For the last talk of the day at #iwHRMM25, we're hearing about resistance to bispecific antibodies, with a focus on high-risk immune profile, from @RossFirestone of @MSKCancerCenter. #MMSM #MultipleMyeloma #Myeloma #HemOnc #ImmunoOnc

We're pleased to welcome @FrancescoMaura4 of @MSKCancerCenter to our Multiple Myeloma Editorial Board on VJHemOnc - thank you for sharing your expert opinions and helping to shape our content. Explore his interviews here: 👉 https://t.co/y2BRKUY8RR👈 #MMsm #HemOnc

Genomics Define Malignant Transformation in Myeloma. Co-authored by @FrancescoMaura4, @VincentRK, @szusmani and @Leif_Bergsagel Read the full article.

Big, beautiful trees!! SMART-PTA for whole-genome+transcriptome on thousand of single cells from the normal human esophagus 🤯 Massively scaling up the power of scWGS to build deep phylogenies and chart somatic evolution from birth throughout life. https://t.co/pciw5yME0x

#OnlineFirst Timing Genomic Antigen Loss in #MultipleMyeloma Treated with T Cell–Redirecting Immunotherapies https://t.co/RBGZzjG1Gu

Thansk @RaabMarc for this nice editorial highlighting our recent paper on @BCD_AACR @NBahlis ⁦@hollyleeYJ ⁩ #PaolaNeri #MariosPapdimitious @BenDiamondMD #mmsm @MSKCancerCenter 👇👇👇

Fantastic event w discussion, debates, & exchange of knowledge, ideas, and opinions at the Kyle Barlogie #PlasmaCellDisorders symposium #MMSM @MSK_DeptOfMed @MayoClinic #MedTwitter #MedEd @szusmani @VincentRK @myelomaMD @FrancescoMaura4 @UrviShahMD @sridevirajeeve & many others

Biallelic antigen escape is a mechanism of resistance to anti-CD38 antibodies in multiple myeloma [Sep 25, 2025] @BenDiamondMD et al. @FrancescoMaura4 @BloodPortfolio https://t.co/KUY1kWvdq7 #mmsm #PrecisionMedicine #cagenome #caxtx

The quest for cure of myeloma starts from the understanding of its initiation and evolution. We contributed to a pivotal work led by @FrancescoMaura4 and @VincentRK Genomics Define Malignant Transformation in Myeloma Precursor Conditions

🧬 Genomics redefine the myeloma spectrum! MGUS ➡️ SMM ➡️ MM- no longer just a clinical continuum, but a genomic one. 🧫 374 pts (84 MGUS | 290 SMM) → WES/WGS 🧠 Key Findings ✅ Introduces “Genomic MGUS” (premalignant) vs “Genomic MM” (malignant at DNA level) 🧩 90 % of

A final thanks to @VincentRK, @Leif_Bergsagel, and @szusmani for their incredible support, mentorship, and the fantastic discussions about these data, myeloma, precursor conditions, and beyond!! 🙏🙏🙏🙏14/14

Thanks to my friend and longtime collaborator @BachisioZic for his patience in working with me, and to all the patients who contributed to this study. 13/14

Truly a fantastic collaboration across multiple institutions. Too many to thank, but a special thanks to those who contributed their invaluable data: @Leif_Bergsagel @Myeloma_Doc #KenShain @DrOlaLandgren @myelomaMD @DrGarethMorgan1 @Rfonsi1 @nickbolli @szusmani @VincentRK 12/14

Importantly , the "prognostication" is different from the "classification". The first aims to predict the patients with evidence of malignant transformation at imminent risk of progression; the second aims to differentiate patients with and without neoplastic transformation 11/14

Notably, in this integrated model, the high-risk group is defined by the presence of both high-risk genomic features and IMWG 2/20/20 high-risk criteria. An important question for future studies is whether such cases should still be considered SMM. 10/14

Specifically integrating of #APOBEC, MYC translocations, complex copy number signatures and RAS mutations with IMWG 2/20/20, we identified a population at high risk of imminent progression 9/14

In line with prior work from @Leif_Bergsagel @IrenemGhobrial @JbAlberge @MarkBustoros @BrunoPaiva_UNAV and others we found that genomics can indeed improve IMWG 2/20/20. 8/14

After reclassifying SMM and MGUS cases based on the presence or absence of malignant transformation, we investigated whether genomic profiling could improve the clinical prediction of which cases would progress earlier. 7/14

While ~90% of SMM already looks genomically similar to MM, some of these cases remain stable for over 10 years!! Why? We don’t know for sure, but we speculate that the immune system may exert selective pressure that blocks these cells from expanding and causing organ damage 6/14

While a pathologist can say if a polyp is benign or not, the same distinction cannot be made in MM/SMM. Our genomic model is designed to provide that information. Using this approach, we did not observe any progressions in cases without evidence of neoplastic transformation. 5/14