bluuebunny/crossref_metadata_2025 huggingface dataset:
Supplementary Figure S3 from MRTX1719 is an MTA-cooperative PRMT5 inhibitor that exhibits synthetic lethality in preclinical models and patients with MTAP deleted cancer
Authors: Engstrom Lars D. , Aranda Ruth , Waters Laura , Moya Krystal , Bowcut Vickie , Vegar Laura , Trinh David , Hebbert Allan , Smith Christopher R. , Kulyk Svitlana , Lawson J David. , He Leo , Hover Laura D. , Fernandez-Banet Julio , Hallin Jill , Vanderpool Darin , Briere David M. , Blaj Alice , Marx Matthew A. , Rodon Jordi , Offin Michael , Arbour Kathryn C. , Johnson Melissa L. , Kwiatkowski David J. , Janne Pasi A. , Haddox Candace L. , Papadopoulos Kyriakos P. , Henry Jason T. , Leventakos Konstantinos , Christensen James G. , Shazer Ronald , Olson Peter
Published: September 2024

Thermal shift PRMT5 inhibitor data
Supplementary Figure S2 from MRTX1719 is an MTA-cooperative PRMT5 inhibitor that exhibits synthetic lethality in preclinical models and patients with MTAP deleted cancer
Authors: Engstrom Lars D. , Aranda Ruth , Waters Laura , Moya Krystal , Bowcut Vickie , Vegar Laura , Trinh David , Hebbert Allan , Smith Christopher R. , Kulyk Svitlana , Lawson J David. , He Leo , Hover Laura D. , Fernandez-Banet Julio , Hallin Jill , Vanderpool Darin , Briere David M. , Blaj Alice , Marx Matthew A. , Rodon Jordi , Offin Michael , Arbour Kathryn C. , Johnson Melissa L. , Kwiatkowski David J. , Janne Pasi A. , Haddox Candace L. , Papadopoulos Kyriakos P. , Henry Jason T. , Leventakos Konstantinos , Christensen James G. , Shazer Ronald , Olson Peter
Published: September 2024

Supplemental biochemical and cellular characterization of MRTX1719
Supplementary Notes 1-5 from The origin of highly elevated cell-free DNA in healthy individuals and patients with pancreatic, colorectal, lung, or ovarian cancer
Authors: Mattox Austin K. , Douville Christopher , Wang Yuxuan , Popoli Maria , Ptak Janine , Silliman Natalie , Dobbyn Lisa , Schaefer Joy , Lu Steve , Pearlman Alexander H. , Cohen Joshua D. , Tie Jeanne , Gibbs Peter , Lahouel Kamel , Bettegowda Chetan , Hruban Ralph H. , Tomasetti Cristian , Jiang Peiyong , Chan K.C. Allen , Lo Yuk Ming Dennis , Papadopoulos Nickolas , Kinzler Kenneth W. , Vogelstein Bert
Published: September 2024

Supplementary Notes 1-5. Supplementary Note 1: Origins of cell-free DNA. Supplementary Note 2: Leukocyte Lysis. Supplementary Note 3: Reference datasets and deconvolution algorithms used to interpret whole genome bisulfite sequencing data. Supplementary Note 4: Turnover rates. Supplementary Note 5: Relationships between ctDNA and tissue specific cfDNA in cancer patients.
Figure S9 from The origin of highly elevated cell-free DNA in healthy individuals and patients with pancreatic, colorectal, lung, or ovarian cancer
Authors: Mattox Austin K. , Douville Christopher , Wang Yuxuan , Popoli Maria , Ptak Janine , Silliman Natalie , Dobbyn Lisa , Schaefer Joy , Lu Steve , Pearlman Alexander H. , Cohen Joshua D. , Tie Jeanne , Gibbs Peter , Lahouel Kamel , Bettegowda Chetan , Hruban Ralph H. , Tomasetti Cristian , Jiang Peiyong , Chan K.C. Allen , Lo Yuk Ming Dennis , Papadopoulos Nickolas , Kinzler Kenneth W. , Vogelstein Bert
Published: September 2024

Supplemental Figure 9. Plasma AST and ALT levels before and ~24 hours after surgery for pancreatic cancer. AST and ALT levels substantially increased in all five patients.
Table S4 from Clinical efficacy of ONC201 in H3K27M-mutant diffuse midline gliomas is driven by disruption of integrated metabolic and epigenetic pathways
Authors: Venneti Sriram , Kawakibi Abed Rahman , Ji Sunjong , Waszak Sebastian M. , Sweha Stefan R. , Mota Mateus , Pun Matthew , Deogharkar Akash , Chung Chan , Tarapore Rohinton S. , Ramage Samuel , Chi Andrew , Wen Patrick Y. , Arrillaga-Romany Isabel , Batchelor Tracy T. , Butowski Nicholas A. , Sumrall Ashley , Shonka Nicole , Harrison Rebecca A. , de Groot John , Mehta Minesh , Hall Matthew D. , Daghistani Doured , Cloughesy Timothy F. , Ellingson Benjamin M. , Beccaria Kevin , Varlet Pascale , Kim Michelle M. , Umemura Yoshie , Garton Hugh , Franson Andrea , Schwartz Jonathan , Jain Rajan , Kachman Maureen , Baum Heidi , Burant Charles F. , Mottl Sophie L. , Cartaxo Rodrigo T. , John Vishal , Messinger Dana , Qin Tingting , Peterson Erik , Sajjakulnukit Peter , Ravi Karthik , Waugh Alyssa , Walling Dustin , Ding Yujie , Xia Ziyun , Schwendeman Anna , Hawes Debra , Yang Fusheng , Judkins Alexander R. , Wahl Daniel , Lyssiotis Costas A. , de la Nava Daniel , Alonso Marta M. , Eze Augustine , Spitzer Jasper , Schmidt Susanne V. , Duchatel Ryan J. , Dun Matthew D. , Cain Jason E. , Jiang Li , Stopka Sylwia A. , Baquer Gerard , Regan Michael S. , Filbin Mariella G. , Agar Nathalie Y.R. , Zhao Lili , Kumar-Sinha Chandan , Mody Rajen , Chinnaiyan Arul , Kurokawa Ryo , Pratt Drew , Yadav Viveka N. , Grill Jacques , Kline Cassie , Mueller Sabine , Resnick Adam , Nazarian Javad , Allen Joshua E. , Odia Yazmin , Gardner Sharon L. , Koschmann Carl
Published: September 2024

