My STEAM project covers the objective of describing the stages of mitosis and its correlation with Lung Cancer. There are five stages of mitosis: prophase, metaphase, anaphase, telophase, and cytokinesis. In these phases, there are checkpoints that ensure the honor of the genome as well as the stability of chromosomes. Lung Cancer tumors develop after abnormalities occur and these checkpoints have been avoided and disrupted (Eymin & Gazzeri, 2010). My art is a drawing using colored pencils and acrylic paints to showcase what normal cells and cancerous cells look like as well as depict how a normal and cancerous lung appears.
Prophase is the chromatin condensing, forming chromosomes and duplicates called sister chromatids as well as the mitotic spindle occurring and synthesizing microtubules propelling the centrosome to the opposite pole of the cell. In late prophase, the nuclear envelope tears apart and the microtubules link with the centromeres. In metaphase, two sister chromatids align at the equator of the cell with the metaphase plate being the center of which the centromeres are located. Anaphase is where both ends of the cell obtain a partner from each pair of chromatids and telophase is the set of chromosomes at the ends of the cell that unravel and configure chromatin. Here, the nucleoli become visible again and the spindles tear apart. The cell divides into half as cytokinesis starts where the cleavage furrow compresses the cell forming two new cells (OpenStax College, Rice University, 2013).
The cell cycle is a strict process requiring checkpoints that essentially ensure each phase is doing what it is supposed to do, including cell size and DNA sincerity. In Lung Cancer, the most prevalent cause of the mutation of normal cells to cancerous cells is the product of smoking. Normal cells undergo an organized cell death known as apoptosis and respond to signals sent from other nearby cells to let them know when to stop growing and when there are enough cells present. This ensures a barrier so that tumors do not develop (Eymin & Gazzeri, 2010; Cooper, 2000; Eldridge, 2019).
Tobacco and nicotine, a type of carcinogen, exposes the bronchial epithelial cells and cause mutations to the p53 gene causing disruptions to the cell cycle, specifically the S phase which is prior to mitosis. With mitosis, it duplicates new cells when they are damaged and normal cells stop growing when there are enough cells present. With the loss of the S phase, entering mitosis does not trigger the spindle checkpoint and only measures the kinetochore attachment. This would cause the loss of chromosome fragments and can be lethal due to the S phase ongoing to mitosis being pertinent for genome integrity (Eymin & Gazzeri, 2010; Barnum & O’Connell, 2016).
Once a cell has mutated, it does not undergo apoptosis, allowing the cell to grow uncontrollably and enabling them to travel through the bloodstream. These cancerous cells fail to compose secreting substances that allow them to stick, which enables them to move freely in the human body. This causes clumps of tumors and allows them to grow despite having enough cells present (Eldridge, 2019).
Barnum, K. J., & O’Connell, M. J. (2014). Cell cycle regulation by checkpoints. Methods in Molecular Biology, 29–40.
OpenStax College, Rice University (2013). Anatomy & Physiology. Cellular Growth and Division, pg. 115.
Cooper, G. M. (2000). The development and causes of cancer – the cell – NCBI bookshelf. The Cell: A Molecular Approach. 2nd Edition.
Eymin, B., & Gazzeri, S. (2010). Role of cell cycle regulators in lung carcinogenesis. Cell Adhesion & Migration, 4(1), 114–123.
Lynne Eldridge, M. D. (2019, December 7). Cancer cells vs. normal cells: How are they different? Verywell Health.