bluuebunny/crossref_metadata_2025 huggingface dataset:
Data from Osimertinib + Savolitinib to Overcome Acquired MET-Mediated Resistance in Epidermal Growth Factor Receptor–Mutated, MET-Amplified Non–Small Cell Lung Cancer: TATTON
Authors: Hartmaier Ryan J. , Markovets Aleksandra A. , Ahn Myung Ju , Sequist Lecia V. , Han Ji-Youn , Cho Byoung Chul , Yu Helena A. , Kim Sang-We , Yang James Chih-Hsin , Lee Jong-Seok , Su Wu-Chou , Kowalski Dariusz M. , Orlov Sergey , Ren Song , Frewer Paul , Ou Xiaoling , Cross Darren A.E. , Kurian Nisha , Cantarini Mireille , Jänne Pasi A.
Published: April 2023

Abstract
MET-inhibitor and EGFR tyrosine kinase inhibitor (EGFR-TKI) combination therapy could overcome acquired MET-mediated osimertinib resistance. We present the final phase Ib TATTON (NCT02143466) analysis (Part B, n = 138/Part D, n = 42) assessing oral savolitinib 600 mg/300 mg once daily (q.d.) + osimertinib 80 mg q.d. in patients with MET-amplified, EGFR-mutated (EGFRm) advanced non–small cell lung cancer (NSCLC) and progression on prior EGFR-TKI. An acceptable safety profile was observed. In Parts B and D, respectively, objective response rates were 33% to 67% and 62%, and median progression-free survival (PFS) was 5.5 to 11.1 months and 9.0 months. Increased antitumor activity may occur with MET copy number ≥10. EGFRm circulating tumor DNA clearance on treatment predicted longer PFS in patients with detectable baseline ctDNA, while acquired resistance mechanisms to osimertinib + savolitinib were mediated by MET, EGFR, or KRAS alterations.
Significance:
The savolitinib + osimertinib combination represents a promising therapy in patients with MET-amplified/overexpressed, EGFRm advanced NSCLC with disease progression on a prior EGFR-TKI. Acquired resistance mechanisms to this combination include those via MET, EGFR, and KRAS. On-treatment ctDNA dynamics can predict clinical outcomes and may provide an opportunity to inform earlier decision-making.

This article is highlighted in the In This Issue feature, p. 1
Data from A Small Molecule Reacts with the p53 Somatic Mutant Y220C to Rescue Wild-type Thermal Stability
Authors: Guiley Keelan Z. , Shokat Kevan M.
Published: April 2023

Abstract
The transcription factor and tumor suppressor protein p53 is the most frequently mutated and inactivated gene in cancer. Mutations in p53 result in deregulated cell proliferation and genomic instability, both hallmarks of cancer. There are currently no therapies available that directly target mutant p53 to rescue wild-type function. In this study, we identify covalent compsounds that selectively react with the p53 somatic mutant cysteine Y220C and restore wild-type thermal stability.
Significance:
The tumor suppressor p53 is the most mutated gene in cancer, and yet no therapeutics to date directly target the mutated protein to rescue wild-type function. In this study, we identify the first allele-specific compound that selectively reacts with the cysteine p53 Y220C to rescue wild-type thermal stability and gene activation.

See related commentary by Lane and Verma, p. 14.

This article is highlighted in the In This Issue feature, p. 1
Data from Intraventricular B7-H3 CAR T Cells for Diffuse Intrinsic Pontine Glioma: Preliminary First-in-Human Bioactivity and Safety
Authors: Vitanza Nicholas A. , Wilson Ashley L. , Huang Wenjun , Seidel Kristy , Brown Christopher , Gustafson Joshua A. , Yokoyama Jason K. , Johnson Adam J. , Baxter Blake A. , Koning Ryan W. , Reid Aquene N. , Meechan Michael , Biery Matthew C. , Myers Carrie , Rawlings-Rhea Stephanie D. , Albert Catherine M. , Browd Samuel R. , Hauptman Jason S. , Lee Amy , Ojemann Jeffrey G. , Berens Michael E. , Dun Matthew D. , Foster Jessica B. , Crotty Erin E. , Leary Sarah E.S. , Cole Bonnie L. , Perez Francisco A. , Wright Jason N. , Orentas Rimas J. , Chour Tony , Newell Evan W. , Whiteaker Jeffrey R. , Zhao Lei , Paulovich Amanda G. , Pinto Navin , Gust Juliane , Gardner Rebecca A. , Jensen Michael C. , Park Julie R.
Published: April 2023

Abstract
Diffuse intrinsic pontine glioma (DIPG) remains a fatal brainstem tumor demanding innovative therapies. As B7-H3 (CD276) is expressed on central nervous system (CNS) tumors, we designed B7-H3–specific chimeric antigen receptor (CAR) T cells, confirmed their preclinical efficacy, and opened BrainChild-03 (NCT04185038), a first-in-human phase I trial administering repeated locoregional B7-H3 CAR T cells to children with recurrent/refractory CNS tumors and DIPG. Here, we report the results of the first three evaluable patients with DIPG (including two who enrolled after progression), who received 40 infusions with no dose-limiting toxicities. One patient had sustained clinical and radiographic improvement through 12 months on study. Patients exhibited correlative evidence of local immune activation and persistent cerebrospinal fluid (CSF) B7-H3 CAR T cells. Targeted mass spectrometry of CSF biospecimens revealed modulation of B7-H3 and critical immune analytes (CD14, CD163, CSF-1, CXCL13, and VCAM-1). Our data suggest the feasibility of repeated intracranial B7-H3 CAR T-cell dosing and that intracranial delivery may induce local immune activation.
Significance:
This is the first report of repeatedly dosed intracranial B7-H3 CAR T cells for patients with DIPG and includes preliminary tolerability, the detection of CAR T cells in the CSF, CSF cytokine elevations supporting locoregional immune activation, and the feasibility of serial mass spectrometry from both serum and CSF.

