BCAC Chair Libby Burgess reflected on this question after attending the premier international breast cancer research conference, SABCS 2023, in San Antonio Texas last month. Triple negative breast cancer (TNBC) is an aggressive subtype lacking HER2 or hormone receptors. It is the most challenging type of breast cancer to treat, particularly at the advanced stage. However, research over the last 20 years has broadened treatment options and improved patient outcomes. 

At SABCS, Libby was able to gain an in-depth understanding of current treatments offered overseas and the scientific evidence backing them, as well as learning about where the research is heading next. Libby noted with dismay how far New Zealand has fallen behind the rest of the developed world in treating both the early and advanced stages of this aggressive breast cancer subtype. Neoadjuvant therapy is not offered to all who would benefit. There is no funded access to immunotherapies such as pembrolizumab (Keytruda) and atezolizumab (Tecentriq), PARP inhibitirs such as olaparib (Lynparza) and talazoparib (Talzenna) or the antibody drug conjugates sacituzumab govitecan (Trodelvy) or T-DXd (Enhertu). BCAC is resolved to continue to advocate strongly for better access to modern treatments for TNBC in Aotearoa New Zealand.

You can read Libby’s essay on this topic below.



Triple-negative breast cancer (TNBC) is an aggressive breast cancer subtype that lacks expression of oestrogen and progesterone receptors and amplification or overexpression of human epidermal growth factor receptor 2 (HER2). The absence of these receptors renders endocrine and HER2-targeted therapies ineffective, leaving cytotoxic chemotherapy as a standard treatment option. However, chemotherapy results in suboptimal antitumor response rates and short overall survival and response durations. TNBC is the most challenging type of breast cancer to treat, particularly at the advanced stage. However, research over recent years has broadened treatment options and improved patient outcomes.

TNBC is now known to be a diverse disease more accurately categorised according to the immune status of the tumour, rather than simply an absence of hormone and HER2 receptors. Firstly, it is now known that TNBC tumours may be either ‘immune-enriched’, or ‘hot’, meaning they exhibit a higher level of tumour-infiltrating lymphocytes (TILs), or ‘cold’, meaning they are low in TILs. The hot tumours have a more favourable prognosis than the cold tumours. Second, TNBC may exhibit high or low levels of the biomarker PD-L1. Finally, TNBC tumours may be positive or negative for BRCA mutations. Importantly, better understanding of TNBC in terms of TIL, PD-L1 and BRCA status have all led to more targeted treatment of TNBC, which is much needed. Research over the last two decades that has led to the development of these new, more effective ways of treating TNBC was summarised at the recent San Antonio Breast Cancer Symposium (SABCS).

Recent research has identified cytotoxic chemotherapy agents that are more effective in treating TNBC, along with indications of the sequencing and combinations likely to provide optimal outcomes while avoiding unnecessary toxicity. These medicines and strategies can be used for all patients in New Zealand (NZ), although some clinics struggle to coordinate the services needed to provide timely neoadjuvant therapy. Novel, effective targeted treatments for TNBC include immune checkpoint inhibitors, PARP inhibitors and antibody drug conjugates. These have been rapidly approved and brought into standard practice in many countries. Unfortunately, none of these breakthrough medicines have yet been funded by NZ’s medicines purchasing agency Pharmac, so they are not available to those treated in our public health system. They can, however, be used to treat patients who can afford to pay for their cancer treatment in private clinics. The lack of modern, targeted therapies in our health system compromises quality of life and reduces the survival of those diagnosed with TNBC, driving socioeconomic and ethnic inequities in health outcomes. 

Recent advances in TNBC

A plenary lecture on Recent Advances in TNBC (PL-02) was presented by Assoc Prof Melinda Telli, Stanford School of Medicine, SF, CA, USA.

