Bio


Dr. Adel Z. I. Mutahar is a postdoctoral researcher in the Department of Surgery at Stanford University, working under the mentorship of Dr. Frederick M. Dirbas. His research focuses on translational breast cancer biology and emerging radiotherapy technologies, with an emphasis on tumor–microenvironment interactions, immuno-oncology, and preclinical therapeutic development. His academic journey spans three countries—beginning in Yemen, advancing through India, and now progressing at Stanford—reflecting his commitment to impactful cancer research and global scientific advancement.
Dr. Mutahar began his career in Yemen, earning his Bachelor’s degree in Medical Laboratory Sciences before joining Abs Community College as a faculty member. From 2007–2013, he held several academic leadership roles, including Academic Director, Head of Evaluation, and Assistant Dean of Students, where he modernized curriculum, expanded hands-on diagnostic training, and strengthened laboratory education infrastructure in resource-limited settings. His work contributed to building a more skilled medical diagnostics workforce and improving pathways for laboratory science education.
Awarded a prestigious national merit scholarship, Dr. Mutahar continued his graduate and doctoral training in India, completing his M.S. and Ph.D. in Biotechnology with a focus on triple-negative breast cancer. During his doctoral work, he developed 3D tumor spheroid models and combinatorial therapeutic strategies, demonstrating synergy between anti-angiogenic agents and chemotherapy in TNBC. He further advanced this research by creating an orthotopic murine model to investigate metastatic progression and demonstrated that knockdown of the MTA1 gene in mesenchymal stem cells (MSCs) significantly suppressed TNBC invasion, angiogenesis, and metastatic spread, introducing a promising stromal-targeted therapeutic concept for aggressive breast cancer. This work earned recognition through travel grants, conference presentations, and a Best Poster Award. His scientific adaptability was further demonstrated during the COVID-19 pandemic, when he uncovered a novel interaction between SARS-CoV-2 Spike RBD and VEGF signaling.
At Stanford, his work emphases on FLASH radiotherapy, an ultrahigh-dose-rate modality with the potential to widen the therapeutic window by minimizing normal-tissue toxicity while maintaining tumor control. Working within Dr. Dirbas’s translational breast oncology program, Dr. Mutahar employs patient-derived xenografts, orthotopic murine models, spatial transcriptomics, single-cell RNA sequencing, and immune profiling to dissect the biological mechanisms governing treatment response. His research integrates multi-omics analysis to map early and late radiotherapy injury pathways—including senescence, apoptosis and fibrosis. His goal is to develop mechanism-driven radio-immunotherapy strategies and durable FLASH-RT combination regimens that can be translated into clinical trials for breast cancer, improving therapeutic durability, minimizing toxicity, and ultimately enhancing patient outcomes.
Dr. Mutahar’s long-term vision is to establish an independent laboratory at the intersection of radiobiology, immuno-oncology, and translational therapeutics. Guided by Dr. Dirbas’s mentorship and shaped by multidisciplinary experience across three continents, he aims to develop biologically informed treatment strategies that eradicate tumors while preserving normal tissue and immune integrity—ultimately improving quality of life and survival for women with aggressive breast cancers.

Honors & Awards


  • Young Investigator Award, San Antonio Breast Cancer Symposium (9-12 December 2025)
  • Travel Award - Immune Responses & DNA Repair - Cancer Fields Converging. Florence, Italy, European Association for Cancer Research (EACR) (16-18 March 2023)
  • Best Poster Presentation Award, Bangalore Tech Summit organized by Government of Karnataka - India at Bangalore. (16th to 18th November 2022)

Boards, Advisory Committees, Professional Organizations


  • Associate Member, American Association of Cancer Research (2020 - Present)
  • Associate Member and Ambassador, European Association of Cancer Research (2019 - Present)
  • Postdoctoral Member, American Society for Radiation Oncology (2025 - Present)
  • Member, Indian Association of Cancer Research (2017 - Present)

Professional Education


  • Doctor of Philosophy, University Of Mysore (2023)
  • Bachelors in Medical Sciences, Faculty of Medicine and Medical Sciences - Hodeida University - Yemen, Medical Laboratories (2006)
  • Master of Science, Bangalore University - India, Biotechnology (2015)
  • PhD, University of Mysore, India, Biotechnology (Cancer Biology and Combination Therapies) (2023)

