Brief Description of Cancer

Cancer is a word that most people think of to be a death sentence. It is one word that nobody wants to hear in a doctor’s office. Sadly, over the past decades, cancer prevalence has continued to rise. It was thought to be more common in elderly people but now it is becoming a lot more common in younger adults and even in children. There are many types of cancer that can develop throughout the body. Luckily, cancer is curable in some cases with treatment. People can be saved at all stages of cancer but sadly, not every person survives. It is a battle that scientists and doctors have been fighting for decades. Cancer is very complex and to get a better understanding of it, first one must have a general idea of what it is, the origin and what causes it.

Cancer is abnormal cell growth within the body. It is when normal cells become mutated and then these mutated cells continue to reproduce. Cancer cells do not differentiate, have abnormal nuclei, and do not undergo apoptosis. What this means is unlike the other cells in our body, cancer cells do not die. They rapidly produce and their nuclei is enlarged. Keep in mind that there are also other abnormal cell growths that can occur within the body and it doesn’t mean that every abnormal cell growth is cancerous. The abnormal cell growth will eventually form tumors. Not all tumors are cancerous. There are two types of tumors; benign and malignant. Benign tumors are noncancerous and malignant tumors are cancerous. Abnormal cells multiply rapidly and cluster up together to form a tumor. Another thing to note is that different kinds of cancers have different mutational signatures (Mike Adams et al.) This is why cancer in general is hard to cure because there are so many types and each type differ from one other in regards to their cells.

The development of cancer isn’t something that happens overnight either. The development of cancer can take years. There are multiple steps or stages that these cells go through to become cancerous. First, the formation of the tumor will occur. Then this tumor will undergo metastasis, which means the tumor will break off into fragments and spread to other parts of the body. Next these tumors will undergo angiogenesis, which is where blood vessels are formed in the tumor and nutrients and oxygen can now be supplied to the tumor. Even though the cancer has spread to different parts of the body from the original starting point, it would still be considered one type of cancer. For example, if a person had a tumor in their pancreas and the cancer spread to the bones or lymph nodes, this cancer would still be called pancreatic cancer because it originated in the pancreas. Knowing this information will make understanding the different stages of cancer much easier. There are technically five stages of cancer and they are: stage 0, stage I, stage II, stage III, and stage IV (‘Stages of Cancer’, 2018). Stage 0 means that the cancer hasn’t spread, it is sedentary in one part of the body. Stage I means that it has started to spread into nearby tissues, but isn’t deep rooted anywhere. Stage II and stage III have spread deeply within the nearby tissues and possibly the lymph nodes. Stage IV is the worst stage of cancer and this means that the cancer has spread to other parts of the body.

The origin of cancer comes from mutated genes. An experiment was performed with mice in an attempt to prove this. Scientists focused on a liver cancer called fibrolamellar hepatocellular carcinoma or fibrolamellar for short. Scientists found that all of the patients with this cancer had the same mutations in their tumor cells. A piece of DNA was missing. This missing DNA is supposed to be between these two genes: DNAJB1 and PRKACA. The deletion of this DNA causes seven other genes to be deleted and a protein to fuse the genes DNAJB1 and PRKACA together. This fusion is call chimera. The formation of chimera is what causes the cancer. This can be clarified by the experiments used on mice. Scientists took the genes of adult mice and mutated their genes. They created the same deletion of DNA missing between DNAJB1 and PRKACA that is found in fibrolamellar patients. After a few months, the mice developed the cancer. Scientists then took another group of mice and added just an extra piece of DNA with the chimera on it and this group of mice also developed the same cancer. These two experiments justify that the formation of chimera in the genes is the cause of fibrolamellar. This is just one example. Referring back to chapter nine, these mutated genes are called ‘oncogenes’. There is another gene called ‘tumor suppressor genes’. An oncogene is a mutated proto-oncogene. This is what can lead to cancer. It basically tells the cells to keep growing and dividing and there is no off switch so a tumor is created. The tumor suppressor genes regulate cell division and reproduction. They tell the cell to stop growing and dividing but if it becomes inactive due to mutation, it can also lead to cancer.

The cause of cancer can be traced back to a number of things. A lot of times doctors can’t even specifically say what caused it because they do not know. It is obvious in some cases; a person who has been diagnosed with lung cancer and also has a vast history of smoking. We are not always that lucky, though. There are many risk factors that have the possibility to lead to cancer. As stated by the National Cancer Institute, some of these factors include: age, diet, sun light, genetics, alcohol, obesity, and etc. Cancer is a lot more common in elderly people. “The median age of a cancer diagnosis is 66 years old. This means that half of cancer cases occur in people below this age and half in people above this age. One-quarter of new cancer cases are diagnosed in people aged 65 to 74” (National Cancer Institute, 2015). Drinking alcohol in excess for long periods of time can possibly lead to the development of multiple cancers such as cancer in the breast, liver, and throat. When it comes to genetics causing cancer, it is because the person has inherited the same genetic mutation that a family member has. Just because the person inherited this genetic mutation does not mean that the person will have cancer. They just have a high risk of getting it or passing on this risk to future offspring. There is some bittersweet hope in this field. If a family has a known history of cancer (not self-induced such as smoking or drinking), genetic testing can be done. The test can tell a person how high the percentage is that they may get cancer. The positive side is that a person can know what to expect but the negative side is there is no preventing it. All one can really do is monitor with regular visits to the doctor and hopefully stop it in time when the time comes. Tobacco is also another leading cause of cancer. When it comes to smokers, not only does the smoker have a high chance of getting cancer but whoever is around that person getting secondhand smoke also has a high chance of developing cancer as well. Tobacco can cause the same cancers as drinking alcohol and more examples also include these cancers: lung (most common), kidney, pancreas, and cervix.

There are some interesting myths when it comes to cancer as well. One myth is, if a person gets cancer, they are going die. Even though a lot of people think of cancer as a death sentence, that is not always the circumstance. Although in some cases it is, depending on how advanced the cancer is. It can reduce a person’s lifespan to numbered years. “Five-year survival rates for some cancers, such as breast, prostate, and thyroid cancers, now are 90 percent or better. The 5-year survival rate for all cancers combined is currently about 67 percent” (National Cancer Institute, 2015). This is very encouraging seeing that the survival rate is increasing. Also, another myth that I myself believed to be true is, eating sugar makes cancer worse. It has not been proven to make cancer worse but the misconception is that eating a lot of sugar all the time can lead to obesity and obesity can lead to several types of cancer. I think this is where people (including myself) mix up sugar worsening cancer. Another big myth that people (including myself) believe to be true is artificial sugars cause cancers. All of the artificial sugars that are used in the United States have been approved by the Food and Drug Administration. Which means that these artificial sweeteners were approved after being evaluated and tested by researchers. There was no evidence that they are linked to cancer. This is why it is important to always check labels of foods when buying especially when they are not fresh foods.

The biggest question is ‘Why isn’t there a cure for cancer yet?’. As I have talked about above, there are many types of cancer and each type of cancer has its own genetic mutation. Since every type of cancer has its own genetic mutation, a cure has to be found for every single type of genetic mutation. In other words, a cure must be found for every type of cancer. Another tricky thing is there can be thousands of genetic mutations within a certain type of cancer. Let’s say two people both have colon cancer; one person may have a different genetic mutation from the other person so generic medication prescribed for colon cancer may not work for both people due to the different genetic mutations. Since this is so common, chemotherapy and radiation are common treatments for cancer. These methods are commonly used because of the many genetic mutations but also if the tumor gets cut out, it may grow back. These treatments can stop potential tumors from growing back. There is also another treatment option called genome sequencing. Scientists test the genes of the cancer cells to determine a specific treatment plan such as developing medications that can combat specific genetic mutations in the genes to stop the cancer. This form of treatment is very helpful compared to chemotherapy and radiation because these treatments are very invasive and have many harmful side effects.

