesis and vasculogenesis are complex processes by which new blood vessels are Key Words formed and expanded. They play a pivotal role not only in physiological development f angiogenesis and growth and tissue and organ repair, but also in a range of pathological conditions, f endothelial cells from tumour formation to chronic inflammation and atherosclerosis. Understanding the f 3D assays multistep cell-differentiation programmes and identifying the key molecular players of physiological angiogenesis/vasculogenesis are critical to tackle pathological mechanisms. While many questions are yet to be answered, increasingly sophisticated in vitro, in vivo and ex vivo models of angiogenesis/vasculogenesis, together with cutting-edge imaging techniques, allowed for recent major advances in the field. This review aims to summarise the three-dimensional models available to study vascular network formation and to discuss advantages and limitations of the current systems. Introduction The major role of the vascular system is to supply sufficient vessels, another type of vasculature exists, which form the levels of oxygen and nutrients to the bodily organs. lymphatic network. Lymphatic vessels are unidirectional, Naturally, any disruption to this system manifests itself blind-ended capillaries, which arise from the venous as a host of diseases including, but not limited to, stroke, vasculature, and they are also formed by endothelial peripheral artery disease and other ischaemic cardiovascular cells.
    [Show full text]
  • Ascites-Induced Compression Alters the Peritoneal Microenvironment
    www.nature.com/scientificreports OPEN Ascites‑induced compression alters the peritoneal microenvironment and promotes metastatic success in ovarian cancer Marwa Asem1,2, Allison Young2, Carlysa Oyama2, Alejandro ClaureDeLaZerda2, Yueying Liu1,2, Matthew. J. Ravosa2,3, Vijayalaxmi Gupta4, Andrea Jewell4, Dineo Khabele4 & M. Sharon Stack1,2* The majority of women with recurrent ovarian cancer (OvCa) develop malignant ascites with volumes that can reach > 2 L. The resulting elevation in intraperitoneal pressure (IPP), from normal values of 5 mmHg to as high as 22 mmHg, causes striking changes in the loading environment in the peritoneal cavity. The efect of ascites-induced changes in IPP on OvCa progression is largely unknown. Herein we model the functional consequences of ascites-induced compression on ovarian tumor cells and components of the peritoneal microenvironment using a panel of in vitro, ex vivo and in vivo assays. Results show that OvCa cell adhesion to the peritoneum was increased under compression. Moreover, compressive loads stimulated remodeling of peritoneal mesothelial cell surface ultrastructure via induction of tunneling nanotubes (TNT). TNT-mediated interaction between peritoneal mesothelial cells and OvCa cells was enhanced under compression and was accompanied by transport of mitochondria from mesothelial cells to OvCa cells. Additionally, peritoneal collagen fbers adopted a more linear anisotropic alignment under compression, a collagen signature commonly correlated with enhanced invasion in solid tumors. Collectively, these fndings elucidate a new role for ascites-induced compression in promoting metastatic OvCa progression. Among gynecologic malignancies, ovarian cancer (OvCa) has the highest mortality rate, resulting in ~ 14,000 deaths in 2019 in the United States alone. Early detection of OvCa is challenging, such that the majority (75%) of women present at diagnosis with metastatic disease.
    [Show full text]
  • Nanoscientificvol 19 SPRING 2020 the Magazine for Nanoscience and Technology
    NANOscientificVOL 19 SPRING 2020 The Magazine for NanoScience and Technology HOW COVID-19 ELECTROCHEMICAL DIAGNOSTIC TESTS WORK p. 6 AFM (EC-AFM): IN SITU MONITOR OF COPPER NANO INFRARED (IR) DEPOSITION/DISSOLUTION PHOTO-INDUCED FORCE ON GOLD p. 9 MICROSCOPY (PIFM) p. 12 DETECTION OF MAGNETIZATION INDUSTRY NEWS: PARK REVERSAL IN MAGNETIC SYSTEMS COMPLETES PATTERNED ARRAY EQUITY INVESTMENT IN USING MAGNETIC FORCE p. 16 MOLECULAR VISTA p. 15 MICROSCOPY USING ATOMIC FORCE MICROSCOPY IN MEDICAL RESEARCH p. 21 PHASE IMAGING OF POLYMER DEPOSITED ON GOLD p. 24 The Most Accurate Atomic Force Microscope ToT olearn learn more more about about Park Park NX10 NX10 or or to to schedule schedule a ademo demo please please visit visit www.parksystems.com/nx10 www.parksystems.com/nx10 oror email email [email protected] [email protected] NANOSCIENTIFIC 2020 EDITORIAL BOARD Dr. Rigoberto Advincula, Professor, Department of Macromolecular Science TABLE and Engineering at Case Western Reserve University. OF CONTENTS NanoScientific Vol 19 Dr. Lane Baker, James L. Jackson Professor of Chemistry Indiana University p. 6 How Covid-19 Diagnostic Tests Work 6 Keibock Lee, Mr. Phil Kaszuba, Global Foundries Senior Member of Technical Staff and Euan McLeod, Assistant Professor College of Optical Sciences, Editor-in-Chief lead engineer in their Scanning Probe University of Arizona Microscopy (SPM) laboratory. Electrochemical AFM (EC-AFM): In Situ Monitor of Copper 9 Dr. John A. Marohn, Professor & Deposition/Dissolution on Gold for the NanoScientific Symposium on Director of Undergraduate Studies, Jiali Zhang, Ben Schoenek, Byong Kim and Keibock Lee, Park Department of Chemistry and Chemical Nano Materials for a Changing World (see Biology Member, Field of Materials Systems Inc., Santa Clara, CA, USA MESSAGE p.
