John L. Cleveland
YOU?
Author Swipe
View article: Lymphoma accelerates T cell and tissue aging
Lymphoma accelerates T cell and tissue aging Open
The combined effects of aging and cancer on immune cells were investigated in young versus aged mice harboring B cell lymphoma, and in T cells from young and aged B cell lymphoma patients. These analyses revealed that lymphoma alone is suf…
View article: Unc-51 Like Kinase 3 (ULK3) is essential for autophagy and cell survival in multiple myeloma
Unc-51 Like Kinase 3 (ULK3) is essential for autophagy and cell survival in multiple myeloma Open
Despite the availability of effective therapies such as proteasome inhibitors, multiple myeloma (MM) patients relapse with refractory disease. To identify new therapeutic targets, we assessed RNA sequencing data from CD138+ MM patient cell…
View article: Comparison of axicabtagene ciloleucel and tisagenlecleucel patient CAR-T cell products by single-cell RNA sequencing
Comparison of axicabtagene ciloleucel and tisagenlecleucel patient CAR-T cell products by single-cell RNA sequencing Open
Background Autologous CD19 chimeric antigen receptor (CAR) T-cell therapy leads to durable responses and improved survival in patients with relapsed or refractory large B-cell lymphoma (R/R LBCL). Among approved CAR T-cell products, axicab…
View article: Epigenetic Plasticity Drives Carcinogenesis and Multi-Therapy Resistance in Multiple Myeloma
Epigenetic Plasticity Drives Carcinogenesis and Multi-Therapy Resistance in Multiple Myeloma Open
We demonstrate that carcinogenesis and multi-therapy resistance in multiple myeloma (MM)—a treatable yet incurable plasma cell malignancy—are driven by epigenetic dysregulation. In this new paradigm, genomic and cytogenetic events unlock e…
View article: Data from The Functional Transcriptomic Landscape Informs Therapeutic Strategies in Multiple Myeloma
Data from The Functional Transcriptomic Landscape Informs Therapeutic Strategies in Multiple Myeloma Open
Several therapeutic agents have been approved for treating multiple myeloma, a cancer of bone marrow–resident plasma cells. Predictive biomarkers for drug response could help guide clinical strategies to optimize outcomes. In this study, w…
View article: Supplementary Data from The Functional Transcriptomic Landscape Informs Therapeutic Strategies in Multiple Myeloma
Supplementary Data from The Functional Transcriptomic Landscape Informs Therapeutic Strategies in Multiple Myeloma Open
This file contains four supplementary tables S1 - S4 and eight supplementary figures S1 - S8.
View article: The Functional Transcriptomic Landscape Informs Therapeutic Strategies in Multiple Myeloma
The Functional Transcriptomic Landscape Informs Therapeutic Strategies in Multiple Myeloma Open
Several therapeutic agents have been approved for treating multiple myeloma, a cancer of bone marrow–resident plasma cells. Predictive biomarkers for drug response could help guide clinical strategies to optimize outcomes. In this study, w…
View article: Supplementary Table S3 from The polyamine-hypusine circuit controls an oncogenic translational program essential for malignant conversion in MYC-driven lymphoma
Supplementary Table S3 from The polyamine-hypusine circuit controls an oncogenic translational program essential for malignant conversion in MYC-driven lymphoma Open
Supplementary Table S3 lists 665 shared differentially translated transcripts (DTT) identified following depletion of eIF5A or DHPS, related to Fig. 5C.
View article: Supplementary Table S4 from The polyamine-hypusine circuit controls an oncogenic translational program essential for malignant conversion in MYC-driven lymphoma
Supplementary Table S4 from The polyamine-hypusine circuit controls an oncogenic translational program essential for malignant conversion in MYC-driven lymphoma Open
Supplementary Table S4 lists oncogenes and tumor suppressor genes analyzed for changes in translation efficiency (TE) following depletion of eIF5A or DHPS, related to Fig. 5E.
View article: Supplementary Tables S1, S2, S5-S13 from The polyamine-hypusine circuit controls an oncogenic translational program essential for malignant conversion in MYC-driven lymphoma
Supplementary Tables S1, S2, S5-S13 from The polyamine-hypusine circuit controls an oncogenic translational program essential for malignant conversion in MYC-driven lymphoma Open
Supplementary Tables S1, S2, S5-S13 includes Supplementary Tables S1, S2, S5-S13. Supplementary Table S1 provides a summary of BL and DHL patient demographics for the immunohistochemistry study presented in Fig. 1, E and F. Supplementary T…
View article: Supplementary Tables S1, S2, S5-S13 from The polyamine-hypusine circuit controls an oncogenic translational program essential for malignant conversion in MYC-driven lymphoma
Supplementary Tables S1, S2, S5-S13 from The polyamine-hypusine circuit controls an oncogenic translational program essential for malignant conversion in MYC-driven lymphoma Open
Supplementary Tables S1, S2, S5-S13 includes Supplementary Tables S1, S2, S5-S13. Supplementary Table S1 provides a summary of BL and DHL patient demographics for the immunohistochemistry study presented in Fig. 1, E and F. Supplementary T…
View article: Supplementary Table S4 from The polyamine-hypusine circuit controls an oncogenic translational program essential for malignant conversion in MYC-driven lymphoma
Supplementary Table S4 from The polyamine-hypusine circuit controls an oncogenic translational program essential for malignant conversion in MYC-driven lymphoma Open
Supplementary Table S4 lists oncogenes and tumor suppressor genes analyzed for changes in translation efficiency (TE) following depletion of eIF5A or DHPS, related to Fig. 5E.