Overall, cancer is a very scary disease to think about or even discuss. However, it should not be something that we live in fear of. We know it can be terminal but we also know it can be treated and managed. It is not something that a person can mentally plan for, even if their chances of becoming diagnosed are high. Even though there isn’t really a preventive measure to getting cancer, a person can get evaluated by a physician regularly and if the cancer does occur, it can be caught in the early stage and hopefully terminated. Living a healthy life free of alcohol and tobacco can help lower the risk of cancer developing in your body. If diagnosed, it does not have to be something that alters the way we live our lives. There is still so much to learn about all the different types of cancers and the genetic mutations that come along with them. I believe that research will have to continue and progress for many years due to the complexity of cancer. I think in the future genome sequencing will become more advanced and hopefully scientists will be able to get rid of the mutated genes that lead to cancer. This could be the cure for cancer we have been searching for. It is only a matter of time before the cure for all cancers is found.

References

  1. https://www.nature.com/scitable/ebooks/essentials-of-cell-biology-14749010/122997842/
  2. https://www.cancer.net/navigating-cancer-care/diagnosing-cancer/stages-cancer
  3. https://www.pnas.org/content/pnas/114/50/13076.full.pdf
  4. https://www.cancer.gov/about-cancer/causes-prevention/risk
  5. https://www.cancer.gov/about-cancer/treatment/types

Analysis of Whether Education Can Affect the Risk of Cancer

Cancer is one of the most well-known life-threatening conditions. The term ‘cancer’ is derived from a Greek word used by Galen in 100-200 AD ‘oncos’ which is Greek for swelling. This term was used to describe tumors. The Greek word, ‘oncos’, has been changed in modern health into oncology which means the study of tumors (Papavramidou N. et al.). A tumor is a swelling on a part of the body which grows abnormally and when there is a growth of abnormal cells in the body due to uncontrolled cell division this is known as cancer. There are many different types of cancers and the most common cancers in humans are; breast, liver, stomach and lung cancer (Dano et al., 2003). Lung cancer is the most common out of all of these cancers listed (Bray et al., 2018). As a result of the fact that cancer is a harmful disease and can spread if not treated properly and quickly. It has been argued that there is a correlation between getting an education and health (Grossman and Kaestner, 1997; Goldman et al., 2011). Education is needed because we would need to learn about what cancer is and once one realizes the symptoms, they would be able to treat it quicker. Getting an education would mean people are more likely to know the risks and ways to prevent themselves from getting cancer (Hemminki et al., 2003; Faggiano et al., 2003; Faggiano et al., 2004). In addition to this, gaining an education means a higher chance of getting a job with a good salary so this means being able to pay for healthcare services if needed. For example, being able to buy sunscreen to protect skin from skin cancer. Therefore, this reduces the risk of cancer for people that have an education as they are more aware of the risks (Levi et al., 1988). In this review, it will be examined on if education can affect the risk of cancer and decide on whether groups that have had an education are likely to get cancer and if there is a causal relationship between the two.

Education Level and Risk of Cancer

Reportedly, it has been suggested that those that have been poorly educated would not receive the proper care and knowledge they need so that they can avoid this life-threatening disease (Braaten et al., 2005). In Lleras-Muney’s 2005 study on education and mortality rates in adults it was shown that there was a causal relationship between education and adult mortality. Researchers found that adding more years to education would decrease percentages of the chances of dying by 3.6%. Lleras-Muney (2005) stated that an extra year of obligatory education would lower death rates after 35 years old by 3% (Lleras-Muney, 2005).

Mouw et al. (2008) further highlighted this in research where it was presented that obtaining a malignant disease, such as lung cancer and other cancers to do with smoking, increased when there was a reduced level of education (Mouw et al., 2008). Mouw et al. conducted a study on 498 455 participants to see the effects of education on the risk of cancer. They found that the more educated the category was the least likely it was that they would get cancer. The most common cancer that they found in less educated people was smoking related cancers like lung cancer. The highly educated group were less likely to smoke therefore they did not have smoking related cancers. They were more likely to have regularly checked themselves in the hospital for any signs of cancer and be fit health wise. Women that were in the study and more educated were said to be non-parous or conceive much later than women that had not had high levels of education. This displays that smoking causes cancer and education can also be a cause of cancer due to education being needed to understand the disease, it’s complications and treatment methods (Wynder EL et al., 1977). This study is more reliable than Lleras-Muney’s study as it is more recent, so it may have more information that is needed.

In a study carried out by Jensen et al. (2008), it was proven that socioeconomic factors had an impact on cancer risk. The study was carried out from 1994-2003 on 3 22 million subjects all aged 30 and above born in the years of 1925-1973 in Denmark, results showed that mortality from cervical cancer was low in women that had a better socioeconomic ranking than women that had a decreased level of education (Jensen et al., 2008). Moreover, endometrial and ovarian cancer death rates increased when linked to women with poor education.

In another similar study carried out by Marsa et al. (2008), socioeconomic position influenced the risk of cancer on male genital organs. This study used the same procedure but on males. It was found that men with higher levels of education had an increased chance of getting prostate cancer (Marsa et al., 2008). However, results showed that the possibility of getting testicular cancer did not depend on socioeconomic factors. Testicular cancer did not show a causal relationship with education in this study. These studies are similar because they are both in Denmark and scientists used male and female participants separately in the two studies.

Opposing Study-Risk of Cancer Linked with Gaining a University Degree

Glioma, a brain tumor that occurs in a big group of cells in the brain called the glial cells (Llaguno et al., 2016). A study carried out in Sweden by Khanolkar et al. (2016) on a large cohort of university students showed that degrees can eventually lead to tumors in the brain (Khanolkar et al., 2016). Demonstrating that, education may not have a causal effect on the risk of cancer. This study is a more recent study so it may be more reliable and have more modern information on the effect of education on cancer. Khanolkar et al.’s study on gliomas and socioeconomic positioning opposes studies such as Mouw et al.’s study and Lleras-Muneys findings as this study claims that high levels of education increase the risk of cancer.

The scientists in this study, Khanolkar et al., used more than 4.3 million Swedish participants in their discoveries and based it on them. Every one of the participants were conceived somewhere in the range of 1911 and 1961 and were also still living in Sweden in 1991. Observations on participants of the study were carried out somewhere in the range of 1993 and 2010 (Khanolkar et al., 2016). This was to check whether they built up a glioma (a brain tumor). Information on their educational level, relationship statuses, income and more were collected via the national census data and labor market. During the time frame given for participants to see if they had gotten a brain tumor, 1.1 million individuals passed on and more than 48,000 emigrated, however 5735 of the men and 7101 of the ladies built up a brain tumor. Men that had achieved a higher-level education such as a university degree for three years, had a 19% higher possibility of being bound to build up a glioma which is a kind of brain tumor emerging in glial cells. Glial cells protect and stay close to neurons in the cerebrum (Llaguno et al., 2016). It was also found that men that did not take part in education or had not been in education for some years of the amount of compulsory years that were meant to be done (9 years) were least likely to build up a glioma. In the women, the possibility of this was 23% higher for getting a glioma in women with an education than women that did not achieve a higher-level education. This study therefore opposes the idea that high levels of education increase risk of cancer but also shows that there is a correlation between cancer and education.

Education Doesn’t Affect the Risk of Cancer

Lund et al.’s (1991) Norwegian study on education and breast cancer carried out on a large cohort of 425,844 married women demonstrated in the results gathered that education had no correlation with cancer. This experiment was carried out from 1970-1985 on Norwegian women aged 35-54 years old (Lund et al., 1991). This opposes arguments that education can affect cancer. However, this study may not be reliable as it is older than other studies arguing that there is a relationship. This means that data is outdated and uses old information which may not be useful. Another limitation is that this study only looks at educations effect on the risk of cancer on a large cohort of married women only and not men too.

To support this a more recent study was carried out by Hemminki et al. (2003). Hemminki et al. (2003) concluded that education had little to no effect on cancer mortality rates in this study as it was found that the development of cancer in men and women in multiple educational levels was 16.7% in women and in men it was 13.8%. This proves that there was not much of a difference between different educational levels. In which further highlighting the point that there is no causal effect between education and cancer. The study took place in Sweden and there were 9 educational groups involved between men and women. There was no specific trend as in all educational levels there was increasing and decreasing risk of cancer in cancer (Hemminki et al., 2003). Scientists in this study used PAF to show educational levels of the experiment (Van Loon et al., 1995).

