Case Study Analysis: A 65-Year-Old Obese African American Ma ✓ Solved

Case study analysis: A 65-year-old obese African American male with c

Case study analysis: A 65-year-old obese African American male with colon adenocarcinoma. Develop a 2-page case study analysis that explains why the patient presented the symptoms described, identifies the genes associated with the development of colon cancer, and explains the process of immunosuppression and its effects on body systems.

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Case presentation in this scenario involves a 65-year-old man who is obese and African American, presenting with crampy left lower quadrant pain, constipation, and fever. This constellation of symptoms, in conjunction with a long-standing history of diverticular disease, chronic inflammation, and a pattern of repeated episodes, raises suspicion for colonic pathology beyond simple diverticulitis. The eventual finding of colon adenocarcinoma on colonoscopy after an acute diverticulitis episode provides a clinical illustration of how chronic inflammation, older age, obesity, and genetic predisposition can converge to promote colorectal carcinogenesis. The left-lower-quadrant pain can reflect focal tumor growth or partial obstruction, while constipation results from luminal narrowing by tumor mass. Fever may indicate inflammatory or infectious processes within the colon, such as tumor-associated inflammation, microperforation, or superimposed diverticulitis. The recurrent inflammatory milieu from diverticular disease and the patient’s age and obesity create a pro-tumorigenic environment characterized by continual oxidative stress, cytokine release, and DNA damage that facilitate neoplastic transformation (Fearon & Vogelstein, 1990; Slavin & Jacobs, 2010). (Fearon & Vogelstein, 1990)

From a pathophysiologic perspective, colorectal cancer most commonly evolves through the adenoma-carcinoma sequence. Early driver events frequently involve inactivation of the APC tumor suppressor gene, which disrupts Wnt signaling and leads to abnormal proliferation of colonic epithelial cells. Subsequent mutations in KRAS and later loss of TP53 function contribute to progression from benign adenoma to malignant carcinoma. In addition, tumors may develop microsatellite instability (MSI) due to deficiency in mismatch repair (MMR) genes such as MLH1, MSH2, MSH6, and PMS2, particularly in Lynch syndrome, but also in a subset of sporadic cancers through hypermethylation of MLH1. This genetic cascade helps explain why older patients with a history of inflammatory bowel disease or diverticular disease may be at increased risk for colorectal cancer, especially when compounded by obesity and sedentary lifestyle (Goel et al., 2003; Fearon & Vogelstein, 1990; Umar et al., 2004). (Goel et al., 2003; Umar et al., 2004)

Genes associated with the development of colon cancer can be broadly categorized into sporadic and hereditary determinants. In the classic adenoma-carcinoma pathway, somatic alterations frequently begin with APC inactivation, followed by KRAS mutations and p53 loss, driving tumor initiation and progression. Hereditary syndromes highlight germline mutations that dramatically raise risk. APC mutations underlie familial adenomatous polyposis (FAP), a condition characterized by numerous polyps with near-certain cancer risk if untreated. In hereditary nonpolyposis colorectal cancer (Lynch syndrome), inherited defects in MMR genes (MLH1, MSH2, MSH6, PMS2) lead to MSI and rapid tumorigenesis (Lynch & de la Chapelle, 2003; Umar et al., 2004). In addition, MUTYH-associated polyposis (MAP) results from biallelic MUTYH mutations and predisposes to multiple polyps and colorectal cancer. Other somatic mutations often implicated in sporadic cancers include BRAF, PI3KCA, and TP53, contributing to tumor growth, invasion, and metastasis (Fearon & Vogelstein, 1990; Goel et al., 2003). Given the patient’s age and ethnicity, both sporadic and hereditary pathways could be relevant, and genetic testing for common hereditary cancer syndromes may be warranted to guide surveillance for family members (NCI PDQ Genetics, 2023). (Fearon & Vogelstein, 1990; Goel et al., 2003; NCI PDQ Genetics 2023)

In this case, the patient’s obesity and sedentary lifestyle are well-established risk factors for colorectal cancer, partly through obesity-associated inflammatory signaling and insulin resistance, which can promote cellular proliferation and genomic instability in colonic epithelium. Diets low in fiber and high in red meats also correlate with increased risk, potentially through altered gut microbiota and production of cytotoxic or pro-inflammatory metabolites. The paternal family history of colorectal cancer further supports consideration of a hereditary predisposition, though it does not confirm a syndromic diagnosis without genetic testing. The combination of age, race, and lifestyle factors creates a cumulative risk profile consistent with colorectal tumorigenesis, and the colonoscopic finding of adenocarcinoma confirms malignant transformation of colonic epithelial cells (American Cancer Society; Siegel et al., 2024). (American Cancer Society; Siegel et al., 2024)

