Does Estradiol Make an Existing Breast Cancer Grow? What I Found When I Followed the Evidence From the Petri Dish to Real Women

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"Even a drop of estrogen could feed your cancer."

I hear some version of this almost every week. A woman tells me she was handed this sentence at diagnosis, or at a follow-up visit, or when she asked about help for hot flashes, sleep, joint pain, or vaginal dryness. Sometimes she was told it years after her breast cancer treatment ended. Often it was said with total certainty.

That sentence carries a lot of weight. It shapes decisions women make for decades. It can mean living for decades without a hormone that helps run your bones, brain, heart, blood vessels, metabolism, and immune system. So I think it is fair to ask a simple question: where is the proof?

If we are going to tell women that estradiol (the main estrogen your ovaries made for most of your life) will make an existing cancer grow, we should be able to show it happening in women. Not in a dish. Not in a mouse with a broken immune system. In women.

So I went looking. I went back through the research I have been collecting for years. I went back through my notes and my conversations with Dr. Zsuzsanna Suba, a cancer researcher whose work on estrogen has changed how I think. And I put it all in order, from the weakest kind of evidence to the strongest.

This is what I found. My hope is that you can read it, understand it, and take it to your doctor.

What the warning rests on

The idea that estrogen "feeds" breast cancer did not come from nowhere. It comes from a few real observations:

• Most breast cancers have estrogen receptors. A receptor is like a docking station on the cell. "ER-positive" means the cancer has these docking stations.

• In the lab, estradiol can make some breast cancer cells divide faster.

• In some mouse studies, giving estradiol made human breast tumors grow.

• Drugs that block estrogen, or lower it, help some women with ER-positive cancer.

Each of these is true as far as it goes. The question is how far it goes. A docking station tells you a cell can hear estrogen. It does not tell you what the cell will do with that message inside a whole, living woman.

So let's walk up the ladder of evidence one rung at a time.

Rung one: cells in a dish

Much of what we "know" about estrogen and breast cancer started with cells growing in a lab dish.

The most famous of these cells is called MCF-7. The name stands for Michigan Cancer Foundation-7. These cells came from one woman.

In 1970, doctors drained fluid from around her lung. Her breast cancer had already spread there. Researchers grew her cancer cells in the lab, and they have been copied and shared around the world ever since [1]. MCF-7 is now the most studied breast cancer cell line in the world. By 2015, it had been used in nearly 25,000 scientific papers [2].

In the 1970s, Dr. Marc Lippman and his team showed that estradiol made MCF-7 cells divide [3]. This is one of the starting points for the whole "estrogen feeds cancer" story. But there are details in that early work that rarely get repeated. In a 1976 paper, the team tested six different breast cancer cell lines. Only one, MCF-7, showed a strong growth response to estrogen. And at very high doses, estrogen slowed the cells down and even killed them, though the authors thought that was a general toxic effect of the high dose [4].

So even in the dish, the answer was "it depends."

What is missing in a dish

Think about what a breast cancer cell lives in inside your body. Now think about what it lives in inside a dish.

In your body, a cancer cell is surrounded by its neighborhood. Scientists call this the tumor microenvironment. It includes:

• Blood vessels that bring food and oxygen

• Fat cells and support cells that send their own signals

• Immune cells that patrol, check IDs, and remove cells that do not belong

• A steady flow of hormones and messengers from your liver, gut, pancreas, thyroid, brain, and more

In a dish, almost all of that is gone. The cells sit in a liquid that researchers mix by hand. There is no immune system. There is no liver breaking estrogen down. There are no rising and falling hormone levels. There is no insulin, blood sugar, or stress hormone pattern like a real woman has. It is one kind of cell, alone, in a very strange place.

It also matters that these cells have been living in labs for more than 50 years. Cells change as they are copied over and over. In 2018, researchers compared 27 different batches of MCF-7 cells from labs around the world. They were not the same. Their genes had drifted apart. When the batches were tested against 321 cancer drugs, at least 75% of the drugs that strongly stopped some batches did nothing at all to others [5]. If the "same" cells can react so differently from lab to lab, we should be careful about treating any one result as a law of nature.

One more example shows how much the setting matters. In 1986, a team studied another breast cancer cell line called T47D. Some of these cells needed estrogen to grow into tumors in animals. But in a dish without blood serum, those same cells grew without estrogen at all [6]. Same cells. Different setting. Different answer.