View article: Supplementary Figures S1-S7 from The polyamine-hypusine circuit controls an oncogenic translational program essential for malignant conversion in MYC-driven lymphoma
Supplementary Figures S1-S7 from The polyamine-hypusine circuit controls an oncogenic translational program essential for malignant conversion in MYC-driven lymphoma Open
Supplementary Figures S1-S7 includes Supplementary Figure S1-S7 and the figure legend for each figure. Supplementary Fig. S1 shows that the polyamine-hypusine circuit is activated in many human cancers including MYC-driven lymphoma. Supple…
View article: Supplementary Table S3 from The polyamine-hypusine circuit controls an oncogenic translational program essential for malignant conversion in MYC-driven lymphoma
Supplementary Table S3 from The polyamine-hypusine circuit controls an oncogenic translational program essential for malignant conversion in MYC-driven lymphoma Open
Supplementary Table S3 lists 665 shared differentially translated transcripts (DTT) identified following depletion of eIF5A or DHPS, related to Fig. 5C.
View article: Supplementary Figures S1-S7 from The polyamine-hypusine circuit controls an oncogenic translational program essential for malignant conversion in MYC-driven lymphoma
Supplementary Figures S1-S7 from The polyamine-hypusine circuit controls an oncogenic translational program essential for malignant conversion in MYC-driven lymphoma Open
Supplementary Figures S1-S7 includes Supplementary Figure S1-S7 and the figure legend for each figure. Supplementary Fig. S1 shows that the polyamine-hypusine circuit is activated in many human cancers including MYC-driven lymphoma. Supple…
View article: Engineered BRET-Based Biologic Light Sources Enable Spatiotemporal Control over Diverse Optogenetic Systems
Engineered BRET-Based Biologic Light Sources Enable Spatiotemporal Control over Diverse Optogenetic Systems Open
Light-inducible optogenetic systems offer precise spatiotemporal control over a myriad of biologic processes. Unfortunately, current systems are inherently limited by their dependence on external light sources for their activation. Further…
View article: The Many Faces of Hypusinated eIF5A: Cell Context-Specific Effects of the Hypusine Circuit and Implications for Human Health
The Many Faces of Hypusinated eIF5A: Cell Context-Specific Effects of the Hypusine Circuit and Implications for Human Health Open
The unique amino acid hypusine [Nε-(4-amino-2-hydroxybutyl)lysine] is exclusively formed on the translational regulator eukaryotic initiation factor 5A (eIF5A) via a process coined hypusination. Hypusination is mediated by two enzymes, deo…
View article: Supplementary Figures S1-S4 from Trisomy 8 Defines a Distinct Subtype of Myeloproliferative Neoplasms Driven by the MYC–Alarmin Axis
Supplementary Figures S1-S4 from Trisomy 8 Defines a Distinct Subtype of Myeloproliferative Neoplasms Driven by the MYC–Alarmin Axis Open
Figure S1. Landscape of somatic mutations and cytogenetics in Moffitt MF cohort. Figure S2. Effects of enforced MYC expression in HSCs in vivo. Figure S3. MYC-induced changes in hematopoietic sub-populations and colony forming potential. F…
View article: Supplementary Table S1-16 from Trisomy 8 Defines a Distinct Subtype of Myeloproliferative Neoplasms Driven by the MYC–Alarmin Axis
Supplementary Table S1-16 from Trisomy 8 Defines a Distinct Subtype of Myeloproliferative Neoplasms Driven by the MYC–Alarmin Axis Open
Table S1. Demographics of Moffitt Total Cancer Care MF patients. Table S2. Demographic Profile of trisomy 8+ TN-MF patients and HDs used in scRNA-seq analysis and PDX studies. Table S3. List of genes used for PROGENy analysis of human BM c…
View article: Data from Trisomy 8 Defines a Distinct Subtype of Myeloproliferative Neoplasms Driven by the MYC–Alarmin Axis
Data from Trisomy 8 Defines a Distinct Subtype of Myeloproliferative Neoplasms Driven by the MYC–Alarmin Axis Open
