bluuebunny/crossref_metadata_2025 huggingface dataset:
Fig. S6 from Small-Molecule–Mediated Stabilization of PP2A Modulates the Homologous Recombination Pathway and Potentiates DNA Damage-Induced Cell Death
Authors: Avelar Rita A. , Armstrong Amy J. , Carvette Gracie , Gupta Riya , Puleo Noah , Colina Jose A. , Joseph Peronne , Sobeck Alexander M. , O'Connor Caitlin M. , Raines Brynne , Gandhi Agharnan , Dziubinski Michele L. , Ma Daniel S. , Resnick Kimberly , Singh Sareena , Zanotti Kristine , Nagel Christa , Waggoner Steven , Thomas Daffyd G. , Skala Stephanie L. , Zhang Junran , Narla Goutham , DiFeo Analisa
Published: May 2023

Fig. S6
Fig. S4 from Small-Molecule–Mediated Stabilization of PP2A Modulates the Homologous Recombination Pathway and Potentiates DNA Damage-Induced Cell Death
Authors: Avelar Rita A. , Armstrong Amy J. , Carvette Gracie , Gupta Riya , Puleo Noah , Colina Jose A. , Joseph Peronne , Sobeck Alexander M. , O'Connor Caitlin M. , Raines Brynne , Gandhi Agharnan , Dziubinski Michele L. , Ma Daniel S. , Resnick Kimberly , Singh Sareena , Zanotti Kristine , Nagel Christa , Waggoner Steven , Thomas Daffyd G. , Skala Stephanie L. , Zhang Junran , Narla Goutham , DiFeo Analisa
Published: May 2023

Fig. S4
Fig. S2 from Small-Molecule–Mediated Stabilization of PP2A Modulates the Homologous Recombination Pathway and Potentiates DNA Damage-Induced Cell Death
Authors: Avelar Rita A. , Armstrong Amy J. , Carvette Gracie , Gupta Riya , Puleo Noah , Colina Jose A. , Joseph Peronne , Sobeck Alexander M. , O'Connor Caitlin M. , Raines Brynne , Gandhi Agharnan , Dziubinski Michele L. , Ma Daniel S. , Resnick Kimberly , Singh Sareena , Zanotti Kristine , Nagel Christa , Waggoner Steven , Thomas Daffyd G. , Skala Stephanie L. , Zhang Junran , Narla Goutham , DiFeo Analisa
Published: May 2023

Fig. S2
Fig. S1 from Small-Molecule–Mediated Stabilization of PP2A Modulates the Homologous Recombination Pathway and Potentiates DNA Damage-Induced Cell Death
Authors: Avelar Rita A. , Armstrong Amy J. , Carvette Gracie , Gupta Riya , Puleo Noah , Colina Jose A. , Joseph Peronne , Sobeck Alexander M. , O'Connor Caitlin M. , Raines Brynne , Gandhi Agharnan , Dziubinski Michele L. , Ma Daniel S. , Resnick Kimberly , Singh Sareena , Zanotti Kristine , Nagel Christa , Waggoner Steven , Thomas Daffyd G. , Skala Stephanie L. , Zhang Junran , Narla Goutham , DiFeo Analisa
Published: May 2023

Fig. S1
Supplementary Tables & Figures from Preclinical Evaluation of ON203, A Novel Bioengineered mAb Targeting Oxidized Macrophage Migration Inhibitory Factor as an Anticancer Therapeutic
Authors: Rossmueller Gregor , Mirkina Irina , Maurer Barbara , Hoeld Verena , Mayer Julia , Thiele Michael , Kerschbaumer Randolf J. , Schinagl Alexander
Published: May 2023

Includes Supplementary Tables S1-S3 and Supplementary Figures S1-S6
Figure 5 from Preclinical Evaluation of ON203, A Novel Bioengineered mAb Targeting Oxidized Macrophage Migration Inhibitory Factor as an Anticancer Therapeutic
Authors: Rossmueller Gregor , Mirkina Irina , Maurer Barbara , Hoeld Verena , Mayer Julia , Thiele Michael , Kerschbaumer Randolf J. , Schinagl Alexander
Published: May 2023

ON203 is efficacious in a prophylactic prostate cancer xenograft model. A, Schematic presentation of the prophylactic prostate cancer xenograft model created with www.biorender.com. B, Tumor volume of subcutaneous PC3 tumor-bearing mice treated 15 times every other day intraperitoneally with vehicle, 20 mg/kg isotype IgG control antibody, 20 mg/kg C0008, 5 mg/kg ON203, or 20 mg/kg ON203 followed for 42 days after randomization (n = 9/treatment group). Median tumor volumes with interquartile ranges are shown. Levels of significance were calculated for all groups by ANOVA with Dunnett multiple comparisons test on log-transformed data; ON203 20 mg/kg versus vehicle + isotype IgG 20 mg/kg (black stars), ON203 20 mg/kg versus C0008 20 mg/kg (gray star) *, P < 0.05; **, P < 0.01. C, Relative change in animal body weight (%) from day 0 (n = 9/treatment group, mean ± SEM). D, Representative immunostaining images of 20 mg/kg isotype IgG-, C0008-, or ON203-treated PC3 tumors; scale bar, 100 μm (CD31 and H&E) or 40 μm (Ki67). Top: CD31 immunostaining (red arrows highlight intravascular tumor cells, and black arrows mark CD31-positive blood vessels); middle: H&E; bottom: Ki67 immunostaining. E, Vessel density in non-necrotic areas quantified on CD31-stained IHC slides from 20 mg/kg isotype IgG control-, C0008-, or ON203-treated tumors (n = 3/treatment group, mean ± SEM). F, Percentage of Ki67-positive cells quantified on Ki67-positive stained IHC slides from 20 mg/kg isotype IgG control-, C0008-, or ON203-treated tumors (n = 3/treatment group, mean ± SEM). Levels of significance were calculated by one-sided Student t test, *, P <0.05. i.p., intraperitoneal; SEM, standard error of mean.
Figure 4 from Preclinical Evaluation of ON203, A Novel Bioengineered mAb Targeting Oxidized Macrophage Migration Inhibitory Factor as an Anticancer Therapeutic
Authors: Rossmueller Gregor , Mirkina Irina , Maurer Barbara , Hoeld Verena , Mayer Julia , Thiele Michael , Kerschbaumer Randolf J. , Schinagl Alexander
Published: May 2023