Here is the main point. A dish can show us what a cell is able to do. It cannot show us what that cell will do inside you.

Rung two: mice

The next step up is putting human breast cancer cells into mice. This sounds closer to real life, and in some ways it is. But there is a catch that changes everything.

Why the mice need a weak immune system

A healthy mouse has an immune system. If you put human cancer cells into it, the mouse's body sees those cells as foreign, the same way your body would react to a splinter or a germ. The immune system attacks them, and the tumor usually never takes hold.

So to grow human tumors in mice, researchers use mice whose immune systems have been bred to be weak, or nearly gone. There are a few common types:

• Nude mice are missing most of their T cells. T cells are the "special forces" of the immune system that hunt down specific threats.

• NOD/SCID mice are missing T cells and B cells. B cells make antibodies.

• NSG mice are missing T cells, B cells, and natural killer cells. Natural killer cells are front-line cells that can destroy abnormal cells on sight. NSG mice are one of the most immune-deficient mice ever created, and that is exactly why they are useful for growing human cells [7].

In many of these studies, the mice also have their ovaries removed. Then researchers put a slow-release estradiol pellet under the skin.

The same few women, over and over

This is the part that stopped me in my tracks. When you look at which cancer cells go into these mice, you keep seeing the same names.

MCF-7, the cells from that one woman in 1970, shows up again and again. So does T47D, a line started in the late 1970s from another woman's cancer cells [8]. In the mouse studies I walk through below, two of the three used MCF-7 or a T47D offshoot. The third didn't use a woman's cancer at all. It used normal breast cells that had been turned into cancer in the lab by adding cancer genes.

Think about what that means. Breast cancer in real women is not one disease. Women differ in age, genes, body size, metabolism, menstrual and menopause history, pregnancies, medications, diet, stress, sleep, and immune health. Their tumors differ too. Yet a huge amount of what we "know" about estrogen and breast cancer comes from the cells of one woman, taken more than 50 years ago, after her cancer had already spread, and copied in labs ever since. We would never accept one woman as a stand-in for every woman in a clinical trial. We shouldn't accept it in a lab either.

Researchers do try to fix this by putting pieces of real patients' tumors into mice. But ER-positive tumors, the kind most women have, are very hard to grow this way. On average, fewer than 15% of ER-positive tumor samples take hold in mice, compared with 30% to 80% of triple-negative tumors. The ones that do take hold, tend to be the faster-growing, higher-grade tumors [9]. So even the "real patient" models lean toward the most aggressive cancers, not the slow, low-grade ER-positive cancers that many women are actually living with.

What a missing immune system changes

Think about what this means. The very system that is built to find and remove cancer cells has been turned down or switched off. We then watch what estradiol does to tumor growth in that setting, and try to apply the answer to a woman whose immune system is working.

That is a big leap.

To be fair, in a well-designed mouse study, both the estrogen group and the placebo group have the same weak immune system. So if the estrogen group grows bigger tumors, that difference is real for that model. I am not saying the mouse results are made up. I am saying they answer a narrower question than the one women are being told they answer.

Here are a few examples of what these studies look like:

In one 2007 study, researchers used normal human breast cells that had been engineered in the lab to become cancer. They put them into NOD/SCID mice, and estrogen made these ER-negative tumors grow. ER-negative means the cancer cells did not even have estrogen docking stations. So how could estrogen help them? The researchers found that estrogen was working on the mouse’s own body. It increased new blood vessel growth and pulled in helper cells from the mouse’s bone marrow. Bone marrow cells from estrogen-treated mice were enough to boost tumor growth on their own [10]. In other words, the effect came through the host’s body, not the cancer cell’s receptor. That is a mouse body, with a mouse immune system that has already been weakened, and mouse blood vessels. In that same work, the pellets used gave the mice estrogen blood levels from about 50 up to more than 900 pg/mL.

