Molecular basis for prostate carcinogenesis / 中南大学学报(医学版)

Prostate cancer is the most prevalent male urogenital malignancy.Androgen deprivation therapy is the principal method for initial treatment for the patients,but the majority of them will eventually develop progressive disease,a status called castration-resistant prostate carcinoma.Lots of susceptibility genes,tumor suppressor genes and oncogenes,and their variations rdevant to the occurrence and development of prostate cancer have been revealed by the studies of molecular oncology.These findings on the molecular basis of prostate carcinogenesis will further improve the strategies on prevention,diagnosis and clinical management for prostate carcinoma.

Biochemical basis and emerging molecular targets to treat diabetic retinopathy

Diabetes being considered as an epidemic, long term untreated complicated diabetes resulting in retinopathy will be a leading cause of blindness worldwide. Many cross-sectional studies reported a strong relationship between chronic hyperglycaemia and development, progression of retinopathy, however the underlying mechanism that cause retinal microvascular damage following prolonged hyperglycaemia, yet to be revealed. Continued research worldwide focuses on understanding the molecular basis with the ultimate goal to prevent diabetic retinopathy by developing newer therapeutic targets. This article reviews multiple biochemical pathways that are implicated in diabetic retinopathy. Recent advancement in the molecular basis of the disease as well as clinical trials undertaken to target these molecules in order to block the signalling cascade prevailing in diabetic retinopathy is also discussed. This review highlights the recent therapeutic targets to prevent the onset as well as the progress of retinopathy in diabetes.

Crystal clear: visualizing the intervention mechanism of the PD-1/PD-L1 interaction by two cancer therapeutic monoclonal antibodies

Antibody-based PD-1/PD-L1 blockade therapies have taken center stage in immunotherapies for cancer, with multiple clinical successes. PD-1 signaling plays pivotal roles in tumor-driven T-cell dysfunction. In contrast to prior approaches to generate or boost tumor-specific T-cell responses, antibody-based PD-1/PD-L1 blockade targets tumor-induced T-cell defects and restores pre-existing T-cell function to modulate antitumor immunity. In this review, the fundamental knowledge on the expression regulations and inhibitory functions of PD-1 and the present understanding of antibody-based PD-1/PD-L1 blockade therapies are briefly summarized. We then focus on the recent breakthrough work concerning the structural basis of the PD-1/PD-Ls interaction and how therapeutic antibodies, pembrolizumab targeting PD-1 and avelumab targeting PD-L1, compete with the binding of PD-1/PD-L1 to interrupt the PD-1/PD-L1 interaction. We believe that this structural information will benefit the design and improvement of therapeutic antibodies targeting PD-1 signaling.

Research on molecular genetic basis for Jk(a-b-) phenotype / 中国输血杂志

Objective To investigate the molecular basis for Jk(a b ) phenotype.Methods Routine serologic testing for phenotype.Genomic DNA covering 4～11 exons and partial introns of JK gene was amplified by ploymerase chain reaction.The PCR products were excised and purified from agarose gels with a kit,then fragments were directly sequenced.Results G mutated to A in the 3'acceptor splice site of intron 5;A to G at 78 site from the 3'end of intron 3;C to T at 84 site from the 5'end of intron 8; A to G at 588 site of exons ( exon 7); G to A at 838 site of exons (exon 9).The splice site mutation (G→A) of intron 5 may cause the skipping of exon 6.Conclusion G to A mutation in the 3'acceptor splice site of intron 5 maybe one of the molecular basis for Jk(a-b-) phenotype