bluuebunny/crossref_metadata_2025 huggingface dataset:
Data from Targeting S100A9–ALDH1A1–Retinoic Acid Signaling to Suppress Brain Relapse in EGFR-Mutant Lung Cancer
Authors: Biswas Anup Kumar , Han Seoyoung , Tai Yifan , Ma Wanchao , Coker Courtney , Quinn S. Aidan , Shakri Ahmad Rushdi , Zhong Timothy James , Scholze Hanna , Lagos Galina G. , Mela Angeliki , Manova-Todorova Katia , de Stanchina Elisa , Ferrando Adolfo A. , Mendelsohn Cathy , Canoll Peter , Yu Helena A. , Paik Paul K. , Saqi Anjali , Shu Catherine A. , Kris Mark G. , Massague Joan , Acharyya Swarnali
Published: April 2023

Abstract
The epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI) osimertinib has significantly prolonged progression-free survival (PFS) in patients with EGFR-mutant lung cancer, including those with brain metastases. However, despite striking initial responses, osimertinib-treated patients eventually develop lethal metastatic relapse, often to the brain. Although osimertinib-refractory brain relapse is a major clinical challenge, its underlying mechanisms remain poorly understood. Using metastatic models of EGFR-mutant lung cancer, we show that cancer cells expressing high intracellular S100A9 escape osimertinib and initiate brain relapses. Mechanistically, S100A9 upregulates ALDH1A1 expression and activates the retinoic acid (RA) signaling pathway in osimertinib-refractory cancer cells. We demonstrate that the genetic repression of S100A9, ALDH1A1, or RA receptors (RAR) in cancer cells, or treatment with a pan-RAR antagonist, dramatically reduces brain metastasis. Importantly, S100A9 expression in cancer cells correlates with poor PFS in osimertinib-treated patients. Our study, therefore, identifies a novel, therapeutically targetable S100A9–ALDH1A1–RA axis that drives brain relapse.
Significance:
Treatment with the EGFR TKI osimertinib prolongs the survival of patients with EGFR-mutant lung cancer; however, patients develop metastatic relapses, often to the brain. We identified a novel intracellular S100A9–ALDH1A1–RA signaling pathway that drives lethal brain relapse and can be targeted by pan-RAR antagonists to prevent cancer progression and prolong patient survival.

This article is highlighted in the In This Issue feature, p. 873
Data from Cancer Induces a Stress Ileopathy Depending on β-Adrenergic Receptors and Promoting Dysbiosis that Contributes to Carcinogenesis
Authors: Yonekura Satoru , Terrisse Safae , Alves Costa Silva Carolina , Lafarge Antoine , Iebba Valerio , Ferrere Gladys , Goubet Anne-Gaëlle , Fahrner Jean-Eudes , Lahmar Imran , Ueda Kousuke , Mansouri Gibrail , Pizzato Eugénie , Ly Pierre , Mazzenga Marine , Thelemaque Cassandra , Fidelle Marine , Jaulin Fanny , Cartry Jérôme , Deloger Marc , Aglave Marine , Droin Nathalie , Opolon Paule , Puget Angélique , Mann Fanny , Neunlist Michel , Bessard Anne , Aymeric Laetitia , Matysiak-Budnik Tamara , Bosq Jacques , Hofman Paul , Duong Connie P.M. , Ugolini Sophie , Quiniou Valentin , Berrard Sylvie , Ryffel Bernhard , Kepp Oliver , Kroemer Guido , Routy Bertrand , Lordello Leonardo , Bani Mohamed-Amine , Segata Nicola , Yengej Fjodor Yousef , Clevers Hans , Scoazec Jean-Yves , Pasolli Edoardo , Derosa Lisa , Zitvogel Laurence
Published: April 2023

Abstract
Gut dysbiosis has been associated with intestinal and extraintestinal malignancies, but whether and how carcinogenesis drives compositional shifts of the microbiome to its own benefit remains an open conundrum. Here, we show that malignant processes can cause ileal mucosa atrophy, with villous microvascular constriction associated with dominance of sympathetic over cholinergic signaling. The rapid onset of tumorigenesis induced a burst of REG3γ release by ileal cells, and transient epithelial barrier permeability that culminated in overt and long-lasting dysbiosis dominated by Gram-positive Clostridium species. Pharmacologic blockade of β-adrenergic receptors or genetic deficiency in Adrb2 gene, vancomycin, or cohousing of tumor bearers with tumor-free littermates prevented cancer-induced ileopathy, eventually slowing tumor growth kinetics. Patients with cancer harbor distinct hallmarks of this stress ileopathy dominated by Clostridium species. Hence, stress ileopathy is a corollary disease of extraintestinal malignancies requiring specific therapies.
Significance:
Whether gut dysbiosis promotes tumorigenesis and how it controls tumor progression remain open questions. We show that 50% of transplantable extraintestinal malignancies triggered a β-adrenergic receptor–dependent ileal mucosa atrophy, associated with increased gut permeability, sustained Clostridium spp.–related dysbiosis, and cancer growth. Vancomycin or propranolol prevented cancer-associated stress ileopathy.

This article is highlighted in the In This Issue feature, p. 873
Data from Spatial Positioning and Matrix Programs of Cancer-Associated Fibroblasts Promote T-cell Exclusion in Human Lung Tumors
Authors: Grout John A. , Sirven Philemon , Leader Andrew M. , Maskey Shrisha , Hector Eglantine , Puisieux Isabelle , Steffan Fiona , Cheng Evan , Tung Navpreet , Maurin Mathieu , Vaineau Romain , Karpf Lea , Plaud Martin , Begue Anne-Laure , Ganesh Koushik , Mesple Jérémy , Casanova-Acebes Maria , Tabachnikova Alexandra , Keerthivasan Shilpa , Lansky Alona , Berichel Jessica Le , Walker Laura , Rahman Adeeb H. , Gnjatic Sacha , Girard Nicolas , Lefevre Marine , Damotte Diane , Adam Julien , Martin Jerome C. , Wolf Andrea , Flores Raja M. , Beasley Mary Beth , Pradhan Rachana , Muller Soren , Marron Thomas U. , Turley Shannon J. , Merad Miriam , Kenigsberg Ephraim , Salmon Hélène
Published: April 2023

Abstract
It is currently accepted that cancer-associated fibroblasts (CAF) participate in T-cell exclusion from tumor nests. To unbiasedly test this, we used single-cell RNA sequencing coupled with multiplex imaging on a large cohort of lung tumors. We identified four main CAF populations, two of which are associated with T-cell exclusion: (i) MYH11+αSMA+ CAF, which are present in early-stage tumors and form a single cell layer lining cancer aggregates, and (ii) FAP+αSMA+ CAF, which appear in more advanced tumors and organize in patches within the stroma or in multiple layers around tumor nests. Both populations orchestrate a particular structural tissue organization through dense and aligned fiber deposition compared with T cell–permissive CAF. Yet they produce distinct matrix molecules, including collagen IV (MYH11+αSMA+ CAF) and collagen XI/XII (FAP+αSMA+ CAF). Hereby, we uncovered unique molecular programs of CAF driving T-cell marginalization, whose targeting should increase immunotherapy efficacy in patients bearing T cell–excluded tumors.
Significance:
The cellular and molecular programs driving T-cell marginalization in solid tumors remain unclear. Here, we describe two CAF populations associated with T-cell exclusion in human lung tumors. We demonstrate the importance of pairing molecular and spatial analysis of the tumor microenvironment, a prerequisite to developing new strategies targeting T cell–excluding CAF.

