Running head: COLON CANCER CASE STUDY 1
Colon Cancer Case
Study Name
Liberty University
, COLON CANCER CASE STUDY 2
Background
Ms. T is a 43-year-old Caucasian female who began to have abdominal pain with bloody
stools several months ago and made an appointment to see her primary care physician. Ms. T
was sent for a colonoscopy and was subsequently diagnosed with colon cancer. Family history
was found to be positive for colon cancer in the patient’s brother, father, uncle, and ovarian
cancer in her paternal grandmother. Ms. T is a former smoker who quit seven years ago. She
does not regularly drink alcohol or participate in the use of any illegal drugs. In addition to colon
cancer, Ms. T also has a history of hypertension and takes Lisinopril 5 mg every morning. She
denies any other current medications or allergies.
Pathophysiology
The process of changing healthy colon cells and tissue to colon cancer is a process which
does not have one cause, but a multitude of factors which all must come together to create
mutations in genetic expression. According to Doig and Huether (2014),
The gene mutations include: (1) activation of proto-oncogenes (promote cell growth: e.g.,
K-ras [retrovirus-associated DNA sequence] and BRAF); (2) loss of tumor-suppressor
gene activity (inhibit cell growth [e.g., APC, TP53, TFTB and SMAD4, DCC]; and (3)
abnormalities in DNA mismatch repair (MMR) genes (fix errors in DNA replication and
recombination, e.g., TGF, EGFR, hMSH1, hMSH2, hMSH6). (pp. 1470)
Most colon cancers begin in the colon in the form of benign polyps. A polyp is “a mass or
fingerlike projection arising from the intestinal mucosal epithelium” (Doig, & Huether, 2014, pp
1470). A polyp is created as the number of genetic changes begins to increase. The variations in
the genetic material allow the cell to reproduce more quickly than the normal cells within the
Colon Cancer Case
Study Name
Liberty University
, COLON CANCER CASE STUDY 2
Background
Ms. T is a 43-year-old Caucasian female who began to have abdominal pain with bloody
stools several months ago and made an appointment to see her primary care physician. Ms. T
was sent for a colonoscopy and was subsequently diagnosed with colon cancer. Family history
was found to be positive for colon cancer in the patient’s brother, father, uncle, and ovarian
cancer in her paternal grandmother. Ms. T is a former smoker who quit seven years ago. She
does not regularly drink alcohol or participate in the use of any illegal drugs. In addition to colon
cancer, Ms. T also has a history of hypertension and takes Lisinopril 5 mg every morning. She
denies any other current medications or allergies.
Pathophysiology
The process of changing healthy colon cells and tissue to colon cancer is a process which
does not have one cause, but a multitude of factors which all must come together to create
mutations in genetic expression. According to Doig and Huether (2014),
The gene mutations include: (1) activation of proto-oncogenes (promote cell growth: e.g.,
K-ras [retrovirus-associated DNA sequence] and BRAF); (2) loss of tumor-suppressor
gene activity (inhibit cell growth [e.g., APC, TP53, TFTB and SMAD4, DCC]; and (3)
abnormalities in DNA mismatch repair (MMR) genes (fix errors in DNA replication and
recombination, e.g., TGF, EGFR, hMSH1, hMSH2, hMSH6). (pp. 1470)
Most colon cancers begin in the colon in the form of benign polyps. A polyp is “a mass or
fingerlike projection arising from the intestinal mucosal epithelium” (Doig, & Huether, 2014, pp
1470). A polyp is created as the number of genetic changes begins to increase. The variations in
the genetic material allow the cell to reproduce more quickly than the normal cells within the