Discussion

Based on the findings from the studies and on common knowledge, education has an influence on cancer as we would learn about cancer in school and treatments or ways to prevent oneself from getting this disease. Adults that have not had an education in some cases may end up developing cancer as they have not learnt what is taught about cancer in education (Mouw et al., 2008). Furthermore, being in education for longer plays a key role because as one gets older, they learn in more detail and depth (Lleras-Muney, 2005). Therefore, they would learn what cancer is when in for example a science lesson. Later, with more years of education they may have learnt about prevention which some people may miss out on. This was demonstrated in studies and this proves that education can affect the risk of cancer. Future treatments are a vital factor to be considered. Researchers should consider future treatments for education affecting cancer. It can be implemented that everyone does compulsory schooling as that has been proven to have influenced an effect on the risk of cancer (Jensen et al., 2003; Marsa et al., 2003). Another future treatment of education and the risk of cancer could be teaching younger kids about the risk of cancer so that they know the risks earlier in their lives and some can learn to prevent the disease before they have the chance to leave education. Further research should be done on whether there is a trend between education and cancer because some studies are outdated and use old data and figures. Most older studies claim that education cannot affect cancer but more recent studies claim that it can.

Liver Cancer: Research Study

My husband’s father, uncle, and aunt passed away after experiencing liver cancer a couple of years. Saying about liver cancer, you might think about poor lifestyle choices such as diabetes, overweight, over consumption of fatty, alcohol drinking or smoking. However, none of these people were involved in the most common risk factors above. We all were shocked about their fatal disease because they ate balanced diets and lived in healthy environment, and they did not experience any signs or symptoms until it had been diagnosed due to tiredness and digestive problems. I would like to learn more on the causes, symptoms, and treatments of this disease as I have seen it dramatically influences our family members’ lives.

Normal Anatomy and Physiology of the Liver

The liver is the human body’s largest internal organ that lies behind the diaphragm in the upper right quadrant of the abdomen (McKinley, OLoughlin, & Bidle, 2016, p.1078). It has hundreds of functions to support the essential processes such as: drug detoxification; metabolism of carbohydrates, lipids, and proteins; and the production of digestive enzymes (McKinley et al., 2016, p.1078-1081). It plays a key role in maintaining homeostasis by taking in glucose during the absorptive state and releasing glucose into the bloodstream during the post-absorptive state of metabolism (McKinley et al., 2016, p.1078-1081). Carrying out these tasks make it a such important organ that is vital to our overall health.

Effects of Liver Cancer to Homeostasis

Damage to the liver results in serious impacts on the entire human body. When liver cells are cancerous, they divide relentlessly and grow into tumors, invading healthy tissues as well as spreading to other organs (‘Liver Cancer Facts’, n.d.). Tumor cells would interfere the homeostatic balance as they cease producing and releasing glucose (Ohio State University Medical Center, 2012). Also, cancer makes liver not to function correctly leading to bilirubin, fluid, and toxic substances build-up that affects other organs in the body (The American Cancer Society medical and editorial content team, 2016).

Types of Liver Cancer

There are two categories of liver cancer: primary and secondary.

Primary Liver Cancer

Primary liver cancer is the cancer that originate in the liver formed in the liver itself. The most common types of primary liver cancer are hepatocellular carcinoma – also called HCC, hepatocellular cancer, or hepatoma – and intrahepatic cholangiocarcinoma (also called ICC).

  • Hepatocellular carcinoma (HCC) – that represents 85% of the primaries – starts from liver cells called hepatocytes. This type is more common in people who have liver damage (such as by the hepatitis B or C virus or by alcohol abuse) or metabolic syndrome (such as diabetes, obesity, and hyperlipidemia). Hepatic adenomas, also known as benign tumors, can also cause HCCs in some cases (‘Liver Cancer Facts’, n.d.).
  • Intrahepatic cholangiocarcinoma (ICC): this is the second common form of primary liver cancer, which occurs within the bile ducts. People who have chronic liver disease such as cirrhosis, choledochal cysts, or sclerosing cholangitis are more likely to get ICC (‘Liver Cancer Facts’, n.d.).
  • Other uncommon types of primary liver cancer: hepatoblastoma (occurs in children), biliary cystadenocarcinoma (usually found in women), and fibrolamellar hepatocellular carcinoma (affects those younger than age 40) (‘Liver Cancer Facts’, n.d.).

Secondary Liver Cancer

Secondary liver cancer is caused by the cancerous cells that grow from other parts of the body then spreads (metastasizes) to the liver and forms new tumors here; and these tumors are called liver metastases. People with breast, bowel, or lung cancer are more likely to develop this category of liver cancer (‘What Is Secondary Liver Cancer?’, 2017).

Causes

The exact cause is not known, but there are a variety of the risk factors that lead to liver cancer. Illnesses such as hepatitis B or C and hemochromatosis are largely to blame as they often lead to cirrhosis – scarring of liver tissues that prevents flood flow through liver. Over time, the scarring will grow, takeover of the healthy cells and therefore damage the function of the liver. Having alcohol abuse (leading to cirrhosis), diabetes, obesity, low immunity (such as those with AIDS), smoking would raise the risk. Males tend to consume larger quantities of alcohol and smoking more than females, thus having higher risk of liver cancer because the liver is damaged more easily. Environmental factors such as prolonged exposure to arsenic or aflatoxin (toxic substance in drinking water and food) can also be contributors. Hemochromatosis is inheritable, and those with family members having liver cancer will have higher risk of liver cancer (Nordqvist, C., 2017, December 5).

Symptoms

The symptoms of liver cancer do not clearly show until the disease has reached certain stages. Some typical symptoms are: uncontrollable weight loss, loss of appetite, vomiting, pain in the right upper quadrant, a buildup of fluid in the abdomen, quickly to feel full even after eating very little food, lump under the ribcage on the right side, jaundice, dark urine, liver or spleen enlargement, fever, pruritus, cirrhosis or cirrhosis gets worse (‘Liver Cancer Facts’, n.d.).

Differential Diagnosis

Due to similar symptoms with other diseases, liver cancer is hard to diagnosed in early stages, therefore delay its detection. Once discovered, the doctors need to determine its stage, the size and location of the tumor as well as whether it has spread to other organs (‘Liver Cancer Facts’, n.d.).

The stage depends on: number and size of tumors, whether blood vessels have been infected, and whether lymph nodes or other organs have been infected (Mayo Clinic Staff, 2019).

Some tests to diagnose liver cancer include: blood tests (to measure the levels of liver protein or certain enzyme to look for any sign of cancer); imaging tests like ultrasound, computed tomography (CT), or magnetic resonance imaging (MRI) scan can detect cancer; liver biopsy (take tumor’s sample using a needle through skin or surgery then examine the sample under a microscope).

According to ‘Liver Cancer Facts’, stages of liver cancer can be categorized from I (earlier) to IV (later) (one to four). Specifically:

  • Stage I: only one tumor in the liver;
  • Stage II: one tumor that has advanced to blood vessels, or multiple tumors which are smaller than 5cm;
  • Stage III: multiple tumors with at least one larger than 5cm or growing to veins like portal and hepatic, growing to liver’s outer cover or nearby organs except gall-bladder;
  • Stage IV: cancer has spread to other organs and the lymph nodes.

Treatment

The statistics show that, for those are diagnosed, the 5-year survival rate heavily depends on how early the disease has been detected: stage I or II: 31%; stage III: 11%; stage IV: 2% (Cancer.Net Editorial Board, 2019). Notes that, even in later stages, treatments are also available to help maintain a good quality life for the patient. Surgery, if can be done, usually brings a good result (Cancer.Net Editorial Board, 2019).

