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Validation genotyping of 215 metastatic luminal B patients confirms an age-of-diagnosis acceleration of 6.3 years. These findings support considering rs867228 detection in screening to increase examination frequency and 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[https://doi.org/10.1080/2162402X.2023.2189823](https://doi.org/10.1080/2162402X.2023.2189823)  \nBRIEF REPORT     \nRs867228 in FPR1 accelerates the manifestation of luminal B breast cancer  \nVincent Carbonniera*, Julie Le Naoura*, Thomas Bachelotb, Erika Vacchellia,c, Fabrice Andréd,e, Suzette Delalogef, and Guido Kroemer a,c,g  \naEquipe labellisée par la Ligue contrele cancer, Université de Paris, Sorbonne Université, Paris, France; bCentre Léon Bérard, Département de Cancérologie Médicale, Lyon, France; cMetabolomics and Cell Biology Platforms, Gustave Roussy Cancer Campus, Villejuif, France; dUniversité Paris Saclay, Faculty of Medicine Kremlin Bicêtre, Le Kremlin Bicêtre, France; e Department of Medical Oncology, INSERM U981, Gustave Roussy Cancer Campus, Villejuif, France; fDepartment of Cancer Medicine, Gustave Roussy Cancer Campus, Villejuif, France; gHôpital Européen Georges Pompidou, AP-HP, Paris, France  \nABSTRACT  \nFormyl peptide receptor-1 (FPR1) is a pathogen recognition receptor involved in the detection of bacteria, in the control of inflammation, as well as in cancer immunosurveillance. A single nucleotide polymorphism in FPR1, rs867228, provokes a loss-of-function phenotype. In a bioinformatic study performed on The Cancer Genome Atlas (TCGA), we observed that homo-or heterozygosity for rs867228 in FPR1 (which affects approximately one-third of the population across continents) accelerates age at diagnosis of specific carcinomas including luminal B breast cancer by 4.9 years. To validate this finding, we genotyped 215 patients with metastatic luminal B mammary carcinomas from the SNPs To Risk of Metastasis (SToRM) cohort. The first diagnosis of luminal B breast cancer occurred at an age of 49.2 years for individuals bearing the dysfunctional TT or TG alleles (n = 73) and 55.5 years for patients the functional GG alleles (n = 141), meaning that rs867228 accelerated the age of diagnosis by 6.3 years (p=0.0077, Mann & Whitney) . These results confirm our original observation in an independent validation cohort. We speculate that it may be useful to include the detection of rs867228 in breast cancer screening campaigns for selectively increasing the frequency and stringency of examinations starting at a relatively young age.  \nARTICLE HISTORY  \nReceived 24 January 2023 Revised 7 March 2023 Accepted 7 March 2023  \nKeywords  \nCancer screening; immunodeficiency; immunosurveillance; mammary carcinoma; polygenic risk score  \nIntroduction  \nEpidemiological studies suggest that over the past few decades some cancer type tend to manifest relatively early, posing a new challenge for disease detection and management.1 Back in 2015 we published a study in which we screened single nucleotide polymorphisms (SNPs) in immune-relevant genes for their impact on breast cancer prognosis, finding rs867228 in FPR1, the gene coding for formyl peptide receptor-1, to be associated with poor responses to anthracycline-based adjuvant chemotherapy in two distinct cohorts of patients.2–4 This finding was later confirmed for locally advanced rectal cancer, in which rs867228 was associated with poor responses to neoadjuvant chemoradiotherapy.5,6  \nThe knockout of the human FPR1 orthologue in mice, Fpr1, revealed a major defect in chemotherapy-induced immunosurveillance, meaning that mice lacking one or two alleles ofFpr1 were unable to control tumor growth upon chemotherapy with anthracyclines (such as mitoxantrone) alone or combination with cyclophosphamide.3, 7 Exhaustive phenotyping of the tumor microenvironment, responding to chemotherapy in the context of Fpr1-proficient or -deficient immune systems, revealed that FPR1 is required for the function of dendritic cells (DCs), allowing them to approach dying cancer cells that release the FPR1 ligand annexin A1 (ANXA1) and then to  \nengage in the cross-presentation of tumor-associated antigens.3,8 In vitro experiments on peripheral blood mononucle","cbCaisnli67iUOw1","https://ap.wps.com/l/cbCaisnli67iUOw1","pdf",1485097,"English","# Abstract\n# Introduction\n## Background on early cancer manifestation\n## Previous findings on rs867228 and prognosis\n## Mechanistic evidence from models and human cells\n## Evidence linking rs867228 to accelerated breast oncogenesis\n# Article history","[{\"question\":\"What is rs867228 in FPR1, and what does it change biologically?\",\"answer\":\"rs867228 is a single nucleotide polymorphism in FPR1 associated with a loss-of-function phenotype, affecting immune surveillance mechanisms involved in cancer detection and response.\"},{\"question\":\"How does rs867228 affect the age of diagnosis for luminal B breast cancer?\",\"answer\":\"In the SToRM validation cohort, the dysfunctional TT or TG alleles were diagnosed at 49.2 years versus 55.5 years for functional GG alleles, indicating a 6.3-year acceleration (p=0.0077).\"},{\"question\":\"Why do the authors suggest using rs867228 detection in screening?\",\"answer\":\"The results suggest incorporating rs867228 detection could selectively increase the frequency and strictness of examinations starting at a relatively young age, targeting higher-risk individuals.\"}]","Rs867228 in FPR1 accelerates the manifestation of luminal B breast cancer - Brief report | PDF",1790270242]