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)

The inhibition of mTOR is a target for anticancer drugs in posttransplant malignancies. The influence of conversion to sirolimus after malignancy diagnosis was investigated on patient and renal allograft survivals. The 20 renal allograft recipients (4 women, 16 men) of ages 26 to 73 years (mean, 59 years) developed malignancies within 6 to 172 months (mean, 53 months) after transplantation. Three patients developed posttransplant lymphoproliferative disease (PTLD); four, Kaposi sarcoma, three, lung cancer; two, malignant melanoma; two, breast cancer; two, renal cell carcinoma; one, Merkel cell carcinoma; one, cutaneous T-cell lymphoma; one, larynx cancer; and one, gingival cancer. After tumor diagnosis, calcineurin inhibitors, azathioprine, or mycophenolate mofetil (MMF) were discontinued abruptly and sirolimus introduced (2 mg/d; target trough level, 4.0 to 8.0 ng/mL). Prednisone was maintained. The observation time of sirolimus therapy was 4 to 48 months (mean, 14 months). Two patients with PTLD (large B-cell lymphoma) and four with Kaposi sarcoma had full regressions. Eleven patients (larynx cancer, melanoma, breast cancer, T-cell lymphoma, renal cell carcinoma, Merkel cell carcinoma, and skin lymphoma) in addition to sirolimus therapy, underwent oncologic treatment, namely, surgery and/or chemotherapy. Six patients died from disseminated malignancy 4 to 9 months after conversion. One patient with T-cell lymphoma lost his graft; in the remaining patients, serum creatinine level was stable. In conclusion, Conversion to sirolimus resulted in regression of large B-cell lymphoma and Kaposi sarcoma. In patients with advanced or disseminated malignancy, the tumors progressed. Graft function was preserved after conversion to sirolimus.
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PMID:Anticancer effect of sirolimus in renal allograft recipients with de novo malignancies. 1802 73

The present study aimed to investigate microRNA (miR/miRNA)-34c expression and the association of miR-34c with B cell lymphoma 2 (BCL2) in M4e laryngeal carcinoma cell line. M4e laryngeal carcinoma cells were cultured and transfected with lenti-miR-34c or scramble miRNA for 72 h. Cell viability and the percentage of cells undergoing apoptosis of transfected cells were detected using MTT and Annexin V/allophycocyanin and propidium iodide assays, respectively. Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) and western blot analysis were performed to determine BCL2 mRNA and protein expression in transfected M4e cells. In addition, luciferase reporter assay was performed to identify whether BCL2 is a direct target of miR-34c. Transfection of lenti-miR-34c was able to significantly inhibit cell viability (P<0.01), increase the percentage of cells undergoing apoptosis (P<0.001) and downregulate BCL2 protein expression (P<0.01) in M4e cells. RT-qPCR data revealed that lenti-miR-34c transfection did not affect BCL2 mRNA expression. However, data from the luciferase reporter assay revealed that transfection with miR-34c negative control decreased luciferase activity in M4e cells co-transfected with pGL3-BCL2-MUT plasmid, compared with miR-34c inhibitor (P<0.01). Collectively, the results from the present study provided evidence that miR-34c may be involved in the pathogenesis of laryngeal cancer, and BCL2 may be negatively regulated by miR-34c in M4e cells.
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PMID:MiR-34c induces apoptosis and inhibits the viability of M4e cells by targeting BCL2. 2943 79