Dr Telli, Director of the Breast Cancer Program at Stanford Cancer Institute, is a translational scientist with expertise in TNBC. She began her talk by reflecting on a patient she treated when she first began working in this area back in 2007. She acknowledged Sunita, who was 33 years old and breast feeding her second daughter when diagnosed with a locally advanced triple negative breast cancer (TNBC) tumour and a germline BRCA1 mutation (gBRCA1m). Sunita was treated with neoadjuvant (given before surgery) anthracycline and a taxane, but she had minimal response to the treatment. After surgery there was significant residual disease. Based on emerging data she was treated with platinum-based chemotherapy. This strategy proved effective and Sunita is now a teacher, about to turn 50.

From my advocate’s perspective, it is heartening when clinical researchers acknowledge particular patients, as this indicates they care personally about their patients as people with real lives. This further confirms that they are fully committed to achieving the very best possible outcomes for each and every one of them.

Dr Telli noted that, as a result of recent research findings, those with a similar diagnosis today would be treated with a very different standard of care. In 2007, adjuvant therapy (given after surgery) involved the use of anthracycline and taxane-based regimens; the use of other cytotoxics was not optimised.  At that time, there were no approved targeted therapies and no clear treatment standard for metastatic TNBC. Survival for mTNBC was 12 – 18 months. In 2023, carboplatin is regularly used, along with immune checkpoint inhibition (CPI) and PARP inhibition (PARPi) in those with a BRCA mutation. Dr Telli summarised what has been achieved through research in recent years.

Recent advances in treatment

Advances in treatment of early stage TNBC (eTNBC)

  • Adjuvant capecitabine improves disease free survival (DFS)
  • Addition of pembrolizumab to neoadjuvant chemotherapy improves event-free survival (EFS)
  • Adjuvant olaparib in gBRCA1/2m high risk breast cancer improves DFS and overall survival (OS)
  • Addition of carboplatin to neoadjuvant anthracycline and taxane-based chemotherapy improves DFS and OS

Advances in treatment of advanced TNBC (mTNBC)

  • The PARP inhibitors olaparib and talazoparib improve progression-free survival (PFS) in gBRCA1/2m breast cancer
  • Pembrolizumab improves PFS and OS in pre-treated PD-L1+ mTNBC
  • The antibody drug conjugate (ADC) sacituzumab govitecan (SG) improves PFS and OS in pre-treated mTNBC
  • The ADC trastuzumab deruxtecan (T-DXd) improves PFS and OS in pre-treated mHER2 low breast cancer, including TNBC.
Research breakthroughs in TNBC

Dr Telli reviewed the historical research breakthroughs that have led to the knowledge we now have of TNBC and hence our ability to treat it more effectively.

Breast cancer molecular subtypes were first described in 2000, including basal-like, which was frequently hormone receptor negative (HR -) and HER2 -. Around 5 years later the term TNBC was coined to describe breast cancers that were ER-, PR- and HER2-. Clinical features were soon described, including high rates of early recurrence, frequent visceral occurrence at first relapse, along with the fact that TNBC is experienced at higher rates by African-American women, especially in those who are pre-menopausal. It was also noted in 2003 that around 75-80% of gBRCA1m breast cancers are triple negative and basal-like. 

Targeting DNA repair mechanisms - PARP inhibitors and platinum chemotherapy

In 2005, research showed that BRCA1 and 2 deficient cells are highly sensitive to inhibition of the enzyme PARP, which is involved in repair of damaged cells. This discovery led to the initiation of clinical trials and the eventual development of therapies for hereditary breast cancers and for TNBC. In 2009 and 2010 the success of targeting DNA repair mechanism defects in treating gBRCA1/2m breast cancers was clinically demonstrated, using both the platinum-based DNA-damaging cytotoxic chemotherapy cisplatin and the PARPi olaparib. These results raised the possibility that targeting DNA repair could be useful in TNBCs that were not BRCAm. By 2018 a number of homologous recombination defects were demonstrated to be implicated in sporadic TNBC and biomarkers were investigated to better describe the biology involved. The TNT trial tested the use of carboplatin or docetaxel as first line treatments in TNBC and gBRCA1/2m advanced breast cancer. Carboplatin was shown to achieve a higher rate of objective response (ORR) for both germline (inherited) and somatic (sporadic) mutations. Biomarkers were unable to identify a subgroup of patients more likely to benefit from this treatment. 

