Молекулярная и генетическая медицина

The second most common cause of cancer-related fatalities in men is prostate cancer, which is also the most prevalent non-skin cancer. A lot of patients with prostate cancer display an aggressive disease with metastasis and progression, whereas some patients display an indolent illness with little potential to advance. Intraepithelial neoplasia, androgen-dependent adenocarcinoma, androgen-independent adenocarcinoma, sometimes known as castration-resistant adenocarcinoma, are the three phases of development of human prostate malignancies. Our understanding of the genetic events involved for the onset and progression of prostate cancer has advanced very quickly because to developments in molecular technologies. These investigations have demonstrated that, in comparison to other malignancies, the prostate cancer genome has a comparatively low mutation rate and little chromosomal losses or gains. Prostate cancer pathways saw an accumulation and convergence of genomic and epigenomic aberrations as the disease progressed, creating a highly diverse transcriptome landscape that was dominated by an overactive androgen receptor signalling axis. This review emphasises the present level of knowledge and lists options for reducing prostate cancer morbidity and death.

The transfer of genetic information from the archival copy of DNA to the transient messenger RNA, often followed by the creation of protein, is represented by transcription, translation and subsequent protein modification. Despite having fundamentally the same DNA, every cell in an organism has a different kind and function due to qualitative and quantitative variations in gene expression. Therefore, differentiation and development depend on the regulation of gene expression. Although it is believed that epigenetic mechanisms such as DNA methylation, histone modification and different RNA-mediated processes primarily affect gene expression at the level of transcription, other stages of the process (such as translation) may also be regulated by epigenetic factors. The following will describe how epigenetics works on different circumstances, their role in various diseases and disorders.

Traditional identification methods for the soft rot Erwinias are both imprecise and time-consuming. We have used the 16S rDNA to aid in their identification.
Analysis of 16S rDNA-PCR and 16S rDNA-RFLP and gene sequencing was found to be simple, precise, and rapid method compared to other molecular techniques.
Analysis of the isolates genome by using their total DNA by amplifying their genome using the universal primer (fD1/rP2) indicated an amplified product of the
16S rDNA at 450 bp and the amplification using the specific 16S rDNA (EP16A/EP1GTC) was located of 700 bp. The restriction analysis of the universal amplified
product of 450 bp size using Hind III, proved the presence of different RFLP bands with some common bands. Variation in RFLP profile bands is an indication of
polymorphism in between the isolates. Whereas common bands indicates genetic stability among the isolates of the same spices or same genus. Sequencing of
the 16S rDNA universal primer amplified product showed a complete sequence of one isolate out of 10 isolate and the similarity between this isolate and the data
base indicated the presence of high similarity above 95% with other Enterobaceriaceae.