Right, 5 nodes taken. Re response in the primary, went from a 1.3 cm lesion to a 0.2 cm lesion.
Nah, not opposed. Just wondering if there's an argument not to.
If she had not gotten NAC, and had a 0.4 cm focus in a single node, you wouldn't do RNI? But w/ NAC, and same outcome, you're gonna do RNI? I don't get it. One thing I hope we could all admit is that it's really difficult (impossible?) to know what RNI adds in that a robust-but-less-than-CR-to-herceptin leaves out.
Regarding your last comment, yes, it makes no sense. Breast radiation oncology makes no sense.
Gosh. Monica was right. We are obsessed over LR control in breast cancer. What's the specific guideline that says RNI and axillary dissection is "the" SOC for a cT1N0 (axillary ultrasounding cT1N0s unnecessary) breast cancer? One that is <0.5 cm in size after chemo in the primary and a single node? This is still a favorable breast cancer that's "just barely" Stage II. RNI is "a" SOC here, but not "the" SOC, surely. And is axillary dissection even "a" SOC in T1 SLN-positive anymore. Are we still "litigating" that? Time to let it go? How is giving the lady a much higher risk (about 20% overall?) of bad lymphedema via RNI and "brisk" further axillary surgery, and ~double the lung damage risk, vs the absolute benefit of 3-4% re: her oncologic outcome (w/ no OS benefit), a decision that can so readily be "RNI, indubitably." None of this risk/benefit calculus makes great sense compared to other things we do. Especially in an older lady with Her2+ disease that responded to NAC, and with minimal volume disease, and with a 0.4
Lewinski? Anyone know what her dad does?
Wow, wow, wow...
Triple wow. That's like a triple dog dare.
It's tough to predict what The World of Rad Onc will or won't "latch on" to re: treatments. I remember reading e.g. EORTC 22845 the first time. Early radiation was associated with a very significant increase in PFS and less seizures (but no OS advantage). I thought, "I guess that's a win for early RT." Only to read opinions later: not a win/not a SOC. And when I read MA20 and EORTC 22922 for the first back-to-back in NEJM it showed modest PFS benefits, but more toxicities, and no OS benefits. And I thought "I guess 'they' will call this one not a win." We see how all that turned out! My theory: men have brains, but they don't have boobs.
Amen to "contradictory findings." Both MA20 and EORTC 22922 failed to meet their primary endpoints, and as you say for the secondary endpoints there's some conflict (and lackluster improvements where there were improvements.... IMHO of course, and some toxicities, yada yada). All that said, RNI became SOC for a woman with a 4mm focus in a single LN? With a 1.3cm pre-NAC mammographically detected primary? A woman who by my eyes more meets Z0011-type criteria where (some) guidelines state "there are no clear indications for directed axillary radiation in patients with 1-2 positive sentinel nodes who undergo breast conserving surgery." Of course we all know that, too, is "a" guideline: no ENI for single SLN positive patients that are otherwise favorable. Use EORTC 22922 style treatments in ypT1N1 "without thinking twice"? Think twice; beam once.
I just do what I think my breast surgeon wants me to do but I have all those trials in my back pocket to justify whatever it is I end up doing!
This patient does not meet z11 criteria. She underwent neoadjuvant chemotherapy. She’s probably understaged clinically at diagnosis. She also didn’t have a cr to neoadjuvant therapy so this suggests worse biology. The dmfs benefit of rt is likely higher in her than somebody on z11
Axilla staged with US. Hypothetically, had she been cT1N1, I suspect she would have gotten AC then Taxol/Herceptin, which is more aggressive and 3 months longer. Seems like she was on her way to a CR, but we looked too soon after inadequate chemo. (Playing devil's advocate)
she got inadequate chemo or isn’t a complete responder. So she needs further therapy.
I can grant you that the biologies ("biology"≈"natural history"≈"survival") of CR patients are different than PR patients. An important concept which I think we all get. (Still, non-CR is not "bad" biology per se.) OTOH, a concept which seems to sail over rad oncs' heads is that "Variations in loco-regional therapy are unlikely to substantially affect [biology]." This is now, if it wasn't obvious ~20 years ago, a pretty proven concept. There hasn't been a randomized survival-changing this-vs-that-RT breast cancer study in a long time. In addition, IIRC in all the trials we've "played" with the LR therapy (Z0011 e.g.), that hasn't (negatively) affected survival either. She does need further therapy; which I'm sure she'll get. The ones that will affect her survival (biology) will be systemics. Ten different rad oncs employing ten different RT approaches all will see very equivalent long-term survivals with their approaches. I'm also suggesting all 10 rad oncs will see equivalent-ish (within 5% of each other) LR failure patterns... but some of the acute and late toxicity differences will be >>5%. I realize additional data will be coming down the pike this decade, but as of now "SLN after systemic therapy does not lead to higher local regional failure rates"... even with the "risk" that following a NAC-then-SLN approach does certainly "under-therapize" women who'd get more aggressive therapy were they not neoadjuvantly chemotherapized prior to axillary staging of some sort.
