ATF1 (Activating Transcription Factor 1)

The partial reversal of this effect by the MEK/ERK inhibitor PD98059 confirmed the role of this pathway in the transcriptional control of VEGFA...Integrative bioinformatic analyses of GEO and TCGA-LIHC datasets supported these experimental findings, revealing hypoxia-associated upregulation of VEGFA, positive correlations between hypoxia scores and VEGFA/HIF1A expression, and context-dependent associations between ADAMTS1 expression, hypoxia signaling, and angiogenesis-related gene networks. These results identify ADAMTS1 as a hypoxia-responsive gene regulated through VEGFA-driven convergence of MAPK and PI3K/AKT signaling on a transcriptionally complex promoter, providing mechanistic insight into hypoxia-associated extracellular matrix remodeling in cancer.

P1/2, N=31, Active, not recruiting, National Cancer Institute (NCI) | Trial completion date: Nov 2025 --> Mar 2026

This work provides further characterization of ICMT as an important CNS mesenchymal neoplasm that is prone to tumor recurrence, showing 2 prognostically relevant methylation subclasses, and warranting diagnostic distinction from other epigenetically and histologically related tumors. ICMTs show substantial overexpression of the CREM gene, independent of fusion type.

Subsequently, the genes for transketolase I tktA and phosphoenolpyruvate synthase ppsA were further overexpressed to increase the availability of erythrose-4-phosphate and phosphoenolpyruvate, resulting in an increase in trans-anethole production to 223 mg/L. Finally, by knocking out the pheA gene to block the competitive pathway, the titer of trans-anethole was increased to 356 mg/L.

Since stress and obesity cooperate to promote the progression of PDAC, novel combinatorial strategies to prevent this devastating disease could be developed, repositioning FDA-approved drugs that are extensively used to treat cardiovascular and metabolic disorders and diseases. Finally, we review new advances in the treatment of PDAC, focusing on the discovery of novel drugs that directly inhibit KRAS and YAP function.

Given the tumor's extent, she was treated with definitive chemoradiation using weekly cisplatin and 70 Gy in 35 fractions...This case highlights the importance of molecular diagnostics in distinguishing HCCC from other clear cell neoplasms and suggests a potential role for chemoradiation in unresectable cases, though treatment-related toxicity remains a significant concern. Further investigation into systemic and targeted therapies for HCCC is warranted.

Atypical-location AFH (e.g., adrenal) exhibits divergent pathologic phenotypes. Diagnosis requires integrated IHC/molecular analysis (e.g., EWSR1 status). Prognostic implications of genetic alterations (e.g., ALK expression) highlight the need for molecular profiling to guide therapy and prognosis.

On the other hand, neither JNK nor p38 contributed significantly to the cytokine-induced EGR1 expression, suggesting complicated SAPK-signaling mechanisms that regulate immediate-early gene expression. Together, these results demonstrate the utility of the comprehensive multigene KO and sole-survivor KO strategy in dissecting intracellular signaling pathways consisting of multiple family members.

WGS in SGC is achievable in clinically relevant timeframes, providing genomic information for deeper understanding of disease pathophysiology, to clarify histologic subtype and can identify actionable genomic targets which may not be found through routine sequencing technologies. Further use of WGS has the potential to improve care for patients with SGC.

IN-SCT is a diagnostically challenging tumor characterized by the triad of inflammatory stroma, EWSR1::ATF1 fusion, and aggressive clinical behavior. Accurate recognition of its unique features supports its classification as a distinct entity. Surgical excision followed by adjuvant chemotherapy may benefit patients with advanced disease. The distinct molecular profile of IN-SCT may provide future directions for targeted therapy and diagnostic refinement.

Growth defects in the wild-type and sty1, pap1, and atf1 disruptants in the presence of DIM were suppressed by the ROS scavenger N-acetylcysteine...Collectively, the study results suggest that DIM increases ROS levels in mitochondria and suppression of ROS increase in mitochondria via inhibition of mitochondrial translation is the mechanism by which DIM-induced growth defects in wild-type cells are suppressed. Overall, the study highlights the potential use of DIM as an anticancer drug to increase ROS generation in mitochondria in cancer cells.

To date, only 3 cases of CCS have been reported involving the genital region, all originating in deep soft tissues. Our report expands the known anatomical sites of cutaneous clear cell sarcoma involvement.