Soon after this, results from the OlympiAD and EMBRACA trials demonstrated PFS advantages of PARPi over treatment of physician’s choice (TPC), leading to the 2018 approvals of the PARPi olaparib and talazoparib for use in advanced gBRCA1/2m breast cancer. The next step was to test these therapies in the early breast cancer (eBC) setting. The OlympiA trial included 1800 patients recruited worldwide (olaparib N=921, placebo N=915) who were randomised to receive one year of olaparib vs placebo following neoadjuvant or adjuvant therapy. Benefits were demonstrated in invasive DFS (106 vs 178 events; HR=0.58, P<0.001), distant DFS (89 vs 152 events; HR=0.57, P<0.001) and OS (70 vs 103 breast cancer deaths; HR 0.68, P= 0.009). The occurrence of fewer ‘non-breast’ cancers in the olaparib-treated group suggested this medicine might have a preventive effect for other cancers. 

Optimising chemotherapy – Carboplatin and partners

A number of small neoadjuvant studies evaluated the addition of carboplatin to chemotherapy. Most of these demonstrated a PFS advantage. Long-term results were somewhat variable but none of those studies were powered to test this (i.e. not designed to have enough participants to statistically demonstrate this). At SABCS in 2022 important results were reported from a phase 3 (larger) study in which carboplatin was added to neoadjuvant therapy in patients with unselected eTNBC. There were benefits in both EFS and OS with the addition of carboplatin, with results being particularly strong for young pre-menopausal women. Another trial testing this strategy in the adjuvant setting is yet to report. The NeoSTOP trial compared the safety and efficacy of the taxane docetaxel with that of paclitaxel and anthracycline (AC) as the neoadjuvant chemotherapy partners for carboplatin. Rates of pathological complete response (pCR, i.e. absence of tumour and lymph node involvement following neoadjuvant therapy) were very similar in the two trial arms, while docetaxel showed fewer side effects (lower neutropenia, febrile neutropenia, anemia and thrombocytopenia) and was associated with higher rates of therapy completion than the other combination treatment. Such treatments that are effective and cause fewer damaging side effects are clearly needed.

Optimising chemotherapy - Capecitabine

Post-neoadjuvant (treatment following neoadjuvant treatment and surgery) capecitabine was shown in the CREATE-X trial to improve DFS by 14% and OS by 8.5% in patients with TNBC who had residual disease after standard neoadjuvant therapy. This established a new standard of care for such patients.

Immunotherapy - Checkpoint inhibitors

T cells, i.e. lymphocytes, are a type of white blood cell important in mounting an immune response to disease. Around 2013 several studies demonstrated the importance of tumour-infiltrating lymphocytes (TILs) in TNBC, with higher TIL numbers leading to a better prognosis. Immune checkpoint inhibitors (CPIs) targeting cell surface receptor Programmed death-1 (PD-1) and Programmed death ligand-1 (PD-L1) have emerged over the last decade as important oncology agents. Binding of PD-1 to PD-L1 activates downstream signalling pathways and inhibits the activation of T cells. High PD-L1 expression on tumour cells and antigen-presenting cells in the tumour microenvironment mediate tumour immune escape, i.e. the ability of tumours to be masked from the immune system and continue to grow. Anti PD-1/PDL-1 antibodies can be used to prevent this escape. 

PDL-1 expression was shown to be higher in TNBC than other breast cancer tumours. The KEYNOTE-355 clinical trial tested the addition of pembrolizumab to the first line chemotherapy treatment of advanced TNBC. Improvements in PFS (around 4 months) and OS (median gain 7 months) in a subgroup of patients with combined positive score (CPS, a measure of PD-L1 expression) ≥ 10 (around 40% of trial participants) led to FDA giving accelerated approval and then full approval for its use. This is now the standard of care for first line treatment of mTNBC. 

