Facts read from oncc.org · last checked Nov 7, 2026
Area I follows a patient from risk assessment through diagnosis and treatment planning to survivorship and the end of life. At 28% of scored questions it is second only to treatment and supportive care.
Practice questions
60 questions written to the AOCNP outline; each choice is explained once you pick.
Screening and prevention: populations at higher risk, screening and early detection, screening survivors for second cancers, hereditary risk assessment.
Assessment and diagnosis: imaging and other diagnostics, biomarkers, performance status, staging, treatment planning from pathology, reproductive planning.
Plan of care: guideline-based care, navigation, survivorship care plans, surveillance for recurrence, interprofessional care, end-of-life care.
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Hereditary risk: who gets referred
NCCN's genetic and familial high-risk assessment guidelines (one for breast, ovarian, pancreatic and prostate cancer; one for colorectal, endometrial and gastric) set the referral criteria. Two rules come up repeatedly:
Germline testing by diagnosis alone: NCCN supports it for every patient with pancreatic adenocarcinoma or epithelial ovarian cancer, and for metastatic prostate cancer and male breast cancer, whatever the family history.
Universal tumor screening: every colorectal and endometrial cancer is tested for mismatch-repair deficiency or microsatellite instability, which screens for Lynch syndrome.
Family history still matters for everyone else, and the pattern (young ages, several generations, rare tumors) points to which syndrome.
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Survivorship care plans and second cancers
A survivorship care plan sums up the diagnosis and treatment received, names the late effects to watch for, and says who does the follow-up. Surveillance should match the guideline for that cancer rather than a general habit of ordering tests.
Second cancers belong here too. Survivors of chest radiation for a childhood or young-adult cancer follow the Children's Oncology Group long-term follow-up guidelines, which set an earlier and more intensive breast schedule than the average-risk one.
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16 questions from risk to follow-up
0 / 16 answered16 questions
Tap an option: why each one is right or wrong appears under it.
Cancer Continuum · 28%
Which result does the APRN identify as a predictive, rather than purely prognostic, biomarker?
Lymphovascular invasion raises the risk of nodal and distant spread, a prognostic finding rather than a guide to a specific therapy.
High grade predicts aggressive behavior and recurrence risk, but it does not identify which drug will work.
LDH is a prognostic factor in melanoma staging, signaling worse outcome regardless of which therapy is given.
A predictive biomarker forecasts benefit from a specific drug, and HER2 amplification predicts response to trastuzumab and other HER2-directed therapy.
A 25-year-old with a RET pathogenic variant (MEN2A) is scheduled for prophylactic thyroidectomy. Which test must be completed before the operation?
Prolactin screens for pituitary adenoma, another MEN1 feature; MEN2A involves the thyroid C cells, adrenal medulla, and parathyroids.
MEN2A carries a high risk of pheochromocytoma, and an unrecognized one can trigger a hypertensive crisis under anesthesia, so plasma free metanephrines are checked and any tumor removed before thyroidectomy.
Urine 5-HIAA detects serotonin-secreting neuroendocrine (carcinoid) tumors, which are not part of MEN2A.
Gastrin screens for gastrinoma, a MEN1 tumor; ordering it mixes up the two MEN syndromes.
A patient with Hodgkin lymphoma has cervical and mediastinal nodal disease plus splenic involvement, no extranodal disease, and drenching night sweats. The stage is:
IIIA is the right anatomic stage but ignores the night sweats, which add the B designation.
Stage IV means diffuse or disseminated extralymphatic involvement such as liver, lung, or marrow; the spleen is lymphoid and does not make it stage IV.
Stage II requires all disease on one side of the diaphragm; the spleen lies below it, so this is stage III.
Nodes above the diaphragm plus the spleen, which counts as lymphatic tissue, define stage III, and drenching night sweats are a B symptom.
A 45-year-old with Crohn colitis and primary sclerosing cholangitis has a new dominant biliary stricture on MRCP and a rising CA 19-9. The APRN's next step is:
Ursodiol does not change PSC outcomes or treat malignancy, and CA 19-9 alone cannot separate cholangitis from cancer, so trending it delays tissue diagnosis.
A new dominant stricture with rising CA 19-9 in PSC must be sampled for cholangiocarcinoma, and ERCP with brush cytology plus FISH gives tissue and allows stenting in the same procedure.
Annual imaging is the surveillance plan for stable PSC; a new dominant stricture with a rising marker changes that, and waiting a year could miss a resectable cancer.
Liver biopsy samples parenchyma, not the bile duct stricture, so it cannot confirm or exclude cholangiocarcinoma.
A patient with stage III high-grade serous ovarian cancer and a germline BRCA1 variant has a complete response to first-line platinum chemotherapy. The APRN anticipates:
Checkpoint inhibitor maintenance has no established role in first-line high-grade serous ovarian cancer; the BRCA result, not PD-L1, drives the choice.
