Dr. Eric P. Grewal

Physician, Immunologist, Cancer Researcher

Welcome to my site!

Background:

What's up! I am a faculty physician-scientist (immunologist and cell therapy physician) with expertise in immuno-oncology, immunotherapeutics, translational research, and early-phase clinical trials.

Originally from the West Coast, I spent most of my time growing up in the suburbs outside of San Francisco, Seattle, and Los Angeles. My education took me all over the United States, including the Northeast and the Midwest, and I am now based in Boston, Massachusetts. Right now, I am an early-career investigator at Massachusetts General Hospital & Harvard Medical School, where I focus on developing novel therapeutics for brain tumors such as glioblastoma.

Through this journey, I have spent over a decade working as a bench scientist (across all areas of in vitro and in vivo immunology), as a translational study director (conducting clinical trials, biomarker studies, and bioinformatic analyses), and at the patient bedside (in my specialty of clinical pathology, with specific emphasis on clinical immunology, apheresis, and cellular therapy). Within immunology, my specific focus is modulating the T cell response to cancer, breaking tolerance against neoantigens, and leveraging new cellular subsets for immunotherapy using vaccines, CARs, synthetic TCRs, bispecific mAbs, scFvs, and occasionally small molecules.

Outside of immunology, I am also passionate about education and global health, with avocations as a lecturer, study director, and global non-profit clinical laboratory advisor. My ultimate goal is to harness the full potential of cellular therapies to treat patients with no current curative options, helping alleviate the burden of immune-mediated diseases worldwide.

Education:

Undergrad:

Immunology & Pathogenesis

Grad school:

Immunology

MD:

Doctor of Medicine

Residency:

Clinical Pathology and Laboratory Medicine

Skills:

Clinical development (phase I/II trials), preclinical research, translational medicine, biomarker strategy, lab management.

Contact information:

Doximity: https://www.doximity.com/pub/eric-grewal-md

LinkedIn: https://www.linkedin.com/in/eric-grewal

ResearchGate: https://www.researchgate.net/profile/Eric-Grewal

Faculty page: https://researchers.mgh.harvard.edu/profile/16020852/Eric-Grewal

Selected works:

Peptide Vaccine with Glucopyranosyl Lipid A–Stable Oil-in-Water Emulsion for Patients with Resected Melanoma Aim: We tested the safety and immunogenicity of a novel vaccine in patients with resected high-risk melanoma. Patients & methods: HLA-A2-positive patients with resected Stage II–IV melanoma were r...

Mutant IDH Modulates Suppressive Myeloid Populations in Malignant GliomaAbstractPurpose:. Mutations in the isocitrate dehydrogenase (IDH) genes IDH1 and IDH2 have critical diagnostic and prognostic significance in diffuse gliomas. Neomorphic mutant IDH activity has been previously implicated in T-cell suppression; however, the effects of IDH mutations on intratumoral myeloid populations remain underexplored. In this study, we investigate the influence of IDH status on the myeloid compartment using human glioma specimens and preclinical models.Experimental Design:. We performed RNA sequencing and quantitative immunofluorescence on newly diagnosed, treatment-naive IDH-mutant grade 4 astrocytoma and IDH-wild-type (IDH-WT) glioblastoma (GBM) specimens. We also generated a syngeneic murine model, comparing transcriptomic and cell-level changes in paired isogenic glioma lines that differ only in IDH mutational status.Results:. Among patient samples, IDH-mutant tumors displayed an underrepresentation of suppressive myeloid transcriptional signatures, which was confirmed at the cellular level with decreased numbers of intratumoral M2-like macrophages and myeloid-derived suppressor cells. Introduction of the mutant IDH enzyme into murine glioma was sufficient to recapitulate the transcriptomic and cellular shifts observed in patient samples.Conclusions:. We provide transcriptomic and cellular evidence that mutant IDH is associated with a quantitative reduction of suppressive myeloid cells in gliomas and that introduction of the mutant enzyme is sufficient to result in corresponding cellular changes using an in vivo preclinical model. These data advance our understanding of high-grade gliomas by identifying key myeloid cell populations that are reprogrammed by mutant IDH and may be targetable through therapeutic approaches.

Neoadjuvant cobimetinib and atezolizumab with or without vemurafenib for high-risk operable Stage III melanoma: the Phase II NeoACTIVATE trial - Nature CommunicationsImmunotherapy with immune checkpoint inhibitors and targeted therapy with BRAF and MEK inhibition have revolutionized the treatment of melanoma. Here the authors report the results of a phase II trial of neoadjuvant cobimetinib (MEK inhibitor) and atezolizumab (anti-PD-L1) with or without the BRAF inhibitor vemurafenib in patients with resectable Stage III melanoma.

Mesothelin is a surface antigen present on human meningioma and can be effectively targeted by CAR T-cells - PubMedMesothelin is a viable CAR T-cell target for meningiomas, and mesothelin-specific CAR T-cell therapy shows strong preclinical efficacy. These findings provide a rationale for early-phase clinical trials of mesothelin CAR T-cell therapy in patients with refractory meningiomas.

Suppression of antitumor immune signatures and upregulation of VEGFA as IDH-mutant gliomas progress to higher grade - PubMedHere, the authors have provided a transcriptomic analysis of a progression cohort for IDH-mutant glioma. Compared with lower-grade tumors, grade 4 astrocytomas displayed alterations that may inform the timing of antiangiogenic and immune-based therapy as these tumors progress.

Clinical progress in the development of CAR T cells to treat malignant glioma - Journal of Neuro-OncologyContext Chimeric antigen receptor (CAR) T cell therapy is an exciting modality of immunotherapy that has revolutionized the treatment of hematologic malignancies. However, translating this success to malignant gliomas such as glioblastoma (GBM) and diffuse midline glioma (DMG) remains a formidable challenge due to multiple biologic, anatomic, and immunologic factors. Despite these hurdles, a number of clinical trials deployed over the last decade have increased optimism for the potential of CAR T cell therapy in glioma treatment. Evidence synthesis We highlight historical and ongoing clinical trials of CAR T cell therapy in glioma, with a focus on key tumor-associated antigens such as IL-13Rα2, HER2, EGFR, EGFRvIII, EphA2, GD2, and B7-H3. Early studies established proof-of-concept for antigen-specific CAR T cell targeting, yet immune evasion mechanisms such as antigen downregulation and limited CAR T cell persistence remain significant obstacles. Recent approaches, including multiantigen targeting, alternative cell sources, and innovations in delivery routes offer promising strategies to overcome these challenges. Conclusions The rapid evolution of investigational CAR T cell therapies portends great potential for the future of glioma treatment. Future studies will need to refine antigen targeting strategies, optimize CAR T cell persistence, and integrate combinatorial approaches to fully harness the therapeutic potential of this modality and improve the therapeutic window against brain tumors.

A Review of Emerging Immunotherapeutic Strategies for IDH-Mutant GliomaIDH-mutant gliomas are a type of brain tumor that grow more slowly than IDH-wildtype glioblastomas but eventually become more aggressive. Current treatments, such as surgery, chemotherapy, radiation, and the new drug vorasidenib, help manage the ...

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