KEYNOTE-522 was a landmark study that tested the addition of pembrolizumab to neoadjuvant chemotherapy and then continued for a year after surgery in stage 2 or 3 eTNBC. Pembrolizumab led to a 13.6% improvement in pCR in those with PDL1+ tumours and 7.5% in those with PDL1- disease. Recent 5-year follow-up data shows a remarkable EFS benefit of 9% in the whole population treated, with the greatest benefit demonstrated in those who had residual disease following neoadjuvant therapy (62.6% EFS vs 52.3% EFS). Those who achieved pCR had 92.2% EFS with pembrolizumab, 88.2% without. Unfortunately, 15% of those receiving pembrolizumab suffered grade 3 or worse toxicities compared to only 2% in the placebo arm. This is significant as some toxicities can be life-long. 

Questions remain regarding the use of CPIs in eTNBC. It is unknown whether adjuvant CPI use adds any benefit to neoadjuvant therapy. The GeparNUEVO study demonstrated similar long-term benefits to KEYNOTE-522 from neoadjuvant use alone. ALEXANDRA/Impassion 030 showed no benefit of adjuvant CPI in the form of atezolizumab added to chemotherapy (data presented by Ignatiadis et al. in GS01-03 at SABCS 2023, see summary below). A further trial, OptimICE-pCR, will investigate this in patients who achieve pCR. The SWOG1418 trial is comparing the use of 1 year of adjuvant pembrolizumab to no additional treatment in patients with eTNBC who received neoadjuvant therapy and did not achieve pCR. This study is now closed and data on invasive disease free survival (IDFS) is eagerly awaited.

The optimal chemotherapy backbone for CPI is currently unknown. The SCARLET study is designed to assess whether all patients need anthracycline in addition to a taxane and platinum-based chemotherapy.

The search for biomarkers that can predict benefit and toxicity of CPI continues. 

Antibody drug conjugates

Antibody drug conjugates (ADCs), consisting of an antibody, a linker and a chemotherapy payload, have recently been added to the arsenal of treatments for TNBC. The anti-Trop-2 monoclonal antibody (MAB) sacituzumab govitecan (SG) has a high ratio of the cytotoxic drug SN-38 to antibody, ensuring delivery of a high quantity of payload to the tumour. Trop-2 is a common epithelial antigen found on many solid tumours, including TNBC. The ASCENT trial compared SG treatment with TPC in heavily pre-treated patients with refractory or relapsed mTNBC. SG showed clear benefit in both PFS and OS, with a very good ORR shown in heavily pre-treated patients. SG was fully approved by FDA in 2021. SG has a similar side-effect profile to chemotherapy, with patients often experiencing myelosuppression, gastrointestinal (GI) toxicity and alopecia.

Trastuzumab deruxtecan (T-DXd) is another MAB and ADC that targets HER2 using trastuzumab, linked to DX-d, a topoisomerase I inhibitor payload, with a similar chemotherapy payload to antibody ratio to SG. It is effective in HER2 low breast cancer as well as its originally intended target of HER2+ breast cancer, but it’s also relevant to TNBC. In addition to its direct effect on target cells its membrane-permeable payload also enables transfer to nearby cells, causing a beneficial ‘bystander’ effect that kills neighbouring tumour cells. In DESTINY-Breast04, T-DXd was compared with TPC in patients with advanced HER2 low breast cancer who had been treated with one or two prior lines of chemotherapy. The study included 480 patients with refractory HR+ disease but also 60 patients who were HR- and considered to have TNBC. Exploratory analysis of data for the HR- patients showed impressive benefits in both PFS (8.5 vs 2.9 mo) and OS (18.2 vs 8.3 mo) with ORR at 50.0 vs 16.7. On this basis, in 2022 the FDA approved T-DXd for use in advanced HER2 low breast cancer, including TNBC. 

