Potential Novel Ovarian Cancer Treatment Targeting Myeloid-Derived Suppressor Cells
Potential Novel Ovarian Cancer Treatment Targeting Myeloid-Derived Suppressor Cells
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Author Info
Kaoru Abiko Takuma Hayashi Ken Yamaguchi Masaki Mandai Ikuo Konishi
Corresponding Author
Takuma HayashiNational Hospital Organization, Kyoto Medical Center, Kyoto, Japan
A B S T R A C T
Diagnosis by biopsy is difficult in the ovary, since it is located deep in the abdomen. As a result, ovarian cancer is mostly found insidiously during exploratory laparotomy. Consequently, early diagnosis of ovarian cancer is often difficult. The likelihood of peritoneal dissemination increases with the progress of ovarian cancer. With further progression, ovarian cancer metastasizes to the omentum, retroperitoneal lymph nodes, large intestine, small intestine, diaphragm, spleen, and other organs. Ovarian cancer has been considered a tumor that has a favourable response to chemotherapy, but more effective treatments are still being explored. Tumors use their own immune escape mechanism to evade host immunity. The immune checkpoint (IC) mechanism, one of the immune escape mechanisms, is established by programmed cell death-1 (PD-1)/PDligand-1 (PD-L1) communication. It has been shown that inhibiting PD-1/PD-L1 communication in various malignancies produces antitumor effects. However, the antitumor effect of ICI monotherapy on ovarian cancer is limited in actual clinical practice. In this review, we describe a novel cancer immunotherapeutic agent that targets myeloid-derived suppressor cells (MDSCs).
Article Info
Article Type
Mini ReviewPublication history
Received: Mon 23, Nov 2020Accepted: Wed 23, Dec 2020
Published: Wed 30, Dec 2020
Copyright
© 2023 Takuma Hayashi. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Hosting by Science Repository.DOI: 10.31487/j.CROGR.2020.03.03