Biology student WSSU
Let's Talk Cancer Biology
Introduction
Upon my entrance into this course, I had no idea the level of difficulty the course entailed. This course substituted for high intellect courses I needed to graduate. After being referred by my advisor to admit into this course, I assumed this course possessed relevance towards the biology and biotechnology program. Stemming from the labeled name, cancer bio, this course entailed informative information relating to the causes, symptoms, and genetic pathways to cancer. This class taught me the many day to day subjects that we as individuals submit ourselves to, has the ability to trigger cancer. As I leave this class, I find myself becoming aware of the things I eat, the subjects I breathe, and chemical exposure.
Cancer has not impacted my direct family members, in which I am highly grateful for, thus I have witnessed family friends surrender their lives to cancer. Cancer can be a very nasty battle, and one hard to fight. When growing up I saw one of my good friends the day she was diagnosed with cancer. I assumed my friend was just sick, because she threw up on the bus ride home. Later when she did not return to school, I gave her a house visit to make sure she was okay, to only find her terrible diagnosis. Seeing someone so young endure such a mature disease, has the persuasion ability to intrigue anyone. Learning about prevention mechanisms, and the root to these various stems of cancer can help implement preventative tactics in order to avert or fight the battle of cancer.
Outcomes
"Describe the six hallmarks of cancer"
1. Self- sufficiency in growth signals: This hallmark expresses the tumor cell in relation to it’s hypersensitivity to ambient growth factors, and their capability to produce their own growth factors. The cell does not acquire outside growth signals to divide.
2. Insensitivity to anti- growth factors: Tumor cells become resistant to anti- growth factors, in which in a normal cell these factors would inhibit proliferation.
3. Tissue invasion and metastasis: The cancerous cells are relieved from the primary site, and branch to secondary sites. This ability is known as metastasis, in which the cells invade new locations.
4. Limitless replicative potential: Due to the tumor cells telomeres not degrading, the cell is able to replicate indeterminately. The telomeres in the cell never shorten, preventing the cell from dying.
5. Sustained angiogenesis: This hallmark embodies the tumor cells ability to recruit new blood vessels for use. Cancer cells need blood vessels to provide oxygen and nutrients.
6. Evading apoptosis: Through the utilization of genetic mutations, tumor cells can avoid programmed cell death. This allows the tumor cells to live, grow and divide.
"Explain the types of gene mutations possible and how these mutations can contribute to cancer formation"
DNA substitution mutations:
1. Transition: Entails bases of similar shape; The interchange of two- ring purines or of on ring pyrimidines.
2. Transversion: Involves the exchange of one ring and two ring structures; The interchange of purines for pyrimidines bases.
· Transition mutations are generating at higher frequencies than transversions, and are less likely to produce amino acid substitutions.
3. Insertion: Declared a mutation presenting the addition of one or more nucleotides to a DNA sequence.
4. Deletion: When one or more nucleotides is deleted from a DNA sequence during DNA replication.
5. Chromosomal translocations: This mutation involves the rearrangement of nonhomologous chromosomes.
These mutations contribute to cancer because if these genetic mutations occur and are not fixed, they can also be replicated during DNA replication.
"Describe an oncogene and why it is important to cancer"
Oncogenes begin as proto-oncogenes, are primarily identified to support cells in growth, thus when an oncogene undergoes mutations, the gene alters bad. During this process, there can be too many copies formulated, the gene can become indefinitely activated or turned on, when it is not directed to be. This process triggers the cell to uncontrollable growth, in which can lead to cancer. Chromosomal rearrangement and gene duplication normally activates oncogenes.
"Explain the cell cycle, its regulation, and how cell cycle dysfunction can lead to cancer"
The cell cycle is identified as a division cycle that experiences a series of events that comprise DNA in order to produce two daughter cells.
Interphase
G1 Phase: Metabolic changes set up the cell for division. The cell is focused on division and moves into the S stage.
S Phase: DNA replication occurs, replicating genetic material. Each chromosome becomes two sister chromatids.
G2 phase: Metabolic changes gather the cytoplasmic materials that important for mitosis and cytokinesis.
Interphase
G1 Phase: Metabolic changes set up the cell for division. The cell is focused on division and moves into the S stage.
S Phase: DNA replication occurs, replicating genetic material. Each chromosome becomes two sister chromatids.
G2 phase: Metabolic changes gather the cytoplasmic materials that important for mitosis and cytokinesis.
M Phase: (Mitosis) Nuclear Division occurs.
Prophase: The nuclear membrane separates to shape small vesicles and the nucleolus crumbles. A structure known as the centrosome copies itself to form two daughter centrosomes that move to opposite ends of the cell. The centrosomes arrange the creation of microtubules which creates the spindle fibers that constitute the mitotic spindle. The chromosomes gather into smaller structures. Each replicated chromosome is now able to comprise of two indistinguishable chromatids (or sister chromatids) held together by a structure known as the centromere.
Prometaphase: The chromosomes, led by their centromeres, relocate to the equatorial plane in the midline of the cell - at right-points to the pivot formed by the centrosomes. This area of the mitotic spindle is known as the metaphase plate. The spinder fibres binds to a structure associated with the centromere of every chromosome called a kinetochore. Then individual spindle fibres tie to a kinetochore structure on each side of the centromere. The chromosomes keep condensing.
•Metaphase: The chromosomes align along the metaphase plate of the spindle apparatus.
•Anaphase: The centromeres divide, and the sister chromatids of each chromosome are detached and move to the opposite ends of the cell, pulled by spindle fibres connected to the kinetochore regions. The isolated sister chromatids are presently alluded to as daughter chromosomes.