Future priorities in TNBC research

Looking towards the near future, Dr Telli noted that there are many new agents in clinical development that will play a part in future treatment regimens. There is an urgent need to understand the optimal sequencing and duration of treatments and to diversify antibody targets and payloads. She stated that as multiple new agents show benefit, their safety and tolerability profiles will determine which are chosen for clinical use. She noted the real progress made in TNBC over the last 20 years, the many new medicine approvals over the past 5 years and the likelihood of many more in the next 5 – 10 years. 

Dr Telli acknowledged the many researchers who had tested important hypotheses that did not lead to clinical advances, noting that their work has taught us more about the disease. An important conclusion was that TNBC research has included collaborating participants from around the world and that the focus on this subtype has enabled significant advances to be made. 

In her final consideration of future directions, challenges and opportunities, Dr Telli noted that ctDNA (circulating tumour DNA, i.e. tumour-derived fragmented DNA circulating in the bloodstream) to detect Minimal Residual Disease (MRD) holds incredible promise to optimise therapy in eTNBC. This is because presence of MRD is closely associated with disease recurrence, so ctDNA MRD is a prognostic biomarker that will help to identify those at greatest risk and in need of further treatment as well as those at reduced risk, enabling avoidance of overtreatment. Collaboration and partnering will be needed to include this element in trial design.

Dr Telli stressed that research into mTNBC must continue to seek curative therapies. Survival gains are obviously desirable but the goal should be to cure. She encouraged new researchers to engage in research on TNBC given the huge opportunity to make a positive difference for the many patients with this breast cancer. 

Is adjuvant immunotherapy needed after neoadjuvant in eTNBC?

Associate Professor Michail Ignatiadis, Institut Jules Bordet and l’ Université Libre de Bruxelles, reported results from a trial testing the benefits of adjuvant (as opposed to neoadjuvant) CPI therapy. 

(GS01-03) Adding atezolizumab to adjuvant chemotherapy for stage II and III triple-negative breast cancer is unlikely to improve efficacy: interim analysis of the ALEXANDRA/IMpassion030 phase 3 trial

Early stage TNBC is known to have a high rate of relapse and checkpoint inhibition is known to improve patient outcomes, although optimal sequencing has needed elucidation. To test the safety and efficacy of adding CPI to adjuvant chemotherapy in eTNBC, the ALEXANDRA/Impassion030 trial randomised 2,199 patients with operable stage II-III TNBC into two study arms. Both arms received adjuvant paclitaxel for 12 weeks followed by dose dense anthracycline (epirubicin or doxorubicin) and cyclophosphamide (AC chemotherapy) for 4 doses every 2 weeks.  Half the participants also received atezolizumab every 2 weeks with chemotherapy, followed by maintenance atezolizumab every 3 weeks until completion of 1 year of atezolizumab. 

After a median follow-up of 25 months, range 0 – 53 months, the study was closed because the hazard ratio for IDFS in the intention to treat population (all those initially randomised to receive the treatment in the clinical trial) crossed the pre-specified futility boundary (HR>1). In this event-driven study no differences had emerged in outcomes for those receiving the CPI vs those who received chemotherapy alone. The same applied for all secondary endpoints. Safety data were consistent with the known profile of atezolizumab, with fatigue, diarrhoea, rash and liver enzyme changes being numerically higher in the CPI arm. 

The results of this study support other emerging data suggesting that in early TNBC, checkpoint inhibitors appear to have their greatest efficacy in the neoadjuvant setting and not when used as adjuvant therapies (see summary of Dr Telli’s plenary lecture presented above). 

Immunotherapy with chemotherapy or a PARPi in mTNBC?

Professor Hope Rugo, Department of Medicine (Haematology/Oncology); Director, Breast Oncology and Clinical Trials Education; Medical Director of Cancer Infusion Services, University of California San Francisco reported emerging results from a phase 2 trial comparing the efficacy and safety of pembrolizumab plus olaparib with pembrolizumab plus chemotherapy as maintenance therapy following induction therapy of pembrolizumab plus chemotherapy in an unselected population of patients with mTNBC that was responding to treatment or stable. 

