Hey Steemers!
The following work is an academic paper I wrote while at UCD. It explains and analyzes research into cancer treatment. I chose to investigate and write about cancer for several reasons. I will one day become a Nurse Practitioner and hope to specialize in Oncology. It is a horrific and fascinating disease, one that has driven researchers to concoct creative treatment approaches. I so admire these humans. Additionally, I lost my grandmother to cancer. I know many others who have had similar experiences, and wanted to offer hope to this community in the form of empirical data.
Each cell in our bodies contains the genetic information necessary to become any other cell. Those that compose our eyes and allow us to see could just as easily set up shop in our hearts and aid in the pumping of blood. So, why don’t they? Context. Cells receive cues from their environment that direct their course of growth. Likewise, whether or not cancer develops is determined by intercellular communication. While normal cell homeostasis inhibits tumor proliferation, dysfunctional immune signaling creates pro—tumorigenic regions (those that are conducive to aberrant growth). Our own defense system is corrupted to promote the cancerous agenda of metastasis. The good news: maladaptive immune responses have been shown to be reversible, which reveals potential therapeutic strategies. Scientists have begun to experiment with targeting surrounding cells instead of the tumors themselves.
Past therapeutic approaches have targeted cancerous cells directly. This was a missed opportunity, as surrounding cells are more genetically stable and easier to manipulate predictably. Current techniques focus on reeducating surrounding cells to promote anti- tumorigenic qualities. This includes stimulating the immune system, reconfiguring maladaptive cell distribution, and encouraging white blood cells to perform their programmed roles. A 2013 study linked cell reeducation to the regression of tumors in “an ovarian cancer model”.
Our immune systems defend against cancer by flooding suspicious regions with macrophage, the infantry of our defenses. Their mission: consume and eliminate deregulated cells. Macrophage are anti- tumorigenic, but only in the early stages of tumor development. Over time these cells begin to produce chemical compounds that create regions conducive to tumor growth. Macrophage levels are positively correlated with rates of angiogenesis- the formation of new blood vessels to supply the tumor- in established cancers. Macrophage functioning becomes maladaptive as local oxygen levels are depleted by high numbers of cancerous and immune cells. Such is the dark irony of the immune system: tumors are able to develop because of the body’s own defenses.
Irony is a prevalent theme in our bodies’ response to tumorigenesis. Inflammation is an innate immune mechanism, yet chronically enflamed tissues show cancer more frequently. Our own regulatory mechanisms are corrupted to promote aberrant growth. Normally, intercellular chemical messengers maintain patterned cell division. In the later stages of tumorigenesis, however, they enhance tumor migration, invasion, and survival. This occurs because the messengers fail to correctly alert the body, which allows aggressive cancer cells to ‘move freely about the cabin’. Poor patient prognosis and rapid disease progression are predicted once this stage is reached.
In order to reeducate cells in regions of tumorigenesis, scientists have experimented with imitating bacterial exposure to the immune system. Surrounding cells are plastic enough to differentiate into several cell types. Each of which has the ability to promote normal cell homeostasis in response to this exposure. This method has been shown to lead to tumor reduction in cases of high- grade, established gliomas.
The ability of our cells to differentiate in form and function offers us a therapeutic opportunity. No cell exists in isolation: target the surrounding microenvironment in order to maintain aggressively anti- tumorigenic conditions.
References
Bissell, Mina J, and William C Hines. "Why Don't We Get More Cancer? A Proposed Role of the Microenvironment in Restraining Cancer Progression." Nature Medicine Nat Med (2011): 320-29.Nature. Web. 2 Nov. 2015.
Joshi, Amit. "TGF-ß Signaling, Tumor Microenvironment and Tumor Progression: The Butterfly Effect."Frontiers in Bioscience Front Biosci (2010): 180. Web. 2 Nov. 2015.
Quail, Daniela F, and Johanna A Joyce. "Microenvironmental Regulation of Tumor Progression and Metastasis." Nature Medicine Nat Med (2013): 1423-437. NCBI. Web. 2 Nov. 2015.
Whiteside, T L. "The Tumor Microenvironment And Its Role In Promoting Tumor Growth." Oncogene: 5904-912. Nature. Web. 2 Nov. 2015.