In a lab model of HER2-positive breast
cancer, cells are treated with trastuzumab. Initially, most cells are killed,
but a subset survives and continues proliferating. Sequencing and protein analysis
reveal that the HER2 receptor lacks the extracellular domain required for
trastuzumab binding, though downstream signalling remains active.

Which explanation best accounts for
this resistance?

Question

In a lab model of HER2-positive breast
cancer, cells are treated with trastuzumab. Initially, most cells are killed,
but a subset survives and continues proliferating. Sequencing and protein analysis
reveal that the HER2 receptor lacks the extracellular domain required for
trastuzumab binding, though downstream signalling remains active.

Which explanation best accounts for
this resistance?

Answer

Cells overexpress
efflux pumps that remove trastuzumab from the extracellular environment

Answer

Truncation
of the HER2 extracellular domain prevents trastuzumab binding, allowing
continuous signalling

Answer

Antibody-dependent
cell-mediated cytotoxicity kills immune cells instead of tumour cells

Answer

Loss-of-function PI3K
mutations reduce signalling, protecting cells from antibody effects

Crowdly

In a lab model of HER2-positive breast cancer, cells are treated with trastuzum...

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