(GS01-05) Pembrolizumab + Olaparib vs Pembrolizumab + Chemotherapy After Induction With Pembrolizumab + Chemotherapy for Locally Recurrent Inoperable or Metastatic TNBC: Randomized Open-Label Phase 2 KEYLYNK-009 Study

After median follow-up of 17.2 months in this small study (N=271) neither PFS nor OS were improved in the olaparib-treated group. In patients with a BRCA mutation, there was a positive trend for PFS and OS for those who received olaparib. A lower rate of adverse events was experienced by those receiving olaparib than experienced by those receiving chemotherapy. 

In conclusion, in patients with responding or stable mTNBC after induction chemotherapy and pembrolizumab, maintenance with pembrolizumab and olaparib shows similar efficacy to maintenance with chemotherapy and pembrolizumab, with those receiving the PARPi experiencing a more favourable safety profile. 

Sequencing ADCs in later line mTNBC – SG or T-DXd first?

Poster 1

François Poumeaud Department of Medical Oncology, Oncopole Claudius Régaud IUCT-O, Toulouse, Midi-Pyrenees, France reported on a small retrospective study that examined the sequencing of SG and T-DXd.

(PS08-02) Efficacy of Sacituzumab-Govitecan (SG) post Trastuzumab-deruxtecan (T-DXd) and vice versa for HER2 low advanced or metastatic breast cancer (MBC): a French multicentre retrospective study.

I was hoping that this study would provide an early indication of whether SG before T-DXd or vice versa would be more safe or efficacious than the other as a later line treatment for mTNBC. However, the study only tested SG first followed by T-DXd in 82 HR-/HER2 low patients and did not test T-DXd followed by SG in this group. Some received other chemotherapy following progression on SG and before T-DXd, while others switched immediately from SG to T-DXd, so the trial design did not allow many conclusions to be drawn.

There was a suggestion from the author that there could be cross-resistance between these ADCs as they carry similar payloads, and a better strategy could be to sequentially use ADCs that deliver chemotherapies with distinct targets. 

Poster 2 

Rachel O. Abelman, MD, Massachusetts General Hospital, Boston, MA reported on a similar exploration of sequencing and mechanisms of cross resistance among ADCs.

(PS08-03) Sequencing Antibody-Drug Conjugate after Antibody-Drug Conjugate in Metastatic Breast Cancer (A3 study): Multi-Institution Experience and Biomarker Analysis

Dr Abelman noted that there are already multiple ADCs being used in mBC and that many more are in development. Best practices for sequencing these are unknown. This study was designed to test whether the same antibody target or same payload would influence the likelihood of cross resistance. Cross resistance between ADCs was scored if there was progression on the second sequential ADC at the first subsequent staging or progression within 60 days of treatment initiation. 

Results suggested that cross resistance was driven by the antibody target in some patients vs the payload in others, highlighting the heterogeneity of mechanisms related to ADC resistance. Sequencing of tumours revealed candidate resistance mutations that could guide optimal sequencing for individual patients. 

Real World effects of immunotherapy on black vs white American patients with TNBC

Poster 3

Mara Hofherr, PharmD, Oncology clinical pharmacist, Washington University, St. Louis, Missouri, United States reported interesting Real-World Evidence on black vs white patients receiving neoadjuvant pembrolizumab according to the KEYNOTE-522 study.

(PS14-02) Real-world analysis comparing Black and White patients with triple-negative breast cancer receiving therapy per KEYNOTE-522

Real world evidence refers to data collected on the outcomes of implementing the findings of clinical trials in patients outside the strict settings and criteria of a clinical trial. Across the world there is growing recognition of the need for greater inclusiveness of diversity in ethnicity, age, gender, physiological and disease state in clinical trial design. Only 4.5% of the original KEYNOTE-555 trial participants were black women, so it was important to gather data to discover the true effects of this treatment on the black population. In this study, neoadjuvant CPI was given to 86 black women and 200 white women across 16 cancer treatment sites. Rates of pCR and toxicity were compared.

