bluuebunny/crossref_metadata_2025 huggingface dataset:
Data from Genomes for Kids: The Scope of Pathogenic Mutations in Pediatric Cancer Revealed by Comprehensive DNA and RNA Sequencing
Authors: Newman Scott , Nakitandwe Joy , Kesserwan Chimene A. , Azzato Elizabeth M. , Wheeler David A. , Rusch Michael , Shurtleff Sheila , Hedges Dale J. , Hamilton Kayla V. , Foy Scott G. , Edmonson Michael N. , Thrasher Andrew , Bahrami Armita , Orr Brent A. , Klco Jeffery M. , Gu Jiali , Harrison Lynn W. , Wang Lu , Clay Michael R. , Ouma Annastasia , Silkov Antonina , Liu Yanling , Zhang Zhaojie , Liu Yu , Brady Samuel W. , Zhou Xin , Chang Ti-Cheng , Pande Manjusha , Davis Eric , Becksfort Jared , Patel Aman , Wilkinson Mark R. , Rahbarinia Delaram , Kubal Manish , Maciaszek Jamie L. , Pastor Victor , Knight Jay , Gout Alexander M. , Wang Jian , Gu Zhaohui , Mullighan Charles G. , McGee Rose B. , Quinn Emily A. , Nuccio Regina , Mostafavi Roya , Gerhardt Elsie L. , Taylor Leslie M. , Valdez Jessica M. , Hines-Dowell Stacy J. , Pappo Alberto S. , Robinson Giles , Johnson Liza-Marie , Pui Ching-Hon , Ellison David W. , Downing James R. , Zhang Jinghui , Nichols Kim E.
Published: April 2023

Abstract
Genomic studies of pediatric cancer have primarily focused on specific tumor types or high-risk disease. Here, we used a three-platform sequencing approach, including whole-genome sequencing (WGS), whole-exome sequencing (WES), and RNA sequencing (RNA-seq), to examine tumor and germline genomes from 309 prospectively identified children with newly diagnosed (85%) or relapsed/refractory (15%) cancers, unselected for tumor type. Eighty-six percent of patients harbored diagnostic (53%), prognostic (57%), therapeutically relevant (25%), and/or cancer-predisposing (18%) variants. Inclusion of WGS enabled detection of activating gene fusions and enhancer hijacks (36% and 8% of tumors, respectively), small intragenic deletions (15% of tumors), and mutational signatures revealing of pathogenic variant effects. Evaluation of paired tumor–normal data revealed relevance to tumor development for 55% of pathogenic germline variants. This study demonstrates the power of a three-platform approach that incorporates WGS to interrogate and interpret the full range of genomic variants across newly diagnosed as well as relapsed/refractory pediatric cancers.
Significance:
Pediatric cancers are driven by diverse genomic lesions, and sequencing has proven useful in evaluating high-risk and relapsed/refractory cases. We show that combined WGS, WES, and RNA-seq of tumor and paired normal tissues enables identification and characterization of genetic drivers across the full spectrum of pediatric cancers.

This article is highlighted in the In This Issue feature, p. 2945
Data from Enhancer Hijacking Drives Oncogenic BCL11B Expression in Lineage-Ambiguous Stem Cell Leukemia
Authors: Montefiori Lindsey E. , Bendig Sonja , Gu Zhaohui , Chen Xiaolong , Pölönen Petri , Ma Xiaotu , Murison Alex , Zeng Andy , Garcia-Prat Laura , Dickerson Kirsten , Iacobucci Ilaria , Abdelhamed Sherif , Hiltenbrand Ryan , Mead Paul E. , Mehr Cyrus M. , Xu Beisi , Cheng Zhongshan , Chang Ti-Cheng , Westover Tamara , Ma Jing , Stengel Anna , Kimura Shunsuke , Qu Chunxu , Valentine Marcus B. , Rashkovan Marissa , Luger Selina , Litzow Mark R. , Rowe Jacob M. , den Boer Monique L. , Wang Victoria , Yin Jun , Kornblau Steven M. , Hunger Stephen P. , Loh Mignon L. , Pui Ching-Hon , Yang Wenjian , Crews Kristine R. , Roberts Kathryn G. , Yang Jun J. , Relling Mary V. , Evans William E. , Stock Wendy , Paietta Elisabeth M. , Ferrando Adolfo A. , Zhang Jinghui , Kern Wolfgang , Haferlach Torsten , Wu Gang , Dick John E. , Klco Jeffery M. , Haferlach Claudia , Mullighan Charles G.
Published: April 2023

Abstract
Lineage-ambiguous leukemias are high-risk malignancies of poorly understood genetic basis. Here, we describe a distinct subgroup of acute leukemia with expression of myeloid, T lymphoid, and stem cell markers driven by aberrant allele-specific deregulation of BCL11B, a master transcription factor responsible for thymic T-lineage commitment and specification. Mechanistically, this deregulation was driven by chromosomal rearrangements that juxtapose BCL11B to superenhancers active in hematopoietic progenitors, or focal amplifications that generate a superenhancer from a noncoding element distal to BCL11B. Chromatin conformation analyses demonstrated long-range interactions of rearranged enhancers with the expressed BCL11B allele and association of BCL11B with activated hematopoietic progenitor cell cis-regulatory elements, suggesting BCL11B is aberrantly co-opted into a gene regulatory network that drives transformation by maintaining a progenitor state. These data support a role for ectopic BCL11B expression in primitive hematopoietic cells mediated by enhancer hijacking as an oncogenic driver of human lineage-ambiguous leukemia.
Significance:
Lineage-ambiguous leukemias pose significant diagnostic and therapeutic challenges due to a poorly understood molecular and cellular basis. We identify oncogenic deregulation of BCL11B driven by diverse structural alterations, including de novo superenhancer generation, as the driving feature of a subset of lineage-ambiguous leukemias that transcend current diagnostic boundaries.

