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BY: LEEVI SYMISTER  Cancer is a general term that refers to a spectrum of over 100 types of diseases that arise in various parts of the body [1]. In general, all cancers include the uncontrolled formation of new damaged or abnormal cells within the body. We are made up of trillions of cells meaning that cancer can start and proliferate almost anywhere inside of the body [1]. This disease discriminates against neither age nor gender. Prostate Cancer is the most common type of cancer that occurs in men while in women Breast Cancer is most common. In children, however, the most common type of cancers are ones that relate to the blood, brain, and lymph nodes [2]. Cancer is the leading cause of death worldwide [9] and in 2021 alone an estimated 1.9 million people will have been diagnosed with cancer in the United States. Over six hundred thousand people are expected to die from cancer this same year [3]. So what exactly makes this disease so widespread and potent for many people every single year despite our seemingly advanced clinical technology and immune health? The answer lies in cancer's evasiveness to our immune system's defenses.  Cells usually form through a process called Mitosis in which a cell divides producing two daughter cells of the same number and kind of chromosomes. When cells become old or damaged, they die and are replaced with new cells. Our body's cells run off of chemical signals that tell them when they should grow or divide and signals that tell them when they should die or stop dividing, a process known as Apoptosis. In cancer, however, this process can become hijacked where damaged and atypical cells grow without restriction. These cells then can accumulate and eventually form tissues called tumors [6]. What causes this behavior in cancerous cells are mutations (or alterations) of genes inside the DNA. The three main genes altered are Proto-oncogenes, Tumor Suppressor genes, and DNA Repair genes [1]. Proto-oncogenes are responsible for restricting cell growth. Mutated genes of this type are called Oncogenes and can allow cells to proliferate uncontrollably and resist the immune system [1]. Tumor Suppressor genes are responsible for preventing tumors. Mutations of this gene force it to become inactive allowing cells to divide uncontrollably [1]. DNA Repair genes can also be altered allowing mutations in the DNA to go unresolved leading to more damaged and abnormal cells. Mutations affecting these three types of genes can be in the form of rearrangements, duplications, and deletions [5] of sections of chromosomes that comprise our DNA. These mutations can even be inherited from an individual's parents if they are present in the gametes, or reproductive cells, that will later form the offspring [4]. With these changes cancer cells can spread and form tumors throughout the body in a process known as Metastasis [1]. Now that we understand what causes cancer inside of the body, let's look at the factors outside the body that can lead to cancer. Cancer is caused by different carcinogens or substances capable of causing the mutations that develop cancer. It is these that alter the body's DNA and lead to tumors. Environmental carcinogens are things in the environment that can cause cancer. Ultraviolet rays from the sun, for example, can damage DNA and lead to certain skin cancers. Nuclear radiation is another environmental carcinogen that with prolonged exposure can lead to cancer development. DNA and RNA viruses that can hijack a cell's DNA and protein development mechanisms and subsequently duplicate themselves can also lead to cancers [6]. Notably DNA viruses such as the Epstein-Barr, Human Papilloma, Hepatitis B, and Human Herpesvirus-8 and RNA viruses such as Human T Lymphotropic Virus Type 1 and Hepatitis C [7] contribute to cancer rates. Carcinogens can also be things such as one's diet and smoking habits [6]. Potential treatments for cancer include Biomarker testing, Hormone therapy, Immunotherapy, Chemotherapy, Radiation therapy, Stem Cell transplant, Surgery, or Targeted Therapy. Most people will have a combination of these treatments [8] in order to either ease their cancer symptoms or eliminate cancer from their body entirely. What treatment(s) a person will need depends upon the type of cancer they have and how much it has progressed [8]. Each treatment comes with its own risks and side effects which the patient will have to evaluate before receiving their treatment. Cancer is a deadly disease that claims the lives of millions of people worldwide every single year. Despite this discouraging figure, it is important that people remain vigilant in preventing cancer from entering their lives in any way that they can. This can be through a change in one's diet, quitting smoking, and avoiding exposure to environmental carcinogens to the best of one's ability. With this and the continued research and advancement of science and technology, we can hope to one day live in a world where cancer is not a dominant occurrence in our everyday lives. Works Cited "What Is Cancer?" National Cancer Institute. Web.
