Free OCN Physiology Practice Questions with Answers

5-FU is an S-phase specific antimetabolite. It acts as a pyrimidine analog that inhibits thymidylate synthase, preventing the synthesis of thymidine, which is essential for DNA replication. Because it is phase-specific, it is most effective during active DNA synthesis. Exam Strategy: ONCC often tests the timing of antimetabolites. Remember that S-phase agents are frequently administered via continuous infusion to maximize the number of cells caught during the vulnerable DNA synthesis window. Common distractors include G2 or M-phase mechanisms.

Most cytotoxic agents target actively dividing cells (specifically those in S or M phase). Cells in G0 are metabolically active but not replicating DNA or dividing, making them invisible to phase-specific drugs. Slow-growing tumors (e.g., indolent lymphomas) often have a large G0 population, leading to lower initial response rates compared to high-growth tumors (e.g., Burkitt lymphoma). Exam Strategy: This explains why liquid tumors often respond faster than solid tumors. Recurrence is often driven by G0 cancer stem cells that re-enter the cycle after treatment ends.

Synthetic lethality occurs when the individual loss of either of two genes is compatible with cell viability, but the simultaneous loss of both leads to cell death. BRCA1/2 are needed for Homologous Recombination (HR) repair of double-strand breaks. PARP is needed for single-strand break repair. In BRCA-mutant cells, inhibiting PARP leaves the cell with no viable way to repair DNA, leading to selective apoptosis of cancer cells. Exam Strategy: This is a cornerstone of 2026 precision oncology. It explains why PARP inhibitors (e.g., olaparib) are highly effective in BRCA+ breast/ovarian/prostate cancers but less so in HR-proficient cells.

NK cells possess inhibitory receptors that recognize MHC Class I (self-markers) on healthy cells, which prevents NK activation. Many tumors downregulate MHC Class I to hide from CD8+ T-cells. However, the absence of this self signal triggers NK cell activation, leading to the release of perforins and granzymes to induce apoptosis. Exam Tip: Tumors use MHC downregulation as an Escape mechanism from T-cells, but this makes them vulnerable to NK-mediated missing self recognition.

VEGF is inherently immunosuppressive. High VEGF levels inhibit dendritic cell maturation (reducing antigen presentation) and promote the recruitment of MDSCs and Tregs. By blocking VEGF, the TME becomes more immunosupportive, allowing better T-cell infiltration and more effective antigen-presenting cell (APC) function. Exam Tip: This is the physiological rationale for combining anti-angiogenic agents (like bevacizumab) with checkpoint inhibitors (like atezolizumab).