bluuebunny/crossref_metadata_2025 huggingface dataset:
Data from Tyrosine Kinase Inhibitors Diminish Renal Neoplasms in a Tuberous Sclerosis Model via induction of Apoptosis
Authors: Unachukwu Uchenna , Sonett Jarrod , Woode Denzel , Shiomi Takayuki , Chada Kiran , D'Armiento Jeanine M.
Published: July 2023

Abstract
Tuberous Sclerosis Complex (TSC) tumors are presently incurable despite a cytostatic response to mTOR pathway inhibition since recurrence of disease occurs after discontinuation of treatment. Here, we explored the hypothesis that inhibiting tyrosine kinase activity in mesenchymal lineage specific platelet derived growth factor receptor beta (PDGFRβ) signaling in TSC tumors is cytocidal and attenuates tumorigenesis at significantly higher levels than treatment with an mTOR inhibitor. Rapamycin- versus tyrosine kinase inhibitor (TKI)-induced renal angiomyolipoma (AML) and pulmonary lymphangioleiomyomatosis (LAM) tumor cells were comparatively analyzed using cell survival assays, and RNA sequencing and bioinformatics to distinguish tumoricidal mechanisms adopted by each drug type. The efficacy of imatinib therapy was validated against spontaneously developing renal cystadenomas in Tuberous Sclerosis Tsc2+/- mouse models (C57BL/6J mice; N=6; 400mg/kg/day; oral gavage) compared to Tsc2+/- mice treated with phosphate buffered saline (PBS) (C57BL/6J mice; N=6). Our study revealed that TKIs imatinib and nilotinib were cytocidal to both pulmonary LAM and renal AML cell cultures through the downregulation of the glycoprotein GPVI pathway and resultant disruption in mitochondrial permeability, increased cytosolic cytochrome C, and caspase 3 activation. Importantly, renal tumor growth was significantly attenuated in imatinib-treated Tsc2+/- mice compared to PBS treatment. The preclinical studies reported here provide evidence documenting the effectiveness of TKIs in limiting LAM and AML cell growth and viability with important clinical potential. Furthermore, these drugs elicit their effects by targeting a PDGF pathway-dependent apoptotic mechanism supporting the investigation of these drugs as a novel class of TSC therapeutics.
Data from Efficacy and Imaging Enabled Pharmacodynamic Profiling of KRAS G12C Inhibitors in Xenograft and Genetically Engineered Mouse Models of Cancer
Authors: Lee Catherine , Jiang Ziyue Karen , Planken Simon , Manzuk Lisa K. , Ortiz Roberto , Hall Michael , Noorbehesht Kavon , Ram Sripad , Affolter Timothy , Troche Gabriel E. , Ihle Nathan T. , Johnson Theodore , Ahn Youngwook , Kraus Manfred , Giddabasappa Anand
Published: July 2023

Abstract
KRAS is one of the most commonly mutated oncogenes in lung, colorectal, and pancreatic cancers. Recent clinical trials directly targeting KRAS G12C presented encouraging results for a large population of non-small cell lung cancer (NSCLC), but resistance to treatment is a concern. Continued exploration of new inhibitors and preclinical models is needed to address resistance mechanisms and improve duration of patient responses. To further enable the development of KRAS G12C inhibitors, we present a preclinical framework involving translational, non-invasive imaging modalities (CT and PET) and histopathology in a conventional xenograft model and a novel KRAS G12C knock-in mouse model of NSCLC. We utilized an in-house developed KRAS G12C inhibitor (Compound A) as a tool to demonstrate the value of this framework in studying in vivo pharmacokinetic/pharmacodynamic (PK/PD) relationship and anti-tumor efficacy. We characterized the Kras G12C-driven genetically engineered mouse model (GEMM) and identify tumor growth and signaling differences compared to its Kras G12D-driven counterpart. We also find that Compound A has comparable efficacy to sotorasib in the Kras G12C-driven lung tumors arising in the GEMM, but like observations in the clinic, some tumors inevitably progress on treatment. These findings establish a foundation for evaluating future KRAS G12C inhibitors that is not limited to xenograft studies and can be applied in a translationally relevant mouse model that mirrors human disease progression and resistance.
Data from The Preclinical Pharmacology of Tepotinib—A Highly Selective MET Inhibitor with Activity in Tumors Harboring MET Alterations
Authors: Albers Joachim , Friese-Hamim Manja , Clark Anderson , Schadt Oliver , Walter-Bausch Gina , Stroh Christopher , Johne Andreas , Karachaliou Niki , Blaukat Andree
Published: July 2023

Abstract
The mesenchymal–epithelial transition factor (MET) proto-oncogene encodes the MET receptor tyrosine kinase. MET aberrations drive tumorigenesis in several cancer types through a variety of molecular mechanisms, including MET mutations, gene amplification, rearrangement, and overexpression. Therefore, MET is a therapeutic target and the selective type Ib MET inhibitor, tepotinib, was designed to potently inhibit MET kinase activity. In vitro, tepotinib inhibits MET in a concentration-dependent manner irrespective of the mode of MET activation, and in vivo, tepotinib exhibits marked, dose-dependent antitumor activity in MET-dependent tumor models of various cancer indications. Tepotinib penetrates the blood–brain barrier and demonstrates strong antitumor activity in subcutaneous and orthotopic brain metastasis models, in-line with clinical activity observed in patients. MET amplification is an established mechanism of resistance to EGFR tyrosine kinase inhibitors (TKI), and preclinical studies show that tepotinib in combination with EGFR TKIs can overcome this resistance. Tepotinib is currently approved for the treatment of adult patients with advanced or metastatic non–small cell lung cancer harboring MET exon 14 skipping alterations. This review focuses on the pharmacology of tepotinib in preclinical cancer models harboring MET alterations and demonstrates that strong adherence to the principles of the Pharmacological Audit Trail may result in a successful discovery and development of a precision medicine.
Supplementary Table 9 from Disruption of the MYC Superenhancer Complex by Dual Targeting of FLT3 and LSD1 in Acute Myeloid Leukemia
Authors: Yashar William M. , Curtiss Brittany M. , Coleman Daniel J. , VanCampen Jake , Kong Garth , Macaraeg Jommel , Estabrook Joseph , Demir Emek , Long Nicola , Bottomly Daniel , McWeeney Shannon K. , Tyner Jeffrey W. , Druker Brian J. , Maxson Julia E. , Braun Theodore P.
Published: July 2023

Differential Phosphoprotein Network Enrichment in MOLM13 Cells (24 Hours After Drug Treatment)
Supplementary Table 8 from Disruption of the MYC Superenhancer Complex by Dual Targeting of FLT3 and LSD1 in Acute Myeloid Leukemia
Authors: Yashar William M. , Curtiss Brittany M. , Coleman Daniel J. , VanCampen Jake , Kong Garth , Macaraeg Jommel , Estabrook Joseph , Demir Emek , Long Nicola , Bottomly Daniel , McWeeney Shannon K. , Tyner Jeffrey W. , Druker Brian J. , Maxson Julia E. , Braun Theodore P.
Published: July 2023

