Advanced Oncology Nursing Exam –
Certification Competency Review.
Original practice questions covering AOCNP competency domains.
Not actual ONCC exam questions.
Total Questions: 50
DOMAIN BREAKDOWN:
• Cancer Biology & Pathophysiology: Q1-Q7
• Systemic Therapies: Q8-Q17
• Symptom Management: Q18-Q29
• Oncologic Emergencies: Q30-Q36
• Survivorship & Palliative Care: Q37-Q42
• Genetics & Hereditary Syndromes: Q43-Q46
• Evidence-Based Practice & Clinical Trials: Q47-Q50
QUESTION 1 — Cancer Biology & Pathophysiology
------------------------------------------------------------
A 58-year-old patient is diagnosed with stage III colon adenocarcinoma. Molecular testing reveals
microsatellite instability-high (MSI-H) status and BRAF V600E mutation. Which underlying
molecular mechanism best explains the MSI-H phenotype?
A. Defective DNA mismatch repair (MMR) leading to accumulation of replication errors
B. Activation of the PI3K/AKT/mTOR pathway promoting cell survival
C. Overexpression of human epidermal growth factor receptor 2 (HER2)
D. Homologous recombination deficiency causing double-strand break repair failure
✓ CORRECT ANSWER: A
RATIONALE: MSI-H results from defective DNA mismatch repair, most commonly due to MLH1
promoter hypermethylation or germline mutations in MMR genes (Lynch syndrome). This leads to
accumulation of insertion/deletion mutations in microsatellite regions. BRAF V600E often co-
occurs with sporadic MLH1-methylated tumors and helps distinguish sporadic from hereditary
cases.
,================================================================================
QUESTION 2 — Cancer Biology & Pathophysiology
------------------------------------------------------------
A patient with metastatic melanoma has a tumor biopsy showing BRAF V600E mutation. The
oncologist explains that this mutation leads to constitutive activation of which signaling cascade?
A. JAK-STAT pathway
B. RAS-RAF-MEK-ERK (MAPK) pathway
C. Wnt/β-catenin pathway
D. NF-κB pathway
✓ CORRECT ANSWER: B
RATIONALE: BRAF is a serine/threonine kinase that activates MEK1/2, which then phosphorylates
ERK1/2. The V600E mutation causes constitutive activation of this RAS-RAF-MEK-ERK cascade,
driving uncontrolled cellular proliferation. BRAF/MEK inhibitors (vemurafenib, dabrafenib,
trametinib) target this pathway.
================================================================================
QUESTION 3 — Cancer Biology & Pathophysiology
------------------------------------------------------------
A breast cancer specimen demonstrates strong, complete membrane staining for HER2 on
immunohistochemistry (IHC 3+). Which molecular event is primarily responsible for the oncogenic
effects of HER2 overexpression?
A. Activation of receptor tyrosine kinase signaling promoting cell proliferation and survival
B. Inhibition of apoptosis via downregulation of caspase enzymes
C. Enhanced DNA repair through upregulation of BRCA1/2 expression
D. Promotion of angiogenesis through direct VEGF receptor activation
✓ CORRECT ANSWER: A
RATIONALE: HER2 (ERBB2) is a receptor tyrosine kinase. Overexpression leads to
homodimerization/heterodimerization and constitutive activation of downstream signaling via
, PI3K/AKT and RAS-RAF-MEK-ERK pathways, driving proliferation, survival, and metastasis.
Trastuzumab and pertuzumab target the extracellular domain to inhibit this signaling.
================================================================================
QUESTION 4 — Cancer Biology & Pathophysiology
------------------------------------------------------------
During tumor board discussion, the pathologist notes that a patient's lung adenocarcinoma
expresses PD-L1 (TPS 75%). Which immunologic concept explains how PD-L1 expression on
tumor cells promotes immune evasion?
A. PD-L1 binding to PD-1 on T cells induces T-cell exhaustion and anergy
B. PD-L1 activates regulatory T cells to suppress cytotoxic T-cell function
C. PD-L1 directly inhibits natural killer cell-mediated cytotoxicity
D. PD-L1 promotes dendritic cell maturation and antigen presentation
✓ CORRECT ANSWER: A
RATIONALE: PD-L1 on tumor cells binds to PD-1 on activated T cells, delivering an inhibitory
signal that promotes T-cell exhaustion, reduces cytokine production (IFN-γ), and induces
apoptosis. High PD-L1 expression (≥50% TPS) predicts better response to PD-1/PD-L1 inhibitors
like pembrolizumab in NSCLC.
================================================================================
QUESTION 5 — Cancer Biology & Pathophysiology
------------------------------------------------------------
A patient with ovarian cancer has germline testing that identifies a pathogenic BRCA1 variant.
Which DNA repair mechanism is primarily impaired in this patient?
A. Base excision repair
B. Nucleotide excision repair
C. Homologous recombination repair
D. Non-homologous end joining
✓ CORRECT ANSWER: C
Certification Competency Review.
