Why is chemo on the table after BC removed?

I had chemo after bilateral mastectomy.  I was stage 1, small 7mm tumor.  Chemo was advised to prevent reoccurrence after my Oncotype score came back 30.  Even with mastectomy, it's not 100% guarantee that all breast tissue has been removed or some cancer cells may have escaped.

Depends on what kind of cancer you had (DCIS almost never gets chemo), tumor size & location (the latter may warrant radiation despite MX if close to the chest wall, clavicle or axillary tail), and cytology: hormone-receptor status, degree of HER2 expression, grade, mitotic rate (division, therefore “growth" speed), whether there was lymphovascular invasion (LVI—i.e., though nodes may have been negative the sample showed tumor cells in blood or lymph vessels—or a blood or lymph supply in the tumor).

If you had IDC or ILC, generally with ER+/PR+/HER2-, grade 1 or 2, mitotic rate 1, tumor <1cm, clean margins and negative nodes, chemo's benefits would likely be too small to be worth its risks. If you're in a “gray area" of tumor >1cm, grade 2, &/or 1-3 nodes positive, etc., a sample from your tumor would be sent out for OncotypeDX testing. A score of 0-17 is “low risk," no chemo (unless it's at the higher end of “low" and you are young, because tumors are more aggressive in younger women), 18-29 “intermediate risk" (often a second test like Mammaprint, which has no middle ground, is ordered to decide on chemo), 29+ almost certainly chemo.

But OncotypeDX is only done on hormone-receptor-positive, HER2-neg., invasive tumors with 3 or fewer positive nodes. If your tumor was ER+/PR- you might get chemo, especially if grade 3 and/or larger than 2cm. But chemo is a must if your tumor lacked hormone-receptors, was HER2+ (including “triple-positive") or was triple-negative. The “targeted therapy" (Herceptin, Perjeta) that attacks HER-2+ cells needs chemo to help it work, even if your tumor was also hormone-receptor-positive.

Why get chemo if “they got it all?" Because not only might some breast tissue (and therefore possibly local tumor cells)remain despite clean margins & nodes, the chances are you have micromets already in the bloodstream, lymph system or elsewhere in the body. We all do. Sometimes a few tiny “seed" cells spread before a tumor forms—often years or even decades earlier. We're probably all born with some, because the “tunneling" process of building milk ducts in the breast (as early as during gestation) involves intermittent turning on & off of genetic “switches" that tell cells to divide and stop dividing. Sometimes those cells “go off the reservation" and lie dormant elsewhere in the body—and usually never wake up, whether or not a tumor forms in the breast first. But sometimes they do, in which case they become actual metastases.

But why not give everybody chemo if we all theoretically have dormant micromets somewhere, even before birth? Because it has very real risks, and unless there’s a good chance of actual metastases that need prevention, those risks would outweigh its benefits.

Chemotherapy is “cytotoxic"—it kills a certain type of cell, namely those that divide rapidly (e.g., epithelial tissue such as digestive linings, mucous membranes, hair follicle cells, bone marrow, etc.). Because they might be anywhere in the body, it's called a “systemic" rather than “local" therapy (e.g., surgery & radiation). If your tumor also was hormone-receptor-positive, another form of systemic therapy called “endocrine" therapy (sometimes misnamed “hormonal," when it should be more properly called “anti-hormonal") is administered in the form of a pill, taken long-term, to starve the tumor cells of the estrogen on which they'd feed. (Some cells might remain even after chemo, which is why endocrine therapy is administered after chemo).

There are two types of anti-hormonal meds: SERMS (selective estrogen receptor modulators) like Tamoxifen, and AIs (aromatase inhibitors) like anastrazole, letrozole & exemestane. If you are postmenopausal you will be prescribed an AI; if pre-or-perimenopausal, a SERM (usually Tamoxifen). SERMs block the estrogen receptors so that the estrogen made in your ovaries & elsewhere (we'll get to that in a minute) can't feed those stray tumor cells. AIs work differently. Even if you no longer have working ovaries, you still make estrogen. Your adrenal glands and fat cells make androgens that an enzyme secreted by the liver called aromatase uses as a catalyst to turn those androgens into estrogens. AIs inhibit aromatase's catalytic activity. In postmenopausal women they work better than Tamoxifen—but in premenopausal women the process of blocking aromatase increases production of gonadotropin, which in turn makes the ovaries crank out more estrogen. Not good. So because AIs work better than Tamox. in postmenopausal women, peri-menopausal women take both Tamoxifen and an ovarian suppressor (or have their ovaries removed) to hasten menopause.

If your tumor was hormone-receptor-negative, endocrine therapy is useless. And if it was also HER2-, so is “targeted" therapy. Chemo is the only weapon in the systemic-therapy arsenal for triple-negative cancer.