It’s worth stopping on those numbers. A young adult female mouse weighs less than an ounce and normally runs an average estradiol level of about 3 pg/mL [11]. So 300 to 400 pg/mL is roughly 100 times what her body would make on its own, and over 900 pg/mL is around 300 times. One lab that tested a common pellet found it kept mice 18 to 40 times above their normal range for the whole experiment [12]. Another found that 0.72 mg and 1.7 mg pellets, the same sizes used in this study, caused urine retention, kidney swelling, and early death [13]. For comparison, postmenopausal women not on estrogen usually run about 1 to 18 pg/mL [14]. A level of 300 to 400 pg/mL is like a woman’s pre-ovulation peak, except a woman reaches that for a day or two, not around the clock for weeks.

In a 2014 study, researchers injected human breast cancer cells (MCF-7 and an offshoot of T47D) into the hearts of NSG mice with their ovaries removed, so the cells would spread through the body. Mice without estrogen did not grow large tumors in other organs, but some still carried small, sleeping groups of cancer cells. In other words, taking estrogen away did not stop the cells from spreading and hiding. In one experiment with the T47D offshoot, when estrogen was given after a delay, visible spread showed up in 8 of 16 mice (50%), compared with 1 of 11 mice (9%) that never got hormones [15]. This study is often used to argue that estrogen “wakes up” sleeping cancer. But remember: these are mice with no T cells, no B cells, and no natural killer cells. The authors said it themselves: because NSG mice are immunodeficient, waking up from dormancy in their model was “unlikely to involve immune mechanisms.” The study can’t tell us what an intact immune system would have done with those cells.

Other mouse models study what happens to leftover cancer cells when estrogen is taken away, to mimic aromatase inhibitors. A 2020 study like this used MCF-7, three other cell lines, and one patient tumor, grown in NSG or nude mice. The authors wrote plainly that “the model systems used herein are immunodeficient,” and that models with working immune systems are needed [16].

And models can point in the other direction too. In a 2016 lab model of the bone marrow, where sleeping breast cancer cells often hide, taking estrogen away caused the support cells to release a signal that helped ER-positive cancer cells wake up and grow. In human tumor samples, higher levels of that signal were linked to more spread only in women who had taken estrogen-lowering therapy [17].

Why the immune system matters so much

There is a real human case that shows how powerful the immune system is in breast cancer. In 2018, doctors reported that four people received organs from one donor. Nobody knew the donor had breast cancer. Over the next 16 months to 6 years, all four recipients developed the same type of breast cancer, which came from the donor’s cells. Organ recipients take drugs to weaken their immune system so they don’t reject the new organ. Three of the four died. The fourth had the organ removed, stopped the immune-weakening drugs, and had chemotherapy. That person went into complete remission [18].

Hidden breast cancer cells were held in check in the donor’s body, then grew in bodies with a weakened immune system. When one person got their immune system back, the cancer went away.

So when we take results from a mouse that has almost no immune system and apply them to a woman, we are leaving out one of the most important parts of the story.

Rung three: a quick word on Ki-67

Almost every human study on this question uses a marker called Ki-67, so we need to understand it before we look at those studies. I wrote a whole article on this, with pictures of the cell cycle, called “Ki-67 Went Down. So What? What This Number Can and Can’t Tell You About Breast Cancer.” If you want the details, start there. Here is the short version.

Ki-67 is a protein inside cells that have left their resting state and entered the cell cycle, the series of steps a cell goes through to copy itself. On a pathology report, it shows up as a percentage: out of the cancer cells counted on a slide, how many had the Ki-67 stain.

Ki-67 does not equal growth. It tells you a cell is active. It doesn’t tell you what the cell will do next. Along the cell cycle there are checkpoints, and at each one a cell can keep going, pause to repair damage, go back to rest, or self-destruct. Ki-67 can’t tell those apart. It also doesn’t measure tumor size. A tumor grows or shrinks based on how many cells are made minus how many die or are cleared away.

Ki-67 is also a single snapshot of one small piece of tissue at one moment. In a very large trial, women who got no drug at all still had Ki-67 scores about 18% lower when their second sample came from the surgery specimen instead of another needle biopsy, just because of how the tissue was collected [19].

And a change in Ki-67 doesn’t reliably change outcomes. In the POETIC trial, 4,480 women with ER-positive breast cancer were split into two groups. About two-thirds took an aromatase inhibitor for about 2 weeks before and after surgery, which lowered Ki-67 a lot. After about 5 years, breast cancer had come back in 280 of 2,976 women who took the drug (9%) and 154 of 1,504 women who did not (10%), a difference that was not meaningful [20]. Ki-67 does carry some information about groups of women. But it is one clue, not the outcome.