This article is highlighted in the In This Issue feature, p. 1
Data from Creating MHC-Restricted Neoantigens with Covalent Inhibitors That Can Be Targeted by Immune Therapy
Authors: Hattori Takamitsu , Maso Lorenzo , Araki Kiyomi Y. , Koide Akiko , Hayman James , Akkapeddi Padma , Bang Injin , Neel Benjamin G. , Koide Shohei
Published: April 2023

Abstract
Intracellular oncoproteins can be inhibited with targeted therapy, but responses are not durable. Immune therapies can be curative, but most oncogene-driven tumors are unresponsive to these agents. Fragments of intracellular oncoproteins can act as neoantigens presented by the major histocompatibility complex (MHC), but recognizing minimal differences between oncoproteins and their normal counterparts is challenging. We have established a platform technology that exploits hapten–peptide conjugates generated by covalent inhibitors to create distinct neoantigens that selectively mark cancer cells. Using the FDA-approved covalent inhibitors sotorasib and osimertinib, we developed “HapImmune” antibodies that bind to drug–peptide conjugate/MHC complexes but not to the free drugs. A HapImmune-based bispecific T-cell engager selectively and potently kills sotorasib-resistant lung cancer cells upon sotorasib treatment. Notably, it is effective against KRASG12C-mutant cells with different HLA supertypes, HLA-A*02 and A*03/11, suggesting loosening of MHC restriction. Our strategy creates targetable neoantigens by design, unifying targeted and immune therapies.
Significance:
Targeted therapies against oncoproteins often have dramatic initial efficacy but lack durability. Immunotherapies can be curative, yet most tumors fail to respond. We developed a generalizable technology platform that exploits hapten–peptides generated by covalent inhibitors as neoantigens presented on MHC to enable engineered antibodies to selectively kill drug-resistant cancer cells.

See related commentary by Cox et al., p. 19.

This article is highlighted in the In This Issue feature, p. 1
Data from Cell Competition Shapes Metastatic Latency and Relapse
Authors: Kim Kangsan , Huang Huocong , Parida Pravat Kumar , He Lan , Marquez-Palencia Mauricio , Reese Tanner C. , Kapur Payal , Brugarolas James , Brekken Rolf A. , Malladi Srinivas
Published: April 2023

Abstract
Cell competition, a fitness-sensing process, is essential for tissue homeostasis. Using cancer metastatic latency models, we show that cell competition results in the displacement of latent metastatic (Lat-M) cells from the primary tumor. Lat-M cells resist anoikis and survive as residual metastatic disease. A memodeled extracellular matrix facilitates Lat-M cell displacement and survival in circulation. Disrupting cell competition dynamics by depleting secreted protein and rich in cysteine (SPARC) reduced displacement from orthotopic tumors and attenuated metastases. In contrast, depletion of SPARC after extravasation in lung-resident Lat-M cells increased metastatic outgrowth. Furthermore, multiregional transcriptomic analyses of matched primary tumors and metachronous metastases from patients with kidney cancer identified tumor subclones with Lat-M traits. Kidney cancer enriched for these Lat-M traits had a rapid onset of metachronous metastases and significantly reduced disease-free survival. Thus, an unexpected consequence of cell competition is the displacement of cells with Lat-M potential, thereby shaping metastatic latency and relapse.
Significance:
We demonstrate that cell competition within the primary tumor results in the displacement of Lat-M cells. We further show the impact of altering cell competition dynamics on metastatic incidence that may guide strategies to limit metastatic recurrences.

This article is highlighted in the In This Issue feature, p. 1
Data from The Impact of Inflammation-Induced Tumor Plasticity during Myeloid Transformation
Authors: Yeaton Anna , Cayanan Geraldine , Loghavi Sanam , Dolgalev Igor , Leddin Emmett M. , Loo Christian E. , Torabifard Hedieh , Nicolet Deedra , Wang Jingjing , Corrigan Kate , Paraskevopoulou Varvara , Starczynowski Daniel T , Wang Eric , Abdel-Wahab Omar , Viny Aaron D , Stone Richard M. , Byrd John C. , Guryanova Olga A. , Kohli Rahul M. , Cisneros G. Andrés , Tsirigos Aristotelis , Eisfeld Ann-Kathrin , Aifantis Iannis , Guillamot Maria
Published: April 2023

Abstract
Clonal hematopoiesis (CH) is an aging-associated condition characterized by the clonal outgrowth of mutated preleukemic cells. Individuals with CH are at an increased risk of developing hematopoietic malignancies. Here, we describe a novel animal model carrying a recurrent TET2 missense mutation frequently found in patients with CH and leukemia. In a fashion similar to CH, animals show signs of disease late in life when they develop a wide range of myeloid neoplasms, including acute myeloid leukemia (AML). Using single-cell transcriptomic profiling of the bone marrow, we show that disease progression in aged animals correlates with an enhanced inflammatory response and the emergence of an aberrant inflammatory monocytic cell population. The gene signature characteristic of this inflammatory population is associated with poor prognosis in patients with AML. Our study illustrates an example of collaboration between a genetic lesion found in CH and inflammation, leading to transformation and the establishment of blood neoplasms.
Significance:
Progression from a preleukemic state to transformation, in the presence of TET2 mutations, is coupled with the emergence of inflammation and a novel population of inflammatory monocytes. Genes characteristic of this inflammatory population are associated with the worst prognosis in patients with AML. These studies connect inflammation to progression to leukemia.