Observation was the standard before PARP inhibitors; with a germline BRCA1 variant it now gives up a proven benefit.
In SOLO-1, olaparib maintenance after response to first-line platinum gave a large, durable progression-free survival benefit in BRCA-mutated advanced ovarian cancer, so a PARP inhibitor is standard here.
Letrozole maintenance is used mainly for low-grade serous carcinoma, which is hormone-driven; high-grade serous BRCA-associated disease is managed with a PARP inhibitor.
A patient with stage IV lung cancer can manage limited self-care but spends more than half of waking hours in bed or a chair. The ECOG performance status is:
ECOG 3 describes a patient capable of only limited self-care who is confined to bed or chair for more than half of waking hours, exactly this description.
ECOG 4 means completely disabled, with no self-care and total confinement to bed or chair; this patient still manages some self-care.
ECOG 1 is restriction only in strenuous activity with full ambulation, a far more functional patient.
ECOG 2 patients are ambulatory, capable of all self-care, and up and about more than half of waking hours; the 50% line is crossed the other way here.
A 32-year-old has about 100 colorectal adenomas. His parents have no polyps, and his brother has 40 adenomas. The APRN suspects biallelic pathogenic variants in:
About 100 adenomas in two brothers with unaffected parents fits autosomal recessive inheritance, the hallmark of MUTYH-associated polyposis, which needs biallelic variants.
APC causes dominant familial adenomatous polyposis, so an affected parent is expected unless the variant is de novo; two affected siblings with clear parents point to recessive MUTYH.
MLH1 causes Lynch syndrome, which produces few adenomas that progress quickly, not a polyposis picture of dozens to hundreds.
STK11 causes Peutz-Jeghers syndrome with hamartomatous polyps and mucocutaneous pigmentation, not adenomatous polyposis.
A 34-year-old with many dysplastic nevi has a mother with two primary melanomas and a maternal uncle with pancreatic cancer. The APRN suspects:
BAP1 variants cause uveal and cutaneous melanoma with mesothelioma and renal cancer; dysplastic nevi with pancreatic cancer is the CDKN2A picture.
Peutz-Jeghers does raise pancreatic cancer risk, but it shows lip and buccal freckling with hamartomatous polyps rather than atypical moles and melanoma.
Multiple dysplastic nevi, melanoma in relatives, and pancreatic cancer in the family are the pattern of familial atypical multiple mole melanoma from CDKN2A variants, which also warrant pancreatic surveillance.
Cowden syndrome presents with trichilemmomas, macrocephaly, and breast, thyroid, and endometrial cancer, not dysplastic nevi with melanoma.
A 62-year-old had stage III colon cancer resected 18 months ago. CEA has risen from 2.1 to 9.8 ng/mL on two draws, and the exam is normal. The APRN orders:
PET/CT is used when CT is negative or equivocal, or before metastasectomy, not as the first test for a rising CEA.
Waiting 6 months after a confirmed rise lets potentially resectable recurrence grow beyond cure; a reproducible rise needs imaging now.
Systemic therapy is not restarted on a marker alone; the disease is located and its resectability judged first.
A confirmed CEA rise after resection signals likely recurrence, and contrast CT of the chest, abdomen, and pelvis is the first step to find disease that may still be resected, such as an isolated liver or lung metastasis.
A 58-year-old embalmer with 30 years of formaldehyde exposure has new unilateral serous otitis media and a painless upper neck mass. The APRN orders:
A neck mass brings the thyroid to mind, but the ear finding localizes the problem to the nasopharynx, which ultrasound cannot see.
Treating adult unilateral effusion as routine otitis media is the classic delay in nasopharyngeal cancer; a new effusion with a neck mass needs direct visualization.
New unilateral serous otitis media with a neck mass in an adult suggests a nasopharyngeal tumor blocking the eustachian tube, and formaldehyde exposure adds to that risk, so the nasopharynx is examined and biopsied.
Upper endoscopy examines the esophagus and stomach and does not reach the nasopharynx behind the nose.
A patient with newly diagnosed lung adenocarcinoma has headaches and word-finding difficulty; a noncontrast head CT shows a 1.2 cm left frontal lesion. The APRN orders:
Whole-body PET-CT stages the body, but normal gray matter takes up FDG avidly, so it is poor at detecting brain metastases.
Contrast CT is better than noncontrast CT but still misses small metastases that MRI shows, so it is kept for patients who cannot have MRI.
Gadolinium-enhanced MRI is the most sensitive test for brain metastases; it finds additional small lesions that decide between radiosurgery and whole-brain radiation.
Repeating the same noncontrast study adds nothing about lesion number or enhancement.