forums.studentdoctor.net
This is some great stuff! I have absolutely nothing to add to these titan wars. I’m just going to eat my popcorn and continue to enjoy the show.View attachment 326115
Scarb just quoted Z0011, I am triggered.
ECE and Z11. Has anything changed?
50 year old. Seeing a 1/1 SLN with microscopic ECE for radiation. No discussion of dissection by surgeon. Mammaprint low-risk so no chemo (gulp). Is this someone you just treat without discussing dissection? Just curious of opinions.
Well yes. "Damn lies" etc. But we cherry pick a bit, don't we? To wit, I could say (leaving subset patient number sizes out of it), "On the basis of MA.20, DFS is not affected (p=0.65) by RNI regardless of nodal positivity or numbers of nodes positive; ergo, it's fallacious to base RNI decisions on nodal status in breast cancer."
Great point - but remind me, were these prespecified subgroup analyses? Or did they pull a Dan Spratt and start propagating that post-hoc subset analyses are just as good as direct randomized data?We are just never going to routinely see surgeons doing axillary dissections again in cT1N0 breast cancer except in very rare cases. And that is because of Z0011. And that is the world in which we now live. And, surgically speaking, it's how this patient was approached (ie she had a SLN biopsy, one node was "slightly" positive, and she didn't get her whole dang axilla whacked out).
For cT1N0 breast cancer, "axillary management" is minutiae in the extreme. It's like arguing over the Gatorade temperature on the sidelines in football. The axilla is not a halfway house for cancer cells. It is not some intermediate step on the way to metastatic failure. For cT1N0 patients, the axilla is prognostic. It is not therapeutic for the surgeon or the rad onc. There've been enough randomized trials and scientific data surely to convince folks of this. Or so I thought. We can whine over Z0011 as rad oncs, but the surgeons have moved on. This is how they think now, and they apply this thinking even in situations (ie w/ NAC) where we as rad oncs are saying "It was inappropriate to cite/use Z0011 here." The rest of the oncologic world is like "cool story bro."
The main reason "believers" cite to treat axillae here is local control/DFS ("You don't need to care about radiation therapy-induced arm lymphedema if you... have a big axillary recurrence"); survival improvement, obviously, never gets mentioned. The DFS advantage disappeared with longer followup in EORTC 22922. (Although very few patients got axillary RT in EORTC 22922; hence why the trial was entitled "Internal Mammary and Medial Supraclavicular Irradiation in Breast Cancer" I reckon.) So re: MA.20, and this patient. She presented as cT1N0 and got NAC. She then had surgery and had one out of five lymph nodes positive. Let's say, for argument's sake, she had zero out of five lymph nodes positive. When we look at subset analysis for DFS from MA.20, which group of patients had the BIGGEST benefit from RNI? Zero-LN patients or 1-positive-node patients? What I'm saying ("breast cancer is the worst") is that while we are arguing whether or not she should get RNI because she had one lymph node positive, I could make the argument from MA.20 that ***all*** cT1N0 patients who get NAC, or don't, and have zero lymph nodes positive have ***more*** DFS benefit from RNI than patients who have one lymph node positive.
So give RNI to all negative LN patients? We "should," because of all the subsets in MA.20, it was zero LN+ patients who had the most* DFS benefit from RNI. But I don't really ever hear rad oncs arguing for RNI in pT1N0 patients.
* hazard ratio
Wasn't there a 5% DFS benefit at 10 years in the NEJM pub?Well yes. "Damn lies" etc. But we cherry pick a bit, don't we? To wit, I could say (leaving subset patient number sizes out of it), "On the basis of MA.20, DFS is not affected (p=0.65) by RNI regardless of nodal positivity or numbers of nodes positive; ergo, it's fallacious to base RNI decisions on nodal status in breast cancer."
To remind us all re: MA.20....
This is the best/biggest modern argument for IMNs. OTOH, it conflicts with a bunch of other data.
