Cancer Biology Questions

Cancer Biology Questions

Cancer Biology Questions

The Biology of Cancer

Discussion Topic 1:

1). Explain in your own words how errors in mitosis could lead to the formation of cancerous cells as an organism (humans in particular for our focus) ages, and why errors in meiosis would not.

            Mitosis is a delicate process that requires high fidelity to ensure the stability of the genome. Recent studies have revealed how errors in mitosis shape cancer genomes by driving both structural and numerical alterations in chromosomes contributing to the initiation of tumor formation and progression as an individual ages (Levine & Holland, 2018). However, errors during meiosis only alter the number of chromosomes, with no structural alteration, and only occur in reproductive organs leading to infertility and human birth defects rather than cancer.

2) Explain in your own words why cancer is often referred to as a disease of the cell cycle.

            Cancer is normally referred to as a disease of the cell cycle because of the process of tumor formation from uncontrollable cell division and spread into neighboring tissues (Mercadante & Kasi, 2020). Cancer is usually caused by an alteration to the DNA.

3) Describe the relationship between hyperplasia and benign tumor growth. 

Hyperplasia refers to an increase in the number of cells abnormally (Nandalur et al., 2021). Hyperplasia can result in a grossly enlarged organ which can lead to the formation of a benign tumor. Benign tumors are non-cancerous but considered an abnormal collection of cells.


Discussion Topic 2:

1). What are the 5 most common cancers based on 2020 data?  What gender, race/ethnicity, and environmental/behavioral disparities exist according to the 2020 data regarding cancer and mortality rates?

            According to the National Cancer Institute (2020), the most common cancers globally include breast cancer, lung cancer, prostate cancer, Colorectal cancer, and skin melanoma respectively. Among women, breast, lung, and colorectal cancer are the top three most common while men have reported high cases of prostate, colorectal, and lung cancer. Mortality rates due to cancer are however high among men than women. Regarding race and ethnicity, African American men have recorded the highest number of deaths from cancer, while Asian/Pacific Islander women have recorded the least. It is also reported that the rates of cancer are generally high in countries with high standards of living and educational levels. Additional disparities include financial burden and low screening rates.

2). As a society, how do you think we could decrease some of these disparities?  How would you approach doing so?  Would you begin at the local, state, national, or international level, so bottom-up approach or a top-down approach?  Why?  Give a brief proposal of where you would start and what you would do.

            Evidence demonstrates that the best way of reducing cancer disparities is by promoting equitable healthcare (National Cancer Institute, 2020). I will start at the local level, by ensuring that healthcare facilities do not discriminate against cancer patients before I advocate for policy change at the national level. The policy change will help overcome racial, systemic social, and institutional inequalities.




Levine, M. S., & Holland, A. J. (2018). The impact of mitotic errors on cell proliferation and tumorigenesis. Genes & Development32(9-10), 620–638.

Mercadante, A. A., & Kasi, A. (2020). Genetics, Cancer Cell Cycle Phases. PubMed; StatPearls Publishing.

Nandalur, K. R., Colvin, R., Walker, D., Nandalur, S. R., Seifman, B., Gangwish, D., & Hafron, J. (2021). Benign prostate hyperplasia as a potentially protective factor against prostate cancer: Insights from a magnetic resonance imaging study of compositional characteristics. The Prostate81(14), 1097–1104.

National Cancer Institute. (2020, September 25). Cancer Statistics. National Cancer Institute;

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Question 1: A) What is the definition of a quantitative trait? Use the example of twin heritability model to explain how this underlying assumption is inaccurate.

B) Explain how the experiment with Agouti mice, demonstrates that the biology of gene x environment interactions is not additive.