Summary of historical control datasets.
Table S13 from Clinical efficacy of ONC201 in H3K27M-mutant diffuse midline gliomas is driven by disruption of integrated metabolic and epigenetic pathways
Authors: Venneti Sriram , Kawakibi Abed Rahman , Ji Sunjong , Waszak Sebastian M. , Sweha Stefan R. , Mota Mateus , Pun Matthew , Deogharkar Akash , Chung Chan , Tarapore Rohinton S. , Ramage Samuel , Chi Andrew , Wen Patrick Y. , Arrillaga-Romany Isabel , Batchelor Tracy T. , Butowski Nicholas A. , Sumrall Ashley , Shonka Nicole , Harrison Rebecca A. , de Groot John , Mehta Minesh , Hall Matthew D. , Daghistani Doured , Cloughesy Timothy F. , Ellingson Benjamin M. , Beccaria Kevin , Varlet Pascale , Kim Michelle M. , Umemura Yoshie , Garton Hugh , Franson Andrea , Schwartz Jonathan , Jain Rajan , Kachman Maureen , Baum Heidi , Burant Charles F. , Mottl Sophie L. , Cartaxo Rodrigo T. , John Vishal , Messinger Dana , Qin Tingting , Peterson Erik , Sajjakulnukit Peter , Ravi Karthik , Waugh Alyssa , Walling Dustin , Ding Yujie , Xia Ziyun , Schwendeman Anna , Hawes Debra , Yang Fusheng , Judkins Alexander R. , Wahl Daniel , Lyssiotis Costas A. , de la Nava Daniel , Alonso Marta M. , Eze Augustine , Spitzer Jasper , Schmidt Susanne V. , Duchatel Ryan J. , Dun Matthew D. , Cain Jason E. , Jiang Li , Stopka Sylwia A. , Baquer Gerard , Regan Michael S. , Filbin Mariella G. , Agar Nathalie Y.R. , Zhao Lili , Kumar-Sinha Chandan , Mody Rajen , Chinnaiyan Arul , Kurokawa Ryo , Pratt Drew , Yadav Viveka N. , Grill Jacques , Kline Cassie , Mueller Sabine , Resnick Adam , Nazarian Javad , Allen Joshua E. , Odia Yazmin , Gardner Sharon L. , Koschmann Carl
Published: September 2024

GSEA analysis of genes with significantly lower chromatin accessibility at promoters and enhancers and reduced gene expression in DIPG007 cells treated with ONC201 versus vehicle.
Table S11 from Clinical efficacy of ONC201 in H3K27M-mutant diffuse midline gliomas is driven by disruption of integrated metabolic and epigenetic pathways
Authors: Venneti Sriram , Kawakibi Abed Rahman , Ji Sunjong , Waszak Sebastian M. , Sweha Stefan R. , Mota Mateus , Pun Matthew , Deogharkar Akash , Chung Chan , Tarapore Rohinton S. , Ramage Samuel , Chi Andrew , Wen Patrick Y. , Arrillaga-Romany Isabel , Batchelor Tracy T. , Butowski Nicholas A. , Sumrall Ashley , Shonka Nicole , Harrison Rebecca A. , de Groot John , Mehta Minesh , Hall Matthew D. , Daghistani Doured , Cloughesy Timothy F. , Ellingson Benjamin M. , Beccaria Kevin , Varlet Pascale , Kim Michelle M. , Umemura Yoshie , Garton Hugh , Franson Andrea , Schwartz Jonathan , Jain Rajan , Kachman Maureen , Baum Heidi , Burant Charles F. , Mottl Sophie L. , Cartaxo Rodrigo T. , John Vishal , Messinger Dana , Qin Tingting , Peterson Erik , Sajjakulnukit Peter , Ravi Karthik , Waugh Alyssa , Walling Dustin , Ding Yujie , Xia Ziyun , Schwendeman Anna , Hawes Debra , Yang Fusheng , Judkins Alexander R. , Wahl Daniel , Lyssiotis Costas A. , de la Nava Daniel , Alonso Marta M. , Eze Augustine , Spitzer Jasper , Schmidt Susanne V. , Duchatel Ryan J. , Dun Matthew D. , Cain Jason E. , Jiang Li , Stopka Sylwia A. , Baquer Gerard , Regan Michael S. , Filbin Mariella G. , Agar Nathalie Y.R. , Zhao Lili , Kumar-Sinha Chandan , Mody Rajen , Chinnaiyan Arul , Kurokawa Ryo , Pratt Drew , Yadav Viveka N. , Grill Jacques , Kline Cassie , Mueller Sabine , Resnick Adam , Nazarian Javad , Allen Joshua E. , Odia Yazmin , Gardner Sharon L. , Koschmann Carl
Published: September 2024

Volcano plot of differentially expressed genes in DIPG007 cells treated with ONC201 versus vehicle.
Fig. S4 from Senescent CAFs Mediate Immunosuppression and Drive Breast Cancer Progression
Authors: Ye Jiayu , Baer John M. , Faget Douglas V. , Morikis Vasilios A. , Ren Qihao , Melam Anupama , Delgado Ana Paula , Luo Xianmin , Bagchi Satarupa Mullick , Belle Jad I. , Campos Edward , Friedman Michael , Veis Deborah J. , Knudsen Erik S. , Witkiewicz Agnieszka K. , Powers Scott , Longmore Gregory D. , DeNardo David G. , Stewart Sheila A.
Published: September 2024

Supplementary figure S4 shows CAF gating strategy and PCA analysis or sorted CAF populations following bulk RNA-Seq.
Data from Splicing Factor SRSF1 Promotes Pancreatitis and KRASG12D-Mediated Pancreatic Cancer
Authors: Wan Ledong , Lin Kuang-Ting , Rahman Mohammad Alinoor. , Ishigami Yuma , Wang Zhikai , Jensen Mads A. , Wilkinson John E. , Park Youngkyu , Tuveson David A. , Krainer Adrian R.
Published: September 2024

Abstract
Inflammation is strongly associated with pancreatic ductal adenocarcinoma (PDAC), a highly lethal malignancy. Dysregulated RNA splicing factors have been widely reported in tumorigenesis, but their involvement in pancreatitis and PDAC is not well understood. Here, we report that the splicing factor SRSF1 is highly expressed in pancreatitis, PDAC precursor lesions, and tumors. Increased SRSF1 is sufficient to induce pancreatitis and accelerate KRASG12D-mediated PDAC. Mechanistically, SRSF1 activates MAPK signaling—partly by upregulating interleukin 1 receptor type 1 (IL1R1) through alternative-splicing-regulated mRNA stability. Additionally, SRSF1 protein is destabilized through a negative feedback mechanism in phenotypically normal epithelial cells expressing KRASG12D in mouse pancreas, and in pancreas organoids acutely expressing KRASG12D, buffering MAPK signaling and maintaining pancreas-cell homeostasis. This negative-feedback regulation of SRSF1 is overcome by hyperactive MYC, facilitating PDAC tumorigenesis. Our findings implicate SRSF1 in the etiology of pancreatitis and PDAC, and point to SRSF1-misregulated alternative splicing as a potential therapeutic target.
Data from C/EBPa confers dependence to fatty acid anabolic pathways and vulnerability to lipid oxidative stress-induced ferroptosis in FLT3-mutant leukemia
Authors: Sabatier Marie , Birsen Rudy , Lauture Laura , Mouche Sarah , Angelino Paolo , Dehairs Jonas , Goupille Lea , Boussaid Ismael , Heiblig Mael , Boet Emeline , Sahal Ambrine , Saland Estelle , Santos Juliana C. , Armengol Marc , Fernandez-Serrano Miranda , Farge Thomas , Cognet Guillaume , Simonetta Federico , Pignon Corentin , Graffeuil Antoine , Mazzotti Celine , Avet-Loiseau Herve , Delos Oceane , Bertrand-Michel Justine , Chedru Amelie , Dembitz Vilma , Gallipoli Paolo , Anstee Natasha S. , Loo Sun , Wei Andrew H. , Carroll Martin , Goubard Armelle , Castellano Remy , Collette Yves , Vergez Francois , Mansat-De Mas Veronique , Bertoli Sarah , Tavitian Suzanne , Picard Muriel , Recher Christian , Bourges-Abella Nathalie , Granat Fanny , Kosmider Olivier , Sujobert Pierre , Colsch Benoit , Joffre Carine , Stuani Lucille , Swinnen Johannes V. , Guillou Herve , Roue Gael , Hakim Nawad , Dejean Anne S. , Tsantoulis Petros , Larrue Clement , Bouscary Didier , Tamburini Jerome , Sarry Jean-Emmanuel
Published: September 2024

