Targeted therapies for breast cancer: HER2, CDK4/6, PARP

Section 01 · Understanding

What is a targeted therapy?

Every breast cancer is unique. Targeted therapies are medications selected based on the specific features of your disease, in order to offer you the treatment most suited to your situation.

A targeted therapy is a drug that acts specifically on what drives a cancer's growth : a particular protein on the surface of cancer cells (such as HER2), a biological pathway they use to multiply, or a weakness specific to their DNA. Unlike chemotherapy, which acts broadly on all rapidly dividing cells (hair, blood, mucosa), targeted therapy concentrates its action on the tumour — with greater efficacy and, most often, better tolerance.

In breast cancer, there are three main families of targeted therapies:

→ anti-HER2 drugs — when your tumour « catches » too much of a growth signal called HER2. The best-known drug is Herceptin (scientific name: trastuzumab).
→ CDK4/6 inhibitors — when your tumour is hormone-sensitive. They slow down cancer cell division. Three names to remember: Ibrance, Kisqali, Verzenio.
→ PARP inhibitors — when you carry a BRCA genetic mutation. They exploit a specific weakness of tumour cells to destroy them. Known as Lynparza and Talzenna.

How do you know which one is for you? It's your biopsy that decides. The pathology lab analyses your tumour and writes its « identity card »: HER2 positive or negative, hormone receptors present or not, BRCA mutation tested if needed. These results guide treatment choice.

The final decision is never made by a single doctor. It is taken at the MDT — a meeting where surgeon, oncologist, radiation oncologist and pathologist discuss your case together, following French (SENORIF, INCa) and European guidelines.

Section 02 · Anti-HER2

Anti-HER2 — the archetype of targeted therapy

About one breast cancer in six has a particular feature : its cells produce large amounts of a protein called HER2. Located on the surface of the cancer cells, this protein continuously captures signals that drive the tumour to grow more rapidly.

For a long time, these cancers were considered more difficult to treat. Everything changed with the arrival of trastuzumab (brand name: Herceptin), a drug designed to block precisely this HER2 protein. Today, HER2-positive breast cancers are among the best managed, with remarkable results.

How do we know a tumour is HER2 positive? The pathology lab analyses your biopsy and assigns a score from 0 to 3+. A score of 3+ means HER2 positive — you are then eligible for anti-HER2 treatment. A score of 0 or 1+ is considered HER2 negative. A score of 2+ requires a confirmatory test.

A recent advance to note: certain cancers with low HER2 levels (called « HER2-low ») can now also benefit from targeted treatments.

The pioneer

Herceptin (trastuzumab)

The drug that transformed the prognosis. It binds to the HER2 protein on the surface of cancer cells and blocks the signal driving them to multiply. Administered by infusion or subcutaneous injection for one year after surgery. Regular cardiac monitoring is set up — a simple ultrasound every 3 months as a precaution.

The partner

Perjeta (pertuzumab)

A second anti-HER2 drug, which binds to the HER2 protein at a different spot from trastuzumab. Combining both blocks the growth signal more completely. Combined with trastuzumab and chemotherapy in higher-risk situations or in advanced disease.

The « Trojan horse »

Kadcyla (T-DM1)

Imagine a drug that delivers chemotherapy directly inside cancer cells — like a parcel addressed specifically to them. That's Kadcyla: Herceptin carries a chemotherapy molecule to HER2+ cells, and releases it only there. Healthy cells are spared. Used especially when tumour remains after chemotherapy given before surgery.

Next generation Major breakthrough

Enhertu (T-DXd)

The next-generation version of this same approach, more powerful. Same principle: targeted delivery of chemotherapy directly into HER2+ cells. In recent studies (DESTINY-Breast), it has shown spectacular results compared with previous treatments. Even more important: it also works on cancers that until now were thought HER2 negative (the « HER2-low » category), extending the benefit to many more patients. Monitoring of the lungs is needed (any unusual cough or shortness of breath should be reported).

For brain metastases

Tukysa (tucatinib)

A tablet that blocks HER2 from inside the cell. Its particularity: it crosses the brain barrier. It is therefore the treatment of choice when cancer has spread to the brain — a situation where many other drugs do not penetrate well (HER2CLIMB trial).