Despite advances in understanding the genetic abnormalities in myeloproliferative neoplasms (MPN) and the development of JAK2 inhibitors, there is an urgent need to devise new treatment strategies, particularly for patients with triple-neg…
View article: Supplementary Table S1-16 from Trisomy 8 Defines a Distinct Subtype of Myeloproliferative Neoplasms Driven by the MYC–Alarmin Axis
Supplementary Table S1-16 from Trisomy 8 Defines a Distinct Subtype of Myeloproliferative Neoplasms Driven by the MYC–Alarmin Axis Open
Table S1. Demographics of Moffitt Total Cancer Care MF patients. Table S2. Demographic Profile of trisomy 8+ TN-MF patients and HDs used in scRNA-seq analysis and PDX studies. Table S3. List of genes used for PROGENy analysis of human BM c…
View article: Data from Trisomy 8 Defines a Distinct Subtype of Myeloproliferative Neoplasms Driven by the MYC–Alarmin Axis
Data from Trisomy 8 Defines a Distinct Subtype of Myeloproliferative Neoplasms Driven by the MYC–Alarmin Axis Open
Despite advances in understanding the genetic abnormalities in myeloproliferative neoplasms (MPN) and the development of JAK2 inhibitors, there is an urgent need to devise new treatment strategies, particularly for patients with triple-neg…
View article: Supplementary Figures S1-S4 from Trisomy 8 Defines a Distinct Subtype of Myeloproliferative Neoplasms Driven by the MYC–Alarmin Axis
Supplementary Figures S1-S4 from Trisomy 8 Defines a Distinct Subtype of Myeloproliferative Neoplasms Driven by the MYC–Alarmin Axis Open
Figure S1. Landscape of somatic mutations and cytogenetics in Moffitt MF cohort. Figure S2. Effects of enforced MYC expression in HSCs in vivo. Figure S3. MYC-induced changes in hematopoietic sub-populations and colony forming potential. F…
View article: Supplementary Table S8 from Trisomy 8 Defines a Distinct Subtype of Myeloproliferative Neoplasms Driven by the MYC–Alarmin Axis
Supplementary Table S8 from Trisomy 8 Defines a Distinct Subtype of Myeloproliferative Neoplasms Driven by the MYC–Alarmin Axis Open
Comparison of gene expression profiles of Mx1-Cre+/-;Rosa26LSL-MYC/LSL-MYC vs. Mx1-Cre+/-;Rosa26+/+ mouse.
View article: Supplementary Table S10 from Trisomy 8 Defines a Distinct Subtype of Myeloproliferative Neoplasms Driven by the MYC–Alarmin Axis
Supplementary Table S10 from Trisomy 8 Defines a Distinct Subtype of Myeloproliferative Neoplasms Driven by the MYC–Alarmin Axis Open
Cell-cell interaction analyses.
View article: Supplementary Table S8 from Trisomy 8 Defines a Distinct Subtype of Myeloproliferative Neoplasms Driven by the MYC–Alarmin Axis
Supplementary Table S8 from Trisomy 8 Defines a Distinct Subtype of Myeloproliferative Neoplasms Driven by the MYC–Alarmin Axis Open
Comparison of gene expression profiles of Mx1-Cre+/-;Rosa26LSL-MYC/LSL-MYC vs. Mx1-Cre+/-;Rosa26+/+ mouse.
View article: Supplementary Figures S5-S9 from Trisomy 8 Defines a Distinct Subtype of Myeloproliferative Neoplasms Driven by the MYC–Alarmin Axis
Supplementary Figures S5-S9 from Trisomy 8 Defines a Distinct Subtype of Myeloproliferative Neoplasms Driven by the MYC–Alarmin Axis Open
Figure S5. Changes in signaling in BM of trisomy 8+ TN-MF patient and MYC MF mice. Figure S6. Effects of silencing S100a9 in MYC-driven MF or overexpression of S100a9. Figure S7. Effects of inhibition of S100a9 or MYC in MYC-driven MF. Fig…
View article: Supplementary Figures S5-S9 from Trisomy 8 Defines a Distinct Subtype of Myeloproliferative Neoplasms Driven by the MYC–Alarmin Axis
Supplementary Figures S5-S9 from Trisomy 8 Defines a Distinct Subtype of Myeloproliferative Neoplasms Driven by the MYC–Alarmin Axis Open
Figure S5. Changes in signaling in BM of trisomy 8+ TN-MF patient and MYC MF mice. Figure S6. Effects of silencing S100a9 in MYC-driven MF or overexpression of S100a9. Figure S7. Effects of inhibition of S100a9 or MYC in MYC-driven MF. Fig…