Original practice questions covering AOCNP competency domains.
Not actual ONCC exam questions.
Total Questions: 50
DOMAIN BREAKDOWN:
• Cancer Biology & Pathophysiology: Q1-Q7
• Systemic Therapies: Q8-Q17
• Symptom Management: Q18-Q29
• Oncologic Emergencies: Q30-Q36
• Survivorship & Palliative Care: Q37-Q42
• Genetics & Hereditary Syndromes: Q43-Q46
• Evidence-Based Practice & Clinical Trials: Q47-Q50
QUESTION 1 — Cancer Biology & Pathophysiology
------------------------------------------------------------
A 58-year-old patient is diagnosed with stage III colon adenocarcinoma. Molecular testing reveals
microsatellite instability-high (MSI-H) status and BRAF V600E mutation. Which underlying
molecular mechanism best explains the MSI-H phenotype?
A. Defective DNA mismatch repair (MMR) leading to accumulation of replication errors
B. Activation of the PI3K/AKT/mTOR pathway promoting cell survival
C. Overexpression of human epidermal growth factor receptor 2 (HER2)
D. Homologous recombination deficiency causing double-strand break repair failure
✓ CORRECT ANSWER: A
RATIONALE: MSI-H results from defective DNA mismatch repair, most commonly due to MLH1
promoter hypermethylation or germline mutations in MMR genes (Lynch syndrome). This leads to
accumulation of insertion/deletion mutations in microsatellite regions. BRAF V600E often co-
occurs with sporadic MLH1-methylated tumors and helps distinguish sporadic from hereditary
cases.
,================================================================================
QUESTION 2 — Cancer Biology & Pathophysiology
------------------------------------------------------------
A patient with metastatic melanoma has a tumor biopsy showing BRAF V600E mutation. The
oncologist explains that this mutation leads to constitutive activation of which signaling cascade?
A. JAK-STAT pathway
B. RAS-RAF-MEK-ERK (MAPK) pathway
C. Wnt/β-catenin pathway
D. NF-κB pathway
✓ CORRECT ANSWER: B
RATIONALE: BRAF is a serine/threonine kinase that activates MEK1/2, which then phosphorylates
ERK1/2. The V600E mutation causes constitutive activation of this RAS-RAF-MEK-ERK cascade,
driving uncontrolled cellular proliferation. BRAF/MEK inhibitors (vemurafenib, dabrafenib,
trametinib) target this pathway.
================================================================================
QUESTION 3 — Cancer Biology & Pathophysiology
------------------------------------------------------------
A breast cancer specimen demonstrates strong, complete membrane staining for HER2 on
immunohistochemistry (IHC 3+). Which molecular event is primarily responsible for the oncogenic
effects of HER2 overexpression?
A. Activation of receptor tyrosine kinase signaling promoting cell proliferation and survival
B. Inhibition of apoptosis via downregulation of caspase enzymes
C. Enhanced DNA repair through upregulation of BRCA1/2 expression
D. Promotion of angiogenesis through direct VEGF receptor activation
✓ CORRECT ANSWER: A
RATIONALE: HER2 (ERBB2) is a receptor tyrosine kinase. Overexpression leads to
homodimerization/heterodimerization and constitutive activation of downstream signaling via
, PI3K/AKT and RAS-RAF-MEK-ERK pathways, driving proliferation, survival, and metastasis.
Trastuzumab and pertuzumab target the extracellular domain to inhibit this signaling.
================================================================================
QUESTION 4 — Cancer Biology & Pathophysiology
------------------------------------------------------------
During tumor board discussion, the pathologist notes that a patient's lung adenocarcinoma
expresses PD-L1 (TPS 75%). Which immunologic concept explains how PD-L1 expression on
tumor cells promotes immune evasion?
A. PD-L1 binding to PD-1 on T cells induces T-cell exhaustion and anergy
B. PD-L1 activates regulatory T cells to suppress cytotoxic T-cell function
C. PD-L1 directly inhibits natural killer cell-mediated cytotoxicity
D. PD-L1 promotes dendritic cell maturation and antigen presentation
✓ CORRECT ANSWER: A
RATIONALE: PD-L1 on tumor cells binds to PD-1 on activated T cells, delivering an inhibitory
signal that promotes T-cell exhaustion, reduces cytokine production (IFN-γ), and induces
apoptosis. High PD-L1 expression (≥50% TPS) predicts better response to PD-1/PD-L1 inhibitors
like pembrolizumab in NSCLC.
================================================================================
QUESTION 5 — Cancer Biology & Pathophysiology
------------------------------------------------------------
A patient with ovarian cancer has germline testing that identifies a pathogenic BRCA1 variant.
Which DNA repair mechanism is primarily impaired in this patient?
A. Base excision repair
B. Nucleotide excision repair
C. Homologous recombination repair
D. Non-homologous end joining
✓ CORRECT ANSWER: C
