Colorectal Cancer Risk Assessment Essay

Colorectal Cancer Risk Assessment Essay

The study was conducted to identify the risk factors for colorectal cancer. The discussion is based on the objectives, the review of literature and research hypotheses specified in this study.
5.1 The objective of the study was to find the association between the case and control groups and various factors such as clinical variability, genetic, environmental, life style and dietary factors, and to identify significant risk factors of colo rectal cancer among the groups.
The chi square of the above specified objectives results report showed as below,
5.1.1. Clinical variability:

It includes factors like Diabetes mellitus, duration of DM, pregnancy, age at first pregnancy, number of live birth and duration of breast feeding.
5.1.1 (a). Diabetes mellitus

The analysis in table no 4.2.1(a) depicts association of the case and control group with their clinical variability like diabetes mellitus and duration of diabetes mellitus.

With regard to Diabetes mellitus, there is a significant association between years of DM and CRC at the level of p<0.05.

With regard to duration of diabetes mellitus, there is a significant association between duration of DM and colo rectal cancer at the level of p<0.05, and the corresponding odds ratio is 2.48 (DM for more than 5 years was referred to less than or equal to 5 years of DM). This shows that patients with DM for more than 5 years are having 2.48 times risk of developing colo rectal cancer.
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Mechanisms through which diabetes may be linked with the risk of colorectal cancer include the bowel transit times for diabetes patients is slower, this contribute increased exposure of colon on and rectal mucosa to carcinogenic substances, another mechanism involved is increased blood glucose level in diabetic patients elevates fecal bile acid concentrations which promotes CRC.

This finding was consistent with the results of meta analysis conducted by Yuhara, h., et al (2011) from EMBASE and MEDLINE databases of case control and cohort studies, in december 2009, analysis of those studies depicted that DM was significantly associated CRC, also from the results of 11 studies in men and 10 studies in women, DM is an risk factor for CRC.
5.1.1 (b).Breast feeding

The analysis in table no 4.2.1(b), there is a significant association between duration of breast feeding and CRC at the level of p<0.05 and its corresponding odds ratio is 0.11(breast feeding more than 12 months was referred to feeding for less than or equal to 12 months). Thus Breast feeding for more than 12 months was protective against colo rectal cancer.

The mechanism behind this factor is during breast feeding the estrodial level will fall. It is hypothesized that the estrogen causes cellular proliferation leading to CRC. Breast feeding result in lower lifetime estradiol exposure. Thus breast feeding reduces the risk of CRC.

This finding was supported by Lo, AC., et al (2010) conducted a case control study on lifestyle, occupational and reproductive factors and risk of CRC in Egypt. Lifestyle information was obtained from 421 CRC patients and 439 hospital controls history of pesticides exposure, increased frequency of eating food directly from farms were associated with CRC risk and parous women who have 7 or more live births or breast fed for 19 months or more has a significant lower risk of CRC, thus results depicted that agricultural and industrial exposure were associated with CRC, whereas prolonged lactation and increased parity were inversely associated with CRC.
5.1.1(c). Past history of colo rectal polyps

With regard to colo rectal polyps, 4.2.1(c) shows there is a significant association between past history of colo rectal polyps and CRC at the level of p <0.05.

Dr. Bert Vogelstein Scientists IN Johns Hopkins, discovered the procees of progression of colo rectal polyps into CRC, it occurs due to mutation of genes or due to any chemical changes resulting. Due to this change Colo rectal polyps develops then gradually turns to CRC. The genetic mutation occurs due to chromosomal alteration thus reducing tumor suppressor genes like P53, K-ras and APC and initiating more tumor promoter genes.
Fig 5.1.1.(c).i. OVogelgramÓ showing colo rectal polyp transition into CRC

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Vogelgram shows, colo rectal adenoma is belived as precursor of CRC..
5.1.1. (d) Past history of other cancer

With regard to history of any other cancer, table no 4.2.1(c) shows there is a significant association between past history of other cancer and colorectal cancer at the level of p <0.05.

The mechanism behind this either by metastasize or due to side effects treatment modalities like chemotherapy or radiation therapy which leads to cancers in other site like colon, rectum etc.
5.1.1.(e) History of constipation

With regard to constipation, table no 4.2.1(c) shows a significant association between constipation and CRC at the level of p <0.01and the corresponding odds ratio was 11.5(patients with the history of constipation was referred with patients without history of constipation), this suggests that patients with the history of constipation are 11.5 times risk of developing CRC.