See related commentary by Sherman, p. 2501.

This article is highlighted in the In This Issue feature, p. 2483
Data from Developmental Deconvolution for Classification of Cancer Origin
Authors: Moiso Enrico , Farahani Alexander , Marble Hetal D. , Hendricks Austin , Mildrum Samuel , Levine Stuart , Lennerz Jochen K. , Garg Salil
Published: April 2023

Abstract
Cancer is partly a developmental disease, with malignancies named based on cell or tissue of origin. However, a systematic atlas of tumor origins is lacking. Here we map the single-cell organogenesis of 56 developmental trajectories to the transcriptomes of over 10,000 tumors across 33 cancer types. We deconvolute tumor transcriptomes into signals for individual developmental trajectories. Using these signals as inputs, we construct a developmental multilayer perceptron (D-MLP) classifier that outputs cancer origin. D-MLP (ROC-AUC: 0.974 for top prediction) outperforms benchmark classifiers. We analyze tumors from patients with cancer of unknown primary (CUP), selecting the most difficult cases in which extensive multimodal workup yielded no definitive tumor type. Interestingly, CUPs form groups distinguished by developmental trajectories, and classification reveals diagnosis for patient tumors. Our results provide an atlas of tumor developmental origins, provide a tool for diagnostic pathology, and suggest developmental classification may be a useful approach for patient tumors.
Significance:
Here we map the developmental trajectories of tumors. We deconvolute tumor transcriptomes into signals for mammalian developmental programs and use this information to construct a deep learning classifier that outputs tumor type. We apply the classifier to CUP and reveal the developmental origins of patient tumors.

See related commentary by Wang, p. 2498.

This article is highlighted in the In This Issue feature, p. 2483
Data from The Single-Cell Immunogenomic Landscape of B and Plasma Cells in Early-Stage Lung Adenocarcinoma
Authors: Hao Dapeng , Han Guangchun , Sinjab Ansam , Gomez-Bolanos Lorena Isabel , Lazcano Rossana , Serrano Alejandra , Hernandez Sharia D. , Dai Enyu , Cao Xuanye , Hu Jian , Dang Minghao , Wang Ruiping , Chu Yanshuo , Song Xingzhi , Zhang Jianhua , Parra Edwin R. , Wargo Jennifer A. , Swisher Stephen G. , Cascone Tina , Sepesi Boris , Futreal Andrew P. , Li Mingyao , Dubinett Steven M. , Fujimoto Junya , Solis Soto Luisa M. , Wistuba Ignacio I. , Stevenson Christopher S. , Spira Avrum , Shalapour Shabnam , Kadara Humam , Wang Linghua
Published: April 2023

Abstract
Tumor-infiltrating B and plasma cells (TIB) are prevalent in lung adenocarcinoma (LUAD); however, they are poorly characterized. We performed paired single-cell RNA and B-cell receptor (BCR) sequencing of 16 early-stage LUADs and 47 matching multiregion normal tissues. By integrative analysis of ∼50,000 TIBs, we define 12 TIB subsets in the LUAD and adjacent normal ecosystems and demonstrate extensive remodeling of TIBs in LUADs. Memory B cells and plasma cells (PC) were highly enriched in tumor tissues with more differentiated states and increased frequencies of somatic hypermutation. Smokers exhibited markedly elevated PCs and PCs with distinct differentiation trajectories. BCR clonotype diversity increased but clonality decreased in LUADs, smokers, and with increasing pathologic stage. TIBs were mostly localized within CXCL13+ lymphoid aggregates, and immune cell sources of CXCL13 production evolved with LUAD progression and included elevated fractions of CD4 regulatory T cells. This study provides a spatial landscape of TIBs in early-stage LUAD.
Significance:
While TIBs are highly enriched in LUADs, they are poorly characterized. This study provides a much-needed understanding of the transcriptional, clonotypic states and phenotypes of TIBs, unraveling their potential roles in the immunopathology of early-stage LUADs and constituting a road map for the development of TIB-targeted immunotherapies for the treatment of this morbid malignancy.

This article is highlighted in the In This Issue feature, p. 2483
Data from Molecular Characterization of Acquired Resistance to KRASG12C–EGFR Inhibition in Colorectal Cancer
Authors: Yaeger Rona , Mezzadra Riccardo , Sinopoli Jenna , Bian Yu , Marasco Michelangelo , Kaplun Esther , Gao Yijun , Zhao HuiYong , Paula Arnaud Da Cruz , Zhu Yingjie , Perez Almudena Chaves , Chadalavada Kalyani , Tse Edison , Chowdhry Sudhir , Bowker Sydney , Chang Qing , Qeriqi Besnik , Weigelt Britta , Nanjangud Gouri J. , Berger Michael F. , Der-Torossian Hirak , Anderes Kenna , Socci Nicholas D. , Shia Jinru , Riely Gregory J. , Murciano-Goroff Yonina R. , Li Bob T. , Christensen James G. , Reis-Filho Jorge S. , Solit David B. , de Stanchina Elisa , Lowe Scott W. , Rosen Neal , Misale Sandra
Published: April 2023

Abstract
With the combination of KRASG12C and EGFR inhibitors, KRAS is becoming a druggable target in colorectal cancer. However, secondary resistance limits its efficacy. Using cell lines, patient-derived xenografts, and patient samples, we detected a heterogeneous pattern of putative resistance alterations expected primarily to prevent inhibition of ERK signaling by drugs at progression. Serial analysis of patient blood samples on treatment demonstrates that most of these alterations are detected at a low frequency except for KRASG12C amplification, a recurrent resistance mechanism that rises in step with clinical progression. Upon drug withdrawal, resistant cells with KRASG12C amplification undergo oncogene-induced senescence, and progressing patients experience a rapid fall in levels of this alteration in circulating DNA. In this new state, drug resumption is ineffective as mTOR signaling is elevated. However, our work exposes a potential therapeutic vulnerability, whereby therapies that target the senescence response may overcome acquired resistance.
Significance:
Clinical resistance to KRASG12C–EGFR inhibition primarily prevents suppression of ERK signaling. Most resistance mechanisms are subclonal, whereas KRASG12C amplification rises over time to drive a higher portion of resistance. This recurrent resistance mechanism leads to oncogene-induced senescence upon drug withdrawal and creates a potential vulnerability to senolytic approaches.