This article is highlighted in the In This Issue feature, p. 2659
Data from PTP1B Is an Intracellular Checkpoint that Limits T-cell and CAR T-cell Antitumor Immunity
Authors: Wiede Florian , Lu Kun-Hui , Du Xin , Zeissig Mara N. , Xu Rachel , Goh Pei Kee , Xirouchaki Chrysovalantou E. , Hogarth Samuel J. , Greatorex Spencer , Sek Kevin , Daly Roger J. , Beavis Paul A. , Darcy Phillip K. , Tonks Nicholas K. , Tiganis Tony
Published: April 2023

Abstract
Immunotherapies aimed at alleviating the inhibitory constraints on T cells have revolutionized cancer management. To date, these have focused on the blockade of cell-surface checkpoints such as PD-1. Herein we identify protein tyrosine phosphatase 1B (PTP1B) as an intracellular checkpoint that is upregulated in T cells in tumors. We show that increased PTP1B limits T-cell expansion and cytotoxicity to contribute to tumor growth. T cell–specific PTP1B deletion increased STAT5 signaling, and this enhanced the antigen-induced expansion and cytotoxicity of CD8+ T cells to suppress tumor growth. The pharmacologic inhibition of PTP1B recapitulated the T cell–mediated repression of tumor growth and enhanced the response to PD-1 blockade. Furthermore, the deletion or inhibition of PTP1B enhanced the efficacy of adoptively transferred chimeric antigen receptor (CAR) T cells against solid tumors. Our findings identify PTP1B as an intracellular checkpoint whose inhibition can alleviate the inhibitory constraints on T cells and CAR T cells to combat cancer.
Significance:
Tumors subvert antitumor immunity by engaging checkpoints that promote T-cell exhaustion. Here we identify PTP1B as an intracellular checkpoint and therapeutic target. We show that PTP1B is upregulated in intratumoral T cells and that its deletion or inhibition enhances T-cell antitumor activity and increases CAR T-cell effectiveness against solid tumors.

This article is highlighted in the In This Issue feature, p. 587
Data from Atezolizumab Treatment of Tumors with High Tumor Mutational Burden from MyPathway, a Multicenter, Open-Label, Phase IIa Multiple Basket Study
Authors: Friedman Claire F. , Hainsworth John D. , Kurzrock Razelle , Spigel David R. , Burris Howard A. , Sweeney Christopher J. , Meric-Bernstam Funda , Wang Yong , Levy Jonathan , Grindheim Jessica , Shames David S. , Schulze Katja , Patel Arisha , Swanton Charles
Published: April 2023

Abstract
High tumor mutational burden (TMB-H) correlates with improved immunotherapy response. We assessed atezolizumab 1,200 mg every 3 weeks for TMB-H tumors from MyPathway (NCT02091141), a phase IIa multibasket study. One hundred twenty-one patients had advanced solid tumors with TMB ≥10 mut/Mb by any Clinical Laboratory Improvement Amendments (CLIA)–certified assay. The preplanned primary endpoint was objective response rate (ORR) in patients with TMB ≥16 mut/Mb tumors by FoundationOne TMB testing [F1(CDx)]. Patients with F1(CDx) TMB ≥10 and <16 mut/Mb were also evaluated. Ninety patients with 19 tumor types and F1(CDx) TMB ≥10 mut/Mb were efficacy evaluable. In 42 patients with F1(CDx) TMB ≥16 mut/Mb, confirmed ORR was 38.1% [16/42; 95% confidence interval (CI), 23.6–54.4], and disease control rate was 61.9% (26/42; 95% CI, 45.6–76.4) versus 2.1% (1/48; 95% CI, 0.1–11.1) and 22.9% (11/48; 95% CI, 12.0–37.3) for 48 patients with TMB ≥10 and <16 mut/Mb. Responses were observed in nine different tumor types (47%; 9/19).
Significance:
Atezolizumab monotherapy had promising, durable clinical activity across a variety of advanced solid tumor types in patients with TMB ≥16 mut/Mb tumors lacking other suitable treatment options and who were immunotherapy-naïve at enrollment, regardless of microsatellite instability status. Limited activity was observed in tumors with TMB ≥10 and <16 mut/Mb.

See related commentary by Maron and Klempner, p. 602.

This article is highlighted in the In This Issue feature, p. 587
Data from Longitudinal Undetectable Molecular Residual Disease Defines Potentially Cured Population in Localized Non–Small Cell Lung Cancer
Authors: Zhang Jia-Tao , Liu Si-Yang , Gao Wei , Liu Si-Yang Maggie , Yan Hong-Hong , Ji Liyan , Chen Yu , Gong Yuhua , Lu Hong-Lian , Lin Jun-Tao , Yin Kai , Jiang Ben-Yuan , Nie Qiang , Liao Ri-Qiang , Dong Song , Guan Yanfang , Dai Pingping , Zhang Xu-Chao , Yang Jin-Ji , Tu Hai-Yan , Xia Xuefeng , Yi Xin , Zhou Qing , Zhong Wen-Zhao , Yang Xue-Ning , Wu Yi-Long
Published: April 2023

Abstract
The efficacy and potential limitations of molecular residual disease (MRD) detection urgently need to be fully elucidated in a larger population of non–small cell lung cancer (NSCLC). We enrolled 261 patients with stages I to III NSCLC who underwent definitive surgery, and 913 peripheral blood samples were successfully detected by MRD assay. Within the population, only six patients (3.2%) with longitudinal undetectable MRD recurred, resulting in a negative predictive value of 96.8%. Longitudinal undetectable MRD may define the patients who were cured. The peak risk of developing detectable MRD was approximately 18 months after landmark detection. Correspondingly, the positive predictive value of longitudinal detectable MRD was 89.1%, with a median lead time of 3.4 months. However, brain-only recurrence was less commonly detected by MRD (n = 1/5, 20%). Further subgroup analyses revealed that patients with undetectable MRD might not benefit from adjuvant therapy. Together, these results expound the value of MRD in NSCLC.
Significance:
This study confirms the prognostic value of MRD detection in patients with NSCLC after definitive surgery, especially in those with longitudinal undetectable MRD, which might represent the potentially cured population regardless of stage and adjuvant therapy. Moreover, the risk of developing detectable MRD decreased stepwise after 18 months since landmark detection.

