Breast Cancer
Core concepts
Know receptor biology as the decision tree: ER/PR status drives endocrine therapy, HER2 status drives trastuzumab/pertuzumab and antibody-drug conjugates, and triple-negative disease pivots to chemotherapy, immunotherapy (PD-L1–positive), and germline BRCA-directed PARP inhibitors or sacituzumab govitecan. Stage-based logic: early-stage disease is about local control plus adjuvant systemic therapy guided by anatomic stage, tumor grade, genomic assays (e.g., 21-gene recurrence score), and menopausal status; metastatic disease is about palliating and prolonging life with sequential lines chosen by biomarker and prior exposure. Understand the CDK4/6 inhibitor backbone for hormone receptor–positive metastatic disease, ovarian suppression in premenopausal high-risk disease, and the role of neoadjuvant therapy for HER2-positive and triple-negative tumors (with residual disease guiding adjuvant capecitabine or T-DM1).
Traps
Questions love flipping menopausal status, confusing adjuvant versus metastatic indications, or testing whether a genomic assay changes chemotherapy decisions in node-positive versus node-negative disease. Watch for "which therapy is contraindicated" items (e.g., tamoxifen and thromboembolic history) and for HER2-low versus HER2-positive distinctions. Also expect bone-modifying agent indications and the difference between endocrine therapy for ductal carcinoma in situ versus invasive disease.
Rule of thumb
Ask three questions in order: What is the stage and intent (curative vs palliative)? What are the receptors? What has the patient already received? The answer almost always follows from those three.
Worked example
A postmenopausal woman with ER-positive, HER2-negative metastatic breast cancer progressing on an aromatase inhibitor plus a CDK4/6 inhibitor: next line is typically endocrine therapy with a different mechanism (fulvestrant, possibly with a targeted agent if PIK3CA-mutant) before chemotherapy, unless visceral crisis dictates chemotherapy.