Rung four: the human studies

Now we finally get to women. There are only a handful of studies where women with an existing breast cancer were given estrogen, and their tumors were checked. Let’s look at all of them, starting with the ones where Ki-67 went down.

When Ki-67 went down

Stopping HRT. In 2003, researchers looked at women who were taking hormone therapy when they were diagnosed. They stopped it before surgery. In 106 women with ER-positive cancer, Ki-67 went down after stopping. In the 15 women who kept taking their hormones until surgery, Ki-67 did not change [21]. The authors concluded HRT should be stopped at diagnosis, and this study is often used to argue that hormones were “fueling” the tumor. But notice that continuing hormones did not push Ki-67 up, and Ki-67 is the same snapshot measure we just talked about. It does not tell us whether those women would have had more recurrence if they kept going.

The PRESTO study. This is the study I find most interesting. In 2022, a Canadian team gave 19 postmenopausal women with newly diagnosed, low-grade, ER-positive, HER2-negative breast cancer a high dose of estradiol: 6 mg a day for about 2 weeks before surgery (on average 12.7 days). That is several times higher than the 1 to 2 mg a day many women use for menopause symptoms.

If “one drop of estrogen feeds cancer” were true, you would expect these tumors to light up. They did not. Ki-67 went down in 13 of the 19 women (68%). In the 13 tumors that had a gene test done, the recurrence-risk score went down in 8 (62%). The tumors also turned on genes linked to a resting, quiet state [22].

This was a small study with no comparison group. I don’t want to overstate it. But it is real estradiol, in real women, with real tumors in their bodies, and the signal pointed the other way.

The PROMISE study. This one used a pill that combines conjugated estrogens (from horse urine) with bazedoxifene, a drug that blocks estrogen in some tissues. Women with ER-positive DCIS (early, non-invasive cancer in the milk ducts) took it or a placebo for about 4 weeks before surgery. The findings were presented at a cancer conference in 2025. In the 94 women included in the results, Ki-67 dropped by about 5.6 points in the estrogen group and about 1.1 points in the placebo group. The researchers called it “a safe option to manage menopausal symptoms for women concerned about their risk of developing breast cancer” [23]. This has only been shared as a conference summary so far, not a full published paper.

The double standard

Here is something I want you to notice. When estrogen lowers Ki-67, we are told, “Well, that’s just Ki-67. It doesn’t prove anything.” And that’s fair, for all the reasons above.

But we have to apply the same rule both ways. If a lower Ki-67 doesn’t prove estrogen is safe, then a higher Ki-67 doesn’t prove estrogen is dangerous. You can’t use the same measure as weak evidence in one direction and strong evidence in the other.

When Ki-67 went up

There are human studies where estrogen pushed more cancer cells into the cell cycle. I want to show you these, because they are the closest thing we have to the evidence people mean when they warn women. And when you look at them closely, you see why they were done.

Fabian and colleagues, 1994. Fifty women with advanced breast cancer were given estradiol through vaginal suppositories. The goal was not to treat menopause. The goal was to push cancer cells into the dividing phase on purpose, right before chemotherapy. Chemotherapy works best on cells that are actively dividing, so doctors wanted to “recruit” sleeping cells into the cycle where the chemo could hit them. Their blood estrogen levels reached about 136 to 1,362 pg/mL. After 48 hours, in women with ER-positive tumors, the share of cells copying DNA went up in 20 of 29 women (69%), and the proliferation measure went up in 23 of 29 (79%) [24].

Of the 28 women with locally advanced cancer, 25 went on to have a complete response to the full treatment plan of estradiol, chemotherapy, surgery, and radiation. There was no comparison group, so we can’t credit the estradiol for that. But this was not a study where estrogen made the cancer run away. That tells us estrogen can move cancer cells into the cycle. It didn’t measure whether the tumors got bigger over time. It was a 48-hour snapshot, and the whole point was to set those cells up to be killed.

