Metastasis
Staging (FIGO) is largely clinical, based on the extent of local spread, parametrial/pelvic sidewall involvement, and distant metastasis.
What our notes say
- Staging (FIGO) is largely clinical, based on the extent of local spread, parametrial/pelvic sidewall involvement, and distant metastasis. (General & Systemic Pathology SAQ Paper II — 15 July 2025 (MBPA 3500, MKU Year 3,)
- | Small cell lung cancer (SCLC) ≈ 15% | Central; very strong smoking link; neuroendocrine origin; very rapid growth and early metastasis; paraneoplastic syndromes (ectopic ACTH, SIADH, Lambert–Eaton); chemotherapy-sensitive | (Lung Cancer)
- B—true, serum acid phosphatase (particularly prostatic acid phosphatase) rises in prostate carcinoma, especially with metastasis. (bchem EOY 2011 — Past Paper Questions & Answers)
- Local invasion into surrounding tissues and potential lymphatic or hematogenous metastasis. (Female rep y3 — Past Paper Questions & Answers)
- 42b) Outline the sequential steps in mechanisms of tumor invasion and metastasis. (10 Marks) (Chemical path 2021 — Past Paper Questions & Answers)
- M (Metastasis) — describes presence or absence of distant metastasis (Medical MCQs: Chemical Pathology & Haematology Exam Review)
Study material on Metastasis
- ONCOPATHOLOGY - 30 KEY SHORT ANSWER QUESTIONS Hallmarks 1,2 & 3
- Genetic Disorders Pathology Crash Course: Exam Revision Notes
- Hallmarks of Cancer: Molecular Basis, Cell Cycle & Oncogenes
- Medical MCQs: Chemical Pathology & Haematology Exam Review
- General Pathology Revision: Cell Injury, Inflammation & Adaptation (MBPA 3500 Paper 1)
- Cancer Pharmacology: Cell Cycle, Oncogenes & Drug Targets
- ONCOPATHOLOGY - SHORT ANSWER QUESTIONS (SAQs)
- Ovarian & Colorectal Cancer: Risks, Pathogenesis, Staging
- Oncopathology MCQs: Test Your Knowledge on Cancer Pathology
- ADRENAL NEOPLASMS — Adenoma vs Carcinoma
- ONCOPATHOLOGY MCQs - HALLMARKS OF CANCER
- Oncopathology Hallmarks of Cancer MCQs
- ONCOPATHOLOGY MCQ EXAMINATION HAllmarks of Cancer 1,2 &3
- Weekly Pathology Exam - May 15, 2026 (Section A: MCQs)
- Weekly Pathology Exam - May 1, 2026 (Section A: MCQs)
- Weekly Pathology Exam - April 10, 2026 (Section A: MCQs)
Practice questions on Metastasis
In pancreatic cancer, TGF-β pathway mutations are found in 100% of cases. However, in late-stage tumors, intact TGF-β signaling promotes metastasis. This apparent contradiction occurs because
- TGF-β always promotes tumor growth
- TGF-β switches from growth inhibition to promoting EMT and invasion
- Late-stage tumors revert their mutations
- Early and late-stage tumors are genetically unrelated
Answer: B. TGF-β has dual roles: in normal/early cancer cells it inhibits growth, but in late-stage tumors it can activate epithelial-to-mesenchymal transition (EMT), promoting migration and metastasis. ---
The invasion-metastasis cascade can be interrupted at multiple points. Which is NOT a step in this cascade?
- Local invasion
- Intravasation
- Increased cell-cell adhesion
- Extravasation
Answer: C. The metastatic cascade involves loosening of cell-cell contacts (not increased adhesion), local invasion, intravasation, transit, extravasation, and growth at distant sites. ---
What cellular process does TGF-β activate in late-stage tumors that promotes metastasis?
- Apoptosis
- Senescence
- Epithelial-to-mesenchymal transition (EMT)
- Differentiation
- Limited to a single tissue compartment
Answer: C. In late-stage tumors, TGF-β signaling can paradoxically activate epithelial-to-mesenchymal transition (EMT), promoting migration, invasion, and metastasis. ---
A metastatic tumor cell must successfully complete multiple steps to establish a distant metastasis. At which stage do MOST tumor cells fail?
- Initial detachment from the primary tumor
- Intravasation into blood vessels
- Survival in circulation
- Colonization and growth at distant sites
Answer: D. ** Tumor cells are quite inefficient at colonizing distant organs. Millions of tumor cells are shed daily from even small tumors, but gross metastatic lesions don't always develop. The target tissue must provide a receptive stroma, and most sites are non-permissive environments for tumor growth. ---
Loss of E-cadherin function promotes metastasis through which TWO mechanisms?
- Loss of intercellular adhesion and loss of β-catenin sequestration
- Increased apoptosis and enhanced immune recognition
- Decreased MMP production and reduced invasion
- Enhanced thrombospondin production and inhibited angiogenesis
Answer: A. ** E-cadherin loss promotes metastasis by: (1) loosening tumor cell-to-cell contacts (loss of "intercellular glue"), and (2) failing to sequester β-catenin, which can then promote proliferation. E-cadherin also transmits anti-growth signals when functioning normally. ---
Why are skeletal muscles rarely sites of metastasis despite being well-vascularized?
- Muscle cells produce high levels of TSP-1
- The target tissue provides a non-permissive environment
- Tumor cells cannot adhere to muscle endothelium
- Skeletal muscle has no basement membrane
Answer: B. ** Despite being well-vascularized, skeletal muscles are rarely metastatic sites because the target tissue is non-permissive. This demonstrates that vascularization alone is insufficient - tumor cells depend on a receptive stroma for growth, which skeletal muscle fails to provide. ---