RNA PolII Pause Index Analysis from MOLM13 RBP1 CUT&Tag (6 Hours After Drug Treatment)
Supplementary Table 6 from Disruption of the MYC Superenhancer Complex by Dual Targeting of FLT3 and LSD1 in Acute Myeloid Leukemia
Authors: Yashar William M. , Curtiss Brittany M. , Coleman Daniel J. , VanCampen Jake , Kong Garth , Macaraeg Jommel , Estabrook Joseph , Demir Emek , Long Nicola , Bottomly Daniel , McWeeney Shannon K. , Tyner Jeffrey W. , Druker Brian J. , Maxson Julia E. , Braun Theodore P.
Published: July 2023

Normalized Read Pileup and Differential Enrichment Clusters of MOLM13 H3K27Ac CUT&Tag (6 Hours After Drug Treatment) at Enhancers and Promoters
Supplementary Figure 6 from BZW2 Inhibition Reduces Colorectal Cancer Growth and Metastasis
Authors: Agarwal Sumit , Afaq Farrukh , Bajpai Prachi , Behring Michael , Kim Hyung-Gyoon , Varambally Amith , Chandrashekar Darshan S. , Peter Shajan , Diffalha Sameer Al , Khushman Moh'd , Seeber Andreas , Varambally Sooryanarayana , Manne Upender
Published: July 2023

S6. MYC regulates BZW2 in CRC cells.
Supplementary Figure 5 from BZW2 Inhibition Reduces Colorectal Cancer Growth and Metastasis
Authors: Agarwal Sumit , Afaq Farrukh , Bajpai Prachi , Behring Michael , Kim Hyung-Gyoon , Varambally Amith , Chandrashekar Darshan S. , Peter Shajan , Diffalha Sameer Al , Khushman Moh'd , Seeber Andreas , Varambally Sooryanarayana , Manne Upender
Published: July 2023

S5. MALAT1 and NEAT1 are downstream target genes of BZW2 in CRC.
Supplementary Figure 4 from BZW2 Inhibition Reduces Colorectal Cancer Growth and Metastasis
Authors: Agarwal Sumit , Afaq Farrukh , Bajpai Prachi , Behring Michael , Kim Hyung-Gyoon , Varambally Amith , Chandrashekar Darshan S. , Peter Shajan , Diffalha Sameer Al , Khushman Moh'd , Seeber Andreas , Varambally Sooryanarayana , Manne Upender
Published: July 2023

S4. BZW2 is involved in CRC tumor growth.
Supplementary Table 2 from Disruption of the MYC Superenhancer Complex by Dual Targeting of FLT3 and LSD1 in Acute Myeloid Leukemia
Authors: Yashar William M. , Curtiss Brittany M. , Coleman Daniel J. , VanCampen Jake , Kong Garth , Macaraeg Jommel , Estabrook Joseph , Demir Emek , Long Nicola , Bottomly Daniel , McWeeney Shannon K. , Tyner Jeffrey W. , Druker Brian J. , Maxson Julia E. , Braun Theodore P.
Published: July 2023

Transcription Factor Enrichment Analysis of MOLM13 Bulk RNA-Seq (24 Hours After Drug Treatment)
Supplementary Figure 3 from BZW2 Inhibition Reduces Colorectal Cancer Growth and Metastasis
Authors: Agarwal Sumit , Afaq Farrukh , Bajpai Prachi , Behring Michael , Kim Hyung-Gyoon , Varambally Amith , Chandrashekar Darshan S. , Peter Shajan , Diffalha Sameer Al , Khushman Moh'd , Seeber Andreas , Varambally Sooryanarayana , Manne Upender
Published: July 2023

S3. BZW2-knockdown reduces cell invasion.
Supplementary Table 17 from Disruption of the MYC Superenhancer Complex by Dual Targeting of FLT3 and LSD1 in Acute Myeloid Leukemia
Authors: Yashar William M. , Curtiss Brittany M. , Coleman Daniel J. , VanCampen Jake , Kong Garth , Macaraeg Jommel , Estabrook Joseph , Demir Emek , Long Nicola , Bottomly Daniel , McWeeney Shannon K. , Tyner Jeffrey W. , Druker Brian J. , Maxson Julia E. , Braun Theodore P.
Published: July 2023

GSEA of Primary AML Bulk RNA-Seq (24 Hours After Drug Treatment)
Supplementary Data from BZW2 Inhibition Reduces Colorectal Cancer Growth and Metastasis
Authors: Agarwal Sumit , Afaq Farrukh , Bajpai Prachi , Behring Michael , Kim Hyung-Gyoon , Varambally Amith , Chandrashekar Darshan S. , Peter Shajan , Diffalha Sameer Al , Khushman Moh'd , Seeber Andreas , Varambally Sooryanarayana , Manne Upender
Published: July 2023

Supplementary figure legends 1-8, and supplementary tables 1-5
Supplementary Table 15 from Disruption of the MYC Superenhancer Complex by Dual Targeting of FLT3 and LSD1 in Acute Myeloid Leukemia
Authors: Yashar William M. , Curtiss Brittany M. , Coleman Daniel J. , VanCampen Jake , Kong Garth , Macaraeg Jommel , Estabrook Joseph , Demir Emek , Long Nicola , Bottomly Daniel , McWeeney Shannon K. , Tyner Jeffrey W. , Druker Brian J. , Maxson Julia E. , Braun Theodore P.
Published: July 2023

Log2 Normalized Counts of Differentially Expressed Genes from Primary AML Blast Bulk RNA-seq (24 Hours After Drug Treatment)
Supplementary Table 12 from Disruption of the MYC Superenhancer Complex by Dual Targeting of FLT3 and LSD1 in Acute Myeloid Leukemia
Authors: Yashar William M. , Curtiss Brittany M. , Coleman Daniel J. , VanCampen Jake , Kong Garth , Macaraeg Jommel , Estabrook Joseph , Demir Emek , Long Nicola , Bottomly Daniel , McWeeney Shannon K. , Tyner Jeffrey W. , Druker Brian J. , Maxson Julia E. , Braun Theodore P.
Published: July 2023

MYC Blood Enhancer Complex (BENC) Module Cooordinates in Hg38
Supplementary Table 1 from Disruption of the MYC Superenhancer Complex by Dual Targeting of FLT3 and LSD1 in Acute Myeloid Leukemia
Authors: Yashar William M. , Curtiss Brittany M. , Coleman Daniel J. , VanCampen Jake , Kong Garth , Macaraeg Jommel , Estabrook Joseph , Demir Emek , Long Nicola , Bottomly Daniel , McWeeney Shannon K. , Tyner Jeffrey W. , Druker Brian J. , Maxson Julia E. , Braun Theodore P.
Published: July 2023

