EGFR expression

When administered above the microdose, ABY-029 demonstrated high correlation to EGFR expression and contrast values that were encouraging for translation to clinical practice. Contrast was similar to those observed with antibody agents, but with substantially reduced imaging-to-resection time, and no drug-related adverse events.

Single-cell RNA, bulk RNA and IHC data demonstrated the high expression levels and co-expression patterns of EGFR and MUC1 in tumors but not normal tissues. Therefore, it is a promising TAA combination for therapeutic targeting which could enhance on-tumor efficacy while reducing off-tumor toxicity.

The study finds more CD44 and EGFR co-expressing exosome subgroups in breast cancer cell lines, while immune-evasion PD-L1 high-phenotype exosome subgroups are primarily presented in complex tumor microenvironments, especially in HER2-positive tissues. This platform offers powerful single-cell isolation, exosome quantification, and phenotypic analysis capabilities, making it a powerful tool for advancing single-cell exosome analysis in cancer research.

Importantly, Cambogin not only efficiently blocks the replication and virion production of SARS-CoV-2 in vitro and in vivo by reducing the expression of EGFR and Cyclin A2, but also simultaneously inhibits both SARS-CoV-2 infection and the growth of KSHV-induced tumors in vivo using a murine xenograft model. These findings provide an alternative strategy for the potential use of Cambogin in the treatment of SARS-CoV-2 patients, particularly those with KSHV co-infection.

High SUOX expression may be a new indicator of recurrence risk in surgically resected lung adenocarcinomas.

An osimertinib and ICI-induced irAE mouse model was constructed that showed osimertinib combined with ICIs inhibited EGFR phosphorylation and activated the IL-6/JAK/STAT3 signaling pathway in mouse liver macrophages, which led to the release of relevant cytokines.

Our studies demonstrate that the small molecule MIF inhibitor CPSI-1306 potently inhibits T cell immunosuppression in the tumor microenvironment and reduces tumor growth in HNSCC. These studies open a novel therapeutic option for modulating anti-tumoral T cell immunity to improve HNSCC outcomes by targeting MIF.

The results of this study show that the combination can synergistically induce apoptosis of NSCLC by regulating ROS production. EGFR downregulation and AKT/ERK signaling pathway inhibition are linked to the synergistic effect.

Our findings suggest that both C-MYC and EGFR may be overexpressed and/or amplified in GISTs, indicating their potential prognostic role. This could also pave the way for therapeutic strategies targeting these proteins.

Finally, we found that three active ingredients (ferulic acid, luteolin, and quercetin) could inhibit the proliferation of non-small cell lung cancer cells and decrease the protein expression of EGFR in a concentration-dependent manner. All these results shed light on the bioactive components, pharmacological effects, and drug development and utilization of Zhe-Ba-Wei, aiming to provide useful support for its further research and clinical application.

Notably, CDDO-Me attenuates TNBC progression by accelerating EGFR degradation in cell-derived xenografts and patient-derived organoid models, highlighting its clinical application potential. Consequently, induction of EGFR degradation through MG degraders represents a viable therapeutic strategy for TNBC.

Combined treatment of PTX-resistant A549 cells with ivermectin and PTX may circumvent PTX resistance caused by P-gp induction, highlighting a novel therapeutic avenue for drug repurposing.

The predictive performance of the combined model established by integrating ultrasomics features and clinical baseline characteristics was improved, with the AUC, sensitivity, specificity, and accuracy of the RF machine learning combined model for the training and test dataset reaching 0.937 (95%CI, 0.884-0.971), 0.822 (95%CI, 0.702-0.909); 0.857, 0.833; 0.857, 0.800; 0.857, 0.817, respectively. To predict the status of EGFR expression in HCC patients, the ultrasomics model and combined model created by five machine learning algorithms can be utilized as efficient and noninvasive techniques, and the ultrasomics model and combined model established by RF classifier have the best predictive performance.