Anti-HER2 pills

Lapatinib, neratinib

Other tablets that block HER2 from the inside. Used less often today than newer drugs, but still useful in certain specific situations, or as a follow-on when other treatments haven't fully resolved the disease.

In practice for you

How infusions work

Infusions take place in a day hospital, in a comfortable chair, usually every 3 weeks. Each session lasts between 30 and 90 minutes. The care team is present throughout the treatment: nurse, oncologist, secretariat. For trastuzumab, a subcutaneous injection form (faster, about 5 minutes) is also available — this is discussed together based on your preference.

Cardiac monitoring

Trastuzumab can, in some cases, slightly tire the heart. This is generally reversible — but we prefer to detect it early. A simple, painless cardiac ultrasound is performed before starting treatment, then every 3 months. It measures the strength of cardiac contraction (LVEF). If a decrease is observed, treatment is adapted; in the vast majority of cases, everything returns to normal.

Section 03 · CDK4/6

CDK4/6 inhibitors — blocking the cell cycle

Three molecules, one revolution in HR+ HER2− breast cancer.

CDK4/6 inhibitors are pills that slow down cancer cell division: they block an enzyme essential for cell division. When combined with hormone therapy, they double the time during which the cancer stays under control, in patients whose tumour is hormone-sensitive and HER2 negative.

Three drugs exist in this family, similar but not identical: each has its own « profile » of side effects. All are taken as tablets, in 28-day cycles (with or without a weekly break depending on the drug), always combined with hormone therapy.

The three drugs:

The first

Ibrance (palbociclib)

The pioneer of the family. Schedule: 3 weeks of tablets, then 1 week off, then the cycle resumes. The most common side effect is a drop in white blood cells — not dangerous in general, but monitored with regular blood tests.

The next one

Kisqali (ribociclib)

Identical schedule: 3 weeks of treatment, 1 week off. Things to watch: drop in white blood cells, a bit more monitoring of the heart (a regular ECG is done) and the liver. Note: in France, this drug is not reimbursed for recurrence prevention after surgery — your oncologist will present the available alternatives.

To prevent recurrence Adjuvant

Verzenio (abemaciclib)

The only one in the family reimbursed for recurrence prevention in France, after surgery, for cancers at higher risk of coming back. Taken continuously (no weekly break). Main side effect: diarrhoea, which is well controlled with guidance from the medical team. Also used in advanced disease.

Which option for your situation?

In the advanced setting, all three drugs work about as well. The choice is mainly based on what suits you best: your health profile (heart, digestion), your lifestyle (do you prefer a weekly break or continuous treatment?), and your team's experience with each drug.

For recurrence prevention after surgery, in France today, Verzenio is the reimbursed option (for 2 years). The choice is made at MDT based on your personal risk of recurrence.

Section 04 · PARP

PARP inhibitors — synthetic lethality

PARP inhibitors exploit an astonishing feature of cancers linked to a BRCA mutation. To understand: our cells constantly have small breaks in their DNA, which they know how to repair thanks to several « repair teams ». When you carry a BRCA mutation (5 to 10% of breast cancers), one of these teams doesn't work — cancer cells compensate by using another team, called PARP.

The drug then does something very clever: it blocks this second PARP team. The result? Tumour cells with BRCA mutation, with no remaining way to repair their DNA, self-destruct. Healthy cells, however, keep their first team and continue to function normally.

This is a major step forward for patients with a BRCA mutation. Taken for 1 year after surgery and chemotherapy, olaparib (Lynparza) significantly reduces the risk of cancer coming back, and improves survival. In advanced disease, it is often better tolerated than standard chemotherapy.

To find out if you are concerned, a BRCA genetic test is needed. It is done on a simple blood sample, in oncogenetic consultation. This test is systematically offered in certain situations: triple-negative cancer, young age, family history. Results take several weeks.

Recurrence prevention + advanced

Lynparza (olaparib)

The most widely used drug in this family. Taken as tablets twice a day, for 1 year, after surgery and chemotherapy, in patients carrying a BRCA mutation whose cancer is at higher risk of coming back. It significantly reduces this risk. Generally better tolerated than standard chemotherapy.