Stanford Advisors


All Publications


  • Effectiveness of FLASH vs. Conventional Dose Rate Radiotherapy in a Model of Orthotopic, Murine Breast Cancer. Cancers Melemenidis, S., Viswanathan, V., Dutt, S., Kapadia, N., Lau, B., Soto, L. A., Ashraf, M. R., Thakur, B., Mutahar, A. Z., Skinner, L. B., Yu, A. S., Surucu, M., Casey, K. M., Rankin, E. B., Horst, K. C., Graves, E. E., Loo, B. W., Dirbas, F. M. 2025; 17 (7)

    Abstract

    Introduction: Radiotherapy is effective for breast cancer treatment but often causes undesirable side effects that impair quality of life. Ultra-high dose rate radiotherapy (FLASH) has shown reduced normal tissue toxicity while achieving comparable tumor growth delay compared to conventional dose rate radiotherapy (CONV). This study evaluated whether FLASH could achieve similar tumor control as CONV with tumor eradication as the primary endpoint, in an orthotopic breast cancer model. Methods: Non-metastatic, orthotopic tumors were generated in the left fourth mammary fat pad using the Py117 mammary tumor cell line in syngeneic C57BL/6J mice. Two sequential irradiation studies were performed using FLASH (93-200 Gy/s) and CONV (0.08 Gy/s) electron beams. Single fractions of 20, 25, or 30 Gy were applied to tumors with varying abdominal wall treatment fields (~3.75 or 2.5 mm treatment margin to tumor). Results: Both FLASH and CONV demonstrated comparable efficacy. Small tumors treated with 30 Gy and larger abdominal wall treatment fields appeared to have complete eradication at 30 days but also exhibited the highest skin toxicity, limiting follow-up and preventing confirmation of eradication. Smaller abdominal wall treatment fields reduced skin toxicity and allowed for extended follow-up, which resulted in 75% tumor-free survival at 48 days. Larger tumors showed growth delay but no eradication. Conclusions: In this preclinical, non-metastatic orthotopic breast cancer model, FLASH and CONV demonstrated equivalent tumor control with single-fraction doses of 20, 25, or 30 Gy. Overall, 30 Gy achieved the highest eradication rate but also resulted in the most pronounced skin toxicity.

    View details for DOI 10.3390/cancers17071095

    View details for PubMedID 40227580

  • In-vitro multicellular 3D-Spheroid model demonstrates the synergistic effect of 2-domain soluble FMS-like Tyrosine Kinase-1 (2d-sFlt-1) for breast cancer targeted therapies Mutahar, A. I. AMER ASSOC CANCER RESEARCH. 2023
  • Vascular Endothelial Growth Factor Receptor, fms-Like Tyrosine Kinase-1 (Flt-1), as a Novel Binding Partner for SARS-CoV-2 Spike Receptor-Binding Domain. Frontiers in immunology Mutahar, A. Z., Devaramani, M., Dayal, R., Saini, D. K., Salimath, P. V., Salimath, B. P. 2022; 13: 906063

    Abstract

    Angiotensin-converting enzyme 2 (ACE2) and neuropilin 1, a vascular endothelial growth factor (VEGF) receptor, were identified to bind to the SARS-CoV-2 spike receptor-binding domain (spike RBD). In silico analysis based on 3D structure, multiple sequence alignment, and molecular docking of second domain of soluble Flt-1 (sFlt-1) and spike RBD revealed structural similarities, sequence homology, and protein-protein interaction. Interaction and binding of recombinant spike RBD (rspike RBD) and recombinant sFlt-1 (rsFlt-1) in vitro induced a conformational change, as revealed by spectrofluorimetric data, with increased fluorescence intensity in emission spectra as compared to either of the proteins alone. Results on ELISA confirmed the binding and cross-reactivity of rspike-RBD and rsFlt-1 as determined by using either specific antibodies towards each protein or immunized human serum. We found that polyclonal or monoclonal anti-spike RBD antibodies can recognize either rsFlt-1 or rspike RBD, showing cross-reactivity for the two proteins in a dose-dependent binding response. Recognition of bound rspike RBD or rsFlt-1 by anti-Flt-1 or anti-spike RBD antibodies, respectively, as observed by immunoblotting, further confirmed interaction between the two proteins. Immunoprecipitation and immunoblot analysis demonstrated the identification of rspike RBD binding to the Flt-1 receptor on A549 cells. Further, the binding of rspike RBD to Flt-1 receptor was shown using immunofluorescence on 2D-culture or 3D-spheroid of MDA-MB-231 cells, which over-express Flt-1 receptor. Together, our study concludes that the Flt-1 receptor is a novel binding partner for SARS-CoV-2 spike RBD.

    View details for DOI 10.3389/fimmu.2022.906063

    View details for PubMedID 35874709

    View details for PubMedCentralID PMC9304886