See related commentary by Pietras and DeGregori, p. 2234.

This article is highlighted in the In This Issue feature, p. 2221
Data from Escherichia coli–Specific CXCL13-Producing TFH Are Associated with Clinical Efficacy of Neoadjuvant PD-1 Blockade against Muscle-Invasive Bladder Cancer
Authors: Goubet Anne-Gaëlle , Lordello Leonardo , Alves Costa Silva Carolina , Peguillet Isabelle , Gazzano Marianne , Mbogning-Fonkou Maxime Descartes , Thelemaque Cassandra , Lebacle Cédric , Thibault Constance , Audenet François , Pignot Géraldine , Gravis Gwenaelle , Helissey Carole , Campedel Luca , Roupret Morgan , Xylinas Evanguelos , Ouzaid Idir , Dubuisson Agathe , Mazzenga Marine , Flament Caroline , Ly Pierre , Marty Virginie , Signolle Nicolas , Sauvat Allan , Sbarrato Thomas , Filahi Mounia , Davin Caroline , Haddad Gabriel , Bou Khalil Jacques , Bleriot Camille , Danlos François-Xavier , Dunsmore Garett , Mulder Kevin , Silvin Aymeric , Raoult Thibault , Archambaud Baptiste , Belhechmi Shaima , Gomperts Boneca Ivo , Cayet Nadège , Moya-Nilges Maryse , Mallet Adeline , Daillere Romain , Rouleau Etienne , Radulescu Camelia , Allory Yves , Fieschi Jacques , Rouanne Mathieu , Ginhoux Florent , Le Teuff Gwénaël , Derosa Lisa , Marabelle Aurélien , Van Dorp Jeroen , Van Dijk Nick , Van Der Heijden Michiel S. , Besse Benjamin , Andre Fabrice , Merad Miriam , Kroemer Guido , Scoazec Jean-Yves , Zitvogel Laurence , Loriot Yohann
Published: April 2023

Abstract
Biomarkers guiding the neoadjuvant use of immune-checkpoint blockers (ICB) are needed for patients with localized muscle-invasive bladder cancers (MIBC). Profiling tumor and blood samples, we found that follicular helper CD4+ T cells (TFH) are among the best therapeutic targets of pembrolizumab correlating with progression-free survival. TFH were associated with tumoral CD8 and PD-L1 expression at baseline and the induction of tertiary lymphoid structures after pembrolizumab. Blood central memory TFH accumulated in tumors where they produce CXCL13, a chemokine found in the plasma of responders only. IgG4+CD38+ TFH residing in bladder tissues correlated with clinical benefit. Finally, TFH and IgG directed against urothelium-invasive Escherichia coli dictated clinical responses to pembrolizumab in three independent cohorts. The links between tumor infection and success of ICB immunomodulation should be prospectively assessed at a larger scale.
Significance:
In patients with bladder cancer treated with neoadjuvant pembrolizumab, E. coli–specific CXCL13 producing TFH and IgG constitute biomarkers that predict clinical benefit. Beyond its role as a biomarker, such immune responses against E. coli might be harnessed for future therapeutic strategies.

This article is highlighted in the In This Issue feature, p. 2221
Data from Distinct Tumor Necrosis Factor Alpha Receptors Dictate Stem Cell Fitness versus Lineage Output in Dnmt3a-Mutant Clonal Hematopoiesis
Authors: SanMiguel Jennifer M. , Eudy Elizabeth , Loberg Matthew A. , Young Kira A. , Mistry Jayna J. , Mujica Kristina D. , Schwartz Logan S. , Stearns Timothy M. , Challen Grant A. , Trowbridge Jennifer J.
Published: April 2023

Abstract
Clonal hematopoiesis resulting from the enhanced fitness of mutant hematopoietic stem cells (HSC) associates with both favorable and unfavorable health outcomes related to the types of mature mutant blood cells produced, but how this lineage output is regulated is unclear. Using a mouse model of a clonal hematopoiesis–associated mutation, DNMT3AR882/+ (Dnmt3aR878H/+), we found that aging-induced TNFα signaling promoted the selective advantage of mutant HSCs and stimulated the production of mutant B lymphoid cells. The genetic loss of the TNFα receptor TNFR1 ablated the selective advantage of mutant HSCs without altering their lineage output, whereas the loss of TNFR2 resulted in the overproduction of mutant myeloid cells without altering HSC fitness. These results nominate TNFR1 as a target to reduce clonal hematopoiesis and the risk of associated diseases and support a model in which clone size and mature blood lineage production can be independently controlled to modulate favorable and unfavorable clonal hematopoiesis outcomes.
Significance:
Through the identification and dissection of TNFα signaling as a key driver of murine Dnmt3a-mutant hematopoiesis, we report the discovery that clone size and production of specific mature blood cell types can be independently regulated.

See related commentary by Niño and Pietras, p. 2724.