    [Show full text]
  • Thermodynamically Constrained Averaging Theory for Cancer Growth
    6th IFAC Conference on View metadata,6th IFAC citation Conference and similar on papers at core.ac.uk brought to you by CORE 6thFoundations IFAC Conference of Systems on Biology in Engineering FoundationsOctober 9-12, of 2016. Systems Magdeburg, Biology Germany in EngineeringAvailable online at www.sciencedirect.com OctoberFoundations 9-12, of 2016. Systems Magdeburg, Biology Germany in Engineering provided by Open Repository and Bibliography - Luxembourg October 9-12, 2016. Magdeburg, Germany ScienceDirect IFAC-PapersOnLine 49-26 (2016) 289–294 Thermodynamically constrained averaging Thermodynamically constrained averaging theory for cancer growth modelling theory for cancer growth modelling Marco Albrecht ∗ Giuseppe Scium`e ∗∗ Philippe Lucarelli ∗ Marco Albrecht ∗ Giuseppe Scium`e ∗∗ Philippe Lucarelli ∗ Marco Albrecht ∗ GiuseppeThomas Scium`e Sauter∗∗∗ Philippe Lucarelli ∗ Thomas Sauter ∗ Thomas Sauter ∗ ∗ University of Luxembourg, Belvaux, 4367 Luxembourg ∗ University of Luxembourg, Belvaux, 4367 Luxembourg (e-mail:∗ University [email protected] of Luxembourg, Belvaux, or [email protected]). 4367 Luxembourg (e-mail:∗ University [email protected] of Luxembourg, Belvaux, or [email protected]). 4367 Luxembourg ∗∗ University(e-mail: of [email protected] Bordeaux I2M-TREFLE, or [email protected]). Talence Cedex, 33405 France ∗∗ University of Bordeaux I2M-TREFLE, Talence Cedex, 33405 France ∗∗ University of(e-mail: Bordeaux [email protected]) I2M-TREFLE, Talence Cedex, 33405 France ∗∗ University of(e-mail: Bordeaux [email protected]) I2M-TREFLE, Talence Cedex, 33405 France (e-mail: [email protected]) Abstract: In Systems Biology, network models are often used to describe intracellular mechanismsAbstract: In at Systems the cellular Biology, level. network The obtained models results are often are difficult used to to describe translate intracellular into three mechanismsAbstract: In at Systems the cellular Biology, level.
    [Show full text]
  • Computational Models of Melanoma Marco Albrecht1, Philippe Lucarelli1, Dagmar Kulms2 Andthomassauter1*
    Albrecht et al. Theoretical Biology and Medical Modelling (2020) 17:8 https://doi.org/10.1186/s12976-020-00126-7 REVIEW Open Access Computational models of melanoma Marco Albrecht1, Philippe Lucarelli1, Dagmar Kulms2 andThomasSauter1* Abstract Genes, proteins, or cells influence each other and consequently create patterns, which can be increasingly better observed by experimental biology and medicine. Thereby, descriptive methods of statistics and bioinformatics sharpen and structure our perception. However, additionally considering the interconnectivity between biological elements promises a deeper and more coherent understanding of melanoma. For instance, integrative network-based tools and well-grounded inductive in silico research reveal disease mechanisms, stratify patients, and support treatment individualization. This review gives an overview of different modeling techniques beyond statistics, shows how different strategies align with the respective medical biology, and identifies possible areas of new computational melanoma research. Keywords: Melanoma, Systems biology, Physical oncology, Tumor growth Background An approach to better understand causative relations, to Melanoma is a neoplasm of the skin and originates from check hypothesis consistency, but also to reveal miss- transformed melanocytes. It causes the loss of 1.6 mil- ing qualitative information is constructing evidence-based lion disease-adjusted life-years worldwide, and the inci- models of these biological systems [9]. Models depict dence rate will increase in the next decades [1]. Since several interconnected biological elements with a struc- the discovery of the high prevalence of mutations in b- ture, which is derived from the current understanding, Raf proto-oncogene (BRAF) and NRAS protooncogene, and parameters, which are based on data. While many GTPase (NRAS) [2, 3], small-molecule inhibitors such life-scientists still rely on straight-forward relationships as dabrafenib and vemurafenib have been developed.