Log2 Normalized Counts of Differentially Expressed Genes from MOLM13 Bulk RNA-seq (24 Hours After Drug Treatment)
Supplementary Materials and Methods from Disruption of the MYC Superenhancer Complex by Dual Targeting of FLT3 and LSD1 in Acute Myeloid Leukemia
Authors: Yashar William M. , Curtiss Brittany M. , Coleman Daniel J. , VanCampen Jake , Kong Garth , Macaraeg Jommel , Estabrook Joseph , Demir Emek , Long Nicola , Bottomly Daniel , McWeeney Shannon K. , Tyner Jeffrey W. , Druker Brian J. , Maxson Julia E. , Braun Theodore P.
Published: July 2023

Supplementary Materials and Methods
Supplementary Fig. 9 from Disruption of the MYC Superenhancer Complex by Dual Targeting of FLT3 and LSD1 in Acute Myeloid Leukemia
Authors: Yashar William M. , Curtiss Brittany M. , Coleman Daniel J. , VanCampen Jake , Kong Garth , Macaraeg Jommel , Estabrook Joseph , Demir Emek , Long Nicola , Bottomly Daniel , McWeeney Shannon K. , Tyner Jeffrey W. , Druker Brian J. , Maxson Julia E. , Braun Theodore P.
Published: July 2023

SPI1 knockdown does not disrupt dual FLT3/LSD1 inhibition synergy.
Supplementary Fig. 8 from Disruption of the MYC Superenhancer Complex by Dual Targeting of FLT3 and LSD1 in Acute Myeloid Leukemia
Authors: Yashar William M. , Curtiss Brittany M. , Coleman Daniel J. , VanCampen Jake , Kong Garth , Macaraeg Jommel , Estabrook Joseph , Demir Emek , Long Nicola , Bottomly Daniel , McWeeney Shannon K. , Tyner Jeffrey W. , Druker Brian J. , Maxson Julia E. , Braun Theodore P.
Published: July 2023

Combined FLT3/LSD1 inhibition does not substantially alter myeloid differentiation.
Supplementary Fig. 6 from Disruption of the MYC Superenhancer Complex by Dual Targeting of FLT3 and LSD1 in Acute Myeloid Leukemia
Authors: Yashar William M. , Curtiss Brittany M. , Coleman Daniel J. , VanCampen Jake , Kong Garth , Macaraeg Jommel , Estabrook Joseph , Demir Emek , Long Nicola , Bottomly Daniel , McWeeney Shannon K. , Tyner Jeffrey W. , Druker Brian J. , Maxson Julia E. , Braun Theodore P.
Published: July 2023

Stat5 over-expression diminishes the efficacy of combined FLT3/LSD1 inhibition.
Supplementary Fig. 1 from Disruption of the MYC Superenhancer Complex by Dual Targeting of FLT3 and LSD1 in Acute Myeloid Leukemia
Authors: Yashar William M. , Curtiss Brittany M. , Coleman Daniel J. , VanCampen Jake , Kong Garth , Macaraeg Jommel , Estabrook Joseph , Demir Emek , Long Nicola , Bottomly Daniel , McWeeney Shannon K. , Tyner Jeffrey W. , Druker Brian J. , Maxson Julia E. , Braun Theodore P.
Published: July 2023

Drug synergy between FLT3 and LSD1 inhibitors in FLT3-ITD and FLT3-wildtype cell lines.
Supplementary Table S1, S2 from MACdb: A Curated Knowledgebase for Metabolic Associations across Human Cancers
Authors: Sun Yanling , Zheng Xinchang , Wang Guoliang , Wang Yibo , Chen Xiaoning , Sun Jiani , Xiong Zhuang , Zhang Sisi , Wang Tianyi , Fan Zhuojing , Bu Congfan , Bao Yiming , Zhao Wenming
Published: July 2023

Supplementary Table S1, S2
Supplementary Tables and Figures from Triple-Negative Breast Cancer-Derived Extracellular Vesicles Promote a Hepatic Premetastatic Niche via a Cascade of Microenvironment Remodeling
Authors: Heo Woohang , Lee Woochan , Cheun Jong Ho , Lee Eun-Shin , Li Songbin , Kim Hoe suk , Son Hye-Youn , Kim Ju Hee , Woo Yeon Duk , Chung Doo Hyun , Yun Jihui , Jung Ji Gwang , Lee Han-Byoel , Han Wonshik , Kim Hong-Kyu , Kim Jong-Il , Moon Hyeong-Gon
Published: July 2023

Supplementary Table 1. Information about patients derived xenograft models and derived patient.Supplementary Table 2. Ontology of differentially expressed genes in metastasis-harboring liver of PDX models.Supplementary Table 3. Differentially expressed genes in liver and lung of metastasis-harboring PDX models.Supplementary Table 4. Human ratio in lung and liver of additional PDX models identified by RNA sequencing.Supplementary Table 5. Gene ontology of co-expressed genes with Cx3cr1 in liver of PDX models identified by RNA sequencing.Supplementary Table 6. Top ranked genes having significant correlation with Cx3cr1 in liver of PDX models identified by RNA sequencing.Supplementary Table 7. Demographic and clinical characteristics of all patients.Supplementary Table 8. Information about used primer sequences for quantitative real-time PCRSupplementary Figure 1. Liver and lung H&E staining pictures of eight nonmetastatic PDX models a. Microscopic images of non-metastasis harboring PDX mouse model's liver (left) and lung (right) taken at 400x magnification.Supplementary Figure 2. Immunohistochemistry about CX3CR1 in liver and lung of breast cancer metastasis patients.Supplementary Figure 3. Hepatic metastasis after four weeks after orthotopic injection of 4T1 breast cancer cells identified by H&E staining.Supplementary Figure 4. Identification of pre-metastatic niche in liver tissues of 4T1 bearing mice a. mRNA expression of inflammation associated genes identified by real-time PCR in liver tissues of 4T1 bearing mice.Supplementary Figure 5. Identification of CX3CR1 positive cell population.Supplementary Figure 6. FACS analysis with anti-CX3CR1 of Raw264.7 macrophage cell lines.Supplementary Figure 7. Trans-well migration assay of BMDM with or without CX3CL1.Supplementary Figure 8. Mmp9 mRNA expression having significant correlation with Cx3cr1 mRNA expression in liver of PDX models.Supplementary Figure 9. MMP9 expression of macrophages with CX3CL1 treatment.Supplementary Figure 10. Signaling pathway of CX3CL1 treated macrophages.Supplementary Figure 11. Splenic injection of 4T1 cells inducing hepatic metastasis within two weeks in most cases.Supplementary Figure 12. mRNA expression about Cx3cr1 and Mmp9 in liver of vehicle or AZD8797 treated BALB/C mice identified by real-time PCR.Supplementary Figure 13. Correlation plot of Tnfa and Cx3cr1 mRNA expression in liver and lung of PDX models.Supplementary Figure 14. EVs isolation of CD63-mRuby-4T1.
Supplementary Figure 2 from Tumor-Derived CCL5 Recruits Cancer-Associated Fibroblasts and Promotes Tumor Cell Proliferation in Esophageal Squamous Cell Carcinoma
Authors: Dunbar Karen J. , Karakasheva Tatiana A. , Tang Qiaosi , Efe Gizem , Lin Eric W. , Harris Michael , Sahu Varun , Sachdeva Uma M. , Hu Jianhua , Klein-Szanto Andres J. , Henick Brian , Diehl J. Alan , Nakagawa Hiroshi , Rustgi Anil K.
Published: July 2023