Lipton and colleagues, 1987. Thirty-nine women with metastatic breast cancer were all on a drug that strongly blocked estrogen production, plus a steroid, plus chemotherapy. Women in the “stimulation” group were also given 2 mg of estradiol under the tongue twice a day for 3 days before each round of chemo, again to try to push cells into the dividing phase. This is the study that often gets used to say estrogen is unsafe. But let's call it what it is. The researchers didn't report measuring the tumors getting bigger. They based "appeared to accelerate" on signs and symptoms: bone pain, high blood calcium, and changes in skin lesions. And when the tumors were formally measured for response to treatment, the two groups responded at similar rates. And it does not show that estradiol makes an existing cancer grow. [25].

Rung five: when estrogen shrank tumors

This is the part of the story most women have never heard. Long before the drugs we use now, estrogen itself was used to treat breast cancer.

In 1944, Dr. Alexander Haddow reported that high-dose synthetic estrogens caused some advanced breast cancers to shrink [26]. For decades after that, high-dose estrogen was a standard treatment for advanced breast cancer in older women.

In 1981, a Dutch trial compared ethinyl estradiol (a synthetic estrogen found in birth control pills) with tamoxifen in 63 women with advanced breast cancer. Tumors shrank in 31% of women on estrogen and 33% on tamoxifen. Median survival was 31 months on estrogen and 25 months on tamoxifen, a difference that was not statistically meaningful [27].

In 1999, a Mayo Clinic team looked at long-term results from a trial of DES (diethylstilbestrol, another synthetic estrogen) versus tamoxifen in 143 women with advanced breast cancer. Tumors responded in 42% on DES and 33% on tamoxifen, which was not a meaningful difference. But at 5 years, 35% of women on DES were alive, compared with 16% on tamoxifen. After adjusting for other factors, that survival difference held up [28].

These were synthetic estrogens, not the estradiol your ovaries make, and they came with real side effects. I’m not suggesting anyone take them. I’m sharing them for one reason: they show that “estrogen makes breast cancer grow” was never the whole truth. Estrogen signaling could also shrink breast cancer.

And this did not stop in the past. In 2009, researchers tested real estradiol in 66 women whose metastatic breast cancer had stopped responding to aromatase inhibitors. Women took either 6 mg or 30 mg of estradiol a day. In the 6 mg group, 10 of 34 women (29%) had their cancer shrink or stay stable for at least 6 months. In the 30 mg group, it was 9 of 32 (28%). Serious side effects were less common with the lower dose: 4 of 34 women (12%) versus 11 of 32 (34%) [29]. This was estradiol, given to women with cancer actively spreading in their bodies, and in close to 30% of women, the cancer was held back or shrank.

Scientists think part of this effect comes from cells that have adapted to living with very little estrogen. When estrogen suddenly returns, some of these cells can’t handle it, and they self-destruct. So the very same hormone we are told always fuels cancer can, in some settings, trigger cancer cell death.

Rung six: the bigger picture in women

A few other pieces of human data help round out the picture.

The Women’s Health Initiative tested conjugated estrogens alone (without a progestin) in women who had had a hysterectomy. These women did not have breast cancer when they started. After long-term follow-up, there were 238 breast cancers in the estrogen group and 296 in the placebo group. There were 30 breast cancer deaths in the estrogen group and 46 in the placebo group [30]. So in the largest trial we have of estrogen alone, fewer women got breast cancer and fewer died of it. This was not estradiol, and these women did not have a known cancer. But it is very hard to square with the idea that estrogen on its own is a powerful fuel for breast cancer.

Another study looked at women whose cancer cells had spread to their bone marrow. Most of those marrow cells were ER-negative, even when the main tumor was ER-positive. Only 12 of 88 women with ER-positive tumors (14%) also had ER-positive marrow cells [31]. The cells that travel and hide are often not the same as the main tumor. That makes it harder to assume they are all waiting for estrogen to wake up and cause a recurrence.

What your doctor might bring up

If you raise this with your doctor, there is a good chance they will mention the HABITS trial. I think you should know about it.

HABITS gave hormone therapy to women who had already had breast cancer. It was stopped early. New breast cancer events happened in 39 of 221 women on hormones (18%) and 17 of 221 women not on hormones (8%). Most women in the hormone group took estradiol together with a synthetic progestin. Breast cancer deaths were similar: 6 in the hormone group and 5 in the other group [32]. It should be noted that the HABITS study was another heavily flawed study that had many issues:

• Participants were not required to have any baseline imaging, so no one knows whether the participants had breast cancer when they began the study.

