Abstract Colon cancer is one of the leading causes of cancer-related deaths worldwide. Therefore, it is not a surprise that when Frank C. Garland proposed in 1980 that colon cancer risk is related to decreased Vitamin D levels in individuals, researchers worldwide rushed to test out his hypothesis. One environmental factor important in the production of Vitamin D, and therefore colon cancer research, is sunlight. It is common knowledge that exposure to sunlight is crucial for animals to make vitamin D out of sterols found on the skin. Through analyzing different research and data obtained from scholarly articles and research institutions, it is evident that higher exposure to sunlight correlates to a decreased chance in obtaining colorectal cancer.
Key words: Colorectal cancer, Vitamin D, CYP27B1, CYP24A1
Introduction Colon cancer, also known as colorectal cancer, is the third most commonly diagnosed cancer among men and women in the United States with an estimated account for 8-9% of cancer deaths (Dong et al, 2009). Despite screenings and
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Although the exact cause is unknown, it has been highly linked to low levels of vitamin D which may be caused due to low sunlight exposure. Many studies such as of that published by Dong et al in 2009 shows there to be a correlation between the colon cancer cases having a reduced exposure to UV sunlight per week than the colon cancer-free controls. Other evidence is found in a map of colon cancer cases by states in which one could observe that colon cancer cases tend to me more common in states within the Unites States with limited sunlight year round due to geographical and environmental reasons. Although finding a cure is very hard, the results of multiple studies show a significant association between an increase in colon cancer risk and decreased sun exposure and therefore decreased vitamin
Cancer is one of the 9 National Health Priority Areas (NHPA), areas which account for a significant portion of the burden of disease, but have sizeable potential for improvement. In Australia, CRC is the second most common cancer, after prostate (in men) and breast cancer (in women) (AIHW, Cancer incidence projections). The incidence has gradually increased (by 13% in males from 1982-2007) (AIHW, Cancer in Australia an overview). This is compounded by the ageing population and population growth, with 14,860 new cases in 2010 (http://www.cancer.org.au/about-cancer/types-of-cancer/bowel-cancer). This graph demonstrates this upward trend ((AIHW, Cancer incidence projections):
Marks, R., P.A. Foley, D. Jolley, K.R. Knight, and J. Harrison. 1995. The effect of regular sunscreen use on vitamin D levels in an Australian population: results of a randomized controlled trial. Archives of Dermatology 131: 415-421.
Colorectal cancer, or CRC, affects African American men and women more than Caucasians, at a rate 20% higher. This is concerning when faced with the mortality rates among African Americans, 28% higher for women and 14% higher for men than for Whites. African Americans are also more likely to be in later stages of the disease when diagnosed. There is a need to study and evaluate why these factors exist, as proper screening and early diagnosis can severely impact survival rates for CRC. One study attempts to find the solution through testing, however, this study slightly discredits itself along the way.
Colorectal cancers are thought to develop slowly over a period of several years. Before a true cancer develops, there usually are precancerous changes in the lining of the colon or rectum. These changes might be dysplasia or adenomatous polyps. A polyp is a growth of tissue into the center of the colon or rectum. Some types of polyps (hyperplastic polyps and inflammatory polyps) are not precancerous. However, having adenomatous polyps, also known as adenomas, does increase a person’s risk of developing cancer, especially if there are many polyps or they are large.
Since ancient times vitamin D has been the predominant cause of bone deficiencies.1 However, it was not in till the seventeenth century when both Dr. Daniel Whistler and Professor Francis Glisson made the first scientific description of a vitamin D deficiency.2 During the mid-seventeenth century there was an increase amount of children that were diagnosed with the bone disease called rickets.2 The cause of the rickets was determined to be associated to the lack of sunlight. A German researcher Kurt Huldschinsky came to the conclusion that when infants were exposed to ultraviolet light rays they became cured of rickets2. He stated that a substance in the skin was the potential source of the cure.2 In 1922, American scientist Elmer McCollum proved that when cod liver oil was heated; the beneficial effects of vitamin A in the oil were reduced.2 However, the oil remained effective in curing rickets leading McCollum to reason that a nutrient different from vitamin A was present in the oil. As a result, he named this nutrient vitamin D, which became the fourth vitamin to be discovered and named.2 Additionally, shortly after 1918, vitamin D was also discovered by an accidental experiment that included a group of scientists curing dogs affected with rickets by feeding cod liver oil to them.1
Colon cancer develops in the part of the gastrointestinal tract that absorbs water and minerals before waste products are disposed via the rectum. In women endometrial cancer is related to colon cancer. This type of cancer is the second leading cause of death due to cancer in the United States. Over one-hundred fifty thousand individuals will be diagnosed this year and this cancer will probably be responsible for about 47,900 deaths in 1999 (http://www.cancer.org). Most colon cancers are adenocarcinomas that develop from the glandular cells. Ninety percent of all colon cancer cases will develop in individuals after 50 years of age. Ninety percent of all tumors arise from polyps that are commonly found in people older than 50. Prevention includes regular exercise and a diet high in fiber. The most important risk factor is age. Medical screening includes a yearly blood occult test after age 50 and a colonoscopy every 3 years after age 50. Regular screening detects polyps that have become precancerous. If regular screening is not done, the cancer is not detected until blood is found in the...