Question 2: Design an experiment to look at the timing of MT1-MMP expression in stromal cancer in the tumor microenvironment in response to tumor growth, making use of small animal optical imaging system (i.e. IVIS). This experiment should include an orthotopic xenograft in a reporter mouse.
• Describe the tumor cells that you will use in this experiment. Consider characteristic such as the cell type and species.
• Explain where the tumor will be implanted and specifically how you will non-invasively monitor tumor progression over time using optical imaging.
• Describe the reporter mouse you would like to design to monitor MMT-MP1 expression in the host stromal cells surrounding the tumor.
• Explain which strain of mice you will use and why it was chosen. Consider characteristics such as color and immune status.
• Describe the gene that will serve as the reporter, how the expression of that gene will be regulated (think about the promoter) and how the reporter will be monitored over time using optical imaging.
• Explain the expected result and least one control for these experiments.

Question 3: Design experimental steps to identify potential genes whose transcriptional are in carcinogenesis of a population exposed to certain environment carcinogens (i.e. mineral dust). After the candidate gene markers are determined from your chosen experimental platform. Describe a second experimental plan to confirm your result using a different gene expression assay platform. Next, please list bioinformatic tools (databases) which can be used to confirm the differential expression patterns of the identified genes in cancer development and progression. Give a brief description of the steps taken in the analysis and anticipated results.

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Question 4: Dr. Davis;

– How is metabolic activity reprogrammed in cancer?
Not all reprogrammed metabolic activities contribute equally to cancer. With many metabolic activities under oncogenic control, categorizing them based on whether they are transforming, enabling, or neutral can clarify the role of each activity in cancer biology and predict how it might be exploited in basic research and clinical oncology.
1: Transforming Activities: These activities directly contribute to cell transformation and blocking them might prevent tumorigenesis in susceptible patients or antagonize disease progression.
2: Enabling Activities: These activities are altered in cancer cells but are not involved in the transformation. They carry out conventional metabolic tasks such as supporting energetics, generating macromolecules, and maintaining redox state and are required for tumor progression
3: Neutral Activities: these activities are predicted to be poor therapeutic targets. Fluctuating nutrient access may cause activities to be required in some contexts and dispensable in others. Thus, confidently classifying an activity as neutral is challenging and requires definitive proof that loss of the activity does not impair tumor progression.
– What products are limiting for proliferation?
Targeting activities that supply limiting materials for proliferation is therapeutically attractive, especially if the pathways used are less important in normal proliferative tissues. Although several metabolic products have been proposed as critical outputs of cancer metabolism, which are rate-limiting for proliferation remains controversial.
Ex: ATP, NADPH, Nucleotide Synthesis, Products of the TCA Cycle, and Consequences of Electron Acceptor.
– What determines how different tumors use metabolism?
1: The Environment Can Affect Cancer Cell Metabolism
2: Cell Lineage Can Also Affect Cancer Metabolism
3: Interactions with Benign Cells Can Affect Cancer Cell Metabolism
– Should metabolism be considered during cancer progression?
Yes, it should be considered during cancer progression to supply tumor cells.
– Can cancer metabolism be exploited to improve therapy?
To target metabolism for therapy, limiting metabolic processes must be identified and understood sufficiently to target the process safely and select responsive patients. Using the classifications, transforming and/or enabling activities must be identified with an adequate therapeutic index.
Clinical experience with cytotoxic chemotherapy highlights the challenges that will likely confront new metabolic therapies. Many chemotherapies inhibit nucleotide metabolism.

Case Study Analysis

            The case study features a 24-year-old male patient who comes to the clinic with significant dandruff on his head and pitting of his fingernails.  He also has morning joint soreness, which diminishes somewhat once he gets ready for work.  He has tried many dandruff shampoos but has received no alleviation from his problems. A negative rheumatoid factor was found in the laboratory testing. The rate of erythrocyte sedimentation increased somewhat. This paper examines the patient’s situation and explains the immunosuppressive process and its influence on the human body.

Reasons behind the Patient’s Symptoms

            The patient may have psoriatic arthritis based on the symptoms of finger pitting, scalp dandruff, and morning joint discomfort (Coates et al., 2022). Psoriatic arthritis is a chronic inflammatory disease that predominantly affects the joints and skin. They are triggered by environmental stimuli such as infection or mechanical stress. The body’s production of IL-23, a critical cytokine, is crucial in the progression of these disorders (Soomro et al., 2023). Dendritic cells and macrophages both generate IL-23.  Due to impaired barrier function or changes in the microbiota, the gastrointestinal tract might be the source of IL-23. Psoriatic arthritis is characterized by enthesitis rather than synovitis, the prevailing pathological lesion in rheumatoid arthritis. Psoriatic arthritis often affects the distal interphalangeal joints, but rheumatoid arthritis does not.