Advanced disease

Talzenna (talazoparib)

A related, slightly more potent drug than Lynparza. One tablet per day. Used mainly when the cancer is more advanced. Watch for: a drop in red blood cells (anaemia) which can cause fatigue — easily detected by blood tests.

Side effects to monitor

Haematological Anaemia, thrombocytopenia, neutropenia — regular CBC and platelets.

Digestive Nausea (frequent, usually manageable), taste alterations.

General Fatigue (50-60% of patients), moderate chronic asthenia.

Rare but serious Myelodysplastic syndrome / acute myeloid leukemia (risk < 1%, prolonged surveillance justified).

Section 05 · Other treatments

Other targeted molecules

Research moves fast.

Beyond the three main families, other targeted drugs appear regularly. They broaden the options, especially in advanced or metastatic breast cancers. Here are the main ones to know:

Triple negative

Trodelvy (sacituzumab govitecan)

Same principle as Enhertu but for a different type of cell: it delivers chemotherapy directly inside cancer cells, by targeting a marker called Trop2 (present on most triple-negative cancers). Allows patients with advanced triple-negative disease to live longer than with standard chemotherapy.

Next-generation hormone therapy Innovation

Orserdu (elacestrant)

A pill that destroys the estrogen receptor in cancer cells. Useful when usual hormone therapy and CDK4/6 inhibitors no longer work, and the tumour has developed a particular mutation (ESR1). A new option that sometimes avoids moving to chemotherapy.

For PIK3CA mutation

Piqray (alpelisib)

Targets another signalling pathway called PI3K, present in about one in three patients at an advanced stage. A tumour (or blood) analysis looks for the PIK3CA mutation to see if you are eligible. Main side effect: a rise in blood sugar, managed with regular monitoring.

AKT pathway

Truqap (capivasertib)

A drug closely related to Piqray, which blocks a neighbouring step of the same signalling pathway. Used in advanced disease, combined with hormone therapy, when certain mutations are found in the tumour.

To give hormone therapy another chance

Afinitor (everolimus)

When standard hormone therapy is no longer enough, this drug — taken as a pill — can make it effective again. Things to watch: small mouth ulcers, sometimes lung inflammation.

Immunotherapy Triple negative

Pembrolizumab — waking up the immune system

Although not strictly a targeted therapy: this drug reactivates your own immune defences so they attack the cancer. Indicated in triple-negative cancers, before and after surgery.

Section 06 · Your pathway

From biopsy to the right molecule

The indication for a targeted therapy is never arbitrary: it follows a succession of biological and decision-making steps that translate your tumour biology into a personalised treatment plan. Here is this pathway, from diagnosis to treatment initiation.

01

Histological biopsy

Diagnosis established on biopsy. The report details the histological type (ductal, lobular…), the SBR grade, the Ki67, the hormone receptors ER/PR, and the HER2 status. The biological identity card of your tumour.
02

Staging work-up

Bilateral mammography + ultrasound, MRI if needed. For more advanced stages or aggressive profiles, PET-scanner or complete staging work-up. Blood tests (CBC, renal, hepatic and cardiac function via pre-therapeutic cardiac ultrasound).
03

Oncogenetic consultation

Search for a BRCA1/BRCA2 mutation (sometimes PALB2, TP53) proposed when: triple negative, young age, family history. The result guides not only treatment (PARP inhibitors) but also surgical strategy and family prevention.
04

Breast MDT

Your case is discussed collectively: medical oncologists, radiation oncologists, pathologists, surgeons, sometimes geneticist. The full strategy (surgery first or neoadjuvant? which targeted therapy? which sequence?) is decided according to SENORIF, INCa, ESMO guidelines.
05

Diagnosis disclosure consultation

Presentation of the personalised care plan with the medical oncologist: nature and duration of treatment, administration modalities, expected side effects, monitoring. Opportunity to ask questions, seek a second opinion, take time to consider.
06

Initiation and monitoring

Start of treatment: IV route (anti-HER2), oral (CDK4/6, PARP, SERD), or ADC by infusion. Monitoring adapted to each class: cardiac (anti-HER2 → quarterly LVEF), haematological (CDK4/6, PARP → CBC), respiratory (T-DXd → cough, dyspnoea), biochemical (ribociclib → liver function, QT). Close consultations initially.