This article is highlighted in the In This Issue feature, p. 1
Data from Natural Coevolution of Tumor and Immunoenvironment in Glioblastoma
Authors: Wu Lingxiang , Wu Wei , Zhang Junxia , Zhao Zheng , Li Liangyu , Zhu Mengyan , Wu Min , Wu Fan , Zhou Fengqi , Du Yuxin , Chai Rui-Chao , Zhang Wei , Qiu Xiaoguang , Liu Quanzhong , Wang Ziyu , Li Jie , Li Kening , Chen Apeng , Jiang Yinan , Xiao Xiangwei , Zou Han , Srivastava Rashmi , Zhang Tingting , Cai Yun , Liang Yuan , Huang Bin , Zhang Ruohan , Lin Fan , Hu Lang , Wang Xiuxing , Qian Xu , Lv Sali , Hu Baoli , Zheng Siyuan , Hu Zhibin , Shen Hongbing , You Yongping , Verhaak Roel G.W. , Jiang Tao , Wang Qianghu
Published: April 2023

Abstract
Isocitrate dehydrogenase (IDH) wild-type glioblastoma (GBM) has a dismal prognosis. A better understanding of tumor evolution holds the key to developing more effective treatment. Here we study GBM's natural evolutionary trajectory by using rare multifocal samples. We sequenced 61,062 single cells from eight multifocal IDH wild-type primary GBMs and defined a natural evolution signature (NES) of the tumor. We show that the NES significantly associates with the activation of transcription factors that regulate brain development, including MYBL2 and FOSL2. Hypoxia is involved in inducing NES transition potentially via activation of the HIF1A–FOSL2 axis. High-NES tumor cells could recruit and polarize bone marrow–derived macrophages through activation of the FOSL2–ANXA1–FPR1/3 axis. These polarized macrophages can efficiently suppress T-cell activity and accelerate NES transition in tumor cells. Moreover, the polarized macrophages could upregulate CCL2 to induce tumor cell migration.
Significance:
GBM progression could be induced by hypoxia via the HIF1A–FOSL2 axis. Tumor-derived ANXA1 is associated with recruitment and polarization of bone marrow–derived macrophages to suppress the immunoenvironment. The polarized macrophages promote tumor cell NES transition and migration.

This article is highlighted in the In This Issue feature, p. 2711
Data from Reprogrammed Schwann Cells Organize into Dynamic Tracks that Promote Pancreatic Cancer Invasion
Authors: Deborde Sylvie , Gusain Laxmi , Powers Ann , Marcadis Andrea , Yu Yasong , Chen Chun-Hao , Frants Anna , Kao Elizabeth , Tang Laura H. , Vakiani Efsevia , Amisaki Masataka , Balachandran Vinod P. , Calo Annalisa , Omelchenko Tatiana , Jessen Kristjan R. , Reva Boris , Wong Richard J.
Published: April 2023

Abstract
Nerves are a component of the tumor microenvironment contributing to cancer progression, but the role of cells from nerves in facilitating cancer invasion remains poorly understood. Here we show that Schwann cells (SC) activated by cancer cells collectively function as tumor-activated Schwann cell tracks (TAST) that promote cancer cell migration and invasion. Nonmyelinating SCs form TASTs and have cell gene expression signatures that correlate with diminished survival in patients with pancreatic ductal adenocarcinoma. In TASTs, dynamic SCs form tracks that serve as cancer pathways and apply forces on cancer cells to enhance cancer motility. These SCs are activated by c-Jun, analogous to their reprogramming during nerve repair. This study reveals a mechanism of cancer cell invasion that co-opts a wound repair process and exploits the ability of SCs to collectively organize into tracks. These findings establish a novel paradigm of how cancer cells spread and reveal therapeutic opportunities.
Significance:
How the tumor microenvironment participates in pancreatic cancer progression is not fully understood. Here, we show that SCs are activated by cancer cells and collectively organize into tracks that dynamically enable cancer invasion in a c-Jun–dependent manner.

See related commentary by Amit and Maitra, p. 2240.

This article is highlighted in the In This Issue feature, p. 2221
Data from A Molecular Switch between Mammalian MLL Complexes Dictates Response to Menin–MLL Inhibition
Authors: Soto-Feliciano Yadira M. , Sánchez-Rivera Francisco J. , Perner Florian , Barrows Douglas W. , Kastenhuber Edward R. , Ho Yu-Jui , Carroll Thomas , Xiong Yijun , Anand Disha , Soshnev Alexey A. , Gates Leah , Beytagh Mary Clare , Cheon David , Gu Shengqing , Liu X. Shirley , Krivtsov Andrei V. , Meneses Maximiliano , de Stanchina Elisa , Stone Richard M. , Armstrong Scott A. , Lowe Scott W. , Allis C. David
Published: April 2023

Abstract
Menin interacts with oncogenic MLL1-fusion proteins, and small molecules that disrupt these associations are in clinical trials for leukemia treatment. By integrating chromatin-focused and genome-wide CRISPR screens with genetic, pharmacologic, and biochemical approaches, we discovered a conserved molecular switch between the MLL1–Menin and MLL3/4–UTX chromatin-modifying complexes that dictates response to Menin–MLL inhibitors. MLL1–Menin safeguards leukemia survival by impeding the binding of the MLL3/4–UTX complex at a subset of target gene promoters. Disrupting the Menin–MLL1 interaction triggers UTX-dependent transcriptional activation of a tumor-suppressive program that dictates therapeutic responses in murine and human leukemia. Therapeutic reactivation of this program using CDK4/6 inhibitors mitigates treatment resistance in leukemia cells that are insensitive to Menin inhibitors. These findings shed light on novel functions of evolutionarily conserved epigenetic mediators like MLL1–Menin and MLL3/4–UTX and are relevant to understand and target molecular pathways determining therapeutic responses in ongoing clinical trials.
Significance:
Menin–MLL inhibitors silence a canonical HOX- and MEIS1-dependent oncogenic gene expression program in leukemia. We discovered a parallel, noncanonical transcriptional program involving tumor suppressor genes that are repressed in Menin–MLL inhibitor–resistant leukemia cells but that can be reactivated upon combinatorial treatment with CDK4/6 inhibitors to augment therapy responses.

