Posts by Caner Saygin, MD
How should we incorporate molecular data in treatment decisions for ALL?
It is time to pay more attention to genetic heterogeneity of adult ALL before we decide therapy.
Targeted therapies are rapidly emerging, and replacing chemo in ALL.
Our review at Blood Cancer Discovery is out today! Link👇
We are very excited to share our work investigating menin inhibition in T-ALL, led by Kate Shimamoto and Arda Karaoglu, just published in Mol Cancer Therapeutics.
We found that high p-MEF2C S222 can predict menin inhibitor response, better than HOX gene expression levels, in T-ALL. rb.gy/oroosm
very cool work led by @canersaygin.bsky.social lab looking at the potential for targeting menin in T-cell ALL!
aacrjournals.org/mct/article/...
In a recent study, Caner Saygin, MD and team examined a large group of adults with a rare, aggressive form of leukemia called TP53-mutant ALL and found key genetic changes that guide doctors to predict which pts may face more serious outcomes. @uchicagomedicine.bsky.social
https://ow.ly/cFsz50YgL2s
Congrats @herranzlab.bsky.social! Very cool story.
InO + TKI has robust activity but limited toxicity when drugs are given sequentially. Great option for older adults with Ph+ ALL in frontline.
Our NCI study of HMA +/- Iadademstat is enrolling briskly for patients with HMA-naive accelerated/blast phase MPNs and overlap syndromes!
www.cancer.gov/research/par...
In a new study, @canersaygin.bsky.social and colleagues show that TP53-mutant ALL is a high-risk, chemo-resistant subtype with poor survival, highlighting the need for tailored strategies.
ow.ly/lvwo50WHJIr
We’re thrilled to announce the 2025–2027 New Investigator Research Grant recipients—13 outstanding scientists from across the country who are pushing the boundaries of leukemia research.
Meet the 2025–2027 awardees: bit.ly/474sfGP
#LeukemiaResearch #ScientificDiscovery #FundingtheFuture
Proud of our cancer program for being #1 in Illinois for the 3rd year in a row!!
Learn more about our USNWR rankings at www.uchicagomedicine.org/forefront/ne...
We are thankful to the funding sources that supported the key personnel and helped us complete this project.
@ash.hematology.org, @preventcancer.org, LLS and CRF
Altogether, serial monitoring of CH may complement MRD assessment in myeloma to identify individuals who are candidates for treatment de-escalation due to risk for SPHM.
Dynamic CH assessment should be further validated as a potential endpoint for future interventional CH trials.
Patients with progressive TP53-mutant CH clones progressed to therapy-related ALL or myeloid neoplasms, while stable clones had lower leukemogenic potential. The data suggest that serial monitoring is more informative than cross-sectional assessment of CH in pts receiving MM tx.
The meticulous work co-led by Jen Cooperrider and Arda Karaoglu revealed that ongoing lenalidomide maintenance selectively expands TP53-mutant CH clones as opposed to age-related CH (DTA muts).
Discontinuation of lenalidomide led to stability or regression of TP53-mutant CH.
We needed a sensitive NGS assay to monitor clones in pts treated with R or KRd maintenance (ATLAS) and in pts who stopped R after MRD negativity (MRD2STOP).
This was achieved in collaboration with @alexbick.bsky.social at Vanderbilt, using their targeted CH panel.
To understand the impact of lenalidomide on evolution of therapy-related CH, we studied prospectively obtained samples from two major MM trials (ATLAS and MRD2STOP), run by
Ben Derman, Andrzej Jakubowiak and Jen Cooperrider.
Very excited to share our paper investigating the evolution of therapy-related CH in myeloma pts treated w/ or w/o LEN.
Can we predict the risk for second blood cancer in myeloma pts?
Grateful for the collaboration with
@uchicagocancer.bsky.social myeloma program.
www.nature.com/articles/s41...
Nice data but OS curves do not seem to have a plateau. They keep going down. I still don`t think CAR-T cures ALL. Unlike allo curves below showing ~1/3 of pts may be cured. www.nature.com/articles/s41...
Interesting. Sounds like this may be best classified as T/myeloid MPAL (bilineal).
Do they share a fusion (e.g. ETV6::ABL1)?
Myeloid mutations are very common in T-ALL, especially with age.
T-ALL and AML can sometimes mingle/differentially interpreted by different pathologists. They are more similar than different, evidenced by T-ALL response to myeloid drugs (Aza/ven, IDH inh)