KRAS wild-type

P2/3, N=574, Recruiting, SUNHO（China）BioPharmaceutical CO., Ltd. | N=90 --> 574 | Trial completion date: Jul 2028 --> Jul 2029 | Trial primary completion date: Jul 2026 --> Jul 2028

P1, N=47, Terminated, BeOne Medicines | N=514 --> 47 | Trial completion date: Dec 2026 --> Apr 2026 | Recruiting --> Terminated | Trial primary completion date: Dec 2026 --> Apr 2026; The Sponsor has made the decision to terminate this study due to the lack of promising efficacy, internal prioritization, and highly competitive landscape.

Poor survival outcomes were observed across all 1 L treatment options. Patients with KRAS-mutated NSCLC and low PD-L1 expression had especially poor outcomes, highlighting the need for more effective treatment options.

This review summarizes current evidence on the crosstalk between KRAS signaling and Furin-like enzymes, emphasizing their cooperative roles in tumour progression and immune escape. Targeting protein maturation by these enzymes may therefore represent a therapeutic approach for KRAS-mutant colorectal cancer, offering new opportunities for personalized treatment.

Nonetheless, K. rosea emerges as a candidate taxon differentially enriched in PDAC, with potential stage- and KRAS-associated patterns. These findings highlight the need for orthogonal validation (qPCR, FISH, culture) and larger prospective cohorts to differentiate true biological associations from residual contamination or stochastic noise in low-biomass settings.

High Cdc42 expression may serve as an adverse prognostic marker in CRC. Cdc42 shows moderate concordance between primary tumors and matched metastases without a consistent directional shift.

Oncologists should consider broad next-generation sequencing, including fusion detection, for patients with KRAS-wildtype PDAC. When an ALK fusion is identified, ALK inhibitor therapy can yield durable disease control.

The modulation of these NF1-SPRED1/2-dependent downstream signaling effectors were further corroborated in Schwann cell models derived from Neurofibromatosis type I patients that consisted of either plexiform neurofibroma cells or unaffected nerve cells abrogated of NF1 or neurofibromin RAS-GAP activity. Taken together, this study provides RAS-independent functions that are dependent on the cooperation of NF1 and SPRED1/2 in a manner that is uncoupled from canonical MAPK signaling.

In plasma, twelve genes were consistently detected, and SHOC2, YAP1, LZTR1, RGS3, and ZDHHC7 were significantly upregulated at week 6. Low tumor LIFR expression was associated with poorer survival, supporting its potential as a prognostic biomarker and highlighting the feasibility of plasma-based gene expression monitoring.

Successful generation of a BrM-derived organoid line enabled high-throughput drug screening, which recapitulated the patient's clinical resistance to standard therapies [gemcitabine/nab-paclitaxel, 5-fluorouracil (5-FU)], and showed sensitivity to afatinib, everolimus and RMC-6236...Physicians should also be aware that KRAS wild-type pancreatic cancer with atypical amplifications is likely to exhibit unique metastatic tropisms. Finally, we suggest that patient-derived organoids pharmacotyping can mirror clinical drug responses and help evaluate therapeutic avenues for patient treatment.

Survival analysis showed no significant difference between serrated-MAC and MAC-NOS. We have confirmed that a large majority of colorectal MAC have similar characteristics to SAC.

Adjuvant chemotherapy was classified as fluoropyrimidine monotherapy (5FU) or oxaliplatin-based therapy (Ox+)...Outcomes were similar between Ox+ and 5FU in double wild-type (KRAS and BRAF wild-type) tumors (OS HR = 1.11, 95% CI, 0.82-1.50). These findings suggest molecular heterogeneity in treatment associations that may inform adjuvant therapy selection.