Skin Cancer is caused by hereditary factors, overexposure to the sun, and weak immune systems. (“Skin Cancer” infotrac.com) One reason people tend to get skin cancer is when someone in your family has passed their genes down to you, known as hereditary. Normally hereditary is one of the causes in the development of melanoma. For all types of skin cancers, overexposure of the skin to UV radiation in sunlight is the most frequently blamed source of skin cancer. “Research suggests that sunburns received early in one’s childhood can lead to skin cancer later in life” (“Skin Cancer” infotrac.com). For example, when someone gets sunburned, you usually don’t know till ten to twenty years after and that’s why people don’t get skin cancer till they reach their twenties.
Vitamin D can often be obtained with two different methods. The main method is the conversion of 7-dehydrocholesterol in the skin into Vitamin D3 via sun exposure to absorb ultraviolet B radiation with a wavelength of 290-315nm (Holick 2007). The other method, is through consumption in diets through plants in the form of Vitamin D2; or fatty fishes, supplements or fortified vitamin D products in the form of Vitamin D3 (Lavie, Lee & Milani 2011). Vitamin D undergoes hydroxylation twice; first with the enzyme 25-hydroxylase to form 25-hydroxyvitamin D (Calcidiol) (Al Mheid et al. 2013). Then, Calcidiol is converted to the most active form of Vitamin D, 1,25-dihidroxyvitamin D Hormone (Calcitriol) with the help of renal 1--hydroxylase in the kidney (Al Mheid et al. 2013). Vitamin D2 and D3 are relatively similar since share the same hydroxylation pathway to produce Calcitriol (Tripkovic 2013), however, D3 has shown to have a greater influence on Calcidiol levels and thus more effective in maintaining Vitamin D health (Heaney et al. 2011).
The patient education brochure that I choose for this assignment connects colorectal cancer screening and scheduling colonoscopies. It was designed as an educational instrument as a health prevention tool by Indiana University Health for adult men and women. This brochure is specifically targeted for adult women and men, aged 50 and older with the special considerations of African American population beginning at age 45 and those who have had a family history of colon cancer to screen 10 years prior to when the family member had precancerous polyps, cancer or the age of 40 whichever comes first (Indiana University Health, 2012).
Cancer develops when cells in a part of the body begin to grow out of
How could your gut bacteria cause you colon cancer? According to the article, “Gut Microbes Combine to cause Colon Cancer, Study Suggests” They reported that there is two type of bacteria causing colon cancer according to recent research publications. There are two type of bacteria associated with colon cancer Bacteroides fragilis and E. coli, they are known to produce a layer in the intestine lining. According to this article, E. coli have toxin that can damage DNA of the colon cells. Additionally, B. fragilis produce another toxin that damage the DNA and inflames the cells. There bacteria are not common to everyone, but some people have them in their intestine. In their study, these toxins expel from bacteria cause cancer when put into mice.
Everyone is born with certain genetic mutations that make the them more likely to develop cancer in a later time in life. Though they might have a genetic feature, cancer will not develop unless triggered by environmental factors such as air and water pollution. As a matter of fact, my grandfather started smoking alongside consuming heavy amounts of alcohol around the age of 15, smoking and heavy alcohol intake have been considered as one of the potential causes of colon
The Authors, members of the Curtis Lab at Stanford University, propose and justify the Big Bang model for colorectal tumor growth. This model is dependent on several characteristics found in samples including the absence of selective sweeps, uniformly high intratumoral heterogeneity (ITH) and subclone mixing in distant regions. The model concludes that mutations occurring early in the tumor development will have a larger effect on overall tumor composition compared to later mutations in spite of the fitness advantages presented by either mutation. This model also provides a possible biomarker for determination of malignant vs benign phenotypes from the primordial tumor. Carcinomas were
It is a very fascinating thought that a single cell zygote contains all information required for the development of an organism. HOX genes called Homeobox are family of 39 transcription factors divided into 4 clusters A, B, C and D and are located on different chromosomes 7p15, 17q21.2, 12q13 and 2q31 (De Souza et al., 2010). HOX genes control the body plan of embryo along anterior-posterior axis and are expressed during embryonic development in highly coordinated manner and continue to express in virtually all tissues and organ throughout adult life (Terence et al., 2006). In addition of its role in development and subsequently in stem cell differentiation the HOX genes are
... into four different groups. The first group was given 400IU/day vitamin E alone, the second; 200ug/day selenium alone, the third; both and the fourth group; a placebo. The men were monitored over a median of six years. 529 men developed prostate cancer in the placebo group as compared to the 620 men in the vitamin E group who developed the disease. 575 men in the selenium group developed prostate cancer and 555 men in the combination group. The risk of prostate cancer in the United States is currently 16%. The results of the study showed that the risk of prostate cancer increased by 1.6% in men taking the vitamin E supplementation [6].