    [Show full text]
  • Reviewphysical Oncology: New Targets for Nanomedicine
    Biomaterials 150 (2018) 87e99 Contents lists available at ScienceDirect Biomaterials journal homepage: www.elsevier.com/locate/biomaterials Review Physical oncology: New targets for nanomedicine * Alba Nicolas-Boluda a, Amanda K.A. Silva a, Sylvie Fournel b, Florence Gazeau a, a Laboratoire Matiere et Systemes Complexes (MSC), CNRS-UMR 7057, Universite Paris Diderot, Sorbonne Paris Cite, 10 Rue Alice Domon et Leonie Duquet, F-75205 Paris Cedex 13, France b Laboratoire de Conception et Application de Molecules Bioactives- Equipe de Biovectorologie UMR 7199 CNRS-Universite de Strasbourg, Facultede Pharmacie, 74 Route du Rhin, BP 60024-67401 Illkirch Cedex, France article info abstract Article history: Physical oncology is an emerging paradigm which recognizes tissue mechanics, per se, as an active Received 9 July 2017 modulator of tumorigenesis, treatment resistance and clinical outcome, mediated by mechanosignaling Received in revised form pathways, matrix remodeling and physical barriers to drugs. The tumor microenvironment displays 28 September 2017 abnormal physical properties in comparison to healthy tissue which contribute to cancer progression and Accepted 2 October 2017 resistance to current treatments. Physical aberrancies comprise the chaotic organization of tumor Available online 6 October 2017 vasculature, an increased interstitial pressure, an increased solid stress, hypoxia, an abundant extracel- lular matrix and a progressive stiffening of solid tumors. The physical barriers in tumors are of critical Keywords: fi Physical oncology importance, as tissue mechanics compromises drug delivery, reduces immune cell in ltration and pro- Mechanobiology motes disease aggressiveness. All these physical hallmarks of cancer, although not fully understood, are Tumor microenvironment inspiring new anticancer strategies aiming to target and normalize the physical anomalies of solid tu- Extracellular matrix mors, particularly in the field of nanomedicine.
    [Show full text]
  • Multiscale Modelling of Solid Tumour Growth: the Effect of Collagen
    Noname manuscript No. (will be inserted by the editor) Multiscale modelling of solid tumour growth: the effect of collagen micromechanics Peter A. Wijeratne · Vasileios Vavourakis · John H. Hipwell · Chrysovalantis Voutouri · Panagiotis Papageorgis · Triantafyllos Stylianopoulos · Andrew Evans · David J. Hawkes Received: date / Accepted: date Abstract Here we introduce a model of solid tumour was reduced by adding a load-bearing non-collagenous growth coupled with a multiscale biomechanical de- component to the fibre network constitutive equation. scription of the tumour microenvironment, which facil- itates the explicit simulation of fibre-fibre and tumour- Keywords Tumour mechanics · Microenvironment · fibre interactions. We hypothesise that such a model, Fibre remodelling · Finite element analysis which provides a purely mechanical description of tumour- host interactions, can be used to explain experimen- tal observations of the effect of collagen micromechan- 1 Introduction ics on solid tumour growth. The model was specified to mouse tumour data and numerical simulations were The tumour microenvironment is now widely accepted performed. The multiscale model produced lower stresses as being an important factor in the development, pro- than an equivalent continuum-like approach, due to a gression and invasion of cancerous cells (Liotta and more realistic remodelling of the collagen microstruc- Kohn, 2001). Whilst historically the focus of cancer re- ture. Furthermore, solid tumour growth was found to search has been on studying the relationship between cause a passive mechanical realignment of fibres at the intrinsic genomic properties and extrinsic chemical stim- tumour boundary from a random to a circumferential uli, observed epigenetic effects of force transmission be- orientation. This is in accordance with experimental tween cells and their microenvironment have established observations, thus demonstrating that such a response the idea of a mechanical phenotype (Butcher et al, 2009); can be explained as purely mechanical.
