ASCL2 (Achaete-Scute Family BHLH Transcription Factor 2)

These changes promote the expansion of persister stem cells that help the intestine recover after radiation. This study shows how fasting and gut bacteria work together to protect healthy tissue and suggests that diet or microbial treatments could help reduce side effects of cancer radiotherapy.

The present study revealed five prognostic genes and constructed a predictive model, which provided a theoretical basis for the correlation linking Tolerogenic dendritic cells to gastric cancer, and established potential therapeutic strategies in managing gastric cancer. Single-cell analysis revealed that INHBA, ASCL2, and CD36 exhibited marked differential expression in dendritic cells.

SCLC exhibits molecular heterogeneity, with ASCL1- and NEUROD1-driven tumors representing the most frequent subtypes. A distinct subset of ASCL1/NEUROD1 double-negative tumors showed high POU2F3 expression together with LRMP and TRPM5, supporting a tuft cell-like subtype and refining the immunohistochemical characterization of this rare SCLC subset.

A genetic diagnostic model constructed based on ten genes (RIF1, GDPD5, DBNDD1, RCCD1, CLDN5, ASCL2, IFITM3, IFITM1, SMPDL3A, and SUCLG2) demonstrates strong predictive performance. This model holds significant potential for the early diagnosis and intervention of colorectal cancer, contributing to the implementation of third-tier prevention strategies.

Rescue experiments demonstrated that overexpression of CLDN3 could partly reverse the inhibitory effects of ASCL2 deletion on the malignant capacities of BC cells, suggesting their synergistic effects. Collectively, ASCL2 is a pivotal biomarker for successful individualized cancer therapy, targeting ASCL2 has enormous therapeutic potential.

Our multi-omics approach identified a malignant epithelial subset, C5, and a five-gene signature that stratifies gastric cancer prognosis and immune response. Functional assays showed that SRI knockdown impairs tumor cell growth, migration and invasion.

Reverse transcription quantitative polymerase chain reaction and Western blot analyses confirmed that CTHRC1, APOD, and S100A12 were significantly upregulated in the tumor group, whereas ASCL2 expression was significantly downregulated. We developed a TME-related gene signature that can predict the prognosis of patients with GC.

Moreover, we discovered that the transcription factor ASCL2 is required for recruitment of NK cells into the spleen and white pulp. These results provide improved tools and novel insights into NK cell biology.

Altogether, our analysis indicates a suboptimal design of several cancer vaccines currently in clinical development: ATP128, BNT111, BNT112, BNT116, INO-5401. We recommend that next-generation cancer vaccines should integrate rigorous epitope filtering strategies to eliminate shared sequences in TAAs.

Notably, FAT1-mutant HNSCC cells exhibit resistance to the TCA cycle inhibitor CPI-613 through activation of CPT1A-mediated FAO, whereas genetic ablation of mutant FAT1 restores sensitivity to CPI-613...Collectively, these findings establish that mutant FAT1 drives CPT1A-dependent FAO, facilitating a metabolic bypass that confers resistance to TCA cycle inhibition in HNSCC. This mechanistic insight highlights promising opportunities for combinatorial therapeutic strategies co-targeting genetic and metabolic vulnerabilities in cancer.

APT cell depletion improved MAPKi treatment efficacy and extended MAPKi response durability in mice. These findings uncover a cellular program that mitigates the impact of MAPKi therapies and highlights the importance of addressing tumor plasticity to improve clinical outcomes.

In this issue of the JCI, Luo and colleagues used genetically engineered mouse models to show that high mobility group A (HMGA1) is a critical mediator in the development of colon tumors driven by the loss of the Apc gene. HMGA1 activated the transcription of Achaete-Scute Family BHLH Transcription Factor 2 (ASCL2), which regulated intestinal stemness and promoted colon tumorigenesis.