Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0079731 (B-cell lymphoma)
 16,671 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We report here a case of fatal respiratory failure developed during chemotherapy for diffuse large B cell lymphoma that occurred late after lung transplantation. 25-year- old man underwent lung transplantation from brain death donor for respiratory failure due to interstitial pneumonia at the age of 16 years old. Two years after transplantation, his respiratory function decreased gradually. Chronic lung allograft dysfunction including bronchiolitis obliterans( BOS) and restrictive allograft syndrome was suspected and immunosuppression was enhanced. Nine years after transplantation, he had abdominal pain and physical examination suggested intestinal obstruction. Small intestine endoscopy revealed an ulcer at jejunum and diffuse large B cell lymphoma( DLBCL) was finally diagnosed by biopsy. Chemotherapy was planned for lymphoma, but respiratory failure progressed just before chemotherapy. Chest computed tomography showed infiltrative shadow in right lung, so we suspected presence of lymphoma and chemotherapy was carried out. After chemotherapy, abnormal shadow in the right lung disappeared. Although chemotherapy was effective, respiratory failure progressed and he died. Pathological examination from autopsy showed mixture of BOS, diffuse alveolar damage, invasion of aspergillus and acute fibrinoid organizing pneumonia but no residual DLBCL was found in the lung.
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PMID:[Fatal Respiratory Failure Developed during Chemotherapy for Diffuse Large B Cell Lymphoma that Occurred Late after Lung Transplantation]. 2771 1

The novel bromophenol derivative, 3-(3-bromo-5-methoxy-4-(3-(piperidin-1-yl)propoxy)benzylidene)-N-(4-bromophenyl)-2-oxoindoline-5-sulfonamide (BOS-93), was synthesized in the CAS Key Laboratory of Experimental Marine Biology, Institute of Oceanology, Chinese Academy of Sciences (Qingdao, China). Experimental studies have demonstrated that it could induce apoptosis and autophagy in human A549 lung cancer cells, and it could also inhibit tumor growth in human A549 lung cancer xenograft models. In the present study, the molecular pathways underlying these effects were identified. The results demonstrated that BOS-93 could inhibit cell proliferation in A549 cells and block A549 cells at the G0/G1 phase. Furthermore, BOS-93 could induce apoptosis, activate caspase-3 and poly ADP ribose polymerase, and increase the B cell lymphoma (Bcl)-2 associated X protein/Bcl-2 ratio. Notably, BOS-93 could also induce autophagy in A549 cells. BOS-93-induced autophagy was confirmed by detecting light chain 3 (LC3)-I/LC3-II conversion and increasing expression of beclin1 and autophagy-related gene 14. Notably, BOS-93-induced autophagy could be inhibited by the autophagy inhibitor 3-MA. Flow cytometry, transmission electron microscopy (TEM) and western blot analysis indicated that BOS-93 induced apoptosis and autophagy activities by deactivating phosphoinositide 3-kinase/protein kinase B/mechanistic target of rapamycin and activating the mitogen-activated protein kinase signaling pathway. The present findings indicated that BOS-93 might be a novel anti-cancer agent for treatment of human lung cancer.
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PMID:BOS-93, a novel bromophenol derivative, induces apoptosis and autophagy in human A549 lung cancer cells via PI3K/Akt/mTOR and MAPK signaling pathway. 3098 70