This article is highlighted in the In This Issue feature, p. 1599
Data from Tumor-Derived Lysophosphatidic Acid Blunts Protective Type I Interferon Responses in Ovarian Cancer
Authors: Chae Chang-Suk , Sandoval Tito A. , Hwang Sung-Min , Park Eun Sil , Giovanelli Paolo , Awasthi Deepika , Salvagno Camilla , Emmanuelli Alexander , Tan Chen , Chaudhary Vidyanath , Casado Julia , Kossenkov Andrew V. , Song Minkyung , Barrat Franck J. , Holcomb Kevin , Romero-Sandoval E. Alfonso , Zamarin Dmitriy , Pépin David , D'Andrea Alan D. , Färkkilä Anniina , Cubillos-Ruiz Juan R.
Published: April 2023

Abstract
Lysophosphatidic acid (LPA) is a bioactive lipid enriched in the tumor microenvironment of immunosuppressive malignancies such as ovarian cancer. Although LPA enhances the tumorigenic attributes of cancer cells, the immunomodulatory activity of this phospholipid messenger remains largely unexplored. Here, we report that LPA operates as a negative regulator of type I interferon (IFN) responses in ovarian cancer. Ablation of the LPA-generating enzyme autotaxin (ATX) in ovarian cancer cells reprogrammed the tumor immune microenvironment, extended host survival, and improved the effects of therapies that elicit protective responses driven by type I IFN. Mechanistically, LPA sensing by dendritic cells triggered PGE2 biosynthesis that suppressed type I IFN signaling via autocrine EP4 engagement. Moreover, we identified an LPA-controlled, immune-derived gene signature associated with poor responses to combined PARP inhibition and PD-1 blockade in patients with ovarian cancer. Controlling LPA production or sensing in tumors may therefore be useful to improve cancer immunotherapies that rely on robust induction of type I IFN.
Significance:
This study uncovers that ATX–LPA is a central immunosuppressive pathway in the ovarian tumor microenvironment. Ablating this axis sensitizes ovarian cancer hosts to various immunotherapies by unleashing protective type I IFN responses. Understanding the immunoregulatory programs induced by LPA could lead to new biomarkers predicting resistance to immunotherapy in patients with cancer.

See related commentary by Conejo-Garcia and Curiel, p. 1841.

This article is highlighted in the In This Issue feature, p. 1825
Data from Deconvolving Clinically Relevant Cellular Immune Cross-talk from Bulk Gene Expression Using CODEFACS and LIRICS Stratifies Patients with Melanoma to Anti–PD-1 Therapy
Authors: Wang Kun , Patkar Sushant , Lee Joo Sang , Gertz E. Michael , Robinson Welles , Schischlik Fiorella , Crawford David R. , Schäffer Alejandro A. , Ruppin Eytan
Published: April 2023

Abstract
The tumor microenvironment (TME) is a complex mixture of cell types whose interactions affect tumor growth and clinical outcome. To discover such interactions, we developed CODEFACS (COnfident DEconvolution For All Cell Subsets), a tool deconvolving cell type–specific gene expression in each sample from bulk expression, and LIRICS (Ligand–Receptor Interactions between Cell Subsets), a statistical framework prioritizing clinically relevant ligand–receptor interactions between cell types from the deconvolved data. We first demonstrate the superiority of CODEFACS versus the state-of-the-art deconvolution method CIBERSORTx. Second, analyzing The Cancer Genome Atlas, we uncover cell type–specific ligand–receptor interactions uniquely associated with mismatch-repair deficiency across different cancer types, providing additional insights into their enhanced sensitivity to anti–programmed cell death protein 1 (PD-1) therapy compared with other tumors with high neoantigen burden. Finally, we identify a subset of cell type–specific ligand–receptor interactions in the melanoma TME that stratify survival of patients receiving anti–PD-1 therapy better than some recently published bulk transcriptomics-based methods.
Significance:
This work presents two new computational methods that can deconvolve a large collection of bulk tumor gene expression profiles into their respective cell type–specific gene expression profiles and identify cell type–specific ligand–receptor interactions predictive of response to immune-checkpoint blockade therapy.

This article is highlighted in the In This Issue feature, p. 873
Data from MYC Levels Regulate Metastatic Heterogeneity in Pancreatic Adenocarcinoma
Authors: Maddipati Ravikanth , Norgard Robert J. , Baslan Timour , Rathi Komal S. , Zhang Amy , Saeid Asal , Higashihara Taku , Wu Feng , Kumar Angad , Annamalai Valli , Bhattacharya Saurav , Raman Pichai , Adkisson Christian A. , Pitarresi Jason R. , Wengyn Maximilian D. , Yamazoe Taiji , Li Jinyang , Balli David , LaRiviere Michael J. , Ngo Tuong-Vi C. , Folkert Ian W. , Millstein Ian D. , Bermeo Jonathan , Carpenter Erica L. , McAuliffe John C. , Oktay Maja H. , Brekken Rolf A. , Lowe Scott W. , Iacobuzio-Donahue Christine A. , Notta Faiyaz , Stanger Ben Z.
Published: April 2023

Abstract
The degree of metastatic disease varies widely among patients with cancer and affects clinical outcomes. However, the biological and functional differences that drive the extent of metastasis are poorly understood. We analyzed primary tumors and paired metastases using a multifluorescent lineage-labeled mouse model of pancreatic ductal adenocarcinoma (PDAC)—a tumor type in which most patients present with metastases. Genomic and transcriptomic analysis revealed an association between metastatic burden and gene amplification or transcriptional upregulation of MYC and its downstream targets. Functional experiments showed that MYC promotes metastasis by recruiting tumor-associated macrophages, leading to greater bloodstream intravasation. Consistent with these findings, metastatic progression in human PDAC was associated with activation of MYC signaling pathways and enrichment for MYC amplifications specifically in metastatic patients. Collectively, these results implicate MYC activity as a major determinant of metastatic burden in advanced PDAC.
Significance:
Here, we investigate metastatic variation seen clinically in patients with PDAC and murine PDAC tumors and identify MYC as a major driver of this heterogeneity.

This article is highlighted in the In This Issue feature, p. 275
Data from Adjuvant Pembrolizumab versus IFNα2b or Ipilimumab in Resected High-Risk Melanoma
Authors: Grossmann Kenneth F. , Othus Megan , Patel Sapna P. , Tarhini Ahmad A. , Sondak Vernon K. , Knopp Michael V. , Petrella Teresa M. , Truong Thach-Giao , Khushalani Nikhil I. , Cohen Justine V. , Buchbinder Elizabeth I. , Kendra Kari , Funchain Pauline , Lewis Karl D. , Conry Robert M. , Chmielowski Bartosz , Kudchadkar Ragini R. , Johnson Douglas B. , Li Hongli , Moon James , Eroglu Zeynep , Gastman Brian , Kovacsovics-Bankowski Magdalena , Gunturu Krishna S. , Ebbinghaus Scot W. , Ahsan Sama , Ibrahim Nageatte , Sharon Elad , Korde Larissa A. , Kirkwood John M. , Ribas Antoni
Published: April 2023

