P1/2, N=45, Recruiting, West China Hospital | Not yet recruiting --> Recruiting | Trial completion date: Apr 2028 --> Sep 2028 | Initiation date: Apr 2025 --> Sep 2025 | Trial primary completion date: Apr 2027 --> Sep 2027

The efficacy of NAT regimens containing trastuzumab plus pertuzumab (HP) and trastuzumab plus pyrotinib (HPy) was compared. Both HP and HPy combined with chemotherapy can be considered as optional NAT regimens for HER2-positive BC. The nomogram incorporating common clinical indicators provides a basis for clinicians to predict NAT efficacy at an earlier stage.

P2, N=18, Recruiting, Peking Union Medical College Hospital | N=45 --> 18 | Trial completion date: Dec 2025 --> Dec 2026 | Trial primary completion date: Dec 2023 --> Dec 2026

Likewise, a combination of selective inhibitors of KRAS (RMC-6236/daraxonrasib), EGFR family (afatinib), and STAT3 (SD36) induced the complete regression of orthotopic PDAC tumors with no evidence of tumor resistance for over 200 d posttreatment...Of importance, this combination therapy was well tolerated. In sum, these results should guide the development of new clinical trials that may benefit PDAC patients.

Pyrotinib plus trastuzumab demonstrates clinically meaningful efficacy and a manageable safety profile in heavily pretreated HER2-positive metastatic colorectal cancer. These findings support advancing this regimen as a potential alternative in refractory HER2-positive mCRC, particularly in the RAS/BRAF wild-type subgroup.

The patient achieved a prolonged period of disease stability, who was treated with various anti-HER2 targeted therapy, such as trastuzumab combined with pyrotinib and HER2-targeted antibody-drug conjugate (ADC). Dynamic CA199 levels paralleled the treatment efficacy. This report underscores the significance of molecular profiling-guided personalized therapy and integrated multidisciplinary management in the treatment of biliary tract cancers.

Notably, no adverse events were observed, and the patient has maintained a partial response for over eight months. This case suggests that afatinib can be administered without major dose modification in HD patients, with PK data indicating minimal impact of dialysis and underscoring the importance of accumulating real-world evidence in this underrepresented population.

The study identified multiple genomic characteristics associated with primary and secondary resistance to first-line afatinib treatment in EGFR- and ERBB2-positive subpopulations.

Spatially distinct and simultaneous resistance mechanisms, namely, EGFR L718V mutation and SCLC transformation, contributed to osimertinib resistance. The detection of RB1 2.4 kb small deletion in RB1 gene highlights the importance of deep genomic profiling. Multi-site biopsy and molecular diagnostics are necessary to guide treatment decisions in EGFR-TKI-resistant NSCLC.

P2, N=0, Withdrawn, West China Hospital | N=98 --> 0 | Recruiting --> Withdrawn

CRM197 markedly inhibited cell proliferation, induced G₀/G₁ arrest, and outperformed cetuximab and matched or exceeded afatinib in vitro; in vivo, CRM197 reduced tumor volume and weight more effectively than afatinib, with extensive necrosis. These data establish CRM197 as a potent, multi‑targeted inhibitor of arsenic‑driven LSCC and highlight novel therapeutic targets for further drug development.

This study represents the largest cohort of NSCLC patients with EGFR G719X + S768I co-mutations treated with first-line afatinib. Our findings confirmed the effectiveness and safety of afatinib in this patient population. Furthermore, the presence of the G719X + S768I co-mutations serves as an independent predictor of favorable PFS for NSCLC patients. This study will provide new clinical evidence supporting afatinib therapy for patients with EGFR G719X + S768I co-mutations, both in China and globally. This study fills an important gap in the existing literature by providing robust, large-scale clinical data, offering new insights for the treatment of NSCLC patients with these uncommon mutations.