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Cereblon loss and up-regulation of c-Myc are associated with lenalidomide resistance in multiple myeloma patients

HAEMATOLOGICA (2018)

Journal

HAEMATOLOGICA

Volume 103, Issue 8, Pages E368-E371

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FERRATA STORTI FOUNDATION

DOI: 10.3324/haematol.2017.186601

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SUMOylation inhibition enhances multiple myeloma sensitivity to lenalidomide

Li Du, Wei Liu, Flavia Pichiorri, Steven T. Rosen

Summary: This study identified SUMOylation as a potential mechanism regulating lenalidomide resistance in multiple myeloma. Inhibition of SUMOylation can enhance sensitivity to lenalidomide by downregulating IRF4 expression.

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miR-22 Modulates Lenalidomide Activity by Counteracting MYC Addiction in Multiple Myeloma

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Summary: The MYC-driven deregulation of microRNAs, particularly the repression of miR-22, plays a critical role in multiple myeloma (MM) and resistance to immunomodulatory imide drugs (IMiDs). Lenalidomide treatment enhances miR-22 activity by reducing MYC inhibition, which restores drug sensitivity and leads to synergistic anti-MM activity.

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Daratumumab, Bortezomib, Lenalidomide, and Dexamethasone for Multiple Myeloma

Pieter Sonneveld, Meletios A. Dimopoulos, Mario Boccadoro, Hang Quach, P. Joy Ho, Meral Beksac, Cyrille Hulin, Elisabetta Antonioli, Xavier Leleu, Silvia Mangiacavalli, Aurore Perrot, Michele Cavo, Angelo Belotti, Annemiek Broijl, Francesca Gay, Roberto Mina, Inger S. Nijhof, Niels W. C. J. van de Donk, Eirini Katodritou, Fredrik Schjesvold, Anna Sureda Balari, Laura Rosinol, Michel Delforge, Wilfried Roeloffzen, Tobias Silzle, Annette Vangsted, Hermann Einsele, Andrew Spencer, Roman Hajek, Artur Jurczyszyn, Sarah Lonergan, Tahamtan Ahmadi, Yanfang Liu, Jianping Wang, Diego Vieyra, Emilie M. J. van Brummelen, Veronique Vanquickelberghe, Anna Sitthi-Amorn, Carla J. de Boer, Robin Carson, Paula Rodriguez-Otero, Joan Blade, Philippe Moreau

Summary: The addition of subcutaneous daratumumab to VRd induction and consolidation therapy and to lenalidomide maintenance therapy showed significant improvement in progression-free survival among transplantation-eligible patients with newly diagnosed multiple myeloma.

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Multiple cereblon genetic changes are associated with acquired resistance to lenalidomide or pomalidomide in multiple myeloma

Sarah Gooding, Naser Ansari-Pour, Fadi Towfic, Maria Ortiz Estevez, Philip P. Chamberlain, Kao-Tai Tsai, Erin Flynt, Marissa Hirst, Dan Rozelle, Paula Dhiman, Paola Neri, Karthik Ramasamy, Nizar Bahlis, Paresh Vyas, Anjan Thakurta

Summary: The study found that in patients with myeloma, as the exposure to IMiD drugs increased, the frequency of CRBN abnormalities also increased gradually, with almost one-third of patients having CRBN alterations by the time they were refractory to pomalidomide (POM). These CRBN abnormalities were associated with inferior outcomes to POM in patients already refractory to lenalidomide (LEN).

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GFI1-Dependent Repression of SGPP1 Increases Multiple Myeloma Cell Survival

Daniela N. Petrusca, Patrick L. Mulcrone, David A. Macar, Ryan T. Bishop, Evgeny Berdyshev, Attaya Suvannasankha, Judith L. Anderson, Quanhong Sun, Philip E. Auron, Deborah L. Galson, G. David Roodman

Summary: This study identifies a novel mechanism by which GFI1 regulates the growth and survival of high risk multiple myeloma (MM) cells through modulation of sphingolipid metabolism. Regardless of p53 status, GFI1 increases intracellular levels of sphingosine-1-phosphate, stabilizing c-Myc and promoting MM cell viability. This finding suggests GFI1 as a potential therapeutic target for the treatment of MM, specifically in patients with non-functional p53.

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Targeting an MDM2/MYC Axis to Overcome Drug Resistance in Multiple Myeloma

Omar Faruq, Davidson Zhao, Mariusz Shrestha, Andrea Vecchione, Eldad Zacksenhaus, Hong Chang

Summary: High expression of MDM2 is associated with poor prognosis and drug resistance in human myeloma cell lines (HMCLs). MDM2 inhibition can sensitize resistant cells to anti-myeloma drugs and induce apoptosis. The study demonstrates the oncogenic regulatory loop between MDM2 and c-Myc, and suggests targeting the MDM2/c-Myc axis as a potential therapeutic strategy for refractory/relapsed MM.

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Cilta-cel or Standard Care in Lenalidomide-Refractory Multiple Myeloma

Jesus San-Miguel, Binod Dhakal, Kwee Yong, Andrew Spencer, Sebastien Anguille, Maria-Victoria Mateos, Carlos Fernandez de Larrea, Joaquin Martinez-Lopez, Philippe Moreau, Cyrille Touzeau, Xavier Leleu, Irit Avivi, Michele Cavo, Tadao Ishida, Seok Jin Kim, Wilfried Roeloffzen, Niels W. C. J. van de Donk, Dominik Dytfeld, Surbhi Sidana, Luciano J. Costa, Albert Oriol, Rakesh Popat, Abdullah M. Khan, Yael C. Cohen, P. Joy Ho, James Griffin, Nikoletta Lendvai, Carolina Lonardi, Ana Slaughter, Jordan M. Schecter, Carolyn C. Jackson, Kaitlyn Connors, Katherine Li, Enrique Zudaire, Diana Chen, Jane Gilbert, T. Yeh, Sarah Nagle, Erika Florendo, Lida Pacaud, Nitin Patel, Simon J. Harrison, Hermann Einsele

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Molecular Mechanisms of Cereblon-Interacting Small Molecules in Multiple Myeloma Therapy

Matteo Costacurta, Jackson He, Philip E. Thompson, Jake Shortt

Summary: Thalidomide analogues, or IMiDs, are crucial in treating multiple myeloma by modifying substrate specificity through binding with CRBN. Recent research has advanced our understanding of CRBN's physiological functions, new IMiD derivatives like CELMoDs, and the use of PROTACs to target cancer dependencies. These CRBN-interacting small molecules offer a powerful tool for precision medicine.

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The Prognostic Role of MYC Structural Variants Identified by NGS and FISH in Multiple Myeloma

Neeraj Sharma, James B. Smadbeck, Nadine Abdallah, Cinthya Zepeda-Mendoza, Moritz Binder, Kathryn E. Pearce, Yan W. Asmann, Jess F. Peterson, Rhett P. Ketterling, Patricia T. Greipp, P. Leif Bergsagel, S. Vincent Rajkumar, Shaji K. Kumar, Linda B. Baughn

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Cereblon loss and up-regulation of c-Myc are associated with lenalidomide resistance in multiple myeloma patients

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