• 43 of the 171 women in the placebo (no-HRT) arm of the study decided to use HRT.

• 11 of the 174 women in the HRT arm of the study decided not to take HRT.

• There was no agreed upon HRT regimen for those in the HRT arm of the study – it was left up to the discretion of the provider. (As you now know, the type of HRT matters!)

A similar trial from Stockholm, which used less progestin, also stopped early. It found 60 new breast cancer events in the hormone group and 48 in the other group. That difference was not statistically meaningful. Much of the gap came from new cancers in the other breast (14 versus 4). The number of women whose cancer spread to distant organs was the same, 12 in each group, and there was no difference in deaths [33].

These trials are real and worth discussing. They also mixed estradiol with synthetic progestins, counted new cancers along with recurrences, and did not show a difference in deaths. They can’t tell us what estradiol alone or estradiol with bioidentical progesterone does to an existing cancer.

What happens when we take estrogen away

Everything above is about one side of the scale: does estradiol make an existing cancer grow? But there is another side, and it gets far less attention. What happens to a woman’s body when we take estrogen away, or block it, for years?

Estrogen is not just a breast hormone or a “reproductive” hormone. Its receptors are found in tissues all over the body. It helps run bone strength, heart and blood vessel health, the brain, mood, and metabolism, including how the body handles insulin [34]. Estrogen receptors also sit on immune cells, and estradiol helps shape how those cells develop and respond [35]. That matters here. If the immune system is one of our best defenses against cancer cells that don’t belong, then estrogen is part of that defense system, not just a signal to a tumor.

We can see what losing estrogen early does when we look at women who lose their ovaries before menopause. In a long-running study in Minnesota, women who had both ovaries removed before age 45 for reasons other than cancer had a 67% higher risk of dying over the following decades than women who kept their ovaries. That extra risk showed up mainly in women who were not given estrogen [36]. In the same population, women who had ovaries removed before menopause had a 46% higher risk of memory problems or dementia, and the younger they were when it happened, the higher the risk [37]. A review of 32 studies with more than 310,000 women found that menopause before age 45 was tied to a 50% higher risk of coronary heart disease and a 12% higher risk of dying from any cause [38]. These are observational studies, so they show strong links, not proof of cause. But they all point the same way.

Breast cancer treatment often does this on purpose. Aromatase inhibitors lower estrogen to very low levels. Tamoxifen blocks estrogen in some tissues. Ovarian suppression shuts down the ovaries. For some women, these treatments lower the chance of cancer coming back, and that matters. But they come at a cost. In the large ATAC trial, 375 women on the aromatase inhibitor anastrozole had fractures during treatment, compared with 234 on tamoxifen [39]. In a study of 8,769 women prescribed endocrine therapy, only 49% took it for the full time as prescribed [40]. Women don’t stop these drugs on a whim. Many stop because of how they feel.

This is why I don’t take the decision to stop or block estrogen lightly. Estrogen got tagged as the “fuel” for breast cancer early on, and that label stuck. I think we’ve misunderstood it, and there is still so much we don’t understand about what it does. But we know enough to say this: estrogen works in nearly every system of a woman’s body. Removing it, for any length of time, is a major medical act with real consequences. If we are going to ask a woman to do that, the reason has to be compelling, and it has to be weighed against everything she gives up.

What Dr. Suba helped me see

Over the past few months, Dr. Suba and I have gone back and forth on many of these studies. I want to share her view in my own words, because it has shaped how I read this research.

Dr. Suba sees estrogen not as a fuel, but as a regulator: a hormone that helps run many systems in the body at once, including blood sugar control, the immune system, and the cell’s DNA repair machinery, which includes the BRCA genes. In her model, when a breast cell is under stress or damaged, it may turn up its estrogen signaling as a way of trying to repair itself. A rising Ki-67 could reflect a cell working hard on that repair, not just a cell racing to divide. And when estrogen is cut off, she believes that repair effort can become exhausted.

This is her model, and it is not settled science. But it gives a very different way to read the same data. And it reminds me that Ki-67 is only one piece of a much larger picture.

What we don’t have

After going through all of this, here is what I can say: I have not found a human study showing that estradiol alone, at doses used for menopause, in a woman with a working immune system, causes an existing breast cancer to grow bigger or come back.

