Bio

→ HCP Graduate Chemical Engineering part time student. Full time Process Engineer at Kite, a Gilead Company.
→ Bachelors in Biomedical Engineering at the University of Texas, Austin.
→ 5 years of experience working in cGMP pharmaceutical manufacturing and upstream process development. Working knowledge of cell and gene therapy, lean manufacturing, risk assessment &mitigation, IOPQ Validation, quality systems, eQRMS, asset lifecycle management, SAP ERP, Syncade MES, Oracle EBS, LIMS, ISO standards and FDA regulations.
→ Through Stanford's MS program, I aim to build upon my biomanufacturing experience, further developing my skillsets in bioreactor design and data analytics to model and improve standardized development of therapeutics for patients

Honors & Awards

  • Cockrell School of Engineering College Scholar, The University of Texas at Austin (2018)
  • CPRIT Cancer Research Grant Receiptent, Cancer Prevention and Research Institute of Texas (2018)
  • ThinkSwiss Research Scholarship, Embassy of Switzerland in the USA (2019)

Education & Certifications

  • B.S., University of Texas, Austin, Biomedical Engineering (2021)

Contact

  • Academic
    alayshah@stanford.edu
    University - Student Department: Chemical Engineering Position: Graduate

Links

Work Experience

  • Manufacturing Sciences and Technology (MSAT) Process Engineer I, Kite, A Gilead Company (January 2022 - Present)

    Location

    El Segundo, CA

  • Manufacturing Bioprocessing Associate, Bristol Myers Squibb (May 2021 - January 2022)

    Location

    Bothell, WA

  • R&D Innovation (Upstream Pilot Manufacturing) Co-Op, Genentech (January 2020 - September 2020)

    Location

    South San Francisco, CA

All Publications

  • Experimentally-driven mathematical modeling to improve combination targeted and cytotoxic therapy for HER2+ breast cancer. Scientific reports Jarrett, A. M., Shah, A., Bloom, M. J., McKenna, M. T., Hormuth, D. A., Yankeelov, T. E., Sorace, A. G. 2019; 9 (1): 12830

    Abstract

    The goal of this study is to experimentally and computationally investigate combination trastuzumab-paclitaxel therapies and identify potential synergistic effects due to sequencing of the therapies with in vitro imaging and mathematical modeling. Longitudinal alterations in cell confluence are reported for an in vitro model of BT474 HER2+ breast cancer cells following various dosages and timings of paclitaxel and trastuzumab combination regimens. Results of combination drug regimens are evaluated for drug interaction relationships based on order, timing, and quantity of dose of the drugs. Altering the order of treatments, with the same total therapeutic dose, provided significant changes in overall cell confluence (p < 0.001). Two mathematical models are introduced that are constrained by the in vitro data to simulate the tumor cell response to the individual therapies. A collective model merging the two individual drug response models was designed to investigate the potential mechanisms of synergy for paclitaxel-trastuzumab combinations. This collective model shows increased synergy for regimens where trastuzumab is administered prior to paclitaxel and suggests trastuzumab accelerates the cytotoxic effects of paclitaxel. The synergy derived from the model is found to be in agreement with the combination index, where both indicate a spectrum of additive and synergistic interactions between the two drugs dependent on their dose order. The combined in vitro results and development of a mathematical model of drug synergy has potential to evaluate and improve standard-of-care combination therapies in cancer.

    View details for DOI 10.1038/s41598-019-49073-5

    View details for PubMedID 31492947

    View details for PubMedCentralID PMC6731321

  • The biomechanical basis of biased epithelial tube elongation in lung and kidney development. Development (Cambridge, England) Conrad, L., Runser, S. V., Fernando Gómez, H., Lang, C. M., Dumond, M. S., Sapala, A., Schaumann, L., Michos, O., Vetter, R., Iber, D. 2021; 148 (9)

    Abstract

    During lung development, epithelial branches expand preferentially in a longitudinal direction. This bias in outgrowth has been linked to a bias in cell shape and in the cell division plane. How this bias arises is unknown. Here, we show that biased epithelial outgrowth occurs independent of the surrounding mesenchyme, of preferential turnover of the extracellular matrix at the bud tips and of FGF signalling. There is also no evidence for actin-rich filopodia at the bud tips. Rather, we find epithelial tubes to be collapsed during early lung and kidney development, and we observe fluid flow in the narrow tubes. By simulating the measured fluid flow inside segmented narrow epithelial tubes, we show that the shear stress levels on the apical surface are sufficient to explain the reported bias in cell shape and outgrowth. We use a cell-based vertex model to confirm that apical shear forces, unlike constricting forces, can give rise to both the observed bias in cell shapes and tube elongation. We conclude that shear stress may be a more general driver of biased tube elongation beyond its established role in angiogenesis. This article has an associated 'The people behind the papers' interview.

    View details for DOI 10.1242/dev.194209

    View details for PubMedID 33946098

    View details for PubMedCentralID PMC8126414