This article is highlighted in the In This Issue feature, p. 1
Data from CD19/CD20 Bispecific Chimeric Antigen Receptor (CAR) in Naive/Memory T Cells for the Treatment of Relapsed or Refractory Non-Hodgkin Lymphoma
Authors: Larson Sarah M. , Walthers Christopher M. , Ji Brenda , Ghafouri Sanaz N. , Naparstek Jacob , Trent Jacqueline , Chen Jia Ming , Roshandell Mobina , Harris Caitlin , Khericha Mobina , Schweppe Thomas , Berent-Maoz Beata , Gosliner Stanley B. , Almaktari Amr , Ceja Melanie Ayala , Allen-Auerbach Martin S. , Said Jonathan , Nawaly Karla , Mead Monica , de Vos Sven , Young Patricia A. , Oliai Caspian , Schiller Gary J. , Timmerman John M. , Ribas Antoni , Chen Yvonne Y.
Published: April 2023

Abstract
To address antigen escape and loss of T-cell functionality, we report a phase I clinical trial (NCT04007029) evaluating autologous naive and memory T (TN/MEM) cells engineered to express a bispecific anti-CD19/CD20 chimeric antigen receptor (CAR; CART19/20) for patients with relapsed/refractory non-Hodgkin lymphoma (NHL), with safety as the primary endpoint. Ten patients were treated with 36 × 106 to 165 × 106 CART19/20 cells. No patient experienced neurotoxicity of any grade or over grade 1 cytokine release syndrome. One case of dose-limiting toxicity (persistent cytopenia) was observed. Nine of 10 patients achieved objective response [90% overall response rate (ORR)], with seven achieving complete remission [70% complete responses (CR) rate]. One patient relapsed after 18 months in CR but returned to CR after receiving a second dose of CART19/20 cells. Median progression-free survival was 18 months and median overall survival was not reached with a 17-month median follow-up. In conclusion, CART19/20 TN/MEM cells are safe and effective in patients with relapsed/refractory NHL, with durable responses achieved at low dosage levels.
Significance:
Autologous CD19/CD20 bispecific CAR-T cell therapy generated from TN/MEM cells for patients with NHL is safe (no neurotoxicity, maximum grade 1 cytokine release syndrome) and demonstrates strong efficacy (90% ORR, 70% CR rate) in a first-in-human, phase I dose-escalation trial.

This article is highlighted in the In This Issue feature, p. 517
C/EBPα Confers Dependence to Fatty Acid Anabolic Pathways and Vulnerability to Lipid Oxidative Stress–Induced Ferroptosis inFLT3-Mutant Leukemia
Authors: Sabatier Marie , Birsen Rudy , Lauture Laura , Mouche Sarah , Angelino Paolo , Dehairs Jonas , Goupille Léa , Boussaid Ismael , Heiblig Maël , Boet Emeline , Sahal Ambrine , Saland Estelle , Santos Juliana C. , Armengol Marc , Fernández-Serrano Miranda , Farge Thomas , Cognet Guillaume , Simonetta Federico , Pignon Corentin , Graffeuil Antoine , Mazzotti Céline , Avet-Loiseau Hervé , Delos Océane , Bertrand-Michel Justine , Chedru Amélie , Dembitz Vilma , Gallipoli Paolo , Anstee Natasha S. , Loo Sun , Wei Andrew H. , Carroll Martin , Goubard Armelle , Castellano Rémy , Collette Yves , Vergez François , Mansat-De Mas Véronique , Bertoli Sarah , Tavitian Suzanne , Picard Muriel , Récher Christian , Bourges-Abella Nathalie , Granat Fanny , Kosmider Olivier , Sujobert Pierre , Colsch Benoit , Joffre Carine , Stuani Lucille , Swinnen Johannes V. , Guillou Hervé , Roué Gael , Hakim Nawad , Dejean Anne S. , Tsantoulis Petros , Larrue Clément , Bouscary Didier , Tamburini Jerome , Sarry Jean-Emmanuel
Published: April 2023

Although transcription factor CCAAT-enhancer binding protein α (C/EBPα) is critical for normal and leukemic differentiation, its role in cell and metabolic homeostasis is largely unknown in cancer. Here, multiomics analyses uncovered a coordinated activation of C/EBPα 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/EBPα regulated the fatty acid synthase (FASN)–stearoyl-CoA desaturase (SCD) axis to promote fatty acid (FA) biosynthesis and desaturation. We further demonstrated that FLT3 or C/EBPα inactivation decreased monounsaturated 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/EBPα function in lipid homeostasis and adaptation to redox stress, and a previously unreported vulnerability of FLT3-mutant AML to ferroptosis with promising therapeutic application.

Significance:

FLT3 mutations are found in 30% of AML cases and are actionable by tyrosine kinase inhibitors. Here, we discovered that C/EBPα regulates FA biosynthesis and protection from lipid redox stress downstream mutant-FLT3 signaling, which confers a vulnerability to ferroptosis upon FLT3 inhibition with therapeutic potential in AML.

This article is highlighted in the In This Issue feature, p. 1501
Suppl Movie 3 from Cytotoxic T Lymphocyte Antigen-4 Blockade Enhances Antitumor Immunity by Stimulating Melanoma-Specific T-cell Motility
Authors: Pentcheva-Hoang Tsvetelina , Simpson Tyler R. , Montalvo-Ortiz Welby , Allison James P.
Published: April 2023

Pmel-1 dynamics in TDLN prior to acute CTLA-4 blockade.
Suppl Movie 13 from Cytotoxic T Lymphocyte Antigen-4 Blockade Enhances Antitumor Immunity by Stimulating Melanoma-Specific T-cell Motility
Authors: Pentcheva-Hoang Tsvetelina , Simpson Tyler R. , Montalvo-Ortiz Welby , Allison James P.
Published: April 2023

Pmel-1 dynamics in TDLN prior to injection of α-CTLA-4 Fab fragments.
Supplementary Figures 1 - 4 from Anti-CTLA-4 Antibodies of IgG2a Isotype Enhance Antitumor Activity through Reduction of Intratumoral Regulatory T Cells
Authors: Selby Mark J. , Engelhardt John J. , Quigley Michael , Henning Karla A. , Chen Timothy , Srinivasan Mohan , Korman Alan J.
Published: April 2023

