Ruben D. Carrasco
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View article: Supplementary Tables from <i>In Vivo</i> Modeling of CLL Transformation to Richter Syndrome Reveals Convergent Evolutionary Paths and Therapeutic Vulnerabilities
Supplementary Tables from <i>In Vivo</i> Modeling of CLL Transformation to Richter Syndrome Reveals Convergent Evolutionary Paths and Therapeutic Vulnerabilities Open
Supplementary file contains all supplementary tables S1-S16 in Excel format in the order in which they appear in the text.
View article: SF3B1 mutation accelerates the development of CLL via activation of the mTOR pathway
SF3B1 mutation accelerates the development of CLL via activation of the mTOR pathway Open
RNA splicing factor SF3B1 is one of the most recurrently mutated genes in chronic lymphocytic leukemia (CLL) and frequently co-occurs with chromosome 13q deletion [del(13q)]. This combination is associated with poor prognosis in CLL, sugge…
View article: Paclitaxel-induced mitotic arrest results in a convergence of apoptotic dependencies that can be safely exploited by BCL-X<sub>L</sub>degradation to overcome cancer chemoresistance
Paclitaxel-induced mitotic arrest results in a convergence of apoptotic dependencies that can be safely exploited by BCL-X<sub>L</sub>degradation to overcome cancer chemoresistance Open
Paclitaxel and other microtubule-targeting agents are cornerstone therapies for diverse cancers, including lung, breast, cervical, pancreatic, and ovarian malignancies. Paclitaxel induces tumor cell apoptosis during mitosis by disrupting m…
View article: The Evolution and Subtypes of Waldenstrom Macroglobulinemia: Findings from a Multi-omic Analysis of 249 Treatment Naive MYD88L265P Mutated Patients.
The Evolution and Subtypes of Waldenstrom Macroglobulinemia: Findings from a Multi-omic Analysis of 249 Treatment Naive MYD88L265P Mutated Patients. Open
To study the heterogeneity of transcriptional and genomic traits that underlie the clinical presentation of untreated Waldenstrom’s Macroglobulinemia (WM), we performed multi-omic studies in 249 treatment-naive patients with WM. For all pa…
View article: Development and characterization of the novel <i>MYD88</i> mutated, 6q deleted <scp>BCWM</scp>.2 cell line for Waldenström macroglobulinaemia
Development and characterization of the novel <i>MYD88</i> mutated, 6q deleted <span>BCWM</span>.2 cell line for Waldenström macroglobulinaemia Open
Summary Cell lines have enabled a comprehensive understanding of disease biology and the advancement of new therapeutics in Waldenström macroglobulinaemia (WM). Herein, we report the development of BCWM.2, a novel WM cell line derived from…
View article: Characterization and Experimental Use of Multiple Myeloma Bone Marrow Endothelial Cells and Progenitors
Characterization and Experimental Use of Multiple Myeloma Bone Marrow Endothelial Cells and Progenitors Open
Multiple myeloma (MM) is a plasma cell malignancy that resides within the bone marrow microenvironment, relying heavily on interactions with its cellular components. Among these, endothelial cells (ECs) play a pivotal role in MM progressio…
View article: Characterization and Experimental Use of Multiple Myeloma Bone Marrow Endothelial Cells and Progenitors
Characterization and Experimental Use of Multiple Myeloma Bone Marrow Endothelial Cells and Progenitors Open
Multiple myeloma (MM) is a plasma cell malignancy that resides within the bone marrow microenvironment, relying heavily on interactions with its cellular components. Among these, endothelial cells (ECs) play a pivotal role in MM progressio…
View article: Loss of GABARAP mediates resistance to immunogenic chemotherapy in multiple myeloma
Loss of GABARAP mediates resistance to immunogenic chemotherapy in multiple myeloma Open
Immunogenic cell death (ICD) is a form of cell death by which cancer treatments can induce a clinically relevant antitumor immune response in a broad range of cancers. In multiple myeloma (MM), the proteasome inhibitor bortezomib is an ICD…
View article: Editor's Note: Eph-B2/Ephrin-B2 Interaction Plays a Major Role in the Adhesion and Proliferation of Waldenstrom's Macroglobulinemia