Hassanpour, Seyed Hossein, and Mohammadamin Dehghani. "Review of Cancer from Perspective of Molecular." Journal of Cancer Research and Practice. No Longer Published by Elsevier, 10 July 2017. Web. "Common Cancer Sites - Cancer Stat Facts." SEER. Web. "The Genetics of Cancer." National Cancer Institute. Web. Lobo, I. (2008) Chromosome abnormalities and cancer cytogenetics. Nature Education 1(1):68 Trichopoulos, Dimitrios, et al. “What Causes Cancer?” Scientific American, vol. 275, no. 3, 1996, pp. 80–87. JSTOR, www.jstor.org/stable/24993351. Accessed 12 Sept. 2021. Liao, John B. “Viruses and human cancer.” The Yale journal of biology and medicine vol. 79,3-4 (2006): 115-22. "Types of Cancer Treatment." National Cancer Institute. Web. "Cancer." World Health Organization. World Health Organization. Web.
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BY: CAMERON YUEN  Imagine this: it’s an early Saturday morning with birds chirping and the sun’s rays just beginning to peer through your blinds. Still groggy, you decide to indulge in a proper breakfast, as you prepare your favorite: avocado toast. You recently became vegan, and have found a fond appreciation for the green fruit for its high nutritional value, and of course, its sustainable nature — right? While the former is true, you may want to reconsider your perceptions of the latter. Between avocado production causing mass deforestation, demanding unruly amounts of water, and leaving a dark carbon footprint, the seemingly perennial face of veganism might only be a façade to a world of wasteful realities. But how can this be possible? You switched to veganism to help the environment, so why do so many modern cooking blogs keep telling us to use avocados if they don’t actually achieve that goal? The problem is, many people don’t even realize avocados’ toll on the world, which has disillusioned the public into a green frenzy. The rapid increase in demand has provoked farmers internationally to level up their supply of avocados, which is where we already see the first problem. Avocado trees are quite particular about their growing conditions, some of which being “stable [weather] conditions… [and] 1 metre deep soils,” and they don’t fare well with a “decline in humidity [or] to salinity” (Eldridge). There are very few available areas that meet all of those conditions, so farmers have cleared “forests lands with diverse wildlife” at varying degrees of legality to expand their enterprise (Ayala). Mexico, the avocado haven of the world, is most guilty of this. Some people have “intentionally burned [the forests] to bypass a Mexican law allowing producers to change the land-use permit to commercial agriculture instead of forest land if it was lost to burning” (Ayala). But not only that, the rapid commercialization of avocados has caused “high agrochemical inputs and exploitative practices that degrade soil fertility” (Eldridge).  But among all avocado producers, the struggle for sufficient quantities of water continues to plague them. “Avocados are among the 3 crops causing more water stress in their region of production, [as they] have a global average water footprint of 1981 m3/ton. [To compare,] grape crops have a water footprint 608 m3/ton” (Gonçalves). So now along with having nutrient-deficient soil, the surrounding plants also lack water, damaging their growth and the ecosystem’s biodiversity. And to parallel its water footprint, avocados also leave a significant carbon footprint as well. “Carbon Footprint Ltd estimates that two small avocados in a packet have a CO2 footprint of 846.36 grams (almost twice the amount of a kilo of bananas),” due to the fact that avocados are an international trend (Eldridge). Trade for this product has been increasing through the years, requiring more shipments, at the expense of heightened fuel consumption. But how do we help solve this problem? In no way shape or form should we completely refrain from having avocados. People all over the world depend entirely on avocado production for their income, but we need to be able to find a healthy medium. The root of the environmental distress stems from soaring consumer demand, so local farmers and big corporations have tried to take advantage. If we can decrease, but not nullify, the profitability of avocados, that may guide us out of the frenzy, and give the environment space to adjust. So instead of having that avocado toast breakfast every day, maybe shrink that to once a week. Or instead of buying ungodly amounts of guacamole for Super Bowl Sunday, try to balance that out with some salsa. But regardless of the way you do it, the more you can control that urge to slice open another avocado, the more you’re doing for the environment. Works Cited Eldridge, Honor May. “Why Our Love for Avocados Is Not Sustainable.” Sustainable Food Trust, 31 Jan. 2020, sustainablefoodtrust.org/articles/why-our-love-for-avocados-is-not-sustainable/.