    [Show full text]
  • Matrix Degradation and Cell Proliferation Are Coupled to Promote Invasion and Escape from an Engineered Human Breast Microtumor Emann M
    Integrative Biology, 2021, 1–13 doi: 10.1093/intbio/zyaa026 Original Article ORIGINAL ARTICLE Downloaded from https://academic.oup.com/ib/advance-article/doi/10.1093/intbio/zyaa026/6120551 by guest on 27 January 2021 Matrix degradation and cell proliferation are coupled to promote invasion and escape from an engineered human breast microtumor Emann M. Rabie1,2, Sherry X. Zhang3, Andreas P. Kourouklis3, A. Nihan Kilinc3, Allison K. Simi3, Derek C. Radisky4,JoeTien5,6,*,and Celeste M. Nelson2,3,* 1Rutgers Robert Wood Johnson Medical School, Piscataway, NJ, USA, 2Department of Molecular Biology, Princeton University, Princeton, NJ, USA, 3Department of Chemical & Biological Engineering, Princeton University, Princeton, NJ, USA, 4Department of Cancer Biology, Mayo Clinic, Jacksonville, FL, USA, 5Department of Biomedical Engineering, Boston University, Boston, MA, USA, and 6Division of Materials Science and Engineering, Boston University, Boston, MA, USA *Corresponding authors. E-mail: [email protected] and [email protected] Abstract Metastasis, the leading cause of mortality in cancer patients, depends upon the ability of cancer cells to invade into the extracellular matrix that surrounds the primary tumor and to escape into the vasculature. To investigate the features of the microenvironment that regulate invasion and escape, we generated solid microtumors of MDA-MB-231 human breast carcinoma cells within gels of type I collagen. The microtumors were formed at defined distances adjacent to an empty cavity, which served as an artificial vessel into which the constituent tumor cells could escape. To define the relative contributions of matrix degradation and cell proliferation on invasion and escape, we used pharmacological approaches to block the activity of matrix metalloproteinases (MMPs) or to arrest the cell cycle.
    [Show full text]
  • Abstracts of Talks at Mini-Symposia
    Abstracts of talks presented at mini-symposia at the 8-th European Conference on Mathematical and Theoretical Biology, and Annual Meeting of the Society for Mathematical Biology, Kraków, June 28 - July 2, 2011 Contents Mini-symposium 1. Vector-borne diseases 19 Mario Recker 19 Erida Gjini 19 Daniel Coffield Jr. 20 Yves Dumont 21 Ben Adams 22 Mini-symposium 2. Modelling dengue fever epidemiology 23 Maira Aguiar 23 Eduardo Massad 24 Helena Sofia Rodrigues 25 Jose Lourenço 26 Nico Stollenwerk 26 Mini-symposium 3. Recent developments in the study of Lotka- Volterra and Kolmogorov systems 29 Janusz Mierczynski 29 Zhanyuan Hou 29 Yasuhiro Takeuchi 30 Joanna Balbus 30 Stephen Baigent 31 Mini-symposium 4. Connecting microscale and macroscale models of cellular migration 33 Ruth Baker 33 Matthew Simpson 34 John Fozard 34 Evgeniy Khain 35 Alistair Middleton 36 Mini-symposium 5. The emergence of resistance in cancer using mathematical modelling 37 Alexander Anderson 37 Edward Flach 37 Jasmine Foo 38 Heiko Enderling 39 David Basanta 39 Mini-symposium 6. Modeling physiological systems: model validation and experimental design issues 41 Jerry Batzel 41 3 European Conference on Mathematical and Theoretical Biology 2011 Mette Olufsen 42 Mostafa Bachar 43 Franz Kappel 43 Johnny Ottesen 44 Julian King 45 Mini-symposium 7. Ecology and evolution of infectious diseases 47 Troy Day 47 Akira Sasaki 47 Andy White 48 Samuel Alizon 49 Eva Kisdi 50 Mini-symposium 8. Game theoretical modelling and optimization in evolution and ecology I 51 Magnus Lindh 51 Maciej Jan Ejsmond 52 Frédéric Grognard 52 Krzysztof Argasinski 53 Mini-symposium 9.
    [Show full text]