MYC expression

Validation through the HPA database further supported these findings, confirming the potential of MYC and STAT3 as diagnostic biomarkers for CRC. Our results suggest that MYC and STAT3 are promising diagnostic biomarkers for CRC, offering new insights into its pathophysiology and potential for targeted therapies.

LDHAα, LDHA and c-MYC expression was significantly higher in human acute lymphocytic leukemia and colorectal cancer tissue specimens compared to normal controls. In conclusion, our study identified LDHAα as a subtype of LDHA and highlighted its critical role in tumor metabolism, providing a potential new therapeutic target for tumor diagnosis and treatment.

Mechanistically, sildenafil restrained GC growth by directly activating PKG through PDE5 inhibition for regulating c-MYC expression via its phosphorylation and ubiquitination degradation, thereby suppressing c-MYC stability for IL-6 transcription within the downstream IL-6/JAK/STAT3 signalling pathway. The PDE5 inhibitor sildenafil may serve as a promising adjuvant for GC therapy if further randomized clinical trials confirm its efficacy.

We examine the evidence that highlights how dysfunctions in PERs activities initiate cancer development, aid tumor growth, and modify cancer cell metabolism through pathways involved in oxidative stress and immune system. Comprehending these connections opens new pathways for the development of circadian rhythm-based therapeutic strategies, with the aims of boosting immune responses and enhancing cancer treatments.

When combined with etoposide/cisplatin, it synergistically inhibited SCLC growth. Mechanistic studies revealed that c-Myc expression may be a key factor influencing the effect of tinengotinib in SCLC-N. This study provides reliable preclinical data and a new direction for tinengotinib as a promising therapy for SCLC, either alone or in combination with chemotherapy.

Additionally, our data suggest a link between the induced expression of MICA and the regulation of both, KLF4 and c-MYC, which might represent a mechanism underlying the induction of NKG2D-L expression upon treatment with APTO253. These results may contribute to the potential use of APTO253 as a treatment to improve tumor cell-mediated NK cell cytotoxicity in various cancers.

The results of molecular docking showed that the predicted drugs can bind well to the core targets. In conclusion, cadmium is associated with NAFLD; the identified cadmium-toxicity targets, HCK, MYC, and DUSP6, may serve as biomarkers for the diagnosis of NAFLD and predicted drugs, decitabine and retinoic acid may have a potential role in the treatment of NAFLD.

Following induction with R-CHOP chemotherapy, BCL6-DHL patients demonstrated a poor OS similar to BCL2-DHL patients and worse than that of DLBCL patients (p = 0.024)...The data also suggest that BCL6-DHL as currently defined, is heterogeneous and that neoplasms with a GCB immunophenotype are more likely to have DH-like signature and behave more aggressively. Lastly, we suggest that BCL6-DHL cases deserve to be recognized separately in a lymphoma classification to facilitate further understanding of these neoplasms and for optimal patient management.

More importantly, 40 exhibited robust antitumor efficacy in the MSTO-211H mouse xenograft model. Collectively, our results suggest that TEAD PROTACs have therapeutic potential for the treatment of cancers associated with TEAD overactivation.

High expression of BRD3 or Ku70 is closely associated with poor prognosis in HCC patients. Overall, we reveal the important role of the Ku70-BRD3 complex in the onset and progression of HCC, suggesting that the Ku70-BRD3 complex is a promising target for clinical intervention in HCC.

These mechanisms collectively boost anaerobic glycolysis and the hexosamine biosynthetic pathway (HBP), providing essential energy and metabolites for rapid liver cell proliferation. Our findings not only elucidate the central role of HA in regulating cellular metabolism but also lay a solid theoretical foundation for developing therapeutic strategies targeting HA-related metabolic pathways.

The microRNA pro-file of HGBCL-11q differs from those of BL and GCB-DLBCL-NOS, exhibiting greater heterogeneity compared to BL. The microRNA profile further supports that HGBCL-11q is a distinct subtype of B-cell lymphoma.