Loss of tumor-derived CCL5 reduces tumor cell proliferation in TE-1 cells.
Supplementary Figure Legend 1 and Supplementary Table 1 from Non-Essential Amino Acid Availability Influences Proteostasis and Breast Cancer Cell Survival During Proteotoxic Stress
Authors: Sannino Sara , Manuel Allison M. , Shang Chaowei , Wendell Stacy G. , Wipf Peter , Brodsky Jeffrey L.
Published: July 2023

Legend to supplementary figure S1 and Table S1 containing a list of reagents and chemicals used to perform the experiments in the manuscript
Supplementary Figure 1 from Non-Essential Amino Acid Availability Influences Proteostasis and Breast Cancer Cell Survival During Proteotoxic Stress
Authors: Sannino Sara , Manuel Allison M. , Shang Chaowei , Wendell Stacy G. , Wipf Peter , Brodsky Jeffrey L.
Published: July 2023

S1. Amino acid modulation orchestrates apoptosis when proteostasis is compromised.
Data from Downregulation of BASP1 Promotes Temozolomide Resistance in Gliomas via Epigenetic Activation of the FBXO32/NF-κB/MGMT Axis
Authors: Liao Xinyi , Li Ziwen , Zheng Haiqing , Qian Wanying , Zhang Shuxia , Chen Suwen , Li Xincheng , Tang Miaoling , Xu Yingru , Yu Ruyuan , Li Man , Song Libing , Li Jun
Published: July 2023

Abstract
The chemoresistance of temozolomide-based therapy is a serious limitation for lasting effective treatment of gliomas, while the underlying mechanisms remain unclear. In this study, we showed that downregulation of BASP1 correlated negatively with the response to temozolomide therapy and disease-free survival (DFS) of patients with gliomas. Silencing BASP1 significantly enhanced the temozolomide resistance of glioma cells both in vitro and in vivo through repair of temozolomide-induced DNA damage via activation of the FBXO32/NF-κB/MGMT axis in both MGMT-methylated and -unmethylated gliomas. We demonstrated that loss of BASP1 resulted in removal of TRIM37/EZH2 complex–induced repressive histone modifications, including H2A-ub and H3K27me3, but addition of WDR5/MLL complex–mediated active histone modifications, including H3K4me3 and H3K9ac, on the FBXO32 promoter, which elicited in FBXO32 upregulation and further activated NF-κB/MGMT signaling via ubiquitin-dependent degradation of IκBα. Importantly, treatment with OICR-9429, an antagonist of the WDR5–MLL interaction, impaired the FBXO32/NF-κB/MGMT axis–mediated repair of temozolomide-induced DNA damage, leading to significant apoptosis of BASP1-downregulated glioma cells. These findings shed light on the molecular mechanism underlying BASP1-mediated epigenetic transcriptional repression and may represent a potential strategy in the fight against temozolomide-resistant gliomas.
Implications:
BASP1 downregulation promotes temozolomide resistance in gliomas through WDR5/MLL complex–mediated epigenetic activation of the FBXO32/NF-κB/MGMT axis, providing new target for improving outcomes in patients with temozolomide-resistant gliomas.
Data from Non-Essential Amino Acid Availability Influences Proteostasis and Breast Cancer Cell Survival During Proteotoxic Stress
Authors: Sannino Sara , Manuel Allison M. , Shang Chaowei , Wendell Stacy G. , Wipf Peter , Brodsky Jeffrey L.
Published: July 2023

Abstract
Protein homeostasis (proteostasis) regulates tumor growth and proliferation when cells are exposed to proteotoxic stress, such as during treatment with certain chemotherapeutics. Consequently, cancer cells depend to a greater extent on stress signaling, and require the integrated stress response (ISR), amino acid metabolism, and efficient protein folding and degradation pathways to survive. To define how these interconnected pathways are wired when cancer cells are challenged with proteotoxic stress, we investigated how amino acid abundance influences cell survival when Hsp70, a master proteostasis regulator, is inhibited. We previously demonstrated that cancer cells exposed to a specific Hsp70 inhibitor induce the ISR via the action of two sensors, GCN2 and PERK, in stress-resistant and sensitive cells, respectively. In resistant cells, the induction of GCN2 and autophagy supported resistant cell survival, yet the mechanism by which these events were induced remained unclear. We now report that amino acid availability reconfigures the proteostasis network. Amino acid supplementation, and in particular arginine addition, triggered cancer cell death by blocking autophagy. Consistent with the importance of amino acid availability, which when limited activates GCN2, resistant cancer cells succumbed when challenged with a potentiator for another amino acid sensor, mTORC1, in conjunction with Hsp70 inhibition.
Implications:
These data position amino acid abundance, GCN2, mTORC1, and autophagy as integrated therapeutic targets whose coordinated modulation regulates the survival of proteotoxic-resistant breast cancer cells.
Supplemental Table S3 from Cost-effectiveness of p16/Ki-67 Dual-Stained Cytology Reflex Following Co-testing with hrHPV Genotyping for Cervical Cancer Screening
Authors: Harper Diane M. , Anderson Rye J. , Baker Ed , Yu Tiffany M.
Published: July 2023

Supplemental Table S3 shows the procedure codes, CMS fee schedule payments, and usage information used to develop cost inputs for screening visits, tests, and procedures
Supplementary Table S2 from Reallocating Cervical Cancer Preventive Service Spending from Low- to High-Value Clinical Scenarios
Authors: Rockwell Michelle S. , Armbruster Shannon D. , Capucao Jillian C. , Russell Kyle B. , Rockwell John A. , Perkins Karen E. , Huffstetler Alison N. , Mafi John N. , Fendrick A. Mark
Published: July 2023

Supplementary Table S2 displays specifications for high and low-value cervical cancer screening as specified by the Milliman Medinsight Health Waste Calculator.
Supplementary Table S1 from Reallocating Cervical Cancer Preventive Service Spending from Low- to High-Value Clinical Scenarios
Authors: Rockwell Michelle S. , Armbruster Shannon D. , Capucao Jillian C. , Russell Kyle B. , Rockwell John A. , Perkins Karen E. , Huffstetler Alison N. , Mafi John N. , Fendrick A. Mark
Published: July 2023