Abstract
While transcription factor C/AAT-enhancer binding protein a (C/EBPa) is critical for normal and leukemic differentiation, its role on cell and metabolic homeostasis is largely unknown in cancer. Here, multi-omics analyses uncovered a coordinated activation of C/EBPa and Fms-like tyrosine kinase 3 (FLT3) that increased lipid anabolism in vivo and in patients with FLT3-mutant acute myeloid leukemia (AML). Mechanistically, C/EBPa regulated FASN-SCD axis to promote fatty acid (FA) biosynthesis and desaturation. We further demonstrated that FLT3 or C/EBPa inactivation decreased mono-unsaturated FA incorporation to membrane phospholipids through SCD downregulation. Consequently, SCD inhibition enhanced susceptibility to lipid redox stress that was exploited by combining FLT3 and glutathione peroxidase 4 inhibition to trigger lipid oxidative stress, enhancing ferroptotic death of FLT3-mutant AML cells. Altogether, our study reveals a C/EBPa function in lipid homeostasis and adaptation to redox stress, and a previously unreported vulnerability of FLT3-mutant AML to ferroptosis with promising therapeutic application
Supplementary Figures from Netrin-1 promotes the immunosuppressive activity of MDSCs in colorectal cancer
Authors: Xia Xueli , Mao Zhenwei , Wang Wenxin , Ma Jie , Tian Jie , Wang Shengjun , Yin Kai
Published: September 2024

Supplementary Figures S1-S9
Supplementary Tables from Microparticle-delivered Cxcl9 prolongs Braf inhibitor efficacy in melanoma
Authors: Romano Gabriele , Paradiso Francesca , Li Peng , Shukla Pooja , Barger Lindsay N. , El Naggar Olivia , Miller John P. , Liang Roger J. , Helms Timothy L. , Lazar Alexander J. , Wargo Jennifer A. , Taraballi Francesca , Costello James C. , Kwong Lawrence N.
Published: September 2024

Supplementary Tables S1-S3
Supplementary Tables from SWI/SNF complex genomic alterations as a predictive biomarker for response to immune checkpoint inhibitors in multiple cancers
Authors: Wang Di , Wang Jianchao , Zhou Dongmei , Wu Zhixian , Liu Wei , Chen Yanping , Chen Gang , Zhang Jing
Published: September 2024

Supplementary Tables S1-S12
Supplementary Data Table 2 from Driver mutations dictate the immunological landscape and response to checkpoint immunotherapy of glioblastoma
Authors: Yeo Alan T. , Shah Rushil , Aliazis Konstantinos , Pal Rinku , Xu Tuoye , Zhang Piyan , Rawal Shruti , Rose Christopher M. , Varn Frederick S. , Appleman Vicky A. , Yoon Joon , Varma Hemant , Gygi Steven P. , Verhaak Roel G.W. , Boussiotis Vassiliki A. , Charest Al
Published: September 2024

Supplementary table 2
Supplementary Figures from Discovery of podofilox as a potent cGAMP–STING signaling enhancer with antitumor activity
Authors: Zhang Conggang , Han Jing , Hu Shuiqing , Hu Yawei , Xu Yifang , Hou Yanfei , Yang Yinlong , Su Huili , Zhang Zhengyin , Liu Peng , Sun Xuxu
Published: September 2024

Supplementary Figures S1 to S9 with Legends
Supplementary Table 4 from The immunopeptidome from a genomic perspective: Establishing the non-canonical landscape of MHC class I–associated peptides
Authors: Bedran Georges , Gasser Hans-Christof , Weke Kenneth , Wang Tongjie , Bedran Dominika , Laird Alexander , Battail Christophe , Zanzotto Fabio Massimo , Pesquita Catia , Axelson Håkan , Rajan Ajitha , Harrison David J. , Palkowski Aleksander , Pawlik Maciej , Parys Maciej , O'Neill J Robert. , Brennan Paul M. , Symeonides Stefan N. , Goodlett David R. , Litchfield Kevin , Fahraeus Robin , Hupp Ted R. , Kote Sachin , Alfaro Javier A.
Published: September 2024

Comparison data of COD-dipp ncMAPs with 4 other studies.
Supplementary Table 3 from The immunopeptidome from a genomic perspective: Establishing the non-canonical landscape of MHC class I–associated peptides
Authors: Bedran Georges , Gasser Hans-Christof , Weke Kenneth , Wang Tongjie , Bedran Dominika , Laird Alexander , Battail Christophe , Zanzotto Fabio Massimo , Pesquita Catia , Axelson Håkan , Rajan Ajitha , Harrison David J. , Palkowski Aleksander , Pawlik Maciej , Parys Maciej , O'Neill J Robert. , Brennan Paul M. , Symeonides Stefan N. , Goodlett David R. , Litchfield Kevin , Fahraeus Robin , Hupp Ted R. , Kote Sachin , Alfaro Javier A.
Published: September 2024

Annotation of the COD-dipp ncMAPs.
Supplementary Table 2 from The immunopeptidome from a genomic perspective: Establishing the non-canonical landscape of MHC class I–associated peptides
Authors: Bedran Georges , Gasser Hans-Christof , Weke Kenneth , Wang Tongjie , Bedran Dominika , Laird Alexander , Battail Christophe , Zanzotto Fabio Massimo , Pesquita Catia , Axelson Håkan , Rajan Ajitha , Harrison David J. , Palkowski Aleksander , Pawlik Maciej , Parys Maciej , O'Neill J Robert. , Brennan Paul M. , Symeonides Stefan N. , Goodlett David R. , Litchfield Kevin , Fahraeus Robin , Hupp Ted R. , Kote Sachin , Alfaro Javier A.
Published: September 2024