This article is highlighted in the In This Issue feature, p. 2711
Data from Epigenome Programming by H3.3K27M Mutation Creates a Dependence of Pediatric Glioma on SMARCA4
Authors: Mo Yan , Duan Shoufu , Zhang Xu , Hua Xu , Zhou Hui , Wei Hong-Jian , Watanabe Jun , McQuillan Nicholas , Su Zhenyi , Gu Wei , Wu Cheng-Chia , Vakoc Christopher R. , Hashizume Rintaro , Chang Kenneth , Zhang Zhiguo
Published: April 2023

Abstract
Patients with diffuse midline gliomas that are H3K27 altered (DMG) display a dismal prognosis. However, the molecular mechanisms underlying DMG tumorigenesis remain poorly defined. Here we show that SMARCA4, the catalytic subunit of the mammalian SWI/SNF chromatin remodeling complex, is essential for the proliferation, migration, and invasion of DMG cells and tumor growth in patient-derived DMG xenograft models. SMARCA4 colocalizes with SOX10 at gene regulatory elements to control the expression of genes involved in cell growth and the extracellular matrix (ECM). Moreover, SMARCA4 chromatin binding is reduced upon depletion of SOX10 or H3.3K27M, a mutation occurring in about 60% DMG tumors. Furthermore, the SMARCA4 occupancy at enhancers marked by both SOX10 and H3K27 acetylation is reduced the most upon depleting the H3.3K27M mutation. Taken together, our results support a model in which epigenome reprogramming by H3.3K27M creates a dependence on SMARCA4-mediated chromatin remodeling to drive gene expression and the pathogenesis of H3.3K27M DMG.
Significance:
DMG is a deadly pediatric glioma currently without effective treatments. We discovered that the chromatin remodeler SMARCA4 is essential for the proliferation of DMG with H3K27M mutation in vitro and in vivo, identifying a potentially novel therapeutic approach to this disease.

See related commentary by Beytagh and Weiss, p. 2730.

See related article by Panditharatna et al., p. 2880.

This article is highlighted in the In This Issue feature, p. 2711
Data from Efficacy of a Small-Molecule Inhibitor of KrasG12D in Immunocompetent Models of Pancreatic Cancer
Authors: Kemp Samantha B. , Cheng Noah , Markosyan Nune , Sor Rina , Kim Il-Kyu , Hallin Jill , Shoush Jason , Quinones Liz , Brown Natalie V. , Bassett Jared B. , Joshi Nikhil , Yuan Salina , Smith Molly , Vostrejs William P. , Perez-Vale Kia Z. , Kahn Benjamin , Mo Feiyan , Donahue Timothy R. , Radu Caius G. , Clendenin Cynthia , Christensen James G. , Vonderheide Robert H. , Stanger Ben Z.
Published: April 2023

Abstract
Mutations in the KRAS oncogene are found in more than 90% of patients with pancreatic ductal adenocarcinoma (PDAC), with Gly-to-Asp mutations (KRASG12D) being the most common. Here, we tested the efficacy of a small-molecule KRASG12D inhibitor, MRTX1133, in implantable and autochthonous PDAC models with an intact immune system. In vitro studies validated the specificity and potency of MRTX1133. In vivo, MRTX1133 prompted deep tumor regressions in all models tested, including complete or near-complete remissions after 14 days. Concomitant with tumor cell apoptosis and proliferative arrest, drug treatment led to marked shifts in the tumor microenvironment (TME), including changes in fibroblasts, matrix, and macrophages. T cells were necessary for MRTX1133's full antitumor effect, and T-cell depletion accelerated tumor regrowth after therapy. These results validate the specificity, potency, and efficacy of MRTX1133 in immunocompetent KRASG12D-mutant PDAC models, providing a rationale for clinical testing and a platform for further investigation of combination therapies.
Significance:
Pharmacologic inhibition of KRASG12D in pancreatic cancer models with an intact immune system stimulates specific, potent, and durable tumor regressions. In the absence of overt toxicity, these results suggest that this and similar inhibitors should be tested as potential, high-impact novel therapies for patients with PDAC.

See related commentary by Redding and Grabocka, p. 260.

This article is highlighted in the In This Issue feature, p. 247
Data from Geospatial Immune Heterogeneity Reflects the Diverse Tumor–Immune Interactions in Intrahepatic Cholangiocarcinoma
Authors: Lin Youpei , Peng Lihua , Dong Liangqing , Liu Dongbing , Ma Jiaqiang , Lin Jian , Chen Xiaofang , Lin Penghui , Song Guohe , Zhang Mao , Liu Yuming , Rao Junhua , Wei Chen , Lu Ye , Zhang Shu , Ding Guangyu , Peng Zhenyu , Lu Haorong , Wang Xiaoying , Zhou Jian , Fan Jia , Wu Kui , Gao Qiang
Published: April 2023

Abstract
Intrahepatic cholangiocarcinoma (iCCA) exhibits extensive intratumoral heterogeneity and an extremely high mortality rate. Here, we performed whole-exome sequencing, RNA sequencing, T-cell receptor (TCR) sequencing, and multiplexed immunofluorescence on 207 tumor regions from 45 patients with iCCA. Over half of iCCA displayed intratumoral heterogeneity of immune infiltration, and iCCA were classified into sparsely, heterogeneously, and highly infiltrated subgroups with distinct immunogenomic characteristics. Sparsely infiltrated tumors displayed active copy-number loss of clonal neoantigens, and heterogeneous immune infiltration played an important role in the subclonal evolution across tumor subregions. Highly infiltrated tumors were characterized by extensive immune activation and a similar TCR repertoire across tumor subregions, but counteracted with T-cell exhaustion and pervasive antigen presentation defects. Notably, FGFR2 mutations and fusions correlated with low mutation burden and reduced immune infiltration. Our work delineated the dynamic tumor–immune interactions and developed a robust classification system to divide patients with iCCA into high and low immune evasion groups with different prognoses.
Significance:
This study elucidates the impact of spatial immune heterogeneity upon tumor evolution of iCCA and reveals distinct immune evasion mechanisms developed in different immune microenvironments, which can be exploited for the development of personalized immunotherapy strategies.