There is a wide range of treatments for liver cancer. The target is to remove the tumors (for people whose have good liver function and the tumors are within the liver and small), replace the liver (transplant for those with early-stage liver cancer), or kill the cancer cells using different therapies depending on the stage and severity of the disease (for those who cannot get surgery or whose cancer has spread) (Mayo Clinic Staff, 2019). According to Mayo Clinic, the typical therapies are:

  • Localized treatments: the cells of the tumors will be destroyed by applying heat to them, freezing them, injecting alcohol to them, or even injecting drugs to the tumor area.
  • Chemotherapy: instead of injecting drugs to tumor area locally, this method injects drugs to the entire body, but the drugs are aimed to kill rapidly-growing cells.
  • Targeted drug therapy: these drugs help block the abnormalities of cancer cells and eventually kill them; however, additional test may need to be done first to confirm the efficiency of these drugs on each patient.
  • Radiation therapy: using high-powered energy beam (e.g., X-rays) to kill cancer cells at small areas in the liver, that might help control symptoms for advanced liver cancer or if other treatments cannot help (Mayo Clinic Staff, 2019).

To lower liver cancer risk, there are some strategies that might help, including avoiding excessive alcohol use, getting Hepatitis B vaccine, avoiding hepatitis C virus by practicing safe sex (because there is no vaccine against hepatitis C), watching your body weight, preventing and treating diabetes as well as hemochromatosis (Nordqvist, C., 2017, December 19).

Conclusion

There are about 42,000 cases have been diagnosed with primary liver cancer in the U.S. in 2019, and, of those, about two-third are men (Cancer.Net Editorial Board, 2019). The number of liver cancer patients keeps increasing, and compared to 1980, it has increased three times, that could result in the death of about 31,000 people this year in the U.S. (Cancer.Net Editorial Board, 2019). Liver cancer is ranked the fifth in cancer death for men and the seventh for women (Cancer.Net Editorial Board, 2019). This disease has a high mortality rate and being on the rise, thus knowing the facts will help rise our awareness to avoid risk factors. To bring awareness and raise funds for liver cancer research, October is chosen as the Liver Cancer Awareness Month, and emerald green is the color of liver cancer ribbon (Johnson, J., 2018, October 24).

This research also gives me an insight at what happened to my husband’s father, uncle, and aunt. Although they lived healthy lifestyles, they might be affected by unknown causes such as infection with the hepatitis B and C viruses or ate aflatoxin-tainted foods. Furthermore, I realize how important to detect the disease early because it decides the survival rate of the patient and gives patients the best chance to be supported and treated.

References

  1. Cancer.Net Editorial Board. (2019). ‘Liver Cancer: Statistics’. Cancer.net. Retrieved April 27, 2019, from https://www.cancer.net/cancer-types/liver-cancer/statistics
  2. Johnson, J. (2018, October 24). ‘Cancer Ribbon Colors: A Guide.’ Medical News Today. Retrieved from https://www.medicalnewstoday.com/articles/323448.php.
  3. ‘Liver Cancer Facts’. (n.d). Seattle Cancer Care Alliance. Retrieved April 26, 2019, from https://www.seattlecca.org/diseases/liver-tumors-cancer/liver-cancer-facts
  4. Mayo Clinic Staff. (2019). ‘Liver Cancer – Diagnosis & Treatment’. Mayoclinic.org. Retrieved April 27, 2019, from https://www.mayoclinic.org/diseases-conditions/liver-cancer/diagnosis-treatment/drc-20353664
  5. McKinley, M. P., OLoughlin, V. D., & Bidle, T. S. (2016). Anatomy & Physiology: An Integrative Approach (2nd ed). New York, NY: McGraw-Hill Education.
  6. Nordqvist, C. (2017, December 5). ‘Everything You Need to Know About Cirrhosis’. Medical News Today. Retrieved from https://www.medicalnewstoday.com/articles/172295.php.
  7. Ohio State University Medical Center. (2012). ‘Liver Cancer Cells Stop Making Glucose as They Become Cancerous’. ScienceDaily. Retrieved April 26, 2019, from http://www.sciencedaily.com/releases/2012/07/120730141635.htm
  8. Torborg, L. (2018). A Medical Illustration of Liver Cancer. [Digital Image]. Retrieved from https://newsnetwork.mayoclinic.org/discussion/mayo-clinic-q-and-a-treatment-for-liver-cancer/
  9. The American Cancer Society medical and editorial content team. (2016). ‘Managing Symptoms of Advanced Cancer’. Cancer.org. Retrieved April 27, 2019, from https://www.cancer.org/treatment/understanding-your-diagnosis/advanced-cancer/managing-symptoms.html
  10. ‘What Is Secondary Liver Cancer?’ (2017). Cancer Research UK. Retrieved April 27, 2019, from https://www.cancerresearchuk.org/about-cancer/secondary-cancer/secondary-liver-cancer/about

Why Is Cancer So Difficult to Treat?

Cancer is defined as a disease caused by uncontrollable cell division of abnormal defective body cells. Cancerous cells have the ability to destroy and damage surrounding organs and healthy tissues. Some cancers metastasize, beginning in one area and then invading and damaging other areas of the body. Cancer cells which group together form tumors, which can be benign (don’t spread) or malignant (metastasize to different areas). Random mutations can often occur in the genetic encoding of cells, but these mutations are quickly detected and cause the cell to undergo apoptosis or ‘cell suicide’. Cancerous cells have mutations which bypass the detection process, allowing for rapid and incontrollable cell division of cells with incorrect genetic coding. The unique difference between cancer and any other illness is that it is caused by the body’s own cells, rather than foreign contaminants or pathogens, such as bacteria or virus. This makes it difficult for the body’s immune system to detect cancerous cells and target them, as well as finding drugs or treatments which will only affect cancerous cells, rather than also killing healthy, functioning body cells.

Treatments for most cancers usually include a combination of surgery to remove tumors, radiotherapy (ionizing radiation is used to kill cancerous cells) and chemotherapy (medication used to kill cancer cells or stop them dividing). A problem with chemotherapy and radiotherapy is that they are treatments designed to target dividing cancer cells. However, some cancer cells lie dormant for long periods of time. This results in cancers returning after many years, despite multiple rounds of treatment. Hormone therapies, immunotherapy (enhancing the body’s natural defense mechanisms to target cancer cells), and targeted treatments tailored for specific types of cancer can also be used. Most cancer treatments are developed using cell cultures grown in labs from samples of human tumors. These cultured cells have allowed oncologists to study the genetics and biology of many different cancers. These cells often lack the complexity of tumors and cancerous cells within patients and other living organisms, meaning drugs designed to target cancers, which show positive results in the lab, often have no effect on real-life patients and fail clinical drug trials.

One of the complexities of aggressive tumors is that they can have multiple populations with slight variations in genetic coding of cancer cells. Over time, distinct genetic mutations arise in cells, in different parts of the tumor, creating unique subclones. For example, aggressive brain tumors called glioblastomas can have up to six different subclones in a single patient. This is called clonal heterogeneity, and it makes treatment difficult because a drug that works on one subclone may have no effect on another due to the wide variation of genes in the mutated DNA of the cells. A tumor is a dynamic interconnected ecosystem where cancerous and healthy cells communicate with each other. Tumors can encourage normal cells to form blood vessels that ‘feed’ the tumor (with essential nutrients and oxygen) and remove waste products (such as carbon dioxide). Tumors can also act as immunosuppressants, keeping the immune system from recognizing and destroying the cancer, as well as pathogenic contaminants. Cancer stem cells have given way to a large array of problems also. These cells, although rare, have special properties which have made them resistant to chemo and radiotherapy. In theory, even if the rest of the tumor minimizes beyond detection, during treatment, a single residual cancer stem cell could seed the growth of a new tumor.