ON203 shows target-dependent cytokine release from PBMCs and reduced unspecific cytokine release compared with C0008 in an ADCR assay. ON203 and C0008 were incubated with human PBMCs for 24 hours in the presence (A–D) or in the absence (E–H) of HCT116/pMIF target cancer cells, and supernatants were analyzed for the release of TNFα (A and E), IFNγ (B and F), MCP-1 (C and G), and IL6 (D and H) using LegendPlex cytometric bead assays (BioLegend). Cytokine concentrations in supernatants (pg/mL) were plotted against mAb concentrations (nmol/L) in GraphPad Prism. Values represent mean ± SEM of n = 3 (PBMCs from 3 healthy donors). ADCR, antibody-dependent cytokine release; PBMC, peripheral blood mononuclear cell; SEM, standard error of mean.
Figure 3 from Preclinical Evaluation of ON203, A Novel Bioengineered mAb Targeting Oxidized Macrophage Migration Inhibitory Factor as an Anticancer Therapeutic
Authors: Rossmueller Gregor , Mirkina Irina , Maurer Barbara , Hoeld Verena , Mayer Julia , Thiele Michael , Kerschbaumer Randolf J. , Schinagl Alexander
Published: May 2023

ON103 and ON203 mAbs with engineered Fc induce potent ADCC and ADCP. A, ON103 and ON203 trigger potent effector cell activation in ADCC reporter bioassays. Serial dilutions of mAbs were incubated for 6 hours with HCT116/pMIF target cells and Jurkat effector cells engineered to stably express human FcγRIIIA of high responder (V158) genotype, or of low responder (F158) genotype, and an NFAT response element driving expression of firefly luciferase. Effector cell activation was quantified through luciferase (RLU) produced as the result of NFAT pathway activation in effector cells (mean and range of n = 2). ON203 (B) and ON103 (C) induce ADCP in an ADCP reporter bioassay. Serial dilutions of mAbs were incubated for 6 hours with target cells (HCT116/pMIF) and Jurkat effector cells engineered to stably express human FcγRIIA (high responder H131 genotype), and an NFAT response element driving expression of firefly luciferase. Effector cell activation was quantified as described in A (mean and range of n = 2). D–F, ON103 and ON203 induce significant target cell lysis in an ADCC assay with human PBMCs. Target cells HCT116/HiBiT/pMIF were incubated with serial dilutions of mAbs and with isolated PBMCs from 3 different healthy human donors at the ratio of PBMCs to target cells of 50:1. PBMCs genotyped having V158/V158 high responder genotype of FcγRIIIA and 7% NK cells (D); nongenotyped PBMCs, 22.5% NK cells (E); nongenotyped PBMCs, 22.1% NK cells (F). After 24 hours, target cell lysis was measured by using NanoGlo HiBiT extracellular detection. Results are expressed in RLU (mean and range of n = 2). NFAT, nuclear factor of activated T cells.
Figure 2 from Preclinical Evaluation of ON203, A Novel Bioengineered mAb Targeting Oxidized Macrophage Migration Inhibitory Factor as an Anticancer Therapeutic
Authors: Rossmueller Gregor , Mirkina Irina , Maurer Barbara , Hoeld Verena , Mayer Julia , Thiele Michael , Kerschbaumer Randolf J. , Schinagl Alexander
Published: May 2023

Pharmacokinetics and BD of C0008, C0083, and C0090. A, BALB/c nude mice received a single intravenous injection of C0008, C0083, and C0090 mAbs (10 mg/kg), and plasma samples were collected 4, 10, 24, 48, and 96 hours thereafter. The plasma concentration of mAbs was determined by a quantitative anti-oxMIF mAb ELISA. B, mAb half-lives were calculated by a two-phase decay model, where plateau was constrained to 0 and Y0 to the theoretical Cmax. Total exposure was calculated from the AUC from the two-phase decay model from 0 to 96 hours. C and D, Tumor penetration and retention of anti-oxMIF mAbs was assessed by infrared in vivo imaging. C, Female BALB/c mice bearing subcutaneous CT26 syngeneic tumors received a single intravenous injection of 5 mg/kg IRDye 800CW-labeled C0008 or C0083 mAbs. D, Female BALB/c nude mice bearing subcutaneous HCT116 xenografts received a single intravenous injection of 5 mg/kg IRDye 800CW-labeled C0008 or C0090 mAbs. C and D, Mice were imaged at 1, 6–8, 24, 48, 72, 96, and 168 hours after dosing. One representative mouse from each treatment group (n = 3) is shown. E and F, Digital image analysis of tumor ROIs from images C and D in LI-COR Pearl Trilogy Software and calculation of total exposure of the tumor (AUC) to the anti-oxMIF mAbs and tumor half-life of mAbs using a monoexponential decay model in GraphPad Prism.
Figure 1 from Preclinical Evaluation of ON203, A Novel Bioengineered mAb Targeting Oxidized Macrophage Migration Inhibitory Factor as an Anticancer Therapeutic
Authors: Rossmueller Gregor , Mirkina Irina , Maurer Barbara , Hoeld Verena , Mayer Julia , Thiele Michael , Kerschbaumer Randolf J. , Schinagl Alexander
Published: May 2023

Physicochemical characterization of the mAb variants revealed identical binding properties and reduced hydrophobicity of the bioengineered anti-oxMIF antibodies compared with C0008 (imalumab). A, Antibody specificity of oxMIF versus redMIF in solution using 50 ng/mL of an oxMIF surrogate (TNB-MIF) by ELISA. B, Antibody apparent affinity to human oxMIF immobilized to an ELISA plate. C, Antibody affinity to human and mouse oxMIF in solution (using ProClin300 to induce oxMIF structure) by ELISA. D, Real-time binding kinetics of immobilized ON103 and ON203 versus C0008 for soluble human and mouse oxMIF by SPR. Data are represented as mean ± SD of the calculated association constants [ka, 1/(mol/L s)], dissociation constants (kd, 1/second), and equilibrium constants (KD, nmol/L) of flow cells 2–4 (after the subtraction of background from the reference cell (FC1). E, HIC of bioengineered antibodies compared with imalumab (C0008). EC50, effective concentration at 50% signal.
Supplementary Table 1 from Comparison of Three Transcytotic Pathways for Distribution to Brain Metastases of Breast Cancer
Authors: Khan Imran , Gril Brunilde , Paranjape Anurag N. , Robinson Christina M. , Difilippantonio Simone , Biernat Wojciech , Bieńkowski Michał , Pęksa Rafał , Duchnowska Renata , Jassem Jacek , Brastianos Priscilla K. , Metellus Philippe , Bialecki Emilie , Woodroofe Carolyn C. , Wu Haitao , Swenson Rolf E. , Steeg Patricia S.
Published: May 2023

Supplementary Table 1
Supplementary Material and Methods from Comparison of Three Transcytotic Pathways for Distribution to Brain Metastases of Breast Cancer
Authors: Khan Imran , Gril Brunilde , Paranjape Anurag N. , Robinson Christina M. , Difilippantonio Simone , Biernat Wojciech , Bieńkowski Michał , Pęksa Rafał , Duchnowska Renata , Jassem Jacek , Brastianos Priscilla K. , Metellus Philippe , Bialecki Emilie , Woodroofe Carolyn C. , Wu Haitao , Swenson Rolf E. , Steeg Patricia S.
Published: May 2023

