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DNA replication is a key event in the cell cycle. Although our knowledge is far from complete and many elusive regulatory mechanisms still remain beyondour grasp, many enzymes and a multiplicity of biochemical mechanisms involved have been discovered. Recent findings in E. coli have confirmed and yet surpassed the original hypothesis of F. Jacob. In yeast and higher eucaryotes, the apparent redundancy in putative origins and initiators has made an estimation of the importance of each identified element difficult to access. In spite of well established methodologies - which are also described in the book - the origin identification in mammalian chromosomes is still a controversial subject. On the other hand, considerable advances have been made in our understanding of virus DNA replication and this continues to deepen and broaden our understanding of the controls of cellular DNA replication.
Oncolytic viruses (OVs) have emerged as a promising anticancer treatment. OVs selectively infect, replicate in, and kill tumor cells. Oncolytic viral therapy occurs in two phases: an initial phase where the virus mediates direct oncolysis of tumor cells, and a second phase where an induced post-oncolytic immune response continues to mediate tumor destruction and retards progression of the disease. For a long time, the therapeutic efficacy was thought to depend mainly on the direct viral oncolysis based on their tumor selective replication and killing activities. But the post-oncolytic anti-tumor activity induced by the OV therapy is also a key factor for an efficient therapeutic activity. The topic adresses various strategies how to optimize OVs anti-tumor activity.
In line with recent evidence, the development of cancer has been described as uncontrolled cell growth that results from gradual accumulation of genetic and epigenetic alterations, involving aberrations in oncogenes, tumor suppressor genes, and defects in genes engaged in DNA repair. As a result, cancer cells acquire a neoplastic phenotype and tumor-associated antigens (TAAs) are presented on their surface. These target structures should be recognized by cells of the immune system. However, a sequence of events at the genetic and epigenetic level disturb immune cells, and in consequence, make them unable to eliminate cancer cells. Both innate and adaptive immunity are mobilized against cance...
The ability to genetically engineer oncolytic viruses in order to minimize side effects and improve the selective targeting of tumor cells has opened up novel opportunities for treating cancer. Understanding the mechanisms involved and the complex interaction between the viruses and the immune system will undoubtedly help guide the development of new strategies. Theranostic biomarkers to monitor these therapies in clinical trials serve an important need in this innovative field and demand further research.
Metabolism of glucose, lipids, amino acids, and nucleotides represents the fundamental capability of host to utilize distinct nutrients and energy to support diverse function of different cell lineages. Cancer cells undergo the Warburg Effect to adapt to the microenvironment composed by stromal cells and immune cells. The crosstalk among cancer cells and immune cells orchestrate tumor progression. In the tumor microenvironment, immune cells also show metabolic reprogramming. For example, naive or memory T cells switch from the oxidation of fatty acids to glycolysis and glutaminolysis after activation; meanwhile massive glucose and glutamine are transported into cells to meet their metabolic ...
Topic Editor Dr. Monteiro is the co-founder of Inatherys. Topic Editor Dr. Zarrin declares no conflict of interest with regard to the Research Topic theme.