BIOL 304 Week 2 Discussion

Greetings Class,

In your own words, explain how cancer cells differ from normal cells in regard to the following:

1. Telomeres, which are products of telomerase enzyme – Telomeres are at the end of all human chromosomes. Telomeres are essential to controlling the number of cell divisions for a particular cell which determines the cell’s overall lifespan. The telomeres’ length determines the cell’s lifespan. In normal cells, a small portion of the telomeres is discarded following each cell division until the telomeres reach a shortened length signaling the cell to refrain from future cell division leading to cell death. Meanwhile, cancer cells employ deceptive tactics by producing a telomerase enzyme that lengthens its telomere. As a result, cancer cells experience the luxury of limitless cell divisions, paving the way for an eternal lifespan.
2. Cell to cell communication – In normal cells, cell to cell communication is achieved by sending chemical messages (ligands) to receptors (proteins) located on the target cell. The intracellular signals from the chemical message binding with the receptor provide cell cycle instructions to keep the target cell healthy and are expressed in genes. Cancer cell genes are mutated, leading to erroneous instructions and the inability to execute the cell cycle, specifically continuous cell division.
3. Apoptosis – Apoptosis is the body’s mechanism for destroying damaged or mutated cells. In normal cells, the body will attempt to correct damaged and mutated cells during the cell cycle. However, if repair efforts are unsuccessful, the cell begins to break down, ultimately destroying itself. Otherwise, cancer cells exhibit immunity to the cell cycle’s ability to execute apoptosis against the damaged and mutated cells. The immunity is achieved through the production of particular proteins and failure to produce effective self-destruct signals. This is problematic because the cancer cells continue to execute cell division, creating additional mutated cells. Furthermore, the continued division leads to the excess formation of mutated cells known as tumors.
4. Molecular controls of the cell cycle (include Cdk and Cdk/cyclin complexes, p53 gene/protein, Rb gene/protein in response) – In normal cells, Cdk is an inactive protein combined with its active protein counterpart, cyclin, to regulate the cell cycle. These proteins cannot perform proper regulation independently of each other. Cdk/cyclin complexes are employed throughout each cell cycle stage to confirm requirements are met to proceed to the next stage of the cell cycle. The p53 gene/protein is the enforcer that stops the cell cycle and directs the cell for repair. If cell repair is not feasible, then the p53 gene/protein initiates the apoptosis process for the damaged cells. Rb gene/protein performs the vetting process for all antigrowth signals. This protein is commonly referred to as the tumor suppressor. However, cancer cells can bypass the Cdk/cyclin complexes screening before moving to the next stage of the cell cycle. Cancer cells alter or lose their p53 gene/protein as a tactic to bypass apoptosis. Rb gene/protein in cancer cells are typically damaged, leading to inaccurate processing of the antigrowth signals facilitating unregulated cell division.

Discussion Topic 2:

In your own words, explain each of the hallmarks of cancer below:

1. Immortality – a cancer cell demonstrates the ability to execute cell division infinitely.
2. Produce go signals – cancer cells’ ability to internally and autonomously modify their growth signal, change their growth factor receptors, or trigger the continuous activation of a mutant version of the RAS protein.
3. Override stop signals – cancer cells can consistently defy all antigrowth signals presented at the G1/S checkpoint and G2/M checkpoint. This is problematic because stop signals exist to restrict cell growth.
4. Resist cell death – is characterized by a cell that successfully and consistently avoids “cell suicide.” Cancer cells mastered the art of evading apoptosis.
5. Angiogenesis and how it relates to metastasis (more details about these in upcoming week). Angiogenesis and how it relates to metastasis (more details about these in the upcoming week). Angiogenesis describes the process initiated by cancerous cells to create blood vessels essential to the cancerous tumor’s life cycle. Angiogenesis facilitates cancer’s ability to successfully execute metastasis by relocating other areas within the body and establishing the vital blood supply.

Which of these hallmarks of cancer do you think would be the ultimate targets for cancer therapy and why?  In my opinion, the ultimate targets for cancer therapy are to override stop signals and resist cell death. Success in either area can potentially prevent the other hallmarks from occurring, ultimately ending the rapid duplication of mutated cells.

Reference

Lynne Eldridge, M. D. (2022, July 4). Cancer cells vs. normal cells: How are they different? Verywell Health. Retrieved August 29, 2022, from

Discussion Topic 1:

In your own words, explain how cancer cells differ from normal cells in regard to the following:

1. Telomeres, which are products of telomerase enzyme
2. Cell to cell communication
3. Apoptosis
4. Molecular controls of the cell cycle (include Cdk and Cdk/cyclin complexes, p53 gene/protein, Rb gene/protein in response)

Discussion Topic 2:

In your own words, explain each of the hallmarks of cancer below:

1. Immortality
2. Produce go signals
3. Override stop signals
4. Resist cell death
5. Angiogenesis and how it relates to metastasis (more details about these in upcoming week).

Which of these hallmarks of cancer do you think would be the ultimate targets for cancer therapy and why?  Read and respond to one classmate’s post to see if you agree/disagree on this, and justify why you agree/disagree.