{"doi":"10.1016/j.ebiom.2022.104089","title":"Increased neutrophil infiltration as a body-wide effect in pancreatic cancer development","abstract":"Cancer has long been considered a systemic disease that can actively perturb normal host organs even from distant anatomic sites.1McAllister SS Weinberg RA. Tumor-host interactions: a far-reaching relationship.J Clin Oncol. 2010; 28: 4022-4028Crossref PubMed Scopus (225) Google Scholar Such perturbations will likely induce alterations in gene expression and protein networks within those organs that could ultimately affect the organism's physiology1McAllister SS Weinberg RA. Tumor-host interactions: a far-reaching relationship.J Clin Oncol. 2010; 28: 4022-4028Crossref PubMed Scopus (225) Google Scholar and may cause tissue damage beyond the tumor itself.2Baracos VE Martin L Korc M Guttridge DC Fearon KCH. Cancer-associated cachexia.Nat Rev Dis Primers. 2018; 4: 17105Crossref PubMed Scopus (207) Google Scholar We now know a great deal of gene expression landscapes in tumor tissues and the adjacent normal tissues. However, our knowledge of other body-wide non-tumor organs is still limited. An earlier study provided some clues of the tumor effects on body-wide transcriptomes in a subcutaneous brain cancer model.3Kozawa S Ueda R Urayama K et al.The Body-wide Transcriptome Landscape of Disease Models.iScience. 2018; 2: 238-268Summary Full Text Full Text PDF PubMed Scopus (12) Google Scholar In a recent issue of eBioMedicine, Jiang and colleagues provided new insights into the body-wide molecular alterations in early pancreatic intraepithelial neoplasia, (PanIN) and late stage pancreatic ductal adenocarcinoma (PDAC) of mouse models of pancreatic cancer.4Jiang S.LD Hu L. et al.Modeling of cancer-related body-wide effects identifies LTB4 as a diagnostic biomarker for pancreatic cancer.eBioMedicine. 2022; https://doi.org/10.1016/j.ebiom.2022.104050Summary Full Text Full Text PDF Scopus (1) Google Scholar The study found that the number of DEGs (differentially expressed gene) in the non-tumor organs was generally several-fold higher in mice with PDAC than with PanIN. This is not surprising as the degree of tumor-driven systemic perturbations is expected to increase with tumor progression. Comparing the transcriptomes of seven mouse organs: liver, lung, colon, stomach, kidney, heart, and brain, from animals with and without PanIN or PDAC, the number of DEGs varied greatly at the different organs, with the colon having the highest and the brain having the lowest levels affected by cancer or precursors in the pancreas compared to controls. Interestingly, the numbers of DEGs in liver and lung increased substantially from early stage to late stage, and liver and lung showed the highest number of upregulated genes among all seven mouse organs in late stage disease. It is tempting to speculate that the high burden of gene perturbations in the liver and lung in PDAC-bearing animals may in part suggest why liver and lung are the two most common sites of metastasis of pancreatic cancer. In recent years, mounting evidence indicates that neutrophils participate in each step of carcinogenesis, from tumor initiation to growth and metastasis.5Coffelt SB Wellenstein MD de Visser KE. Neutrophils in cancer: neutral no more.Nat Rev Cancer. 2016; 16: 431-446Crossref PubMed Scopus (840) Google Scholar In pancreatic cancer, neutrophils infiltrate pancreatic tumors at higher levels compared to normal pancreas; PDAC patients with high neutrophil infiltration have a worse prognosis.6Ino Y Yamazaki-Itoh R Shimada K et al.Immune cell infiltration as an indicator of the immune microenvironment of pancreatic cancer.Br J Cancer. 2013; 108: 914-923Crossref PubMed Scopus (496) Google Scholar,7Wang Y Fang T Huang L et al.Neutrophils infiltrating pancreatic ductal adenocarcinoma indicate higher malignancy and worse prognosis.Biochem Biophys Res Commun. 2018; 501: 313-319Crossref PubMed Scopus (24) Google Scholar Interestingly, the study by Jiang and colleagues found increased neutrophil infiltration in multiple organs at early stage of PDAC. The neutrophil infiltration w","journal":"EBioMedicine","year":2022,"id":267979,"datarank":0.0,"base_score":0.0,"endowment":0.0,"self_citation_contribution":0.0,"citation_network_contribution":0.0,"self_endowment_contribution":0.0,"citer_contribution":0.0,"corpus_percentile":null,"corpus_rank":null,"citation_count":6,"citer_count":0,"citers_with_citation_signal":0,"citers_with_endowment":0,"datacite_reuse_total":0,"is_dataset":false,"is_dataset_confidence":0.952,"is_data_producer":false,"deposit_databanks":null,"is_oa":true,"file_count":0,"downloads":0,"has_version_chain":false,"published_date":"2022-01-01","fair_score":null,"fair_percentile":null,"algorithm_id":"datarank_citation_only_1hop_v6","ranking_scope":"data_only","authors":[{"id":340708,"name":"Sheng Pan","orcid":null,"position":1,"is_corresponding":false},{"id":339153,"name":"Ru Chen","orcid":"0000-0002-1823-0686","position":0,"is_corresponding":true}],"reference_count":9,"raw_metadata":null,"created_at":"2026-07-19T00:27:10.233250Z","pmid":"35665683","pmcid":null,"fwci":null,"citation_percentile":null,"influential_citations":0,"oa_status":null,"license":null,"views":0,"total_file_size_bytes":0,"version_count":0,"fair_f":null,"fair_a":null,"fair_i":null,"fair_r":null,"fair_zscore":null,"fair_rationale":null,"fair_model":null,"fair_agent_version":null,"fair_fulltext_source":null,"fair_has_llm":null,"fair_computed_at":null,"clinical_trials":[],"software_tools":[],"db_accessions":[],"linked_datasets":[],"topics":[]}