Your questions

Frequently asked questions on targeted therapies

The questions patients ask most often — before treatment, during, or simply to understand what is being offered. If yours is not here, it will find its answer in consultation.

What is a targeted therapy in breast cancer?▾

A targeted therapy is a drug that acts on a precise biological abnormality of the tumour — a receptor, a protein, a signalling pathway. Unlike chemotherapy which attacks all rapidly dividing cells, it targets a specific feature. Three main families exist in breast cancer: anti-HER2 (for HER2+ tumours), CDK4/6 inhibitors (for advanced hormone-dependent tumours), and PARP inhibitors (for BRCA-mutated tumours).

Will I qualify for a targeted therapy?▾

The indication for a targeted therapy depends on the biological profile of your tumour, determined from biopsy and surgical specimen. Three main criteria: HER2 status (positive = anti-HER2 possible), hormone receptors combined with stage (HR+ advanced = CDK4/6 possible), and presence of BRCA mutation (= PARP possible). The decision is made at MDT according to SENORIF, INCa and ESMO guidelines.

How does trastuzumab (Herceptin) work?▾

Trastuzumab is a monoclonal antibody that binds to the HER2 receptor on the surface of tumour cells. It blocks proliferation signals and recruits the immune system to destroy the cell. In adjuvant setting, after surgery, it reduces mortality from HER2+ breast cancer by approximately one third. It is administered by infusion or subcutaneous injection for 1 year. The main side effect to monitor is cardiotoxicity — cardiac ultrasound (LVEF) is performed every 3 months during treatment.

What is T-DXd (trastuzumab deruxtecan, Enhertu)?▾

T-DXd is an antibody-drug conjugate (ADC): an anti-HER2 antibody linked to a chemotherapy payload. The antibody delivers chemotherapy directly inside HER2+ tumour cells. It has demonstrated major efficacy in the DESTINY-Breast trials (substantially prolonged PFS versus comparator). It has transformed the prognosis of HER2+ metastatic breast cancer in second line, and its indication now extends to HER2-low tumours (weakly HER2-expressing). Specific side effect to monitor: interstitial lung disease.

What do CDK4/6 inhibitors do?▾

CDK4/6 inhibitors block the cell cycle of cancer cells by acting on proteins (CDK4 and CDK6) that regulate cell division. They are prescribed orally, in combination with endocrine therapy, in advanced or metastatic HR+/HER2− breast cancer. This combination doubles progression-free survival. Abemaciclib (Verzenio) also has an adjuvant indication in high-risk HR+/HER2− forms (MonarchE trial). In France, ribociclib (Kisqali) has not obtained reimbursement in the early adjuvant setting.

PARP inhibitors: for whom and why?▾

PARP inhibitors (olaparib, talazoparib) target tumour cells deficient in DNA repair — typically those carrying a BRCA1 or BRCA2 mutation (5 to 10% of breast cancers). The principle is synthetic lethality: by blocking one repair mechanism, you selectively kill already-vulnerable cells. In adjuvant setting, 1 year of olaparib after chemotherapy significantly reduces the risk of relapse in high-risk gBRCAm patients (OlympiA trial). In metastatic setting, these molecules have prolonged progression-free survival (OlympiAD, EMBRACA).

Do I need a BRCA genetic test?▾

Yes — the indication for PARP inhibitors relies on demonstrating a pathogenic BRCA1 or BRCA2 mutation (germline, most often). The test is performed at an oncogenetic consultation on a blood sample. Results take several weeks. For triple-negative cancers or high-risk HER2-/HR+ cancers, testing is systematically offered, including in the absence of family history. A BRCA mutation has consequences beyond therapeutic choice: enhanced surveillance, sometimes contralateral prophylactic mastectomy, and family information.

Do targeted therapies replace chemotherapy?▾

Not systematically — they are combined with or substituted for chemotherapy depending on the case. In HER2+ disease, the combination trastuzumab + pertuzumab + chemotherapy remains a standard. In metastatic disease, some targeted therapies (T-DXd, sacituzumab govitecan) have surpassed classical chemotherapy in second line. For HR+/HER2− cancers, the CDK4/6 + endocrine therapy combination often allows chemotherapy to be deferred. For BRCA-mutated cancers, PARP inhibitors can replace chemotherapy in the metastatic setting. The decision is always individualised and discussed at MDT.

