GEOapplication/xmlftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE291nnn/GSE291385/primaryOK200OtherMus musculus Genome binding/occupancy profiling by high throughput sequencing Expression profiling by high throughput sequencingOtherhttps://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE291385GEOGSEfalseHepatic hematopoiesis hijacked by tumor metastasis promotes immunosuppressionCancer-associated hematopoietic abnormalities contribute to systemic immunosuppression. However, whether tumors can initiate localized extramedullary hematopoiesis (EMH) to suppress anti-tumor immunity remains unclear. Here, we identify a distinct form of hepatic hematopoiesis driven by liver metastasis-associated hematopoietic stem cells (LM-HSCs). Liver metastases establish ectopic periportal hematopoietic niches that recruit bone marrow HSCs through Kupffer cell-dependent CCR1 signaling. Although LM-HSCs retain self-renewal and multipotency, CREB activation skews their differentiation toward the myeloid lineage, particularly ANXA1⁺ immature neutrophils. These neutrophils produce glucocorticoids, which activate glucocorticoid receptor (GR) signaling in a paracrine manner and induce immune checkpoint receptor expression and functional anergy in CD8⁺ T and NK cells. Collectively, these findings demonstrate that liver metastases reprogram hepatic hematopoiesis to promote immunosuppression.2026/08/21GSE291385GSM8834138GSM8834139GSM8834134GSM8834135GSM8834136GSM8834137GSM8834130GSM8834152GSM8834153GSM8834131GSM8834154GSM8834132GSM8834133GSM8834155GSM8834150GSM8834151GSM9574953GSM8834127GSM8834149GSM8834128GSM8834129GSM8834145GSM8834146GSM8834147GSM8834148GSM8834126GSM8834141GSM8834142GSM8834143GSM8834144GSM8834140283301311234328291385Mus musculus