About

Sujit Basu, MD, PhD, is a Professor in the Department of Pathology and Division of Medical Oncology at Ohio State University Medical Center. He received his medical degree and PhD from the University of Calcutta, India, and trained as a medical oncologist. His postdoctoral research was conducted in the Department of Molecular Genetics at the University of Illinois at Chicago and in the Department of Pathology at Beth Israel Deaconess Medical Center, Harvard Medical School. Dr. Basu has also undertaken clinical training in Nephrology at Boston Children’s Hospital, as well as in Internal Medicine, Gastroenterology, Hepatology, Nutrition, and Medical Oncology at Beth Israel Deaconess Medical Center. Prior to joining Ohio State University in 2008, he served as an Assistant Professor at Mayo Clinic in Rochester. His research primarily focuses on studying cancer biology, including tumor microenvironment, experimental therapeutics, neural regulation of tumorigenesis, angiogenesis, vasculogenesis, and immunity, particularly neural-immune interactions. His work is supported by grants from the National Institute of Health, DOD, and various research foundations.

Research topics

• Internal medicine
• Medicine
• Pharmacology
• Biology
• Oncology
• Immunology
• Bioinformatics
• Endocrinology
• Cancer research

Selected publications

• Angiotensin II type 1 receptor blockade inhibits gastric cancer metastasis through tight junction restoration

  Cancer Letters · 2026-05-02

  article
  PublisherDOI

• Dopamine <scp>D2</scp> Receptor Agonists as Modulators of <scp>VEGF</scp> ‐A‐Driven Angiogenesis: Mechanisms, Clinical Evidence, and Translational Opportunities

  The FASEB Journal · 2026-05-12

  articleOpen accessSenior author

  Angiogenesis mediated by vascular endothelial growth factor A (VEGF-A) is essential for physiological vascular remodeling but also drives pathological processes, including tumor growth, ocular neovascularization, and inflammation. Emerging evidence has revealed that dopamine D2 receptor (DRD2) activation is a key inhibitory pathway that counterbalances VEGF-A-dependent endothelial activation and vascular permeability. This review integrates current mechanistic insights into the effects of DRD2 agonists on endothelial signaling, focusing on their ability to suppress VEGF-A-induced proangiogenic signaling cascades. Preclinical and translational studies have demonstrated that DRD2 agonists attenuate aberrant angiogenesis, promote vascular normalization, and mitigate VEGF-A-induced vascular leakage in diverse pathological contexts, including malignancy, ovarian hyperstimulation syndrome, endometriosis, and inflammatory lung injury. Particular attention is given to the emerging model of tumor-derived VEGF-A inducing DRD2 expression within the tumor endothelium, establishing a reciprocal paracrine feedback loop with potential biomarker relevance. Finally, the clinical safety profile and pharmacologic repositioning of DRD2 agonists are evaluated, and priorities for translational research are outlined to refine dosing, scheduling, and patient selection strategies in precision antiangiogenic therapy.

  PublisherDOI

• Abstract 4776: The role of angiogenesis in gastric tumorigenesis

  Cancer Research · 2024-03-22

  articleSenior author

  Abstract Introduction: Gastric or stomach cancer remains one of the most lethal malignancies, with an estimated 1,089,103 new cases and 768,793 deaths worldwide in 2020. In the United States, it is estimated that there were 26,500 new cases and 11,130 deaths from stomach cancer in 2023. Unfortunately, despite improved treatment in recent years, ~65% of gastric cancer patients present with aggressive metastatic disease, and they die within one year of diagnosis. Therefore, the identification of newer and effective therapies to target the precancerous stages of the disease promises possibilities for the prevention of gastric cancer in patients harboring these lesions. Gastric metaplasia and dysplasia are precancerous lesions that often progress to gastric cancer. Since anti-VEGF-A anti-angiogenic agents have shown efficacy in advanced gastric cancer patients, we hypothesized that VEGF-A-mediated angiogenesis has a functional role in the pathogenesis of gastric metaplasia and dysplasia. Experimental Procedures: The Initial experiments were undertaken in human gastric metaplasia and dysplasia tissues and murine gastric metaplasia and dysplasia tissues collected from a well-established Helicobacter felis (H. felis) induced murine model of gastric tumorigenesis simulating human patients to detect angiogenesis (CD31/MVD) and identify angiogenic pathways using GeoMx DSP Spatial Proteomics and NanoString nCounter assay. Thereafter, further experiments were undertaken in the H. felis-induced murine model of gastric metaplasia and dysplasia, simulating human patients using VEGF-A hypo mice to determine the role of VEGF-A-induced angiogenesis in the progression of these lesions. Results and Conclusion: Although our results indicated angiogenesis and VEGF-A expression in both human and mouse gastric metaplasia and dysplasia, inhibition in the progression of the precancerous gastric lesions was observed in only 40% of the VEGF-A hypo mice, thereby suggesting that VEGF-A induced angiogenesis might not be the major angiogenic pathway in these precancerous lesions in every patient. A similar phenomenon is also seen in some gastric cancer patients. Citation Format: Venu Akkanapally, SUJIT BASU. The role of angiogenesis in gastric tumorigenesis [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2024; Part 1 (Regular Abstracts); 2024 Apr 5-10; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2024;84(6_Suppl):Abstract nr 4776.