Cancer cells are masters of adaptation, with the ability to adjust their molecular and cellular characteristics to survive under stress. When targeted by radiation or chemotherapy, some cancer cells can effectively switch on ‘protective shields’ by changing their gene expression. Cancer is a disease which does not comply with the ‘one size fits all’ method of treatment, meaning different patients require different treatments and even then, the risk of killing all cancer cells is not always absolute. To conclude, much more in-depth research must be conducted in cancer genetics and biology in order to properly understand how to effectively tackle the problem of cancer, which presents itself in more than 200 different forms.

References

  1. Thallinger, C., Füreder, T., Preusser, M., Heller, G., Müllauer, L., Höller, C., Prosch, H., Frank, N., Swierzewski, R., Berger, W., Jäger, U. and Zielinski, C. (2018). Review of Cancer Treatment with Immune Checkpoint Inhibitors: Current Concepts, Expectations, Limitations and Pitfalls. Wiener klinische Wochenschrift, [online] 130(3–4), pp.85–91. Available at: https://www.ncbi.nlm.nih.gov/pubmed29098404 [Accessed 1 Jan. 2021].
  2. Jackson, H.J., Rafiq, S. and Brentjens, R.J. (2016). Driving CAR T-cells Forward. Nature Reviews Clinical Oncology, [online] 13(6), pp.370–383. Available at: https://www.nature.com/articlesnrclinonc.2016.36 [Accessed 1 Jan. 2021].
  3. Garden, H. HowStuffWorks, Health, Conditions, Cancer and Facts, 2021. Why Is It so Difficult To Find Cancer Cells?. [online] HowStuffWorks.
  4. Wanner, M., 2015. Why Is Cancer so Difficult to Cure?. [online] The Jackson Laboratory.
  5. nhs.uk. 2019. Cancer. [online].

Nutrition and Cancer Risk

Numerous studies have observed at the chance that definite nutritive mechanisms or nutrients relate to increases or decreases in cancer risk. Studies of cancer cells in the laboratory and of animal representations have occasionally provided proof that sequestered mixtures may be carcinogenic (or have anticancer action). However, with few exclusions, studies of human inhabitants have not yet exposed ultimately that any dietary element reasons or safeguards in contradiction of cancer. From time to time the outcomes of epidemiological studies that associate the diets of society with and without cancer have specified that people with and without cancer be at variance in their consumption of a specific dietary element. Especially young children don’t have any idea about this disease and they always end up eating food outside. They should be thought to eat home and to know what kind of food they should eat. Cancer is common in well developed countries because most of the food they consume is artificial. People eat junk food and processed food more often, so I am not surprised that there is a high number of cancer patients in well developed country. People care about how much time they will save from getting outside food for cheaper price or from processed food. They don’t see the bad side which risk their life of having worst diseases.

Conversely, these outcomes demonstration only that the dietary constituent is related with an alteration in cancer risk, not that the dietary element is accountable for, or effects, the regulation in risk. For instance, study members with and without cancer could fluctuate in other ways besides their diet, and it is conceivable that some other modification balance sheet for the metamorphosis in cancer. When data appears from an epidemiological study that a dietary constituent is related with abridged risk of cancer, a randomized experimental might be completed to examine this option. Unsystematic task to dietary assemblages guarantees that any variances among people who have high and low consumption of a nutrient are due to the nutrient itself a little than to other undetected adjustments (for ethical reasons, randomized studies are not commonly completed when data materializes that a dietary constituent may be accompanying with an increased risk of cancer).

Some foods and the vitamins, minerals, and other nutrients found in them may increase or lesser cancer risk. Examiners have been learning how the foods, nutrients, and eating patterns are associated to cancer. These are the main foundations of animal protein in most diets: meat, fish, poultry, shellfish, dairy products, and eggs. Of these, red and processed meats raise the greatest concern in terms of cancer risk. Red meat includes pork, beef, veal, and lamb. Processed meat includes bacon, ham, lunch meats, meat jerky, hot dogs, salami, and other cured meat products. Any quantity of processed meat and more than about 18 ounces of fresh meat per week are greatest powerfully related with a greater risk of cancer. Most of cancer-causing foods are dairy food which is bad because everyone grows up eating them. People don’t afford getting organic products so they will always get low price once which is low in quality and most of them have a higher chance of causing cancer and other diseases.

Drinking alcohol rises the risk of developing certain kinds of cancer. Systems among food and cancer it is stimulating to discovery specific relationships between a food or nutrient and cancer since foods grip several resources that strength both increase and lower cancer risk. Nethermost people eat and drink a variety of foods. This produces interactions that are indissoluble to learning. The movables of a food or nutrient can vary be liable on how much of it you ingest. Roughly investigations establish that how a food is prearranged may stimulus its risk or compensations. Corpulent about cancer risk undercurrents, such as inheritances and surroundings, are out of your regulator, but inspection endorse that proximate 70% of your compeers’ risk of cancer is within your regulator to modification, comprising your diet. Avoiding cigarettes, controlling alcohol, accomplishment a healthy weight, and success steady exercise are altogether excessive ladders for stopping cancer. Complimentary a healthy diet can also play a forceful role. Drinking alcohol usually cause lung cancer because alcohol and smoking affect the lung. I don’t know why people smoke and drink a lot of alcohol knowing the side effect of it.

What you eat—and don’t eat—can have a prevailing consequence on your health, containing your risk for cancer. Despite the fact that examination inclines to point to relations among specific foods and cancer, rather than compact cause-and-effect communications, there are convinced dietary behaviors that can have a main encouragement on your risk. For instance, eating outmoded Mediterranean diet rich in fruit, vegetables, and healthy fats like olive oil can lesser your risk for assortment of conjoint cancers, counting breast cancer. Contrariwise, a diet that take account of a daily portion of administered meat increases your risk of correctional cancer. If you have a history of cancer in your family, making small changes to your diet and behaviors now can make a big alteration to your long-term health. And if you’ve already been diagnosed with cancer, eating a nutritious diet can help support your mood and strengthen your body during this challenging time. It is so surprising that food make a big difference in risk of cancer. Since there is a family history of cancer in my family, I should always be careful of what to eat. The cancer risk accompanying with deal with meat products is even higher. The International Agency for Research on Cancer, a branch of the World Health Organization, classifies processed meat as a Group 1 carcinogen, meaning that like other Group 1 carcinogens – tobacco, UV radiation and alcohol – research has proven that processed meat can cause cancer in humans. Eating just 50 grams of processed meat each day, the IARC reports, can elevate cancer risk by 18%. About four strips of bacon or one hot dog contains about 50 grams of processed meat. Studies have not proven that there is a solid link between a specific diet and whether it may increase or decrease a person’s chance of getting cancer. It can be challenging to find direct links between cancer risk and certain foods because people eat a wide range of foods and cook and prepare them in a variety of ways. Eating meat processed specially eating processed food will make it very risky. People eat processed food and meat warming it in the microwave, which makes the situation of risking of cancer higher because of the microwave radiation. People should decrease the habit of consuming a lot of meat and processed foods. People usually don’t cook in the house because of not having a lot of time but is very dangerous eating outside because we don’t even know the products, they use to cook the food. People also eat raw meat which is very risky for cancer because the meat is not cooked, and it contains a lot of blood inside.

In general, I recommend all people to eat home that is home made, and to buy organic product if they are financially stable. We all must care about our health, so it is very important to always cook in the house and watch what we always eat. If you have a history of any family disease you must be careful and know what kind of foods really increase the risk of getting them. People should really stop eating here and here and always read what they eat.

Cancer Treatment by Nanotechnology

First Draft (Introduction)

Cancer is among the greatest killer diseases of the 21st century. Several factors cause cancer infection. A range of these factors either falls within the category of hormonal factors or behavioral factors. Hormonal factors include genetic mutations and somatic mutations while behavioral factors include smoking and lack of nutrition (Frank and Nowak, 2004, p. 291).

Genetic mutations cause cancer because a range of genetic errors causes the rapid multiplication of cells, which eventually lead to the formation of cancer. For instance, for liver cancer, a perfectly healthy liver may experience excessive injuries to cells because of genetic mutations (Frank and Nowak, 2004, p. 291). Consequently, genetic errors are bound to accumulate and unhealthy cells may rapidly multiply to cause the disorganization of cells. This cell disorganization causes cancerous cells (Gold, Slone, Manley and Ames, 2002).