PDF file - 206K, Supplemental Figure S1. Equivalent binding of anti-CTLA-4 isotypes to cell surface CTLA-4. Supplemental Figure S2. Serum concentrations of anti-CTLA-4 isotypes in C57BL/6 mice. Supplemental Figure S3. Representative FACS plots for peripheral regulatory T cells. Supplemental Figure S4. A. Representative FACS plots for intratumoral regulatory T cells. B. Kinetics of intratumoral Treg reduction following anti-CTLA-4 treatment. Supplemental Figure S5. Isotype-dependent recruitment of MDSCs and IL-1α production.
Supplementary Table 1 from Locally Delivered CD40 Agonist Antibody Accumulates in Secondary Lymphoid Organs and Eradicates Experimental Disseminated Bladder Cancer
Authors: Sandin Linda C. , Orlova Anna , Gustafsson Erika , Ellmark Peter , Tolmachev Vladimir , Tötterman Thomas H. , Mangsbo Sara M.
Published: April 2023

PDF file - 68K, Table 1: In vivo biodistribution 4h (also see Fig. 4A). Statistical differences calculated between anti-CD40 and rat IgG2a and the two administration routes (n=4, Student?s paired t-test).
Figure S4 from Programmed Cell Death Ligand 1 (PD-L1) Signaling Regulates Macrophage Proliferation and Activation
Authors: Hartley Genevieve P. , Chow Lyndah , Ammons Dylan T. , Wheat William H. , Dow Steven W.
Published: April 2023

Supplemental Figure S4. Control antibody treatments for macrophage proliferation and co-stimulatory molecule expression. Macrophages were incubated with irrelevant isotype antibody, macrophage-specific antibody (CD11b), Fc-blocking antibody, or pre-treated with Fc-blocking antibody before treatment with PD-L1 antibody. After 48 hours, proliferation measured by EdU incorporation and surface expression of co-stimulatory molecules (CD86 and MHC II) was compared by flow cytometry with two-way ANOVA and Prism7 software. Statistically significant differences were denoted as P-value **** < 0.0001, and similar results were obtained in 2 independent experiments.
Supplementary Figures 1 - 3 from MEK Inhibition, Alone or in Combination with BRAF Inhibition, Affects Multiple Functions of Isolated Normal Human Lymphocytes and Dendritic Cells
Authors: Vella Laura J. , Pasam Anupama , Dimopoulos Nektaria , Andrews Miles , Knights Ashley , Puaux Anne-Laure , Louahed Jamila , Chen Weisan , Woods Katherine , Cebon Jonathan S.
Published: April 2023

PDF file - 376K, Supplementary Figure 1. Representative flow cytometry data of T-cell proliferation. Supplementary Figure 2. Gating strategy for T-lymphocyte cytokine production. Supplementary Figure 3. Gating strategy for antigen specific T-lymphocytes.
Supplementary Figure Legends from MEK Inhibition, Alone or in Combination with BRAF Inhibition, Affects Multiple Functions of Isolated Normal Human Lymphocytes and Dendritic Cells
Authors: Vella Laura J. , Pasam Anupama , Dimopoulos Nektaria , Andrews Miles , Knights Ashley , Puaux Anne-Laure , Louahed Jamila , Chen Weisan , Woods Katherine , Cebon Jonathan S.
Published: April 2023

PDF file - 79K
Supplementary Table 1 from Assessment of MAGE-A Expression in Resected Non–Small Cell Lung Cancer in Relation to Clinicopathologic Features and Mutational Status of EGFR and KRAS
Authors: Ayyoub Maha , Memeo Lorenzo , Álvarez-Fernández Emilio , Colarossi Cristina , Costanzo Rosario , Aiello Eleonora , Martinetti Daniela , Valmori Danila
Published: April 2023

PDF file - 35K, MAGE-A expression score in NSCLC and correlation with tumor grade and disease stage.
Supplementary Figures from Computational Immune Monitoring Reveals Abnormal Double-Negative T Cells Present across Human Tumor Types
Authors: Greenplate Allison R. , McClanahan Daniel D. , Oberholtzer Brian K. , Doxie Deon B. , Roe Caroline E. , Diggins Kirsten E. , Leelatian Nalin , Rasmussen Megan L. , Kelley Mark C. , Gama Vivian , Siska Peter J. , Rathmell Jeffrey C. , Ferrell P. Brent , Johnson Douglas B. , Irish Jonathan M.
Published: April 2023

Supplementary figures S1-S7.
Figure S6 from Human GUCY2C-Targeted Chimeric Antigen Receptor (CAR)-Expressing T Cells Eliminate Colorectal Cancer Metastases
Authors: Magee Michael S. , Abraham Tara S. , Baybutt Trevor R. , Flickinger John C. , Ridge Natalie A. , Marszalowicz Glen P. , Prajapati Priyanka , Hersperger Adam R. , Waldman Scott A. , Snook Adam E.
Published: April 2023

Figure S6 shows activation marker upregulation by 5F9.m28BBz CAR-T cells stimulated by CT26.hGUCY2C cells.
Figure S3 from Human GUCY2C-Targeted Chimeric Antigen Receptor (CAR)-Expressing T Cells Eliminate Colorectal Cancer Metastases
Authors: Magee Michael S. , Abraham Tara S. , Baybutt Trevor R. , Flickinger John C. , Ridge Natalie A. , Marszalowicz Glen P. , Prajapati Priyanka , Hersperger Adam R. , Waldman Scott A. , Snook Adam E.
Published: April 2023

Figure S3 shows the murine CAR construct sequence used in the paper.
Supplementary Figure 2 from Role of Crosslinking for Agonistic CD40 Monoclonal Antibodies as Immune Therapy of Cancer
Authors: Richman Lee P. , Vonderheide Robert H.
Published: April 2023

PDF file - 72K, Supplementary Figure 2. Dose-dependent B cell activation with CP-870,893 and its F(ab)'2 fragment.
Supplementary Figure 3 from Ipilimumab Treatment Results in an Early Decrease in the Frequency of Circulating Granulocytic Myeloid-Derived Suppressor Cells as well as Their Arginase1 Production
Authors: de Coaña Yago Pico , Poschke Isabel , Gentilcore Giusy , Mao Yumeng , Nyström Maria , Hansson Johan , Masucci Giuseppe V. , Kiessling Rolf
Published: April 2023

PDF file - 213K, This figure shows the gating strategy used for analyzing the arginase staining
Supplemental Figure 1 from PD-L1 microSPECT/CT Imaging for Longitudinal Monitoring of PD-L1 Expression in Syngeneic and Humanized Mouse Models for Cancer
Authors: Heskamp Sandra , Wierstra Peter J. , Molkenboer-Kuenen Janneke D.M. , Sandker Gerwin W. , Thordardottir Soley , Cany Jeannette , Olive Daniel , Bussink Johan , Boerman Otto C. , Dolstra Harry , Aarntzen Erik H.J.G. , Hobo Willemijn A.
Published: April 2023