Open search peptide-spectrum matches (PSMs) information of serine acetylation, cysteinylation, carbamidomethylation, and cysteine trioxidation.
Supplementary Tables from iBRIDGE: A Data Integration Method to Identify Inflamed Tumors from Single-Cell RNAseq Data and Differentiate Cell Type–Specific Markers of Immune-Cell Infiltration
Authors: Turan Tolga , Kongpachith Sarah , Halliwill Kyle , McLaughlin Robert T. , Binnewies Mikhail , Reddy Dhemath , Zhao Xi , Mathew Rebecca , Ye Shiming , Jacob Howard J. , Samayoa Josue
Published: September 2024

Supplementary Tables S1-S16
Supplementary Tables and Figures from Targeting the IL-1β pathway for cancer immunotherapy remodels the tumor microenvironment and enhances antitumor immune responses
Authors: Diwanji Rohan , O'Brien Neil A. , Choi Jiyoung E. , Nguyen Beverly , Laszewski Tyler , Grauel Angelo L. , Yan Zheng , Xu Xin , Wu Jincheng , Ruddy David A. , Piquet Michelle , Pelletier Marc R. , Savchenko Alexander , Charette LaSalette , Rodrik-Outmezguine Vanessa , Baum Jason , Millholland John M. , Wong Connie C. , Martin Anne-Marie , Dranoff Glenn , Pruteanu-Malinici Iulian , Cremasco Viviana , Sabatos-Peyron Catherine , Jayaraman Pushpa
Published: September 2024

Supplementary tables S1-S5 and figures S1-S7
Supplemental Figure 1 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-González Graciela M. , Kebriaei Partow , Shpall Elizabeth J. , Vining David , Hwu Patrick , Singh-Jasuja Harpreet , Reinhardt Carsten , Britten Cedrik M. , Hilf Norbert , Weinschenk Toni , Maurer Dominik , Walter Steffen
Published: September 2024

Supplemental Figure 1
Table S3 from CD69 imposes tumor-specific CD8+ T-cell fate in tumor-draining lymph nodes
Authors: Koyama-Nasu Ryo , Kimura Motoko Y. , Kiuchi Masahiro , Aoki Ami , Wang Yangsong , Mita Yukiyoshi , Hasegawa Ichita , Endo Yukihiro , Onodera Atsushi , Hirahara Kiyoshi , Motohashi Shinichiro , Nakayama Toshinori
Published: September 2024

Table S3
Table S2 from CD69 imposes tumor-specific CD8+ T-cell fate in tumor-draining lymph nodes
Authors: Koyama-Nasu Ryo , Kimura Motoko Y. , Kiuchi Masahiro , Aoki Ami , Wang Yangsong , Mita Yukiyoshi , Hasegawa Ichita , Endo Yukihiro , Onodera Atsushi , Hirahara Kiyoshi , Motohashi Shinichiro , Nakayama Toshinori
Published: September 2024

Table S2
Table S1 from CD69 imposes tumor-specific CD8+ T-cell fate in tumor-draining lymph nodes
Authors: Koyama-Nasu Ryo , Kimura Motoko Y. , Kiuchi Masahiro , Aoki Ami , Wang Yangsong , Mita Yukiyoshi , Hasegawa Ichita , Endo Yukihiro , Onodera Atsushi , Hirahara Kiyoshi , Motohashi Shinichiro , Nakayama Toshinori
Published: September 2024

Table S1
Supplementary Table 3 from Systemic Alterations in Type-2 Conventional Dendritic Cells Leads to Impaired Tumor Immunity in Pancreatic Cancer
Authors: James C. Alston. , Baer John M. , Zuo Chong , Panni Usman Y. , Knolhoff Brett L. , Hogg Graham D. , Kingston Natalie L. , Kang Liang-I , Lander Varintra E. , Luo Jingqin , Tao Yu , Watson Mark A. , Aft Rebecca , Fields Ryan C. , Hawkins William G. , DeNardo David G.
Published: September 2024

Supplementary Table 3
Supplementary Figures from Systemic Alterations in Type-2 Conventional Dendritic Cells Leads to Impaired Tumor Immunity in Pancreatic Cancer
Authors: James C. Alston. , Baer John M. , Zuo Chong , Panni Usman Y. , Knolhoff Brett L. , Hogg Graham D. , Kingston Natalie L. , Kang Liang-I , Lander Varintra E. , Luo Jingqin , Tao Yu , Watson Mark A. , Aft Rebecca , Fields Ryan C. , Hawkins William G. , DeNardo David G.
Published: September 2024

Supplemental Figures and Legends
Supplementary Tables from Small gene networks delineate immune cell states and characterize immunotherapy response in melanoma
Authors: Egan Donagh , Kreileder Martina , Nabhan Myriam , Iglesias-Martinez Luis F. , Dovedi Simon J. , Valge-Archer Viia , Grover Amit , Wilkinson Robert W. , Slidel Timothy , Bendtsen Claus , Barrett Ian P. , Brennan Donal J. , Kolch Walter , Zhernovkov Vadim
Published: September 2024

Supplementary Tables S1 and S2
Supplementary Table S6 from Immunogenetic metabolomics reveals key enzymes that modulate CAR T-cell metabolism and function
Authors: Renauer Paul , Park Jonathan J. , Bai Meizhu , Acosta Arianny , Lee Won-Ho , Lin Guang Han , Zhang Yueqi , Dai Xiaoyun , Wang Guangchuan , Errami Youssef , Wu Terence , Clark Paul , Ye Lupeng , Yang Quanjun , Chen Sidi
Published: September 2024

Supplementary Table S6
Table S2 from Circulating and intratumoral immune determinants of response to atezolizumab plus bevacizumab in patients with variant histology or sarcomatoid renal cell carcinoma
Authors: Saliby Renee Maria , El Zarif Talal , Bakouny Ziad , Shah Valisha , Xie Wanling , Flippot Ronan , Denize Thomas , Kane M. Harry , Madsen Katrine N. , Ficial Miriam , Hirsch Laure , Wei Xiao X. , Steinarter John A. , Harshman Lauren C. , Vaishampayan Ulka N. , Severgnini Mariano , McDermott David F. , Lee Gwo-Shu Mary. , Xu Wenxin , Van Allen Eliezer M. , McGregor Bradley A. , Signoretti Sabina , Choueiri Toni K. , McKay Rana R. , Braun David A.
Published: September 2024

Supplementary table 2
Figure S9 from Circulating and intratumoral immune determinants of response to atezolizumab plus bevacizumab in patients with variant histology or sarcomatoid renal cell carcinoma
Authors: Saliby Renee Maria , El Zarif Talal , Bakouny Ziad , Shah Valisha , Xie Wanling , Flippot Ronan , Denize Thomas , Kane M. Harry , Madsen Katrine N. , Ficial Miriam , Hirsch Laure , Wei Xiao X. , Steinarter John A. , Harshman Lauren C. , Vaishampayan Ulka N. , Severgnini Mariano , McDermott David F. , Lee Gwo-Shu Mary. , Xu Wenxin , Van Allen Eliezer M. , McGregor Bradley A. , Signoretti Sabina , Choueiri Toni K. , McKay Rana R. , Braun David A.
Published: September 2024

