Recently, in order to make chemotherapy, safer and more effective various forms of intervention by pharmacists are needed. In this paper, we report our experience in intervening in the administration of gefitinib to a patient with dysphagia. Chemotherapy with an intravenous drip injection to the 58 year-old woman admitted to our hospital for non-small cell lung cancer (NSCLC) was withdrawn due to severe pancytopenia after the first cycle of pharamcotherapy. Then, as an altermative, oral medication, of gefitinib was suggested by medical doctors. However, the oral administration was inappropriate to the condition of the patient. She was unable to keep taking gefitinib pills because she had been suffering from a progressive swallowing disturbance due to progressive non-small cell lung cancer. Thus, we proposed another oral administration method in which gefitinib was resuspended in thickening agents. This method made it possible for the patient to take gefitinib without any adverse events until the day before the patient died.
Patients ; Chemotherapy-Oncologic Procedure ; Non-small cell lung cancer ; Deglutition Disorders ; Needs

Cellular senescence is an irreversible cell cycle arrest triggered by the activation of oncogenes or mitogenic signaling as well as the enforced expression of tumor suppressors such as p53, p16(INK4A) and promyelocytic leukemia protein (PML) in normal cells. E2F-binding protein 1 (E2FBP1), a transcription regulator for E2F, induces PML reduction and suppresses the formation of PML-nuclear bodies, whereas the down-regulation of E2FBP1 provokes the PML-dependent premature senescence in human normal fibroblasts. Here we report that the depletion of E2FBP1 induces the accumulation of PML through the Ras-dependent activation of MAP kinase signaling. The cellular levels of p16(INK4A) and p53 are elevated during premature senescence induced by depletion of E2FBP1, and the depletion of p16(INK4A), but not p53 rescued senescent cells from growth arrest. Therefore, the premature senescence induced by E2FBP1 depletion is achieved through the p16(INK4A)-Rb pathway. Similar to human normal fibroblasts, the growth inhibition induced by E2FBP1 depletion is also observed in human tumor cells with intact p16(INK4A) and Rb. These results suggest that E2FBP1 functions as a critical antagonist to the p16(INK4A)-Rb tumor suppressor machinery by regulating PML stability.
Cell Line, Tumor ; Cells, Cultured ; Cellular Senescence ; genetics ; physiology ; Cyclin-Dependent Kinase Inhibitor p16 ; antagonists & inhibitors ; genetics ; physiology ; DNA-Binding Proteins ; deficiency ; genetics ; physiology ; Down-Regulation ; Fibroblasts ; Gene Expression Regulation ; Humans ; Intranuclear Inclusion Bodies ; metabolism ; MAP Kinase Signaling System ; Nuclear Proteins ; genetics ; metabolism ; physiology ; Promyelocytic Leukemia Protein ; Protein Isoforms ; Protein Stability ; RNA Interference ; Retinoblastoma Protein ; antagonists & inhibitors ; genetics ; physiology ; Transcription Factors ; deficiency ; genetics ; metabolism ; physiology ; Transfection ; Tumor Suppressor Protein p53 ; physiology ; Tumor Suppressor Proteins ; genetics ; metabolism ; physiology ; Ubiquitination ; ras Proteins ; metabolism