KRAS G12

Knockdown of RCC1 in pancreatic cancer cells restored SIRT3 expression and impaired tumor formation in vivo. Overall, our study has revealed a previously unrecognized mechanism by which oncogenic KRAS promotes tumor development through down-regulation of the SIRT3-mediated tumor suppression pathway, and has also identified RCC1 as a potential therapeutic target for treatment of cancer patients with KRAS mutations.

Histopathological evaluation may aid risk stratification alongside KRAS status. Prognostic assessment in clinical settings should take both TNM staging and KRAS status into account.

Furthermore, we validated the specificity of our approach by successfully detecting various mutations, including KRAS G12C, KRAS G12D, EGFR T790M and TP53 R273H, in simulated clinical samples. These findings highlight a reliable method for precise ctDNA detection, offering high specificity, selectivity, and accuracy, thus paving the way for potential cancer diagnostic application.

Mutational analysis further highlighted the significance of KRAS G12C, G12V, and G12D mutations, which were common between RCC and pancreatic metastasis. Our study provides critical insights into the statistically significant associations between metabolic disorders and malignancies, emphasizing the potential of tailored therapies alongside shared therapies in managing RCC and its progression to pancreatic metastasis.

P2, N=95, Active, not recruiting, Novartis Pharmaceuticals | Trial completion date: Nov 2027 --> Dec 2026

Alterations associated with the formation of a somatic-type malignancy and/or the development of cisplatin resistance include TP53 mutations or MDM2 gene amplifications as well as epigenetic alterations...Additionally, we will provide guidance on how to examine a testicular tumour specimen histopathologically to reach an accurate diagnosis. Finally, we will outline the importance of the content of a histopathological report for the urologists and oncologists.

There is a need to understand how the LUAD TME impacts patient response to immunotherapy. We identified a transcriptional program enacted by TAp73 in tumor alveolar macrophages that supports T-cell activation. Transcriptional and metabolomic data from LUAD patients supports the relevance of this program in response to immune checkpoint inhibition.

PBAE-PEG/LNP delivery of sgRNAs targeting Eml4 (sgEml4) and Alk (sgAlk) into Cas9 mice by IT injection produced autochthonous lung tumors carrying the driver oncogene Eml4-Alk. This approach using PBAE-PEG/LNP to deliver RNA will allow for agile development of lung cancer mouse models.

Additional discussion includes advancements in therapies directed at MET, HER2, RET, ROS1, and FGFR alterations-each representing promising targets in NSCLC. This review concludes by exploring the growing evidence surrounding TROP-2 as a novel therapeutic target, especially relevant in cases where previous targeted treatments have failed.

These findings reveal that Sod2 shapes cellular metabolism in pancreatic cancer through peroxynitrite formation and Myc activation.

We described the genomic landscape of KRASG12D-mutant CRC and PDAC, demonstrating that cases often have additional oncogenic alterations linked to resistance to KRAS inhibition. These alterations are also associated with a worse prognosis. Recognizing these alterations may inform new therapeutic strategies. Further studies are warranted to validate these findings in ongoing clinical trials.

EMP1 plays a crucial role in the pathogenesis of PDAC, as it contributes to the proliferative and metastatic characteristics of PDAC. This study suggests that EMP1 may be a potential therapeutic target gene for aggressive disease.