EGFR and SMAD4 expression were found to be negatively correlated in GBC tissue samples. ERBB2 overexpression/amplification was observed in 30% of the GBC samples. We also found a low percentage of GBC samples to show KRAS codon 12 mutation in Indian GBC patient population, as had been previously documented in pancreatic cancers.

Both deep learning models and radiomic signature-based models offer reasonably accurate non-invasive predictions of EGFR status and its subtypes. Fusion models hold the potential to enhance noninvasive methods for predicting EGFR mutations and subtypes, presenting a more reliable prediction approach.

Significant differences occurred in PFS on the basis of PD-L1 expression with values of 13.6 (95% CI: 10.5-NA), 18.7 (95% CI: 15.1-26.9), and 24.7 (95% CI: 20.7-NA) months for TPS of 0, 1-49, and 50 or higher, respectively (p = 0.02). Durvalumab maintenance therapy after definitive CCRT in unresectable locally advanced NSCLC patients with EGFR or ALK mutation demonstrates comparable clinical outcomes to those with wild-type EGFR/ALK when PD-L1 expression is present.

Strong expression of EGFR in tumours with higher grade validates its prognostic role and can be utilized for targeted therapy with potentially lifesaving consequences in patients presenting with urothelial carcinoma.

Verification of the anticancer activity of CLYF and its potential mechanisms may have important implications for anticancer therapies. Our results may provide a scientific basis for the clinical use of CLYF for cancer treatment and have important implications for developing pharmaceutical preparations, which also need more pharmacological experiments, clinical experiments, and in vivo experiments.

The in vivo tumor targeting ability and imaging also showed that Z239-1907 specifically and selectively targeted NPC xenograft mice models and accumulate at tumor site as early as 30 min and disappeared within 24 h post-injection. Collectively, these results suggest that Z239-1907 dual-target affibody is a promising therapeutic agent and a molecular imaging probe for early diagnosis in NPC.

Our study in Kerala showed PD-L1 expression in NSCLC patients, correlated with clinicopathologic factors. Males, COPD, ALK+, and advanced-stage tumors had higher expression. Females, smokers, poorly differentiated tumors, and stage IV tumors had high PD-L1.

The CR diet inhibited tumor growth by suppressing mTOR and its related upstream and downstream gene signaling pathways, reducing tumor glycolysis, and accelerating tumor cell apoptosis.

Furthermore, GCC2 inhibition compromised Golgi structural integrity in cancer cells, indicating a functional role of GCC2 in regulating intracellular trafficking and signaling to promote lung cancer progression. Together, these findings suggest GCC2 as a potential therapeutic target for the treatment of NSCLC.

In terms of mechanism, we found that mT16A#5 inhibited the phosphorylation of PI3K, AKT and JNK. These results highlight the anti-growth and anti-metastasis capacity of the combination of mT16A#5 and Cetuximab in the treatment of ESCC by targeting TMEM16A and EGFR, and provide a reference for combinational antibody treatment in ESCC.

In conclusion, pedHGG-RTK2A/B tumors are characterized by highly diffuse-infiltrating growth patterns and specific radiological and histo-molecular features. By comprehensively characterizing methylation-based tumors, the chance to develop specific and effective therapy concepts for these detrimental tumors increases.

While Rad-score of Ki-67 expression status in the training group obtained the top accuracy, sensitivity, specificity, and PPV with values of 0.85, 0.80, 0.92, and 0.93. Preoperative MRI-based radiomics analysis has the ability to noninvasively assess the postoperative Ki-67, p53, and EGFR of rectal cancer.

Furthermore, MFMP mediates immunogenic cell death in HCC by synergizing with RFA through cGAS DNA demethylation, EGFR mRNA demethylation, and TBK1 protein phosphorylation, thereby inhibiting recurrence and metastasis and enhancing immune memory. Thus, MFMP is a potential adjunctive therapy requiring clinical validation.

High PD-L1 expression was more commonly found in lung adenocarcinomas with uncommon and complex EGFR mutations. Furthermore, high PD-L1 expression independently predicted poor survival. These findings warrant validation through prospective studies.