  PublisherDOI

• Therapeutic Immunomodulation in Gastric Cancer

  Cancers · 2024-01-28 · 20 citations

  articleOpen accessSenior authorCorresponding

  Gastric carcinoma, being one of the most prevalent types of solid tumors, has emerged as the third leading cause of death worldwide. The symptoms of gastric cancer (GC) are typically complex, which makes early detection challenging. Immune checkpoint inhibition has become the new standard targeted therapy for advanced or metastatic GC. It is currently being explored in various combinations, both with and without chemotherapy, across multiple therapies in clinical trials. Immunotherapy can stimulate immune responses in GC patients, leading to the destruction of cancer cells. Compared with traditional therapies, immunotherapy has shown strong effectiveness with tolerable toxicity levels. Hence, this innovative approach to the treatment of advanced GC has gained popularity. In this review, we have outlined the recent advancements in immunotherapy for advanced GC, including immune checkpoint inhibitors, cancer vaccines, vascular endothelial growth factor-A inhibitors, and chimeric antigen receptor T-cell therapy. Our current emphasis is on examining the immunotherapies presently employed in clinical settings, addressing the existing challenges associated with these therapeutic approaches, and exploring promising strategies to overcome their limitations.

  PublisherOA PDFDOI

• Abstract 3034: Krüppel-like factors in regulation of gastric cancer progression

  Cancer Research · 2024-03-22

  article

  Abstract Introduction: Gastric cancer (GC) is the third leading cause of cancer-associated mortality and the fifth most frequently diagnosed cancer worldwide. The development and progression of GC is a complicated multistage process subjected to dynamic changes in gene regulation. Investigating the effects of these changes is therefore critical for improving our knowledge about GC initiation and progression. Krüppel-like factors (KLFs) are evolutionarily conserved zinc finger-containing transcription factors with altered expressions and diverse regulatory functions in GC. We previously reported that there is loss of KLF4 in GC. Here we report that KLF4 is a crucial regulator of KLF5 expression and vice versa and together they regulate GC cell behavior. Methods: The Cancer Genome Atlas (TCGA) and pan cancer data of differential expressions of KLFs in GC was analyzed. TCGA RNAseq and clinical data for the differential expression status of KLF genes in normal and cancerous tissues and the clinicopathological association was accessed from the UALCAN web portal. The expressions of KLF4 and KLF5 in human normal stomach and GC and orthotopic xenografts were detected by immunohistochemistry (IHC). KLF4, KLF5 cross regulation was evaluated by gene manipulation of each gene individually and checking the expression of the other factor in GC cells. The effect of KLFs on GC cell proliferation, migration, and invasion was determined by Ki67 staining of tissues, PrestoBlue cell viability assay, scratch wound and transwell cell invasion assays. Results and Conclusion: Our results indicated that not only KLF4 and KLF5 have contrasting expressions and effects in GC but also these two factors cross regulate each other. While lower expressions of KLF4 was found in human GC and orthotopic xenografts, increased expression of KLF5 was found in both human GC tissue and orthotopic xenografts. KLF4 silencing and CRISPR/Cas9 knockdown in human GC cells resulted in increased expression of KLF5 which was associated with increased GC cell proliferation and invasiveness. Interestingly, KLF5 knockdown by CRISPR/Cas9 in human GC cells on the other hand resulted in increased expression of KLF4, which was associated with decreased GC cell growth. Our data therefore suggests that the differential expressions of KLF4 and KLF5 might serve as valuable prognostic markers in GC. Citation Format: Sooraj Kakkat, Prabhat Suman, Sandeep Goswami, Sujit Basu, Martin J. Heslin, Elba A. Turbat-Herrera, Veronica Ramirez Alcantara, Chandrani Sarkar, Debanjan Chakroborty. Krüppel-like factors in regulation of gastric cancer progression [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2024; Part 1 (Regular Abstracts); 2024 Apr 5-10; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2024;84(6_Suppl):Abstract nr 3034.