Supplementary Table S1 includes codes used to identify cervical cancer screening tests within claims data.
Supplementary Table 6 from Associations between Physical Activity and Incidence of Cancer among Overweight Adults in Korea: Results from the Health Examinees-G Study
Authors: Choi Jaesung , Park JooYong , Kim Ji-Eun , Lee Miyoung , Kang Daehee , Shin Aesun , Choi Ji-Yeob
Published: July 2023

Supplementary Table 6 shows the association of physical activity with overall cancer incidence in the normal population, defined as those with body mass index between 18.5 and 25.0
Supplementary Table 5 from Associations between Physical Activity and Incidence of Cancer among Overweight Adults in Korea: Results from the Health Examinees-G Study
Authors: Choi Jaesung , Park JooYong , Kim Ji-Eun , Lee Miyoung , Kang Daehee , Shin Aesun , Choi Ji-Yeob
Published: July 2023

Supplementary Table 5 shows the association of physical activity with overall cancer incidence stratified by obesity status
Supplementary Table 2 from Associations between Physical Activity and Incidence of Cancer among Overweight Adults in Korea: Results from the Health Examinees-G Study
Authors: Choi Jaesung , Park JooYong , Kim Ji-Eun , Lee Miyoung , Kang Daehee , Shin Aesun , Choi Ji-Yeob
Published: July 2023

Supplementary Table 2 shows the association of physical activity with overall cancer incidence after excluding those diagnosed with cancer within the first 2 years of follow-up
Supplementary Table 14 from Associations between Physical Activity and Incidence of Cancer among Overweight Adults in Korea: Results from the Health Examinees-G Study
Authors: Choi Jaesung , Park JooYong , Kim Ji-Eun , Lee Miyoung , Kang Daehee , Shin Aesun , Choi Ji-Yeob
Published: July 2023

Supplementary Table 14 shows the association of physical activity with breast cancer incidence stratified by obesity status
Supplementary Table 13 from Associations between Physical Activity and Incidence of Cancer among Overweight Adults in Korea: Results from the Health Examinees-G Study
Authors: Choi Jaesung , Park JooYong , Kim Ji-Eun , Lee Miyoung , Kang Daehee , Shin Aesun , Choi Ji-Yeob
Published: July 2023

Supplementary Table 13 shows the association of physical activity with breast cancer incidence
Supplementary Table 12 from Associations between Physical Activity and Incidence of Cancer among Overweight Adults in Korea: Results from the Health Examinees-G Study
Authors: Choi Jaesung , Park JooYong , Kim Ji-Eun , Lee Miyoung , Kang Daehee , Shin Aesun , Choi Ji-Yeob
Published: July 2023

Supplementary Table 12 shows the association of physical activity with lung cancer incidence stratified by obesity status
Supplementary Table 10 from Associations between Physical Activity and Incidence of Cancer among Overweight Adults in Korea: Results from the Health Examinees-G Study
Authors: Choi Jaesung , Park JooYong , Kim Ji-Eun , Lee Miyoung , Kang Daehee , Shin Aesun , Choi Ji-Yeob
Published: July 2023

Supplementary Table 10 shows the association of physical activity with gastric cancer incidence stratified by obesity status
Supplementary Table 1 from Associations between Physical Activity and Incidence of Cancer among Overweight Adults in Korea: Results from the Health Examinees-G Study
Authors: Choi Jaesung , Park JooYong , Kim Ji-Eun , Lee Miyoung , Kang Daehee , Shin Aesun , Choi Ji-Yeob
Published: July 2023

Supplementary Table 1 shows the categorization of physical activity
Supplementary Figure 11 from Feasibility and Safety of Personalized, Multi-Target, Adoptive Cell Therapy (IMA101): First-in-Human Clinical Trial in Patients with Advanced Metastatic Cancer
Authors: Tsimberidou Apostolia M. , Guenther Kerstin , Andersson Borje S. , Mendrzyk Regina , Alpert Amir , Wagner Claudia , Nowak Anna , Aslan Katrin , Satelli Arun , Richter Fabian , Kuttruff-Coqui Sabrina , Schoor Oliver , Fritsche Jens , Coughlin Zoe , Mohamed Ali S. , Sieger Kerry , Norris Becky , Ort Rita , Beck Jennifer , Vo Henry Hiep , Hoffgaard Franziska , Ruh Manuel , Backert Linus , Wistuba Ignacio I. , Fuhrmann David , Ibrahim Nuhad K. , Morris Van Karlyle , Kee Bryan K. , Halperin Daniel M. , Nogueras-Gonzalez Graciela M. , Kebriaei Partow , Shpall Elizabeth J. , Vining David , Hwu Patrick , Singh Harpreet , Reinhardt Carsten , Britten Cedrik M. , Hilf Norbert , Weinschenk Toni , Maurer Dominik , Walter Steffen
Published: July 2023

Supplementary Figure 11
Supplemental Figure 9 from Feasibility and Safety of Personalized, Multi-Target, Adoptive Cell Therapy (IMA101): First-in-Human Clinical Trial in Patients with Advanced Metastatic Cancer
Authors: Tsimberidou Apostolia M. , Guenther Kerstin , Andersson Borje S. , Mendrzyk Regina , Alpert Amir , Wagner Claudia , Nowak Anna , Aslan Katrin , Satelli Arun , Richter Fabian , Kuttruff-Coqui Sabrina , Schoor Oliver , Fritsche Jens , Coughlin Zoe , Mohamed Ali S. , Sieger Kerry , Norris Becky , Ort Rita , Beck Jennifer , Vo Henry Hiep , Hoffgaard Franziska , Ruh Manuel , Backert Linus , Wistuba Ignacio I. , Fuhrmann David , Ibrahim Nuhad K. , Morris Van Karlyle , Kee Bryan K. , Halperin Daniel M. , Nogueras-Gonzalez Graciela M. , Kebriaei Partow , Shpall Elizabeth J. , Vining David , Hwu Patrick , Singh Harpreet , Reinhardt Carsten , Britten Cedrik M. , Hilf Norbert , Weinschenk Toni , Maurer Dominik , Walter Steffen
Published: July 2023

Supplemental Figure 9
Supplemental Figure 7 from Feasibility and Safety of Personalized, Multi-Target, Adoptive Cell Therapy (IMA101): First-in-Human Clinical Trial in Patients with Advanced Metastatic Cancer
Authors: Tsimberidou Apostolia M. , Guenther Kerstin , Andersson Borje S. , Mendrzyk Regina , Alpert Amir , Wagner Claudia , Nowak Anna , Aslan Katrin , Satelli Arun , Richter Fabian , Kuttruff-Coqui Sabrina , Schoor Oliver , Fritsche Jens , Coughlin Zoe , Mohamed Ali S. , Sieger Kerry , Norris Becky , Ort Rita , Beck Jennifer , Vo Henry Hiep , Hoffgaard Franziska , Ruh Manuel , Backert Linus , Wistuba Ignacio I. , Fuhrmann David , Ibrahim Nuhad K. , Morris Van Karlyle , Kee Bryan K. , Halperin Daniel M. , Nogueras-Gonzalez Graciela M. , Kebriaei Partow , Shpall Elizabeth J. , Vining David , Hwu Patrick , Singh Harpreet , Reinhardt Carsten , Britten Cedrik M. , Hilf Norbert , Weinschenk Toni , Maurer Dominik , Walter Steffen
Published: July 2023

