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New Research - Triple Negative Breast Cancer (TNBC)

Dual therapy against Triple Negative Breast Cancer (TNBC) shows promise

Rayan Afif | CERI Youth Program and CERI Research Team Member, and 
Aygün Sahin, MSc, PhD  | CEO, President, and Cancer Lead, Cancer Education and Research Institute (CERI)

Researchers have found in a preclinical study that dual therapy for Triple Negative Breast Cancer (TNBC) shows promise.

The study has explored the combination of Aurora-A kinase (AURKA) and Programmed Death-Ligand 1 (PD-L1) inhibitors to further advance the effectiveness of the treatment of TNBC.

What is Triple Negative Breast Cancer (TNBC)?

Triple Negative Breast Cancer (TNBC) is one of the most aggressive types of breast cancer that accounts for approximately 15-20% of all breast cancers and is mainly found in younger and minority women [1]. This is because TNBC lacks:
  1. Estrogen receptors (ER) (the lack of estrogen hormonal sensors on the cell surface)
  2. Progesterone receptors (PR) (the lack of progesterone hormone sensors on cells), and
  3. Human epidermal growth factor receptor 2 (HER2) expression (absence of sensors recognizing human epidermal growth factor protein) [1].
Chemotherapy is the main treatment for TNBC, since there is no targeted therapy for this breast cancer type because there are no sensor targets to aim at [1].
​

What are the Three Main Breast Cancers?

Breast cancer can be categorized into three main types: 
  1. Estrogen receptor-positive (ER-positive) breast cancer
  2. HER2-positive breast cancer
  3. Triple Negative Breast Cancer (TNBC) [1]
​

Dual Targeted Therapy for TNBC

This strategy focuses on the use of two therapies to treat cancer at once with the aim to attack the cancerous cells in more than one way [2]. In the case of TNBC, the combination of therapy targeting Aurora-A kinase (AURKA) and Programmed Death-Ligand 1 (PD-L1) is under investigation for better treatment.
​

What is Aurora-A Kinase?

Aurora-A kinase (AURKA) is a protein that is involved in cell cycle regulation, particularly in the control of chromosome segregation2 during cell division3 [3]. In the context of cancer, for instance, in TNBC, AURKA can get amplified, which causes improper cell division and thus results in the formation of tumors. It shows elevated levels in the more aggressive forms of breast cancer and in instances where resistance to chemotherapy is observed [2].
​

What is PD-L1?

PD-L1 is a protein on the surface of cancer cells that puts the immune system to sleep, thus allowing the cancer cells to escape the immune system’s destruction [4]. PD-L1 attaches to PD-1 receptors on immune cells rendering them inactive and thus cannot eliminate cancer cells. Immune checkpoint inhibitors work by preventing the interaction between PD-L1 and PD-1, which helps the immune system find and destroy cancer cells [4].

Dual Targeting Through AURKA and PD-L1 in TNBC

In the last decades, the findings have revealed that the combined inhibition of AURKA and PD-L1 may be effective in the treatment of TNBC [2]. AURKA inhibitors may slow down the development of cancer and make cancer cells more responsive to chemotherapy, which may increase the chance of a positive response.

On the other hand, PD-L1 inhibitors increase the immune system’s ability to detect and destroy TNBC cells since PD-L1 uses immune checkpoints to hide from the immune system. When both of these approaches are used in preclinical models, there is an enhancement of the effects obtained as compared to the use of only one agent [2].
​

Importance of the Study for TNBC

This study is a breakthrough in the search for treatment of TNBC, which has few targeted therapies at the moment. Given these findings, this dual-targeted therapy has the potential to enhance the survival of TNBC patients through the inhibition of AURKA, a protein that fuels cancer cell growth, and PD-L1, which allows cancer cells to escape the body’s immune system [4]. If the strategy works in clinical trials, dual-targeted therapy may decrease the risk of recurrence and metastasis for aggressive forms of breast cancer, thus increasing survival rates and enhancing the quality of life for the patients.
Future studies and additional clinical trials are required to support these findings and translate dual-targeted agents into daily practice for the management of TNBC [4]. One important thing to keep in mind is that although this seems like a genuine approach towards future treatment this is still a phase 1 trial, meaning further steps are required for potential approval.

References:

1. Foulkes WD, Smith IE, Reis-Filho JS. Triple-negative breast cancer. N Engl J Med. (2010) 363:1938–48. 
2. Opyrchal M, Gil M, Salisbury JL, Goetz MP, Suman V, Degnim A, et al. Molecular targeting of the Aurora-A/SMAD5 oncogenic axis restores chemosensitivity in human breast cancer cells. Oncotarget. (2017) 8:91803–16. 
3. Dutertre S, Descamps S, Prigent C. On the role of aurora-A in centrosome function. Oncogene. (2002) 21:6175–83. 
4. Dong P, Xiong Y, Yue J, Hanley SJB, Watari H. Tumor-intrinsic PD-L1 signaling in cancer initiation, development and treatment: beyond immune evasion. Front Oncol. (2018) 8:386. 

We recommend you watch our popular videos below to learn more about Breast Cancer and TNBC:

Early Diagnosis of Breast Cancer

How To Do Breast Self-Examination

Breast Cancer Symposium Takeaways

FDA Approvals for Breast Cancer

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