About

Teju Cole is the Gore Vidal Professor of the Practice of Creative Writing at Harvard University. His academic background includes a B.A. from Kalamazoo College, an M.A. from SOAS, University of London, and an M. Phil. from Columbia University. His interests encompass fiction writing, literary criticism, and photography criticism. Cole has authored works such as 'Blind Spot' (2017), 'Known and Strange Things' (2016), and 'Every...' which reflect his engagement with contemporary literary and visual arts. As a professor, he contributes to the department through his expertise in creative writing and critical analysis, fostering a deeper understanding of narrative and visual storytelling.

Research topics

• Pathology
• Immunology
• Medicine
• Nuclear medicine

Selected publications

• Supplementary Figures S1-S10 from p38MAPKα Stromal Reprogramming Sensitizes Metastatic Breast Cancer to Immunotherapy

  2025-12-11

  articleOpen access

  <p>Contains supplemental figures and legends</p>

  PublisherDOI

• Supplementary Table S1 from p38MAPKα Stromal Reprogramming Sensitizes Metastatic Breast Cancer to Immunotherapy

  2025-12-11

  articleOpen access

  <p>Table containing all of our reagents</p>

  PublisherOA PDFDOI

• Tumor site-directed A1R expression enhances CAR T cell function and improves efficacy against solid tumors

  Nature Communications · 2025-07-03 · 8 citations

  articleOpen access

  Abstract The efficacy of Chimeric Antigen Receptor T cells against solid tumors is limited by immunosuppressive factors in the tumor microenvironment including adenosine, which suppresses Chimeric Antigen Receptor T cells through activation of the A 2A receptor. To overcome this, Chimeric Antigen Receptor T cells are engineered to express A 1 receptor, a receptor that signals inversely to A 2A receptor. Using murine and human Chimeric Antigen Receptor T cells, constitutive A 1 receptor overexpression significantly enhances Chimeric Antigen Receptor T cell effector function albeit at the expense of Chimeric Antigen Receptor T cell persistence. Through a CRISPR/Cas9 homology directed repair “knock-in” approach we demonstrate that Chimeric Antigen Receptor T cells engineered to express A 1 receptor in a tumor-localized manner, enhances anti-tumor therapeutic efficacy. This is dependent on the transcription factor IRF8 and is transcriptionally unique when compared to A 2A receptor deletion. This data provides a novel approach for enhancing Chimeric Antigen Receptor T cell efficacy in solid tumors and provides proof of principle for site-directed expression of factors that promote effector T cell differentiation.

  PublisherOA PDFDOI

• CRISPR engineering of armored CAR T cells enables tumor restricted payload delivery with enhanced efficacy and safety

  Research Square · 2025-04-28

  preprintOpen access
  PublisherOA PDFDOI

• Rewiring endogenous genes in CAR T cells for tumour-restricted payload delivery

  Nature · 2025-07-02 · 53 citations

  articleOpen access

  The efficacy of chimeric antigen receptor (CAR) T cell therapy in solid tumours is limited by immunosuppression and antigen heterogeneity1–3. To overcome these barriers, ‘armoured’ CAR T cells, which secrete proinflammatory cytokines, have been developed4. However, their clinical application has been limited because of toxicity related to peripheral expression of the armouring transgene5. Here, we have developed a CRISPR knock-in strategy that leverages the regulatory mechanisms of endogenous genes to drive transgene expression in a tumour-localized manner. By screening endogenous genes with tumour-restricted expression, we have identified the NR4A2 and RGS16 promoters as promising candidates to support the delivery of cytokines such as IL-12 and IL-2 directly to the tumour site, leading to enhanced antitumour efficacy and long-term survival of mice in both syngeneic and xenogeneic models. This effect was concomitant with improved CAR T cell polyfunctionality, activation of endogenous antitumour immunity and a favourable safety profile, and was applicable in CAR T cells from patients. A CRISPR knock-in strategy that uses endogenous gene regulatory mechanisms can engineer ‘armoured’ CAR T cells that secrete proinflammatory cytokines directly within a tumour without causing toxicity, leading to prolonged survival in mice.

  PublisherOA PDFDOI

• Supplementary Figures S1-S10 from p38MAPKa stromal reprogramming sensitizes metastatic breast cancer to immunotherapy

  2024-09-16

  preprintOpen access

  <p>Contains supplemental figures and legends</p>

  PublisherDOI

• Tumor-site directed A1R expression enhances CAR T cell function and improves efficacy against solid tumors

  Research Square · 2024-03-13

  preprintOpen access
  PublisherOA PDFDOI

• Supplementary Figures S1-S10 from p38MAPKa stromal reprogramming sensitizes metastatic breast cancer to immunotherapy

  2024-09-16

  preprintOpen access

  <p>Contains supplemental figures and legends</p>

  PublisherDOI

• Supplementary Table S1 from p38MAPKa stromal reprogramming sensitizes metastatic breast cancer to immunotherapy

  2024-09-16

  supplementary-materialsOpen access

  <p>Table containing all of our reagents</p>

  PublisherDOI

• Targeting stromal p38MAPKalpha triggers innate-adaptive anti-tumor immunity and sensitizes metastatic breast cancer to immunotherapy

  Journal of bone oncology · 2024-04-01

  articleOpen access
  PublisherDOI

Frequent coauthors

• Michael Berkwits

  897 shared

• Annette Flanagin

  897 shared

• Phil Fontanarosa

  897 shared

• James Madara

  St. Louis County Missouri

  897 shared

• Larry Bryant

  International Rescue Committee

  897 shared

• Deanna Bellandi

  893 shared

• Yolanda Davis

  Advisory Board Company (United States)

  878 shared

• Rick Bell

  University of Washington

  853 shared

Education

• B.A., English

  Yale University

  1996

• M.A., English

  Yale University

  1998

• Ph.D., English

  Yale University

  2004