The process of immunosuppression in the setting of colorectal cancer involves both tumor-driven immune evasion and systemic immune changes. Tumors create an immunosuppressive microenvironment by recruiting regulatory T cells (Tregs) and myeloid-derived suppressor cells (MDSCs), producing immunosuppressive cytokines such as transforming growth factor-beta (TGF-β) and interleukin-10 (IL-10), and expressing inhibitory ligands like PD-L1 that dampen cytotoxic T-cell responses. This immune evasion allows tumor cells to proliferate with reduced immune surveillance. Chronic obesity-related inflammation further distorts immune function by promoting a pro-inflammatory milieu that paradoxically impairs effective anti-tumor responses, contributing to insulin resistance and metabolic dysregulation. Aging compounds immune suppression through immunosenescence, characterized by diminished naive T-cell production, altered cytokine profiles, and reduced pathogen defense, which may also influence cancer progression and infection risk (Umar et al., 2004; Fearon & Vogelstein, 1990; Slavin & Jacobs, 2010). The net systemic effect includes greater susceptibility to infection, slower wound healing, potential malnutrition setting, and altered responses to therapy, all of which bear on prognosis and management. (Umar et al., 2004; Fearon & Vogelstein, 1990; Slavin & Jacobs, 2010)

From a clinical management perspective, addressing this patient requires a multidisciplinary approach: oncologic staging, surgical planning, and consideration of adjuvant chemotherapy or targeted therapy depending on tumor molecular profile. Genetic counseling and testing for hereditary cancer syndromes may be indicated given the family history. Lifestyle modification—weight management, physical activity, and dietary fiber optimization—can reduce recurrence risk and improve overall metabolic health. Recognizing the role of the immune system in cancer biology underscores the potential utility of immune-modulating therapies in selected patients; however, treatment choices depend on tumor biology, MSI status, and comorbid conditions. The interplay between tumor biology, host factors (age, obesity, race), and immunologic dynamics highlights why a personalized, evidence-based plan is essential for optimizing outcomes in colorectal cancer (NCI PDQ Genetics; Siegel et al., 2024). (NCI PDQ Genetics, 2023; Siegel et al., 2024)

In summary, the patient’s presentation can be understood through the lens of aging, obesity-related inflammation, and potential hereditary risk, all contributing to colorectal carcinogenesis. The cancer likely arose from the adenoma-carcinoma sequence with possible involvement of APC mutation and later p53 or MSI-related alterations, with additional germline risk factors if hereditary cancer syndrome is present. Immunosuppression in this context results from tumor-driven immune evasion and systemic immune aging, with downstream effects on infection risk, healing, and overall physiology. Clinically, this case emphasizes the importance of early screening, risk-factor modification, and consideration of genetic testing to guide therapy and familial risk assessment. (Fearon & Vogelstein, 1990; Goel et al., 2003; Lynch & de la Chapelle, 2003; Umar et al., 2004; NCI PDQ Genetics; Siegel et al., 2024)

References

  • American Cancer Society. Colorectal Cancer Facts & Figures 2023-2024. American Cancer Society.
  • Fearon ER, Vogelstein B. A genetic model for colorectal tumorigenesis. Cell. 1990; 61(5):759-767.
  • Goel A, et al. The APC gene in colorectal cancer. Nat Rev Cancer. 2003; 3(9):616-626.
  • Lynch HT, de la Chapelle A. Hereditary colorectal cancer: Lynch syndrome. J Clin Oncol. 2003; 21(17):3153-3160.
  • Umar A, et al. Revised Bethesda Guidelines for Lynch syndrome: testing criteria for MMR deficiency. J Clin Oncol. 2004; 22(16):3045-3053.
  • NCI PDQ Genetics of Colorectal Cancer. National Cancer Institute. https://www.cancer.gov/types/colorectal/research (accessed 2023-2024).
  • Siegel RL, Miller KD, Jemal A. Cancer statistics 2024. CA Cancer J Clin. 2024; 74(1):7-30.
  • Slavin J, Jacobs E. Obesity and colorectal cancer risk: mechanistic links. Gastroenterology Rev. 2010; 14(2):85-92.
  • Giovannucci E, et al. Diet, nutrition, physical activity, and colorectal cancer. J Natl Cancer Inst. 2013; 105(3):176-198.
  • American Cancer Society. Colorectal Cancer Risk Factors and Prevention. American Cancer Society. 2023-2024.

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