While the treatment was equally effective on both groups of patients with equivalent pCRs, white women suffered more grade 3 or worse immune-related adverse events (33.8% vs 20.9%). The authors were unable to determine the reason for this difference. However, despite the variation in adverse events, there were similar rates of hospitalisation and acute care in the two groups.

Matching TNBC patients to the best therapies

Satellite Educational Symposium

Matching the Right Patients to the Right Therapies in TNBC: Case-based applications of immune checkpoint inhibitors, PARP-inhibitors and TROP-2-targeted ADCs

Reassuringly the strategies proposed by a panel of experts in each case study exactly matched Dr Telli’s description of best practice treatment of TNBC described in the Recent Advances in TNBC plenary lecture summarised above. 


Over the past 20 years there has been significant progress in the established standard of treatment for TNBC. This has resulted from the work of many laboratory scientists and clinical researchers around the globe who have focused on understanding the mechanisms that drive this ‘difficult to treat’ breast cancer subtype. Collaboration has been a key to this success. Several new targeted therapies are now known to reduce the rate of metastasis in early disease and to extend both PFS and OS in advanced disease. The use of CPIs, PARPi and ADCs, along with more precisely selected and sequenced cytotoxic chemotherapy agents has significantly improved patient outcomes. Many new therapies will emerge over the next 5 to 10 years that promise further improvement to treatment strategies. Overcoming or avoiding cross resistance among targeted agents will be an important research objective. Minimising side effects is a critical goal for both patients and clinicians. Many biological mysteries remain to be unravelled in the fascinating study of TNBC.

What is BCAC doing to bring modern treatments to New Zealand patients with TNBC?

The evidence presented at SABCS on best practice treatment of TNBC clearly demonstrates how far New Zealand has fallen behind the rest of the developed world in treating both the early and advanced stages of this aggressive breast cancer subtype. Median survival for New Zealanders diagnosed with mTNBC is staggeringly low at only 6.6 months (Breast Cancer Foundation, 2018), lower than the 12 to 18 months experienced by US women back in 2007. The Breast Cancer Aotearoa Coalition (BCAC) is working to change this through our advocacy. We inform through our website as well as our Facebook page and groups. We comment in media and advocate to politicians and health officials, seeking reform and improvements that will benefit patients. 

One of BCAC’s founding committee members is a pharmaco-economist with the skills to make formal evidence-based applications to NZ’s medicines funding agency, Pharmac. Late in 2022 BCAC applied for funding of pembrolizumab for both high-risk early stage and advanced TNBC, citing the PFS and OS benefits demonstrated in the KEYNOTE-355 and KEYNOTE-522 clinical trials. We are also considering preparing an application for sacituzumab govitecan based on the results of the ASCENT trial showing that this medicine improves in both PFS and OS in pre-treated mTNBC. Over the last two years we have encouraged the company that owns this medicine to seek registration and funding in New Zealand. The DESTINY-03 trial demonstrated superiority of T-DXd over T-DM1 in second line treatment of patients with advanced HER2+ breast cancer with advantages in both PFS and OS. DESTINY-04 has demonstrated similar advantages in HER2 low mBC. BCAC has written to Medsafe, our medicines regulator, seeking priority status for the applications to register T-DXd for both these indications and we will support the company’s Pharmac applications. 

New Zealand is a difficult environment for pharmaceutical companies as it takes considerable time, effort and expense to get medicines to market. An important role for BCAC is to encourage and support companies to bring their medicines to our country, to apply for registration by Medsafe, for funding from Pharmac, and to establish cost-share programmes prior to funding. We also collaborate with other patient groups to persuade the government to increase funding for medicines. 

The ability to report the latest expert summary of best practice treatment from SABCS strengthens our work to achieve better outcomes for New Zealanders diagnosed with breast cancer. 

15 January 2024

For more information on treatments available for the different subtypes of advanced breast cancer in Aotearoa New Zealand read our article here.

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