MYC (V-myc avian myelocytomatosis viral oncogene homolog)

The most active compounds were further tested in wound-healing assays, where 3lPd almost completely inhibited A549 cell migration at 24 and 48 h, whereas the reference drug cisplatin induced only partial inhibition...In silico studies were performed to investigate their interactions with p53, GAPDH, and c-MYC proteins. Overall, these results suggest that piperidine-bearing hydrazones and their Pt(II)/Pd(II) complexes represent promising scaffolds for the development of novel anticancer agents.

Reestablishing ATF4 protein expression rescues the diminished viability due to loss of MondoA expression or activity, providing direct evidence of a link between deregulated MYC and the transcriptional machinery of the ISR. Last, we find that small-molecule inhibition of MondoA is lethal in a subset of PDAC cell lines, including patient-derived organoids, suggesting that the ability to target MYC via chemical inhibition of MondoA transcriptional activity may have broad efficacy.

Treatment with a rituximab-bevacizumab combination regimen induced a second complete remission, sustained for six months at the time of reporting. Our case highlights the importance of routine CD5 testing in PCDLBCL-LT to identify this distinct subgroup and to guide appropriate differential diagnosis and patient monitoring.

P1/2, N=174, Active, not recruiting, Monte Rosa Therapeutics, Inc | Recruiting --> Active, not recruiting

P1, N=20, Not yet recruiting, Stanford University

Riluzole disrupts mitochondrial homeostasis by increasing Bax/Bcl-2 ratio, resulting in a drop of mitochondrial membrane potential. In conclusion, riluzole inhibits HCC growth by regulating glucose and glutamine metabolism and inducing autophagic cell death, thereby highlighting its therapeutic potential for HCC treatment.

These findings suggest that C. sinensis infection promotes HCC malignancy and stemness via ESP-induced PTTG1 expression, potentially through Wnt/β-catenin signaling and its downstream targets, including c-MYC and CD44, particularly in the context of the specific carcinogen-driven models used in this study. Further exploration of the PTTG1 pathway may offer insights into potential therapeutic strategies for C. sinensis-associated HCC.

A cisplatin (DDP)-resistant MDA-MB-231 cell line was established using a dose escalation...Mutation of Thr58 not only resulted in lower c-Myc stability, reduced colony formation ability, and increased apoptosis but also resulted in a decrease in both the total expression and O-GlcNAcylation of c-Myc. Therefore, O-GlcNAcylation at Thr-58 regulates c-Myc activity to promote chemoresistance of TNBC cells.

In a murine intrahepatic tumor model, KCTD1 knockdown synergizes with anti-PD-1 therapy, resulting in enhanced tumor infiltration by CD4⁺ and CD8⁺ T lymphocytes and improved anti-tumor efficacy. These findings establish KCTD1 as a key modulator of immune evasion in HCC and a promising target to potentiate immune checkpoint therapy.

HN-NCs had dismal prognosis, especially those originating from oral mucosa. HN-NC should be included in the differential diagnosis when encountering poorly differentiated/undifferentiated malignancies or carcinomas with squamous differentiation.

Moreover, TTFields-induced tumor immunogenicity may enable combination strategies with immunotherapies. A phase 2 clinical trial investigating TTFields with Gem/NabP and immune checkpoint inhibitors (ICIs) for metastatic PDAC is currently underway.

FGFR inhibition reversed these changes and synergized with anti-PD-1 therapy to enhance antitumor immune responses and establish durable immune memory. Collectively, these findings identify FGFR signaling as a key driver of therapeutic resistance and immune escape in SEC and support FGFR-targeted combination strategies.