Somatic mutations are notorious in damaging normal cells. Cell damage leads to cancer formation. Somatic mutations work by altering body cells to cause cancer and other diseases (Frank and Nowak, 2004, p. 291). The theory behind the causes of cancer (through mutation) has been existent for the past 50 years.

This theory notes that cancer primarily develops from a single somatic mutation cell, which has undergone years of DNA mutation (Frank and Nowak, 2004, p. 291). Its link with cancer therefore emanates from the fact that cancer is a disease of cell mutations, which affect the cell cycle, thereby causing the disease. Somatic mutation is at the center of the alterations in cell cycles (Frank and Nowak, 2004, p. 292).

Behaviorally, around the world, smoking has been singled out as the most notorious behavioral cause of cancer (Frank and Nowak, 2004, p. 291). For instance, a fifth of all cancer cases in the world are attributed to smoking (Gold et al., 2002). The most common form of cancer (attributed to smoking) is lung cancer because about four in five lung cancer cases are caused by smoking (Gold et al., 2002).

The link between smoking and cancer can be traced to research studies, which affirm that tobacco smoke (for example) consists of more than 80 cancerous substances (Gold et al., 2002). Nonetheless, proper nutrition is synonymous with good health. In fact, proper nutritional diets do not only help fight cancers; they also help in fighting other diseases as well.

The link between cancer and nutrition is observed from the fact that some types of foods increases one’s risk of developing cancer, while other types of foods support the body in fighting cancer by boosting the immunity (Gold et al., 2002). The lack of certain types of foods may also increase one’s risk of developing cancer. For instance, patients are often advised to take plant-based foods to manage cancer (Gold et al., 2002).

Cancer treatment methods have changed over the years. Old methods of treating cancer include drug administration, radiation and surgery. However, a newer method of cancer treatment includes nanotechnology (and other transitional drug treatment methods).

This paper elaborates on the usefulness of using nanotechnology in the treatment of cancer in Saudi Arabia. To do this, an explanation of the advantages of nanotechnology over other cancer treatment methods will be evaluated. These advantages will be highlighted by explaining how nanotechnology works and how it is fast and efficient in treating cancer.

The latter segment constitutes an explanation of how nanotechnology reduces the side effects of treating cancer and how it facilitates the easy adoption of drugs into the cancerous cells. Consequently, a comprehensive overview of how nanotechnology helps in treating cancer will be explained.

Second Draft (Cancer Treatment Using Nanotechnology)

Saudi Arabia has a relatively lower incidence of cancer when compared to other gulf countries. However, cancer treatment and care in Saudi Arabia is normally different from other countries. The difference emanates from the fact that there is a clash between acceptable and unacceptable cancer treatment methods in the Kingdom.

This difference also stretches to the way cancer education is administered, and the manner cancer patients receive care. Similar to the history of cancer in the US, most cancer cases in Saudi Arabia are diagnosed at a late stage. Often, this problem is influenced by late detection and the use of inefficient and old methods of cancer treatment.

Cancer treatment methods are normally diverse and applicable in different types of situations. Conventional cancer treatment methods include surgery, chemotherapy, and radiation. Surgery works by removing cancerous tumors (surgically) as much as possible (Frank and Nowak, 2004, p. 291). Usually, surgery is used to prevent, treat and diagnose cancer, but ordinarily, during treatment, it is combined with radiation and chemotherapy as auxiliary cancer treatment methods (Frank and Nowak, 2004, p. 291).

Chemotherapy is a drug treatment method for treating cancer but unlike other drug treatment methods, it affects the entire human body. Like other surgery treatment methods, chemotherapy may be used alongside other cancer treatment methods (Frank and Nowak, 2004, p. 291). Lastly, radiation works by killing cancerous cells and shrinking certain types of tumors. Similarly, radiation also works by destroying the DNA of cancerous cells thereby causing their inactivity.

Due to the inefficiencies associated with the above methods of cancer treatment in Saudi Arabia, it is crucial to adopt newer methods of cancer treatment. Nanotechnology is one such method.

Saudi Arabia reports increased causes of cancer every year. For instance, 7,000 new cancer cases are reported every year and it is estimated that in 15 years, the kingdom will report more than 30,000 new cancer cases annually (Gold et al., 2002). These statistics abound, the future of cancer care and treatment in Saudi Arabia rests with nanotechnology.

From an electromagnetic point of view, the adoption of nanotechnology in Saudi Arabia includes the understanding of Paclitaxel-Loaded Gelatin Nanoparticles, Light Absorption by Gold Nanoparticles and Magnetic Nanoparticle Hyperthermia Methods as the main forms of cancer treatment.

Paclitaxel-Loaded Gelatin Nanoparticles is a constituent of electromagnetic cancer treatment method (in nanotechnology), which is commonly used in the treatment of intravesical bladder cancer (Gold et al., 2002). In a study to test the efficiency and use of Paclitaxel-Loaded Gelatin Nanoparticles in treating bladder cancer, it was established that “Paclitaxel-loaded gelatin nanoparticles represent a rapid release, biologically active paclitaxel formulation that can be used for intravesical bladder cancer therapy” (Torchilin, 2007, p. 128).

Its efficacy is therefore undisputed. Gold nanoparticles are exclusive components of cancer treatment using electromagnetic nanotechnology treatment methods. Gold nanoparticles are normally finer than dust particles (Gold et al., 2002). These particles normally contain “peptide” which draws nanospehers directly to the cancerous cells and destroying them (Huang, Jain, El-Sayed and El-Sayed, 2007, p. 681).

Magnetic nanoparticle hyperthermia method is normally used in the early detection of cancer because it is ordinarily contrasted with MRI imaging. The magnetic nanoparticle hyperthermia method works by producing nanoparticle suspensions that are highly effective in the early detection of tumors (Prijic and Sersa, 2011, p. 1). The magnetic nanoparticle hyperthermia method will be useful in the early detection of cancer because most cancer cases in Saudi Arabia are diagnosed late.

Nanotechnology will offer several advantages to the diagnosis, treatment and care of cancer patients in Saudi Arabia. Among the greatest advantages of nanotechnology over other cancer treatment methods is its early detection of cancer. This advantage emanates from the fact that, nanotechnology has a stronger accuracy and precision than conventional cancer detection methods (Mansoori et al, 2007, p. 226).

Precisely, electromagnetic technology aids in detecting DNA alterations at a very early stage in the development of cancer. In fact, advanced electromagnetic technology in cancer treatment helps in exclusively binding cancer cells and isolating normal cells (Mansoori et al, 2007, p. 226).

The second greatest advantage of nanotechnology is its accuracy in treating cancer because it has a stronger sense of precision and thoroughness when compared to conventional cancer treatment methods in Saudi Arabia (Mansoori et al, 2007, p. 226). In fact, the greatest promise that nanotechnology offers in cancer treatment is the fact that, it can destroy dangerous cancer cells, which have been normally resistant to conventional treatment methods.

Advanced electromagnetic nanotechnology is often combined with radiation therapy to focus cancer treatment on the specific cancer cells using laser light technology to destroy the cancer cells from within (Mansoori et al, 2007, p. 226). This treatment method improves cancer treatment.

It is through this technology that nanotechnology helps to focus drug treatment methods on the cancer cells. Future nanotechnology guarantees the alteration of cancer DNA, returning them back to normal cells. The above advantages will significantly improve the diagnosis, treatment and care of cancer patients in Saudi Arabia.

Conclusion

Though there are few statistics regarding the use of nanotechnology cancer treatment in Saudi Arabia, this paper highlights the use of nanotechnology as the future of cancer treatment, diagnosis and care in Saudi Arabia. Weighing the functionality of nanotechnology and its contribution to cancer treatment, we can establish that nanotechnology will greatly improve the efficiency and precision of cancer treatment in Saudi Arabia.

