Indoleamine 2,3- Dioxygenase: A Novel Immunotherapeutic Target for Osteosarcoma

  • Asim Farooq Department of Clinical Research, Shaukat Khanum Memorial Cancer Hospital and Research Centre, Lahore
  • Bilal Zulfiqar Griffith Institute for Drug Discovery, Griffith University, Brisbane
  • Kashif Asghar Department of Basic Sciences Research, Shaukat Khanum Memorial Cancer Hospital and Research Centre, Lahore
Keywords: Indoleamine 2,3-dioxygenase, immunosuppression, immunotherapeutic target, osteosarcoma

Abstract

Introduction: Tumour-emitted molecules induce immunosuppression in the tumour microenvironment. An immunosuppressive enzyme, indoleamine 2,3-dioxygenase (IDO/IDO1), facilitates immune escape in several malignant tumours, including osteosarcoma. Upregulation of IDO establishes a tolerogenic environment in the tumour and the tumour-draining lymph nodes. IDO-induced downregulation of effector T-cells and upregulation of local regulatory T-cells creates immunosuppression and promotes metastasis. Observations: Osteosarcoma is the most common bone tumour characterised by immature bone formation by the tumour cells. Almost 20% of osteosarcoma patients present with pulmonary metastasis at the time of diagnosis. The improvement in therapeutic modalities for osteosarcoma has been in a stagnant phase for two decades. Therefore, the development of novel immunotherapeutic targets for osteosarcoma is emergent. High IDO expression is associated with metastasis and poor prognosis in osteosarcoma patients. Conclusion and Relevance: At present, only a few studies are available describing IDO’s role in osteosarcoma. This review describes the prospects of IDO not only as a prognostic marker but also as an immunotherapeutic target for osteosarcoma.

Published
2022-09-30
How to Cite
1.
Farooq A, Zulfiqar B, Asghar K. Indoleamine 2,3- Dioxygenase: A Novel Immunotherapeutic Target for Osteosarcoma. J Cancer Allied Spec [Internet]. 2022Sep.30 [cited 2023Feb.3];9(1). Available from: https://journals.sfu.ca/jcas/index.php/jcas/article/view/501