KRAS G13

The cancer was refractory to regimens extrapolated from rectal cancer management (capecitabine with oxaliplatin, and irinotecan). Pelvic recurrence and osseous metastases were clearly radiosensitive. Tumor molecular profile showed microsatellite stable cancer with KRAS p.G13D and TP53 p.C176W mutations.

In conclusion, no significant associations between KRAS-G12 and overall survival were found for TAS-102 or TAS-Bev. Further research is needed to assess the impact of these mutations on combined TAS-Bev therapy prior to any clinical application.

We also include a systematic review of cutaneous HS cases, identifying only two cases with underlying hematologic transdifferentiation. The distinct clinical morphology, histopathologic characteristics, and immunohistochemical markers associated with each of these entities highlight a very rare and unique example of histiocytic transdifferentiation in the context of a hematologic malignancy.

Instead, some cases may reflect adult-onset RASopathies or early clonal proliferations with distinct biological behavior. Recognition of such cases warrants refinement of diagnostic criteria and may influence therapeutic decision-making.

Our results support a causal relationship between red meat and CRC and may inform tailored dietary and screening guidelines for CRC prevention.

Despite the historical challenges in targeting KRAS-mutant proteins, the findings of this study support the potential of natural products as scaffolds for anticancer drug discovery as a source for developing novel anticancer therapies. The identified phytochemicals from C. officinalis such as calendasaponin D and procyanidin A2 may serve as potential leads for future preclinical and experimental validation against KRAS-driven malignancies.

This study suggests codon 13 KRAS mutations may be associated with LR in LARC. However, given the small number patients and events, these findings should be cautiously interpreted until confirmed by larger studies. Preoperative genetic testing for KRAS mutations is suggested to enhance risk stratification.

Previously, we developed small molecule ULK1 inhibitors that not only inhibit ULK kinase activity but also induced the degradation of other core members of the ULK complex including ATG101 and ATG13...Finally, immunohistochemical staining of orthotopic pancreatic tumors reveals a significant increase in CD4⁺ and CD8⁺ T cell infiltration upon treatment, suggesting that SBP-1750 enhances anti-tumor immunity. These findings support further development of SBP-1750 as a novel ATG-targeting cancer therapy.

KRASmt and NRASmt are seen in 49% and 4% of mCRC, respectively. No clinically relevant differences were observed between different RASmt. KRASmt is a common subgroup for which the outcome hopefully can be improved with newly developed drugs.

Sensitivity to mutant-specific inhibitors largely overlapped with sensitivity to state-selective agents, suggesting that most RAS-mutant tumors will respond poorly to any currently available RAS inhibitor. Implications: Determining the signaling inhibition index (SII) can inform the design and clinical application of RAS-targeted therapies to improve tumor selectivity and therapeutic outcomes.

Here we present GoDig-LiF, which uses spectra and retention times predicted by the Prosit-TMT model in place of data libraries, enabling targeted proteomics with only a tandem mass tag-labeled sample, target list, and mass spectrometer. We applied GoDig-LiF to the quantification of mutated proteins in cancer cell lines, including KRAS G13D.

Pancreatic cancer driven by the KRASG12D mutation faces therapeutic challenges from KRAS undruggability and acquired resistance to inhibitors like MRTX1133 via secondary mutations (e.g., Q95/Y96)...In vivo, ZJK-807 (30 mg/kg, subcutaneous) achieved 47% tumor growth inhibition in AsPC-1 xenografts with favorable pharmacokinetics. This study presents a CRBN-based PROTAC to selectively target and degrade resistant KRASG12D mutants, establishing a groundbreaking approach for KRAS-driven malignancies.