Supplementary Figure 9
Figure S5 from Circulating and intratumoral immune determinants of response to atezolizumab plus bevacizumab in patients with variant histology or sarcomatoid renal cell carcinoma
Authors: Saliby Renee Maria , El Zarif Talal , Bakouny Ziad , Shah Valisha , Xie Wanling , Flippot Ronan , Denize Thomas , Kane M. Harry , Madsen Katrine N. , Ficial Miriam , Hirsch Laure , Wei Xiao X. , Steinarter John A. , Harshman Lauren C. , Vaishampayan Ulka N. , Severgnini Mariano , McDermott David F. , Lee Gwo-Shu Mary. , Xu Wenxin , Van Allen Eliezer M. , McGregor Bradley A. , Signoretti Sabina , Choueiri Toni K. , McKay Rana R. , Braun David A.
Published: September 2024

Supplementary Figure 5
Figure S2 from Circulating and intratumoral immune determinants of response to atezolizumab plus bevacizumab in patients with variant histology or sarcomatoid renal cell carcinoma
Authors: Saliby Renee Maria , El Zarif Talal , Bakouny Ziad , Shah Valisha , Xie Wanling , Flippot Ronan , Denize Thomas , Kane M. Harry , Madsen Katrine N. , Ficial Miriam , Hirsch Laure , Wei Xiao X. , Steinarter John A. , Harshman Lauren C. , Vaishampayan Ulka N. , Severgnini Mariano , McDermott David F. , Lee Gwo-Shu Mary. , Xu Wenxin , Van Allen Eliezer M. , McGregor Bradley A. , Signoretti Sabina , Choueiri Toni K. , McKay Rana R. , Braun David A.
Published: September 2024

Supplementary Figure 2
Figure S12 from Circulating and intratumoral immune determinants of response to atezolizumab plus bevacizumab in patients with variant histology or sarcomatoid renal cell carcinoma
Authors: Saliby Renee Maria , El Zarif Talal , Bakouny Ziad , Shah Valisha , Xie Wanling , Flippot Ronan , Denize Thomas , Kane M. Harry , Madsen Katrine N. , Ficial Miriam , Hirsch Laure , Wei Xiao X. , Steinarter John A. , Harshman Lauren C. , Vaishampayan Ulka N. , Severgnini Mariano , McDermott David F. , Lee Gwo-Shu Mary. , Xu Wenxin , Van Allen Eliezer M. , McGregor Bradley A. , Signoretti Sabina , Choueiri Toni K. , McKay Rana R. , Braun David A.
Published: September 2024

Supplementary Figure 12
Figure S11 from Circulating and intratumoral immune determinants of response to atezolizumab plus bevacizumab in patients with variant histology or sarcomatoid renal cell carcinoma
Authors: Saliby Renee Maria , El Zarif Talal , Bakouny Ziad , Shah Valisha , Xie Wanling , Flippot Ronan , Denize Thomas , Kane M. Harry , Madsen Katrine N. , Ficial Miriam , Hirsch Laure , Wei Xiao X. , Steinarter John A. , Harshman Lauren C. , Vaishampayan Ulka N. , Severgnini Mariano , McDermott David F. , Lee Gwo-Shu Mary. , Xu Wenxin , Van Allen Eliezer M. , McGregor Bradley A. , Signoretti Sabina , Choueiri Toni K. , McKay Rana R. , Braun David A.
Published: September 2024

Supplementary Figure 11
Figure S10 from Circulating and intratumoral immune determinants of response to atezolizumab plus bevacizumab in patients with variant histology or sarcomatoid renal cell carcinoma
Authors: Saliby Renee Maria , El Zarif Talal , Bakouny Ziad , Shah Valisha , Xie Wanling , Flippot Ronan , Denize Thomas , Kane M. Harry , Madsen Katrine N. , Ficial Miriam , Hirsch Laure , Wei Xiao X. , Steinarter John A. , Harshman Lauren C. , Vaishampayan Ulka N. , Severgnini Mariano , McDermott David F. , Lee Gwo-Shu Mary. , Xu Wenxin , Van Allen Eliezer M. , McGregor Bradley A. , Signoretti Sabina , Choueiri Toni K. , McKay Rana R. , Braun David A.
Published: September 2024

Supplementary Figure 10
Table S1 from β-catenin drives butyrophilin-like molecule loss and γδ T-cell exclusion in colon cancer
Authors: Suzuki Toshiyasu , Kilbey Anna , Casa Rodriguez Nuria , Lawlor Amy , Georgakopoulou Anastasia , Hayman Hannah , Yin Swe Kyi Lai , Nordin Anna , Cantù Claudio , Vantourout Pierre , Ridgway Rachel A. , Byrne Ryan M. , Chen Lei , Verzi Michael P. , Gay David M. , Gil Vazquez Ester , Belnoue-Davis Hayley L. , Gilroy Kathryn , Kostner Anne Helene , Kersten Christian , Thuwajit Chanitra , Andersen Ditte K. , Wiesheu Robert , Jandke Anett , Blyth Karen , Roseweir Antonia K. , Leedham Simon J. , Dunne Philip D. , Edwards Joanne , Hayday Adrian , Sansom Owen J. , Coffelt Seth B.
Published: September 2024

Clinicopathological characteristics of colon cancer patient cohorts.
Figure S6 from β-catenin drives butyrophilin-like molecule loss and γδ T-cell exclusion in colon cancer
Authors: Suzuki Toshiyasu , Kilbey Anna , Casa Rodriguez Nuria , Lawlor Amy , Georgakopoulou Anastasia , Hayman Hannah , Yin Swe Kyi Lai , Nordin Anna , Cantù Claudio , Vantourout Pierre , Ridgway Rachel A. , Byrne Ryan M. , Chen Lei , Verzi Michael P. , Gay David M. , Gil Vazquez Ester , Belnoue-Davis Hayley L. , Gilroy Kathryn , Kostner Anne Helene , Kersten Christian , Thuwajit Chanitra , Andersen Ditte K. , Wiesheu Robert , Jandke Anett , Blyth Karen , Roseweir Antonia K. , Leedham Simon J. , Dunne Philip D. , Edwards Joanne , Hayday Adrian , Sansom Owen J. , Coffelt Seth B.
Published: September 2024

Identification of a WNT responsive element (WRE) in the HNF4G genomic locus.
Data from HDAC3 inhibition promotes anti-tumor immunity by enhancing CXCL10 mediated chemotaxis and recruiting of immune cells
Authors: Li Lili , Hao Shumin , Gao Meiling , Liu Junxiao , Xu Xin , Huang Jianfei , Cheng Genhong , Yang Heng
Published: September 2024