What are the side effects of targeted therapies?▾

Variable depending on the molecule. Anti-HER2 agents may affect cardiac function (monitored by echocardiography). T-DXd can cause interstitial lung disease. CDK4/6 inhibitors cause low white blood cell counts (palbociclib, ribociclib) or diarrhoea (abemaciclib). PARP inhibitors mainly cause anaemia, fatigue and nausea, with a rare but serious long-term risk of myelodysplastic syndrome. Overall, these treatments are better tolerated than classical chemotherapy — less alopecia, less severe nausea — but require specific monitoring.

Are targeted therapies reimbursed?▾

Breast cancer is a long-term condition (ALD 30) in France. Targeted therapies with marketing authorisation and a favourable reimbursement opinion from HAS are covered at 100% by French health insurance based on Sécurité Sociale tariffs. Certain recent treatments are subject to early or compassionate access depending on indications. In 2025, ribociclib (Kisqali) did not obtain reimbursement in the early adjuvant setting — your oncologist will inform you of options based on your situation.

How long does a targeted therapy treatment last?▾

Duration varies depending on indication. In adjuvant setting: trastuzumab 1 year, olaparib 1 year, abemaciclib 2 years, ribociclib 3 years (per validated protocols). In metastatic setting: treatment is continued as long as it remains effective and well tolerated — it may therefore last several months to several years. Monitoring is close (consultations, blood tests, imaging).

What is HER2-low and why does it matter?▾

Historically, tumours were classified as HER2 positive (IHC 3+ or FISH-amplified) or HER2 negative. A new category, HER2-low (IHC 1+ or non-amplified 2+), represents about half of HER2-negative breast cancers and now benefits from T-DXd in metastatic setting after the DESTINY-Breast04 trial. This is a revolution: patients previously ineligible for anti-HER2 therapy can now benefit from it. Ask your oncologist for the precise HER2 status on your report.

Can I have a pregnancy during or after targeted therapy?▾

No pregnancy is possible during treatment, and effective contraception is mandatory. An onco-fertility consultation should be offered before starting treatments if a pregnancy project exists — oocyte or embryo freezing. After completing all treatments, pregnancy is possible, in discussion with the oncology team. The POSITIVE trial confirmed that temporary interruption of endocrine therapy for pregnancy does not worsen prognosis.

What is the role of surgery when receiving targeted therapy?▾

For localised cancers, surgery remains the cornerstone — targeted therapy precedes (neoadjuvant) or follows (adjuvant) surgery. In neoadjuvant setting, some combinations (trastuzumab + pertuzumab + chemotherapy for HER2+) lead to sometimes complete tumour regression (pCR), improving prognosis. For metastatic cancers from the outset, surgery is no longer systematic: targeted therapy takes first place. The strategy is defined at MDT.

Can I request a second opinion?▾

Yes, and it is encouraged. Requesting a second opinion before a major therapeutic decision is legitimate and common. It generally does not delay care. Simply bring your biopsy report, imaging results and any MDT report. I offer second-opinion consultations at the Paris 8th office and at the Clinique Hartmann.

Criterion	Anti-HER2	CDK4/6	PARP
Indication	HER2+ (IHC 3+ or FISH+) — all stages. T-DXd also for HER2-low metastatic.	HR+/HER2− advanced/metastatic. Abemaciclib also adjuvant high-risk.	Germline BRCA1 or BRCA2 mutation, HER2−.
Main drugs	Trastuzumab, pertuzumab, T-DM1, T-DXd, tucatinib	Palbociclib, ribociclib, abemaciclib	Olaparib, talazoparib
Route	IV or subcutaneous (antibodies) — oral (tucatinib)	Oral	Oral
Standard combination	+ chemotherapy (taxane) ± pertuzumab	+ endocrine therapy (aromatase inhibitor or fulvestrant)	Monotherapy
Key benefit	Adjuvant trastuzumab: ≈ −33% mortality (HERA, BCIRG-006)	PFS doubled in metastatic (HR ≈ 0.55)	IDFS and OS improved adjuvant (OlympiA)
Dominant toxicity	Cardiotoxicity (LVEF), interstitial lung disease (T-DXd)	Neutropenia (palbo/ribo), diarrhoea (abema), QT prolongation (ribo)	Anaemia, fatigue, nausea. Rare MDS/AML
Specific monitoring	Quarterly echocardiography	CBC, ECG (ribociclib), liver function	Regular CBC and platelets, prolonged surveillance
Companion test	IHC HER2 ± FISH	ER/PR + HER2 on biopsy	BRCA genetic test (oncogenetic)

