Project description:Using a genome-wide CRISPR activation screen, we identified ZNF296, a transcription factor prominently expressed in epithelial cancers, as a key regulator of tumor resistance to NK cell-mediated cytotoxicity. To investigate the role of ZNF296 in regulating chromatin accessibility and its effects on gene transcription, we performed ATAC-seq on ZNF296-overexpressing (ZNF296-OE) and control A549 cells. These data provide insights into the epigenetic mechanisms underlying ZNF296-mediated tumor immune evasion.

2025-09-06 | GSE283057 | GEO

P2RY2 fuelled by eATP drives cancer immune evasion and therapy resistance

Project description:P2RY2 fuelled by eATP drives cancer immune evasion and therapy resistance

| PRJNA1220715 | ENA

KRAS drives immune evasion in a genetic model of pancreatic cancer

Project description:KRAS drives immune evasion in a genetic model of pancreatic cancer

| PRJNA548394 | ENA

Suppressed cGAS-STING DNA Sensing Drives Immune Evasion in Anaplastic Thyroid Cancer

Project description:Suppressed cGAS-STING DNA Sensing Drives Immune Evasion in Anaplastic Thyroid Cancer

| PRJNA1463273 | ENA

Ubiquitin D drives colorectal cancer immune evasion and resistance to anti PD1 immunotherapy

Project description:Ubiquitin D drives colorectal cancer immune evasion and resistance to anti PD1 immunotherapy by suppressing FBXW7 mediaUbiquitin D drives colorectal cancer immune evasion and resistance to anti PD1 immunotherapy by suppressing FBXW7 mediated CD73 degradation [scRNA-seq] The majority of patients with colorectal cancer (CRC) can’t benefit from anti-PD-1 immunotherapy due to an insufficient T cell response in the tumor microenvironment (TME); however, the underlying mechanism remains unknown. Here, we show that ubiquitin D (UBD) in tumor cells inhibits CD8+ T cell‑mediated anti‑tumor responses, and consequently mediates resistance to anti‑PD‑1 immunotherapy in experimental and clinical CRC. Mechanistically, UBD disrupted E3 ligase F‑box and WD repeat domain‑containing 7 (FBXW7)‑induced proteasome degradation of CD73, thereby increasing the concentration of intracellular adenosine, which subsequently suppressed CD8+ T cell function in the TME. Importantly, blockade of CD73 sensitized UBD‑overexpressed cancer cells to anti-PD‑1 immunotherapy by restoring intratumor CD8+ T cell function. We have thus revealed a previously unrecognized mechanism for CRC resistance to anti‑PD‑1 therapy through UBD‑CD73‑adenosine mediated suppression of CD8+ T cells. This new information potentially provides a novel strategy to overcome resistance to PD‑1 blockade in patients with CRC.

2026-05-23 | GSE233462 | GEO

Breast Cancer Stem Cells Regulated Metabolism Remodeling of Bulk Tumor Drives Immune Evasion

Project description:Breast Cancer Stem Cells Regulated Metabolism Remodeling of Bulk Tumor Drives Immune Evasion

| PRJNA986080 | ENA

Ubiquitin D drives colorectal cancer immune evasion and resistance to anti PD1 immunotherapy

Project description:Ubiquitin D drives colorectal cancer immune evasion and resistance to anti PD1 immunotherapy

| PRJNA976309 | ENA