Study On The P73Gene Polymorphism In Patients With Keloid In Notrheast Han Population

Human genome is composed of22autosomes and2sex chromosomes, itsencoding gene carrying and human development, aging, disease and deathrelated to all the genetic information. The human genome is a structure verystable system, guarantee the human species as a common and stability. At thesame time it is a variant of the system, in the long-term evolution in the processof DNA sequence constantly mutate, some of them are preserved, leads to adifferent race, individual genomic variations or polymorphisms.With the human genome project, a comprehensive understanding ofdifferent individual genome sequence variation or polymorphism has becomepossible, and gradually shows its significance. Polymorphic marker researchhelps to reveal the genetic variants and phenotypes, thereby revealing gene andthe relationship between disease occurrence, this complex disease prevention,diagnosis and treatment is of great significance.Keloid is a secondary to skin lesions such as trauma, burns or operationafter the fibrous connective tissue hyperplasia, fibroblast proliferation causedby local collagen accumulation formation of skin collagen diseases. Withhypertrophic scars, keloids showed excessive growth, exceeding the originalwound boundaries, invading adjacent tissue, a tumor-like hyperplasia, so it isalso called benign skin tumour, keloids causing dysfunction, a good location,more common in people of color, do not undergo degenerative changes andsimple operation after resection of pole characteristics of Yi Fu. Because of itspathogenesis is very complex, treatment is still not a breakthrough, while thedomestic and foreign scholars carried on a large amount of research, but thepathogenesis remains unclear. As for keloid etiological research especially the development of molecular genetics, genetic factors in the occurrence anddevelopment of disease in the role by more and more scholars attention. Manystudies showed, inheritance in the pathogenesis of plays a vital role, and thereare obvious genetic heterogeneity. The traditional operation excision of keloidscar caused by recurrence, continue to increase, the postoperative need ofradiation, freezing, laser treatment, so that the treatment of keloids has becomethe focus and difficulty of plastic surgery.In recent years, some scholars study found, keloids have a strong geneticpredisposition, genetic variability may be an important factor in thepathogenesis of keloid. Domestic and foreign scholars on the keloid relatedgenes were studied. About half of the P53gene mutation in human malignanttumor exists, p73gene is a member of the p53family of proteins in thestructure, p73and p53protein with homology, can activate p53response genetranscription, which are involved in cell cycle regulation, DNA repair andapoptosis, and induction of apoptosis and inhibition of cell division arrest in theG1phase. Inhibition of cell proliferation, so p73is considered as a candidatetumor suppressor gene. Level and p53gene with high homology. As a result ofkeloid infiltration, recurrence, tumor characteristics, make people think ofkeloids may have p53, p73gene change.There is no domestic and foreign p73gene GC/AT polymorphism andnortheast regions of patients with keloid etiology research reports. Therefore,study on the p73gene non-coding area of GC/AT SNP loci and keloidpathogenesis correlation has great potential value.This study collected42cases of keloid patients and a control group of90caseswere health examination, all patients were between unrelated Jilin Han people,are the Third Clinical Medical College of Jilin University outpatients and inpatients. Case group and control group were in the informed consent fromelbow vein blood for DNA extraction. Polymerase chain reaction and Sty Irestriction enzyme digestion method,4%agarose gel electrophoresis, the gelimaging system, based on the restriction map of judging genotypes. Statisticalanalysis in GeneRunner software package for.Objective: To study the Northeast Han population of earlobe keloids with theoccurrence of p73gene related.Results:(1)The Keloid group p73gene GC/AT called genotype and allelefrequencies were compared with the control group, the difference was notstatistically significant.(P>0.05).(2) the different causes of injuries causedby keloid genotype and allele genotype distributions differ significantly (P <0.05).(3) of earlobe keloids group p73gene GC/AT called genotype andallele genotype and other sites of keloids as comparison groups, the differencewas statistically significant (P <0.05)Conclusion: p73gene exon non coding region of GC/AT loci genotype andallele frequencies in May and the northeastern region of earlobe keloidspatients about pathogenesis.This study is to explore the molecular genetic mechanism of keloidpathogenesis for the purpose, the effects of p73gene exon non coding region ofGC/AT polymorphism and keloid(keloid) etiologic relevance. Furtherrevealed keloid pathogenesis molecular genetic mechanisms, for keloid and provide theoretical basis for clinical treatment. Because the p73gene andkeloid clinical study of correlation between less, is not completely defined p73gene exon non coding region of GC/AT polymorphism and other polymorphicsite variability in keloid pathogenesis and the role of mechanisms. P73geneexon non coding region of GC/AT1mutations in other genes such as P53, Fasgene in keloid pathogenesis of synergetic effect? These problems need furtherresearch confirmed that the clinician.