I loved all the best of #ASH21 threads this year, but in this thread I highlight 5 deeply flawed marketing advertisements (studies) that should not change practice. #mmsm 🧵
I will start by saying that it is very hard to criticize studies without offending people, so I apologize sincerely and it is my intention only to call out what I perceive as flawed. I may be wrong, and many of these authors have done more than I ever will for myeloma
We had chance to universally give dara upon progression to control arm in newly diagnosed MM in 3 different trials. But we didn’t. And now we shouldn’t just create a modeled scenario with so many assumptions and say it’s better to give dara up front
As a me-too drug offers little advantages over dara, isatuximab could have ran 3 vs 3 trials, or done modeling comparing vs dara with same backbone. But here we get a comparison of dara/len/dex versus isa/carf/dex. Fundamentally diff studies/patients
Breaks my heart. You compare people that were fit enough and had better biology to stay on Selinexor for longer to people who couldn’t stay on it for longer. Beyond marketing, what is the scientific value of such an inherently flawed analysis?
Study 4:
Cilta-cel is great (for patients with biology stable enough to wait to get therapy).
We don’t need flawed comparisons with patients from different areas of the world, many of whom are getting doublets to know that. What is the value, beyond marketing- of such a study?
No subgroup analysis can salvage a study with a fundamentally unethical control arm.I see efforts made to highlight unique role of seli in del 17p- but remember- it’s compared to doublet that nobody uses, and it’s likely all statistical noise.
Is MGUS more common in patients with osteoporosis? Do patients with MGUS have lower bone density? Should patients with osteoporosis be screened for MGUS? Or patients with MGUS screened for osteoporosis? What does the data (and guidelines) say?
🧵 #mmsm#medtwitter
We know from work done by the gurus of myeloma- that fractures are more common in patients with mgus than general population
But are fractures because of decreased done density or existing osteoporosis? We didn’t know.
More work from the Mayo Group did also show that patients with MGUS had a slightly higher risk of osteoporosis, but you can see- the RR was 1.2 with 95% CI of 1.0-1.4. pubmed.ncbi.nlm.nih.gov/19648385/
I confess that after #ASH21 I likely will use more quads.
but it isnt because Isa-RVD vs RVD showed ⬆️1 timept MRD🙄- or that GRIFFIN (DRVD vs RVD) showed signal for PFS benefit.
Read on for a 🧵on uncertainty, equipoise, decision making as an oncologist @AaronGoodman33 #mmsm
Before we delve in, there are two facts that the evidence seems to indicate:
Fact 1:
-MRD is undoubtedly prognostic, those that achieve (and sustain) MRD neg tend to have better outcomes than those who dont achieve and sustain MRD neg.
Fact 2:
Youd be neglecting the history of myeloma literature, if you looked back and didnt notice that interventions to deepen response (and achieve MRD negativity) havent always translated to increased overall survival, if those interventions were given later in disease course.
So, the FORTE trial was recently published. This is a great trial, and there are many important lessons/concepts/questions that arise from this, which I wanted to highlight in this 🧵
First randomization assesses different types of induction strategies, and lets first focus on that.
Demographics- anything important to note?
See table-
High-risk are well represented, but important to note Gain 1q (which isnt a good player by any means, just not a part of R-ISS high-risk staging), does inflate overall number of HIGH-RISK to almost 60% of enrolled pts!
So as a junior myeloma faculty, I see a lot of consults for MGUS. Heres a tweetorial on how to interpret light chain values in the setting of kidney disease, as light chains are often checked to look for plasma cell disorders when patients have CKD.