TP53 (Tumor protein P53)

Those treated with PD-1/PD-L1 inhibitors (Pembrolizumab) had limited benefit, with a median overall survival of 4.1 ± 2.8 months...Comprehensive genomic profiling may help refine understanding of tumour biology and potentially inform treatment decisions. Larger studies are needed to validate these findings, but integrating genomic, pathologic, and clinical data may advance personalized therapy for these patients.

Both components showed concordant aberrant tumor-suppressor immunoprofiles (p53 overexpression and Rb loss), and high-risk HPV RNA in situ hybridization (RNAscope) was negative. This case expands the recognized morphologic spectrum of bladder neuroendocrine carcinoma to include POU2F3-defined non-small cell neuroendocrine carcinoma with basaloid architecture, supporting the practical value of incorporating POU2F3 into immunohistochemical panels for poorly differentiated basaloid bladder tumors.

We analyzed global and Chinese CRLM clinical trials from the Informa database, focusing on fruquintinib, sintilimab, and dual immunotherapy (CTLA-4 + PD-1). Targets analysis shows most have low safety and specificity, but CD34, FLT1, and TP53 exhibit good profiles and potential for CRLM therapy and prognosis. This study, by integrating and analyzing the clinical trial data related to CRLM, aims to conduct an in-depth investigation and evaluate the safety specificity of the treatment targets through reference.

Although the R-CHOP regimen has significantly improved the prognosis for most patients, a subset continues to experience poor therapeutic outcomes...The key gene TRPV2, associated with favorable prognosis, was found to promote M1-like polarization in monocytes/macrophages and enhance antigen presentation in B cells. This study establishes the NR risk score as a novel prognostic tool for DLBCL and underscores neuro-immune interactions as potential therapeutic targets.

Mdm2 was found mutated heavily in carcinoma, and its variant can have a significant role when associating with p53. Our findings demonstrate a natural living model, to utterly contribute to the mechanistic understanding of the role of p53 in its activation, giving insight on structural properties aiming to target these biomarkers in cancer therapeutics.

These findings clarified that CP-31398 could elevate the transcriptional function of p53 probably by modulating the phase behavior. The study provided new insights into the regulation mechanism of p53 and potential therapeutic avenues for cancer.

HER2-high and HER2-low/TNBC breast cancers demonstrate distinct clinicopathologic and molecular profiles. Therapy-associated enrichment of PIK3CA mutations and their association with aggressive behavior underscore their prognostic and therapeutic significance in HER2-positive disease. Further studies are needed to clarify their role in guiding personalized treatment strategies.

This study is the first to report anticancer potential and mechanism of action of EECTL against breast cancer MDA-MB-231 cells. EECTL shows potential to serve as an adjunct to the main line of treatment in breast cancer and may be of interest for future preclinical and clinical studies aimed at developing integrative breast cancer treatments.

Our data support the clinical implementation of a tailored, histology-driven MP algorithm, potentially optimizing the genomic testing resources in SGCs.

Patients with lung-only metastases had a better OS than others, were more often women, and harbored less KRAS mutations. Our results argue in favor of PDAC with specific characteristics, especially a better prognosis, possibly further enhanced by the possibility to perform local treatments, and less detection of ctDNA.

In conclusion, a subset of CKD-/ESRD-associated iCCAs in Taiwan shows molecular and chemical evidence of AA exposure. However, the modest correlation between AA adducts and SBS22a signatures and the paucity of T>A transversions in driver genes suggests that AA acts as a contributory rather than causal factor, possibly synergizing with aging and liver disease-related mutagenic processes.

Collectively, our data reveal a SMAD-dependent regulatory role of TGFβ-superfamily signaling on hepatocytes that is tightly connected with hepatic growth to ensure proper energy homeostasis and metabolism. This is a critical regeneration parameter, which is closely related to the restoration of hepatic mass, especially following liver injury and fibrosis.