Sources & references

Scientific references

This article is based on the SENORIF 2025-2026 Reference Document (Île-de-France regional breast pathology reference), guidelines from learned societies (INCa, HAS, ESMO, NCCN, ABC, Saint-Gallen) and the international literature from the major pivotal trials.

SENORIF. Reference document diagnostic and therapeutic — BREAST 2025-2026. PDF Curie.
Tutt ANJ, Garber JE, Kaufman B, et al. Adjuvant Olaparib for Patients with BRCA1- or BRCA2-Mutated Breast Cancer (OlympiA). N Engl J Med. 2021;384(25):2394-2405. NEJMoa2105215.
Geyer CE Jr, Garber JE, Gelber RD, et al. Overall survival in the OlympiA phase III trial. Ann Oncol. 2022;33(12):1250-1268. Ann Oncol.
Cortés J, Kim SB, Chung WP, et al. Trastuzumab Deruxtecan versus Trastuzumab Emtansine for Breast Cancer (DESTINY-Breast03). N Engl J Med. 2022;386(12):1143-1154. PubMed 35320644.
Modi S, Jacot W, Yamashita T, et al. Trastuzumab Deruxtecan in Previously Treated HER2-Low Advanced Breast Cancer (DESTINY-Breast04). N Engl J Med. 2022;387(1):9-20. PubMed 35665782.
Tolaney SM, Jiang Z, Zhang Q, et al. T-DXd + pertuzumab vs taxane + trastuzumab + pertuzumab — first line HER2+ MBC (DESTINY-Breast09). J Clin Oncol. 2025;43(suppl 17):LBA1008. FDA approval.
Swain SM, Baselga J, Kim SB, et al. Pertuzumab, trastuzumab and docetaxel in HER2-positive metastatic breast cancer (CLEOPATRA). N Engl J Med. 2015;372(8):724-734. PubMed 25693012.
von Minckwitz G, Procter M, de Azambuja E, et al. Adjuvant pertuzumab and trastuzumab in early HER2-positive breast cancer (APHINITY). N Engl J Med. 2017;377(2):122-131. PubMed 28581356.
von Minckwitz G, Huang CS, Mano MS, et al. Trastuzumab emtansine for residual invasive HER2-positive breast cancer (KATHERINE). N Engl J Med. 2019;380(7):617-628. PubMed 30516102.
Johnston SRD, Toi M, O'Shaughnessy J, et al. Abemaciclib plus endocrine therapy in HR+/HER2- early breast cancer (MonarchE). Lancet Oncol. 2023;24(1):77-90. PubMed 36493792.
Finn RS, Martin M, Rugo HS, et al. Palbociclib and Letrozole in Advanced Breast Cancer (PALOMA-2). N Engl J Med. 2016;375(20):1925-1936. PubMed 27959613.
Litton JK, Rugo HS, Ettl J, et al. Talazoparib in advanced breast cancer with a germline BRCA mutation (EMBRACA). N Engl J Med. 2018;379(8):753-763. PubMed 30110579.
Robson M, Im SA, Senkus E, et al. Olaparib for Metastatic Breast Cancer with a Germline BRCA Mutation (OlympiAD). N Engl J Med. 2017;377(6):523-533. PubMed 28578601.
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HAS — 16 July 2025 Opinion. Information of women on CDK4/6 inhibitors in early breast cancer. HAS — CDK4/6 Opinion.
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Article written and medically reviewed by Dr Jérémie Zeitoun, surgical oncologist and breast specialist in Paris, former senior physician at Institut Gustave Roussy. Last update: 10 May 2026.

