Prognostic value of CD73 expression in resected colorectal cancer liver metastasis.

Messaoudi, Nouredin; Stephen, D Robinson; Cousineau, Isabelle; St-Hilaire, Pierre-Antoine; Vandenbroucke‐Menu, Franck; Dagenais, Michel; Létourneau, Richard; Plasse, M.; Roy, André; Lapointe, Réal; Nguyen, Bich; Trudel, Dominique; Arslanian, Elizabeth; Soucy, Geneviève; Mes‐Masson, Anne‐Marie; Stagg, John; Turcotte, Simon

doi:10.1200/jco.2018.36.15_suppl.3584

Cited by 8 publications

(10 citation statements)

References 3 publications

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“…Liver metastasis occurs in 50% CRC patients (237). Recently, studies have shown high CD73 expression associates with significantly shorter time to recurrence and poor survival (238). In renal cancer patients, an adenosine high (AdenoSig hi ) expression signature was identified in pretreatment biopsies and associated with clinical response to A2AR antagonism (124).…”

Section: Colorectal Cancermentioning

confidence: 99%

CD73's Potential as an Immunotherapy Target in Gastrointestinal Cancers

et al. 2020

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CD73, a cell surface 5 ′ nucleotidase that generates adenosine, has emerged as an attractive therapeutic target for reprogramming cancer cells and the tumor microenvironment to dampen antitumor immune cell evasion. Decades of studies have paved the way for these findings, starting with the discovery of adenosine signaling, particularly adenosine A2A receptor (A2AR) signaling, as a potent suppressor of tissue-devastating immune cell responses, and evolving with studies focusing on CD73 in breast cancer, melanoma, and non-small cell lung cancer. Gastrointestinal (GI) cancers are a major cause of cancer-related deaths. Evidence is mounting that shows promise for improving patient outcomes through incorporation of immunomodulatory strategies as single agents or in combination with current treatment options. Recently, several immune checkpoint inhibitors received FDA approval for use in GI cancers; however, clinical benefit is limited. Investigating molecular mechanisms promoting immunosuppression, such as CD73, in GI cancers can aid in current efforts to extend the efficacy of immunotherapy to more patients. In this review, we discuss current clinical and basic research studies on CD73 in GI cancers, including gastric, liver, pancreatic, and colorectal cancer, with special focus on the potential of CD73 as an immunotherapy target in these cancers. We also present a summary of current clinical studies targeting CD73 and/or A2AR and combination of these therapies with immune checkpoint inhibitors.

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Section: Colorectal Cancermentioning

confidence: 99%

CD73's Potential as an Immunotherapy Target in Gastrointestinal Cancers

et al. 2020

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“…Furthermore, both enzymes regulate the magnitude of the purinergic reaction surrounding the immune cells. High expression of CD73 is therefore associated with low levels of lymphocytes in the TME and poor prognosis in for example colorectal, prostate, and triple-negative breast cancer [44][45][46][47]. Of note, CD73 is regulated by HIF-1alpha and therefore more abundant in a hypoxic microenvironment [48].…”

Section: Main Molecular and Immunological Features Of Icdmentioning

confidence: 99%

Immunogenic cell death and its therapeutic or prognostic potential in high-grade glioma

et al. 2022

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Immunogenic cell death (ICD) has emerged as a key component of therapy-induced anti-tumor immunity. Over the past few years, ICD was found to play a pivotal role in a wide variety of novel and existing treatment modalities. The clinical application of these techniques in cancer treatment is still in its infancy. Glioblastoma (GBM) is the most lethal primary brain tumor with a dismal prognosis despite maximal therapy. The development of new therapies in this aggressive type of tumors remains highly challenging partially due to the cold tumor immune environment. GBM could therefore benefit from ICD-based therapies stimulating the anti-tumor immune response. In what follows, we will describe the mechanisms behind ICD and the ICD-based (pre)clinical advances in anticancer therapies focusing on GBM.

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“…35,36 Previous clinical studies have reported the possibilities of increased CD73 expression in gastric, liver, pancreatic, and colorectal cancers, as biomarkers for poor prognosis and malignancy. 15,20 In this study, we demonstrated for the first time that extracellular adenosine can directly upregulate PD-L1 expression in human macrophages. The immunosuppressive adenosine was potentially produced by the ectoenzymes CD39 and CD73, and accordingly, the CD73 inhibitor AB680 significantly reduced PD-L1 levels in both human macrophages and TAMs obtained from mouse models of CRC.…”

Section: Discussionmentioning

confidence: 62%