Supplementary Material and Methods
Supplementary Figure S1-S10 from Comparison of Three Transcytotic Pathways for Distribution to Brain Metastases of Breast Cancer
Authors: Khan Imran , Gril Brunilde , Paranjape Anurag N. , Robinson Christina M. , Difilippantonio Simone , Biernat Wojciech , Bieńkowski Michał , Pęksa Rafał , Duchnowska Renata , Jassem Jacek , Brastianos Priscilla K. , Metellus Philippe , Bialecki Emilie , Woodroofe Carolyn C. , Wu Haitao , Swenson Rolf E. , Steeg Patricia S.
Published: May 2023

Supplementary Figures S1-S10
Supplementary Data from IMiDs Augment CD3-Bispecific Antibody–Induced CD8+ T-Cell Cytotoxicity and Expansion by Enhancing IL2 Production
Authors: Li Ji , Slaga Dionysos , Johnston Jennifer , Junttila Teemu T.
Published: May 2023

Supplementary Data
Supplementary Data from Discovery of a Small-Molecule Inhibitor Targeting the Androgen Receptor N-Terminal Domain for Castration-Resistant Prostate Cancer
Authors: Yi Qianhui , Liu Weiguo , Seo Jung Hwa , Su Jie , Alaoui-Jamali Moulay A. , Luo Jun , Lin Rongtuan , Wu Jian Hui
Published: May 2023

Supplementary figures and methods
Supplementary Table S3 from Pharmacokinetic/Pharmacodynamic Analysis of Savolitinib plus Osimertinib in an EGFR Mutation–Positive, MET-Amplified Non–Small Cell Lung Cancer Model
Authors: Jones Rhys D.O. , Petersson Klas , Tabatabai Areya , Bao Larry , Tomkinson Helen , Schuller Alwin G.
Published: May 2023

Supplementary Table S3
Supplementary Table S2 from Pharmacokinetic/Pharmacodynamic Analysis of Savolitinib plus Osimertinib in an EGFR Mutation–Positive, MET-Amplified Non–Small Cell Lung Cancer Model
Authors: Jones Rhys D.O. , Petersson Klas , Tabatabai Areya , Bao Larry , Tomkinson Helen , Schuller Alwin G.
Published: May 2023

Supplementary Table S2
Supplementary Materials and Methods from Pharmacokinetic/Pharmacodynamic Analysis of Savolitinib plus Osimertinib in an EGFR Mutation–Positive, MET-Amplified Non–Small Cell Lung Cancer Model
Authors: Jones Rhys D.O. , Petersson Klas , Tabatabai Areya , Bao Larry , Tomkinson Helen , Schuller Alwin G.
Published: May 2023

Supplementary Data text
Supplementary Figure S5 from Pharmacokinetic/Pharmacodynamic Analysis of Savolitinib plus Osimertinib in an EGFR Mutation–Positive, MET-Amplified Non–Small Cell Lung Cancer Model
Authors: Jones Rhys D.O. , Petersson Klas , Tabatabai Areya , Bao Larry , Tomkinson Helen , Schuller Alwin G.
Published: May 2023

Supplementary Figure S5
Supplementary Figure S4 from Pharmacokinetic/Pharmacodynamic Analysis of Savolitinib plus Osimertinib in an EGFR Mutation–Positive, MET-Amplified Non–Small Cell Lung Cancer Model
Authors: Jones Rhys D.O. , Petersson Klas , Tabatabai Areya , Bao Larry , Tomkinson Helen , Schuller Alwin G.
Published: May 2023

Supplementary Figure S4
Supplementary Figure S3 from Pharmacokinetic/Pharmacodynamic Analysis of Savolitinib plus Osimertinib in an EGFR Mutation–Positive, MET-Amplified Non–Small Cell Lung Cancer Model
Authors: Jones Rhys D.O. , Petersson Klas , Tabatabai Areya , Bao Larry , Tomkinson Helen , Schuller Alwin G.
Published: May 2023

Supplementary Figure S3
Supplementary Figure S2 from Pharmacokinetic/Pharmacodynamic Analysis of Savolitinib plus Osimertinib in an EGFR Mutation–Positive, MET-Amplified Non–Small Cell Lung Cancer Model
Authors: Jones Rhys D.O. , Petersson Klas , Tabatabai Areya , Bao Larry , Tomkinson Helen , Schuller Alwin G.
Published: May 2023

Supplementary Figure S2
Data from Targeting Senescence as a Therapeutic Opportunity for Triple-Negative Breast Cancer
Authors: de Paula Bruno , Kieran Rosalind , Koh Samantha Shui Yuan , Crocamo Susanne , Abdelhay Eliana , Muñoz-Espín Daniel
Published: May 2023

Abstract
Triple-negative breast cancer (TNBC) is associated with an elevated risk of recurrence and poor prognosis. Historically, only chemotherapy was available as systemic treatment, but immunotherapy and targeted therapies currently offer prolonged benefits. TNBC is a group of diseases with heterogeneous treatment sensitivity, and resistance is inevitable and early for a large proportion of the intrinsic subtypes. Although senescence induction by anticancer therapy offers an immediate favorable clinical outcome once the rate of tumor progression reduces, these cells are commonly dysfunctional and metabolically active, culminating in treatment-resistant repopulation associated with worse prognosis. This heterogeneous response can also occur without therapeutic pressure in response to damage or oncogenic stress, playing a relevant role in the carcinogenesis. Remarkably, there is preclinical and exploratory clinical evidence to support a relevant role of senescence in treatment resistance. Therefore, targeting senescent cells has been a scientific effort in many malignant tumors using a variety of targets and strategies, including increasing proapoptotic and decreasing antiapoptotic stimuli. Despite promising results, there are some challenges to applying this technology, including the best schedule of combination, assessment of senescence, specific vulnerabilities, and the best clinical scenarios. This review provides an overview of senescence in TNBC with a focus on future-proofing senotherapy strategies.
Data from Preclinical Evaluation of ON203, A Novel Bioengineered mAb Targeting Oxidized Macrophage Migration Inhibitory Factor as an Anticancer Therapeutic
Authors: Rossmueller Gregor , Mirkina Irina , Maurer Barbara , Hoeld Verena , Mayer Julia , Thiele Michael , Kerschbaumer Randolf J. , Schinagl Alexander
Published: May 2023