This article is for information purposes and does not replace an individual medical consultation.

FREQUENTLY ASKED QUESTIONS

Frequently asked questions

What is the difference between targeted therapy and chemotherapy?

Chemotherapy acts on all rapidly dividing cells (cancerous and healthy — hence alopecia, nausea, decreased defences). Targeted therapy aims at a precise biological abnormality (HER2, CDK4/6, BRCA defect), hence increased efficacy on the target and better overall tolerance.

Which targeted therapy for which breast cancer subtype?

HER2+: trastuzumab ± pertuzumab ± T-DXd. HR+/HER2− advanced: CDK4/6 inhibitor + endocrine therapy. BRCA-mutated: PARP inhibitor (olaparib, talazoparib). HER2-low metastatic: T-DXd now possible. Metastatic triple-negative: sacituzumab govitecan, pembrolizumab + chemotherapy.

Does trastuzumab cure HER2+ breast cancer?

In adjuvant setting after surgery, trastuzumab reduces mortality from HER2+ breast cancer by approximately one third (HERA, BCIRG-006 trials). Combined with the other treatments (surgery, chemotherapy, radiotherapy), it allows durable remission in most early-stage patients. In metastatic setting, it significantly prolongs progression-free and overall survival.

Is a targeted therapy reimbursed at 100%?

Breast cancer is a long-term condition in France (ALD 30), covered at 100% by Health Insurance. Targeted therapies with marketing authorisation and a favourable HAS reimbursement opinion are included. Notable cases in 2025: ribociclib (Kisqali) not reimbursed in early adjuvant; abemaciclib (Verzenio) reimbursed in high-risk adjuvant; olaparib reimbursed in adjuvant gBRCAm.

Do I need a BRCA test before any treatment?

Not systematically, but an oncogenetic consultation is offered for triple-negative cancers (regardless of age), young patients (< 50 years), in the presence of significant family history (Eisinger score ≥ 3), or for high-risk HR+/HER2− cancers eligible for adjuvant olaparib. The test determines the indication of a PARP inhibitor.

Is surgery still necessary if I receive a targeted therapy?

Yes — for localised breast cancers, surgery remains the cornerstone. Targeted therapy precedes (neoadjuvant) or follows (adjuvant) surgery. In neoadjuvant HER2+, the combination trastuzumab + pertuzumab + chemotherapy can lead to pathologic complete response (pCR), improving prognosis. For metastatic cancers, surgery is no longer systematic.

Targeted therapies for breast cancer Dr Jérémie Zeitoun · Surgeon Paris 8th

The essentials in 30 seconds

Key figures — Targeted therapies

What is a targeted therapy?

Anti-HER2 — the archetype of targeted therapy

Herceptin (trastuzumab)

Perjeta (pertuzumab)

Kadcyla (T-DM1)

Enhertu (T-DXd)

Tukysa (tucatinib)

Lapatinib, neratinib

How infusions work

Cardiac monitoring

CDK4/6 inhibitors — blocking the cell cycle

Ibrance (palbociclib)

Kisqali (ribociclib)

Verzenio (abemaciclib)

Understanding your situation,choosing the best-suited treatment

PARP inhibitors — synthetic lethality

Lynparza (olaparib)

Talzenna (talazoparib)

Other targeted molecules

Trodelvy (sacituzumab govitecan)

Orserdu (elacestrant)

Piqray (alpelisib)

Truqap (capivasertib)

Afinitor (everolimus)

Pembrolizumab — waking up the immune system

From biopsy to the right molecule

Histological biopsy

Staging work-up

Oncogenetic consultation

Breast MDT

Diagnosis disclosure consultation

Initiation and monitoring

Useful documents

Understanding your pathology report

Breast cancer — overview

BRCA hereditary risk assessment

BRCA prophylactic mastectomy

SENORIF 2025-2026 Reference Document

HAS — Information on CDK4/6 inhibitors

INCa — CDK4/6 inhibitors expert opinion

INCa — Breast cancer patient space

Frequently asked questions on targeted therapies

Comparison of the three main families — Anti-HER2 vs CDK4/6 vs PARP