Abstract
It is generally believed that histone deacetylase (HDAC) inhibitors, which represent a new class of anti-cancer agents, exert their anti-tumor activity by directly causing cell cycle arrest and apoptosis of tumor cells. However, in this study, we demonstrated that class I HDAC inhibitors, such as Entinostat and Panobinostat, effectively suppressed tumor growth in immunocompetent but not immunodeficient mice. Further studies with Hdac1, 2, or 3 knockout tumor cells indicated that tumor-specific inactivation of HDAC3 suppressed tumor growth by activating anti-tumor immunity. Specifically, we found that HDAC3 could directly bind to promotor regions and inhibit the expression of CXCL9, 10, and 11 chemokines. Hdac3-deficient tumor cells expressed high levels of these chemokines, which suppressed tumor growth in immunocompetent mice by recruiting CXCR3+ T cells into the tumor microenvironment (TME). Furthermore, the inverse correlation between HDAC3 and CXCL10 expression in hepatocellular carcinoma (HCC) tumor tissues also suggested HDAC3 might be involved in anti-tumor immune regulation and patient survival. Thus, our studies have illustrated that HDAC3 inhibition suppresses tumor growth by enhancing immune cell infiltration into the TME. This anti-tumor mechanism may be helpful in guiding HDAC3 inhibitor-based treatment.
Data from EBV-upregulated B7-H3 inhibits NK cell–mediated antitumor function and contributes to nasopharyngeal carcinoma progression
Authors: Chen Haiwen , Duan Xiaobing , Deng Xiaohong , Huang Yingping , Zhou Xiang , Zhang Shanshan , Zhang Xiao , Liu Pingjuan , Yang Chaopin , Liu Guojun , Ren Qinqin , Xiong Yan , Zhu Bo , Zhang Jiexia , Xiang Tong
Published: September 2024

Abstract
Nasopharyngeal carcinoma (NPC) is an Epstein–Barr virus (EBV)-associated epithelial malignancy characterized by the presence of prominent infiltration of lymphocytes, including natural killer (NK) cells. Although NK cells can directly target EBV-infected tumor cells without restriction by the MHC, EBV+ NPC cells often develop resistance mechanisms that allow them to evade immune surveillance by NK cells. Elucidating the mechanisms involved in EBV-induced NK-cell dysfunction will contribute to the design of novel NK cell–based immunotherapies to treat NPC. Herein, we confirmed that the cytotoxic function of NK cells was impaired in EBV-positive NPC tissues and found that EBV infection–induced expression of B7-H3 in NPC negatively correlated with NK-cell function. The inhibitory effect of EBV+ tumor expression of B7-H3 on NK-cell function was clarified in vitro and in vivo. Mechanistically, activation of the PI3K/AKT/mTOR signaling pathway via EBV latent membrane protein 1 (LMP1) was responsible for EBV infection–induced upregulation of B7-H3 expression. In an NPC xenograft mouse model with adoptive transfer of primary NK cells, deletion of B7-H3 on tumor cells in combination with anti–PD-L1 treatment restored NK cell–mediated antitumor activity and significantly improved the antitumor efficacy of NK cells. Based on our findings, we conclude that EBV infection can inhibit NK cell–mediated antitumor function by inducing upregulation of B7-H3 expression and provide a rationale for NK cell–based immunotherapies in combination of PD-L1 blockade and overcoming the immunosuppression of B7-H3 to treat EBV-associated NPC.
Data from The immunopeptidome from a genomic perspective: Establishing the non-canonical landscape of MHC class I–associated peptides
Authors: Bedran Georges , Gasser Hans-Christof , Weke Kenneth , Wang Tongjie , Bedran Dominika , Laird Alexander , Battail Christophe , Zanzotto Fabio Massimo , Pesquita Catia , Axelson Håkan , Rajan Ajitha , Harrison David J. , Palkowski Aleksander , Pawlik Maciej , Parys Maciej , O'Neill J Robert. , Brennan Paul M. , Symeonides Stefan N. , Goodlett David R. , Litchfield Kevin , Fahraeus Robin , Hupp Ted R. , Kote Sachin , Alfaro Javier A.
Published: September 2024

Abstract
Tumor antigens can emerge through multiple mechanisms, including translation of non-coding genomic regions. This non-canonical category of antigens has recently gained attention; however, our understanding of how they recur within and between cancer types is still in its infancy. Therefore, we developed a proteogenomic pipeline based on deep learning de novo mass spectrometry to enable the discovery of non-canonical MHC-associated peptides (ncMAPs) from non-coding regions. Considering that the emergence of tumor antigens can also involve post-translational modifications, we included an open search component in our pipeline. Leveraging the wealth of mass spectrometry-based immunopeptidomics, we analyzed 26 MHC class I immunopeptidomic studies of 9 different cancer types. We validated the de novo identified ncMAPs, along with the most abundant post-translational modifications, using spectral matching and controlled their false discovery rate (FDR) to 1%. Interestingly, the non-canonical presentation appeared to be 5 times enriched for the A03 HLA supertype, with a projected population coverage of 54.85%. Here, we reveal an atlas of 8,601 ncMAPs with varying levels of cancer selectivity and suggest 17 cancer-selective ncMAPs as attractive targets according to a stringent cutoff. In summary, the combination of the open-source pipeline and the atlas of ncMAPs reported herein could facilitate the identification and screening of ncMAPs as targeting agents for T-cell therapies or vaccine development.
Table S1 from HTLV-1 bZIP factor-induced reprogramming of lactate metabolism and epigenetic status promote leukemic cell expansion
Authors: Toyoda Kosuke , Yasunaga Jun-ichirou , Shichijo Takafumi , Arima Yuichiro , Tsujita Kenichi , Tanaka Azusa , Salah Tarig , Zhang Wenyi , Hussein Osama , Sonoda Miyu , Watanabe Miho , Kurita Daisuke , Nakashima Kazutaka , Yamada Kyohei , Miyoshi Hiroaki , Ohshima Koichi , Matsuoka Masao
Published: September 2024

Human cluster 2 genes whose H3K27me3 in TSS’s was decreased.
Figure S6 from HTLV-1 bZIP factor-induced reprogramming of lactate metabolism and epigenetic status promote leukemic cell expansion
Authors: Toyoda Kosuke , Yasunaga Jun-ichirou , Shichijo Takafumi , Arima Yuichiro , Tsujita Kenichi , Tanaka Azusa , Salah Tarig , Zhang Wenyi , Hussein Osama , Sonoda Miyu , Watanabe Miho , Kurita Daisuke , Nakashima Kazutaka , Yamada Kyohei , Miyoshi Hiroaki , Ohshima Koichi , Matsuoka Masao
Published: September 2024