Abstract
We conducted a randomized phase III trial to evaluate whether adjuvant pembrolizumab for one year (647 patients) improved recurrence-free survival (RFS) or overall survival (OS) in comparison with high-dose IFNα-2b for one year or ipilimumab for up to three years (654 patients), the approved standard-of-care adjuvant immunotherapies at the time of enrollment for patients with high-risk resected melanoma. At a median follow-up of 47.5 months, pembrolizumab was associated with significantly longer RFS than prior standard-of-care adjuvant immunotherapies [HR, 0.77; 99.62% confidence interval (CI), 0.59–0.99; P = 0.002]. There was no statistically significant association with OS among all patients (HR, 0.82; 96.3% CI, 0.61–1.09; P = 0.15). Proportions of treatment-related adverse events of grades 3 to 5 were 19.5% with pembrolizumab, 71.2% with IFNα-2b, and 49.2% with ipilimumab. Therefore, adjuvant pembrolizumab significantly improved RFS but not OS compared with the prior standard-of-care immunotherapies for patients with high-risk resected melanoma.
Significance:
Adjuvant PD-1 blockade therapy decreases the rates of recurrence, but not survival, in patients with surgically resectable melanoma, substituting the prior standard-of-care immunotherapies for this cancer.

See related commentary by Smithy and Shoushtari, p. 599.

This article is highlighted in the In This Issue feature, p. 587
Data from Melanoma-Secreted Amyloid Beta Suppresses Neuroinflammation and Promotes Brain Metastasis
Authors: Kleffman Kevin , Levinson Grace , Rose Indigo V.L. , Blumenberg Lili M. , Shadaloey Sorin A.A. , Dhabaria Avantika , Wong Eitan , Galán-Echevarría Francisco , Karz Alcida , Argibay Diana , Von Itter Richard , Floristán Alfredo , Baptiste Gillian , Eskow Nicole M. , Tranos James A. , Chen Jenny , Vega y Saenz de Miera Eleazar C. , Call Melissa , Rogers Robert , Jour George , Wadghiri Youssef Zaim , Osman Iman , Li Yue-Ming , Mathews Paul , DeMattos Ronald B. , Ueberheide Beatrix , Ruggles Kelly V. , Liddelow Shane A. , Schneider Robert J. , Hernando Eva
Published: April 2023

Abstract
Brain metastasis is a significant cause of morbidity and mortality in multiple cancer types and represents an unmet clinical need. The mechanisms that mediate metastatic cancer growth in the brain parenchyma are largely unknown. Melanoma, which has the highest rate of brain metastasis among common cancer types, is an ideal model to study how cancer cells adapt to the brain parenchyma. Our unbiased proteomics analysis of melanoma short-term cultures revealed that proteins implicated in neurodegenerative pathologies are differentially expressed in melanoma cells explanted from brain metastases compared with those derived from extracranial metastases. We showed that melanoma cells require amyloid beta (Aβ) for growth and survival in the brain parenchyma. Melanoma-secreted Aβ activates surrounding astrocytes to a prometastatic, anti-inflammatory phenotype and prevents phagocytosis of melanoma by microglia. Finally, we demonstrate that pharmacologic inhibition of Aβ decreases brain metastatic burden.
Significance:
Our results reveal a novel mechanistic connection between brain metastasis and Alzheimer's disease, two previously unrelated pathologies; establish Aβ as a promising therapeutic target for brain metastasis; and demonstrate suppression of neuroinflammation as a critical feature of metastatic adaptation to the brain parenchyma.

This article is highlighted in the In This Issue feature, p. 1171
Data from Genomic and Single-Cell Landscape Reveals Novel Drivers and Therapeutic Vulnerabilities of Transformed Cutaneous T-cell Lymphoma
Authors: Song Xiaofei , Chang Shiun , Seminario-Vidal Lucia , de Mingo Pulido Alvaro , Tordesillas Leticia , Song Xingzhi , Reed Rhianna A. , Harkins Andrea , Whiddon Shannen , Nguyen Jonathan V. , Segura Carlos Moran , Zhang Chaomei , Yoder Sean , Sayegh Zena , Zhao Yun , Messina Jane L. , Harro Carly M. , Zhang Xiaohui , Conejo-Garcia José R. , Berglund Anders , Sokol Lubomir , Zhang Jianhua , Rodriguez Paulo C. , Mulé James J. , Futreal Andrew P. , Tsai Kenneth Y. , Chen Pei-Ling
Published: April 2023

Abstract
Cutaneous T-cell lymphoma (CTCL) is a rare cancer of skin-homing T cells. A subgroup of patients develops large cell transformation with rapid progression to an aggressive lymphoma. Here, we investigated the transformed CTCL (tCTCL) tumor ecosystem using integrative multiomics spanning whole-exome sequencing (WES), single-cell RNA sequencing, and immune profiling in a unique cohort of 56 patients. WES of 70 skin biopsies showed high tumor mutation burden, UV signatures that are prognostic for survival, exome-based driver events, and most recurrently mutated pathways in tCTCL. Single-cell profiling of 16 tCTCL skin biopsies identified a core oncogenic program with metabolic reprogramming toward oxidative phosphorylation (OXPHOS), cellular plasticity, upregulation of MYC and E2F activities, and downregulation of MHC I suggestive of immune escape. Pharmacologic perturbation using OXPHOS and MYC inhibitors demonstrated potent antitumor activities, whereas immune profiling provided in situ evidence of intercellular communications between malignant T cells expressing macrophage migration inhibitory factor and macrophages and B cells expressing CD74.
Significance:
Our study contributes a key resource to the community with the largest collection of tCTCL biopsies that are difficult to obtain. The multiomics data herein provide the first comprehensive compendium of genomic alterations in tCTCL and identify potential prognostic signatures and novel therapeutic targets for an incurable T-cell lymphoma.

