NURS 506 Week 4 Oncology Case Study 1 on Chronic Myeloid Leukemia Example

Oncology Case Study: Chronic-Phase Chronic Myeloid Leukemia in a 46-Year-Old Long-Haul Driver

Patient Background

The patient is a 46-year-old Black long-haul truck driver who presented to a rural clinic with six weeks of fatigue, night sweats, an unintended weight loss of 11 pounds, and fullness under the left ribs that made a full meal uncomfortable. On examination the spleen was palpable 8 cm below the left costal margin. The complete blood count showed a white cell count of 148,000/mm3 with neutrophils at every stage of maturation, increased basophils and eosinophils, 2% blasts in the blood, a platelet count of 612,000/mm3 and a hemoglobin of 11.2 g/dL. Quantitative polymerase chain reaction detected BCR::ABL1 transcripts, and bone marrow cytogenetics confirmed the Philadelphia chromosome with 3% marrow blasts, establishing chronic myeloid leukemia in chronic phase. Past history includes hypertension treated with amlodipine 5 mg daily and occasional omeprazole for heartburn on the road. There are no known drug allergies. Family history includes a parent with type 2 diabetes and no known blood cancers. The patient is married, has two teenagers, drives routes of 10 to 12 days, does not smoke, drinks alcohol rarely and is an active member of a Baptist congregation.

Pathophysiology at the Cellular Level

Chronic myeloid leukemia begins with one event in one pluripotent hematopoietic stem cell: a reciprocal translocation between the long arms of chromosomes 9 and 22, written t(9;22)(q34;q11). The shortened chromosome 22 that results is the Philadelphia chromosome. The break joins the 5' portion of the BCR gene on chromosome 22 to most of the ABL1 gene from chromosome 9, creating the fusion gene BCR::ABL1, which in chronic phase usually encodes a 210-kilodalton protein (Jabbour & Kantarjian, 2024).

The normal ABL1 protein is a tyrosine kinase that is tightly regulated; part of its structure folds back on itself and keeps the enzyme inactive until the cell needs it. In the fusion protein, the BCR segment replaces that regulatory region and adds a coiled-coil domain that makes the proteins pair and phosphorylate each other. The result is a kinase that is permanently on. It transfers phosphate groups from adenosine triphosphate to tyrosine residues on many substrate proteins and activates the main growth and survival pathways of the cell. Through RAS and the mitogen-activated protein kinase cascade, it drives proliferation without a growth factor signal. Through phosphatidylinositol 3-kinase and AKT, it blocks apoptosis, and through STAT5, it switches on genes for survival and cell cycle progression (McCance & Huether, 2019). The fusion protein also weakens the adhesion of progenitor cells to the bone marrow stroma, so immature cells leave the marrow early.

These molecular changes explain the patient's findings one by one. The leukemic clone expands but still matures, which is why the blood holds neutrophils at every stage rather than mainly blasts. The spleen enlarges as it filters and harbors the excess cells, causing the early fullness the patient described. Rapid cell turnover and cytokines produce fatigue, sweats and weight loss, and the crowding of normal red cell production causes the mild anemia. The kinase also impairs DNA repair, so additional mutations accumulate over time; without treatment, the disease tends to progress over several years to an accelerated and then a blast phase that behaves like acute leukemia.

Treatment follows the mechanism. Imatinib and the second-generation drugs dasatinib, nilotinib and bosutinib occupy the kinase's adenosine triphosphate binding site, so the enzyme cannot phosphorylate its substrates. Asciminib binds a different site, the myristoyl pocket, restoring the natural self-inhibition the fusion removed. In the ASC4FIRST trial, 74.1% of patients assigned asciminib reached a major molecular response at 96 weeks, compared with 52.0% of those assigned an investigator-selected inhibitor, and fewer stopped treatment because of side effects (Cortes et al., 2026). Mutations in the kinase domain, such as T315I, can cause resistance by blocking drug binding.