What we have instead:

• Dish studies that show what some cells can do, in a setting that looks nothing like a body

• Mouse studies done in animals whose immune systems have been bred to be weak or nearly absent

• Short-term Ki-67 changes that go both up and down, and that don’t reliably predict outcomes

• Human studies where estrogen was used on purpose to push cells into division before chemo, with no changes in response rate or survival difference

• A long history of estrogen, including real estradiol, shrinking or holding back advanced breast cancer in some women

• Trials of combined hormones in survivors that mixed in synthetic progestins and did not show more deaths

And on the other side of the scale, we have consistent evidence that losing estrogen early is tied to more heart disease, more dementia, more fractures, loss of wuality of life, mood issues, and shorter lives.

If someone can show me clear human evidence that estradiol makes an existing breast cancer grow, I want to see it. But if we are going to tell women to give up estrogen for the rest of their lives, the burden of proof should be on that claim. We need to be certain. Right now, the evidence doesn’t give us that certainty. Not even close.

Questions to bring to your doctor

If you want to have this conversation, here are some questions that may help:

• What human evidence shows that estradiol alone makes an existing breast cancer grow?

• Is that evidence from cells, mice, or women? If it is from mice, did those mice have a working immune system?

• Is the concern based on Ki-67? If so, do we have evidence that the change in Ki-67 led to a worse outcome?

• Were the hormones in that study body-identical estradiol, or synthetic estrogens and progestins?

• What are the risks to my bones, heart, brain, sleep, and quality of life if I go without estrogen for decades?

• Can we look at my own tumor, my own history, and my own goals together, instead of applying one rule to everyone?

A good doctor will welcome these questions. You are not being difficult. You are asking for the evidence behind a decision that will shape the rest of your life.

You deserve the whole story

Women with breast cancer deserve honest information. That means telling them what we know, what we don’t know, and where the evidence comes from. It means taking real risks seriously without turning lab findings into lifelong rules. And it means respecting that the woman living in the body is the one who gets to weigh the tradeoffs.

Breast cancer is not just a cell with a docking station. It lives inside a whole woman, with an immune system, a metabolism, a history, and a future. When we think that big, the question “does estrogen make cancer grow?” becomes a much more interesting, and much more hopeful, conversation.

Want to learn more?

• Read my related articles on estrogen and breast cancer:

  • Besides Endocrine Therapy, What Are My Options? Start With Why the Cancer Grew in the First Place

  • Ki-67 Went Down. So What? What This Number Can and Can’t Tell You About Breast Cancer

  • Could There Be Another Explanation? Rethinking Estrogen, Endocrine Therapy, and Breast Cancer

  • Nobody Has Watched It Happen: What We Really Know About Cancer Cells “Waking Up”

  • The Minority Benefit: Why Hormone Blockers Help Some Women but Fail Many

• Read Dr. Suba’s publications and share with your provider

• Download the Balance App for hormone education, symptom tracking, and tools to prepare for your next appointment. Be sure to check out our series: Breast Cancer: Your Complete Guide.

• Read The Third Opinion on Substack for deeper conversations on hormones, breast cancer, and informed choice.

References

1.        Soule, H. D., et al. (1973). A Human Cell Line From a Pleural Effusion Derived From a Breast Carcinoma. Journal of the National Cancer Institute, 51(5), 1409–1416. https://doi.org/10.1093/jnci/51.5.1409

2.        Lee, A. V., et al. (2015). MCF-7 Cells—Changing the Course of Breast Cancer Research and Care for 45 Years. Journal of the National Cancer Institute, 107(7), djv073. https://doi.org/10.1093/jnci/djv073

3.        Lippman, M. E., & Bolan, G. (1975). Oestrogen-responsive human breast cancer in long term tissue culture. Nature, 256(5518), 592–593. https://doi.org/10.1038/256592a0

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Disclaimer: This article is for educational and informational purposes only and is not intended to replace personalized medical advice or individualized care. It is meant to help you understand your physiology, explore evidence-based options, and make informed choices about your health and wellness. Healthcare should be a partnership, not a permission slip, and proactive care is just as essential as treatment. Use this information to engage in open, collaborative discussions with your provider or to make empowered decisions that align with your own values, goals, and comfort level. You are the ultimate authority on your body.