  PublisherDOI

• IL-27 Gene Therapy Ameliorates IPEX Syndrome Caused by Germline Mutation of Foxp3 Gene: A Major Role for Induction of IL-10

  The Journal of Immunology · 2024-07-08 · 3 citations

  articleOpen access

  Inactivating mutations of Foxp3, the master regulator of regulatory T cell development and function, lead to immune dysregulation, polyendocrinopathy, enteropathy, X-linked (IPEX) syndrome in mice and humans. IPEX is a fatal autoimmune disease, with allogeneic stem cell transplant being the only available therapy. In this study, we report that a single dose of adeno-associated virus (AAV)-IL-27 to young mice with naturally occurring Foxp3 mutation (Scurfy mice) substantially ameliorates clinical symptoms, including growth retardation and early fatality. Correspondingly, AAV-IL-27 gene therapy significantly prevented naive T cell activation, as manifested by downregulation of CD62L and upregulation of CD44, and immunopathology typical of IPEX. Because IL-27 is known to induce IL-10, a key effector molecule of regulatory T cells, we evaluated the contribution of IL-10 induction by crossing IL-10-null allele to Scurfy mice. Although IL-10 deficiency does not affect the survival of Scurfy mice, it largely abrogated the therapeutic effect of AAV-IL-27. Our study revealed a major role for IL-10 in AAV-IL-27 gene therapy and demonstrated that IPEX is amenable to gene therapy.

  PublisherOA PDFDOI

• CD200R signaling contributes to unfavorable tumor microenvironment through regulating production of chemokines by tumor-associated myeloid cells

  iScience · 2023-05-19 · 7 citations

  articleOpen access

  CD200 is overexpressed in many solid tumors and considered as an immune checkpoint molecule dampening cancer immunity. In this study, we found that CD200R−/− mice were significantly more potent in rejecting these CD200+ tumors. scRNA sequencing demonstrated that tumors from CD200R−/− mice had more infiltration of CD4+ and CD8+ T cells, and NK cells but less infiltration of neutrophils. Antibody depletion experiments revealed that immune effector cells are crucial in inhibiting tumor growth in CD200R−/− mice. Mechanistically, we found that CD200R signaling regulates the expression of chemokines in tumor-associated myeloid cells (TAMCs). In the absence of CD200R, TAMCs increased expression of CCL24 and resulted in increased infiltration of eosinophils, which contributes to anti-tumor activity. Overall, we conclude that CD200R signaling contributes to unfavorable TME through chemokine-dependent recruitment of immune suppressive neutrophils and exclusion of anti-cancer immune effectors. Our study has implications in developing CD200-CD200R targeted immunotherapy of solid tumors.

  PublisherOA PDFDOI

• Abstract 5831: CD200R signaling contributes to unfavorable tumor microenvironment through regulating production of chemokines by tumor associated macrophages