This article is highlighted in the In This Issue feature, p. 1171
Data from SETD2 Haploinsufficiency Enhances Germinal Center–Associated AICDA Somatic Hypermutation to Drive B-cell Lymphomagenesis
Authors: Leung Wilfred , Teater Matt , Durmaz Ceyda , Meydan Cem , Chivu Alexandra G. , Chadburn Amy , Rice Edward J. , Muley Ashlesha , Camarillo Jeannie M. , Arivalagan Jaison , Li Ziyi , Flowers Christopher R. , Kelleher Neil L. , Danko Charles G. , Imielinski Marcin , Dave Sandeep S. , Armstrong Scott A. , Mason Christopher E. , Melnick Ari M.
Published: April 2023

Abstract
SETD2 is the sole histone methyltransferase responsible for H3K36me3, with roles in splicing, transcription initiation, and DNA damage response. Homozygous disruption of SETD2 yields a tumor suppressor effect in various cancers. However, SETD2 mutation is typically heterozygous in diffuse large B-cell lymphomas. Here we show that heterozygous Setd2 deficiency results in germinal center (GC) hyperplasia and increased competitive fitness, with reduced DNA damage checkpoint activity and apoptosis, resulting in accelerated lymphomagenesis. Impaired DNA damage sensing in Setd2-haploinsufficient germinal center B (GCB) and lymphoma cells associated with increased AICDA-induced somatic hypermutation, complex structural variants, and increased translocations including those activating MYC. DNA damage was selectively increased on the nontemplate strand, and H3K36me3 loss was associated with greater RNAPII processivity and mutational burden, suggesting that SETD2-mediated H3K36me3 is required for proper sensing of cytosine deamination. Hence, Setd2 haploinsufficiency delineates a novel GCB context–specific oncogenic pathway involving defective epigenetic surveillance of AICDA-mediated effects on transcribed genes.
Significance:
Our findings define a B cell–specific oncogenic effect of SETD2 heterozygous mutation, which unleashes AICDA mutagenesis of nontemplate strand DNA in the GC reaction, resulting in lymphomas with heavy mutational burden. GC-derived lymphomas did not tolerate SETD2 homozygous deletion, pointing to a novel context-specific therapeutic vulnerability.

This article is highlighted in the In This Issue feature, p. 1599
Data from Single-Cell Sequencing Reveals Trajectory of Tumor-Infiltrating Lymphocyte States in Pancreatic Cancer
Authors: Schalck Aislyn , Sakellariou-Thompson Donastas , Forget Marie-Andrée , Sei Emi , Hughes Tara G. , Reuben Alexandre , Bai Shanshan , Hu Min , Kumar Tapsi , Hurd Mark W. , Katz Matthew H.G. , Tzeng Ching-Wei D. , Pant Shubham , Javle Milind , Fogelman David R. , Maitra Anirban , Haymaker Cara L. , Kim Michael P. , Navin Nicholas E. , Bernatchez Chantale
Published: April 2023

Abstract
Pancreatic ductal adenocarcinoma (PDAC) has few effective treatments. Immunotherapy, an attractive alternative strategy, remains challenging with the lack of knowledge on the tumor-infiltrating lymphocyte (TIL) landscape in PDAC. To generate a reference of T-cell subpopulations, we profiled 80,000 T cells from 57 PDAC samples, 22 uninvolved/normal samples, and cultured TIL using single-cell transcriptomic and T-cell receptor analysis. These data revealed 20 cell states and heterogeneous distributions of TIL populations. The CD8+ TIL contained a putative transitional GZMK+ population based on T-cell receptor clonotype sharing, and cell-state trajectory analysis showed similarity to a GZMB+PRF1+ cytotoxic and a CXCL13+ dysfunctional population. Statistical analysis suggested that certain TIL states, such as dysfunctional and inhibitory populations, often occurred together. Finally, analysis of cultured TIL revealed that high-frequency clones from effector populations were preferentially expanded. These data provide a framework for understanding the PDAC TIL landscape for future TIL use in immunotherapy for PDAC.
Significance:
To improve the efficacy of immunotherapy in PDAC, there is a great need to understand the PDAC TIL landscape. This study represents a reference of PDAC TIL subpopulations and their relationships and provides a foundation upon which to base future immunotherapeutic efforts.

This article is highlighted in the In This Issue feature, p. 2221
Data from Genetic Ancestry Correlates with Somatic Differences in a Real-World Clinical Cancer Sequencing Cohort
Authors: Arora Kanika , Tran Thinh N. , Kemel Yelena , Mehine Miika , Liu Ying L. , Nandakumar Subhiksha , Smith Shaleigh A. , Brannon A. Rose , Ostrovnaya Irina , Stopsack Konrad H. , Razavi Pedram , Safonov Anton , Rizvi Hira A. , Hellmann Matthew D. , Vijai Joseph , Reynolds Thomas C. , Fagin James A. , Carrot-Zhang Jian , Offit Kenneth , Solit David B. , Ladanyi Marc , Schultz Nikolaus , Zehir Ahmet , Brown Carol L. , Stadler Zsofia K. , Chakravarty Debyani , Bandlamudi Chaitanya , Berger Michael F.
Published: April 2023

Abstract
Accurate ancestry inference is critical for identifying genetic contributors of cancer disparities among populations. Although methods to infer genetic ancestry have historically relied upon genome-wide markers, the adaptation to targeted clinical sequencing panels presents an opportunity to incorporate ancestry inference into routine diagnostic workflows. We show that global ancestral contributions and admixture of continental populations can be quantitatively inferred using markers captured by the MSK-IMPACT clinical panel. In a pan-cancer cohort of 45,157 patients, we observed differences by ancestry in the frequency of somatic alterations, recapitulating known associations and revealing novel associations. Despite the comparable overall prevalence of driver alterations by ancestry group, the proportion of patients with clinically actionable alterations was lower for African (30%) compared with European (33%) ancestry. Although this result is largely explained by population-specific cancer subtype differences, it reveals an inequity in the degree to which different populations are served by existing precision oncology interventions.
Significance:
We performed a comprehensive analysis of ancestral associations with somatic mutations in a real-world pan-cancer cohort, including >5,000 non-European individuals. Using an FDA-authorized tumor sequencing panel and an FDA-recognized oncology knowledge base, we detected differences in the prevalence of clinically actionable alterations, potentially contributing to health care disparities affecting underrepresented populations.

This article is highlighted in the In This Issue feature, p. 2483
Data from Racial/Ethnic and Sex Differences in Somatic Cancer Gene Mutations among Patients with Early-Onset Colorectal Cancer
Authors: Holowatyj Andreana N. , Wen Wanqing , Gibbs Timothy , Seagle Hannah M. , Keller Samantha R. , Edwards Digna R. Velez , Washington Mary K. , Eng Cathy , Perea Jose , Zheng Wei , Guo Xingyi
Published: April 2023