Genes Associate

Researchers are now investigating the etiology of psoriatic arthritis, precisely the differential vulnerability among persons with psoriasis. The contribution is anticipated to be impacted by an intricate interaction of genetic and environmental factors. A considerable percentage, varying between 33 and 50 percent, of those who have received a diagnosis of psoriasis-related arthritis exhibit a familial pattern, wherein at least one sibling or parent has also been diagnosed with the condition (Curry et al., 2023). Psoriatic arthritis has been linked to several genes on chromosome six’s human leukocyte antigens locus. The immune function is intricately associated with this specific site. In addition, other non-HLA genes have been identified as having a potential involvement in immune function (Helliwell et al., 2023).


Immunosuppression is a physiological state in which the immune system’s capacity to effectively react to exogenous antigens, such as the surface antigens on malignant cells, is compromised. According to Xiao et al. (2023), immunosuppression may result from the destruction of immune cell effector cells or the blocking of intracellular pathways essential for identifying antigens and other immune system reactions. Continued suppression of the immune system raises the probability of acquiring cancer. Immunocompromised individuals may experience evasion of immune surveillance by possibly malignant cells that arise spontaneously or have been modified by carcinogens, which operate via mechanisms such as genotoxicity or various modes of action associated with oncogenic viruses (Schett et al., 2022). As a result, the improved capacity of these cells to survive and multiply dramatically contributes to the development of tumors. Psoriatic arthritis patients undergo immunosuppression due to immune failure during periods of active illness or the use of immunosuppressive medicines during remission, leaving them vulnerable to infections.


            The patient in the case study has symptoms consistent with a diagnosis of psoriatic arthritis. In rare people, psoriatic arthritis may occur before the beginning of psoriasis. In some people, psoriatic arthritis might occur without any visible psoriasis lesions. Chronic psoriasis and psoriatic arthritis are examples of autoimmune diseases brought on by a dysfunctional immune system.




Coates, L. C., Soriano, E. R., Corp, N., Bertheussen, H., Callis Duffin, K., Campanholo, C. B., Chau, J., Eder, L., Fernández-Ávila, D. G., FitzGerald, O., Garg, A., Gladman, D. D., Goel, N., Helliwell, P. S., Husni, M. E., Jadon, D. R., Katz, A., Laheru, D., Latella, J., & Leung, Y.-Y. (2022). Group for Research and Assessment of Psoriasis and Psoriatic Arthritis (GRAPPA): updated treatment recommendations for psoriatic arthritis 2021. Nature Reviews Rheumatology.

Curry, P. D. K., Morris, A. P., Barton, A., & Bluett, J. (2023). Do genetics contribute to TNF inhibitor response prediction in Psoriatic Arthritis? The Pharmacogenomics Journal23(1), 1–7.

Helliwell, P. S., Coates, L. C., & Gladman, D. D. (2023). Psoriatic Arthritis. Springer EBooks, pp. 97–104.

Schett, G., Rahman, P., Ritchlin, C., McInnes, I. B., Elewaut, D., & Scher, J. U. (2022). Psoriatic arthritis from a mechanistic perspective. Nature Reviews Rheumatology.

Soomro, M., Hum, R., Barton, A., & Bowes, J. (2023). Genetic Studies Investigating Susceptibility to Psoriatic Arthritis: A Narrative Review. Clinical Therapeutics45(9), 810–815.

Xiao, Q., Mears, J., Nathan, A., Ishigaki, K., Baglaenko, Y., Lim, N., Cooney, L. A., Harris, K. M., Anderson, M. S., Fox, D. A., Smilek, D. E., Krueger, J. G., & Raychaudhuri, S. (2023). Immunosuppression causes dynamic changes in the expression of QTLs in psoriatic skin. Nature Communications14(1), 6268.