Triple-Negative
Overview of triple-negative breast cancer, including biomarkers, standard treatment logic, and common drug names used in this section
This is the main hub for triple-negative breast cancer, or TNBC, on the site.
TNBC is ER-negative, PR-negative, and HER2-negative on standard testing.
In this section
Jump to:
Our TNBC treatment resistance research section includes pages on:
Natural compounds — microRNA, EMT, blueberry, pterostilbene, and piperlongumine research
Off-label drugs — pitavastatin, melatonin, metformin, aspirin, and related repurposing leads and
Emerging SOC strategies — RNA-targeting and multi-target combinations that may shape the next wave of TNBC resistance work
Why TNBC needs its own treatment logic
TNBC is not one single disease.
It is a mixed group of tumours with different molecular patterns, immune activity, and treatment sensitivities.
Several features come up more often here:
DNA-repair weakness. BRCA1/2 variants and wider HRD can make platinum drugs and PARP inhibitors more relevant.
Immune variability. Some tumours are more immune-active, with higher TILs or PD-L1 expression.
Earlier recurrence risk. Relapse risk is often more front-loaded in the first few years after diagnosis.
Strong neoadjuvant relevance. Response before surgery matters a lot, and pathologic complete response usually signals a better outlook.
Biomarkers that can change treatment decisions
BRCA1, BRCA2, and HRD
BRCA1/2 testing matters in TNBC.
It can affect treatment choice, inherited-risk assessment, and family counselling.
Positive findings may support:
stronger interest in platinum chemotherapy
eligibility for PARP inhibitors
wider family risk assessment
Broader HRD or BRCAness may also matter, even without a classic BRCA variant.
PD-L1
PD-L1 testing helps identify metastatic TNBC patients who may benefit from pembrolizumab plus chemotherapy.
Assays and cut-offs vary.
That makes report interpretation important.
TILs and immune context
Higher tumour-infiltrating lymphocytes, or TILs, often track with better chemotherapy response.
They can also suggest a more active anti-tumour immune environment.
TILs are not a stand-alone treatment selector, but they can still help frame prognosis.
TROP2 and other emerging targets
TROP2 matters because it is the target of sacituzumab govitecan.
Some TNBC tumours also sit in more specialised subgroups, including:
HER2-low or HER2-mutant disease
androgen-receptor-positive or luminal androgen receptor patterns
PI3K/AKT/mTOR-altered tumours
These findings matter most in later-line planning or clinical-trial matching.
Androgen-receptor-positive or LAR-type TNBC
Some TNBCs are strongly positive for the androgen receptor, or AR.
This pattern is often called the luminal androgen receptor, or LAR, subtype.
LAR tumours often show lower proliferation and lower chemotherapy response rates than basal-like TNBC.
They may also carry actionable findings such as PIK3CA or ERBB2 mutations.
If your report shows strong AR staining, low Ki-67, or a non-basal pattern, it is worth asking whether added molecular testing or LAR-focused trials could change the plan.
For the fuller patient guide, see LAR-Subtype Triple-Negative (AR-Positive).
Standard treatment pathway
Treatment varies by stage, country, and prior therapy.
Early-stage TNBC
Treatment often starts with neoadjuvant chemotherapy before surgery in stage II to III disease.
Common regimens combine an anthracycline, cyclophosphamide, a taxane, and sometimes carboplatin.
Pembrolizumab now matters in selected high-risk early-stage settings.
After systemic therapy, treatment usually moves to surgery and then radiation when indicated.
Residual disease can change the next step.
That may include capecitabine, ongoing pembrolizumab, or olaparib in selected gBRCA1/2 cases.
Metastatic or advanced TNBC
Chemotherapy still anchors treatment in metastatic disease.
Pembrolizumab plus chemotherapy matters in PD-L1-positive metastatic TNBC.
PARP inhibitors matter in selected gBRCA1/2-mutated, HER2-negative disease.
Sacituzumab govitecan matters after prior chemotherapy exposure.
Later-line options can also include capecitabine, eribulin, vinorelbine, or gemcitabine.
Palliative radiation, bone support, symptom control, and multidisciplinary care stay central throughout.
Also relevant beyond this sub-type section
These pages live outside this subsection, but they often help frame TNBC questions.
Breast Cancer Pathways Project Free worksheet downloads and pathways-based planning support.
Breast Cancers Overview Main breast-cancer hub for subtype navigation and cross-subtype pages.
Treatment Resistance Overview Wider framework for resistance patterns and escape logic across cancers.
Selected references
Drug and brand names often used with TNBC
Expand the TNBC treatment-name glossary
On this site, drug names usually appear as the generic name first, then the brand name in brackets.
Brand names can vary by country.
Common chemotherapy backbones
Doxorubicin — Adriamycin and epirubicin — Ellence. Anthracyclines often pair with cyclophosphamide in early-stage TNBC.
Paclitaxel — Taxol and docetaxel — Taxotere. Taxanes are used in neoadjuvant, adjuvant, and metastatic settings.
Carboplatin — Paraplatin and cisplatin — Platinol. Platinum drugs matter most when BRCA1/2 or wider HRD is in the picture.
Immunotherapy
Pembrolizumab — Keytruda. A PD-1 inhibitor used with chemotherapy in selected high-risk early-stage and PD-L1-positive metastatic TNBC.
PARP inhibitors
Olaparib — Lynparza. Used in selected gBRCA1/2-mutated, HER2-negative breast cancer settings.
Talazoparib — Talzenna. Another PARP inhibitor used in metastatic HER2-negative disease with germline BRCA variants.
Antibody-drug conjugates
Sacituzumab govitecan — Trodelvy. A TROP2-directed ADC used in previously treated metastatic TNBC.
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