Editor's Note: Eph-B2/Ephrin-B2 Interaction Plays a Major Role in the Adhesion and Proliferation of Waldenstrom's Macroglobulinemia Open
View article: Epigenetic regulation of CD38/CD48 by KDM6A mediates NK cell response in multiple myeloma
Epigenetic regulation of CD38/CD48 by KDM6A mediates NK cell response in multiple myeloma Open
View article: Author Correction: The Cyclophilin A–CD147 complex promotes the proliferation and homing of multiple myeloma cells
Author Correction: The Cyclophilin A–CD147 complex promotes the proliferation and homing of multiple myeloma cells Open
View article: Hyperphosphorylation of BCL-2 family proteins underlies functional resistance to venetoclax in lymphoid malignancies
Hyperphosphorylation of BCL-2 family proteins underlies functional resistance to venetoclax in lymphoid malignancies Open
The B cell leukemia/lymphoma 2 (BCL-2) inhibitor venetoclax is effective in chronic lymphocytic leukemia (CLL); however, resistance may develop over time. Other lymphoid malignancies such as diffuse large B cell lymphoma (DLBCL) are freque…
View article: In vivo bone marrow microenvironment siRNA delivery using lipid–polymer nanoparticles for multiple myeloma therapy
In vivo bone marrow microenvironment siRNA delivery using lipid–polymer nanoparticles for multiple myeloma therapy Open
Multiple myeloma (MM), a hematologic malignancy that preferentially colonizes the bone marrow, remains incurable with a survival rate of 3 to 6 mo for those with advanced disease despite great efforts to develop effective therapies. Thus, …
View article: Data from Bortezomib Induces Anti–Multiple Myeloma Immune Response Mediated by cGAS/STING Pathway Activation
Data from Bortezomib Induces Anti–Multiple Myeloma Immune Response Mediated by cGAS/STING Pathway Activation Open
The proteasome inhibitor bortezomib induces apoptosis in multiple myeloma cells and has transformed patient outcome. Using in vitro as well as in vivo immunodeficient and immunocompetent murine multiple myeloma models, we her…
View article: Supplementary Methods from ROBO1 Promotes Homing, Dissemination, and Survival of Multiple Myeloma within the Bone Marrow Microenvironment
Supplementary Methods from ROBO1 Promotes Homing, Dissemination, and Survival of Multiple Myeloma within the Bone Marrow Microenvironment Open
Supplementary Methods
View article: Supplementary Methods from ROBO1 Promotes Homing, Dissemination, and Survival of Multiple Myeloma within the Bone Marrow Microenvironment
Supplementary Methods from ROBO1 Promotes Homing, Dissemination, and Survival of Multiple Myeloma within the Bone Marrow Microenvironment Open
Supplementary Methods
View article: Data from <i>In Vivo</i> Modeling of CLL Transformation to Richter Syndrome Reveals Convergent Evolutionary Paths and Therapeutic Vulnerabilities
Data from <i>In Vivo</i> Modeling of CLL Transformation to Richter Syndrome Reveals Convergent Evolutionary Paths and Therapeutic Vulnerabilities Open
Transformation to aggressive disease histologies generates formidable clinical challenges across cancers, but biological insights remain few. We modeled the genetic heterogeneity of chronic lymphocytic leukemia (CLL) through multiplexed
View article: Supplementary Figures 1-15, Supplementary Table 1 from ROBO1 Promotes Homing, Dissemination, and Survival of Multiple Myeloma within the Bone Marrow Microenvironment
Supplementary Figures 1-15, Supplementary Table 1 from ROBO1 Promotes Homing, Dissemination, and Survival of Multiple Myeloma within the Bone Marrow Microenvironment Open
Supplementary Figure 1 showing ROBO1 expression in primary MM cells versus normal donor bone marrow plasma cells via gene expression profiling and immunohistochemistry. Supplementary Figure 2 showing distribution of ROBO1 expression in the…
View article: Supplementary Tables from <i>In Vivo</i> Modeling of CLL Transformation to Richter Syndrome Reveals Convergent Evolutionary Paths and Therapeutic Vulnerabilities
Supplementary Tables from <i>In Vivo</i> Modeling of CLL Transformation to Richter Syndrome Reveals Convergent Evolutionary Paths and Therapeutic Vulnerabilities Open
Supplementary file contains all supplementary tables S1-S16 in Excel format in the order in which they appear in the text.
