EGFR amplification

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.

This study demonstrates the feasibility of localized tumor-normal sequencing in Nigerian BC patients, revealing actionable variants with clinical relevance. These findings highlight the need to integrate genomic profiling into routine cancer care and establish molecular tumor boards to advance precision oncology in Nigeria.

This led to the in silico identification of a novel lead compound with a distinct thiazolopyridine-based scaffold and high predicted potency. Our findings demonstrate how integrated bioinformatic pipelines can dissect the complex landscape of GBM resistance, contextualize the roles of key oncogenes, and guide the rational design of potential new inhibitors.

A plasma sample serves as a supplement for identifying GPS when a tissue sample is unavailable. Moreover, the integration of FISH, NGS, and ddPCR provided a comprehensive assessment of MET amplification.

The findings highlight the superior sensitivity and accuracy of SR-based detection in identifying EGFRvIII and capturing intratumor heterogeneity. SR-based analysis is recommended as the method for EGFRvIII detection in both clinical and research settings.

Our study highlights diverging infiltration patterns across glioblastoma tumors, with indications of a GPC-like to AC-like transition occurring in classical-subtyped tumors. This shift is associated with a decrease in cell proliferation and may have implications for clinical treatment.

Single agent therapy in a BT20 xenograft model reduced tumor volume, however only the combination statistically significantly reduced tumor volume compared to control. We conclude that EGFR amplification with co-incident PI3K pathway mutations are driver mutations in a subset of breast cancers and present a subgroup of breast cancers that are more likely to respond to dual targeted therapy.

Subsequently, the patient started gefitinib treatment, and 3 months later, the treatment effect assessment showed a partial response (PR) at regular follow-up according to RECIST evaluation criteria...Two months later, imaging examination showed that the lesions in various parts of the body were stable. Except for dryness of oral and nasal mucosa, the patient did not experience other serious adverse reactions.

P1, N=21, Recruiting, Marcela V. Maus, M.D.,Ph.D. | Trial completion date: Jan 2027 --> Jun 2027 | Trial primary completion date: Jan 2026 --> Jun 2026

Furthermore, patients with higher Ki67 levels had higher rCBV and rCBF (P < 0.05 for both). MR perfusion values (rCBV and rCBF) have statistically significant differences between different grades of meningioma.

This study aimed to assess the safety and efficacy of depatuxizumab mafodotin as a monotherapy or in combination with temozolomide in patients with recurrent epidermal growth factor receptor (EGFR)-amplified glioblastoma multiforme, focusing on overall survival (OS) and progression-free survival (PFS). While depatuxizumab mafodotin shows the potential to improve survival outcomes, the heterogeneity in results highlights the need for further research. Future studies should refine patient selection criteria and explore alternative therapeutic combinations, such as depatuxizumab mafodotin with gemcitabine or cisplatin, to optimize treatment strategies.

Our integrative bioinformatics and histopathological analyses highlight EGFR as a central oncogenic driver and potential immunomodulatory factor in GBM. EGFR amplification correlates with poor prognosis, immune dysregulation, underscoring its utility as both a diagnostic biomarker and a potential therapeutic target in GBM management.