Holistic Plan of Care

Genetic Counseling and Testing

The patient asked whether the children should be tested. Counseling explains that BCR::ABL1 is a somatic mutation acquired in a blood stem cell, not inherited and not passed to offspring, so relatives need no testing. Genetic testing for the patient is ongoing instead: quantitative BCR::ABL1 testing on the International Scale every three months guides treatment, with kinase domain mutation testing if the response falls short (Jabbour & Kantarjian, 2024).

Physical Care

With the hematology team, the advanced practice nurse supports a daily oral inhibitor chosen with attention to comorbidities, goals and cost. Haddad et al. (2026) note that generic imatinib offers excellent value when survival is the goal, while second-generation drugs suit higher-risk disease or a goal of stopping treatment later. Allopurinol and hydration prevent tumor lysis in the first weeks. The plan reviews drug interactions, since omeprazole lowers the absorption of some inhibitors, and amlodipine and the inhibitor share liver metabolism. Blood pressure, glucose, lipids and an electrocardiogram are followed because several agents carry cardiovascular or metabolic risks.

Patient Education

Education centers on taking the drug every day as directed, because adherence predicts molecular response. The patient learns the specific timing and food rules of the chosen drug, how to manage common side effects such as fatigue, muscle cramps, rash and nausea, and when to call, such as for fever, shortness of breath or bleeding. The goal of treatment-free remission is explained honestly: some patients with a deep molecular response sustained for at least two years can stop therapy under close monitoring (Haddad et al., 2026).

Psychosocial Care

A long-haul route complicates laboratory visits and refills, so the plan schedules blood draws at a national laboratory chain along the route and mail-order refills to the patient's truck stops. In a survey of 146 Italian patients, 26% reported low or very low quality of life, with fatigue and muscle pain the most frequent problems, and patients wanted more information about supportive services (Abruzzese et al., 2026). The nurse screens for depression and financial strain, refers the patient to a social worker for copay assistance and discusses whether a temporary change in routes would help.

Spiritual and Cultural Care

The patient described faith as "the steering wheel" in hard times and asked the congregation to pray. The plan honors that by inviting the patient's pastor into the education visit if desired and offering chaplain support. Culturally, the nurse recognizes that Black patients may carry justified distrust from past inequities in research and care, so the plan explains every test plainly, invites questions and confirms that the treatment choice reflects the patient's priorities. Because the clinic is rural, telehealth follow-up reduces lost workdays.

References

Abruzzese, E., Annunziata, M., Bombaci, F., Russo Rossi, A., Galante, A., Misto, A., Valsecchi, D., Gushchina, E., & Fava, C. (2026). Unmet needs and quality of life burden in chronic myeloid leukemia: Results from a nationwide Italian real-world survey. Frontiers in Oncology, 16, Article 1846801. https://doi.org/10.3389/fonc.2026.1846801

Cortes, J. E., Hughes, T. P., Wang, J., Kim, D. W., Kim, D. D. H., Mayer, J., Goh, Y. T., le Coutre, P., Etienne, G., Kim, I., Andorsky, D. J., Bombaci, F., Issa, G. C., Takahashi, N., Kapoor, S., Jinwal, R., Malek, K., McCulloch, T., Yau, L., . . . Hochhaus, A. (2026). Asciminib demonstrates superior efficacy and safety in newly diagnosed chronic myeloid leukemia in the ASC4FIRST trial. Blood, 147(13), 1433-1446. https://doi.org/10.1182/blood.2025029210

Haddad, F. G., Jabbour, E., Breccia, M., Hehlmann, R., Malhotra, H., Nicolini, F. E., Stenke, L., & Kantarjian, H. (2026). SOHO state of the art updates and next questions: Choosing the best frontline BCR::ABL1 tyrosine kinase inhibitor in chronic myeloid leukemia: How to define the treatment value? Clinical Lymphoma, Myeloma and Leukemia, 26(2), 57-65. https://doi.org/10.1016/j.clml.2025.10.001

Jabbour, E., & Kantarjian, H. (2024). Chronic myeloid leukemia: 2025 update on diagnosis, therapy, and monitoring. American Journal of Hematology, 99(11), 2191-2212. https://doi.org/10.1002/ajh.27443

McCance, K. L., & Huether, S. E. (2019). Pathophysiology: The biologic basis for disease in adults and children (8th ed.). Elsevier.