Rectal adenocarcinoma
Introduction
Rectal adenocarcinoma arises from the epithelium cells lining the large intestines. The
main function of the rectum is the temporary storage of fecal matter before elimination. This
cancer is common at an advanced age, especially at age 60 years and above. Statistics show that
this type of cancer is found worldwide but common in areas where people consume food low in
fibre and high in fat content such as Australia, USA and Europe. The prevalence of rectal
adenocarcinoma in Australia is approximately 15,605 new cases every year (Melaku et al. 2018).
Also, as one advance in age, there is increased risk, especially at 85 years ad above. The risk of
being diagnosed with cancer is 1 in every 11 men and 1in every 16 women. The main risk factors
include hereditary conditions, family history of rectal cancer, diet, inflammatory bowel disease
and polyps (Van Den Eynde et al. 2017).
Pathophysiology of rectal adenocarcinoma
Normally, the mucosa of the large intestines regenerates after every six days, where the
crypt cells migrate from the base of the crypt to the surface. They then differentiate and mature
losing their ability to replicate. For adenocarcinoma to develop, three pathways exist. These are
the adenomatous polyposis coli (APC) gene adenoma-carcinoma pathway, hereditary
nonpolyposis colorectal cancer (HNPCC) pathway and ulcerative colitis dysplasia (McCance and
Huether 2018). In the APC pathway, several gene mutations are involved. First, the APC gene
becomes inactivated, allowing cellular replication at the crypt surface to remain unchecked
increasing cell division. With increased cell division, it causes inactivation of the K-ras oncogene
first the P-53 gene later, which are tumor suppressor genes. The loss of these genes then prevents
apoptosis and therefore, cell life is prolonged indefinitely, leading to cancer (Hall 2017).
In the HNPCC pathway, there is a mutation in DNA mismatch repair genes. These genes
are Hmlh1, hMSH2 and 6, hPMS 1and 2. This mutation, therefore, leads to negative DNA repair
resulting in cancer. Finally, in the ulcerative colitis pathway, genetic alteration is caused by
chronic inflammation as in inflammatory bowel disease and ulcerative colitis. This, in turn, leads
to dysplasia and cancer formation (Bullock and Hales 2019).

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