Supplemental Figure 7
Supplemental Figure 5 from Feasibility and Safety of Personalized, Multi-Target, Adoptive Cell Therapy (IMA101): First-in-Human Clinical Trial in Patients with Advanced Metastatic Cancer
Authors: Tsimberidou Apostolia M. , Guenther Kerstin , Andersson Borje S. , Mendrzyk Regina , Alpert Amir , Wagner Claudia , Nowak Anna , Aslan Katrin , Satelli Arun , Richter Fabian , Kuttruff-Coqui Sabrina , Schoor Oliver , Fritsche Jens , Coughlin Zoe , Mohamed Ali S. , Sieger Kerry , Norris Becky , Ort Rita , Beck Jennifer , Vo Henry Hiep , Hoffgaard Franziska , Ruh Manuel , Backert Linus , Wistuba Ignacio I. , Fuhrmann David , Ibrahim Nuhad K. , Morris Van Karlyle , Kee Bryan K. , Halperin Daniel M. , Nogueras-Gonzalez Graciela M. , Kebriaei Partow , Shpall Elizabeth J. , Vining David , Hwu Patrick , Singh Harpreet , Reinhardt Carsten , Britten Cedrik M. , Hilf Norbert , Weinschenk Toni , Maurer Dominik , Walter Steffen
Published: July 2023

Supplemental Figure 5
Supplemental Figure 10 from Feasibility and Safety of Personalized, Multi-Target, Adoptive Cell Therapy (IMA101): First-in-Human Clinical Trial in Patients with Advanced Metastatic Cancer
Authors: Tsimberidou Apostolia M. , Guenther Kerstin , Andersson Borje S. , Mendrzyk Regina , Alpert Amir , Wagner Claudia , Nowak Anna , Aslan Katrin , Satelli Arun , Richter Fabian , Kuttruff-Coqui Sabrina , Schoor Oliver , Fritsche Jens , Coughlin Zoe , Mohamed Ali S. , Sieger Kerry , Norris Becky , Ort Rita , Beck Jennifer , Vo Henry Hiep , Hoffgaard Franziska , Ruh Manuel , Backert Linus , Wistuba Ignacio I. , Fuhrmann David , Ibrahim Nuhad K. , Morris Van Karlyle , Kee Bryan K. , Halperin Daniel M. , Nogueras-Gonzalez Graciela M. , Kebriaei Partow , Shpall Elizabeth J. , Vining David , Hwu Patrick , Singh Harpreet , Reinhardt Carsten , Britten Cedrik M. , Hilf Norbert , Weinschenk Toni , Maurer Dominik , Walter Steffen
Published: July 2023

Supplemental Figure 10
Supplementary Data from NL-201 Upregulates MHC-I Expression and Intratumoral T-cell Receptor Diversity, and Demonstrates Robust Antitumor Activity as Monotherapy and in Combination with PD-1 Blockade
Authors: Mortales Christie , Dutzar Benjamin , Chen Jerry , Chen Alex , Huard Justin , Walkey Carl , Swanson Ryan
Published: July 2023

Supplementary Table S1. Neo-2/15 maximum pSTAT5 signaling (maximal Mean fluorescent intensity, MFI) in human PBMCs and mouse splenocytes.Supplementary Table S2. IL-2 Receptor Signaling in Primary Human and Cynomolgus Monkey CD8+ T Cells induced by IL-2, NL-201, and Neo2/15.Supplementary Figure S1. A-B, Flow cytometric analysis of human PBMCs (A) and mouse splenocytes (B) for cell surface expression of IL-2Rα (CD25), IL-2Rβ (CD122), and IL-2Rγc (CD132).Supplementary Figure S2. Flow cytometric analysis of CT26-hHER2 and CT26 cell death assessed by Annexin V labeling after a 6-hour co-culture with isolated Balb/c NK cells and indicated concentrations of IL-2R agonists.Supplementary Figure S3. NL-201 demonstrates improved in vivo efficacy as compared to Neo-2/15.Supplementary Figure S4. A-B, Flow cytometric analysis of MHC-I (A) and PD-L1 (B) surface expression on in vitro B16F10 cells cultured with the indicated concentrations of cytokines for 1 day.Supplementary Figure S5. A-C, Tumor volume measurements of individual mice bearing subcutaneous B16F10 melanoma (A), EMT6 mammary carcinoma (B), and Renca renal adenocarcinoma (C) tumors.Supplementary Figure S6. A-B, B16F10 tumor-bearing mice were given a single dose of NL-201 by intravenous administration and then harvested 5 days later for ex vivo flow cytometric analysis to measure the abundance of CD45+ cells (A) and CD3+ T cells of CD45+ gate (B).
Table S6 from MYC Induces Immunotherapy and IFNγ Resistance Through Downregulation of JAK2
Authors: Markovits Ettai , Harush Ortal , Baruch Erez N. , Shulman Eldad D. , Debby Assaf , Itzhaki Orit , Anafi Liat , Danilevsky Artem , Shomron Noam , Ben-Betzalel Guy , Asher Nethanel , Shapira-Frommer Ronnie , Schachter Jacob , Barshack Iris , Geiger Tamar , Elkon Ran , Besser Michal J. , Markel Gal
Published: July 2023

Differential gene expression analysis between Interferon Resistance Score (IRS) high and low tumors in four melanoma cohorts. Related to Figure 2.
Table S1 from MYC Induces Immunotherapy and IFNγ Resistance Through Downregulation of JAK2
Authors: Markovits Ettai , Harush Ortal , Baruch Erez N. , Shulman Eldad D. , Debby Assaf , Itzhaki Orit , Anafi Liat , Danilevsky Artem , Shomron Noam , Ben-Betzalel Guy , Asher Nethanel , Shapira-Frommer Ronnie , Schachter Jacob , Barshack Iris , Geiger Tamar , Elkon Ran , Besser Michal J. , Markel Gal
Published: July 2023

Primers and Antibodies used in this paper.
Supplementary Figure 8 from MYC Induces Immunotherapy and IFNγ Resistance Through Downregulation of JAK2
Authors: Markovits Ettai , Harush Ortal , Baruch Erez N. , Shulman Eldad D. , Debby Assaf , Itzhaki Orit , Anafi Liat , Danilevsky Artem , Shomron Noam , Ben-Betzalel Guy , Asher Nethanel , Shapira-Frommer Ronnie , Schachter Jacob , Barshack Iris , Geiger Tamar , Elkon Ran , Besser Michal J. , Markel Gal
Published: July 2023

