Breast cancer is the most common cancer among women.1 About 1.67 million new cases are diagnosed worldwide, and over 500,000 women die of the disease each year.1 This means that one woman is diagnosed with breast cancer somewhere in the world every 20 seconds and more than three women die of breast cancer every five minutes worldwide.1
There are several types of breast cancer, which can be classified based on the proteins (known as receptors) that coat the surface of the cancer cells. These proteins play an important role in tumour development, by signalling cells to grow and divide.
Each type of breast cancer is identified by the presence or absence of three receptors found on the surface of cells: the oestrogen receptor (ER), the progesterone receptor (PR) and the Human Epidermal Growth Factor Receptor 2 (HER2).2 When diagnosed, people can be confirmed as being positive or negative for more than one of these receptors.
HR-positive breast cancer is the most common type of breast cancer, accounting for approximately 80% of cases.2 Breast cancers are considered HR-positive when tumour cells produce abnormal amounts of receptors for the hormones, oestrogen and/or progesterone. As these hormones signal cells to grow and divide, having too many receptors on the surface of a cell can cause uncontrolled growth and the formation of a tumour. HR-positive breast cancers are commonly treated with medicines, known as hormone therapies, that block the activity of ER and/or PR, or that reduce hormone levels.
HER2-positive breast cancer – characterised by cells that over-produce the HER2 protein – represents approximately 20% of all breast cancers. This type of breast cancer can be particularly aggressive. If left untreated, it is associated with faster disease progression and poorer chances of survival compared to HER2-negative disease (i.e. breast cancer cells that are coated with normal amounts of the HER2 protein).3 Today, treatments are available which specifically target HER2, blocking the signals that cause cancer cells to grow and multiply.
Triple-negative breast cancer (TNBC) is a rare form of breast cancer, accounting for around 10-20% of all breast cancers.4 It is a type of breast cancer that lacks oestrogen and progesterone receptors and does not over-produce the HER2 protein. The mechanisms that drive this type of cancer are therefore largely unknown, which makes it a particularly difficult type of breast cancer to treat. Although patients may respond to chemotherapy, overall, treatment options are limited, and the prognosis is often poor.5
Knowing the type of breast cancer a patient has is important, because whilst some treatments such as surgery and radiotherapy may be similar across different types of breast cancer, drug treatments such as chemotherapy, hormonal therapy and targeted therapies will differ between cancer types.6
When diagnosed, patients will be told the ‘stage’ of their breast cancer. This indicates how big it is and how far it has spread (if at all). The stage is important because it helps cancer specialists to decide on the best course of treatment for a patient. Generally, the more advanced the cancer is, the harder it is to treat and the worse the prognosis is likely to be.7
The majority of breast cancer cases are diagnosed at an early stage, before the cancer has spread beyond the breast.8,9 When treated at this early stage, breast cancer may be potentially curable.10 The eBC treatment approach is comprehensive and may involve treatment before and after surgery to remove the cancerous cells and prevent them from returning.
Unfortunately, some patients are initially diagnosed with an advanced stage of disease, or they see their cancer return and worsen after initial treatment for eBC. For patients whose cancer has spread to other parts of the body, such as the brain or liver, cure is sadly no longer a possibility. The goal of treatment for patients with aBC is to prolong life as much as possible, while also trying to keep patients feeling as well as possible by managing symptoms and treatment side-effects.11
Wolff AC, et al. Journal of Clinical Oncology 2013;31(31):3997-4013.
Hammond E. Journal of Clinical Oncology 2011;29,15:e458.
Cardoso F, et al. Annals of Oncology 2012; 23(suppl 7):vii11-9.
Cardoso F, et al. Annals of Oncology 2014;25:1871–1888.