Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: KEGG:D03301 (PDL)
658 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A number of cancer therapy agents are cleared by the kidney and may affect renal function, including cytotoxic chemotherapy agents, molecular targeted therapies, analgesics, antibiotics, radiopharmaceuticals and radiation therapy, and bone-targeted therapies. Many of these agents can be nephrotoxic, including targeted cancer therapies. The incidence, severity, and pattern of renal toxicities may vary according to the respective target of the drug. Here, we review the renal effects associated with a selection of currenty approved targeted cancer therapies, directed to vascular endothelial growth factor or VEGF receptor(s) (VEGF/VEGFR), epidermal growth factor receptor (EGFR), human epidermal growth factor receptor2 (HER2), BRAF, anaplastic lymphoma kinase (ALK), programmed cell death protein-1 or its ligand (PD-1/PDL-1), receptor activator of nuclear factor kappa-B ligand (RANKL), and mammalian target of rapamycin (mTOR). The early diagnosis and prompt treatment of these renal alterations are essential in the daily practice where molecular targeted therapies have a definitive role in the armamentarium used in many cancers.
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PMID:Renal effects of molecular targeted therapies in oncology: a review by the Cancer and the Kidney International Network (C-KIN). 2573 15

A majority of non-small cell lung cancer (NSCLC), especially adenocarcinomas, harbour at least one oncogenic driver mutation that can potentially be a target for therapy. The treatment of these oncogene-addicted tumors has dramatically changed the outcome of these patients, where tyrosine kinase inhibitors (TKIs) of mutated epidermal growth factor receptor (EGFR) and rearranged anaplastic lymphoma kinase (ALK) have paved the way for a new era of precision cancer medicine. Another paradigm shift in the treatment of NSCLC, as well as numerous other tumor types, has been the introduction of immunotherapy (IO) with immune checkpoint inhibitors targeting mainly programmed cell death-1 (PD-1) or its ligand PDL-L1, where studies have demonstrated an increased survival versus standard treatment with chemotherapy, both in the first- and second-line setting. However, the role of IO in oncogene-addicted NSCLC is still unclear where most clinical data come from subgroup analyses with low number of patients in larger randomized trials, and these data do not support the use of IO after TKI in this category of NSCLC patients. The purpose of this review is to summarize the existing evidence about the use of IO in oncogenic-addicted NSCLC and highlight the issues that should be addressed in the future in order to define the role of IO for these patients.
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PMID:Oncogene-addicted non-small cell lung cancer and immunotherapy. 2995 5