Supplementary Figure 8
Supplementary Figure 6 from MYC Induces Immunotherapy and IFNγ Resistance Through Downregulation of JAK2
Authors: Markovits Ettai , Harush Ortal , Baruch Erez N. , Shulman Eldad D. , Debby Assaf , Itzhaki Orit , Anafi Liat , Danilevsky Artem , Shomron Noam , Ben-Betzalel Guy , Asher Nethanel , Shapira-Frommer Ronnie , Schachter Jacob , Barshack Iris , Geiger Tamar , Elkon Ran , Besser Michal J. , Markel Gal
Published: July 2023

Supplementary Figure 6
Supplementary Figure 4 from MYC Induces Immunotherapy and IFNγ Resistance Through Downregulation of JAK2
Authors: Markovits Ettai , Harush Ortal , Baruch Erez N. , Shulman Eldad D. , Debby Assaf , Itzhaki Orit , Anafi Liat , Danilevsky Artem , Shomron Noam , Ben-Betzalel Guy , Asher Nethanel , Shapira-Frommer Ronnie , Schachter Jacob , Barshack Iris , Geiger Tamar , Elkon Ran , Besser Michal J. , Markel Gal
Published: July 2023

Supplementary Figure 4
Supplementary Figure 3 from MYC Induces Immunotherapy and IFNγ Resistance Through Downregulation of JAK2
Authors: Markovits Ettai , Harush Ortal , Baruch Erez N. , Shulman Eldad D. , Debby Assaf , Itzhaki Orit , Anafi Liat , Danilevsky Artem , Shomron Noam , Ben-Betzalel Guy , Asher Nethanel , Shapira-Frommer Ronnie , Schachter Jacob , Barshack Iris , Geiger Tamar , Elkon Ran , Besser Michal J. , Markel Gal
Published: July 2023

Supplementary Figure 3
Supplemental Table 5 from mWTX-330, an IL-12 INDUKINE Molecule, Activates and Reshapes Tumor-Infiltrating CD8+ T and NK Cells to Generate Antitumor Immunity
Authors: Nirschl Christopher J. , Brodkin Heather R. , Domonkos Celesztina , Dwyer Connor J. , Hicklin Daniel J. , Ismail Nesreen , Seidel-Dugan Cynthia , Steiner Philipp , Steuert Zoe , Sullivan Jenna M. , Winston William M. , Salmeron Andres
Published: July 2023

EC50 Values and Fold Change in Activity of WTX-330 in Primary Human Tblasts
Supplemental Figures from mWTX-330, an IL-12 INDUKINE Molecule, Activates and Reshapes Tumor-Infiltrating CD8+ T and NK Cells to Generate Antitumor Immunity
Authors: Nirschl Christopher J. , Brodkin Heather R. , Domonkos Celesztina , Dwyer Connor J. , Hicklin Daniel J. , Ismail Nesreen , Seidel-Dugan Cynthia , Steiner Philipp , Steuert Zoe , Sullivan Jenna M. , Winston William M. , Salmeron Andres
Published: July 2023

Supplemental Figures 1-10
Supplementary Tables from KRT17 Promotes T-lymphocyte Infiltration Through the YTHDF2–CXCL10 Axis in Colorectal Cancer
Authors: Liang Wenfeng , Liu Huashan , Zeng Ziwei , Liang Zhenxing , Xie Hao , Li Wenxin , Xiong Li , Liu Zhihang , Chen Mian , Jie Haiqing , Zheng Xiaobin , Huang Liang , Kang Liang
Published: July 2023

Materials were used in the research.
Supplementary Legends from KRT17 Promotes T-lymphocyte Infiltration Through the YTHDF2–CXCL10 Axis in Colorectal Cancer
Authors: Liang Wenfeng , Liu Huashan , Zeng Ziwei , Liang Zhenxing , Xie Hao , Li Wenxin , Xiong Li , Liu Zhihang , Chen Mian , Jie Haiqing , Zheng Xiaobin , Huang Liang , Kang Liang
Published: July 2023

Detailed descriptions of supplementary figures.
Supplementary Figures from Single-Cell Profiling of CD8+ T Cells in Acute Myeloid Leukemia Reveals a Continuous Spectrum of Differentiation and Clonal Hyperexpansion
Authors: Desai Poonam N. , Wang Bofei , Fonseca Andre , Borges Pamella , Jelloul Fatima Zahra , Reville Patrick K. , Lee Eric , Ly Christopher , Basi Akshay , Root Jessica , Baran Natalia , Post Sean M. , Deng Qing , Sun Hanxiao , Harmanci Arif O. , Burks Jared K. , Gomez Javier A. , DiNardo Courtney D. , Daver Naval G. , Alatrash Gheath , Konopleva Marina , Green Michael R. , Antunes Dinler A. , Futreal Andrew , Hao Dapeng , Abbas Hussein A.
Published: July 2023

All Supplementary Figures
Data from High Expression of MHC Class I Overcomes Cancer Immunotherapy Resistance Due to IFNγ Signaling Pathway Defects
Authors: Kawase Katsushige , Kawashima Shusuke , Nagasaki Joji , Inozume Takashi , Tanji Etsuko , Kawazu Masahito , Hanazawa Toyoyuki , Togashi Yosuke
Published: July 2023

Abstract
IFNγ signaling pathway defects are well-known mechanisms of resistance to immune checkpoint inhibitors. However, conflicting data have been reported, and the detailed mechanisms remain unclear. In this study, we have demonstrated that resistance to immune checkpoint inhibitors owing to IFNγ signaling pathway defects may be primarily caused by reduced MHC-I expression rather than by the loss of inhibitory effects on cellular proliferation or decreased chemokine production. In particular, we found that chemokines that recruit effector T cells were mainly produced by immune cells rather than cancer cells in the tumor microenvironment of a mouse model, with defects in IFNγ signaling pathways. Furthermore, we found a response to immune checkpoint inhibitors in a patient with JAK-negative head and neck squamous cell carcinoma whose HLA-I expression level was maintained. In addition, CRISPR screening to identify molecules associated with elevated MHC-I expression independent of IFNγ signaling pathways demonstrated that guanine nucleotide-binding protein subunit gamma 4 (GNG4) maintained MHC-I expression via the NF-κB signaling pathway. Our results indicate that patients with IFNγ signaling pathway defects are not always resistant to immune checkpoint inhibitors and highlight the importance of MHC-I expression among the pathways and the possibility of NF-κB–targeted therapies to overcome such resistance.