This article is highlighted in the In This Issue feature, p. 2221
Data from Mutant NPM1 Hijacks Transcriptional Hubs to Maintain Pathogenic Gene Programs in Acute Myeloid Leukemia
Authors: Wang Xue Qing David , Fan Dandan , Han Qinyu , Liu Yiman , Miao Hongzhi , Wang Xinyu , Li Qinglan , Chen Dong , Gore Haley , Himadewi Pamela , Pfeifer Gerd P. , Cierpicki Tomasz , Grembecka Jolanta , Su Jianzhong , Chong Shasha , Wan Liling , Zhang Xiaotian
Published: April 2023

Abstract
Nucleophosmin (NPM1) is a ubiquitously expressed nucleolar protein with a wide range of biological functions. In 30% of acute myeloid leukemia (AML), the terminal exon of NPM1 is often found mutated, resulting in the addition of a nuclear export signal and a shift of the protein to the cytoplasm (NPM1c). AMLs carrying this mutation have aberrant expression of the HOXA/B genes, whose overexpression leads to leukemogenic transformation. Here, for the first time, we comprehensively prove that NPM1c binds to a subset of active gene promoters in NPM1c AMLs, including well-known leukemia-driving genes—HOXA/B cluster genes and MEIS1. NPM1c sustains the active transcription of key target genes by orchestrating a transcription hub and maintains the active chromatin landscape by inhibiting the activity of histone deacetylases. Together, these findings reveal the neomorphic function of NPM1c as a transcriptional amplifier for leukemic gene expression and open up new paradigms for therapeutic intervention.
Significance:
NPM1 mutation is the most common mutation in AML, yet the mechanism of how the mutant protein results in AML remains unclear. Here, for the first time, we prove mutant NPM1 directly binds to active chromatin regions and hijacks the transcription of AML-driving genes.

See related article by Uckelmann et al., p. 746.

This article is highlighted in the In This Issue feature, p. 517
Data from Detecting Liver Cancer Using Cell-Free DNA Fragmentomes
Authors: Foda Zachariah H. , Annapragada Akshaya V. , Boyapati Kavya , Bruhm Daniel C. , Vulpescu Nicholas A. , Medina Jamie E. , Mathios Dimitrios , Cristiano Stephen , Niknafs Noushin , Luu Harry T. , Goggins Michael G. , Anders Robert A. , Sun Jing , Meta Shruti H. , Thomas David L. , Kirk Gregory D. , Adleff Vilmos , Phallen Jillian , Scharpf Robert B. , Kim Amy K. , Velculescu Victor E.
Published: April 2023

Abstract
Liver cancer is a major cause of cancer mortality worldwide. Screening individuals at high risk, including those with cirrhosis and viral hepatitis, provides an avenue for improved survival, but current screening methods are inadequate. In this study, we used whole-genome cell-free DNA (cfDNA) fragmentome analyses to evaluate 724 individuals from the United States, the European Union, or Hong Kong with hepatocellular carcinoma (HCC) or who were at average or high-risk for HCC. Using a machine learning model that incorporated multifeature fragmentome data, the sensitivity for detecting cancer was 88% in an average-risk population at 98% specificity and 85% among high-risk individuals at 80% specificity. We validated these results in an independent population. cfDNA fragmentation changes reflected genomic and chromatin changes in liver cancer, including from transcription factor binding sites. These findings provide a biological basis for changes in cfDNA fragmentation in patients with liver cancer and provide an accessible approach for noninvasive cancer detection.
Significance:
There is a great need for accessible and sensitive screening approaches for HCC worldwide. We have developed an approach for examining genome-wide cfDNA fragmentation features to provide a high-performing and cost-effective approach for liver cancer detection.

See related commentary Rolfo and Russo, p. 532.

This article is highlighted in the In This Issue feature, p. 517
Supplementary Tables from Collapse of the Plasmacytoid Dendritic Cell Compartment in Advanced Cutaneous Melanomas by Components of the Tumor Cell Secretome
Authors: Vescovi Raffaella , Monti Matilde , Moratto Daniele , Paolini Lucia , Consoli Francesca , Benerini Luisa , Melocchi Laura , Calza Stefano , Chiudinelli Mariella , Rossi Giulio , Bugatti Mattia , Maio Michele , Fonsatti Ester , Farisoglio Camillo , Simbolo Michele , Almici Camillo , Verardi Rosanna , Scarpa Aldo , Bergese Paolo , Manganoni Ausilia , Facchetti Fabio , Vermi William
Published: April 2023

Supplementary tables
Supplementary Table S5 from Phase II Study of Personalized Peptide Vaccination for Previously Treated Advanced Colorectal Cancer
Authors: Kibe Shiro , Yutani Shigeru , Motoyama Satoru , Nomura Takanobu , Tanaka Natsuki , Kawahara Akihiko , Yamaguchi Tomohiko , Matsueda Satoko , Komatsu Nobukazu , Miura Masatomo , Hinai Yudai , Hattori Satoshi , Yamada Akira , Kage Masayoshi , Itoh Kyogo , Akagi Yoshito , Sasada Tetsuro
Published: April 2023

