🎗️ Triple-Negative Breast Cancer Chemotherapy Simulator

Tumor Receptor Testing

Placeholder: every breast tumor is screened for three receptors first.

• ~15%: TNBC share of breast cancers (placeholder: rough population share)
• ER, PR, HER2: Receptors screened (placeholder: standard IHC/FISH panel)
• <1% staining: ER/PR negativity cutoff (placeholder: ASCO/CAP threshold)
• IHC 0/1+, FISH−: HER2 negative score (placeholder: negative criteria)

Immunohistochemistry panel

Placeholder: pathology lab stains tumor tissue for three receptors.

Why test all three

Placeholder: receptor status decides which drug classes can work.

Placeholder: all three negative defines triple-negative breast cancer.

Result: triple-negative

Placeholder: no ER, PR, or HER2 target found on this tumor.

Hormone Therapy Option Evaluated

Placeholder: hormone-blocking drugs need an ER/PR receptor to act on.

• Tamoxifen, AIs: Hormone therapy examples (placeholder: standard ER/PR drugs)
• ER and/or PR: Requires target (placeholder: receptor dependency)
• Both negative: TNBC ER/PR status (placeholder: no binding site)
• None: Expected efficacy in TNBC (placeholder: mechanism has no target)

How hormone therapy works

Placeholder: these drugs block estrogen/progesterone signaling at the receptor.

No receptor, no binding

Placeholder: without ER/PR, the drug has nowhere to attach.

Placeholder: hormone therapy is ruled out for triple-negative disease.

Option eliminated

Placeholder: one of three major systemic pathways is now closed.

HER2-Targeted Therapy Option Evaluated

Placeholder: trastuzumab-type drugs need HER2 overexpression to function.

• Trastuzumab, T-DM1: HER2 drug examples (placeholder: standard HER2 agents)
• HER2 overexpression: Requires target (placeholder: receptor dependency)
• Negative: TNBC HER2 status (placeholder: no binding site)
• None: Expected efficacy in TNBC (placeholder: mechanism has no target)

How HER2 therapy works

Placeholder: antibodies bind HER2 protein on the cell surface.

No overexpression, no binding

Placeholder: without HER2, the antibody drifts off unbound.

Placeholder: HER2 therapy is ruled out for triple-negative disease.

Second option eliminated

Placeholder: two of three systemic pathways are now closed.

Chemotherapy — The Remaining Option

Placeholder: chemo does not need a receptor, it targets dividing cells.

• AC-T, carboplatin: Common TNBC regimens (placeholder: standard chemo backbones)
• DNA/mitosis disruption: Mechanism (placeholder: general cytotoxicity)
• None (receptor-agnostic): Target requirement (placeholder: works without a receptor)
• All breast cancer subtypes: Applicability (placeholder: broad but nonspecific)

A receptor-agnostic mechanism

Placeholder: chemo attacks rapidly dividing cells generally, not a receptor.

Why it still works here

Placeholder: tumor cells still divide fast even without ER/PR/HER2.

Placeholder: chemotherapy becomes the only remaining systemic option.

Trade-off: less selectivity

Placeholder: healthy dividing cells are also affected, causing side effects.

Chemotherapy as Primary Systemic Treatment

Placeholder: chemo becomes the backbone treatment for triple-negative disease.

• Cytotoxic chemotherapy: Primary systemic option (placeholder: standard of care backbone)
• Immunotherapy (checkpoint): Emerging option (placeholder: for eligible PD-L1+ cases)
• PARP inhibitors: Emerging option (BRCA) (placeholder: for BRCA-mutated cases)
• More limited: Historical option landscape (placeholder: vs receptor-positive subtypes)

Chemo as the backbone

Placeholder: with no receptor target, chemo carries the treatment plan.

A narrower historical landscape

Placeholder: fewer targeted options existed compared to other subtypes.

Expanding options today

Placeholder: immunotherapy and PARP inhibitors now widen the field.

Placeholder: newer therapies are gradually expanding TNBC treatment options.

Systemic option landscape by receptor subtype