OBJECTIVETo improve the diagnosis and treatment of penile metastasis from rectal carcinoma.

METHODSWe reported a case of penile metastasis secondary to rectal adenocarcinoma, reviewed the relevant literature, and discussed the common origins, clinical features, pathogenic mechanisms, diagnosis and treatment of this disease.

RESULTSThe patient was a 54-year-old male, with metastatic penile tumors secondary to rectal adenocarcinoma, with serious adhesion to the surrounding tissue and metastasis to the liver. As treatment, we performed colostomy to relieve voiding difficulty, followed by combination chemotherapy with oxaliplatin, 5-fluorouracil, and levofolinate. The patient died 10 months later as a result of systemic failure.

CONCLUSIONPenile metastatic malignancy has a poor prognosis. Early diagnosis and combined and individualized therapies may improve the quality of life, relieve pain and prolong the life of the patient.

Adenocarcinoma ; secondary ; therapy ; Antineoplastic Combined Chemotherapy Protocols ; therapeutic use ; Combined Modality Therapy ; methods ; Fluorouracil ; administration & dosage ; Humans ; Liver Neoplasms ; secondary ; therapy ; Male ; Middle Aged ; Organoplatinum Compounds ; administration & dosage ; Penile Neoplasms ; secondary ; therapy ; Quality of Life ; Rectal Neoplasms ; pathology

OBJECTIVETo investigate the relationship between -308 genotype polymorphism in the promoter region of the tumor necrosis factor alpha (TNFalpha) gene and asthenospermia in infertile men.

METHODSAllele-specific polymerase chain reaction (ASPCR) and polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) were used to analyze the genotype at position -308 in the promoter region of the TNFalpha gene in 187 infertile male patients, who were divided into Groups A (asthenospermia, n = 60), B (oligoasthenozoospermia, n = 65) and C (infertile patients with normal sperm, n = 62). The levels of TNFalpha in the seminal plasma from these patients were measured by radioimmunoassay, and all the data were statistically analyzed by SPSS16.0.

RESULTSGroups A and B exhibited significant differences from C in the frequency of GA/AA at position 308 in the promoter region of the TNFalpha gene (21.67% and 26.15% versus 8.06%, P < 0.05). Spearman analysis showed a negative correlation between the GA + AA type of the TNFalpha-308 allele and the percentage of grade a + b sperm (r = -0.690, P < 0.05). The level of TNFalpha in the seminal plasma was significantly elevated in Groups A ([4.23 +/- 0.45] ng/ml) and B ([4.29 +/- 0.47] ng/ml) as compared with C ([4.03 +/- 0.66] ng/ml, P < 0.05), but with no significant differences between Groups A and B (P > 0.05). It was also significantly higher in the GA+AA ([4.61 +/- 0.29] ng/ml) than in the GGtype ([4.06 +/- 0.45] ng/ml, P < 0.05).

CONCLUSIONRegardless of sperm density, the frequently of TNFalpha-308 GA/AA is negatively correlated with the percentage of grade a + b sperm, which may be associated with the level of TNFalpha in the seminal plasma. Accordingly, anti-TNFalpha therapy might be effective for asthenospermia, and the measurement of the TNFalpha level in the seminal plasma can be an auxiliary diagnostic marker for male infertility.

Adult ; Alleles ; Asthenozoospermia ; genetics ; Case-Control Studies ; Gene Frequency ; Genotype ; Humans ; Infertility, Male ; genetics ; Male ; Polymorphism, Genetic ; Promoter Regions, Genetic ; Tumor Necrosis Factor-alpha ; genetics

OBJECTIVETo investigate the role of α-enolase (ENO1) in regulating glucose metabolism and cell growth in human glioma cells.

METHODSGlucose uptake and lactate generation were assessed to evaluate the changes in glucose metabolism in human glioma U251 cells with small interfering RNA (siRNA)-mediated ENO1 knockdown. MTT assay and 5-ethynyl-2'-deoxyuridine (EdU) staining were used to examine the cell growth and cell cycle changes following siRNA transfection of the cells.

RESULTSTransfection of U251 cells with siRNA-ENO1 markedly reduced glucose uptake (P=0.023) and lactate generation (P=0.007) in the cells and resulted in significant suppression of cell proliferation (*P<0.05) since the second day following the transfection. Transfection with siRNA-ENO1 also obviously suppressed cell cycle G1/S transition in the cells (P=0.0425). The expressions of HK2 and LDHA, the marker genes for glucose metabolism, were significantly down-regulated in the cells with siRNA-mediated ENO1 knockdown.

CONCLUSIONENO1 as a potential oncogene promotes glioma cell growth by positively modulating glucose metabolism.