A 55-year-old's lung adenocarcinoma was staged cT2a N0 M0 before lobectomy. Pathology shows a 3.8-cm tumor, 3 of 16 nodes positive including mediastinal station 4R, and negative margins; EGFR and ALK testing are negative. The APRN plans:
Adjuvant osimertinib requires an EGFR exon 19 deletion or L858R mutation; with EGFR testing negative it has no role.
Unexpected mediastinal (N2) nodes upstage the cancer to stage III, where platinum-based adjuvant chemotherapy improves survival; with EGFR and ALK negative, PD-L1 and the chosen agent then guide adjuvant immunotherapy.
PORT for completely resected N2 disease did not improve survival in Lung ART and does not treat micrometastases.
Planning by clinical stage after pathology shows nodal disease keeps the patient on a plan for a lower stage; the pathologic stage governs adjuvant therapy.
Plasma ctDNA NGS in a never-smoker with newly diagnosed metastatic lung adenocarcinoma detects no driver alterations. The APRN's next step is:
A negative plasma test can reflect low tumor DNA shedding, so tissue NGS is done before calling a never-smoker's adenocarcinoma driver-negative.
Targeted therapy is given only for a confirmed driver; treating empirically exposes the patient to toxicity without expected benefit.
Starting chemoimmunotherapy before tissue results risks missing a targetable driver, and prior checkpoint inhibitor exposure raises toxicity if a TKI follows.
Repeating the plasma test a week later has the same shedding limitation; the next step is a different sample, tissue.
A 76-year-old with metastatic lung adenocarcinoma, ECOG 1, has a MET exon 14 skipping mutation. The APRN recommends first-line:
MET exon 14 skipping is targeted with a MET inhibitor, capmatinib or tepotinib, which NCCN prefers first-line over immunotherapy.
Alectinib targets ALK rearrangements; choosing it confuses one driver-specific TKI with another.
Older patients with MET exon 14 tumors often have high PD-L1, but driver-positive lung cancers respond poorly to single-agent immunotherapy, so the targeted agent comes first.
Osimertinib targets EGFR mutations, which this tumor does not have.
A 78-year-old with severe COPD and heart failure (life expectancy 3–5 years) had a prostatectomy for Gleason 3+4 cancer 4 years ago; his PSA remains undetectable. The APRN recommends:
Intensive surveillance with imaging is not recommended even for healthy men with an undetectable PSA, let alone with limited life expectancy.
Lifelong testing ignores competing mortality; finding a recurrence he would not live long enough to be harmed by adds anxiety and procedures.
PSMA PET is used to localize disease after a rising PSA, not as routine surveillance with an undetectable PSA.
With an undetectable PSA after prostatectomy for grade group 2 cancer and a life expectancy of 3–5 years, a biochemical recurrence would take years to become metastatic, so surveillance can stop and care can focus on his heart and lung disease.
A 35-year-old survivor of Hodgkin lymphoma treated with chest radiation is found to carry a germline TP53 pathogenic variant. Which surveillance imaging should the APRN recommend?
Low-dose CT is the lung screening test, but TP53 carriers are unusually prone to radiation-induced cancers, and she has already had chest radiation.
TP53 carriers (Li-Fraumeni syndrome) are followed with annual whole-body MRI under the Toronto protocol, which detects early tumors without ionizing radiation; women also get annual breast MRI.
PET/CT gives a larger radiation dose than CT and is not the surveillance standard for Li-Fraumeni syndrome.
Chest radiographs are insensitive for early tumors, still deliver radiation, and cover one region of a syndrome whose cancers can arise anywhere.
A running total sits here; it fills in after your last pick.
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Where area I answers go wrong
Average-risk schedules for high-risk people. USPSTF intervals are written for average risk. Carriers of a hereditary syndrome and survivors of chest radiation follow their own, earlier and more intensive schedules.
ECOG and Karnofsky point opposite ways. ECOG worsens as the number rises (0 is fully active); Karnofsky worsens as it falls (100 is normal). A "high" score means opposite things on the two.
Clinical, pathologic and post-treatment stage. cTNM is assigned before treatment, pTNM after surgery, and a y prefix marks staging after neoadjuvant therapy. The post-treatment stage does not replace the original clinical stage.
Routine tests after breast cancer. ASCO's follow-up guideline advises against routine tumor markers and routine imaging in survivors without symptoms; history, examination and mammography carry surveillance.
Hospice timing. The Medicare hospice benefit requires a prognosis of 6 months or less if the illness runs its usual course. Palliative care has no such requirement (symptom management).
Does the AOCNP test average-risk cancer screening?
Screening and early detection is in area I. On this site the average-risk schedules sit with the FNP-C, and the AOCNP pages cover high-risk, hereditary and survivor screening.
Which staging system does the AOCNP expect?
The outline says "staging guidelines" without naming one. In US practice solid tumors are staged with AJCC TNM and lymphomas with the Lugano classification.