Supplemental Figure 1
Figure S1 from Successful Treatment of HIV-Associated Kaposi Sarcoma with Immune Checkpoint Blockade
Authors: Galanina Natalie , Goodman Aaron M. , Cohen Philip R. , Frampton Garrett M. , Kurzrock Razelle
Published: April 2023

CONSORT diagram
Table S2 from Phase I Trial of Autologous CAR T Cells Targeting NKG2D Ligands in Patients with AML/MDS and Multiple Myeloma
Authors: Baumeister Susanne H. , Murad Joana , Werner Lillian , Daley Heather , Trebeden-Negre Helene , Gicobi Joanina K. , Schmucker Adam , Reder Jake , Sentman Charles L. , Gilham David E. , Lehmann Frédéric F. , Galinsky Ilene , DiPietro Heidi , Cummings Kristen , Munshi Nikhil C. , Stone Richard M. , Neuberg Donna S. , Soiffer Robert , Dranoff Glenn , Ritz Jerome , Nikiforow Sarah
Published: April 2023

Patient therapy details
Table S1 from Phase I Trial of Autologous CAR T Cells Targeting NKG2D Ligands in Patients with AML/MDS and Multiple Myeloma
Authors: Baumeister Susanne H. , Murad Joana , Werner Lillian , Daley Heather , Trebeden-Negre Helene , Gicobi Joanina K. , Schmucker Adam , Reder Jake , Sentman Charles L. , Gilham David E. , Lehmann Frédéric F. , Galinsky Ilene , DiPietro Heidi , Cummings Kristen , Munshi Nikhil C. , Stone Richard M. , Neuberg Donna S. , Soiffer Robert , Dranoff Glenn , Ritz Jerome , Nikiforow Sarah
Published: April 2023

Antibody details
Supplementary Figures 1 - 2 from mTOR Inhibition Improves Antitumor Effects of Vaccination with Antigen-Encoding RNA
Authors: Diken Mustafa , Kreiter Sebastian , Vascotto Fulvia , Selmi Abderraouf , Attig Sebastian , Diekmann Jan , Huber Christoph , Türeci Özlem , Sahin Ugur
Published: April 2023

PDF file - 1926K, Description of effects of Rapamycin on CD8 T cell phenotype.
Supplementary Figure 1 from Splenectomy Promotes Indirect Elimination of Intraocular Tumors by CD8+ T Cells That Is Associated with IFNγ- and Fas/FasL-Dependent Activation of Intratumoral Macrophages
Authors: Miller Maxine R. , Mandell Jonathan B. , Beatty Kelly M. , Harvey Stephen A.K. , Rizzo Michael J. , Previte Dana M. , Thorne Stephen H. , McKenna Kyle C.
Published: April 2023

Measurement of Intraocular Tumor Growth.
Supplementary Figure 2 from Immune Consequences of Decreasing Tumor Vasculature with Antiangiogenic Tyrosine Kinase Inhibitors in Combination with Therapeutic Vaccines
Authors: Farsaci Benedetto , Donahue Renee N. , Coplin Michael A. , Grenga Italia , Lepone Lauren M. , Molinolo Alfredo A. , Hodge James W.
Published: April 2023

Examples of 2 different grades of tumor compactness in MC38-CEA tumors.
Data Supplement from Quantitative Effect of Natural Killer–Cell Licensing on Hepatocellular Carcinoma Recurrence after Curative Hepatectomy
Authors: Tanimine Naoki , Tanaka Yuka , Kobayashi Tsuyoshi , Tashiro Hirotaka , Miki Daiki , Imamura Michio , Aikata Hiroshi , Tanaka Junko , Chayama Kazuaki , Ohdan Hideki
Published: April 2023

One hundred seventy HCC patients who underwent curative hepatectomy were enrolled based on the following inclusion criteria: presence of histologically confirmed HCC; preserved preoperative liver function (Child-Pugh grade A); no residual tumor after surgery; and no evidence of comorbid malignant tumor. Background characteristics and prognoses of the patients and tumors are summarized.
Data Supplement from Quantitative Effect of Natural Killer–Cell Licensing on Hepatocellular Carcinoma Recurrence after Curative Hepatectomy
Authors: Tanimine Naoki , Tanaka Yuka , Kobayashi Tsuyoshi , Tashiro Hirotaka , Miki Daiki , Imamura Michio , Aikata Hiroshi , Tanaka Junko , Chayama Kazuaki , Ohdan Hideki
Published: April 2023

KIR and HLA genotyping was performed using the reverse SSP-PCR method. Presence of the HLA ligand for KIR was determined according to the HLA genotypes.
Data Supplement from Quantitative Effect of Natural Killer–Cell Licensing on Hepatocellular Carcinoma Recurrence after Curative Hepatectomy
Authors: Tanimine Naoki , Tanaka Yuka , Kobayashi Tsuyoshi , Tashiro Hirotaka , Miki Daiki , Imamura Michio , Aikata Hiroshi , Tanaka Junko , Chayama Kazuaki , Ohdan Hideki
Published: April 2023

The effect of each compound genotype (KIR2DL1-C2, KIR2DL2-C1, KIR3DL1-BW4, and KIR3DL2-A3/11) on 5-year OS was analyzed by propensity score-matched studies using nine variables (age, sex, etiology, tumor number, maximum diameter, histological differentiation, vascular invasion, satellite lesion, and surgical margin). The 5-year OS was compared between one-to-two or two-to-one patient pairs with or without each compound KIR-HLA genotype. (A) KIR2DL1-C2; (B) KIR2DL2-C1; (C) KIR3DL1-Bw4; and (D) KIR3DL2-A3/11.
Supplemental Figure 1 legend from Leveraging TCR Affinity in Adoptive Immunotherapy against Shared Tumor/Self-Antigens
Authors: Miller Aaron M. , Bahmanof Milad , Zehn Dietmar , Cohen Ezra E.W. , Schoenberger Stephen P.
Published: April 2023

Legend for supplementary Figure 1 in Word format
Supplementary Table 3 from Alternative Variants of Human HYDIN Are Novel Cancer-Associated Antigens Recognized by Adaptive Immunity
Authors: Laske Karoline , Shebzukhov Yuriy V. , Grosse-Hovest Ludger , Kuprash Dmitry V. , Khlgatian Svetlana V. , Koroleva Ekaterina P. , Sazykin Alexey Y. , Penkov Dmitry N. , Belousov Pavel V. , Stevanović Stefan , Vass Verona , Walter Steffen , Eisel David , Schmid-Horch Barbara D. , Nedospasov Sergei A. , Rammensee Hans-Georg , Gouttefangeas Cécile
Published: April 2023

