Journal of Medical Oncology and Therapeutics

All submissions of the EM system will be redirected to Online Manuscript Submission System. Authors are requested to submit articles directly to Online Manuscript Submission System of respective journal.
Reach Us +441518081136

Rapid Communication - Journal of Medical Oncology and Therapeutics (2023) Volume 8, Issue 4

Cancer and the cell cycle: unraveling the connection

Philip Burrows *

MRC Integrative Epidemiology Unit (IEU), Population Health Sciences, University of Bristol, Bristol, United Kingdom

*Corresponding Author:
Philip Burrows
MRC Integrative Epidemiology Unit (IEU), Population Health Sciences
University of Bristol, Bristol
United Kingdom

Received: 29-Jun-2023, Manuscript No. JMOT-23-109780; Editor assigned: 30-Jun-2023, PreQC No. JMOT-23-109780 (PQ); Reviewed: 18-Jul-2023, QC No. JMOT-23-109780; Revised: 19-Jul-2023, Manuscript No. JMOT-23-109780 (R); Published: 29-Jul-2023, DOI: 10.35841/jmot-8.4.159

Citation: Burrows P. Cancer and the cell cycle: unraveling the connection. J Med Oncl Ther. 2023;8(4):159

Visit for more related articles at Journal of Medical Oncology and Therapeutics




Cancer is a complex and devastating disease that affects millions of people worldwide. It arises when normal, healthy cells undergo uncontrolled growth and division, forming a mass of abnormal cells known as a tumour. To comprehend the roots of cancer, it is essential to delve into the intricate relationship between the disease and the cell cycle—the tightly regulated process that governs cell division and growth. The cell cycle is a meticulously orchestrated series of events that a cell undergoes to reproduce itself. It consists of several distinct phases, including interphase (G1, S, and G2 phases) and mitosis (M phase). Interphase is the period of cell growth and DNA replication, while mitosis is the actual process of cell division [1].

During the G1 phase, the cell grows and prepares for DNA synthesis. The S phase follows, during which the cell duplicates its DNA, ensuring each resulting daughter cell will have the same genetic information. The G2 phase is a checkpoint phase, where the cell assesses whether its DNA has been accurately replicated and is ready for division. If all conditions are met, the cell proceeds to the M phase. The M phase consists of several tightly regulated steps, including prophase, metaphase, anaphase, and telophase, leading to the formation of two genetically identical daughter cells. These daughter cells then enter the G1 phase again, completing the cycle [2].

To ensure the cell cycle progresses smoothly and accurately, a sophisticated network of regulatory mechanisms exists. Key players in this process are cyclins and cyclin-dependent kinases (CDKs). Cyclins are proteins that fluctuate in concentration throughout the cell cycle, while CDKs are enzymes that become active when bound to cyclins. The interaction between cyclins and CDKs forms cyclin-CDK complexes, which act as molecular switches, triggering the cell to move from one phase to another. Additionally, there are checkpoint pathways that act as guardians of the genome, ensuring that damaged or abnormal cells do not progress to the next stage [3].

Cancer arises when these regulatory mechanisms go awry, allowing cells to bypass checkpoints and escape control mechanisms. There are various ways in which this can occur: Genetic Mutations: Mutations in critical genes that regulate the cell cycle can lead to uncontrolled cell division. For example, mutations in the tumour suppressor gene p53, which plays a crucial role in cell cycle arrest and DNA repair, are found in a wide range of cancers. Oncogenes: Oncogenes are altered forms of normal genes (proto-oncogenes) that promote cell growth and division. When proto-oncogenes undergo mutations, they can become overactive, leading to excessive cell proliferation and the development of cancer. Checkpoint Dysregulation: Defects in the checkpoint pathways that monitor DNA integrity and cell division can lead to the survival and proliferation of damaged cells, contributing to tumorigenesis. Telomerase Activation: Telomeres are protective caps at the ends of chromosomes that shorten with each cell division. Cancer cells often activate the telomerase enzyme, allowing them to maintain their telomeres' length and evade the natural aging process of cells [4].

Understanding these underlying molecular mechanisms of cancer provides valuable insights into the development of targeted therapies and treatments. For instance, targeted drugs that inhibit specific overactive kinases derived from mutated oncogenes have shown promising results in treating certain cancers. Moreover, studying the cell cycle and its regulation has paved the way for novel cancer therapies that aim to halt cell proliferation by interfering with specific checkpoints or key players in the cell cycle machinery. These treatments offer a more focused approach, minimizing damage to healthy cells and reducing side effects often associated with traditional chemotherapy [5].


In Conclusion, the cell cycle is a tightly controlled and complex process responsible for the growth, development, and maintenance of living organisms. When its regulation falters, cancer can emerge as a result of uncontrolled cell division and proliferation. By unraveling the connection between cancer and the cell cycle, scientists and researchers have made significant strides in understanding the disease's molecular basis and developing targeted therapies. As we continue to expand our knowledge, we inch closer to more effective and personalized treatments that offer hope in the fight against cancer.


  1. Dunn GP, Old LJ, Schreiber RD. The immunobiology of cancer immunosurveillance and immunoediting. Immunity. 2004;21(2):137-48.
  2. Indexed at, Google Scholar, Cross Ref

  3. Lujambio A, Lowe SW. The microcosmos of cancer. Nature. 2012;482(7385):347-55.

    Indexed at, Google Scholar, Cross Ref

  4. Bailar JC, Gornik HL. Cancer undefeated. N Engl J Med. 1997;336(22):1569-74.
  5. Indexed at, Google Scholar, Cross Ref

  6. Adlercreutz H. Phyto-oestrogens and cancer. Lancet Oncol. 2002;3(6):364-73.
  7. Indexed at, Google Scholar, Cross Ref

  8. Pantel K, Alix-Panabières C, Riethdorf S. Cancer micrometastases. Nat RevClin Oncol. 2009;6(6):339-51.
  9. Indexed at, Google Scholar, Cross Ref

Get the App