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Cancer and the cell cycle

Medicine

Cancer and the cell cycle

Introduction

The topic selected for this assignment is ‘cancer and the cell cycle’ and the specific focus of the essay is the spread of cancer. Cancer cells are majorly characterized by their ability to multiply infinitely without degrading and hence spreading across the body from a point of growth concentration – tumor (tumor Metastases). Most of the treatments for cancer are centered on the premise that destroying the tumor lowers the spread of cancerous cells.

This premise is faulted by Jayatilaka (2017), a post-doctoral researcher at Stanford, in her TED Talk dubbed ‘How cancer cells communicate – and how we can slow them down’. Jayatilaka’s (2017) talk is a follow-up of her research findings that it is possible to alter tumor Metastases – the spread of cancer – by interfering with the communication patterns of cancerous cells in their high concentration zones (tumors).

Literature review

Metastasis and biological dispersal in other ecosystems

A research by Tissot et. al., (2019) explored the foundation of metastasis from a biological perspective of dispersal, that is, the movement of cells from a region of high concentration to another region of lower concentration. The aim of the study was to build an understanding of metastasis in way that could help to contain the spread of cancer.

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The hypothetical stance by Tissot et. al., (2019) is that cancer spread – from tumor to other metastatic sites – can be explained via the concept of cell dispersal in different ecosystems. The study was solving the problem of lack of clarity in how the biological concept of dispersion can be applied to emergence and characteristics of metastasis.

The study, while taking a review approach, accepts the hypothesis because the discussion from secondary literature shows how metastasis follows basic principles of dispersion. However, the review leaves room for further research by recommending the xenograft experiment to test whether deterioration of conditions in the primary cell triggers metastasis or whether altruistic behaviour among kin cells is the source of the trigger.

Tissot et. al.,’s (2019) study relates to the topic of metastasis in class specifically the elaboration of how cancer cells spreads after multiplication to specific regions of the body. Further the article reveals the nature of science on the basis of its collection of evidence from previous research on the topic dating as far back as 1950s. in addition, the article shows the possibility of re-conceptualizing knowledge as it borrows from an already existent field – dispersal in biology – to expand knowledge in a niche – metastasis – and also unlock room for further inquiry into the perception of metastasis as a concept founded on dispersal in biological ecosystems.

Cell collectives and their influence

This study by Nadell et, al., (2013) is an attempt at explaining the powerful influence that cells have when concentrated together as opposed to acting singularly. The authors leverage of the concept of how biofilms – consortium of cancerous cells for instance – can cooperatively secret enzymes that favor their survival. The authors hypothesize that mechanistic theory, theoretical ecology and evolution can be used to explain this cooperative cell behaviour and cognizant of the different – and dauting – antecedents to cooperation.

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The hypothesis is accepted in the study. This is evident in the findings where the analytical model used (mechanistic theory, theoretical ecology and evolution) applies dimensionless numbers to prove that cells cooperate when there is shared benefits from this cooperation in their ecosystem. The findings show that there are cells called ‘cheaters’ and ‘producers’ when it comes to enzyme secretion. While cheaters fail to secret enzymes even as producers continue to do so, the overall benefic of collective behaviour emerges from producers concentrating their enzyme to prolong their survival above the cheaters.

This topic on cell collectives relates to the concept of tumor growth in cancerous cells, the concentration of this cells (the tumor location) and survival of the tumor including its mutation capabilities. A principle of nature of science well exhibited in this article is that of a ‘scientific way of knowing’. This is because the authors use well-established theories in science, that is, mechanistic theory, theoretical ecology and evolution to explain a phenomenon commonly observed in nature – cell collectives.

The study adds to the body of knowledge in collective cells by explaining how such cells can have greater influence in their environment when they remain concentrated in a single location and acting together than when they are spread and acting individually.

Metastasis and immunity against cancer cells

Lin et. al., (2020) in their study focus on the possible detrimental effects of immunity when it comes to growth of cancerous cells. The study took an experimental approach in vivo and vitro, that is, in which case the researchers first used antibodies – from a human combinatorial single-chain variable fragment (scFv) antibody library – capable of affecting tumor cell growth and later used tissue from a breast affected by cancer. The aim of the study was to prove that antibodies play a part in cancer patients experiences of the disease.

The hypothesis put forward is that two related antibodies from B cells of cancer patients would respond differently to the growth factor receptor TrkB (tropomyosin receptor kinase B). The hypothesis was influenced by the already existent body of knowledge of epithelial-mesenchymal transition (EMT) and the existence of antibodies that can influence this process.

The hypothesis was accepted as true because as the researchers had expected, one of the antibodies was capable of reversing epithelial-mesenchymal transition (EMT) – with the target being TrkB receptor – while the other antibody was not. The results labeled one antibody agonist in that it promoted the growth of the cells while the other antibody was antagonistic and inhibited the growth of these cells.

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This article parallels the classroom knowledge on how cancerous cells spread after growth and the essence of antibody resistance – or lack of resistance – to this metastasis process. The article however is a deeper analysis at the possible contribution of certain antibodies to the spread of cancer which is a concept beyond the general perception that antibodies prevent disease from spreading.

The article accurately represents the nature of replication of knowledge in science by adhering to a script set of rules. The authors for example justify using the scFv-fragment crystallizable (Fc) format and not the display–derived scFv both of which are standard scientific methods of antibody selection. Overall, this research by Lin et. al., (2020) improves the already existent body of knowledge on antibodies and resistance to the proliferation of cancer.

Conclusion

Following the TED Talk by Jayatilaka (2017), a research question that would expand the knowledge on the topic of cancer and cell cycle is;

  • Is it possible to exponentially reduce growth and metastasis of collective cells

Hypothesis

  • Interruption of cell communication reduces metastasis while antagonistic antibodies will kill the collective cells

Experiment

Under the first step, I would set up a trial like that of Jayatilaka (2017) where interleukin 6 and 8 will be used as inhibitors to the metastasis process of collective cells.

The second step would be to set up an experiment similar to that of Lin et. al., (2020) where antibodies are introduced to the same batch of collective cells.

I would test the growth/reduction factor of the collective cells.

References

Jayatilaka, H., 2017. How Cancer Cells Communicate — And How We Can Slow Them Down. [online] Ted.com. Available at: <https://www.ted.com/talks/hasini_jayatilaka_how_cancer_cells_communicate_and_how_we_can_slow_them_down#t-386026> [Accessed 19 July 2020].

Lin, C. W., Xie, J., Zhang, D., Han, K. H., Grande, G., Wu, N. C., … & Lerner, R. A. (2020). Immunity against cancer cells may promote their proliferation and metastasis. Proceedings of the National Academy of Sciences, 117(1), 426-431.

Nadell, C. D., Bucci, V., Drescher, K., Levin, S. A., Bassler, B. L., & Xavier, J. B. (2013). Cutting through the complexity of cell collectives. Proceedings of the Royal Society B: Biological Sciences, 280(1755), 20122770.

Tissot, T., Massol, F., Ujvari, B., Alix-Panabieres, C., Loeuille, N., & Thomas, F. (2019). Metastasis and the evolution of dispersal. Proceedings of the Royal Society B, 286(1916), 20192186.

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