From a broader point of view, nanotechnology brings immense hope in the treatment of cancer such that if a person were diagnosed with cancer, this diagnosis should not amount to an automatic death sentence. However, the use of nanotechnology in Saudi Arabia needs to be understood from the understanding of paclitaxel-loaded gelatin nanoparticles, light absorption by gold nanoparticles and magnetic nanoparticle hyperthermia methods as the main forms of cancer treatment.

Since nanotechnology is more efficient and fast in treating cancer, the future of cancer treatment in Saudi Arabia is expected to change dramatically. Among the greatest advantages of nanotechnology treatment in Saudi Arabia, which is identified in this paper, is the efficiency associated with nanotechnology (Frank and Nowak, 2004, p. 291).

In fact, conventional cancer treatment methods (such as chemotherapy and radiation) are synonymous to cancer resurfacing, thereby warranting the use of higher dosages of cancer treatment drugs in the management of the disease. Nanotechnology eliminates the possibility of cancer resurfacing by making the entire treatment process more efficient.

References

Frank, S. A. & Nowak, M. A. (2004). Problems of Somatic Mutation and Cancer. BioEssays, 26(3), 291-299. Web.

Gold, L. S., Slone T. H., Manley, N. B., and Ames, B. N. (2002). Misconceptions about the Causes of Cancer. Vancouver, Canada: Fraser Institute. Web.

Huang, X., Jain, P., El-Sayed, I., & El-Sayed, M. (2007). Gold Nanoparticles: Interesting Optical Properties and Recent Applications in Cancer Diagnostics and Therapy. Nanomedicine, 2(5), 681-693. Web.

Mansoori , G., Mohazzabi, P., McCormack, P., & Jabbari, S. (2007). Nanotechnology in Cancer Prevention, Detection and Treatment: Bright Future Lies Ahead. World Review of Science, Technology and Sustainable Development, 4(2/3), 226-257. Web.

Prijic, S., & Sersa, G. (2011). . Radiol Oncol, 45(1), 1-16. Web.

Torchilin, V. P. (2007). Targeted Pharmaceutical Nanocarriers for Cancer Therapy and Imaging. The AAPS Journal, 9(2), 128-147. Web.

Technologies: Improving the MD Anderson Cancer Center Website

Search Engine Optimization (SEO)

Search engine optimization for the MD Anderson Cancer Center website can be achieved by installing plugins that possess extra features such as page navigation, thumbnail, and customized page numbers (Stokes, 2011). Specifically, this proposed system in Google will consist of a multi-tab page that will serve different areas and services to online customers.

The main categories may be treatment services ordering menu, e-newspaper/magazines, and brochures related to common cancer problems and their solutions, shopping (duty-free) for cancer consultancy options, and a guide on cost for each treatment package.

When implementing SEO in the Google search, it is necessary to revise the algorithms constantly for the search result of the MD Anderson Cancer Center website to remain at the top (Stokes 2011). This can be achieved through revising the content to ensure that all the information on the website pertains directly to the needs of potential clients.

Thus, constant blogging of the website and recruiting other independent bloggers to blog about the website will give the MD Anderson Cancer Center website a competitive advantage in marketing its products. This has been achieved by the Amazon and eBay websites since their SEO have been optimized and easy to access from a single search (Napier, Judd, Rivers, and Adams, 2003).

The SEO may also be tailored to include a unique cookie which is transferable to the users of the MD Anderson Cancer Center website. The unique cookie for the website will be transferred to all primary and secondary visitors of this site hence broadening the spread information on this website (Stokes 2011).

Optimizing the SEO has the potential of making the website go viral within six months since the unique cookie will spread to the primary and secondary users. However, the risk of using this option may be the high cost of constantly optimizing the SEO and hiring unprofessional bloggers who may compromise the elements of trust in dealing with the potential clients (Napier et al. 2003).

Social media advertising

Social media, especially Google, Linkedin, and Twitter, have gained popularity among companies and individuals who uses these sites as interaction modules to share experiences and exchange ideas. In the e-Marketing industry, social media has penetrated the communication environment and currently commands a large following among the users (Stokes 2011).

Reflectively, Google, Linkedin, and Twitter are ideal tools for branding and community following building for the MD Anderson Cancer Center website. Through ‘likes’ and ‘tweets,’ the customer base for the MD Anderson Cancer Center website will expand substantially over a short period.

To increase credibility and maintain professionalism, the current bomb internet channels used by the MD Anderson Cancer website for reaching the consumers should be tailored to encompass processes and features that flawlessly facilitate a healthy and lifetime relationship between the center and its clients.

For instance, the website should carry out a link reference promotion where the website user with the highest number of referral links is rewarded with a free cancer consultancy service or gift hampers. This will create long term loyalty among clients. The potential of the referral link approach is that it will improve the visibility of the MD Anderson Cancer Center website across the globe (Napier et al. 2003).

Finally, the MD Anderson Cancer Center should create a dynamic and functional team within its expansion structure to ensure the sustainability of the gains that will be made when the above recommendations are implemented.

References

Napier, H. A., Judd, P. J., Rivers, O. N., & Adams, A. (2003). E-business technologies. Boston, MA: Course Technology.

Stokes, R. (2011). E-Marketing: The essential guide to digital marketing. London, UK: Quirk e-Marketing (Pty) Ltd.

Progress in Cancer Control: Rhetorical Analysis

Rhetorical Analysis

For my study, I chose the article An assessment of progress in cancer control by Siegel et al. (2018). The article was chosen because of its relevance and societal relevance (2018 is the earliest of all the others). Problems related to cancer prevention and event management are precious for future research. In addition, the article is part of American Cancer Society (ACS) projects, which lends credibility to work because of its status.

Rhetorical Situation

The need for this article is justified by the widespread prevalence of cancer, which haunts many people, so society is concerned about their health. According to Siegel et al. (2018), the fight against cancer has lasted since the early 1900s through prevention and early detection. Consequently, the need for persuasion is justified by the lack of preventive measures to control cancer. The historical reason is the progress of medicine in technological support that can serve as tools to assess the likelihood of cancer.

Author

The authors of this article are ACS staff members who do research coming out of the standard and several visiting MDs. There is no personal credibility, but the collective work provided is credible. It is created by using specialized medical vocabulary, consistency in presentation, and coverage of issues that will be relevant to almost any reader. The authors appear knowledgeable and fair because they make an objective assessment using relevant research data and the openness of information in their work. Since almost all of the contributors are ACS, they create some credibility, and the article looks credible.

Purpose of Speech

The authors’ presentation aims to provide findings on the dynamics of cancer and the relationship to assumptions not previously addressed in medicine. Instead, the authors attack the reader, seeking to discourage drinking alcoholic beverages, smoking, and dietary extremes. According to their study, these behaviors are more likely to lead to cancer, and the authors’ goal is to convince the audience that they should take responsibility for their health and strive to minimize the triggers of cancer (Siegel et al. 2018). The authors seek to teach audiences about health care and show statistically valid connections.

Target Audience

The article’s target audience is the general public, who does not care about minimizing the triggers of cancer development. Siegel et al. (2018) summarize that more preventive measures should be used under the National Cancer Control Act. Based on this, audiences may be presented with a political asset that can influence budget allocation; however, these audiences probably do not fully recognize ethical values. A secondary audience may be individuals who suspect a predisposition to cancer and would like to seek help.

Content

The main message of Siegel et al. (2018) is that there is a need to strive to spread preventive measures because of the breadth of the cancer population. Siegel et al.’s (2018) arguments focus on the presence of high cancer mortality (including undetected), social inequalities (claims of racial and geographic differences), and disease outcomes. They use cause and effect to assess the relationship between prevention and cancer prevalence and compare differences in cancer outcomes across demographics. The authors instead appeal to reason, pointing to statistics as their most potent weapon.

Message Transmission Form

Siegel et al. (2018) use standard review articles, including an introduction, a statistics review, and a closing statement (conclusions). It is a literary genre using a specific technical (medical) style and a persuasive tone so that the audience imagines the seriousness of the issue being discussed. The central figure of speech is comparisons and forms like “if…, then…” to indicate the likely outcome of the course of cancer if no measures are taken to improve its prevention.

