• Arturo Araujo, PhD

    Scientist, artist and film lover.

    I am senior research fellow at Braintree Ltd, an Artificial Intelligence research company based in London UK with close ties to UCL. As leader of the pure research branch, my vision is examine systems related to natural life, its processes, and its evolution, through the use of simulations with computer models, robotics, and biochemistry. This enable us to develop brand new ways of doing natural computation outside of traditional schemes; as well as increase our understanding of life processes.

     

    I have 5 years postdoc experience at the Integrated Mathematical Oncology (IMO) department at H. Lee Moffitt Cancer Center, where I strived to acquire the necessary skills to become a successful independent researcher including cost managing, grant writing, multi project managing, risk assessment and importantly collaborative and people skills. I am fluent in English and Spanish and have experience in IT, programming, cell culture, teaching, art and graphic design. My long-term goal is to computationally explore and understand the complexity in biological systems and diseases such as cancer.

     

    I look forward to meeting and collaborating with new people, as I think we all have important things to contribute to the advancement of science. By working together, we can really make a difference in the world.

  • Cancer Research

    Understanding Colorectal Cancer

    Intestinal glands in the small intestine and colon, or intestine crypts, are an important example of tissue homeostasis regulated by the extracellular environment. The crypts are invaginated structures made of a layer of cells that help absorb nutrients from passing food. However, they are continuously worn away by this process and are being continually renovated by Stem Cells at the bottom of the crypt. These Stem Cells divide to replace worn cells and may even displace other stem cells so that at a given time the whole crypt becomes monoclonal- a descendant of one single Stem Cell. Colorectal Cancer, the second leading cause of cancer-related death in Europe and North America, is thought to start with a mutation of one Stem Cell at the base of the intestinal crypt; which then expands within the crypt until the crypt is composed of monoclonal cells. The time to monoclonality therefore offers a key metric for the successful establishment of mutations.; however, the biggest biological contributor to this feature is highly debated. To tackle this, we have abstracted key biological features and modelled them in a bottom-up Agent-Based Model that allowed us to study the biological first principles that rule the fixation of mutations, offering key spatial and temporal understanding of this process. Our results show that the number of basal Stem Cells have a direct influence on the fixations of mutations and suggesting a lesser role for extracellular influences, while proposing the existence of a threshold to the contribution of cell side displacement. Our results have been published as:

     

    • Araujo, A., Rübben A., Bentley, P., Basanta D. Testing Three Hypotheses of the Contribution of Geometry and Migration Dynamics to Intestine Crypt Evolution. Accepted.
    • Rübben A., Araujo, A. (2017) “Cancer Heterogeneity: Converting a Limitation into a Source of Biologic Information” Journal of Translational Medicine. 2017;15:190. doi:10.1186/s12967-017-1290-9.

     

     

    Modeling Therapies for Prostate to Bone Metastasis

    Bone metastasis is common in prostate cancer progression. In bone, prostate cancer cells derive factors necessary for progression by manipulating bone forming osteoblasts and bone resorbing osteoclasts, resulting in areas of excessive osteogenesis and osteolysis, respectively. Transforming growth factor beta (TGFBeta) is a key factor in the progression of bone metastases. Therapeutic inhibition of TGFBeta however, presents a dilemma since it can have differential effects on various cell types in the tumor-bone microenvironment. In our current study, we have utilised an integrated approach using mathematical and in vivo models to test the impact of TGFBeta inhibition on prostate to bone metastases as a possible therapy. For this, we developed an agent-based mathematical model where the interactions between key cell types and their role on the evolutionary dynamics of the tumour can be studied. Our work has been published in :

    • Araujo, A., Cook, L. M., Lynch, C. C., & Basanta, D. (2018) Establishment of prostate cancer metastases in the bone. Bulletin of Mathematical Biology. https://doi.org/10.1007/s11538-018-0416-4
    • Cook, L. M., Araujo, A.., Pow-Sang, J. M., Budzevich, M. M., Basanta, D., & Lynch, C. C. (2016). Predictive computational modeling to define effective treatment strategies for bone metastatic prostate cancer. Scientific reports, 6.
    • Araujo, A. & Bastanta D. (2016) Hybrid Discrete-Continuum Cellular Automaton (HCA) model of Prostate to Bone Metastasis. bioRxiv. 2016 Jan 1:043620.
    • Gallaher J, Cook LM, Gupta S, Araujo, A., Dhillon D, Park JY, Scott, J, Basanta, D and Lynch CC. (2014). Improving Treatment Strategies for Patients with Metastatic Castrate Resistant Prostate Cancer through Personalized Computational Modeling. Clinical & Experimental Metastasis, 31(8), 991-999.
    • Cook, L. M., Shay, G., Araujo, A., & Lynch, C. C. (2014). Integrating new discoveries into the “vicious cycle” paradigm of prostate to bone metastases. Cancer and Metastasis Reviews.
    • Araujo, A.., Cook, L. M., Lynch, C. C., & Basanta, D. (2014). An Integrated Computational Model of the Bone Microenvironment in Bone-Metastatic Prostate Cancer. Cancer research, 74(9), 2391-2401.