Abstract
Molecular features underlying colorectal cancer disparities remain uncharacterized. Here, we investigated somatic mutation patterns by race/ethnicity and sex among 5,856 non-Hispanic white (NHW), 535 non-Hispanic Black (NHB), and 512 Asian/Pacific Islander (API) patients with colorectal cancer (2,016 early-onset colorectal cancer patients: sequencing age <50 years). NHB patients with early-onset nonhypermutated colorectal cancer, but not API patients, had higher adjusted tumor mutation rates than NHW patients. There were significant differences for LRP1B, FLT4, FBXW7, RNF43, ATRX, APC, and PIK3CA mutation frequencies in early-onset nonhypermutated colorectal cancers between racial/ethnic groups. Heterogeneities by race/ethnicity were observed for the effect of APC, FLT4, and FAT1 between early-onset and late-onset nonhypermutated colorectal cancer. By sex, heterogeneity was observed for the effect of EP300, BRAF, WRN, KRAS, AXIN2, and SMAD2. Males and females with nonhypermutated colorectal cancer had different trends in EP300 mutations by age group. These findings define genomic patterns of early-onset nonhypermutated colorectal cancer by race/ethnicity and sex, which yields novel biological clues into early-onset colorectal cancer disparities.
Significance:
NHBs, but not APIs, with early-onset nonhypermutated colorectal cancer had higher adjusted tumor mutation rates versus NHWs. Differences for FLT4, FBXW7, RNF43, LRP1B, APC, PIK3CA, and ATRX mutation rates between racial/ethnic groups and EP300, KRAS, AXIN2, WRN, BRAF, and LRP1B mutation rates by sex were observed in tumors of young patients.

See related commentary by Shen et al., p. 530.

This article is highlighted in the In This Issue feature, p. 517
Supplementary Figure 5 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 5. Retuning is specific to mature spleen NK cells.
Supplementary figure legends from Neoadjuvant Interferons: Critical for Effective PD-1–Based Immunotherapy in TNBC
Authors: Brockwell Natasha K. , Owen Katie L. , Zanker Damien , Spurling Alex , Rautela Jai , Duivenvoorden Hendrika M. , Baschuk Nikola , Caramia Franco , Loi Sherene , Darcy Phillip K. , Lim Elgene , Parker Belinda S.
Published: April 2023

Figure legends for supplementary figures 1, 2 & 3
Figure S2 from Neoadjuvant Interferons: Critical for Effective PD-1–Based Immunotherapy in TNBC
Authors: Brockwell Natasha K. , Owen Katie L. , Zanker Damien , Spurling Alex , Rautela Jai , Duivenvoorden Hendrika M. , Baschuk Nikola , Caramia Franco , Loi Sherene , Darcy Phillip K. , Lim Elgene , Parker Belinda S.
Published: April 2023

The effect of poly(I:C) on immune cell activation
Supplementary Figure S4 from Safety of Targeting ROR1 in Primates with Chimeric Antigen Receptor–Modified T Cells
Authors: Berger Carolina , Sommermeyer Daniel , Hudecek Michael , Berger Michael , Balakrishnan Ashwini , Paszkiewicz Paulina J. , Kosasih Paula L. , Rader Christoph , Riddell Stanley R.
Published: April 2023

Adoptive transfer, persistence, and migration of autologous control gene-marked T cells.
Supplementary Table 6 from The Tumor Microenvironment Shapes Lineage, Transcriptional, and Functional Diversity of Infiltrating Myeloid Cells
Authors: Elpek Kutlu G. , Cremasco Viviana , Shen Hua , Harvey Christopher J. , Wucherpfennig Kai W. , Goldstein Daniel R. , Monach Paul A. , Turley Shannon J.
Published: April 2023

XLSX file - 1K, Supplementary Table S6: Expression values for neutrophil granular effector molecules from the heatmap in Figure 7A.
Supplementary Table 1 from Bevacizumab plus Ipilimumab in Patients with Metastatic Melanoma
Authors: Hodi F. Stephen , Lawrence Donald , Lezcano Cecilia , Wu Xinqi , Zhou Jun , Sasada Tetsuro , Zeng Wanyong , Giobbie-Hurder Anita , Atkins Michael B. , Ibrahim Nageatte , Friedlander Philip , Flaherty Keith T. , Murphy George F. , Rodig Scott , Velazquez Elsa F. , Mihm Martin C. , Russell Sara , DiPiro Pamela J. , Yap Jeffrey T. , Ramaiya Nikhil , Van den Abbeele Annick D. , Gargano Maria , McDermott David
Published: April 2023

PDF file - 111K, Patient Demographics.
Supplementary Figure Legends from Augmentation of CAR T-cell Trafficking and Antitumor Efficacy by Blocking Protein Kinase A Localization
Authors: Newick Kheng , O'Brien Shaun , Sun Jing , Kapoor Veena , Maceyko Steven , Lo Albert , Puré Ellen , Moon Edmund , Albelda Steven M.
Published: April 2023

Supplementary Figure Legends
Supplementary Materials and Methods from Phase I/II Study of Metastatic Melanoma Patients Treated with Nivolumab Who Had Progressed after Ipilimumab
Authors: Weber Jeffrey , Gibney Geoffrey , Kudchadkar Ragini , Yu Bin , Cheng Pingyan , Martinez Alberto J. , Kroeger Jodie , Richards Allison , McCormick Lori , Moberg Valerie , Cronin Heather , Zhao Xiuhua , Schell Michael , Chen Yian Ann
Published: April 2023

Supplementary Materials and Methods and Supplementary Table 1. This table describes the treatment characteristics of the six cohorts of patients that participated in the study described herein, including what grades of toxicity to prior ipilimumab they might have had.
Supplementary Figure S2 from Neoantigen Load, Antigen Presentation Machinery, and Immune Signatures Determine Prognosis in Clear Cell Renal Cell Carcinoma
Authors: Matsushita Hirokazu , Sato Yusuke , Karasaki Takahiro , Nakagawa Tohru , Kume Haruki , Ogawa Seishi , Homma Yukio , Kakimi Kazuhiro
Published: April 2023

Correlations of gene expression with IFN-gamma and IFN-gamma-inducible immune suppressive molecules in the tumor.
Supplementary Figure 4 from Tasquinimod Modulates Suppressive Myeloid Cells and Enhances Cancer Immunotherapies in Murine Models
Authors: Shen Li , Sundstedt Anette , Ciesielski Michael , Miles Kiersten Marie , Celander Mona , Adelaiye Remi , Orillion Ashley , Ciamporcero Eric , Ramakrishnan Swathi , Ellis Leigh , Fenstermaker Robert , Abrams Scott I. , Eriksson Helena , Leanderson Tomas , Olsson Anders , Pili Roberto
Published: April 2023