Multivariate Cox regression analysis for OS.
Supplementary Figure S2 from Phase II Study of Personalized Peptide Vaccination for Previously Treated Advanced Colorectal Cancer
Authors: Kibe Shiro , Yutani Shigeru , Motoyama Satoru , Nomura Takanobu , Tanaka Natsuki , Kawahara Akihiko , Yamaguchi Tomohiko , Matsueda Satoko , Komatsu Nobukazu , Miura Masatomo , Hinai Yudai , Hattori Satoshi , Yamada Akira , Kage Masayoshi , Itoh Kyogo , Akagi Yoshito , Sasada Tetsuro
Published: April 2023

Prognostic significance of increased peptide-specific CTL and/or IgG responses in aCRC patients after PPV.
Suppl Movie 5 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-B7-1 and α-B7-2 antibodies.
Suppl Movie 4 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 subsequent to acute CTLA-4 blockade.
Suppl Movie 1 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 tumors prior to acute CTLA-4 blockade.
Supplementary Tables 1 - 2 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 - 94K, Supplemental Table S1. Binding affinities of anti-CTLA-4 isotypes to murine FcγR proteins as assessed by surface plasmon resonance. Supplemental Table S2. Summary of pharmacokinetic parameters of anti-CTLA4 isotypes following a single intraperitoneal injection at 10 mg/kg in non-tumor bearing C57BL/6 mice.
Supplementary Tables 1 - 4 from JAK2 Expression Is Associated with Tumor-Infiltrating Lymphocytes and Improved Breast Cancer Outcomes: Implications for Evaluating JAK2 Inhibitors
Authors: Miller Chris P. , Thorpe Jason D. , Kortum Amanda N. , Coy Catherine M. , Cheng Wei-Yi , Yang Tai-Hsien Ou , Anastassiou Dimitris , Beatty J. David , Urban Nicole D. , Blau C. Anthony
Published: April 2023

PDF file - 53K, Supplementary Table S1. Taqman Assays. Supplementary Table S2. Characteristics of Patients by Recurrence Status. Supplementary Table S3. Case-Control Study of JAK2 mRNA Levels and Distant Breast Cancer Recurrence. Supplementary Table S4. JAK2 mRNA vs Protein Levels in Primary Breast Tumors.
Supplementary Table 3 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 3: In vivo biodistribution 48h (also see Supplementary Fig. S3A). Statistical differences calculated between anti-CD40 and rat IgG2a and the two administration routes (n=4, Student?s paired t-test).
Supplementary Table 2 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 - 67K, Table 2: In vivo biodistribution 24h (also see Fig. 4B). Statistical differences calculated between anti-CD40 and rat IgG2a and the two administration routes (n=4, Student?s paired t-test).
Supplementary Methods, Figure Legend 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 - 103K
Supplementary Figure 3 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 - 195K, Figure 3. In vivo biodistribution of target organs 48h and 72h post injection of 125I-CD40-specific and 131I-rat IgG2a control antibody.
Supplementary Figure 2 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 - 404K, Figure 2. Retained CD40 specificity after radiolabeling and modulation of CD40 expression as well as immune cell distribution after repeated injections of FGK4.5 in vivo.
Supplemental Figure Legends 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

Legends for supplemental figures
Supplementary Table 1 from Peptide Vaccination in Montanide Adjuvant Induces and GM-CSF Increases CXCR3 and Cutaneous Lymphocyte Antigen Expression by Tumor Antigen–Specific CD8 T Cells
Authors: Clancy-Thompson Eleanor , King Laura K. , Nunnley Lenora D. , Mullins Irene M. , Slingluff Craig L. , Mullins David W.
Published: April 2023

PDF file - 45K, Supplemental Table I: Effect of GM-CSF in vaccine on the expression of CXCR3 and CLA by tetramer-positive CD8+ T cells.
Supplementary Figure 3 from Peptide Vaccination in Montanide Adjuvant Induces and GM-CSF Increases CXCR3 and Cutaneous Lymphocyte Antigen Expression by Tumor Antigen–Specific CD8 T Cells
Authors: Clancy-Thompson Eleanor , King Laura K. , Nunnley Lenora D. , Mullins Irene M. , Slingluff Craig L. , Mullins David W.
Published: April 2023

PDF file - 551K, Supplemental Figure 3: Representative CXCR3 and CLA staining in tetramer-negative cell populations.
Table S2 from Maelstrom Directs Myeloid-Derived Suppressor Cells to Promote Esophageal Squamous Cell Carcinoma Progression via Activation of the Akt1/RelA/IL8 Signaling Pathway
Authors: Li Pupu , Chen Xinfeng , Qin Guohui , Yue Dongli , Zhang Zhen , Ping Yu , Wang Dan , Zhao Xuan , Song Mengjia , Zhao Qitai , Li Jieyao , Liu Shasha , Wang Dong , Zhang Chaoqi , Lian Jingyao , Cao Ling , Li Feng , Huang Lan , Wang Liping , Yang Li , Huang Jianmin , Li Hong , Zhang Bin , Zhang Yi
Published: April 2023

The construct and primer sequences of MAEL used in the study.
Supplementary Figure 1 from Peptide Vaccination in Montanide Adjuvant Induces and GM-CSF Increases CXCR3 and Cutaneous Lymphocyte Antigen Expression by Tumor Antigen–Specific CD8 T Cells
Authors: Clancy-Thompson Eleanor , King Laura K. , Nunnley Lenora D. , Mullins Irene M. , Slingluff Craig L. , Mullins David W.
Published: April 2023

