Orthotopic KRAS-mutant xenograft models (LOVO-Luc2 (N = 52) and SW480-Luc2 (N = 52)) were treated with standard-of-care regimens (FOLFOX, bevacizumab, or combination) and longitudinally imaged by CT (N = 104 tumour scans, N = 156 liver scans collected over 4 timepoints)...The most predictive features, GLSZM Gray Level Non-Uniformity, GLRLM Run Length Non-Uniformity Normalized, and GLDM Small Dependence Emphasis, were significantly associated with metastatic burden and survival in a clinical CRC cohort (N = 41), indicating species conservation and translational relevance. Collectively, these data demonstrate that preclinical CT radiomics can identify quantitative imaging features associated with treatment sensitivity and early metastatic progression, supporting translational potential.

P1, N=5, Active, not recruiting, City of Hope Medical Center | Trial completion date: Apr 2026 --> Mar 2027 | Trial primary completion date: Apr 2026 --> Mar 2027

P3, N=204, Recruiting, Sixth Affiliated Hospital, Sun Yat-sen University | Not yet recruiting --> Recruiting

P2, N=17, Terminated, University of Southern California | Active, not recruiting --> Terminated; Insufficient Accrual

P1/2, N=482, Recruiting, BioNTech SE | Trial completion date: May 2031 --> Dec 2032

Anti-angiogenic agents targeting VEGF/VEGFR2 (e.g., bevacizumab, TKIs) are used clinically, but their benefit in advanced breast cancer is controversial: progression-free survival (PFS) gains are inconsistent, overall survival (OS) benefits are unclear, and resistance with class-specific toxicities (e.g., hypertension) is common...Benefit is independent of visceral metastasis but reduced in bone metastases. Increased toxicities (hypertension, proteinuria, hand-foot syndrome, diarrhea) warrant proactive management.

Patients with high TEPGS exhibited resistance to immunotherapy but responded to a BRAF V600E inhibitor, while TEPGS showed tentative value for predicting cetuximab response and preliminary utility for bevacizumab. Functional assays confirmed ARPC1B as an oncogene. Our findings establish TEPGS as a valuable biomarker for prognostic stratification and tailored therapy selection in CRC.

The efficacy of anti-EGFR therapy in mCRC appears to exhibit additional intraregional heterogeneity beyond the conventional right-left classification. These findings suggest that anatomical tumour location may reflect underlying biological differences not fully captured by this binary classification.

P2, N=76, Recruiting, Dechang Diao

Kaplan-Meier analysis of OS and progression-free survival (PFS) demonstrated that the AAT score could significantly stratify patients into low (≤1.8), median (>1.8 to ≤3.0), and high (>3.0) risk groups, with distinct 2-year OS rates of 80.0%, 48.0%, and 4.0%, and PFS rates of 63.3%, 56.0%, and 4.0% in the training cohort, validated in the cohort. The AAT model effectively stratifies OS and PFS in uHCC patients undergoing TACE plus sintilimab and bevacizumab, guiding personalized treatment decisions.

In the BRCA+ high-risk population, olaparib monotherapy (median PFS 41.2 months) and olaparib plus bevacizumab (median PFS 42.5 months) demonstrated the greatest PFS benefit, marginally outperforming niraparib (median PFS 31.2 months). RMST analysis also indicated an advantage of 8.5 months for the combination, though this did not reach statistical significance. PARPi treatment benefit in ovarian cancer is meaningfully influenced by genetic profile and relapse risk, supporting biomarker-driven treatment selection in clinical practice.

The phase III KEYNOTE-B96 trial in platinum-resistant disease demonstrated a progression-free survival benefit in the intention-to-treat population and an overall survival benefit in tumors with programmed death ligand 1 (PD-L1) combined positive score ≥1 when pembrolizumab was paired with weekly paclitaxel with or without bevacizumab, underscoring the value of an immunomodulatory chemotherapy backbone in earlier lines. We explain why single-analyte biomarkers-PD-L1, tumor mutational burden, homologous recombination deficiency/BRCA1/2-have not reliably enriched benefit and outline a multidimensional approach integrating genomic scars (e.g., mutational signature 3), immune functional state (Immunoscore, CD8⁺ tumor-infiltrating lymphocyte density and CD8⁺: regulatory T-cell ratio), and spatial architecture (inflamed, excluded, desert phenotypes). This framework aims to move beyond the all-comer era toward context-informed precision immunotherapy in ovarian cancer.