PDF - 49KB, Supplementary Table 3: Epitope prediction for HLA-A*02 binding peptides derived from KIAA1864 and MO-TES391.
Supplementary Table 2 from Alternative Variants of Human HYDIN Are Novel Cancer-Associated Antigens Recognized by Adaptive Immunity
Authors: Laske Karoline , Shebzukhov Yuriy V. , Grosse-Hovest Ludger , Kuprash Dmitry V. , Khlgatian Svetlana V. , Koroleva Ekaterina P. , Sazykin Alexey Y. , Penkov Dmitry N. , Belousov Pavel V. , Stevanović Stefan , Vass Verona , Walter Steffen , Eisel David , Schmid-Horch Barbara D. , Nedospasov Sergei A. , Rammensee Hans-Georg , Gouttefangeas Cécile
Published: April 2023

PDF - 61KB, Supplementary Table 2: Primers used in the study.
Figure S2 from Melanoma Sequentially Suppresses Different DC Subsets in the Sentinel Lymph Node, Affecting Disease Spread and Recurrence
Authors: van den Hout Mari F.C.M. , Koster Bas D. , Sluijter Berbel J.R. , Molenkamp Barbara G. , van de Ven Rieneke , van den Eertwegh Alfons J.M. , Scheper Rik J. , van Leeuwen Paul A.M. , van den Tol M. Petrousjka , de Gruijl Tanja D.
Published: April 2023

Flowcytometric gating strategies for dendritic cells in the melanoma sentinel lymph node
Supplementary data from Simultaneous Targeting of FcγRs and FcαRI Enhances Tumor Cell Killing
Authors: Brandsma Arianne M. , ten Broeke Toine , Nederend Maaike , Meulenbroek Laura A.P.M. , van Tetering Geert , Meyer Saskia , Jansen J.H. Marco , Beltrán Buitrago M. Alejandra , Nagelkerke Sietse Q. , Németh István , Ubink Ruud , Rouwendal Gerard , Lohse Stefan , Valerius Thomas , Leusen Jeanette H.W. , Boross Peter
Published: April 2023

Supplementary figure legends and Tables
Supplementary figure S2 from Broadening Specificity and Enhancing Cytotoxicity of Adoptive T Cells for Nasopharyngeal Carcinoma Immunotherapy
Authors: Faè Damiana Antonia , Martorelli Debora , Mastorci Katy , Muraro Elena , Dal Col Jessica , Franchin Giovanni , Barzan Luigi , Comaro Elisa , Vaccher Emanuela , Rosato Antonio , Dolcetti Riccardo
Published: April 2023

Supplementary figure describing: the release of EBV virionic DNA by LCLs treted with the various drugs; the lysis of DX-CTLS of targets expressing EBNA-1 or LMP2 epitope peptides; the effects of the various drugs used on the differentiaition of CD28+ efector memory T cells.
Supplementary Materials & Methods from Broadening Specificity and Enhancing Cytotoxicity of Adoptive T Cells for Nasopharyngeal Carcinoma Immunotherapy
Authors: Faè Damiana Antonia , Martorelli Debora , Mastorci Katy , Muraro Elena , Dal Col Jessica , Franchin Giovanni , Barzan Luigi , Comaro Elisa , Vaccher Emanuela , Rosato Antonio , Dolcetti Riccardo
Published: April 2023

Supplementary Material and Methods including patients and donors, generation of HLA-A*0201-expressing c666.1 NPC cells, quantitative Real-time PCR, immunoblotting, cytotoxicity assays, HMGB1-release quantification and TLR-4 neutralization experiments. Supplementary Table 1 listing of PCR primer sequence is also included.
Supplementary Figure S4 from Rational Combination of Immunotherapies with Clinical Efficacy in Mice with Advanced Cancer
Authors: Bransi Ali , Salgado Oscar Camilo , Beffinger Michal , Milo Karim , Silina Karina , Yagita Hideo , Becher Burkhard , Knuth Alexander , van den Broek Maries
Published: April 2023

Administration of anti-CD40 + IL-2 complexes + IL-12Fc improves local and systemic tumor-specific immunity.
Figure S2 from Extracellular S100A9 Protein in Bone Marrow Supports Multiple Myeloma Survival by Stimulating Angiogenesis and Cytokine Secretion
Authors: De Veirman Kim , De Beule Nathan , Maes Ken , Menu Eline , De Bruyne Elke , De Raeve Hendrik , Fostier Karel , Moreaux Jérôme , Kassambara Alboukadel , Hose Dirk , Heusschen Roy , Eriksson Helena , Vanderkerken Karin , Van Valckenborgh Els
Published: April 2023

ABR-238901 treatment reduced IL-10 expression in MM cells in vivo.
Supplementary Tables S1 through S3 from The Intratumoral Balance between Metabolic and Immunologic Gene Expression Is Associated with Anti–PD-1 Response in Patients with Renal Cell Carcinoma
Authors: Ascierto Maria Libera , McMiller Tracee L. , Berger Alan E. , Danilova Ludmila , Anders Robert A. , Netto George J. , Xu Haiying , Pritchard Theresa S. , Fan Jinshui , Cheadle Chris , Cope Leslie , Drake Charles G. , Pardoll Drew M. , Taube Janis M. , Topalian Suzanne L.
Published: April 2023

Supplementary Table S1: PD-L1+ RCC specimens used in this study. Supplementary Table S2: Genes differentially expressed in RCC based on whole genome microarray analysis, in patients responding or not to anti-PD-1 therapy (234 probe sets corresponding to 223 genes). Supplementary Table S3: Sixty genes included in custom multiplex qRT-PCR array to assess candidates from RCC whole genome microarray profiling.
Supplementary Materials and Methods from The Intratumoral Balance between Metabolic and Immunologic Gene Expression Is Associated with Anti–PD-1 Response in Patients with Renal Cell Carcinoma
Authors: Ascierto Maria Libera , McMiller Tracee L. , Berger Alan E. , Danilova Ludmila , Anders Robert A. , Netto George J. , Xu Haiying , Pritchard Theresa S. , Fan Jinshui , Cheadle Chris , Cope Leslie , Drake Charles G. , Pardoll Drew M. , Taube Janis M. , Topalian Suzanne L.
Published: April 2023

Supplementary Materials and Methods
ntary Methods, Figure Legends from TLR7 Ligand Augments GM-CSF–Initiated Antitumor Immunity through Activation of Plasmacytoid Dendritic Cells
Authors: Narusawa Megumi , Inoue Hiroyuki , Sakamoto Chika , Matsumura Yumiko , Takahashi Atsushi , Inoue Tomoko , Watanabe Ayumi , Miyamoto Shohei , Miura Yoshie , Hijikata Yasuki , Tanaka Yoshihiro , Inoue Makoto , Takayama Koichi , Okazaki Toshihiko , Hasegawa Mamoru , Nakanishi Yoichi , Tani Kenzaburo
Published: April 2023

