# Role of necroptosis and immune infiltration in essential thrombocytosis

## TL;DR

This study explores how necroptosis, a type of cell death, and immune cell infiltration contribute to the progression of essential thrombocytosis, a blood cancer.

## Contribution

The study identifies specific necroptosis genes and their link to immune infiltration in essential thrombocytosis.

## Key findings

- Five necroptosis genes were found to be enriched in the necroptosis pathway in essential thrombocytosis.
- Th1/Th17 immune cell imbalance was observed in ET patients.
- Necroptosis genes correlated positively with immune cell infiltration in ET.

## Abstract

Necroptosis, a recently identified form of programmed cell death involved in the pathogenesis of a variety of tumor and non-tumor diseases. Nevertheless, the function of necroptosis in essential thrombocytosis (ET) remains unclear, which is a classic myeloproliferative tumor.

The role of necroptosis in ET was determined via bioinformatics combined with qRT-PCR analysis of clinical samples. GSE57793 and GSE26049 datasets were recruited to identify necroptosis differentially expressed genes based on differential gene identification, necroptosis gene sets and data machine learning. Enrichment analysis (GSEA) was used to evaluate the gene enrichment signaling pathway of ET, immune infiltration analysis was used to explore the abundance of immune cell infiltration in ET, and the correlation between necroptosis differential genes and immune cell infiltration was studied.

Five necroptosis genes were recognized to be remarkably enriched in the necroptosis pathway, including CHMP1B, FTH1, HSP90AB1, IL1A, and RBCK1. The imbalance of invasion of Th1/Th17 cells was identified in ET, and the differential necroptosis gene was positively correlated with the infiltration of multiple immune cells. There is significant necroptosis in ET, which is enriched in the necrotizing apoptotic pathway, and is associated with immune infiltration.

Necroptosis might drive the progression of ET via stimulating immune infiltration and immune responses. The findings bring new insights into the treatment mechanism and treatment strategy of ET in the future.

The online version contains supplementary material available at 10.1186/s41065-025-00428-1.