Abstract
High levels of macrophage migration inhibitory factor (MIF) in patients with cancer are associated with poor prognosis. Its redox-dependent conformational isoform, termed oxidized MIF (oxMIF), is a promising tumor target due to its selective occurrence in tumor lesions and at inflammatory sites. A first-generation anti-oxMIF mAb, imalumab, was investigated in clinical trials in patients with advanced solid tumors, where it was well tolerated and showed signs of efficacy. However, imalumab has a short half-life in humans, increased aggregation propensity, and an unfavorable pharmacokinetic profile. Here, we aimed to optimize imalumab by improving its physicochemical characteristics and boosting its effector functions. Point mutations introduced into the variable regions reduced hydrophobicity and the antibodies’ aggregation potential, and increased plasma half-life and tumor accumulation in vivo, while retaining affinity and specificity to oxMIF. The introduction of mutations into the Fc region known to increase antibody-dependent cellular cytotoxicity resulted in enhanced effector functions of the novel antibodies in vitro, whereas reduced cytokine release from human peripheral blood mononuclear cells in the absence of target antigen by the engineered anti-oxMIF mAb ON203 versus imalumab reveals a favorable in vitro safety profile. In vivo, ON203 mAb demonstrated superior efficacy over imalumab in both prophylactic and established prostate cancer (PC3) mouse xenograft models. In summary, our data highlight the potential of the second-generation anti-oxMIF mAb ON203 as a promising immunotherapy for patients with solid tumors, warranting clinical evaluation.
Data from IMiDs Augment CD3-Bispecific Antibody–Induced CD8+ T-Cell Cytotoxicity and Expansion by Enhancing IL2 Production
Authors: Li Ji , Slaga Dionysos , Johnston Jennifer , Junttila Teemu T.
Published: May 2023

Abstract
Although CD3-bispecific antibodies have shown promising activity in the treatment of hematological cancers, insufficient T-cell costimulation may limit long-term responses. Immunomodulatory drugs (IMiDs), routinely used in treating multiple myeloma, possess pleiotropic antimyeloma properties and have been described to enhance T-cell responses similar to costimulatory signaling and may therefore have synergistic effects when combined with T-cell bispecifics. In this report, we demonstrate that IMiDs substantially enhance tumor cell killing induced by CD3 bispecifics and increase CD8+ T-cell proliferation and expansion. We further show that the beneficial effects of IMiDs on T-cell function and expansion are mediated by enhanced IL2 production by CD4+ T cells. Our studies provide mechanistic insight into the costimulatory properties of IMiDs and support combination treatments with T-cell agonist therapies in a broad spectrum of indications.
Data from Discovery of a Small-Molecule Inhibitor Targeting the Androgen Receptor N-Terminal Domain for Castration-Resistant Prostate Cancer
Authors: Yi Qianhui , Liu Weiguo , Seo Jung Hwa , Su Jie , Alaoui-Jamali Moulay A. , Luo Jun , Lin Rongtuan , Wu Jian Hui
Published: May 2023

Abstract
The current mainstay therapeutic strategy for advanced prostate cancer is to suppress androgen receptor (AR) signaling. However, castration-resistant prostate cancer (CRPC) invariably arises with restored AR signaling activity. To date, the AR ligand-binding domain (LBD) is the only targeted region for all clinically available AR signaling antagonists, such as enzalutamide (ENZ). Major resistance mechanisms have been uncovered to sustain the AR signaling in CRPC despite these treatments, including AR amplification, AR LBD mutants, and the emergence of AR splice variants (AR-Vs) such as AR-V7. AR-V7 is a constitutively active truncated form of AR that lacks the LBD; thus, it can not be inhibited by AR LBD-targeting drugs. Therefore, an approach to inhibit AR through the regions outside of LBD is urgently needed. In this study, we have discovered a novel small molecule SC428, which directly binds to the AR N-terminal domain (NTD) and exhibits pan-AR inhibitory effect. SC428 potently decreased the transactivation of AR-V7, ARv567es, as well as full-length AR (AR-FL) and its LBD mutants. SC428 substantially suppressed androgen-stimulated AR-FL nuclear translocation, chromatin binding, and AR-regulated gene transcription. Moreover, SC428 also significantly attenuated AR-V7–mediated AR signaling that does not rely on androgen, hampered AR-V7 nuclear localization, and disrupted AR-V7 homodimerization. SC428 inhibited in vitro proliferation and in vivo tumor growth of cells that expressed a high level of AR-V7 and were unresponsive to ENZ treatment. Together, these results indicated the potential therapeutic benefits of AR-NTD targeting for overcoming drug resistance in CRPC.
Discovery of a Small-Molecule Inhibitor Targeting the Androgen Receptor N-Terminal Domain for Castration-Resistant Prostate Cancer
Authors: Yi Qianhui , Liu Weiguo , Seo Jung Hwa , Su Jie , Alaoui-Jamali Moulay A. , Luo Jun , Lin Rongtuan , Wu Jian Hui
Published: May 2023

The current mainstay therapeutic strategy for advanced prostate cancer is to suppress androgen receptor (AR) signaling. However, castration-resistant prostate cancer (CRPC) invariably arises with restored AR signaling activity. To date, the AR ligand-binding domain (LBD) is the only targeted region for all clinically available AR signaling antagonists, such as enzalutamide (ENZ). Major resistance mechanisms have been uncovered to sustain the AR signaling in CRPC despite these treatments, including AR amplification, AR LBD mutants, and the emergence of AR splice variants (AR-Vs) such as AR-V7. AR-V7 is a constitutively active truncated form of AR that lacks the LBD; thus, it can not be inhibited by AR LBD-targeting drugs. Therefore, an approach to inhibit AR through the regions outside of LBD is urgently needed. In this study, we have discovered a novel small molecule SC428, which directly binds to the AR N-terminal domain (NTD) and exhibits pan-AR inhibitory effect. SC428 potently decreased the transactivation of AR-V7, ARv567es, as well as full-length AR (AR-FL) and its LBD mutants. SC428 substantially suppressed androgen-stimulated AR-FL nuclear translocation, chromatin binding, and AR-regulated gene transcription. Moreover, SC428 also significantly attenuated AR-V7–mediated AR signaling that does not rely on androgen, hampered AR-V7 nuclear localization, and disrupted AR-V7 homodimerization. SC428 inhibited in vitro proliferation and in vivo tumor growth of cells that expressed a high level of AR-V7 and were unresponsive to ENZ treatment. Together, these results indicated the potential therapeutic benefits of AR-NTD targeting for overcoming drug resistance in CRPC.
Table 1 from Patterns of Oncogene Coexpression at Single-Cell Resolution Influence Survival in Lymphoma
Authors: Hoppe Michal Marek , Jaynes Patrick , Shuangyi Fan , Peng Yanfen , Sridhar Shruti , Hoang Phuong Mai , Liu Clementine Xin , De Mel Sanjay , Poon Limei , Chan Esther Hian Li , Lee Joanne , Ong Choon Kiat , Tang Tiffany , Lim Soon Thye , Nagarajan Chandramouli , Grigoropoulos Nicholas F. , Tan Soo-Yong , Hue Susan Swee-Shan , Chang Sheng-Tsung , Chuang Shih-Sung , Li Shaoying , Khoury Joseph D. , Choi Hyungwon , Harris Carl , Bottos Alessia , Gay Laura J. , Runge Hendrik F.P. , Moutsopoulos Ilias , Mohorianu Irina , Hodson Daniel J. , Farinha Pedro , Mottok Anja , Scott David W. , Pitt Jason J. , Chen Jinmiao , Kumar Gayatri , Kannan Kasthuri , Chng Wee Joo , Chee Yen Lin , Ng Siok-Bian , Tripodo Claudio , Jeyasekharan Anand D.
Published: May 2023

