Recurrence Risk Decreases Over Time?

Hi Colt45 - I think it was you that was asking questions about recurrence in a previous thread? 

Anyways, for sure recurrence rates are highest in the first three years and the further you get from the diganosis the lower the risk.  Most studies state if they are measuring time since diagnosis or treatment.  For example, on cancer.org the survival rates are for overall survival (not recurrence) from diagnosis.  Note that I believe these rates include people who have a recurrence and die within the five-years after diagnosis.  By this I mean, I don't believe you are re-classified as Stage IV if you were originally diagnosed at Stage II and then had a recurrence and died.  If you were, the survival rates for Stage I through III would be the same as the general population.

There is one interesting article which shows that the residual risk of recurrence five years after completing adjuvant treatment.  http://jnci.oxfordjournals.org/content/100/16/1179.full

It shows that grade 1 tumors tend to recur later than grade 3 tumors, something which has been confirmed by other studies.  Tumors that also tend to recur later are hormone positive and HER2-.  Most medical oncs will consider you cured after 10 years, although there is always a residual risk.  My great aunt had breast cancer in her early 50s and died in her late 80s of brain cancer.  I always wondered if it was a late recurrence of her breast cancer.  Likely not, but who knows!

I've come to terms with my risk of recurrence.  Anybody could be diagnosed with a stage IV cancer (or hit by a bus, or die in a plane crash) tomorrow.  Sure, my chances of dying of breast cancer are on average higher than somebody else, but I've done all I can do to minimize that risk.  Now it's about enjoying and not worrying about the things that may or may not happen tomorrow that are out of my control.  Before I came to this conclusion, I read almost every study about prognosis and survival on Google, so it took a while.   I hope that you can come to the same conclusion!

Won't the 10 yr Tamoxifen help the premenopausal women extending the benefit?

Colt... my understanding is that hormone-positive breast cancer cells have little "radar dishes" on them called receptors that allow the cell to attach itself to an estrogen cell and fuel itself.  Tamoxifen pretends to be an estrogen cell and allows the breast cancer cell to attach to it.  By the time the breast cancer cell realises that whoops!  This isn't an estrogen cell and I can't feed from it, the tamoxifen has bound itself to the cancer cell and the cancer cell can't jettison it.  Thus, what happens is the cancer cell slowly "starves" and dies off.

Unfortunately, some breast cancer cells - rather than die off - go dormant.  Although they can remain dormant for a long time, sometimes, something triggers them and brings them out of dormancy; hence, recurrence.  It's thought that certain breast cancer stem cells are responsible for this, but research is still ongoing.

Hormone-positive cancers tend to be more "survivable" in the short term than other, more aggressive breast cancers, but - in exchange for that benefit - they do have the tendency to recur late in the game.  That is the conundrum that emerged when more women started surviving breast cancer long-term.

The metformin clinical trial - which is ongoing - is investigating the theory that breast cancer cells, also, have insulin receptors that attach to blood sugar and use that to fuel growth.  Since metformin is a diabetes drug that stabilises insulin levels, it is hoped that the study will show that - by keeping blood sugar levels stable - metformin can be added to the arsenal of weapons already in place to fight breast cancer and prevent recurrence.  The trial ends in 2017, I believe.

colt45 -when in doubt or confused, especially for newbies, BCO has great explanations for many aspects of chemo, treatment, etc.  Here is the excerpt on Tamoxifen:

Selective estrogen receptor modulators, called SERMs for short, block the effects of estrogen in the breast tissue. SERMs work by sitting in the estrogen receptors in breast cells. If a SERM is in the estrogen receptor, there is no room for estrogen and it can't attach to the cell. If estrogen isn't attached to a breast cell, the cell doesn't receive estrogen's signals to grow and multiply.

Cells in other tissues in the body, such as bones and the uterus, also have estrogen receptors. But each estrogen receptor has a slightly different structure, depending on the kind of cell it is in. So breast cell estrogen receptors are different from bone cell estrogen receptors and both of those estrogen receptors are different from uterine estrogen receptors. As their name says, SERMs are "selective" – this means that a SERM that blocks estrogen's action in breast cells can activate estrogen's action in other cells, such as bone, liver, and uterine cells.

There are three SERMs:

• tamoxifen (also called tamoxifen citrate; brand name: Nolvadex)
• Evista (chemical name: raloxifene)
• Fareston (chemical name: toremifene)

Each is a pill, usually taken once a day. Tamoxifen is the oldest, most well-known, and most-prescribed SERM.

SERMs can be used to treat women both before and after menopause.

In terms of counting the time elapsed - I think a lot of people start after surgery because that is when the cancer is removed - none of us knows if there is still any cancer remaining if we receive adjuvent chemo/rads. I count from the time I had my axillary node dissection surgery 5 weeks after BMX, since I still had cancer in those nodes and it was not known at the BMX.  In terms of recurrence and stats there are no absolutes.  I can have the same size tumor, same nodal status, as someone else and receive the same treatment, but one of us may recur and one may not.  Differing hormonal status and Her2 status have different sets of stats.  For me personally, my Her2+ aspect means I may have a recurrence early due to the aggressiveness of Her2, but my long term danger for recurrence due to my ER+ is also a factor, so what it amounts to is a big who knows?