GATA6 (GATA Binding Protein 6)

Treatment-induced EMT reduces GATA6+ populations and MHCI expression, which is restored by combining MEKi with HDAC inhibitors, enhancing GATA6+ tumor cells, MHCI, CD8+ T cell infiltration, tumor suppression, and survival. These findings suggest that therapeutic strategies promoting a GATA6-driven tumor cell state improve immune recognition of PDAC cells and potentiate anti-tumor cytotoxic effects.

Conclusions By enabling rapid, cost-effective molecular stratification from routine H&E-stained slides, PanSubNet offers a clinically deployable and interpretable tool for genetic subtyping. We are gathering data from two institutions to validate and assess real-world performance, supporting integration into digital pathology workflows and advancing precision oncology for PDAC.

One hundred and ninety-three patients with resected pancreatic ductal adenocarcinoma from the ESPAC-4 trial of adjuvant gemcitabine and capecitabine were included. GATA6 expression was not associated with differential treatment effects. GATA6 expression measured by immunohistochemistry with digital assistance was a prognostic biomarker among people with pancreatic adenocarcinoma treated with surgical resection and adjuvant chemotherapy.

It is the first pancreatic carcinoma type in which a basal molecular phenotype can be indicated clinically by both imaging and histopathology, with major potential management implications (as it is also enriched in actionable targets like ARID1A). Recognition of this category is critical for cancer research, as it offers an invaluable group to study plasticity, stroma versatility, necrosis mechanisms, and the basal type in pancreatic cancer.

This study defines a spatially organized stromal-immune signaling axis that drives immune exclusion and immunotherapy resistance in ccRCC. Targeting the POSTN⁺ CAF-CCL3⁺ macrophage interaction offers a promising strategy to remodel the fibrotic barrier and restore antitumor immunity.

In the context of cancer biology, VIM-AS1 did not affect the antiproliferative actions of TGF-β, yet had an impact on the epithelial-mesenchymal transition gene program, and increased the invasion and motility of tumor cells, whereas its silencing sensitized cancer cells to chemotherapeutic agents. The molecular mechanism highlights how a lncRNA can modulate the nuclear pore's capacity to import SMAD complexes, by facilitating their capture by Nup358/RanBP2 and thereby enhancing nuclear accumulation of SMADs with distinct isoform composition, thus promoting selectively TGF-β signaling responses.

By enabling rapid, cost-effective molecular stratification from routine H&E-stained slides, PanSubNet offers a clinically deployable and interpretable tool for genetic subtyping. We are gathering data from two institutions to validate and assess real-world performance, supporting integration into digital pathology workflows and advancing precision oncology for PDAC.

Furthermore, we have shown STAT3/GATA6 axis as a key mediator of anti-inflammatory effects of butyrate. These findings provide mechanistic insight into butyrate's protective role and highlight its potential to mitigate Aβ and TNF-α-induced cerebrovascular inflammation in AD.

Cancers with high co-expression of ELF3 and HNF4A were frequently chromosomally instability (CIN), intestinal-type adenocarcinomas, and harbored TP53 mutations and WWOX deletions. Expression of E74 like ETS transcription factor 3 (ELF3), an ETS transcription family member, correlates with expression of other key factors in gastric cancer and confers specific characteristics that may become exploited in targeted therapeutic interventions.

Our findings demonstrate the tumor-promoting function of SPDEF in NSCLC by transcriptionally activating BIRC5, highlighting SPDEF as a candidate target for future NSCLC-directed therapies.

In contrast, RepID depletion resulted in a marked upregulation of GATA6 expression due to the loss of these repressive modifications. Collectively, these findings establish RepID as a pivotal upstream regulator of osteosarcoma metastasis through modulation of the PRC1-GATA6 axis, and highlight its potential as a promising therapeutic target.

Our study identifies how oncogenic KRAS/ERK signaling suppresses GATA6 to cause dedifferentiation in pancreatic cancer. Combining KRAS/ERK inhibitors with standard-of-care chemotherapies could be a promising therapeutic strategy for treating pancreatic cancers.