Multivariate analysis of continuous M+2+6− percentage extent at 5% increments as a predictor of OS in the NUH, SGH, and MDA cohorts of DLBCL (Cox proportional hazards model)
Supplementary tables from Patterns of Oncogene Coexpression at Single-Cell Resolution Influence Survival in Lymphoma
Authors: Hoppe Michal Marek , Jaynes Patrick , Shuangyi Fan , Peng Yanfen , Sridhar Shruti , Hoang Phuong Mai , Liu Clementine Xin , De Mel Sanjay , Poon Limei , Chan Esther Hian Li , Lee Joanne , Ong Choon Kiat , Tang Tiffany , Lim Soon Thye , Nagarajan Chandramouli , Grigoropoulos Nicholas F. , Tan Soo-Yong , Hue Susan Swee-Shan , Chang Sheng-Tsung , Chuang Shih-Sung , Li Shaoying , Khoury Joseph D. , Choi Hyungwon , Harris Carl , Bottos Alessia , Gay Laura J. , Runge Hendrik F.P. , Moutsopoulos Ilias , Mohorianu Irina , Hodson Daniel J. , Farinha Pedro , Mottok Anja , Scott David W. , Pitt Jason J. , Chen Jinmiao , Kumar Gayatri , Kannan Kasthuri , Chng Wee Joo , Chee Yen Lin , Ng Siok-Bian , Tripodo Claudio , Jeyasekharan Anand D.
Published: May 2023

Supplementary table 1. Per-patient mfIHC MYC, BCL2 and BCL6 single oncogene and subpopulation scores for normal tonsil tissue and reactive lymph node tissue.
Supplementary table 2. Per-patient mfIHC MYC, BCL2 and BCL6 single oncogene and subpopulation scores for DLBCL tissue (NUH, CMMC, SGH, MDA, BCA and UP).
Supplementary table 6. Inferred percentage extents of MYC, BCL2, BCL6 and sub-population metrics in GEP cohorts.
Supplementary table 11. Correlation of M+2+6- metric with gene expression in GEP cohorts.
Supplementary table 12. Differential gene expression analysis of primary germinal center (GC) B-cells with M+2+ and M+2+6+ overexpression.
Supplementary table 13. Differentially expressed genes between M+2+6- and all other malignant cells in scRNA-seq samples of DLBCL. Dichotomized non-parametric comparison, Wilcoxon rank sum test.
Supplementary table 14. Analysis of positive enrichment of Wikipathways terms between M+2+6- and all other malignant cells in scRNA-seq samples of DLBCL by gprofiler2.
Figure 5 from Patterns of Oncogene Coexpression at Single-Cell Resolution Influence Survival in Lymphoma
Authors: Hoppe Michal Marek , Jaynes Patrick , Shuangyi Fan , Peng Yanfen , Sridhar Shruti , Hoang Phuong Mai , Liu Clementine Xin , De Mel Sanjay , Poon Limei , Chan Esther Hian Li , Lee Joanne , Ong Choon Kiat , Tang Tiffany , Lim Soon Thye , Nagarajan Chandramouli , Grigoropoulos Nicholas F. , Tan Soo-Yong , Hue Susan Swee-Shan , Chang Sheng-Tsung , Chuang Shih-Sung , Li Shaoying , Khoury Joseph D. , Choi Hyungwon , Harris Carl , Bottos Alessia , Gay Laura J. , Runge Hendrik F.P. , Moutsopoulos Ilias , Mohorianu Irina , Hodson Daniel J. , Farinha Pedro , Mottok Anja , Scott David W. , Pitt Jason J. , Chen Jinmiao , Kumar Gayatri , Kannan Kasthuri , Chng Wee Joo , Chee Yen Lin , Ng Siok-Bian , Tripodo Claudio , Jeyasekharan Anand D.
Published: May 2023

Transcriptomic analysis of M+2+6− high cases and potential role of CCND2. A, Correlation of observed M+2+6− percentage extent in the BCA cohort with the cell-of-origin (COO) DLBCL90-COO signature. Bonferroni corrected Kruskal–Wallis test for ABC vs. others. B, Correlation of M+2+6− metric in GEP cohorts with COO signatures. Mean M+2+6− metric value per group per cohort is shown. Bonferroni corrected paired-samples t test. C, Correlation of the M+2+6− percentage extent and metric evaluated by mfIHC and mRNA inference, respectively, with genetic subtypes (LymphGen classification). D, Sankey plot of M+2+6− dichotomized grouping matched with molecular features. E, Volcano plot of pooled direct correlation of gene mRNA expression and M+2+6− metric across seven GEP cohorts. Genes highly correlated with M+2+6− metric across datasets at absolute Spearman rho ≥0.2 and FDR≤0.001 are shown (see also Supplementary Table S11). The abscissa is scaled exponentially. F, Differential gene expression between primary GC B cells overexpressing M+2+ and M+2+6+ (see also Supplementary Table S12). Analysis is generated from 4 biological replicates from each condition, from cells of independent donors. G, Genes highly enriched in M+2+6− cells: correlation of results from E and F. H,CCDN2 gene expression in GEP cohorts in patients dichotomized by M+2+6− 15% metric (left) and in primary B cells (right). Paired t test (left); mean with standard deviation and FDR (FDR as per Supplementary Table S12) for t test (right). I, Single-cell RNA-seq of GC primary B cells transduced either with BCL2 and MYC (MYC-transduced) or BCL2 and BCL6 (BCL6-transduced). Untransduced GC primary B cells are also included. Expression of CCND2 is indicated in color. J, Proliferation analysis of M+2+6+ primary GC B cells overexpressing cyclin D2 (CCND2) compared with M+2+6+ primary GC B cells transduced with an empty vector (EV). Analysis performed with 3 biological replicates for each condition, using cells from 3 independent patients; mean with standard deviation; t test. UMAP, Uniform Manifold Approximation and Projection.
Figure 3 from Patterns of Oncogene Coexpression at Single-Cell Resolution Influence Survival in Lymphoma
Authors: Hoppe Michal Marek , Jaynes Patrick , Shuangyi Fan , Peng Yanfen , Sridhar Shruti , Hoang Phuong Mai , Liu Clementine Xin , De Mel Sanjay , Poon Limei , Chan Esther Hian Li , Lee Joanne , Ong Choon Kiat , Tang Tiffany , Lim Soon Thye , Nagarajan Chandramouli , Grigoropoulos Nicholas F. , Tan Soo-Yong , Hue Susan Swee-Shan , Chang Sheng-Tsung , Chuang Shih-Sung , Li Shaoying , Khoury Joseph D. , Choi Hyungwon , Harris Carl , Bottos Alessia , Gay Laura J. , Runge Hendrik F.P. , Moutsopoulos Ilias , Mohorianu Irina , Hodson Daniel J. , Farinha Pedro , Mottok Anja , Scott David W. , Pitt Jason J. , Chen Jinmiao , Kumar Gayatri , Kannan Kasthuri , Chng Wee Joo , Chee Yen Lin , Ng Siok-Bian , Tripodo Claudio , Jeyasekharan Anand D.
Published: May 2023

