Targeted Therapy & Immunotherapy in Oncology Flashcards

Which immune checkpoint molecule does pembrolizumab (Keytruda) target?

Answer: PD-1

Pembrolizumab is a humanized monoclonal antibody that targets PD-1 on T cells, blocking the PD-1/PD-L1 interaction and restoring anti-tumor T cell activity.

Ipilimumab was the first FDA-approved immune checkpoint inhibitor (2011) and targets which molecule?

Answer: CTLA-4 on T cells

Ipilimumab targets CTLA-4, a negative regulator of T cell activation in lymph nodes, thereby amplifying anti-tumor immune responses in melanoma.

What is the first procedural step in manufacturing autologous CAR-T cell therapy for a patient?

Answer: Perform leukapheresis to collect the patient's T cells

Leukapheresis to collect the patient's own T cells is the first manufacturing step; these cells are then genetically engineered to express the chimeric antigen receptor.

Which biomarker is most commonly used to predict response to PD-1/PD-L1 checkpoint inhibitors across multiple tumor types?

Answer: PD-L1 expression by immunohistochemistry (tumor proportion score)

PD-L1 expression measured by IHC is an established predictive biomarker for checkpoint inhibitor response, with higher expression generally correlating with greater benefit.

Atezolizumab differs from pembrolizumab and nivolumab in that it targets which molecule?

Answer: PD-L1 on tumor and immune cells

Atezolizumab targets PD-L1 (the ligand) rather than PD-1 (the receptor), blocking the interaction from the antigen-presenting or tumor cell side.

Blinatumomab is a bispecific T-cell engager (BiTE) that simultaneously binds CD19 on B cells and which molecule on T cells?

Answer: CD3

Blinatumomab bridges CD19-expressing malignant B cells and CD3-expressing T cells, forcing T cells to recognize and destroy the B cell tumor targets.

Microsatellite instability-high (MSI-H) status predicts response to PD-1 inhibitors. Which enzyme deficiency causes MSI-H tumors?

Answer: Mismatch repair (MMR) protein deficiency

MSI-H tumors arise from deficient mismatch repair (dMMR), leading to accumulation of mutations that generate neoantigens, making them highly responsive to PD-1 blockade.