    Aneuploidy in Cancer

    Many cancers are aneuploid (have chromosomal aberrations). However, the precise role that chromosomal instability plays in the development of cancer and in the response of tumours to treatment is still hotly debated. To explore this question from a theoretical standpoint we have developed an agent-based model of tissue homeostasis in which to test the likely effects of whole chromosome mis-segregation during cancer development. In stochastic simulations, chromosome mis-segregation events at cell division lead to the generation of a diverse population of aneuploid clones that over time exhibit hyperplastic growth. Significantly, the course of cancer evolution depends on genetic linkage, as the structure of chromosomes lost or gained through mis-segregation events and the level of genetic instability function in tandem to determine the trajectory of cancer evolution. As a result, simulated cancers differ in their level of genetic stability and in their growth rates. We used this system to investigate the consequences of these differences in tumour heterogeneity for anti-cancer therapies based on surgery and anti-mitotic drugs that selectively target proliferating cells. Our model highlights the difficulties of predicting the outcome of a given anti-cancer treatment, even in cases in which it is possible to determine the genotype of the entire set of cells within the developing tumour. This work was published in :

     

    • Araujo, A.., Baum, B., & Bentley, P. (2013). The Role of Chromosome Missegregation in Cancer Development: A Theoretical Approach Using Agent-Based Modelling. PloS one, 8(8), e72206.
    • Araujo, A., Bentley, P. J. and Baum, B. (2010) Modelling the Role of Chromosome Missegregation in Cancer Therapies. 3rd Complex Systems Modelling and Simulation Workshop. 2010. Luniver Press. 
    • Araujo, A., Bentley, P. J. and Baum, B. (2010) Modelling the Role of Aneuploidy in Tumour Evolution. 12th International Conference on the Synthesis and Simulation of Living Systems. 2010. MIT Press. 
  • Arturo in the Media

    I aim to use all of my interdisciplinary training and viewpoints to successfully bridge the gap between theory, experiments and the clinic with integrated computational models in tight collaboration with biologists and clinicians. Together with Dr. Leah Cook, we successfully modelled Prostate Bone Metastasis at the interphase between mathematics, biology and the clinic. The cutting-edge computational techniques I developed have been highlighted in the media at:

    I was also interviewed by Univision (in Spanish) on Adaptive Treatments:

    And on my science outreach efforts when organising the Pint of Science Festival in Tampa, FL USA:

  • Call me, maybe?

    I'll get back to you as soon as possible.

  • About me

    Really interested? Well...

     

    I have the ability to think abstractly. This is my main feature :P. It is easy for me to see the grey areas and the blurred lines. I’m also a planer and enjoy structure and order with a dash of spontaneity. I’m an introverted thinker but an extroverted feeler. this means I need plenty of time to ponder a question and organise my thoughts into words.

     

    I sometimes struggle with social norms and, because I find it difficult to put my thoughts into words, I’m uncomfortable being in situations where I have to interact in a spontaneous manner (such as meeting someone new), but I always try my best hoping it’ll be enough.

     

    I spend most of my time thinking through stuff. I love to talk about culture, life stories and sincere issues. I strive to see the other persons point-of-view on any situation.

     

     

    I am private and enjoy only opening up to my closest friends. I’ve been told that I take ”how are you” too literal, but when I answer and when I ask this, I mean it.

     

    I have travelled.

     

    I call my mum in Mexico once a week.

     

    I have rarely been at complete peace with myself, but I have often feel happiest and most fulfilled when making models to help others understand their problems, be it scientific, artistic, social or personal.

     

    My passions are coffee, red wine and watching films. Lots of films. I also build lightsabers.