•Telophase: The last phase of mitosis and an inversion of many of the procedures observed during prophase. The nuclear membrane reforms around the chromosomes grouped at either pole of the cell, the chromosomes uncoil and end up diffuse, and the spindle fibres vanish.
•Cytokinesis: The last cell division to create two new cells. In plants a cell plate form along the line of the metaphase plate. Whereas animals, there is a constriction of the cytoplasm. The cell at that point enters interphase; the interval between mitotic divisions.
In terms of the production of cancerous cells, a cell travels through different check points depicted within the cell cycle. As the cell maneuvers through these check points, in order to proceed checkpoints, the cell receives a signal triggering division. If the cell does is not granted access to the next check point, apoptosis is signaled. Apoptosis is defined as programmed cell death. If the cell dodges apoptosis, it can also avoid further checkpoints. The cell will be replicated with errors, and cancerous tumors are the outcome.
"Describe the function of tumor suppressor genes"
Tumor suppressor genes are identified as normal genes that are responsible for braking cell division, repairing DNA mistakes, and signaling the cell to undergo apoptosis. In doing so, when the tumor suppressor gene is mutated the “brakes are released”, causing the cell to experience uncontrollable growth, leading to cancer. This gene differs from an oncogene, due its ability to cause cancer when deactivated. Primarily mutations in the tumor suppressor genes are acquired and not inherited.
"Explain how external and internal stimuli can lead to apoptosis"
Intrinsic Pathway: Notified as a pathway to signal apoptosis or programmed cell death. Intrinsic pathway is implemented when signals from the mitochondria are released within the cell.
Extrinsic Pathway: This pathway is initiated through the outside transmembrane death receptors, in which targets apoptosis or programmed cell death. Articulating such a process outside of the cell, the death receptors binds to death factor, in which involves the receptor to change its shape. The receptors come together in order to transfer a message to the inside of the cell. The process of changing shape, exposes the death domain to be exposed on the receptor. This allows other proteins to bind relevant to apoptosis. Through the utilization of caspases inside the cell, the process of apoptosis proceeds.
•Why apoptosis is important?
•Apoptosis, also known as programmed cell death. It decimates cells, which may show a risk to our health. For example, cells with DNA damage that could lead to tumors forming frequently due to cancer cells restrain apoptosis, making them extremely hazardous and immortal.
"List and describe the steps that lead to metastasis"
1. Invasion: Cancer cells leave primary tumor and leaves the area.
2. Intravasation: The cancer cells enter the blood and the blood vessels.
3. Transport: Cancer cells travel through the lymphatic system or blood line to reach other parts of the body.
4. Extravasation: The cancer cell is finished traveling through the blood stream or lymphatic system and settles in an area in the body.
5. Metastatic colonization: Cancer cell settles in new location, grows, and divides.
"Clarify how cancer cells escape cell death"
This topic addresses hallmark three, in which displays the evasion of apoptosis or programmed cell death. In order for a cancer cell to grow uncontrollable and divide, the cell must capture the cellular pathways, and avoid cellular death. All types of cancer cells acquire the ability to resist apoptosis. Cellular suicide acts as a required function in normal cells, especially in the presence of DNA mutations. If a DNA mutation is detected, the cell will experience cellular suicide. Apoptosis involves the breaking of cellular membranes, degradation of chromosomes, and DNA breaks into fragments. The shrunken cell is then swallowed by a neighboring cell or immune cell. The p53 gene, is known as a tumor suppressor gene, in which when activated inhibits proliferation. Most cancers involve a defect in this gene, in which the p53 gene acta as a gatekeeper for apoptosis. The cancer cells can increase the inhibitors of p53 and silence the activators, causing a compromise in apoptosis. Cancer cells can hijack the function of genes controlling cell division and cell death. In addition, evading apoptosis can be expressed when an excessive amount of anti-apoptotic proteins, resulting in a short circuit in the extrinsic death receptor apoptotic pathway.
"Give details on how chronic inflammation and infectious agents can lead to cancer"
An oxidant is recognized as a oxidizing agent that removes one or more electron from a chemical reactions. In relation to cancer, oxidants can be an outcome to chronic inflammation. The build up of oxidants results in a mutation in normal DNA. When a DNA mutation is detected the cell will receive a signal for repair causing the production and release of toxins. These toxins cause more inflammation to occur, enabling cellular food of nutrients and oxygen, causing growth of cancer cells. The cancer cell can maneuver through the blood stream causing more trouble in surrounding areas.
"Explain the role of diet in cancer development and prevention"
Studies show that diet plays a key role in the implementation of cancer. The dietary components and nutrients have the ability to reduce or induce cancer. Starting with the harsh risk of alcohol causing cancer of the mouth, larynx, pharynx, liver, breast, colon, and esophagus. The more alcohol intake, the larger risk an individual has of gaining cancer. Another risk agent is Acrylamide, found in foods and tobacco sources. A vital dietary chemical, responsible for blocking the activity of other chemicals, Antioxidants are found in a large number of foods causing risk to cancer. Furthermore, Polycyclic Aromatic Hydrocarbons are indirect carcinogens that can cause cancer, found in grilled food.
References
All photos from Google images
All videos from youtube
All assignments have individual references
•“The Cell Cycle, Mitosis and Meiosis.” University of Leicester, 17 Aug. 2017, www2.le.ac.uk/projects/vgec/highereducation/topics/cellcycle-mitosis-meiosis.\
•“Why Do We Need 'Programmed Cell Death' (Apoptosis)?” NIMR History, 2009, www.historyofnimr.org.uk/mill-hill-essays/essays-yearly-volumes/2009-2/why-do-we-need-programmed-cell-death-apoptosis/.
•https://www.cancer.gov/types/breast/patient/breast-treatment-pdq
Pecorino, L. , Molecular Biology of Cancer. Oxford University Press. (4th Edition)
