There was a good article for the lay public a week ago in the New York Times "With a Tiny Bit of Cancer, Debate on How to Proceed" about the phenomena and controversy over breast cancer "micrometastasis" to lymph nodes. I do a lot of breast cancer related surgery and have this kind of discussion frequently with patients. I've tried over the years to come up with simple concepts for these women who often feel overwhelmed with ideas and terms that have been poorly explained to them.
If you're trying to keep things simple for patients with invasive breast cancer (meaning it has acquired characteristics on microscopic exam suggesting it has the potential to spread elsewhere), it's important to come up with a simple way to explain what their diagnosis really means. There's 3 things that really affect whether or not you're likely to do well when you're diagnosed with invasive breast cancer.
Tumor size and nodal status are proxies for metastatic potential. A larger tumor is more likely to have spread to the lymph nodes at the time of diagnosis. A tumor present in the lymph nodes is in turn more likely to have spread elsewhere and show up again down the road as systemic terminal disease. Breast cancer, like most solid tumors that spread via lymphatic tissue, is conceptually really only "cured" if you remove it surgically before it gets to lymph nodes. This basic fact is essentially unchanged despite steady refinement in radiation (XRT) and chemotherapy (CRT) treatments for 60 years. XRT or CRT do not cure anything, but rather decrease/delay recurrence or palliate symptoms. (I'm simplifying this greatly, but that's the skinny in a nutshell).
Estrogen receptors (ER) are conceptually an "on/off" switch for normal breast tissue cells. A breast cancer cell that still maintains this normal regulatory switch offers a target for hormone manipulation. This "killswitch" provides the basis for medicines like Tamoxifen or Arimidex to show improvements in local recurrence after surgery by blocking these receptors or interrupting estrogen metabolism by essentially "starving" the tumor. We're increasingly seeing how important having this receptor is, particularly in post-menopausal women. It's looking more and more from tumor databases that many older women with ER+ tumors may be able to avoid chemotherapy altogether after surgery, and this observation is currently being tested in prospective trials. A breast cancer that's ER- (missing the receptor) suggests a more "primitive" tumor that's lost some of it's normal regulatory mechanisms and implies a worse prognosis. I found a really nice primer on this for people over at "Cancer Geeks"
BACK TO THE TIMES ON "MICROMETS"
Complicating treatment options now is our increasing ability to detect infinitesimal amounts of cancer cells (micrometastasis) in some lymph nodes that would have been labeled normal just a few years ago. Do we treat this the way we traditionally did positive nodes or are we over treating? We just don't know. It has played a little havoc with interpreting some breast cancer data that was suggesting we were doing better with our treatment.
Why? Well if you suddenly take these micromet positive patients and up the stage of their diagnosis like you would normally with positive nodes, you make both the node - and node + groups look like things are getting better. Nothings really changed except you're removing people who do worse from one group and putting them into a group of node + cancer patients where they will do better then their peers. (I cannot for the life of me think of the name for this statistical phenomena....)
Anyway, read the article (click here) as it's interesting.
Rob
Rob
If you're trying to keep things simple for patients with invasive breast cancer (meaning it has acquired characteristics on microscopic exam suggesting it has the potential to spread elsewhere), it's important to come up with a simple way to explain what their diagnosis really means. There's 3 things that really affect whether or not you're likely to do well when you're diagnosed with invasive breast cancer.
- the size of your tumor
- the presence or absence of cancer in your lymph nodes
- the presence of Estrogen hormone receptors on the cancer cells
Tumor size and nodal status are proxies for metastatic potential. A larger tumor is more likely to have spread to the lymph nodes at the time of diagnosis. A tumor present in the lymph nodes is in turn more likely to have spread elsewhere and show up again down the road as systemic terminal disease. Breast cancer, like most solid tumors that spread via lymphatic tissue, is conceptually really only "cured" if you remove it surgically before it gets to lymph nodes. This basic fact is essentially unchanged despite steady refinement in radiation (XRT) and chemotherapy (CRT) treatments for 60 years. XRT or CRT do not cure anything, but rather decrease/delay recurrence or palliate symptoms. (I'm simplifying this greatly, but that's the skinny in a nutshell).
Estrogen receptors (ER) are conceptually an "on/off" switch for normal breast tissue cells. A breast cancer cell that still maintains this normal regulatory switch offers a target for hormone manipulation. This "killswitch" provides the basis for medicines like Tamoxifen or Arimidex to show improvements in local recurrence after surgery by blocking these receptors or interrupting estrogen metabolism by essentially "starving" the tumor. We're increasingly seeing how important having this receptor is, particularly in post-menopausal women. It's looking more and more from tumor databases that many older women with ER+ tumors may be able to avoid chemotherapy altogether after surgery, and this observation is currently being tested in prospective trials. A breast cancer that's ER- (missing the receptor) suggests a more "primitive" tumor that's lost some of it's normal regulatory mechanisms and implies a worse prognosis. I found a really nice primer on this for people over at "Cancer Geeks"
BACK TO THE TIMES ON "MICROMETS"
Complicating treatment options now is our increasing ability to detect infinitesimal amounts of cancer cells (micrometastasis) in some lymph nodes that would have been labeled normal just a few years ago. Do we treat this the way we traditionally did positive nodes or are we over treating? We just don't know. It has played a little havoc with interpreting some breast cancer data that was suggesting we were doing better with our treatment.
Why? Well if you suddenly take these micromet positive patients and up the stage of their diagnosis like you would normally with positive nodes, you make both the node - and node + groups look like things are getting better. Nothings really changed except you're removing people who do worse from one group and putting them into a group of node + cancer patients where they will do better then their peers. (I cannot for the life of me think of the name for this statistical phenomena....)
Anyway, read the article (click here) as it's interesting.
Rob
Rob
2 comments:
Rob...good discussion on how my supposedly "easy" specialty is becoming more and more complicated seemingly by the hour. As surgeons we sometimes find ourselves at odds with what the medical oncologists (or a specific med onc) wants. Its hard for some of them to resist treating that positive node, even if its a micromet.
But we could "get away" with not treating that < 2 mm node. Until now...remember the patient with the skin recurrence I asked you about in regards to wound coverage? She had breast conservation with a 1.9 mm micromet. Then there was my patient with the 5 mm tumor with bony mets. Try as I might to simply things, as you have, for patients, with pictures, there comes a point at which you have to say, "sometimes tumors don't follow the rules."
Winged Scapula (KSC)
"Breast cancer, like most solid tumors that spread via lymphatic tissue, is conceptually really only "cured" if you remove it surgically before it gets to lymph nodes. This basic fact is essentially unchanged despite steady refinement in radiation (XRT) and chemotherapy (CRT) treatments for 60 years. XRT or CRT do not cure anything, but rather decrease/delay recurrence or palliate symptoms."
Really? That's not what oncs tell us patients. They show an 80% recurrance free 10 year survival rate for stage IIA and 75% for stage IIB. I'm stage IIA and my onc says I am probably cured (after surgery, chemo, etc.).
Do you really think all node positive younger women are destined to recur?
Another question: how do you compare positive nodes with lympho vascular invasion? My onc says that there is no data that LVI is as negative an indicator as nodes.
Thanks.
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