Hormone therapy is a systemic treatment as well, it can prevent recurrence for hormone positive cancers.

I think the OP mentioned she had surgery—BMX—first. It is not at all unusual to not see an MO until after surgery, especially if there are no hereditary mutations, the tumor is small and the core biopsy indicates likely Luminal A Stage I.

For example: I saw my surgeon first, then her NP who did the “teaching session” and selected the MO (and scheduled my first appt. with her); next came my surgery, and both the surgeon’s follow-up and first MO visit one week post-op. The MO ordered the OncotypeDX and genetic counseling (despite lack of family history, my ethnicity put me at risk for a mutation). Got the genetic test, then got first the OncotypeDX and genetic results back. Saw the MO again, who prescribed endocrine therapy after radiation, then the RO and finally my radiation treatments. When I’d recovered from those, I started the endocrine therapy.

ChiSandy,

I really appreciate your detailed explanation of topics I/probably most of us, are unfamiliar with. Thank you, thank you. How do you have so much knowledge? Again, you are appreciated!

Westthebest

ChiSandy, can I ask your source for this?

"Sometimes a few tiny "seed" cells spread before a tumor forms—often years or even decades earlier. We're probably all born with some, because the "tunneling" process of building milk ducts in the breast (as early as during gestation) involves intermittent turning on & off of genetic "switches" that tell cells to divide and stop dividing. Sometimes those cells "go off the reservation" and lie dormant elsewhere in the body—and usually never wake up, whether or not a tumor forms in the breast first. But sometimes they do, in which case they become actual metastases."

I know that you mentioned something similar to this with regard to the following research study: Researchers Reveal How Cancer Can Spread Even Before a Tumor Develops. If this is the study that you are using as the basis for this statement, I would have to disagree. I don't believe that this is at all what the researchers are suggesting. What I believe the researchers are hypothesizing is that the same process that leads to the development of the ductal system when we are in the womb, might later on in life activate (although it shouldn't) and thereby create an environment in which cancer cells can move out of the breast into the body at the very earliest stage of the cancer's development, well before the cancer is detected. I don't see this study to be saying that the development of cancer cells and this movement of cancer cells happens before we are born. They are simply suggesting that this is a possibly pathway for cancer cells to leave the breast and enter the body early in the development of the cancer.

One other thing to keep in mind about this study is that it was a small lab study involving the manipulation of the cells in a petri dish, and then placement of the cells into mice and some human tissue. Is it an interesting hypothesis? Yes. Did the first test of this hypothesis suggest that it might actually be possible for cancer cell migration to happen this way? Yes. But this still all happened in a lab environment with a lot of manipulation. This was likely the first test out of many tests that will be necessary before anyone can say that this actually happens in humans. I have been reading up on the process of breast cancer development since I was diagnosed almost 12 years ago. I've been bookmarking these types of studies since the beginning and have a big pile of them. For the past few years, I've actually given up bookmarking them because there are just so many - and because almost inevitably, they are one-shot wonders. The hypothesis is interesting and the first test is successful and gets written up in a medical journal and mentioned in the press... and then the hypothesis is never heard about again. Why? Probably because the next round of testing fails. I'm not saying that this will happen in this case - this might be the 1 in 1000 that proves to be correct - but I'm just saying that at this stage of the research, it's way too early to take the results to the bank and suggest that metastasis develops the way that it did after those cell manipulations in the petri dish.

Now, on the other hand, if your information come from a different study, one that is further down the line in terms of proving the hypothesis, that would be very interesting to know.

Steph, sorry for diverting your thread. To your question, even if cancer cells aren't moving into our bodies while we are in the womb, they can possibly move into our bodies, either through the blood stream or the lymphatic system, while the cancer is developing and well before the cancer is discovered. If it's just a few cells, they could easily slip through undetected by any testing or even a pathological assessment. This is why hormone therapy (a systemic treatment) is recommended for pretty much everyone who has ER+ invasive cancer and it's why chemo (another systemic treatment) is recommended for those who have aggressive cancers (ER-/PR- or HER2+ or as indicated by the Oncotype score), even when there is no evidence of lymph node involvement or mets. The idea is that if there are any of those rogue cells lying around dormant somewhere in the body, these systemic treatments will hopefully find them and kill them off before they have an opportunity to take hold, grow and spread.

I had the same question, and thanks for all your responses. It has helped me accept that chemo is a likely treatment for my situation. I am 2 weeks post-op and will meet with my MO in a couple of weeks. Tumor board unanimously recommended chemo for me and this helped me better understand the reasons.

Newer research is showing that premenopausal women might have greater benefit from doing ovarian suppression (ie Lupron shots) and AI instead of Tamoxifen. I am a premenopausal woman (diagnosed at age 43) and that is what I am doing. I take monthly Lupron shots and Aromasin.

Very helpful and thorough information!