Correlation of Form and Content

It is a review article; Siegel et al.’s (2018) primary purpose is to reinforce the effects of the statistics and point out their potential and deterioration. Through the presence of comparisons, appeals to facts and statistics, and links to social inequalities, the authors reinforce their stance on cancer control. The presence of images and tables is one of the most vital tools of the form to help the reader visualize the harms of cancer and imagine the magnitude of the problem.

Implementation of Intent

The article’s message is spectacular and transparent because it contains facts and legitimate conclusions. The authors’ intent is achievable because it is non-contradictory, makes sense to themselves and the audience, and has a particular purpose. The authors reflect their messages because they belong to the scientific community, and their research is generally focused on the proposed topic, cancer control. The intended audience may react in two ways. Only a fraction will listen because political and economic circumstances impede prevention; however, secondary audiences will respond positively.

Nature of Communication

Siegel et al.’s (2018) communication is respectful and accessible; despite the terms they use, the authors express concerns clearly, grounding them in facts. According to the article, one can make assumptions about the scientific community as a whole: scientists are hardworking, persistent, operate with statistics, and genuinely care about the health of society. The article’s scientific style and form speak to the authors’ orderliness and their desire to deliver the material in an accessible format and to avoid lies or fabrications to embellish research results.

Reference

Siegel, R. L., Jemal, A., Wender, R. C., Gansler, T., Ma, J., & Brawley, O. W. (2018). . CA: A Cancer Journal for Clinicians, 68(5), 329–339. Web.

Reverse Mutation Concept in Cancer Biology

Evaluating 2-Aminoanthracene as a Possibly Cancerogenic Compound

In the environment where animal testing is not allowed, determining possible genotoxicity of a compound is possible with the help of the Ames test (Samiei et al. 121). The specified instrument represents a “bacterial reverse mutation assay” (Samiei et al. 121), which will ostensibly help detect a mutagenic compound. The test involves using the strains of Salmonella/E.coli. As a rule, the following strains are used to detect the presence of cancerogenic elements: “TA97, TA98, TA100, TA102, TA104, TA1535, TA1537, and TA1538” (U.S. Department of Health and Human Services). The test is based on the concept of reverse (back) mutation. The bacteria are cultured in the presence of 2-Aminoanthracene as a supposedly mutagenic compound and without histidine. In case Salmonella/E.coli becomes capable of producing histidine and continues to proliferate, the mutagenic nature of 2-Aminoanthracene will be proven (Ruiz-Pérez et al. 6743). Since the test is known for delivering false-positive results, the control tools such as TA98, TA98 and TA1538, TA100 and TA1535, and TA102 will have to be utilized (U.S. Department of Health and Human Services).

Human Oncogene in Fibroblasts: Cloning, Activity Analysis, and the Human Genome

To determine whether it is the human cellular oncogene that affects the development of the fibroblasts, one will have to consider using the DNA sequences known as Alu sequences as the key tool (Yang et al. 5812). Since Alu elements are typically viewed as the cause of human mutations, they will have to be used as the testing tool (Yang et al. 5812). The DNA sequence from the mouse cells will be isolated so that it could be cloned into the bacteriophage (Sherif and Broome 124). Using the transposon tagging framework, which implies tagging the genes that do not coincide with the regular process of gene expression, one will be able to detect the presence of the human cellular oncogene in the fibroblasts developed by the mice (Zhang et al. 3134). The hybridization of phage and the Alu probe will point to the presence of the human mutagen in the cell (Yang et al. 5813).

Defining the Possibility of Ras Being Responsible for the Cell Transformation

To test whether the phenotype was transformed by Ras, one will have to consider using a signaling inhibitor that will allow detecting the possibility of Ras being responsible for the malignant transformations in cells. Particularly, the application of the KIF2C protein will have to be considered to identify the ostensible connection between Ras and the transformation of cells. To be more specific, the use of KIF2C as the kinesin family member will allow inhibiting the activation of ERK1/2, which, in turn, spurs the mTORC1 activity in a mutated gene (Zaganjor 10568). Therefore, in case the activity mentioned above is observed in the mutant gene, the fact that it was Ras that triggered the transformation can be considered proven.

Mechanistic Role of Rb and Protein Mutations: What Produces the Transformed Phenotype

The Rb mechanism causes alterations in chromatin structures of cells (Scott et al. 28972). The abnormal expression of the gene may lead to cancer cells developing the ability to either activate or repress the process of gene transcription (Ferraro 196). As a result, the genomes of cancer cells can be reprogrammed so that the development of malignant elements could be stopped, activated, or aggravated (Lin and Zhao 388). The synonymous mutations that occur in the process include “G12, G13, and G60” (Waters e0163272).

Works Cited

Ferraro, Angelo. “Altered Primary Chromatin Structures and Their Implications in Cancer Development.” Cellular Oncology, vol. 39, no. 3, 2016, pp. 195-210. Web.

Lin, Run-Long, and Lu-Jun Zhao. “Mechanistic Basis and Clinical Relevance of the Role of Transforming Growth Factor-β in Cancer.” Cancer Biology & Medicine, vol. 12, no. 4, 2015, pp. 385-393. Web.

Ruiz-Pérez, Nancy J., et al. “Mutagenic and Antimutagenic Effects of Heterotheca Inuloides.” Scientific Reports, vol. 4, no. 1, 2014, pp. 6743-6748. Web.

Samiei, Mohammad, et al. “Investigating the Mutagenic Effects of Three Commonly Used Pulpotomy Agents Using the Ames Test.” Advanced Pharmaceutical Bulletin, vol. 5, no. 1, 2015, pp. 121-125. Web.

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The Cancer Cell Development: Causes and Sources

Conducting a reflective analysis after a section or topic is covered is a successful strategy for mastering academic material. It allows you to summarize the available data and structure them. Thus, it has been found that proto-oncogenes can turn into oncogenes by point mutations, chromosomal insertions, or deletions. At the same time, while suppressor genes are designed to inhibit oncogenesis, mutations in them can, on the contrary, lead to the amplification of harmful mutations. Loss of function of suppressor genes resulting from mutations becomes the cause of cancer development: the cell divides abnormally, increasing the cell mass of the tissue. In the same way, numerical statistics for oncogenes and suppressor genes were passed in class. I must admit that, in general, these are the numbers that I expected: a large number of suppressor genes are necessary to suppress oncogenes. At the same time, the survival rate for both categories is equal, which suggests that they are mutually related. It has also been shown that the maintenance gene can catalyze cancer development. It is worth noting that this is not a straightforward process: mutations in the maintenance system entail profound changes in defense mechanisms. The more significant number of oncogenes and suppressor genes responsible for cell survival determines the evolutionary driving forces that make cells remain viable even in the face of mutation. Zero oncogenes have been found in the support system, confirming the deleterious nature of such oncogenes. Finally, the dominance of suppressor genes over oncogenes in fate cells also has an explanation. Since differentiation is accompanied by mutations, the cell must protect itself in case of an unforeseen increase in oncogenicity.

Three key ideas have been assimilated by me within this topic. The first one concerns the diversity of sources of cancer cell development. In fact, it is a mistake to believe that cancer is initiated by only one factor: on the contrary, a combination of biological, physical, infectious, and even chemical causes can trigger cancer development. Secondly, I have learned that there is a complex mechanism of cancer cell formation involving proto-oncogenes, which, when amplified, can be modified to oncogenes. To suppress them, suppressor genes are activated, among which p53 is the best known. Finally, I have learned the relationship between age and the likelihood of developing cancer. As life expectancy increases, the number of mutations increases, and thus the likelihood of cancer increases. I found it amazing that science knows precisely what the frequency of mutations is: 1 error in a billion bases is deficient. In addition, I was struck by the information that the mutated gene is dominant. The question I still have involves the refinement of numerical statistics. If human DNA includes 3 billion base pairs — a total of six per DNA molecule — does this mean that only three harmful mutations are possible in a single cell?