  Cancer Research · 2023-04-04

  article

  Abstract CD200 is overexpressed in human solid tumors such as neuroblastoma and melanoma and is considered as an immune checkpoint molecule for dampening cancer immunity. However, how CD200 affects tumor microenvironment (TME) and host immunity is incompletely understood. In the present study, we evaluated the role of the CD200-CD200R pathway in TME using loss-of-function CD200R-/- mice, along with two clinically relevant, CD200-positive murine tumor models: the mouse neuroblastoma NB9464D and melanoma Yummer1.7. We found that comparing with the wild type mice, CD200R-/- mice were significantly more potent in rejecting these CD200+ tumors. Transcriptome analysis by single cell RNA sequencing demonstrated that tumors from CD200R-/- mice had more infiltration of CD45+ immune cells, including CD4+ and CD8+ T cells, and NK cells but less infiltration of neutrophils. Antibody depletion experiments revealed that immune effectors including CD8+ T cells and NK cells in combination, are crucial in inhibiting tumor growth in CD200R-/- mice. Mechanistically, we found that CD200R signaling differentially regulates the expression of chemokines in tumor-associated macrophages (TAMs). In the absence of CD200R, TAMs up-regulate CCL24 and CCL8 and down-regulate CXCL3, CXCL2, and CCL3 via activation of ERK and/or p38 MAP kinases. Increased expression of CCL24 in CD200R-deficient tumors resulted in increased infiltration of eosinophils, which also contributes to anti-tumor activity. Overall, we conclude that CD200R-mediated signaling, via interaction with CD200 on tumor cells, contributes to unfavorable TME primarily through chemokine-dependent recruitment of immune suppressive neutrophils and exclusion of anti-cancer immune effectors. Our study has significant implications in developing CD200-targeted immunotherapy of solid tumors. Citation Format: Cho-Hao Lin, Fatemeh Talebian, Yang Li, Jianmin Zhu, Bolin Zhao, Jin-Qing Liu, Sujit Basu, Xueling Pan, Xi Chen, Pearlly Yan, William E. Carson, Gang Xin, Haitao Wen, Ruoning Wang, Zihai Li, Qin Ma, Xue-Feng Bai. CD200R signaling contributes to unfavorable tumor microenvironment through regulating production of chemokines by tumor associated macrophages [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2023; Part 1 (Regular and Invited Abstracts); 2023 Apr 14-19; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2023;83(7_Suppl):Abstract nr 5831.

  PublisherDOI

• Neuropeptide Y, a paracrine factor secreted by cancer cells, is an independent regulator of angiogenesis in colon cancer

  British Journal of Cancer · 2022-07-28 · 28 citations

  articleOpen access
  PublisherOA PDFDOI

• VEGF-A controls the expression of its regulator of angiogenic functions, dopamine D2 receptor, on endothelial cells

  Journal of Cell Science · 2022-05-20 · 17 citations

  articleOpen accessSenior authorCorresponding

  We have previously demonstrated significant upregulation of dopamine D2 (DAD2) receptor (DRD2) expression on tumor endothelial cells. The dopamine D2 receptors, upon activation, inhibit the proangiogenic actions of vascular endothelial growth factor-A (VEGF-A, also known as vascular permeability factor). Interestingly, unlike tumor endothelial cells, normal endothelial cells exhibit very low to no expression of dopamine D2 receptors. Here, for the first time, we demonstrate that through paracrine signaling, VEGF-A can control the expression of dopamine D2 receptors on endothelial cells via Krüppel-like factor 11 (KLF11)-extracellular signal-regulated kinase (ERK) 1/2 pathway. These results thus reveal a novel bidirectional communication between VEGF-A and DAD2 receptors.

  PublisherOA PDFDOI

Recent grants

• NIH Grant R01CA169158

  NIH · $1.6M · 2020

• NIH Grant R01CA124763

  NIH · $1.4M · 2014

• NIH Grant R01HL131405

  NIH · $1.5M · 2021

• NIH Grant R21CA118265

  NIH · $303k · 2008

• NIH Grant R01DK098045

  NIH · $1.6M · 2019

Frequent coauthors

• Partha Dasgupta

  56 shared

• Chandrani Sarkar

  University of South Alabama

  46 shared

• Debanjan Chakroborty

  Michigan State University

  45 shared

• Biswarup Basu

  Chittaranjan National Cancer Institute

  20 shared

• Saurav Shome

  Chittaranjan National Cancer Institute

  14 shared

• Subhalakshmi Ganguly

  12 shared

• Uttio Roy Chowdhury

  Mayo Clinic

  9 shared

• Sandeep Goswami

  University of South Alabama

  9 shared

Labs

• AI4PathPI

  From Pixels to Prognosis: AI in Action!

Education

• M.D., Medicine/Cancer Research

  University of Calcutta, India

• Ph.D., Medicine/Cancer Research

  University of Calcutta, India