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Marek’s disease virus (MDV) and avian leucosis virus (ALV) are known to cause tumours in egg-laying hens. Here, we investigated the aetiology of tumours in a flock of egg-laying hens vaccinated against MDV. We carried out gross pathology and histopathological examinations of the diseased tissues, identified virus antigen and sequenced viral oncogenes to elucidate the cause of death in 21–22-week-old hens. At necropsy, diseased hens had distinctly swollen livers, spleens, and proventriculus, and white tumour nodules in the liver. The spleen and liver had been infiltrated by lymphoid tumour cells, while the proventriculus had been infiltrated by both lymphoid tumour cells and myeloblastic cells. Subtype J ALV (ALV-J) and MDV were widely distributed in the proventricular gland cells, and the lymphoid tumour cells in the liver and the spleen. In addition, positive ALV-J signals were also observed in parts of the reticular cells in the spleen. MDV and ALV-J antigens were observed in the same foci of the proventricular gland cells; however, the two antigens were not observed in the same foci from the spleen and liver. The amino acid sequence of the AN-1 (the representative liver tumour tissue that was positive for both ALV-J and MDV) Meq protein was highly similar to the very virulent MDV QD2014 from China. Compared to the ALV-J HPRS-103 reference strain, 10 amino acids (224-CTTEWNYYAY-233) were deleted from the gp85 protein of AN-1. We concluded that concurrent infection with MDV and ALV-J contributed to the tumorigenicity observed in the flock. [ABSTRACT FROM PUBLISHER]

The phosphatase and tensin homology deleted on chromosome 10 (PTEN) gene is a novel tumor suppressor gene of the phosphatase family. Studies have shown that the PTEN gene is probably involved in human malignant disease pathogenesis, multidrug resistance, angiogenesis and extramedullary infiltration. This study was designed to investigate the effect of wild-type PTEN gene transfection on drug resistance reversal in K562/ADM leukemia cells in vitro and the possible mechanism. A recombinant adenovirus containing green fluorescent protein gene and wild-type PTEN gene (Ad-PTEN-GFP) or a recombined adenovirus containing green fluorescent protein gene only (Ad-GFP) was transfected into K562/ADM cells. These cells were then treated with different concentrations of adriamycin, cytarabine or arsenic trioxide, respectively. The half-maximal inhibitory concentration (IC50) of each drug was detected by MTT assay and the drug resistance reversal factor (RF) was calculated. The proliferation inhibition rate of these K562/ADM cells treated with or without the above-mentioned drugs was determined by MTT assay and the apoptosis rate was evaluated by flow cytometry. PTEN, nuclear factor-κB (NF-κB), I-κB, p53, multidrug resistance genes MDR1 and MRP, and apoptosis related genes Bcl-2, Bcl-xL and Bax mRNA levels were detected by real-time fluorescence relative-quantification reverse transcription polymerase chain reaction (FQ-PCR). PTEN, Akt, p-Akt and NF-κB (p65) protein levels were detected by Western blot. Results showed that PTEN gene transfection could increase the sensitivity of K562/ADM cells to chemotherapeutic drugs. The drug resistance reversal index of adriamycin, cytarabine and arsenic trioxide was 3.8-fold, 2.65-fold and 2.64-fold, respectively, after PTEN gene transfection. NF-κB, MDR1, Bcl-2 and Bcl-xL mRNA levels as well as p-Akt and NF-κB (p65) protein levels were down-regulated, while p53 and Bax mRNA levels were up-regulated in K562/ADM cells after transfection with Ad-PTEN-GFP. Therefore, wild-type PTEN gene transfection might increase drug sensitivity or reverse drug resistance via inhibiting the PI3K/Akt pathway and regulating downstream molecules of the cell signaling transduction pathway in K562/ADM cells, such as down-regulating NF-κB, MDR1, Bcl-2 expression but up-regulating the expression of p53 and Bax. [ABSTRACT FROM AUTHOR]