DDIT3 (DNA-damage-inducible transcript 3)

Emerging tools, such as radiomics and artificial intelligence-based approaches, are briefly addressed as evolving adjuncts. By integrating classical imaging principles with contemporary classification frameworks, this article aims to serve as a comprehensive and clinically relevant reference for radiologists involved in the assessment and management of fat-containing soft-tissue tumors.

To address this, an antioxidant-enriched hydrogel (PG-gel) was developed from N-acetylcysteine-modified gelatin and poly (ethylene glycol) succinimidyl succinate, loaded with conditioned medium from umbilical cord mesenchymal stem cells (CM-UCMSCs)...Transcriptomic analysis revealed downregulation of apoptosis-related genes (e.g., Ddit3, Trib3 and Hmox1) and upregulation of mitochondrial metabolism genes (e.g., Mt-atp8, Mt-nd1 and Mt-cyb). In conclusion, the PG + CM-UCMSCs system provided comprehensive protection to cryopreserved ovarian tissue by mitigating oxidative stress, fibrosis, and apoptosis, likely through regulation of apoptotic signaling and enhancement of mitochondrial energy metabolism, thereby offering a promising strategy to improve OTCT outcomes.

We provide the first systematic single-cell atlas of UPR heterogeneity in PCa and develop a clinically translatable UPRRS prognostic model. IFRD1, a key driver, emerges as a dual diagnostic and therapeutic target, offering both theoretical and experimental foundations for precision stratification and individualized management of PCa.

To encapsulate our findings, we have determined eight MAPK pathway-associated CRC prognostic biomarkers and developed a prognostic model accordingly. This model has proven effective in stratifying the risk levels among CRC patients.

This study examined the effects of five anticancer agents-cisplatin, 5-fluorouracil, vincristine, irinotecan, and cyclophosphamide-on mouse skeletal muscle. Targeting ER stress may help prevent chemotherapy-induced muscle wasting. Further studies are needed to clarify mechanisms and develop protective strategies.

This led to the downregulation of key oncogenic effectors including Slug, FN1, CDH2, F2RL1, CDK6, CCND1, MMP9, CDKN2A, and SQSTM1, while upregulating tumor suppressors CDKN1B, CDKN1A, and DDIT3. In conclusion, COPB2 acts as an oncogene in GC, driving tumor progression through modulation of the cell cycle and key signaling pathways, highlighting its potential as a therapeutic target.

The efficacy of GLJ and GLK on lung cancer cell proliferation was further demonstrated in a zebrafish xenograft model. Collectively, the absolute configurations of GLJ and GLK were identified and they exerted lethal effects on lung cancer cells to the same extent via ROS-ER stress-mitochondrial apoptosis signaling, suggesting that GLJ and GLK might be used as potential modulating agents in lung cancer treatments.

This review provides information about the clinicoradiological features, pathogenesis, histopathology, and management currently available for MPLPS. In addition, we discuss the differential diagnosis of this novel entity.

This study established an integrated model "multicomponents-multitargets-multiactivities" and offered a theoretical framework to elucidate its molecular mechanisms of antitumor and alleviating chemotherapy-induced toxicities in CRC patients.

Our findings highlight the prognostic relevance of PET-derived MPs via GC signaling dysregulation, providing mechanistic insights into how environmental pollutants exacerbate cancer risks. This study advances strategies for refining MPs toxicity assessments and developing targeted interventions to mitigate CRC progression linked to MPs exposure.

(4) In summary, a tumor-intrinsic TF network cooperates with SPP1+ macrophage signaling to promote a permissive microenvironment and HCC progression. This integrated axis highlights tractable vulnerabilities for therapeutic intervention.

The prototypic EPRS inhibitor halofuginone demonstrated significant tumour growth inhibition in an in vivo patient-derived xenograft model. These results suggest that targeting metabolic stress pathways via ATF4 activation presents a novel therapeutic approach for chordoma, warranting further clinical investigation.