The Underlying Pathophysiology of Cancer

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Introduction

Fundamentally cancer occurs from accumulated mutations in the genes which control cell proliferation and differentiation (Croce, 2008). Normal cells slowly and systemically replace dead ones via cell cycle consisting of growing, dividing, and dying phases, whereas cancer cells keep reproducing, and do not surrender to signals from body control (Cancer Research UK, 2010). Cancerous cells could invade nearby tissues, and even spread to other organs through lymph nodes or blood vessels, which might eventually lead to loss of adequate functions in the body system (Chang, Daly, & Elliott, 2006) As the second most common cancer in Australia, colorectal cancer is a major medical issue in Australia (Portelli, 2008). It is reported that Australia has more than 13,500 new cases of colorectal cancer every year (Cancer Council Australia, 2010). In this report, I will present the pathophysiology and adjuvant chemotherapy of colorectal cancer, how the gastrointestinal system might be influenced by it, and how a clinician should assess the symptoms and signs of patients in the course of post-surgery care, regarding a 65 year old indigenous woman.

Discuss the underlying pathophysiology of cancer and how this applies to Mrs Lane

1 Development of colorectal cancer

Colorectal cancer is a malignant neoplasm in the large intestine and generally limited locally for a long term before invasion and metastasis (The Cancer Council Australia & Australian Cancer Network, 2005). Adenomatous polyps on the wall of large intestine have possibility to grow into colorectal cancer and around 80% of tumours in the colon are developed through adenoma-carcinoma sequence over years (Kumar, Abbas, Fausto, & Aster, 2010). For instance, the loss of TSG on chromosome 5 or other in mucosa cells of the colon could lead normal epithelium to become hyperproliferative, making small, benign polyps. Further combinations of the loss of DNA methylation, activation of ras oncogene on chromosome 12, and loss of DCC on chromosome 18, transforms small polyps into larger benign polyps, or adenoma. On top of that, the loss of p53 TSG on chromosome 17 culminates in carcinoma (Marieb & Hoehn, 2010). Molecular alterations in the adenoma-carcinoma sequence are demonstrated in Figure 1 (Kumar, et al., 2010). Additional mutations contribute to metastasis, in which cancerous cells travel to other body organs via lymphatic or blood vessels, forming secondary cancer masses (Chang, et al., 2006). Intrusion into adjacent tissues and spreading to other organs differentiate cancer from benign neoplasm. Stage grouping of colorectal cancer according to the TNM (for tumours/nodes/metastasis) system is described in Table 1 (American Joint Committee on Cancer, 2009). Table 1. Stage grouping of colorectal cancer

|Stage |T |N |M | |Stage 0 |Tis |N0 |M0 | |Stage I |T1 |N0 |M0 | | |T2 |N0 |M0 | |Stage IIA |T3 |N0 |M0 | |Stage IIB |T4a |N0 |M0 | |Stage IIC |T4b |N0 |M0 | |Stage IIIA |T1–T2 |N1/N1c |M0 | |Stage IIIA |T1 |N2a...
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