MYC, BCL2, and BCL6 protein coexpression in DLBCL can be inferred from individual marker data. A, Schematic of possible relationships between expression of three oncogenes in a population of cells. The distribution of these oncogenes can either reflect interdependent expression, independent/stochastic expression, or mutually exclusive expression. These relationships result in the percentage extent of oncogenes in the tumor being either strongly positively correlated, not correlated, or strongly negatively correlated, respectively. Created with BioRender.com. B, Correlation of MYC, BCL2, and BCL6 percentage extent across patients in DLBCL cohorts. Spearman correlation; axes are equivalent in all panels. C, Good correlation between probabilistically predicted subpopulation percentage extent based on single oncogene positivity and observed percentage extent in the NUH cohort. Cases of double-hit lymphoma (DHL, MYC+BCL2+ translocations or MYC+BCL6+ translocations) or triple-hit lymphoma (THL) are highlighted. Spearman rho for each correlation is shown; axes are equivalent in all panels. Correlation for other cohorts can be found in Supplementary Fig. S7. D, Prospective evaluation of an optimal dichotomization cutoff for M+2+6− percentage extent in the BCA cohort. Univariate Cox PH model at 1% extent positivity increment, HR for death with 95% CI. HR scale is exponential. Optimal dichotomization cutoff is highlighted in blue. E, Kaplan–Meier OS analysis of the chromogenic IHC BCA cohort evaluation stratified into M+2+6− metric high and low groups across an absolute value of 15% M+2+6−metric. Log-rank test, shading denotes 95% confidence interval. CMMC, Chi-Mei Medical Center.
Figure 2 from Patterns of Oncogene Coexpression at Single-Cell Resolution Influence Survival in Lymphoma
Authors: Hoppe Michal Marek , Jaynes Patrick , Shuangyi Fan , Peng Yanfen , Sridhar Shruti , Hoang Phuong Mai , Liu Clementine Xin , De Mel Sanjay , Poon Limei , Chan Esther Hian Li , Lee Joanne , Ong Choon Kiat , Tang Tiffany , Lim Soon Thye , Nagarajan Chandramouli , Grigoropoulos Nicholas F. , Tan Soo-Yong , Hue Susan Swee-Shan , Chang Sheng-Tsung , Chuang Shih-Sung , Li Shaoying , Khoury Joseph D. , Choi Hyungwon , Harris Carl , Bottos Alessia , Gay Laura J. , Runge Hendrik F.P. , Moutsopoulos Ilias , Mohorianu Irina , Hodson Daniel J. , Farinha Pedro , Mottok Anja , Scott David W. , Pitt Jason J. , Chen Jinmiao , Kumar Gayatri , Kannan Kasthuri , Chng Wee Joo , Chee Yen Lin , Ng Siok-Bian , Tripodo Claudio , Jeyasekharan Anand D.
Published: May 2023

Prognostic significance of subpopulations after R-CHOP therapy. A, Pooled univariate Cox PH model analysis for MYC, BCL2, and BCL6 single oncogene and subpopulations percentage extent as predictors of OS across multiple DLBCL cohorts. Percentage extent was used as a continuous variable in the model at 5% increments (see Survival Analysis) for an unbiased comparison between the variables. Pooled P values were Bonferroni corrected for single oncogenes and subpopulations independently to adjust for multiple testing and are shown for each variable. Hazard ratio (HR) with 95% confidence interval (CI) per 5%-positivity increment is shown (see also Supplementary Table S4). B, Kaplan–Meier OS analysis of dichotomized into M+2+6− high and low groups. Log-rank test, shading denotes 95% CI. An optimal dichotomization cutoff was used for stratification; total patient numbers in each group are shown.
Supplementary Tables S1-S3 from A View on Drug Development for Cancer Prevention
Authors: Reynolds Andrew R. , Moschetta Michele , Yohannes Alula R. , Walcott Farzana , Ashford Marianne , Szucs Zoltan , Sarbajna Tina , Hadfield James , Harrison Eden , Challis Benjamin G. , Hernandez Amaya Gasco , Schiavon Gaia , Germa Caroline , Zorenyi Gyorgy , Crean Barry , Galbraith Susan
Published: May 2023

Tables that provide additional information to support the main article
Table S2 from Addressing Tumor Heterogeneity by Sensitizing Resistant Cancer Cells to T cell–Secreted Cytokines
Authors: Ito Yoshinaga , Pan Deng , Zhang Wubing , Zhang Xixi , Juan Tiffany Y. , Pyrdol Jason W. , Kyrysyuk Oleksandr , Doench John G. , Liu X. Shirley , Wucherpfennig Kai W.
Published: May 2023

Supplementary Table S2: ## Raw count matrix of mini-pool CRISPR screens. ## Normalized gene scores in mini-pool screens.
Table S1 from Addressing Tumor Heterogeneity by Sensitizing Resistant Cancer Cells to T cell–Secreted Cytokines
Authors: Ito Yoshinaga , Pan Deng , Zhang Wubing , Zhang Xixi , Juan Tiffany Y. , Pyrdol Jason W. , Kyrysyuk Oleksandr , Doench John G. , Liu X. Shirley , Wucherpfennig Kai W.
Published: May 2023

Supplementary Table S1: # Raw count of the genome-wide CRISPR screen for identifying T cell-mediated tumor killing in B2m-deficient cells. # MAGeCK results (Gene summary) for the genome-wide CRISPR screen from the B2m-deficient cells. # Gene log2FC in CRISPR screens from B2m-WT cells and B2m-KO cells. ## Common regulators of T cell mediated tumor killing in both B2m-WT and B2m-KO cells
Supplementary Fig. S9 from Addressing Tumor Heterogeneity by Sensitizing Resistant Cancer Cells to T cell–Secreted Cytokines
Authors: Ito Yoshinaga , Pan Deng , Zhang Wubing , Zhang Xixi , Juan Tiffany Y. , Pyrdol Jason W. , Kyrysyuk Oleksandr , Doench John G. , Liu X. Shirley , Wucherpfennig Kai W.
Published: May 2023

Supplementary Fig. S9 shows enhanced IFNg and TNFa expression by T cells and NK cells in Rnf31/Atg5-dKO tumors.
Supplementary Fig. S8 from Addressing Tumor Heterogeneity by Sensitizing Resistant Cancer Cells to T cell–Secreted Cytokines
Authors: Ito Yoshinaga , Pan Deng , Zhang Wubing , Zhang Xixi , Juan Tiffany Y. , Pyrdol Jason W. , Kyrysyuk Oleksandr , Doench John G. , Liu X. Shirley , Wucherpfennig Kai W.
Published: May 2023

