Permissiveness Paradox in Cell Cycle Progression Towards Genome Instability and Malignant Transformation

Journal Title: Open Access Journal of Oncology and Medicine - Year 2018, Vol 2, Issue 2

Abstract

Dimensional representation of events actively executing the cell cycle dynamics of progression in carcinogenesis allow for a paradoxical emergence of highly permissive elements in the establishment of the mitotic spindle and the separation of chromatids. In such terms, ongoing processes of dissolution of the nuclear membrane betray an essential permissiveness in cell cycling that is paramount constitutional characterization of a process as “passenger” event in defining malignant transformation. In real terms, incremental progression of the cell cycle is specific hallmark for the events that constitutionally permit the system machinery in mitosis to conclusively establish potential re-setting of events as non-re-replication of the cell cycle in the re-emerging G1 phase of mitotic activity. The cell cycle dynamics and its relative interactions with states of instability of the genome acquire significant relevance in regard to cellular malignant transformation. There appears to be a tumor suppressor role effect of apoptosis, DNA repair by homozygous recombination and cell cycle arrest in G2 in simple epithelia subject to ionizing radiation-induced DNA damage [1]. The attributes of such interface effects include the dimensional shifts in phosphorylation of the retinoblastoma suppressor gene activities in a manner that prevents re-replication of the nuclear DNA within the same cell cycle. Such processes are linked to inhibitory effects of phosphorylation in relative measure to rephosphorylation. The dimensional connotations relative to genomic instability underlie progression of a cell-cycle series of events relative to the stabilization of CDK1/Cyclin B1 that progresses as alternate modes of representation and constitution of the cell replicative machinery components. In such measure, the inclusion of integral genomic participation in each of the cell cycle stages allows for phosphorylation and other post-translational events to assume transforming attributes to stage identity and potential.

Authors and Affiliations

Lawrence M Agius

Keywords

Related Articles

Somatic Mutations in Cancer-Free Individuals: A Liquid Biopsy Connection

Somatic mutations have been perceived as the causal event in the origin of the vast majority of cancers. Advanced massively parallel, highthroughput DNA sequencing have enabled the comprehensive characterization of somat...

Percutaneous nephrostomy in the management of malignant ureteral obstruction: an alternative using central venous catheter and “zero irradiation”

Introduction and Objective: Percutaneous Nephrostomy (NP) is a procedure that involves the placement of a drainage catheter in the renal pelvis by puncture through the skin guided by an imaging method. The objective of t...

Re-Purposing Evodiamine as an Anti-Cancer Drug: Effects on Migration and Apoptosis

Introduction: Evodiamine is a quinolone alkaloid compound obtained from a fruit described in traditional Chinese medicine. It has been in use for many centuries for the treatment of headaches, menstrual problems, abdomin...

Promising Role of Fractional Calculus in Biomedicine and Biophysics

The study of complex systems and investigation of their structural and dynamical properties have attracted considerable interests among scientists in general and physicists, biologists and medical researchers in particul...

Permissiveness Paradox in Cell Cycle Progression Towards Genome Instability and Malignant Transformation

Dimensional representation of events actively executing the cell cycle dynamics of progression in carcinogenesis allow for a paradoxical emergence of highly permissive elements in the establishment of the mitotic spindle...

Download PDF file
  • EP ID EP589078
  • DOI 10.32474/OAJOM.2018.02.000133
  • Views 63
  • Downloads 0

How To Cite

Lawrence M Agius (2018). Permissiveness Paradox in Cell Cycle Progression Towards Genome Instability and Malignant Transformation. Open Access Journal of Oncology and Medicine, 2(2), 135-137. https://www.europub.co.uk/articles/-A-589078