Writing and Publishing Scientific Articles Course Workbook

3-16

Writing and Publishing Scientific Articles

Example of an Introduction Needing Improvement (Basic Science Study)

UC [Abbreviation should be defined] is a chronic disease characterized by inflammation of the mucosa and submucosa of the large intestine. UC and Crohn’s disease are the 2 main types of inflammatory bowel disease. The incidence of UC is approximately the same in men and women. [Preceding 2 sentences provide unnecessary background information] Increasing duration and severity of UC correlate directly with an increased propensity to develop CR [What does “CR” mean?] carcinoma (1,2). For patients who have had UC for >20 years, the incidence of colorectal cancer is 10- to 20-fold greater than that of the general population, and the average age of onset is 20 years earlier (3). Sporadic CR carcinoma arises from adenomatous polyps. UC-associated CR carcinoma progresses from areas of dysplastic mucosa. [Transition words could be added to preceding sentences to help show how they are connected] The molecular events that facilitate the progression of adenoma to carcinoma in sporadic CR cancer have been well investigated (4). Identifying the events involved in progression of UC mucosa to dysplasia and carcinoma would allow us to identify patients with UC at increased risk for developing CR carcinoma. [Gap is implied (there must not be much information available about molecular events in progression of UC to colorectal carcinoma) but not explicitly stated] Inactivation of the p53 tumor suppressor gene is common in both sporadic and UC-associated CR carcinoma (4–6). Point mutation and loss of heterozygosity are the most commonly reported mechanisms resulting in p53 inactivation. Other genetic and epigenetic factors have been shown to modify p53 activity as well. [What is the connection between the preceding paragraph and the first paragraph of the Introduction?] MDM-2 is inhibited by p14 ARF (8). Homozygous deletion of the p14 ARF locus has been reported in a variety of cancers (9–13), and gene knockout of p14 ARF correlates with tumorigenesis (14). [What is the relationship between MDM-2 and UC?] In addition to mutation, the p14 ARF gene can be epigenetically inactivated through hypermethylation of its normally unmethylated CpG island. Esteller et al. (15) demonstrated that p14 ARF hypermethylation occurs frequently in sporadic colorectal cancer. In the study reported here, we examined p14 ARF hypermethylation in clinical samples ranging from nonneoplastic UC mucosa to CR carcinoma. [Why did they do this? What was their hypothesis?]

Adapted from the well-written introduction in Fumiaki Sato F et al. Hypermethylation of the p14 ARF gene in ulcerative colitis–associated colorectal carcinogenesis. Cancer Res 62:1148–1151, 2002.

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