PDF file - 705K, Supplemental Figure 1: Representative gating strategy for the evaluation of patient-derived samples.
Supplementary Figure 5 from Novel Mechanism of Tumor Suppression by Polarity Gene Discs Large 1 (DLG1) Revealed in a Murine Model of Pediatric B-ALL
Authors: Sandoval Gabriel J. , Graham Daniel B. , Gmyrek Grzegorz B. , Akilesh Holly M. , Fujikawa Keiko , Sammut Benedicte , Bhattacharya Deepta , Srivatsan Shuba , Kim Alfred , Shaw Andrey S. , Yang-Iott Katherine , Bassing Craig H. , Duncavage Eric , Xavier Ramnik J. , Swat Wojciech
Published: April 2023

PDF file - 181K, Supplemental Figure 5: Histopathology analysis of lymph node and spleen of p53 KO, DKO, and B6/CTRL mice.
Supplementary Figure 2 from Novel Mechanism of Tumor Suppression by Polarity Gene Discs Large 1 (DLG1) Revealed in a Murine Model of Pediatric B-ALL
Authors: Sandoval Gabriel J. , Graham Daniel B. , Gmyrek Grzegorz B. , Akilesh Holly M. , Fujikawa Keiko , Sammut Benedicte , Bhattacharya Deepta , Srivatsan Shuba , Kim Alfred , Shaw Andrey S. , Yang-Iott Katherine , Bassing Craig H. , Duncavage Eric , Xavier Ramnik J. , Swat Wojciech
Published: April 2023

PDF file - 76K, Supplemental Figure 2: Conditional deletion of Dlg1 results in a developmental "bottleneck" at the C/C' stage of B cell differentiation.
Supplementary Table 1 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 Table 1 with updated patient sample information
Figure S11 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 S11 shows that hGUCY2C-specific 5F9.m28BBz CAR-T cells do not recognize murine GUCY2C.
Supplementary Tables 1 and 2 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 - 51K, These tables show the additional untreated melanoma patients and the antibodies used in flow cytometry
Supplemental Table 2 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 Table 2
Supplemental Figure 3 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 3
Supplemental Figure 2 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 2
Table S1 and S2 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

S1: Staging Classification for AIDS-related KS S2: Kaposi Sarcoma Response Criteria
Table 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

SLN characteristics of patients with 2 SLNs
Figure S6 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

Differences in SLN-resident DCs between patients with and without distant recurrence
Figure S5 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

Differences in frequency and phenotype of skin-derived SLN DCs between patients with and without local recurrence
Sup Figure 1 from Expanded CD56superbrightCD16+ NK Cells from Ovarian Cancer Patients Are Cytotoxic against Autologous Tumor in a Patient-Derived Xenograft Murine Model
Authors: Poznanski Sophie M. , Nham Tina , Chew Marianne V. , Lee Amanda J. , Hammill Joanne A. , Fan Isabella Y. , Butcher Martin , Bramson Jonathan L. , Lee Dean A. , Hirte Hal W. , Ashkar Ali A.
Published: April 2023

Expanded NK cell activation and inhibitory receptor expression with increasing CD56 brightness.
Supplementary Table 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

P815 tumor cell line authentication.
Supplementary Figure 1 from PD-L1 Expression in Triple-Negative Breast Cancer
Authors: Mittendorf Elizabeth A. , Philips Anne V. , Meric-Bernstam Funda , Qiao Na , Wu Yun , Harrington Susan , Su Xiaoping , Wang Ying , Gonzalez-Angulo Ana M. , Akcakanat Argun , Chawla Akhil , Curran Michael , Hwu Patrick , Sharma Padmanee , Litton Jennifer K. , Molldrem Jeffrey J. , Alatrash Gheath
Published: April 2023

PDF file - 30K, Supplementary figure 1. Extent of increased PD-L1 expression following PTEN knockdown. MDA-MB-231 breast cancer cells were treated with interferon-gamma (10 ng/ml) for 48 hours (positive control), or transduced with PTEN shRNA, after which PD-L1 cell surface expression was determined using flow cytometry. The mean ? SD fold-change in MFI of PD-L1 expression for IFN-γ-treated and shRNA-transduced MDA-MB-231 cells was compared to surface PD-L1 expression in untreated cells.
Supplementary Figure 3 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

Characterization of myeloid cells in Luc-E.G7 tumor bearing eyes.
Supplementary Figure legends from Suboptimal T-cell Therapy Drives a Tumor Cell Mutator Phenotype That Promotes Escape from First-Line Treatment
Authors: Evgin Laura , Huff Amanda L. , Kottke Timothy , Thompson Jill , Molan Amy M. , Driscoll Christopher B. , Schuelke Matthew , Shim Kevin G. , Wongthida Phonphimon , Ilett Elizabeth J. , Smith Karen Kaluza , Harris Reuben S. , Coffey Matt , Pulido Jose S. , Pandha Hardev , Selby Peter J. , Harrington Kevin J. , Melcher Alan , Vile Richard G.
Published: April 2023

Suppl Fig legends
Supplementary Figure 1 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 - 395KB, Supplementary Figure 1: Structure of MO-TES391 and KIAA1864 transcripts.
Supplementary Figure 5 from Chimeric Antigen Receptor T Cells with Dissociated Signaling Domains Exhibit Focused Antitumor Activity with Reduced Potential for Toxicity In Vivo
Authors: Lanitis Evripidis , Poussin Mathilde , Klattenhoff Alex W. , Song Degang , Sandaltzopoulos Raphael , June Carl H. , Powell Daniel J.
Published: April 2023

