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EGFR

Heterogeneity of Programmed Death-Ligand 1 Expression and Infiltrating Lymphocytes in Paired Resected Primary and Metastatic Non-Small Cell Lung Cancer

[Modern Pathology] In this study, 64 surgically resected specimens of paired primary tumors and metastatic tumors were obtained from 28 patients with non-small cell lung cancer. Multiplex immunofluorescence was performed on whole sections.

Expression of LGR5 in Mammary Myoepithelial Cells and in Triple-Negative Breast Cancers

[Scientific Reports] Scientists investigated LGR5 expression in normal, benign, and malignant lesions of the human breast using RNA in situ hybridization, and suggested that LGR5 marked facultative stem cells that were involved in post injury regeneration instead of homeostatic stem cells.

Oncogenic Switch and Single-Agent MET Inhibitor Sensitivity in a Subset of EGFR-Mutant Lung Cancer

[Science Translational Medicine] Researchers identified and characterized six patient-derived models of epidermal growth factor receptor (EGFR)-mutant, MET-amplified lung cancer that have switched oncogene dependence to rely exclusively on MET activation for survival.

The Potential Targeted Drugs for Fusion Genes including NRG1 in Pancreatic Cancer

[Critical Reviews in Oncology/Hematology] Pancreatic cancer (PC) remains an incurable disease with few treatment options. Recently, promising targets have been identified and novel therapeutic drugs are currently under development in KRAS wild-type PC.

Targeting DNA Damage Repair Pathways in Pancreas Cancer

[Cancer and Metastasis Reviews] Scientists outline the current treatment landscape for pancreas ductal adenocarcinoma patients with DNA damage repair gene-mutated tumors, highlight novel therapeutic approaches focused on surmounting tumor resistance, and explore new strategies which may lead to an expansion in the number of patients who benefit from these targeted treatments.

Effect of Aerobic Exercise on Acquired Gefitinib Resistance in Lung Adenocarcinoma

[Translational Oncology] Scientists successfully established lung adenocarcinoma cell lines with gefitinib resistance. Long-term gefitinib induction could increase the level of oxidative stress in lung adenocarcinoma cells and reduce the antioxidant capacity, resulting in the high expression of HIF-1 and ALDH1 and leading to the enrichment of CSCs, and a decreased response to gefitinib.

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