Supplementary Figure 4. The effect of tasquinimod on T cell proliferation and regulatory T cells.
Supplemental Figure 1 from Generation of Potent T-cell Immunotherapy for Cancer Using DAP12-Based, Multichain, Chimeric Immunoreceptors
Authors: Wang Enxiu , Wang Liang-Chuan , Tsai Ching-Yi , Bhoj Vijay , Gershenson Zack , Moon Edmund , Newick Kheng , Sun Jing , Lo Albert , Baradet Timothy , Feldman Michael D. , Barrett David , Puré Ellen , Albelda Steven , Milone Michael C.
Published: April 2023

Cytotoxicity induced by SS1-KIRS2, but not receptor expression at the cell surface, depends upon DAP12 co-expression.
Tables S1 to S12 from VEGF Neutralization Plus CTLA-4 Blockade Alters Soluble and Cellular Factors Associated with Enhancing Lymphocyte Infiltration and Humoral Recognition in Melanoma
Authors: Wu Xinqi , Giobbie-Hurder Anita , Liao Xiaoyun , Lawrence Donald , McDermott David , Zhou Jun , Rodig Scott , Hodi F. Stephen
Published: April 2023

Supplementary Table S1. H-scores of ICAM-1, VCAM-1 and IP-10 expression in tumors of melanoma patients before and after ipilimumab or Ipi-Bev treatment. Supplementary Table S2. CXCR3 expression on circulating CD4+ and CD8+ T cells before and after Ipi-Bev treatment. Supplementary Table S3. Pre-treatment serum levels of cytokines/chemokines were not associated with response (CR/PR vs. SD/PD/Uneval) to Ipi-Bev. Supplementary Table S4. Pre-treatment serum levels of cytokines/chemokines were not associated with disease control (CR/PR/SD vs. PD/Uneval) in Ipi-Bev-treated patients. Supplementary Table S5. Fold-changes of serum cytokines/chemokines were not associated with response (CR/PR vs. SD/PD/Uneval) to Ipi-Bev. Supplementary Table S6. Fold-changes of serum cytokines/chemokines were not associated with disease control (CR/PR/SD vs. PD/Uneval) in Ipi-Bev-treated patients. Supplementary Table S7. Response (CR/PR vs. SD/PD/Uneval) to Ipi-Bev by cytokine expression category. Supplementary Table S8. Disease control (CR/PR/SD vs. PD/Uneval) in Ipi-Bev-treated patients by cytokine expression category. Supplementary Table S9. Pre-treatment cytokine levels according to immune related adverse events (irAEs). Supplementary Table S10. Relationship between cytokine fold-changes according to irAEs. Supplementary Table S11. Clinical responses and survival of patients whose plasma samples were used in antibody response analyses. Supplementary Table S12. Effects of ipilimumab alone and Ipi-Bev on circulating cytokine/chemokine levels.
Supplemental Table 1 from Shifting the Balance of Activating and Inhibitory Natural Killer Receptor Ligands on BRAFV600E Melanoma Lines with Vemurafenib
Authors: Frazao Alexandra , Colombo Marina , Fourmentraux-Neves Emmanuelle , Messaoudene Meriem , Rusakiewicz Sylvie , Zitvogel Laurence , Vivier Eric , Vély Frédéric , Faure Florence , Dréno Brigitte , Benlalam Houssem , Bouquet Fanny , Savina Ariel , Pasmant Eric , Toubert Antoine , Avril Marie-Françoise , Caignard Anne
Published: April 2023

List of antibodies used for flow cytometry.
Supplementary Materials and Methods from IL2 Variant Circumvents ICOS+ Regulatory T-cell Expansion and Promotes NK Cell Activation
Authors: Sim Geok Choo , Liu Chengwen , Wang Ena , Liu Hui , Creasy Caitlin , Dai Zhimin , Overwijk Willem W. , Roszik Jason , Marincola Francesco , Hwu Patrick , Grimm Elizabeth , Radvanyi Laszlo
Published: April 2023

Additional information for materials and methods
Supplementary Figure from The Antitumor Effects of Vaccine-Activated CD8+ T Cells Associate with Weak TCR Signaling and Induction of Stem-Like Memory T Cells
Authors: Wu Sha , Zhu Wei , Peng Yibing , Wang Lan , Hong Yuan , Huang Lei , Dong Dayong , Xie Junping , Merchen Todd , Kruse Edward , Guo Zong Sheng , Bartlett David , Fu Ning , He Yukai
Published: April 2023

Supplementary Figure from The Antitumor Effects of Vaccine-Activated CD8+ T Cells Associate with Weak TCR Signaling and Induction of Stem-Like Memory T Cells
Supplementary Figure Legends from Complement Factor H Antibodies from Lung Cancer Patients Induce Complement-Dependent Lysis of Tumor Cells, Suggesting a Novel Immunotherapeutic Strategy
Authors: Campa Michael J. , Gottlin Elizabeth B. , Bushey Ryan T. , Patz Edward F.
Published: April 2023

Supplementary Figure Legends
Supplemental Figure and Table Legends from Soluble PD-L1 as a Biomarker in Malignant Melanoma Treated with Checkpoint Blockade
Authors: Zhou Jun , Mahoney Kathleen M. , Giobbie-Hurder Anita , Zhao Fengmin , Lee Sandra , Liao Xiaoyun , Rodig Scott , Li Jingjing , Wu Xinqi , Butterfield Lisa H. , Piesche Matthias , Manos Michael P. , Eastman Lauren M. , Dranoff Glenn , Freeman Gordon J. , Hodi F. Stephen
Published: April 2023

Supplemental Figure and Table Legends
Supplementary Data for publication from A Four-Factor Immunoscore System That Predicts Clinical Outcome for Stage II/III Gastric Cancer
Authors: Wen Ti , Wang Zhenning , Li Yi , Li Zhi , Che Xiaofang , Fan Yibo , Wang Shuo , Qu Jinglei , Yang Xianghong , Hou Kezuo , Zhou Wenyang , Xu Ling , Li Ce , Wang Jin , Liu Jing , Chen Liqun , Zhang Jingdong , Qu Xiujuan , Liu Yunpeng
Published: April 2023

Supplementary Data for publication
Figure S6 from Assessing the Magnitude of Immunogenic Cell Death Following Chemotherapy and Irradiation Reveals a New Strategy to Treat Pancreatic Cancer
Authors: Ye Jian , Mills Bradley N. , Zhao Tony , Han Booyeon J. , Murphy Joseph D. , Patel Ankit P. , Johnston Carl J. , Lord Edith M. , Belt Brian A. , Linehan David C. , Gerber Scott A.
Published: April 2023