The upregulation of ENAH through a PI3K/AKT/β-catenin signaling cascade enhances oral cancer cell migration and growth via the ITGB5/Src axis. These findings offer a new interpretation of the ENAH function in the OSCC progression and provide crucial information for developing new OSCC treatment strategies.

P1, N=62, Active, not recruiting, National Cancer Institute (NCI) | Trial completion date: Oct 2024 --> Oct 2025

In conclusion, SH3BGRL3 is upregulated in GC, particularly in EBVnGC. Higher SH3BGRL3 expression is closely associated with hyperglycemia and poor outcomes in patients with EBVnGC, suggesting its potential as a biomarker and prognostic predictor.

MiRNA-218-5p up-regulates ErbB2 and EGFR expression by suppressing LRIG1 expression, thus promoting the malignant behaviors of BC. miRNA-218-5p may exert a pro-tumor effect on BC and serve as a therapeutic target for BC treatment.

Additionally, SLCDS inhibits the expressions of EGFR, PDGFR, Ki67, and Vimentin in gliomas. Our findings offer a potential approach for treating glioma.

This drug resistance feedback loop could be mitigated by the synergistic action of agents targeting PI3K-AKT-mTOR and EGFR for HGSOC with CAV1 and EGFR expression. Using this workflow could enable the personalized testing of patient-derived tumor samples at single-cell resolution.

BXD has the effect of inhibiting tumor growth rate and delaying the development of GC. Its mechanism of action may be related to the regulation of PI3K-Akt signaling pathway.

In conclusion, benzothiazole derivatives exhibited potent inhibitory effects on breast cancer in vitro by promoting apoptosis, downregulating EGFR activity, and modulating key signaling pathways, including JAK/STAT, ERK/MAPK, and PI3K/Akt/mTOR. These results highlighted the potential of benzothiazole derivatives as novel therapeutic agents for breast cancer treatment.

C12 also exhibited tumor growth inhibition in an ovarian cancer xenograft mouse model. Consistent with its selective tumor cell binding in vitro, radioimmuno PET (positron emission tomography) imaging with 89Zr-DFO-C12 in mouse xenograft models confirmed tumoral accumulation of the C12 mAb.

Women may develop more aggressive tumors, and extralaryngeal tumors often present with more challenging prognoses. Low Cx43 expression may be more likely to coincide with higher Ki67 and COX-2 levels, possibly indicating a link with more aggressive tumor behavior.

our study elucidated the therapeutic mechanism of CKI in treating liver cancer and unveiled the underlying principles of its TCM compatibility through its mode of action.

Protein expression analysis revealed that hyperthermia decreased EGFR expression and increased levels of apoptosis-related proteins, including cleaved PARP and caspase-3. IPHC with cisplatin demonstrated enhanced antitumor efficacy in vitro models, particularly in drug-resistant lung cancer, indicating its potential as a valuable adjunct to existing treatment regimens for lung cancer and for improving patient outcomes in advanced lung cancer with MPE or pleural metastasis.

Furthermore, CyH inhibited the activation of JAK3/STAT signaling pathway. Taken together, our findings suggest that CyH promotes the sensitivity to gefitinib in NSCLC cells through the inhibition of EGFR activation and PD-L1 expression.

Among agents targeting one or more members of the HER family, the pan‑HER family blocker afatinib was the most effective, inhibiting the proliferation of three out of seven human liver cancer cell lines (LCCLs), while the CDK inhibitor dinacicilib was the most effective agent, inhibiting the proliferation of all human LCCLs tested. Taken together, the present results suggested that EGFRvIII expression and its co‑expression with wtEGFR or CD44 was of prognostic significance. These results also support further investigations of the therapeutic potential of drugs targeting EGFRvIII and other members of the HER family in patients with HCC.

P1, N=701, Active, not recruiting, Janssen Research & Development, LLC | Recruiting --> Active, not recruiting | N=460 --> 701