See related Spotlight by Haugh and Daud, p. 864
Supplementary Table S4 from The Polyamine–Hypusine Circuit Controls an Oncogenic Translational Program Essential for Malignant Conversion in MYC-Driven Lymphoma
Authors: Nakanishi Shima , Li Jiannong , Berglund Anders E. , Kim Youngchul , Zhang Yonghong , Zhang Ling , Yang Chunying , Song Jinming , Mirmira Raghavendra G. , Cleveland John L.
Published: July 2023

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.
Supplementary Table S3 from The Polyamine–Hypusine Circuit Controls an Oncogenic Translational Program Essential for Malignant Conversion in MYC-Driven Lymphoma
Authors: Nakanishi Shima , Li Jiannong , Berglund Anders E. , Kim Youngchul , Zhang Yonghong , Zhang Ling , Yang Chunying , Song Jinming , Mirmira Raghavendra G. , Cleveland John L.
Published: July 2023

Supplementary Table S3 lists 665 shared differentially translated transcripts (DTT) identified following depletion of eIF5A or DHPS, related to Fig. 5C.
Supplementary Figures S1-S7 from The Polyamine–Hypusine Circuit Controls an Oncogenic Translational Program Essential for Malignant Conversion in MYC-Driven Lymphoma
Authors: Nakanishi Shima , Li Jiannong , Berglund Anders E. , Kim Youngchul , Zhang Yonghong , Zhang Ling , Yang Chunying , Song Jinming , Mirmira Raghavendra G. , Cleveland John L.
Published: July 2023

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. Supplementary Fig. S1 is related to Fig. 1.
Supplementary Fig. S2 shows that inhibition of DHPS enzyme activity, or silencing eIF5A or DHPS, suppresses the growth of mouse MYC-driven lymphoma. Supplementary Fig. S2 is related to Fig. 2.
Supplementary Fig. S3 shows that hypusinated eIF5A (eIF5AHyp) contributes to the tumorigenic potential and maintenance of MYC-driven lymphoma. Supplementary Fig. S3 is related to Fig. 3.
Supplementary Fig. S4 shows the effects of eIF5A or DHPS depletion on the transcriptional landscape of MYC-driven lymphoma. Supplementary Fig. S4 is related to Fig. 4.
Supplementary Fig. S5 shows that depletion of eIF5A or DHPS impairs the translation efficiency of subsets of mRNA in MYC-driven lymphoma. Supplementary Fig. S5 is related to Fig. 5.
Supplementary Fig. S6 shows the validation of select eIF5AHyp translation targets identified by the multi-omics analyses, and that the translation of key regulatory cell cycle factors is controlled by hypusinated eIF5A. Supplementary Fig. S6 is related to Fig. 6.
Supplementary Fig. S7 shows that hypusinated eIF5A is essential for the development of MYC-driven lymphoma. Supplementary Fig. S7 is related to Fig. 7.
Supplementary Tables 1-6 from Patient-Derived iPSCs Faithfully Represent the Genetic Diversity and Cellular Architecture of Human Acute Myeloid Leukemia
Authors: Kotini Andriana G. , Carcamo Saul , Cruz-Rodriguez Nataly , Olszewska Malgorzata , Wang Tiansu , Demircioglu Deniz , Chang Chan-Jung , Bernard Elsa , Chao Mark P. , Majeti Ravindra , Luo Hanzhi , Kharas Michael G. , Hasson Dan , Papapetrou Eirini P.
Published: July 2023

Table S1. Patient characteristics. AML: acute myeloid leukemia; MDS: myelodysplastic syndrome; MPN: myeloproliferative neoplasm; ET: essential thrombocythemia; PBMCs: peripheral blood mononuclear cells; BMMCs: bone marrow mononuclear cells; PDX: patient-derived xenografts
Table S2. All patient samples used in this study with genetic characterization and reprogramming outcomes. Blue font denotes partially reprogrammed (as opposed to bona fide iPSC) colonies and clones.
Table S3. All AML-iPSC lines phenotypically characterized.
Table S4. Top 50 upregulated genes (highest log2 fold change) in each cluster.
Table S5. Primers used for genotyping.
Table S6. Primers used for qRT-PCR analyses.
TABLE 3 from Evaluating Work Impairment as a Source of Financial Toxicity in Cancer Healthcare and Negative Impacts on Health Status
Authors: Mudaranthakam Dinesh Pal , Nollen Nicole , Wick Jo , Hughes Dorothy , Welch Danny , Calhoun Elizabeth
Published: July 2023

Logistic regression of full model of main effects
TABLE 2 from Evaluating Work Impairment as a Source of Financial Toxicity in Cancer Healthcare and Negative Impacts on Health Status
Authors: Mudaranthakam Dinesh Pal , Nollen Nicole , Wick Jo , Hughes Dorothy , Welch Danny , Calhoun Elizabeth
Published: July 2023

The best-fit model – evaluating the financial factors across four cancer type patients (breast, lung, prostate, and colon)
Functional and Clinical Importance of SGLT2-inhibitors in Frailty: From the Kidney to the Heart
Authors: Santulli Gaetano , Varzideh Fahimeh , Forzano Imma , Wilson Scott , Salemme Luigi , de Donato Antonio , Lombardi Angela , Rainone Antonio , Nunziata Luigi , Jankauskas Stanislovas S. , Tesorio Tullio , Guerra Germano , Kansakar Urna , Mone Pasquale
Published: July 2023

SGLT2 (sodium-glucose cotransporter 2) enables glucose and sodium reabsorption in the kidney. SGLT2-inhibitors (also known as gliflozins, which include canagliflozin, dapagliflozin, empagliflozin, and ertugliflozin) act by increasing glycosuria, thereby reducing glycemia. These drugs are critical to reach and keep glycemic control, a crucial feature, especially in patients with comorbidities, like frail individuals. Several studies evaluated the effects of SGLT2-inhibitors in different settings beyond diabetes, revealing that they are actually pleiotropic drugs. We recently evidenced the favorable effects of SGLT2-inhibition on physical and cognitive impairment in frail older adults with diabetes and hypertension. In the present overview, we summarize the latest clinical and preclinical studies exploring the main effects of SGLT2-inhibitors on kidney and heart, emphasizing their potential beneficial actions in frailty.
Publications Trends in Society & Animals from 2009–2019: A Bibliometric Analysis
Authors: Rousseau Camille Xinmei , Binfet John-Tyler
Published: July 2023

This bibliometric analysis of Society & Animals (SOAN) publications from 2009–2019 generated a portrait of publishing trends including prevalent authors (i.e., Who?), institutions publishing HAI research (i.e., Where?), and salient themes of research showcased (i.e., What?). Pete Porter and Randy Malamud emerged as preeminent authors and collaborators. Researchers with prevalent citations included Pavol Prokop, Christoph Randler, and Randy Malamud. Özel et al. (2009) had the most cited publication of SOAN articles whereas Haraway (2008) was the most cited reference across SOAN publications. The University of Melbourne, Georgia State University, and the Slovakian Academy of Science emerged as key organizations, and the top three countries central to SOAN publications were the USA, Australia, and England. Salient keywords included animal welfare, companion animals, and animals. Text analysis of titles and abstracts revealed that dog, article, and companion animal were prevalent. The findings are discussed within the broader context of HAI research.