When you hear the words ‘breast cancer’, your mind can start racing. Then often come the labels. ‘Hormone-sensitive’. ‘Estrogen-driven’. ’It feeds on estrogen’. These words are said so often, and usually with so much certainty, that they start to sound like facts. Many women walk away believing their own estrogen has turned against them and caused their breast cancer. Many doctors and clinicians think this too.
That’s not what those words mean, and estrogen does not cause breast cancer. So let's slow down and look at what this really means, and what it does not.
First, what was actually found
After a biopsy or surgery, a laboratory examines a sample of the cancer. One of the things it looks for is receptors: proteins on or inside cells that receive signals.
Routine testing for invasive breast cancer usually checks three markers: the estrogen receptor (ER), the progesterone receptor (PR), and HER2. HER2 is a different type of receptor involved in growth signaling [1].
But these are not the only receptors a cancer cell may carry. They are the ones routinely tested.
Breast cancer cells can also have androgen receptors, which respond to hormones such as testosterone, as well as receptors for insulin and insulin-like growth factors. In one large research review, about 75% of ER-positive breast cancers also had androgen receptors [2]. Researchers have also identified insulin and IGF-1 receptors in human breast tumours, though these are not part of the routine three-marker panel.
The report provides useful information, but it is not a complete map of the cell’s biology. An ‘ER-positive’ result tells us that estrogen receptors are present. It doesn’t tell us every signal the cell can receive or how those signals work together.
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What we routinely measure is only part of the picture
‘ER-positive’ tells us that estrogen receptors are present. It does not describe every signal the cell can receive, or explain, by itself, everything that shapes the cancer’s behaviour.
If enough of the tested cells have the ER or PR receptor, the report says ‘positive’ [3]. All that really means is that the tumour has hormone receptors. It does not tell us what caused the cancer. It does not tell us what is making it grow. Keep that in mind as we go through five of the most common myths.
Myth 1: ‘Hormone-sensitive means hormones caused my cancer’
The truth: ‘hormone-sensitive’ and ‘hormone-responsive’ only mean the lab found hormone receptors in the cancer cells. Having a receptor for a hormone is not the same as the cancer being caused by that hormone [3].
Healthy cells have these hormone receptors too. Normal breast tissue has two main types of estrogen receptors. The one doctors look for on a breast cancer report, ER-alpha, is found in about 10 to 15% of [DLN1.1]the cells that line the milk ducts [4, 5]. The second type, ER-beta, is far more common. About 80% of those cells have it, and so does the tissue around them [4, 6, 7]. Most healthy breast cells carry an estrogen receptor. Your bones, heart, blood vessels, and brain have them as well [8]. An estrogen receptor is not a sign that something went wrong. It is how your body hears one of its most important messengers.
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Myth 2: ‘My cancer is estrogen-driven,’ or ‘it's ER-driven’
The truth: a receptor test cannot tell us that. It shows the estrogen receptor is there. It does not mean that estrogen is driving the cancer, or that it is the only signal the cancer listens to [9].
Breast cancer cells listen to many signals at once. Finding estrogen receptors tells us those receptors are present. It does not, by itself, tell us what is driving the cancer. Calling the cancer ‘estrogen-driven’ goes beyond what the test actually shows.
Myth 3: ‘My cancer feeds on estrogen’
The truth: estrogen is not food. It's a messenger.
Estrogen has many roles in your body. It helps your cells take in sugar for energy [10]. It sends messages to your bones, heart, blood vessels, and brain [8]. Calling it ‘food for cancer’ turns one of your body's key messengers into a villain, which is not accurate.
Dr Zsuzsanna Suba, a pathologist and cancer researcher, goes further. She points out that ER-positive cancers tend to be more organised and less likely to spread, while cancers without estrogen receptors tend to be more aggressive. In her view, the estrogen receptor is likely to be part of the cell's effort to stay in control, not the cause of the problem [10].
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Myth 4: ‘Estrogen is the only signal that matters’
The truth: cancer cells have receptors for many hormones and proteins, not just estrogen.
Progesterone. When progesterone switches on its own receptor (PR), PR can steer the estrogen receptor toward a calmer set of genes. In lab studies and samples of real tumours, progesterone slowed the growth in many ER-positive tumours [12].
Testosterone and other androgens. In laboratory models of ER-positive breast cancer, switching on the androgen receptor slowed cancer growth. Researchers now describe it as a tumour suppressor, a kind of brake, in this type of cancer [13[DLN2.1]]. Studies of women using testosterone point the same way. In studies by Dr Rebecca Glaser and Dr Gary Donovitz, women using testosterone pellets had fewer breast cancers than expected for women their age [14, 15]. A 2024 trial points the same way. In women with advanced ER-positive breast cancer, a medicine that switches on the androgen receptor shrank or stalled the cancer in about 30% of women [16].
Other growth signals. HER2 is one example. There are many more [1].
IGF-1 can even activate the estrogen receptor without estrogen binding to it [11]. Think of a busy switchboard receiving many messages at once. Some signals encourage growth; others help slow or stop it. Estrogen is one part of that larger network. Routine receptor tests look at a few key markers, not what is switching those signals on.
Myth 5: ‘Estrogen positive is bad news’
The truth: here, ‘positive’ is usually the better result.
On most medical tests, ‘estrogen positive’ sounds like bad news. On a breast cancer report, a hormone receptor-positive result usually points the other way. These cancers tend to grow more slowly. They tend to have a better outlook than cancers without hormone receptors.
Progesterone receptors add another piece of encouraging information. Cancers that are both ER-positive and PR-positive tend to have better outcomes than those that are ER-positive but PR-negative [17].
These receptors also interact. In laboratory research, the progesterone receptor worked with the estrogen receptor, changing which genes it switched on [12]. That helps us see why looking at estrogen receptors alone gives us only part of the picture. The way receptors work together matters, too.
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Words matter in medicine
Even a small change in wording can change what a reader understands. That is why we need to be precise: progesterone and synthetic progestins are not interchangeable terms. Neither are bioidentical estradiol and synthetic estrogens. When we group them together without naming the differences, we can blur what the research actually studied, and what it can tell us.
The same care matters when we describe breast cancer. ‘ER-positive’ tells us that the cells tested positive for estrogen receptors. Calling that cancer ‘estrogen-driven’ adds an interpretation beyond the lab finding itself.
Going forward, we can choose words that describe what we know:
- Instead of ‘hormone-sensitive cancer,’ we can say, ‘a cancer with hormone receptors’
- Instead of ‘estrogen-driven’ or ‘ER-driven,’ we can say, ‘ER-positive’
- Instead of ‘it feeds on estrogen,’ we can say, ‘the cells have estrogen receptors’
- And instead of the vague phrase ‘hormonal cancer,’ we can say ‘hormone receptor-positive cancer’.
These terms describe what the testing found without claiming to explain the cancer’s entire biology. They also avoid language that can leave women feeling that their own bodies, or their hormones, are to blame.