View article: Data from <i>In Vivo</i> Modeling of CLL Transformation to Richter Syndrome Reveals Convergent Evolutionary Paths and Therapeutic Vulnerabilities
Data from <i>In Vivo</i> Modeling of CLL Transformation to Richter Syndrome Reveals Convergent Evolutionary Paths and Therapeutic Vulnerabilities Open
Transformation to aggressive disease histologies generates formidable clinical challenges across cancers, but biological insights remain few. We modeled the genetic heterogeneity of chronic lymphocytic leukemia (CLL) through multiplexed
View article: Supplementary Figure 1-9 from Bortezomib Induces Anti–Multiple Myeloma Immune Response Mediated by cGAS/STING Pathway Activation
Supplementary Figure 1-9 from Bortezomib Induces Anti–Multiple Myeloma Immune Response Mediated by cGAS/STING Pathway Activation Open
Supp. Fig. 1 shows that bortezomib induces ICD in vitro. Suppl. Fig.2 shows that bortezomib treatment of co-culture of dendritic and T cells does not induce T cell maturation. Suppl. Fig. 3 shows that bortezomib-induced MM cell death promo…
View article: Supplementary Figure 1-9 from Bortezomib Induces Anti–Multiple Myeloma Immune Response Mediated by cGAS/STING Pathway Activation
Supplementary Figure 1-9 from Bortezomib Induces Anti–Multiple Myeloma Immune Response Mediated by cGAS/STING Pathway Activation Open
Supp. Fig. 1 shows that bortezomib induces ICD in vitro. Suppl. Fig.2 shows that bortezomib treatment of co-culture of dendritic and T cells does not induce T cell maturation. Suppl. Fig. 3 shows that bortezomib-induced MM cell death promo…
View article: Supplementary Tables from <i>In Vivo</i> Modeling of CLL Transformation to Richter Syndrome Reveals Convergent Evolutionary Paths and Therapeutic Vulnerabilities
Supplementary Tables from <i>In Vivo</i> Modeling of CLL Transformation to Richter Syndrome Reveals Convergent Evolutionary Paths and Therapeutic Vulnerabilities Open
Supplementary file contains all supplementary tables S1-S16 in Excel format in the order in which they appear in the text.
View article: Data from Bortezomib Induces Anti–Multiple Myeloma Immune Response Mediated by cGAS/STING Pathway Activation
Data from Bortezomib Induces Anti–Multiple Myeloma Immune Response Mediated by cGAS/STING Pathway Activation Open
The proteasome inhibitor bortezomib induces apoptosis in multiple myeloma cells and has transformed patient outcome. Using in vitro as well as in vivo immunodeficient and immunocompetent murine multiple myeloma models, we her…
View article: Data from ROBO1 Promotes Homing, Dissemination, and Survival of Multiple Myeloma within the Bone Marrow Microenvironment
Data from ROBO1 Promotes Homing, Dissemination, and Survival of Multiple Myeloma within the Bone Marrow Microenvironment Open
The bone marrow (BM) microenvironment actively promotes multiple myeloma pathogenesis, and therapies targeting both cancer cells and the niche are highly effective. We were interested in identifying novel signaling pathways supporting mult…
View article: Supplementary Figures 1-15, Supplementary Table 1 from ROBO1 Promotes Homing, Dissemination, and Survival of Multiple Myeloma within the Bone Marrow Microenvironment
Supplementary Figures 1-15, Supplementary Table 1 from ROBO1 Promotes Homing, Dissemination, and Survival of Multiple Myeloma within the Bone Marrow Microenvironment Open
Supplementary Figure 1 showing ROBO1 expression in primary MM cells versus normal donor bone marrow plasma cells via gene expression profiling and immunohistochemistry. Supplementary Figure 2 showing distribution of ROBO1 expression in the…
View article: Data from ROBO1 Promotes Homing, Dissemination, and Survival of Multiple Myeloma within the Bone Marrow Microenvironment
Data from ROBO1 Promotes Homing, Dissemination, and Survival of Multiple Myeloma within the Bone Marrow Microenvironment Open
The bone marrow (BM) microenvironment actively promotes multiple myeloma pathogenesis, and therapies targeting both cancer cells and the niche are highly effective. We were interested in identifying novel signaling pathways supporting mult…
View article: Supplementary Table S1 from Bortezomib Induces Anti–Multiple Myeloma Immune Response Mediated by cGAS/STING Pathway Activation
Supplementary Table S1 from Bortezomib Induces Anti–Multiple Myeloma Immune Response Mediated by cGAS/STING Pathway Activation Open
Supp. table S1 shows immune genes regulated after treatment with bortezomib in vivo.
View article: Supplementary Table S1 from Bortezomib Induces Anti–Multiple Myeloma Immune Response Mediated by cGAS/STING Pathway Activation
Supplementary Table S1 from Bortezomib Induces Anti–Multiple Myeloma Immune Response Mediated by cGAS/STING Pathway Activation Open
Supp. table S1 shows immune genes regulated after treatment with bortezomib in vivo.
View article: Supplementary Figures from <i>In Vivo</i> Modeling of CLL Transformation to Richter Syndrome Reveals Convergent Evolutionary Paths and Therapeutic Vulnerabilities
Supplementary Figures from <i>In Vivo</i> Modeling of CLL Transformation to Richter Syndrome Reveals Convergent Evolutionary Paths and Therapeutic Vulnerabilities Open
Supplementary file contains a PDF version of supplementary figures S1-S7 and associated figure legends.