The postulated causal link between constipation and increased colorectal cancer risk is that constipation causes longer transit times and which increase the duration of contact between the mucosa of colon and rectum and carcinogens like bile acids.

This finding was supported by Nicholas., et al (2011) conducted a case control study among 28,854 patients with chronic constipation and 86,562 controls without chronic constipation, results showed both colo rectal cancer and benign neoplasm were more prevalent among chronic constipation patients also analyses the risk of developing colo rectal cancer among patients with chronic constipation, was 1.78 times and risk of developing benign tumors was 2.7 times higher.
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5.1.2. Genetic factors:
5.1.2(a). Family history of colorectal polyps

The analysis in table 4.2.2 depicts association between family history of colo rectal polyps and CRC at the level of p <0.05.
5.1.2(b).Family history of CRC

The analysis in table 4.2.2 shows there is a significant association between family history of CRC and CRC at p<0.05.
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5.1.2(c).Family history of CRC

The analysis in table 4.2.2 depicts significant association between family history of cancer and CRC at p<0.001, the corresponding odds ratio was 17.4(patients with family history of cancer was referred with patients without family history of cancer).This shows that family history of cancer increases the risk of getting CRC by 17.4 times.

These finding was supported by Johns, LE., et al (2001) conducted a systematic review and meta-analysis of familial CRC risk in UK among 27 case control and cohort studies, weighted average was calculated from relative risk of all these studies result shows pooled estimates of relative risk as follows: a first-degree relative with CRC 2.25 (95% CI = 2.00-2.53), colon 2.42 (95% CI = 2.20-2.65), and rectal 1.89 (95% CI = 1.62-2.21) cancer; parent with CRC 2.26 (95% CI = 1.87-2.72); sibling with CRC 2.57 (95% CI = 2.19-3.02); more than one relative with CRC 4.25 (95% CI = 3.01-6.08); relative diagnosed with CRC before age 45, 3.87 (95% CI = 2.40-6.22); and a relative with colo rectal adenoma 1.99 (95% CI = 1.55-2.55), thus this study provides a strong evidence that CRC is more among those with family history of CRC and colo rectal adenoma.

The mechanism behind all the above genetic factors involves, there are certain Colon Cancer Genes , mutations of these genes known to cause predisposition to CRC and are inherited in an autosomal dominant fashion or autosomal recessive fashion. Inheritance risk is 50% for both males and females. When a parent carries an autosomal dominant genetic predisposition, each child has a 50% chance of inheriting the predisposition. The risk is the same for both male and female children.
5.1.3.Lifestylefactors:
5.1.3(a).Smoking

Table no 4.2.3(a) shows association of smoking and CRC.

With regard to smoking status, shows, there is a significant association between smoking status and CRC at p<0.01.

With regard to forms of smoking, there is a significant association between forms of smoking and CRC at p<0.001. Odds ratio is 6.7(beedi smokers referred to other forms of smokers).Thus it is evident that beedi smokers are 6.7 times risk of developing CRC.

With regard to duration of smoking, there is a significant association between duration of smoking and colo rectal cancer at p < 0.01.

With regard to frequency of smoking, there is a significant association between frequency of smoking and Colo rectal cancer at p<0.01, Odds ratio is 3(smoking more than 6 times per day was referred to smoking less than or equal to 6 times per day).This shows that smokers who smokes more than 6 times are 3 times risk of developing colorectal cancer.

The mechanism of smoking towards its causation of CRC involves: Tobacco and nicotine present in cigarettes are carcinogens disseminated throughout your body while inhaling, this mutate the cells and causes cellular changes that lead to cancer of colon or rectum and the bits of tobacco swallowed result in mixing up of chemicals with saliva which ends up in the colon, thus these carcinogens comes direct contact with mucosa of colon or rectum resulting in cancer.

This result was supported by Phipps, AI., et al (2011) conducted a case control study samples were selected from 13 countries of USA during the year 1998-2007 who were diagnosed to have CRC and selected by registry of epidemiology, surveillance and End result cancer through telephone. Information was collected regarding history of smoking and alcohol consumption. The result showed CRC related mortality was higher among smokers than non smokers.
5.1.3(b). Alcoholism

Table 4.2.3(b) depicts association of alcoholism and CRC.

With regard to type of alcohol intake, there is a significant association between type of drinkers and colo rectal cancer at p < 0.01. Odds ratio is 10.66(regular drinkers referred to other type of drinkers).This shows that regular drinkers are 10.66 times risk of developing colorectal cancer.