PDF file - 854K, Figure S5. F-28z CART cells produce dramatically less IFN-γ in response to stimulation with A1847 (M+/F-) cells compared to A1847 (M+/F+) cells. A. F-28z CAR expression on human CD3+ T cells upon transduction with lentivirus compared to untransduced T cells. F-28z CART transduced T cells were detected using biotinylated-protein L followed by SA-PE. B. Transduced T cells (1 x 105 T cells) were cultured alone (none) or stimulated overnight with an equal number of either FRa-negative PEO-1 cells or A1847 (M+/F-) cells, or FRa-positive A1847 (M+/F+) cancer cells. Cell-free supernatant was harvested after ~20 hours of incubation and the IFN-γ levels were measured with ELISA. Mean IFN-γ concentration plus-minus SEM (pg/ml) from triplicate cultures is shown. ***P < 0.001 comparing the IFN-γ secretion produced by M-z/F-28 CART cells against A1847M+/F+ versus A1847M+/F- or PEO cells.
Supplementary Table 2 from Antigen-Specific Culture of Memory-like CD8 T Cells for Adoptive Immunotherapy
Authors: Litterman Adam J. , Zellmer David M. , LaRue Rebecca S. , Jameson Stephen C. , Largaespada David A.
Published: April 2023

XLSX - 276K, Supplementary Table 2. Differentially expressed genes between sorted populations of memory cocktail and IL-2 grown OT-I CD8 T cells.
Supplementary Materials and Methods and Supplementary Figure Legends from Retuning of Mouse NK Cells after Interference with MHC Class I Sensing Adjusts Self-Tolerance but Preserves Anticancer Response
Authors: Wagner Arnika Kathleen , Wickström Stina Linnea , Tallerico Rossana , Salam Sadia , Lakshmikanth Tadepally , Brauner Hanna , Höglund Petter , Carbone Ennio , Johansson Maria Helena , Kärre Klas
Published: April 2023

Supplementary Materials and Methods and Supplementary Figure Legends
Supplementary Figure 2 from Retuning of Mouse NK Cells after Interference with MHC Class I Sensing Adjusts Self-Tolerance but Preserves Anticancer Response
Authors: Wagner Arnika Kathleen , Wickström Stina Linnea , Tallerico Rossana , Salam Sadia , Lakshmikanth Tadepally , Brauner Hanna , Höglund Petter , Carbone Ennio , Johansson Maria Helena , Kärre Klas
Published: April 2023

Supplementary Figure 2. Expresssion of MHC class I and activating receptor ligands on RMA and RMA-S.
Supplementary Figure 1 from Retuning of Mouse NK Cells after Interference with MHC Class I Sensing Adjusts Self-Tolerance but Preserves Anticancer Response
Authors: Wagner Arnika Kathleen , Wickström Stina Linnea , Tallerico Rossana , Salam Sadia , Lakshmikanth Tadepally , Brauner Hanna , Höglund Petter , Carbone Ennio , Johansson Maria Helena , Kärre Klas
Published: April 2023

Supplementary Figure 1. Spleen cell number after inhibitory receptor blockade.
Supplementary Figure 3 from Loss of Host Type-I IFN Signaling Accelerates Metastasis and Impairs NK-cell Antitumor Function in Multiple Models of Breast Cancer
Authors: Rautela Jai , Baschuk Nikola , Slaney Clare Y. , Jayatilleke Krishnath M. , Xiao Kun , Bidwell Bradley N. , Lucas Erin C. , Hawkins Edwin D. , Lock Peter , Wong Christina S. , Chen Weisan , Anderson Robin L. , Hertzog Paul J. , Andrews Daniel M. , Möller Andreas , Parker Belinda S.
Published: April 2023

Immune suppressor cell and T lymphocyte accumulation in the peripheral blood of WT and Ifnar1-/- mice.
Supplementary Figure 1 from Loss of Host Type-I IFN Signaling Accelerates Metastasis and Impairs NK-cell Antitumor Function in Multiple Models of Breast Cancer
Authors: Rautela Jai , Baschuk Nikola , Slaney Clare Y. , Jayatilleke Krishnath M. , Xiao Kun , Bidwell Bradley N. , Lucas Erin C. , Hawkins Edwin D. , Lock Peter , Wong Christina S. , Chen Weisan , Anderson Robin L. , Hertzog Paul J. , Andrews Daniel M. , Möller Andreas , Parker Belinda S.
Published: April 2023

Loss of hematopoietic Ifnar1 reduces metastasis-free survival in the 4T1.2 model.
Supplementary Figure Legends from Restoration of miR17/20a in Solid Tumor Cells Enhances the Natural Killer Cell Antitumor Activity by Targeting Mekk2
Authors: Jiang Hong , Wang Ping , Li Xiaohua , Wang Qilong , Deng Zhong-Bin , Zhuang Xiaoying , Mu Jingyao , Zhang Lifeng , Wang Baomei , Yan Jun , Miller Donald , Zhang Huang-Ge
Published: April 2023

PDF file - 194K
Supplementary Table 2 from TCR Sequencing Can Identify and Track Glioma-Infiltrating T Cells after DC Vaccination
Authors: Hsu Melody S. , Sedighim Shaina , Wang Tina , Antonios Joseph P. , Everson Richard G. , Tucker Alexander M. , Du Lin , Emerson Ryan , Yusko Erik , Sanders Catherine , Robins Harlan S. , Yong William H. , Davidson Tom B. , Li Gang , Liau Linda M. , Prins Robert M.
Published: April 2023

TCR Sequencing data of each patient
Supplementary Figure S7 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

Gating strategy for flow cytometry analysis.