Supplemental figure 6
Figure S5 from Assessing the Magnitude of Immunogenic Cell Death Following Chemotherapy and Irradiation Reveals a New Strategy to Treat Pancreatic Cancer
Authors: Ye Jian , Mills Bradley N. , Zhao Tony , Han Booyeon J. , Murphy Joseph D. , Patel Ankit P. , Johnston Carl J. , Lord Edith M. , Belt Brian A. , Linehan David C. , Gerber Scott A.
Published: April 2023

Supplemental figure 5
Table S4 from CD47 Expression Defines Efficacy of Rituximab with CHOP in Non–Germinal Center B-cell (Non-GCB) Diffuse Large B-cell Lymphoma Patients (DLBCL), but Not in GCB DLBCL
Authors: Bouwstra Renée , He Yuan , de Boer Janneke , Kooistra Hilde , Cendrowicz Ewa , Fehrmann Rudolf S.N. , Ammatuna Emanuele , zu Eulenburg Christine , Nijland Marcel , Huls Gerwin , Bremer Edwin , van Meerten Tom
Published: April 2023

Uni- and multivariate analysis of R-CHOP treated DLBCL patients
Table S3 from CD47 Expression Defines Efficacy of Rituximab with CHOP in Non–Germinal Center B-cell (Non-GCB) Diffuse Large B-cell Lymphoma Patients (DLBCL), but Not in GCB DLBCL
Authors: Bouwstra Renée , He Yuan , de Boer Janneke , Kooistra Hilde , Cendrowicz Ewa , Fehrmann Rudolf S.N. , Ammatuna Emanuele , zu Eulenburg Christine , Nijland Marcel , Huls Gerwin , Bremer Edwin , van Meerten Tom
Published: April 2023

Uni- and multivariate analysis of R-CHOP treated DLBCL patients
Supplementary Tables and Figure Legends from Myeloid-Derived Suppressive Cells Promote B cell–Mediated Immunosuppression via Transfer of PD-L1 in Glioblastoma
Authors: Lee-Chang Catalina , Rashidi Aida , Miska Jason , Zhang Peng , Pituch Katarzyna C. , Hou David , Xiao Ting , Fischietti Mariafausta , Kang Seong Jae , Appin Christina L. , Horbinski Craig , Platanias Leonidas C. , Lopez-Rosas Aurora , Han Yu , Balyasnikova Irina V. , Lesniak Maciej S.
Published: April 2023

Supplementary Tables and Supplementary Figure Legends
Supplementary Tables and Data from Tumor-Derived α-Fetoprotein Suppresses Fatty Acid Metabolism and Oxidative Phosphorylation in Dendritic Cells
Authors: Santos Patricia M. , Menk Ashley V. , Shi Jian , Tsung Allan , Delgoffe Greg M. , Butterfield Lisa H.
Published: April 2023

Supplementary tables 1 and 2, Supplementary figures 1-4
Figure S2 from Hypoxia-Induced VISTA Promotes the Suppressive Function of Myeloid-Derived Suppressor Cells in the Tumor Microenvironment
Authors: Deng Jie , Li Jiannan , Sarde Aurelien , Lines J. Louise , Lee Yu-Chi , Qian David C. , Pechenick Dov A. , Manivanh Richard , Le Mercier Isabelle , Lowrey Christopher H. , Varn Frederick S. , Cheng Chao , Leib David A. , Noelle Randolph J. , Mabaera Rodwell
Published: April 2023

Figure S2. Vista expression is correlated with myeloid infiltration in the TME of colon cancer patients. Volcano plot of CLS differences (granulocytic, monocytic, and αβ T cells) between VISTAhigh and VISTAlow cohorts and the associated significance values obtained using Mann-Whitney tests.
Figure S1 from Hypoxia-Induced VISTA Promotes the Suppressive Function of Myeloid-Derived Suppressor Cells in the Tumor Microenvironment
Authors: Deng Jie , Li Jiannan , Sarde Aurelien , Lines J. Louise , Lee Yu-Chi , Qian David C. , Pechenick Dov A. , Manivanh Richard , Le Mercier Isabelle , Lowrey Christopher H. , Varn Frederick S. , Cheng Chao , Leib David A. , Noelle Randolph J. , Mabaera Rodwell
Published: April 2023

Figure S1. VISTA is an independent predictor of survival in cohort of colon cancer patients. Kaplan-Meier plot of disease specific survival stratified by VISTA expression with optimized cut-off of high/low expression. A log-rank test with subsequent Monte Carlo simulations was used to determine significance
Supplementary Data from The Impact of High-Dose Glucocorticoids on the Outcome of Immune-Checkpoint Inhibitor–Related Thyroid Disorders
Authors: Ma Chanjuan , Hodi F. Stephen , Giobbie-Hurder Anita , Wang Xiaocheng , Zhou Jing , Zhang Amy , Zhou Ying , Mao Fei , Angell Trevor E. , Andrews Chelsea P. , Hu Jiani , Barroso-Sousa Romualdo , Kaiser Ursula B. , Tolaney Sara M. , Min Le
Published: April 2023

Supplementary data, tables and figures
Supplementary Data from RORγ Agonists Enhance the Sustained Antitumor Activity through Intrinsic Tc17 Cytotoxicity and Tc1 Recruitment
Authors: Liu Xikui , Zawidzka Elizabeth M. , Li Hongxiu , Lesch Charles A. , Dunbar Jenna , Bousley Dick , Zou Weiping , Hu Xiao , Carter Laura L.
Published: April 2023

Supplemental Table 1, Figure 1-5
Supplementary Table S2 from TCR Repertoire Diversity of Peripheral PD-1+CD8+ T Cells Predicts Clinical Outcomes after Immunotherapy in Patients with Non–Small Cell Lung Cancer
Authors: Han Jiefei , Duan Jianchun , Bai Hua , Wang Yuqi , Wan Rui , Wang Xin , Chen Si , Tian Yanhua , Wang Di , Fei Kailun , Yao Zhuoran , Wang Shuhang , Lu Zhimin , Wang Zhijie , Wang Jie
Published: April 2023

Univariable and multivariable analysis of progression-free survival (PFS).
Figure S5 from Virus-Like Particle–Drug Conjugates Induce Protective, Long-lasting Adaptive Antitumor Immunity in the Absence of Specifically Targeted Tumor Antigens
Authors: Kines Rhonda C. , Thompson Cynthia D. , Spring Sean , Li Zhenyu , de los Pinos Elisabet , Monks Stephen , Schiller John T.
Published: April 2023

Examples of gating strategy to determine proportions and viability of tumor infiltrating cell populations shown in Figure 4.