Concorde Career College Case Study – Peer Comment – Description
Expectations (Danielle)
Length: A minimum of 180 words, not including references
Citations: At least one high-level scholarly reference in APA from within the last 5 years (Pls don’t use same reference)
A 47-year-old female presents with Stage IV breast cancer. Today, the PET scan reveals brain metastasis.
Define proliferation and differentiation and relate these changes to cancer.
Differentiation also known as cell maturation is a process by which cells become specialized in terms of cell type, function, structure, and cell cycle (McCance et al., 2019). Proliferation is the regulated process by which cells divide and reproduce (McCance et al., 2019). If proliferation happens rapidly with no control, then it can mean the cancer cells are dividing rapidly, and the cancer is growing faster. Deregulation of differentiation and proliferation processes leads to carcinogenesis.
Describe invasion, angiogenesis and metastasis.
Invasion: Tumor cells eventually acquire the ability to penetrate the surrounding tissues, known as the process of invasion. These motile cancer cells pass through basement membrane and extracellular matrix, progressing to intravasation as they penetrate the lymphatic or vascular circulation (Martin et al., 2013).
Angiogenesis: Angiogenesis (blood vessel formation) is essential for tissue growth in both normal development and physiology and in some diseases such as inflammation and cancer (Koltai et al., 2022).
Metastasis: Metastasis can be defined as the spread of cancer cells to tissues and organs beyond where the tumor originated and thus leads to the subsequent formation of new tumors (Martin et al., 2013).
There are three underlying causes of growth and maturity abnormalities: telomerase, pRB changes and 53 changes. Discuss these in relation to the patient.
pRB is a tumor suppressor protein. Normal function of the pRb is to prevent excessive cell growth by inhibiting cell cycle progression until a cell is ready (McCance et al., 2019). Dysfunction with this protein leads to cancer spread.
P53 tumor suppressor gene is similar to the pRB gene. It stops the formation of tumors. It is often noted as the most mutated gene in cancer and is seen in approximately half of all cancers (McCance et al., 2019). It is particularly mutated in some of the most aggressive cancers such as triple negative breast cancer.
Telomerase are protective ends of repeating nucleotide units on each chromosome. When non-germ cells begin to proliferate abnormally their telomere caps shorten with each cell division. Short telomeres typically signal the cell to cease cell division. If the telomeres become critically small the chromosomes become unstable and fragment (McCance et al., 2019). This can lead to cellular mutations.
Discuss tumor suppressor genes, oncogenes and DNA repair genes.
Tumor suppressor genes: The normal function of tumor suppressor genes is to regulate the cell cycle so that cells do not divide in an uncontrolled manner. When a mutation alters the protein, its tumor suppressing capability is lost and tumors can therefore form (McCance et al., 2019).
Oncogenes: Proto-oncogenes are genes that are designed to regulate normal cellular proliferation. When a proto-oncogene is changed so that too many copies are made or it becomes more active than normal and is then called oncogenes (McCance et al., 2019). Oncogenes do not operate like proto-oncogenes and thus the cell is driven into a state of unregulated expression of proliferation signals and uncontrolled cell growth (McCance et al., 2019).
DNA repair genes: DNA repair genes are essential for the maintenance of cell integrity. These genes function in a diverse pathway that involves the recognition and removal of DNA lesions, tolerance to DNA damage and protection from errors of incorporation made during DNA replication (Glickman, 2001).
References
Glickman, R. A. (2001). Human DNA repair genes. Environmental and molecular mutagenesis. https://pubmed.ncbi.nlm.nih.gov/11317342
Koltai, T., Reshkin, S. J., & Cardone, R. A. (2022). Antiangiogenic Drugs as Chemosensitizers in Cancer Therapy, 18, 147–197. https://doi.org/10.1016/c2020-0-03561-9
Martin, T. A., Ye, L., Sanders, A. J., Lane, J., & Jiang, W. G. (2013). Cancer invasion and metastasis: Cellular, molecular and clinical aspects. SpringerReference. https://doi.org/10.1007/springerreference_33863
McCance, K. L., Huether, S. E., Brashers, V. L., & Rote, N. S. (2019). Pathophysiology: The biologic basis for disease in adults and children. Elsevier.
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