Will 30% of Early Stage (1-IIIA) go on to metastasize??

What a wonderful discussion. I can vaguely remember when I was in the decision making process over single or double mastectomy for what we then thought was DCIS. At that point, I didn't have this information, I was reacting to having dense breast tissue that was hard to image and hiding the little monster. This data is so valuable for us to understand. Beesie we need a risk primer boiled down in easy speak for those newly diagnosed (hint hint)

And, as Beesie has repeatedly tried to point out, there is a big difference in this (outdated) statistic if you were Stage 1a vs. Stage 3

Beesie, I always appreciate your posts and I have for years. Thank you.

Nola, I hope you'll start a new thread & let us know what is happening with your armpit lump & where you're at with getting it diagnosed.

PS: Here's a key excerpt from the 2021 article I mentioned above, proposing an additional model of metastasis—what they refer to as a "parallel" vs a linear model of tumor cell dissemination. It fits w/ a lot of discussion on this thread and to me, rather than promoting a sense of helplessness, will enable much more personalized treatment from the earliest phase as more precise genetic and biologic featuers of tumors are understood.

Excerpt from 2021  https://www.nature.com/articles/s41416-020-01161-4  :

"When do tumour cells disseminate? Early versus late dissemination….

The first step of the metastatic cascade refers to the ability of cancer cells to escape from the primary tumour. In regard to the ‘when’, two different models of metastatic dissemination—linear and parallel—have been proposed33 (Fig. 2.1). The linear model, based on the natural stepwise progression of cancer40 and on the aforementioned correlation between primary tumour size and the risk of relapse,30 surmises that only advanced neoplasms contain enough molecular aberrations to facilitate all of the obligate steps of the metastatic cascade. Accordingly, only fully malignant cancer cells (termed ‘late’ DTCs) can break away from the primary source and give rise to deadly metastases.41 

The parallel model, by contrast, posits that metastatic dissemination can be a precocious event in tumorigenesis in which incipient tumour cells (termed ‘early’ DTCs) can develop into deadly metastases in parallel with each other and the primary tumour. Accordingly, early DTCs would simultaneously, yet independently, acquire genetic and epigenetic alterations as compared with their tumour of origin, perhaps based on the specific niche-related microenvironments they lodge in ref. 33. This model is supported by a plethora of tumour-growth rate studies asserting that some metastases were too big to have been initiated by late-stage tumours,42,43 as well as by the detection of secondary lesions in patients with cancers of unknown origin.33 Furthermore, DTCs have been detected in the bone marrow of patients with early-stage cancer,44,45,46,47,48,49 wherein their presence did not correlate with tumour stage, subtype, histological grade nor axillary lymph node status.50

Altogether, these results suggest that the parallel model of cancer cell dissemination is a much more common phenomenon than previously thought (Fig. 2.1). Although more compelling data are needed to elucidate the temporal pattern of DTC spread, the majority of metastatic human neoplasms appear to have already disseminated—albeit without being detected—at the time of diagnosis,51 despite the fact that metastases tend to be associated with larger tumours (as mentioned above30). Thus, both parallel and linear dissemination might occur, even within the same patient. Importantly, despite the fact that both models assume a clonal relationship between primary tumours and metastases, they differ not only in regard to the timing of the emergence of metastasis-prone DTCs (as discussed above), but also in the expected genetic divergence between paired sites—bigger in the case of parallel dissemination, smaller in the case of linear progression.35 Consequently, phenotypic differences that distinguish early and late DTC functions have been reported,45,46,52 the implications of which are discussed later in the text."

May 28, 202

Relationship between tumor size and metastatic site in patients with stage IV breast cancer: A large SEER-based study..... studies are now coming out to show how and where mets occurs. I read a study on size of tumor that metastasized. It was 5mm. Most stage 1a are around 1 cm so 2 times that size. So ablility to tumor metastasis has already occured in nearly all breast cancers by the time they are seen on a scan. https://ascopubs.org/doi/10.1200/JCO.2021.39.15_suppl.e13065#:~:text=At%20the%20same%20time%2C%20the%20results%20indicated%20that%20Luminal%20A,likely%20to%20develop%20liver%20metastasis.

Yes, it’s important to remember that there are no guarantees and though the overall recurrence rate is too high*, the majority of early stage patients are treated and don’t recur. That 30% is not broken down by stage either. The most difficult part? None of those stats have any predictive value for how an individual will do.
* Many who’ve been lulled into pretty pink land are shocked to find out recurrences can and do happen even decades after treatment and that while most early stagers don’t recur, a not insignificant subset do. And there seems to be little known rhyme or reason to recurrences. The unpredictability is hugely frustrating, coupled with no cure for stage IV.

Thanks herb. Unfortunately, why I have done so well is completely unknown. That may give hope to others but provides no actual help.