Efficacy of the MCT1/4 inhibitor syrosingopine on ATL cells.
Figure S3 from HTLV-1 bZIP factor-induced reprogramming of lactate metabolism and epigenetic status promote leukemic cell expansion
Authors: Toyoda Kosuke , Yasunaga Jun-ichirou , Shichijo Takafumi , Arima Yuichiro , Tsujita Kenichi , Tanaka Azusa , Salah Tarig , Zhang Wenyi , Hussein Osama , Sonoda Miyu , Watanabe Miho , Kurita Daisuke , Nakashima Kazutaka , Yamada Kyohei , Miyoshi Hiroaki , Ohshima Koichi , Matsuoka Masao
Published: September 2024

Regulation of TP73 by BATF3 and IRF4.
Table S5 from A SINGLE-CELL TAXONOMY PREDICTS INFLAMMATORY NICHE REMODELING TO DRIVE TISSUE FAILURE AND OUTCOME IN HUMAN AML
Authors: Chen Lanpeng , Pronk Eline , van Dijk Claire , Bian Yujie , Feyen Jacqueline , van Tienhoven Tim , Yildirim Meltem , Pisterzi Paola , De Jong Madelon M E. , Bastidas Alejandro , Hoogenboezem Remco M. , Wevers Chiel , Bindels Eric M. , Löwenberg Bob , Cupedo Tom , Sanders Mathijs A. , Raaijmakers Marc HGP.
Published: September 2024

Table S5 Differentially expressed genes in residual normal/pre-leukemic HSCs in AML vs. HSCs from NBM (scRNAseq)
Table S2 from A SINGLE-CELL TAXONOMY PREDICTS INFLAMMATORY NICHE REMODELING TO DRIVE TISSUE FAILURE AND OUTCOME IN HUMAN AML
Authors: Chen Lanpeng , Pronk Eline , van Dijk Claire , Bian Yujie , Feyen Jacqueline , van Tienhoven Tim , Yildirim Meltem , Pisterzi Paola , De Jong Madelon M E. , Bastidas Alejandro , Hoogenboezem Remco M. , Wevers Chiel , Bindels Eric M. , Löwenberg Bob , Cupedo Tom , Sanders Mathijs A. , Raaijmakers Marc HGP.
Published: September 2024

Table S2 Differentially expressed genes in the HSC (low-output) cluster 0 vs. (high-output) HSC/MPP clusters 1-4
Table S1 from A SINGLE-CELL TAXONOMY PREDICTS INFLAMMATORY NICHE REMODELING TO DRIVE TISSUE FAILURE AND OUTCOME IN HUMAN AML
Authors: Chen Lanpeng , Pronk Eline , van Dijk Claire , Bian Yujie , Feyen Jacqueline , van Tienhoven Tim , Yildirim Meltem , Pisterzi Paola , De Jong Madelon M E. , Bastidas Alejandro , Hoogenboezem Remco M. , Wevers Chiel , Bindels Eric M. , Löwenberg Bob , Cupedo Tom , Sanders Mathijs A. , Raaijmakers Marc HGP.
Published: September 2024

Table S1 patient characteristics
Figure 4 from Synergistic Effects of PARP Inhibition and Cholesterol Biosynthesis Pathway Modulation
Authors: Rutkowska Anna , Eberl H. Christian , Werner Thilo , Hennrich Marco L. , Sévin Daniel C. , Petretich Massimo , Reddington James P. , Pocha Shirin , Gade Stephan , Martinez-Segura Amalia , Dvornikov Dmytro , Karpiak Joel , Sweetman Gavain M.A. , Fufezan Christian , Duempelfeld Birgit , Braun Florian , Schofield Christopher , Keles Hakan , Alvarado David , Wang Zhuo , Jansson Keith H. , Faelth-Savitski Maria , Curry Edward , Remlinger Katja , Stronach Euan A. , Feng Bin , Sharma Geeta , Coleman Kevin , Grandi Paola , Bantscheff Marcus , Bergamini Giovanna
Published: September 2024

Co-inhibition of PARP and cholesterol biosynthesis pathway improves efficiency in tumor cell killing. A, Viability (ATP levels) of HCC70 triple-negative breast cancer (TNBC) cell line after 7-day treatment with niraparib (6.25 μmol/L) and olaparib (6.25 μmol/L) as a single agent or in combination with LSS inhibitor Ro-48-8071 (300 nmol/L). Mean (n = 3) for four independent biological experiments is shown (linear mixed-effect model with TukeyHSD contrasts, ****, P ≤ 0.0001). Niraparib is more efficient than olaparib in reducing cell viability. Addition of an LSS inhibitor improves both niraparib and especially olaparib efficiency in reducing the viability and makes both inhibitors comparable. B, 3-D surface Bliss synergy response for niraparib–atorvastatin and olaparib–atorvastatin combinations after 7-day treatment in MDA-MB-231 TNBC cell line. Red indicates the region of synergy, and green indicates the region of antagonism. Representative of three independent biological experiments (each n = 3) is shown as well as the mean BSmatrix and P value reported (see Supplementary Fig. S5F and S5G for details including other replicates and statistical analysis). Both combinations with lipophilic atorvastatin resulted in a significant synergistic response (significance criteria: mean BSmatrix > 3, P < 0.05). C, 3D surface Bliss synergy response for niraparib–pravastatin, details as in B. Combination with hydrophilic pravastatin shows no synergy. D, 3D surface Bliss synergy response for niraparib–atorvastatin combination after 7-day treatment in HGS1 (HUB-19-C2-008) patient-derived ovarian cancer organoids (n = 4). This combination resulted in significant synergy (see Supplementary Fig. S5H for details). E, Model: inhibition of PARP combined with inhibition of cholesterol biosynthesis pathway (e.g., through the niraparib off-target activity on LSS or by combination with LSS inhibitors or more strongly with HMGCR inhibitors such as lipophilic statins) can result in increased cell death of tumors subtypes, which depend on steroid metabolism, like TNBC and/or highly metastatic tumors.
Data from Synergistic Effects of PARP Inhibition and Cholesterol Biosynthesis Pathway Modulation
Authors: Rutkowska Anna , Eberl H. Christian , Werner Thilo , Hennrich Marco L. , Sévin Daniel C. , Petretich Massimo , Reddington James P. , Pocha Shirin , Gade Stephan , Martinez-Segura Amalia , Dvornikov Dmytro , Karpiak Joel , Sweetman Gavain M.A. , Fufezan Christian , Duempelfeld Birgit , Braun Florian , Schofield Christopher , Keles Hakan , Alvarado David , Wang Zhuo , Jansson Keith H. , Faelth-Savitski Maria , Curry Edward , Remlinger Katja , Stronach Euan A. , Feng Bin , Sharma Geeta , Coleman Kevin , Grandi Paola , Bantscheff Marcus , Bergamini Giovanna
Published: September 2024

