Top Tweets for #smarcb1
On the cover of the September 15 issue—#SMARCB1 Deficiency in Tumors Confers Vulnerability to H3K27 Demethylase Inhibitors via Autophagy Disruption https://t.co/8xfkkUL5pX @CespedesMontse @Romero_Ferraro
#SMARCB1-deficient #RMC: wtEGFR emerges as a targetable dependency. #Panitumumab-based therapy achieved ORR 53.9% (4 CRs) in heavily pretreated pts, outperforming historical outcome w/manageable toxicity. Compelling preclinical/clinical rationale for a new SOC in RMC #ASCO26
1/5 New in @CCR_AACR: Results of the 1st prospective trial of a targeted agent in #SMARCB1-deficient #RenalMedullaryCarcinoma (RMC). We tested ixazomib + gemcitabine + doxorubicin in 30 patients https://t.co/LyGS55EfcV #endRMC #MsaouelLab
Powerful story raising awareness for SMARCB1-deficient sinonasal carcinoma (#SDSC). Like #renalmedullarycarcinoma, SDSC is driven by loss of #SMARCB1 and deserves dedicated research. Grateful to @chubbyemu for consistently supporting #rarecancers 👉https://t.co/yG8d4A3yWx
We identified PHF6 as a critical #dependency for the survival of #SMARCB1-mutant cancers through #CRISPR screenings conducted in collaboration with @cancerdepmap.
SCI leader Nathanael Gray & others reversed aggressive cancer, reverting malignant cells to a more normal state, suggesting a new approach to curing cancer rather than killing cancer cells with toxic therapies. https://t.co/lI8JLnezuU #SMARCB1
Appreciate the @TheVFoundation’s support of our research into crosstalks between rare #Kidneycancer subtypes such as #RenalMedullaryCarcinoma with #SMARCB1-deficient #bladdercancer subtypes. Details in recent @NatureComms publication 👉 https://t.co/RW0HWQxSd9
Our researchers really know how to be bold. Here’s the impactful work that is truly game-changing. 👇
https://t.co/hVDwp1CiaE
@VeredStearns | @RoisinMConnolly | @PavlosMsaouel | @fjsanchezrivera
Just in time for #HumpDay: Our study Targeting DCAF5 suppresses #SMARCB1-mutant #cancer via stabilizing SWI/SNF is online now in @Nature. Congratulations 🎉 to co-first authors Sandi-Radko-Juettner and @HongYue88665668 and all co-authors on this story! 1/
https://t.co/f3fJfiPjiM
What is a #radonc doing at @NANOStweets? Learning from the best diagnosticians in the world! #eyetwitter Today @ Walsh Mystery Cases-excellent relevant pearls today about #SMARCB1 histology, use of #dotatatePET for RT planning for meningioma, and a LOT of Ddx!
Excited to share the latest #MsaouelLab collaborative effort in @NatureComms characterizing #SMARCB1 deficiency as a driver of urothelial carcinoma subsets at least in part via IL6/JAK/STAT signaling 👉https://t.co/RW0HWQxSd9
Six papers that improved our understanding of Renal Medullary Carcinoma - @PavlosMsaouel
#Bevacizumab #Cancer #Immunotherapy #KidneyCancer #OncoDaily #Oncology #Pembrolizumab #SMARCB1 #RenalMedullaryCarcinoma
https://t.co/VjBuVNDCOm
Orgulloso y emocionado tras la defensa de la Tesis Doctoral de la Dra. Andrea Vilarrubí Porta.Afortunado de haber co-Dirigido la tesis con @CespedesMontse y esperanzado por el futuro que que abre está tesis en la #medicinadeprecision en #oncologiapediatrica
#IJC #SMARCB1 #SJD
Our latest #MsaouelLab collaboration with @LabGenovese @MDAndersonNews elucidates the connection between #SickleCellTrait and #SMARCB1 loss in #RenalMedullaryCarcinoma 👉https://t.co/aTDmp1BU3t
👇Those are quite rare but tricky #kidneycancer entities to diagnose and treat. The #SMARCB1 loss can induce a vulnerability to replication stress making cytotoxic chemotherapy a reasonable option in our toolbox as shown here: https://t.co/t0Aort0FeU
6/6 Our findings open new avenues for prevention and therapy by explaining why #SMARCB1 loss is a consistent hallmark of #RenalMedullaryCarcinoma in individuals with #SickleCellTrait & why these tumors are so distinctly refractory to hypoxia-inducing anti-VEGF therapies. #endRMC
5/6 Notably, SMARCB1-proficient tumors showed #SMARCB1 reduction and increased growth & aggressiveness in presence of #SickleCellTrait, while they failed to grow in mice with wild-type human hemoglobin.
4/6 Loss of #SMARCB1 conferred a survival advantage in renal tumor cells under hypoxic stress. Conversely, disruption of ubiquitin-mediated degradation of SMARCB1 conferred a growth disadvantage to #RenalMedullaryCarcinoma tumor cells in vivo.
3/6 We noted that #SMARCB1 is reduced in the renal medullary tubule cells of nephrectomy samples in patients with #RenalMedullaryCarcinoma and mouse models with #SickleCellTrait suggesting a selective pressure to decrease SMARCB1 protein levels under hypoxic conditions.
2/6 We identified in our #SickleCellTrait mouse models that red blood cell sickling induces chronic renal medullary hypoxia leading to degradation of #SMARCB1 via the ubiquitin–proteasome system which can be prevented by K62R mutation.
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