Supplementary Fig. S8 shows CD8 T cell-dependent control of tumors containing a B2m-/- population with inactivated Rnf31 and Atg5 genes.
Supplementary Fig. S7 from Addressing Tumor Heterogeneity by Sensitizing Resistant Cancer Cells to T cell–Secreted Cytokines
Authors: Ito Yoshinaga , Pan Deng , Zhang Wubing , Zhang Xixi , Juan Tiffany Y. , Pyrdol Jason W. , Kyrysyuk Oleksandr , Doench John G. , Liu X. Shirley , Wucherpfennig Kai W.
Published: May 2023

Supplementary Fig. S7 shows effect of PD-1 inhibition on treatment of tumors containing a B2m-/- population.
Supplementary Fig. S6 from Addressing Tumor Heterogeneity by Sensitizing Resistant Cancer Cells to T cell–Secreted Cytokines
Authors: Ito Yoshinaga , Pan Deng , Zhang Wubing , Zhang Xixi , Juan Tiffany Y. , Pyrdol Jason W. , Kyrysyuk Oleksandr , Doench John G. , Liu X. Shirley , Wucherpfennig Kai W.
Published: May 2023

Supplementary Fig. S6 shows functional links between autophagy and cytokine signaling pathways.
Supplementary Fig. S5 from Addressing Tumor Heterogeneity by Sensitizing Resistant Cancer Cells to T cell–Secreted Cytokines
Authors: Ito Yoshinaga , Pan Deng , Zhang Wubing , Zhang Xixi , Juan Tiffany Y. , Pyrdol Jason W. , Kyrysyuk Oleksandr , Doench John G. , Liu X. Shirley , Wucherpfennig Kai W.
Published: May 2023

Supplementary Fig. S5 shows association of Atg5-KO and Rnf31/Atg5-dKO signatures with patient survival.
Supplementary Fig. S4 from Addressing Tumor Heterogeneity by Sensitizing Resistant Cancer Cells to T cell–Secreted Cytokines
Authors: Ito Yoshinaga , Pan Deng , Zhang Wubing , Zhang Xixi , Juan Tiffany Y. , Pyrdol Jason W. , Kyrysyuk Oleksandr , Doench John G. , Liu X. Shirley , Wucherpfennig Kai W.
Published: May 2023

Supplementary Fig. S4 shows differentially expressed genes revealed by RNA-seq analysis.
Supplementary Fig. S3 from Addressing Tumor Heterogeneity by Sensitizing Resistant Cancer Cells to T cell–Secreted Cytokines
Authors: Ito Yoshinaga , Pan Deng , Zhang Wubing , Zhang Xixi , Juan Tiffany Y. , Pyrdol Jason W. , Kyrysyuk Oleksandr , Doench John G. , Liu X. Shirley , Wucherpfennig Kai W.
Published: May 2023

Supplementary Fig. S3 generation of tumor cell lines with multiple gene edits.
Supplementary Fig. S2 from Addressing Tumor Heterogeneity by Sensitizing Resistant Cancer Cells to T cell–Secreted Cytokines
Authors: Ito Yoshinaga , Pan Deng , Zhang Wubing , Zhang Xixi , Juan Tiffany Y. , Pyrdol Jason W. , Kyrysyuk Oleksandr , Doench John G. , Liu X. Shirley , Wucherpfennig Kai W.
Published: May 2023

Supplementary Fig. S2 shows efficiency of gene editing in tumor cell lines for co-dependency screen.
Supplementary Fig. S11 from Addressing Tumor Heterogeneity by Sensitizing Resistant Cancer Cells to T cell–Secreted Cytokines
Authors: Ito Yoshinaga , Pan Deng , Zhang Wubing , Zhang Xixi , Juan Tiffany Y. , Pyrdol Jason W. , Kyrysyuk Oleksandr , Doench John G. , Liu X. Shirley , Wucherpfennig Kai W.
Published: May 2023

Supplementary Fig. S11 shows pharmacological sensitization of human melanoma cell line to T cell cytokines.
Supplementary Fig. S10 from Addressing Tumor Heterogeneity by Sensitizing Resistant Cancer Cells to T cell–Secreted Cytokines
Authors: Ito Yoshinaga , Pan Deng , Zhang Wubing , Zhang Xixi , Juan Tiffany Y. , Pyrdol Jason W. , Kyrysyuk Oleksandr , Doench John G. , Liu X. Shirley , Wucherpfennig Kai W.
Published: May 2023

Supplementary Fig. S10 shows pharmacological sensitization to T cell cytokines in vitro and in vivo.
Supplementary Fig. S1 from Addressing Tumor Heterogeneity by Sensitizing Resistant Cancer Cells to T cell–Secreted Cytokines
Authors: Ito Yoshinaga , Pan Deng , Zhang Wubing , Zhang Xixi , Juan Tiffany Y. , Pyrdol Jason W. , Kyrysyuk Oleksandr , Doench John G. , Liu X. Shirley , Wucherpfennig Kai W.
Published: May 2023

Supplementary Fig. S1 shows regulators of MHC-I independent and MHC-I dependent T cell mediated killing.
Supplemental Table 1 from Reprogramming Cancer into Antigen-Presenting Cells as a Novel Immunotherapy
Authors: Linde Miles H. , Fan Amy C. , Köhnke Thomas , Trotman-Grant Aaron C. , Gurev Sarah F. , Phan Paul , Zhao Feifei , Haddock Naomi L. , Nuno Kevin A. , Gars Eric J. , Stafford Melissa , Marshall Payton L. , Dove Christopher G. , Linde Ian L. , Landberg Niklas , Miller Lindsay P. , Majzner Robbie G. , Zhang Tian Yi , Majeti Ravindra
Published: May 2023

Summary of clinical features of primary B-ALL specimens
Supplemental Figure S8 from Reprogramming Cancer into Antigen-Presenting Cells as a Novel Immunotherapy
Authors: Linde Miles H. , Fan Amy C. , Köhnke Thomas , Trotman-Grant Aaron C. , Gurev Sarah F. , Phan Paul , Zhao Feifei , Haddock Naomi L. , Nuno Kevin A. , Gars Eric J. , Stafford Melissa , Marshall Payton L. , Dove Christopher G. , Linde Ian L. , Landberg Niklas , Miller Lindsay P. , Majzner Robbie G. , Zhang Tian Yi , Majeti Ravindra
Published: May 2023

TR-APC induction in solid tumor models attenuates tumor growth kinetics and prolongs survival
Supplementary Tables S1-S9 and Figures S1-S9 from Dimeric p53 Mutant Elicits Unique Tumor-Suppressive Activities through an Altered Metabolic Program
Authors: Gencel-Augusto Jovanka , Su Xiaoping , Qi Yuan , Whitley Elizabeth M. , Pant Vinod , Xiong Shunbin , Shah Vrutant , Lin Jerome , Perez Encarnacion , Fiorotto Marta L. , Mahmud Iqbal , Jain Abhinav K. , Lorenzi Philip L. , Navin Nicholas E. , Richie Ellen R. , Lozano Guillermina
Published: May 2023