Ayala, Manuel Ochoa. “Avocado: the 'Green Gold' Causing Environment Havoc.” World Economic Forum, www.weforum.org/agenda/2020/02/avocado-environment-cost-food-mexico/. Gonçalves, André. “Avocado Lovers: Your Precious Fruit Is Far from Being Sustainable.” Youmatter, 22 July 2020, youmatter.world/en/benefits-avocados-production-bad-people-planet-27107/. BY: MORGAN ATKINSON  During the cell cycle (both mitosis and meiosis), there are many proteins involved, but Polo-like Kinases have been shown to be regulators of the different stages of the cell cycle, ensuring that it occurs correctly. There are five total Polo-like kinases (PLK’s), each of which has a unique role in regulating cell division (de Cárcer, Guillermo et al. 2011). It is incredibly important that cell division occurs without error, as errors in DNA or other cell structures have critical, and possible fatal consequences, and because of this the proper function of PLK’s 1-5 is vital. Overall, the structure of all five PLK’s are very similar with key structures being the polo-box domain (PBD), which activates the properties of the PLK and also is the site of localization (de Cárcer, Guillermo et al. 2011). In addition, PLK’s also have a serine/threonine kinase domain. Both of these domains are sites of binding, and modification by proteins, which is important to understanding how they regulate the cell cycle (de Cárcer, Guillermo et al. 2011). However, there are some significant differences among all five of the PLKS, both in structure and function. Firstly, PLK1 is involved in several key parts of the cell cycle, including chromosome regulation, the beginning of mitosis, bi-polar spindle formation and cytokinesis (Barr, Siljie & Nigg 2004). PLK2 has been studied and been found to regulate the G1 phase of cell division and it has important roles in centrosome and centriole replication. There have also been shown to be interactions between PLK2 and PLK4, but not much is known (Barr, Siljie & Nigg 2004). PLK3 is involved with the S phase of cell division, specifically DNA replication and mitotic entry via golgi apparatus. PLK4 is involved in centriole replication, similar to PLK2. Finally, PLK5 so far has not been identified as regulating the cell cycle, but instead has an incomplete PDB and is involved in neuron differentiation (de Cárcer, Guillermo et al. 2011). While PLK regulation is key to having a proper cell cycle and division, PLK’s, specifically PLK1 has been linked to tumorigenesis and cancer outcome. PLK1 has been found to be overexpressed in samples of many different types of cancer (Lee et al 2014). One of the theories is that since PLK1 is involved in centrosome maturation and chromosome maturation, if it does not function properly, abnormal chromosome separation can occur, causing cancer cells, which is due to the loss of oncogenes (Lee et al 2014). PLK1 has also been shown to bind to, and inhibit the anti-tumor gene, P53. In addition, PLK1 is also involved with apoptosis, since it interacts with FAAD (which controls apoptosis), and inhibits it, preventing proper apoptosis and leading to cancer cells (Lee et al 2014). The combination of the inhibition of apoptosis, inhibition of P53 and abnormal chromosome division creates the perfect conditions for cancer cells (Lee et al 2014). However, other PLK’s are also implicated in cancer cells, as PLK2 is silenced in several types of cancer, and mice studies have shown that decreased levels of PLK3 and PLK4 make mice more susceptible to tumors (PMC3230524). Finally, PLK5 has been shown to be silenced in brain tumors, but not much more is known about its role (Lee et al 2014). The role of PLK1 in cancer has also been shown through several successful inhibitors, as it is a key target in anti-cancer therapies (Lee et al 2014). Some of these inhibitors include BI2536, Volasertib, Poloxin and others (Gutteridge et al 2016). All of these are effective inhibitors as BI2536 was shown to inhibit and prevent tumor growth, Volasertib was shown to be a competitive ATP-inhibitor and work on preventing cancer, and finally, Poloxin was shown to be a competitive inhibitor by binding to the Polo Box Domain and interfering with the structure and function of PLK1 (Gutteridge et al 2016). Currently, there are also other PLK inhibitors being studied, with the goal to have cancer treatments that are targeted and have significantly less side effects than chemotherapy Gutteridge et al 2016). Overall, the PLK group has incredibly important roles in cell division; however, they also have the potential to go awry and cause both tumors and cancers of many types. While PLK1 has been shown to have the clearest link between elevated levels and cancer, other PLK’s have been implicated in cancer growth (Lee et al 2014). Finally, PLK’s offer a specific drug target that allow for cancer therapies without as many side effects as chemotherapy (Gutteridge et al 2016). More research needs to be, and is being, conducted regarding the role of PLK’s in cancer and the potential for targeted drug therapies. Works Cited Barr, F., Silljé, H. & Nigg, E. Polo-like kinases and the orchestration of cell division. Nat Rev Mol Cell Biol 5, 429–441 (2004). https://doi.org/10.1038/nrm1401
