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. 2021 Apr 1;40:119. doi: 10.1186/s13046-021-01919-5

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© The Author(s) 2021

Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 1 — Circadian markers and their influences on immune-oncology pathways. Diagram represents a simplified depiction highlighting immune cells and receptors of interest. Circadian effects supported by experimental evidence are depicted, with connectors representing the direction of relationships (i.e., arrows represent positive or upregulatory relationships, flat connectors represent negative or inhibitory relationships). Not depicted, disruption or tumor reprogramming of circadian gene signals has been associated with tumor immunophenotype patterns and glucocorticoids have been implicated in poorer response to anti-PD-(L)1 therapy. *“Clock Index” refers to a combined index score of BMAL1, PER1/2/3, CRY1/2, and CLOCK expression levels across multiple cancer types [56]