PDF file - 146K
Supplementary Figures 1 - 9, Table 1 from Microtubule-Depolymerizing Agents Used in Antibody–Drug Conjugates Induce Antitumor Immunity by Stimulation of Dendritic Cells
Authors: Müller Philipp , Martin Kea , Theurich Sebastian , Schreiner Jens , Savic Spasenija , Terszowski Grzegorz , Lardinois Didier , Heinzelmann-Schwarz Viola A. , Schlaak Max , Kvasnicka Hans-Michael , Spagnoli Giulio , Dirnhofer Stephan , Speiser Daniel E. , von Bergwelt-Baildon Michael , Zippelius Alfred
Published: April 2023

PDF file - 2651K, Supp. Fig. 1. Dolastatins induce phenotypic DC maturation in vitro. Supp. Fig. 2. Dolastatins induce phenotypic and functional maturation of BM-DCs in vitro. Supp. Fig. 3. Immuno-stimulatory effect of dolastatin 10 is independent of MyD88 signaling. Supp. Fig. 4. Dolastatin-induced DC homing is limited to tumor-draining LNs. Supp. Fig. 5. Dolastatin 10 treatment requires intact host immunity for full therapeutic efficacy. Supp. Fig. 6. Dolastatin 10 treatment synergizes with tumor-antigen-specific vaccination. Supp. Fig. 7. Combined effects of Dolastatin 10 and anti-CTLA-4/PD-1 treatment on tumor infiltrating lymphocyte subsets. Supp. Fig. 8. MMAE induces phenotypic and functional maturation in murine and human DCs. Supp. Fig. 9. Anti-Thy1.1-MMAE ADC-induced DC homing is limited to tumor-draining LNs. Supp. Table 1. Tumor histology and CD86/MHC-II up-regulation on intratumoral CD11c+ DCs upon treatment with Dolastatin 10, MMAE and LPS.
Supplementary Fig. S1 from Regulatory T Cells from Colon Cancer Patients Inhibit Effector T-cell Migration through an Adenosine-Dependent Mechanism
Authors: Sundström Patrik , Stenstad Hanna , Langenes Veronica , Ahlmanner Filip , Theander Lisa , Ndah Tapuka Gordon , Fredin Kamilla , Börjesson Lars , Gustavsson Bengt , Bastid Jérémy , Quiding-Järbrink Marianne
Published: April 2023

This supplementary figure shows the gating strategy to analyze T cell transendothelial migration (A), and the migration of CD4+ (B) and CD8+ T cells (C) after endothelial activation.
Supplemental Figure 1 from Neutrophils Increase Oral Squamous Cell Carcinoma Invasion through an Invadopodia-Dependent Pathway
Authors: Glogauer Judah E. , Sun Chun X. , Bradley Grace , Magalhaes Marco A.O.
Published: April 2023

UMSCC1 and UMSCC47 invasion. Transwell assays were performed as described previously (19). Briefly, 50,000 UMSCC1 or UMSCC47 cells were resuspended in 250 Î¼l 10% FBS/DMEM and plated in the upper chamber. The bottom chamber was filled with 1 ml 10% FBS/DMEM. Where indicated, 50,000 neutrophils (1:1 ratio) were added to the bottom chamber. A- Comparison between UMSCC1 and UMSCC47 baseline invasion without neutrophils. B- UMSCC1 invasion in the presence of neutrophils (indirect co-culture). Results shown are normalized to control.
Supplementary Dataset from Rational Selection of Syngeneic Preclinical Tumor Models for Immunotherapeutic Drug Discovery
Authors: Mosely Suzanne I.S. , Prime John E. , Sainson Richard C.A. , Koopmann Jens-Oliver , Wang Dennis Y.Q. , Greenawalt Danielle M. , Ahdesmaki Miika J. , Leyland Rebecca , Mullins Stefanie , Pacelli Luciano , Marcus Danielle , Anderton Judith , Watkins Amanda , Coates Ulrichsen Jane , Brohawn Philip , Higgs Brandon W. , McCourt Matthew , Jones Hazel , Harper James A. , Morrow Michelle , Valge-Archer Viia , Stewart Ross , Dovedi Simon J. , Wilkinson Robert W.
Published: April 2023

Supplementary dataset containing raw data from targeted sequencing, whole exome sequencing, array CGH and transcriptomic analysis
Supplementary Methods and Figure Legends from Mast Cells Boost Myeloid-Derived Suppressor Cell Activity and Contribute to the Development of Tumor-Favoring Microenvironment
Authors: Danelli Luca , Frossi Barbara , Gri Giorgia , Mion Francesca , Guarnotta Carla , Bongiovanni Lucia , Tripodo Claudio , Mariuzzi Laura , Marzinotto Stefania , Rigoni Alice , Blank Ulrich , Colombo Mario P. , Pucillo Carlo E.
Published: April 2023

Supplemental material and figure legend
Supplemental Figure 5 from Inhibition of Fatty Acid Oxidation Modulates Immunosuppressive Functions of Myeloid-Derived Suppressor Cells and Enhances Cancer Therapies
Authors: Hossain Fokhrul , Al-Khami Amir A. , Wyczechowska Dorota , Hernandez Claudia , Zheng Liqin , Reiss Krzystoff , Valle Luis Del , Trillo-Tinoco Jimena , Maj Tomasz , Zou Weiping , Rodriguez Paulo C. , Ochoa Augusto C.
Published: April 2023

Supplemental Figure 5: FAO inhibitors do not affect the activation and function of T cells.
Supplementary Figure Legends from Optimization of Peptide Vaccines to Induce Robust Antitumor CD4 T-cell Responses
Authors: Kumai Takumi , Lee Sujin , Cho Hyun-Il , Sultan Hussein , Kobayashi Hiroya , Harabuchi Yasuaki , Celis Esteban
Published: April 2023

File contains the supplemental figure legends
Supplementary Fig. S3 from Salmonella-Based Therapy Targeting Indoleamine 2,3-Dioxygenase Coupled with Enzymatic Depletion of Tumor Hyaluronan Induces Complete Regression of Aggressive Pancreatic Tumors
Authors: Manuel Edwin R. , Chen Jeremy , D'Apuzzo Massimo , Lampa Melanie G. , Kaltcheva Teodora I. , Thompson Curtis B. , Ludwig Thomas , Chung Vincent , Diamond Don J.
Published: April 2023

Key replicate treatment groups (A) Replicate IVIS images of key treatment groups emphasizing reproducibility of treatment in KPC orthotopic model. Numbers above images represent days post-tumor implantation. (B) Quantitation of IVIS luciferase signal for individual mice in key groups represented in Fig. 1A and Supplementary Fig. S3A.