de Cárcer, Guillermo et al. “From Plk1 to Plk5: functional evolution of polo-like kinases.” Cell cycle (Georgetown, Tex.) vol. 10,14 (2011): 2255-62. doi:10.4161/cc.10.14.16494 Gutteridge, Rosie Elizabeth Ann et al. “Plk1 Inhibitors in Cancer Therapy: From Laboratory to Clinics.” Molecular cancer therapeutics vol. 15,7 (2016): 1427-35. doi:10.1158/1535-7163.MCT-15-0897 Lee, Su-Yeon et al. “Polo-like kinases (plks), a key regulator of cell cycle and new potential target for cancer therapy.” Development & reproduction vol. 18,1 (2014): 65-71. doi:10.12717/DR.2014.18.1.065 BY: DAVID KHAWAND  Breast cancer is a phenomenon in which breast cells grow uncontrollably (CDC). In a normal cell, the cell cycle is regulated by signaling pathways that determine whether it will grow, replicate its DNA, or divide. Throughout the cycle, checkpoints allow the cell to decide whether it should proceed to the next step, fix any errors, or commit cell death. In cancer cells, the whole checkpoint system is neglected, permitting the cell to divide uncontrollably. This is due to mutations in the DNA of healthy breast cells that allow them to evade the cell cycle checkpoints and apoptosis (cell death). One in eight women in the U.S. will be affected by this disease in her lifetime. In 2021, 281,550 new cases are expected to be diagnosed in women and 2,650 new cases in men. 43,600 women are projected to die from this disease (U.S. Breast Cancer Statistics). Hundreds of organizations are working to find a cure for this illness. Cancer cell’s rate of growth is measured by a TNM scale. This progression is broken up into four stages. The first through third stage signifies that cancer is present. The greater the stage, the larger the tumor becomes and the more it has spread into nearby tissue. In the fourth and final stage, metastasis occurs (NIH). Metastasis is the process in which cancer spreads from its original primary site of growth. When this happens, doctors can do very little to reverse the cancer progression and the patient has a very low chance of survival. Invasive breast cancer is the most frequent type of breast cancer. This particular cancer originates in the milk ducts and can spread into the surrounding breast tissue. The symptoms that may be associated with this kind of malignancy include lumps in the breast or underarm area, rashes or redness of the breast, swelling, and nipple pain. The two main categories of invasive breast cancer include invasive ductal carcinoma (IDC) and invasive lobular carcinoma (ILC). IDC is more common than ILC, constituting about 8 in 10 invasive breast cancer cases (American Cancer Society). Invasive ductal carcinoma begins in the milk duct cell lining in the breast. Then, it breaks through the milk duct wall, growing around the breast tissues and may metastasize through the bloodstream. Invasive lobular carcinoma impacts 1 in 10 invasive breast cancer patients (American Cancer Society). ILC starts in the milk-producing glands and can metastasize similarly to IDC. In addition, ILC is harder to detect on a physical examination and imaging. In this article review, the topic of breast cancer has been discussed. The two types mentioned were invasive ductal carcinoma and invasive lobular carcinoma. In a typical process of cancer development, it follows four steps on the TNM scale. Metastasis is the process of cancer cells leaving its original site and traveling throughout the body via the bloodstream. Once this occurs, very few treatments are available to control the spread. Works Cited "Breast Cancer Treatment: Treatment Options for Breast Cancer." American Cancer Society. Web. 07 Sept. 2021.
Brown, Ken. "Invasive Ductal Carcinoma (IDC) Breast Cancer: Johns Hopkins BREAST CENTER." Breast Cancer: Johns Hopkins Breast Center. 03 Nov. 2017. Web. 07 Sept. 2021. "Cancer Staging." National Cancer Institute. Web. 07 Sept. 2021. "Cell Cycle in Cancer." Cyclacel. Web. 07 Sept. 2021. "Invasive Breast Cancer (idc/ilc): Types of Invasive Breast Carcinoma." American Cancer Society. Web. 07 Sept. 2021. "U.S. Breast Cancer Statistics." Breastcancer.org. 04 Feb. 2021. Web. 07 Sept. 2021. "What Is Breast Cancer?" Centers for Disease Control and Prevention. Centers for Disease Control and Prevention, 14 Sept. 2020. Web. 07 Sept. 2021. |
Quest Student Research InstituteOn Science, Computation, Medicine, and Academic Success Archives
January 2022
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