Immune system in cancer + drugs Flashcards
(17 cards)
What are the “3 E’s” of cancer development?
Escape, Edit (mutations), Exploit (immune evasion)
Why might twins with identical CLL mutations have different disease courses?
Differences in tumor microenvironment (TME) (immune cell infiltration, matrix, conditions)
What is the mechanism of rituximab?
Anti-CD20 monoclonal antibody → B-cell death via complement/antibody-dependent cytotoxicity
How do bispecific T-cell engagers (BiTEs) work?
Bind CD3 (T-cell) + tumor antigen (e.g., CD20) → T-cell activation → tumor lysis (e.g., blinatumomab for ALL)
What is the target of pembrolizumab?
PD-1 inhibitor → blocks T-cell exhaustion (used in melanoma, NSCLC, HL)
Compare CTLA-4 vs. PD-1 inhibitors
CTLA-4 (e.g., ipilimumab): Early T-cell activation check.
PD-1 (e.g., nivolumab): Late T-cell exhaustion check.
What is the benefit of combining nivolumab + ipilimumab?
Synergistic T-cell activation → improved OS in RCC/metastatic melanoma
How do CAR-T cells work?
Engineered T-cells with chimeric antigen receptors (e.g., CD19) → target tumor cells (refractory B-cell malignancies).
Name 2 cancer-preventive vaccines.
Cervarix (HPV-16/18), Gardasil (HPV) → prevent cervical/GU cancers
Gardasil is a non-infectious recombinant vaccine
What is the #1 red flag for hematologic malignancy?
Unexplained cytopenias (e.g., anemia, thrombocytopenia) + B symptoms (fever, weight loss, night sweats)
What is the tumor microenvironment (TME) role in therapy resistance?
Permissive TME = immune evasion; restrictive TME = limits drug infiltration
How to remember monoclonal antibody suffixes?
-mab = monoclonal antibody
-zu- = humanized (e.g., obinutuzumab)
-xi- = chimeric (e.g., rituximab)
-u- = fully human (e.g., nivolumab).
Vincristine MOA
Vincristine binds to tubulin (protein that polymerises to form microtubules); inhibits mitotic spindle formation
Methotrexate MOA
MTX inhibits enzymes responsible for nucleotide synthesis; inhibits dihydrofolate reductase which catalyses reduction of dihydrofolate to tetrahydrofolate. It also inhibits thymidylate synthetase which catalyses formation of thymidine residues
Doxorubicin MOA
Doxorubicin disrupts DNA + RNA synthesis; inhibits topoisomerase II this prevents relaxation of supercoiled DNA during transcription + replication= DNA strand breaks + cumulative DNA damage triggers apoptotic pathways
Cyclophosphamide MOA
Cyclophosphamide is a prodrug activated by hepatic cytochrome P450 enzymes to form 4-hydroxycyclophosphamide which is converted to phosphoramide mustard + acrolein= phosphoramide INHIBITS DNA replication + transcription= cell cycle arrest + apoptosis
Cisplatin MOA
It enters cells + is hydrolysed to form a reactive platinum complex. It binds to DNA at N7 position of guanine bases it forms GG and GA crosslink thus distorting the DNA helix= this inhibits DNA polymerase activity which halts replication + transcription