Table S1 shows predicted off target sites for p53TD mutant mice.
Table S2 shows upregulated PPAR target genes in p53AD vs p53-null.
Table S3 shows ATAC-seq and RNA-seq congruent genes in p53AD vs p53 null.
Table S4 shows p53half site analysis in PPAR target genes
Table S5 shows control sequences used for p53 half site analysis
Table S6 shows altered genes in p53AD-derived thymic lymphomas
Table S7 shows primers used for genotyping of p53 mutant mice
Table S8 shows primers used for qRT-PCR
Table S9 shows antibodies used for flow cytometry
Figure S1 shows extended data for generation of knock-in mouse models and features of p53TD mutant proteins and mice.
Figure S2 shows homozygous mutant mice survival curves as well as tumor data.
Figure S3 shows exome sequencing results for thymic lymphomas and hemangiosarcomas derived from p53 monomer and dimer mutant mice.
Figure S4 shows characterization of stress responses of p53TD mutants.
Figure S5 shows RNA-sequencing results for p53AD and p53RP, and Mdm2 genetic deletion rescue experiments.
Figure S6 shows RNA-seq results of basal p53AD vs p53-null thymi, upstream regulator analysis, and ATAC-seq results for specific loci.
Figure S7 shows extended data for p53 dimer mutant novel activities (co-IP, motif analysis, other dimer mutants activities, and tumor data)
Figure S8 shows ferroptosis and scRNA-seq extended data
Figure S9 shows diagram summarizing findings within this study.
Supplemental Figure S7 from Reprogramming Cancer into Antigen-Presenting Cells as a Novel Immunotherapy
Authors: Linde Miles H. , Fan Amy C. , Köhnke Thomas , Trotman-Grant Aaron C. , Gurev Sarah F. , Phan Paul , Zhao Feifei , Haddock Naomi L. , Nuno Kevin A. , Gars Eric J. , Stafford Melissa , Marshall Payton L. , Dove Christopher G. , Linde Ian L. , Landberg Niklas , Miller Lindsay P. , Majzner Robbie G. , Zhang Tian Yi , Majeti Ravindra
Published: May 2023

Benchmarking antigen presentation by TR-APCs
Supplemental Figure S6 from Reprogramming Cancer into Antigen-Presenting Cells as a Novel Immunotherapy
Authors: Linde Miles H. , Fan Amy C. , Köhnke Thomas , Trotman-Grant Aaron C. , Gurev Sarah F. , Phan Paul , Zhao Feifei , Haddock Naomi L. , Nuno Kevin A. , Gars Eric J. , Stafford Melissa , Marshall Payton L. , Dove Christopher G. , Linde Ian L. , Landberg Niklas , Miller Lindsay P. , Majzner Robbie G. , Zhang Tian Yi , Majeti Ravindra
Published: May 2023

TR-APC induction results in inflammatory rewiring of the tumor
microenvironment.
Supplemental Figure S4 from Reprogramming Cancer into Antigen-Presenting Cells as a Novel Immunotherapy
Authors: Linde Miles H. , Fan Amy C. , Köhnke Thomas , Trotman-Grant Aaron C. , Gurev Sarah F. , Phan Paul , Zhao Feifei , Haddock Naomi L. , Nuno Kevin A. , Gars Eric J. , Stafford Melissa , Marshall Payton L. , Dove Christopher G. , Linde Ian L. , Landberg Niklas , Miller Lindsay P. , Majzner Robbie G. , Zhang Tian Yi , Majeti Ravindra
Published: May 2023

In vitro re-exposure of T cells from surviving mice demonstrates TR-APC-mediated generation of tumor-specific memory.
Supplemental Figure S3 from Reprogramming Cancer into Antigen-Presenting Cells as a Novel Immunotherapy
Authors: Linde Miles H. , Fan Amy C. , Köhnke Thomas , Trotman-Grant Aaron C. , Gurev Sarah F. , Phan Paul , Zhao Feifei , Haddock Naomi L. , Nuno Kevin A. , Gars Eric J. , Stafford Melissa , Marshall Payton L. , Dove Christopher G. , Linde Ian L. , Landberg Niklas , Miller Lindsay P. , Majzner Robbie G. , Zhang Tian Yi , Majeti Ravindra
Published: May 2023

In vivo TR-APC induction results in expansion of activated and memory T cells, and decreased frequency of Tregs
Supplemental Figure S10 from Reprogramming Cancer into Antigen-Presenting Cells as a Novel Immunotherapy
Authors: Linde Miles H. , Fan Amy C. , Köhnke Thomas , Trotman-Grant Aaron C. , Gurev Sarah F. , Phan Paul , Zhao Feifei , Haddock Naomi L. , Nuno Kevin A. , Gars Eric J. , Stafford Melissa , Marshall Payton L. , Dove Christopher G. , Linde Ian L. , Landberg Niklas , Miller Lindsay P. , Majzner Robbie G. , Zhang Tian Yi , Majeti Ravindra
Published: May 2023

Primary B-ALL-derived TR-APCs activate T cells in an MHC-restricted manner according to the inflammatory milieu
Supplemental Figure S1 from Reprogramming Cancer into Antigen-Presenting Cells as a Novel Immunotherapy
Authors: Linde Miles H. , Fan Amy C. , Köhnke Thomas , Trotman-Grant Aaron C. , Gurev Sarah F. , Phan Paul , Zhao Feifei , Haddock Naomi L. , Nuno Kevin A. , Gars Eric J. , Stafford Melissa , Marshall Payton L. , Dove Christopher G. , Linde Ian L. , Landberg Niklas , Miller Lindsay P. , Majzner Robbie G. , Zhang Tian Yi , Majeti Ravindra
Published: May 2023

In vivo doxycycline administration results in significant TR-APC
induction throughout tumors
Table S6 from Abatacept/Ruxolitinib and Screening for Concomitant Respiratory Muscle Failure to Mitigate Fatality of Immune-Checkpoint Inhibitor Myocarditis
Authors: Salem Joe-Elie , Bretagne Marie , Abbar Baptiste , Leonard-Louis Sarah , Ederhy Stéphane , Redheuil Alban , Boussouar Samia , Nguyen Lee S. , Procureur Adrien , Stein Frederic , Fenioux Charlotte , Devos Perrine , Gougis Paul , Dres Martin , Demoule Alexandre , Psimaras Dimitri , Lenglet Timothee , Maisonobe Thierry , De Chambrun Marc Pineton , Hekimian Guillaume , Straus Christian , Gonzalez-Bermejo Jesus , Klatzmann David , Rigolet Aude , Guillaume-Jugnot Perrine , Champtiaux Nicolas , Benveniste Olivier , Weiss Nicolas , Saheb Samir , Rouvier Philippe , Plu Isabelle , Gandjbakhch Estelle , Kerneis Mathieu , Hammoudi Nadjib , Zahr Noel , Llontop Claudia , Morelot-Panzini Capucine , Lehmann Lorenz , Qin Juan , Moslehi Javid J. , Rosenzwajg Michelle , Similowski Thomas , Allenbach Yves
Published: May 2023

Treatment modalities and reported adverse events by quartile of period of inclusion.