Breast Cancer
The 'triple negative' breast cancers (ER, PR, HER2 negative) are harder to treat, but there are chemotherapy protocols that can be employed.
Treatment at a glance
- Early: surgery ± chemotherapy (anthracycline then taxane), then endocrine therapy for hormone-receptor-positive disease
- HER2-positive: add trastuzumab
What our notes say
- The 'triple negative' breast cancers (ER, PR, HER2 negative) are harder to treat, but there are chemotherapy protocols that can be employed. (Breast mcqs — Past Paper Questions & Answers)
- Counsel on risks of hormone therapy (breast cancer, venous thrombosis, stroke) and review regularly. (Year 4 Gynaecology CAT 1 (MBOG 4212): 2 July 2021)
- Benign breast disease and breast cancer risk (11 marks) (General Surgery CAT 2 (MBSG 4600): 4 October 2021)
- A family history of breast cancer increases the risk for breast cancer the most. (Breast mcqs — Past Paper Questions & Answers)
- Discuss the three major pathways of breast cancer development and their resultant immunohistochemical staining patterns. (Eoy paper 2 gen systemic Patho 2025 — Past Paper Questions & Answers)
- Lymphatic obstruction (lymphoedema) — e.g. filariasis, and post-surgical/post-radiotherapy lymph node dissection (e.g. after axillary clearance in breast cancer) or tumour infiltration of lymphatics. (General & Systemic Pathology SAQ Paper II — 15 July 2025 (MBPA 3500, MKU Year 3,)
Study material on Breast Cancer
- Breast Cancer Guide: Epidemiology, Risk Factors & Classification
- Breast Carcinoma: Understanding Types, Receptors & Treatment
- Breast mcqs
- Disorders of the Vagina and Breast
- Exam Prep: Skin Infections, Psoriasis & Pemphigus
- Cancer Pharmacology: Cell Cycle, Oncogenes & Drug Targets
- Skin & Breast Pathology CAT: MKU Year 3 Medicine Exam
- Molecular Basis of Cancer: Cell Cycle, Apoptosis & Angiogenesis
- General & Systemic Pathology SAQ Paper II — 15 July 2025 (MBPA 3500, MKU Year 3, With Answers)
- Genetics & Disease: Muscular Dystrophy, CF, Marfan, Diabetes, Cancer
- ONCOPATHOLOGY MCQ EXAMINATION HAllmarks of Cancer 1,2 &3
- ONCOPATHOLOGY MCQs - HALLMARKS OF CANCER
- Disorders of the Vagina and Breast
- Weekly Pathology Exam - October 9, 2026 (Section A: MCQs)
- Weekly Pathology Exam - October 2, 2026 (Section A: MCQs)
- Weekly Pathology Exam - September 25, 2026 (Section A: MCQs)
Practice questions on Breast Cancer
A 48-year-old woman with breast cancer develops a right pleural effusion. Thoracentesis yields fluid protein of 5.2 g/dL, serum protein 6.8 g/dL, fluid LDH 420 U/L, and serum LDH 310 U/L. Cytology shows malignant cells. What is the most likely type of effusion?
- Transudative
- Exudative
- Malignant
- Serous
Answer: C. Using Light's criteria, this is an exudative effusion: Fluid protein/serum protein ratio is 5.2/6.8 = 0.76 ( > 0.5), and fluid LDH/serum LDH ratio is 420/310 = 1.35 ( > 0.6). The presence of malignant cells in the cytology confirms it as a malignant effusion, which is a subtype of exudative effusion.
A 33-year-old woman with breast cancer is found to have HER2/neu gene amplification. Which of the following best describes the mechanism by which HER2/neu promotes oncogenesis?
- It acts as a transcription factor to promote cell growth.
- It is a receptor tyrosine kinase that stimulates downstream signaling pathways involved in cell proliferation and survival.
- It inhibits apoptosis by stabilizing p53.
- It directly causes DNA mutations leading to genomic instability.
Answer: B. HER2/neu (ERBB2) is a receptor tyrosine kinase. Amplification leads to increased expression and constitutive activation, which drives downstream signaling pathways (e.g., PI3K/Akt, MAPK) promoting cell growth, survival, and angiogenesis, contributing to oncogenesis.
A 48-year-old woman with breast cancer develops a right pleural effusion. Thoracentesis yields fluid protein of 5.2 g/dL, serum protein 6.8 g/dL, fluid LDH 420 U/L, and serum LDH 310 U/L. Cytology shows malignant cells. Most likely type of effusion?
- Transudate
- Exudate
- Chylothorax
- Hemothorax
Answer: B. Using Light's criteria: Fluid protein/serum protein ratio (5.2/6.8 ≈ 0.76) is >0.5. Fluid LDH (420 U/L) is >2/3 the upper limit of normal serum LDH (assuming upper limit is ~200 U/L, 420 is > ~133). These findings are characteristic of an exudative effusion. Given the history of breast cancer and malignant cells on cytology, this is a malignant pleural effusion.
A 33-year-old woman with breast cancer is found to have HER2/neu gene amplification. Which of the following best describes the mechanism by which HER2/neu promotes oncogenesis?
- Increased cell proliferation and survival signaling
- Inhibition of apoptosis
- Promotion of angiogenesis
- Induction of genomic instability
Answer: A. HER2/neu is a receptor tyrosine kinase. Amplification of its gene leads to overexpression of the HER2 protein, which then dimerizes and activates downstream signaling pathways (e.g., PI3K/Akt, MAPK) that promote uncontrolled cell proliferation, survival, and growth.
A 48-year-old woman with breast cancer develops a right pleural effusion. Thoracentesis yields fluid protein of 5.2 g/dL, serum protein 6.8 g/dL, fluid LDH 420 U/L, and serum LDH 310 U/L. Cytology shows malignant cells. Most likely type of effusion?
- Transudate
- Exudate
- Chylothorax
- Hemothorax
Answer: B. This effusion is an exudate. Using Light's criteria: Fluid protein/serum protein ratio (5.2/6.8 = 0.76) is >0.5. Fluid LDH/serum LDH ratio (420/310 = 1.35) is >0.6. The presence of malignant cells further supports an exudate, specifically a malignant effusion.
A 33-year-old woman with breast cancer is found to have HER2/neu gene amplification. Which of the following best describes the mechanism by which HER2/neu promotes oncogenesis?
- Activation of growth factor signaling pathways
- Inhibition of tumor suppressor genes
- Promotion of angiogenesis
- Induction of apoptosis
Answer: A. HER2/neu (ERBB2) is a receptor tyrosine kinase. Amplification of its gene leads to overexpression of the HER2 protein, which then signals aberrantly through downstream pathways (e.g., PI3K/Akt, MAPK) promoting cell proliferation, survival, and invasion, thereby driving oncogenesis.