Abstract
An in-depth multiomic molecular characterization of PARP inhibitors revealed a distinct poly-pharmacology of niraparib (Zejula) mediated by its interaction with lanosterol synthase (LSS), which is not observed with other PARP inhibitors. Niraparib, in a similar way to the LSS inhibitor Ro-48-8071, induced activation of the 24,25-epoxysterol shunt pathway, which is a regulatory signaling branch of the cholesterol biosynthesis pathway. Interestingly, the combination of an LSS inhibitor with a PARP inhibitor that does not bind to LSS, such as olaparib, had an additive effect on killing cancer cells to levels comparable with niraparib as a single agent. In addition, the combination of PARP inhibitors and statins, inhibitors of 3-hydroxy-3-methylglutaryl-coenzyme A reductase, an enzyme catalyzing the rate-limiting step in the mevalonate pathway, had a synergistic effect on tumor cell killing in cell lines and patient-derived ovarian tumor organoids. These observations suggest that concomitant inhibition of the cholesterol biosynthesis pathway and PARP activity might result in stronger efficacy of these inhibitors against tumor types highly dependent on cholesterol metabolism.
Significance:
The presented data indicate, to our knowledge, for the first time, the potential benefit of concomitant modulation of cholesterol biosynthesis pathway and PARP inhibition and highlight the need for further investigation to assess its translational relevance.
The Impact of Age and Body Composition on the Agreement between Estimated and Measured GFR in Heart Transplant Recipients
Authors: Hornum Mads , Jørgensen Morten Buus , Sidenius Nelson Lærke Marie , Feldt-Rasmussen Bo , Rossing Kasper , Porrini Esteban , Oturai Peter , Gustafsson Finn
Published: September 2024

Background: Estimated GFR (eGFR) has shown poor agreement with measured GFR (mGFR) in several populations. We investigated the impact of age and body composition on the accuracy and precision of eGFR in heart transplant (HTx) recipients. Methods: In a longitudinal, observational, retrospective study design, patients receiving first-time HTx with at least one registered mGFR value within 15 months after HTx and a corresponding plasma creatinine were included. GFR was measured by 51Cr-EDTA and eGFR calculated by creatinine-based CKD-EPI formula. Results: A total of 150 patients with a total of 723 mGFR measurements were included. During the first year after HTx, mean weight increased by 4.2 kg (CI: 3.2 to 5.1) followed by an annual decrease of 0.35 kg/year (Cl: −0.05 to 0.74). mGFR increased by 7.5 mL/min (Cl: 3.2 to 11.8) the first year but was stable hereafter (0.0 mL/min/year; CI: −1.0 to 1.0). The initial weigh gain and increase in mGFR were most pronounced in patients <45 years. Neither eGFR adjusted nor unadjusted for BSA detected the initial increase in mGFR. At 1 year after HTx, limits of agreement on the Bland-Altman plot were −37.2 to 33.1 mL/min with a bias of −2.1 mL/min (Cl: −5.0 to 0.9). In patients <45 years, eGFR significantly overestimated mGFR by 7.1 mL/min (Cl: 1.0 to 13.2) and showed a significant lower precision than patients >45 years. There was no effect of BMI class, weight, BSA, or change in BMI class on the difference between eGFR and mGFR. Conclusion: eGFR is, on average, accurate but imprecise in HTx patients. The agreement is affected by age but not body composition.
The Study of Pro-Inflammatory Molecules Induced by Genetically and Phenotypically Diverse Strains of Haemophilus influenzae Type a in an in vitro Infection Model
Authors: Huska Brenda , Ferris Courtney , Shahid Zaid , Ulanova Marina
Published: September 2024

Introduction: Haemophilus influenzae type a (Hia) has recently emerged as a cause of invasive disease in North American Indigenous children. Factors determining the outcomes of exposure to the pathogen, from asymptomatic carriage to fatal disease, are poorly understood. The role of innate immune activation in the pathogenesis of invasive Hia disease remains unexplored. We used clinical Hia isolates to determine whether innate immune responses depended on the presence of the capsule, strain genetic background, and abilities to cause invasive disease. Methods: Differentiated THP-1 cells and HL-60 neutrophil-like cells were stimulated with four Hia strains (invasive or noninvasive; encapsulated or nonencapsulated), in comparison to 1 invasive and 1 noninvasive non-typeable H. influenzae. Surface expression of ICAM-1 and CD64 and release of pro-inflammatory cytokines TNF-α and IL-1β were quantified. Results: In vitro Hia infection resulted in robust activation of inflammatory responses in terms of expression of ICAM-1 and release of TNF-α and IL-1β, irrespective of the presence or absence of the capsule, or abilities to cause invasive disease. Inhibition of TLR4 decreased TNF-α release by THP-1 cells stimulated by Hia. Conclusion: Powerful activation of pro-inflammatory responses induced by Hia may contribute to the pathogenesis of invasive Hia disease. As the activation of macrophages and neutrophils did not depend on encapsulation or source of Hia isolation, the functional abilities of phagocytic cells unlikely represent a limiting factor in host defenses. The development of invasive versus noninvasive disease may depend on the functional abilities of the adaptive immune system.
Relationship Between Attitude to Global Risks, Belief in the Paranormal and Self-Efficacy among Students
Authors: Sachkova Marianna E. , Semenova Lidiya E.
Published: September 2024

Background. There is a growing concern about global risks, including among young people in the modern world. At the same time, there also appears information about the wide spread of superstitions and other variants of belief in the paranormal among young people. The appeal to the paranormal occurs primarily in situations of instability and is aimed at reducing anxiety and achieving a sense of security. However, there is still an unspecified question about the nature of the relationship between the attitude to global risks and a number of personal characteristics, including belief in the paranormal and self-efficacy, which in terms of active actions can be considered as the opposite of superstition. Objective. The goal is to identify the specifics of the relationship between attitudes to global risks and the belief in the paranormal and self-efficacy among students. Methods. The empirical research was conducted in an online format using psychodiagnostic techniques: “The scale of belief in the paranormal” by J. Tobacyk in the adaptation of D.S. Grigoriev, “The scale of general self-efficacy” by R. Schwarzer and M. Yerusalem in the adaptation of V.G. Romek, the questionnaire “Attitude to global risks” by T.A. Nestik. Statistically significant connections between the structural components of the attitude to global risks with the variants of belief in the paranormal and the personal evaluation of self-efficacy among students were established. Results. It is found that the attitude of students to global risks is associated with various manifestations of belief in the paranormal. The strongest positive links were found in such components of the attitude to global risks as religious authoritarianism and apocalypticism. On the contrary, negative connections are recorded between the readiness to participate in risk prevention, on the one hand, and faith in predictions and the traditional religious belief of students, on the other hand. A positive relationship between self-efficacy and the cognitive components of the attitude to global risks — optimism and religious authoritarianism — was also found. Conclusions. The results obtained indicate the substantial proximity of religious authoritarianism and apocalypticism with a belief in the supernatural among students. At the same time, general self-efficacy is a personal characteristic associated with optimism and religious authoritarianism as a strategy for preventing global risks and threats.