bluuebunny/crossref_metadata_2025 huggingface dataset:
Data from Resistance to Durvalumab and Durvalumab plus Tremelimumab Is Associated with Functional STK11 Mutations in Patients with Non–Small Cell Lung Cancer and Is Reversed by STAT3 Knockdown
Authors: Pore Nabendu , Wu Song , Standifer Nathan , Jure-Kunkel Maria , de los Reyes Melissa , Shrestha Yashaswi , Halpin Rebecca , Rothstein Raymond , Mulgrew Kathy , Blackmore Stephen , Martin Philip , Meekin John , Griffin Matthew , Bisha Ina , Proia Theresa A. , Miragaia Ricardo J. , Herbst Ronald , Gupta Ashok , Abdullah Shaad E. , Raja Rajiv , Frigault Melanie M. , Barrett J. Carl , Dennis Phillip A. , Ascierto Maria Libera , Oberst Michael D.
Published: April 2023

Abstract
Mutations in the STK11 (LKB1) gene regulate resistance to PD-1/PD-L1 blockade. This study evaluated this association in patients with nonsquamous non–small cell lung cancer (NSCLC) enrolled in three phase I/II trials. STK11 mutations were associated with resistance to the anti–PD-L1 antibody durvalumab (alone/with the anti-CTLA4 antibody tremelimumab) independently of KRAS mutational status, highlighting STK11 as a potential driver of resistance to checkpoint blockade. Retrospective assessments of tumor tissue, whole blood, and serum revealed a unique immune phenotype in patients with STK11 mutations, with increased expression of markers associated with neutrophils (i.e., CXCL2, IL6), Th17 contexture (i.e., IL17A), and immune checkpoints. Associated changes were observed in the periphery. Reduction of STAT3 in the tumor microenvironment using an antisense oligonucleotide reversed immunotherapy resistance in preclinical STK11 knockout models. These results suggest that STK11 mutations may hinder response to checkpoint blockade through mechanisms including suppressive myeloid cell biology, which could be reversed by STAT3-targeted therapy.
Significance:
Patients with nonsquamous STK11-mutant (STK11mut) NSCLC are less likely than STK11 wild-type (STK11wt) patients to respond to anti–PD-L1 ± anti-CTLA4 immunotherapies, and their tumors show increased expression of genes and cytokines that activate STAT3 signaling. Preclinically, STAT3 modulation reverses this resistance, suggesting STAT3-targeted agents as potential combination partners for immunotherapies in STK11mut NSCLC.

This article is highlighted in the In This Issue feature, p. 2659
Data from Spatiotemporal Immune Landscape of Colorectal Cancer Liver Metastasis at Single-Cell Level
Authors: Wu Yingcheng , Yang Shuaixi , Ma Jiaqiang , Chen Zechuan , Song Guohe , Rao Dongning , Cheng Yifei , Huang Siyuan , Liu Yifei , Jiang Shan , Liu Jinxia , Huang Xiaowu , Wang Xiaoying , Qiu Shuangjian , Xu Jianmin , Xi Ruibin , Bai Fan , Zhou Jian , Fan Jia , Zhang Xiaoming , Gao Qiang
Published: April 2023

Abstract
Liver metastasis, the leading cause of colorectal cancer mortality, exhibits a highly heterogeneous and suppressive immune microenvironment. Here, we sequenced 97 matched samples by using single-cell RNA sequencing and spatial transcriptomics. Strikingly, the metastatic microenvironment underwent remarkable spatial reprogramming of immunosuppressive cells such as MRC1+ CCL18+ M2-like macrophages. We further developed scMetabolism, a computational pipeline for quantifying single-cell metabolism, and observed that those macrophages harbored enhanced metabolic activity. Interestingly, neoadjuvant chemotherapy could block this status and restore the antitumor immune balance in responsive patients, whereas the nonresponsive patients deteriorated into a more suppressive one. Our work described the immune evolution of metastasis and uncovered the black box of how tumors respond to neoadjuvant chemotherapy.
Significance:
We present a single-cell and spatial atlas of colorectal liver metastasis and found the highly metabolically activated MRC1+ CCL18+ M2-like macrophages in metastatic sites. Efficient neoadjuvant chemotherapy can slow down such metabolic activation, raising the possibility to target metabolism pathways in metastasis.

This article is highlighted in the In This Issue feature, p. 1
Data from A CRISPR/Cas9-Engineered ARID1A-Deficient Human Gastric Cancer Organoid Model Reveals Essential and Nonessential Modes of Oncogenic Transformation
Authors: Lo Yuan-Hung , Kolahi Kevin S. , Du Yuhong , Chang Chiung-Ying , Krokhotin Andrey , Nair Ajay , Sobba Walter D. , Karlsson Kasper , Jones Sunny J. , Longacre Teri A. , Mah Amanda T. , Tercan Bahar , Sockell Alexandra , Xu Hang , Seoane Jose A. , Chen Jin , Shmulevich Ilya , Weissman Jonathan S. , Curtis Christina , Califano Andrea , Fu Haian , Crabtree Gerald R. , Kuo Calvin J.
Published: April 2023

Abstract
Mutations in ARID1A rank among the most common molecular aberrations in human cancer. However, oncogenic consequences of ARID1A mutation in human cells remain poorly defined due to lack of forward genetic models. Here, CRISPR/Cas9-mediated ARID1A knockout (KO) in primary TP53−/− human gastric organoids induced morphologic dysplasia, tumorigenicity, and mucinous differentiation. Genetic WNT/β-catenin activation rescued mucinous differentiation, but not hyperproliferation, suggesting alternative pathways of ARID1A KO-mediated transformation. ARID1A mutation induced transcriptional regulatory modules characteristic of microsatellite instability and Epstein–Barr virus–associated subtype human gastric cancer, including FOXM1-associated mitotic genes and BIRC5/survivin. Convergently, high-throughput compound screening indicated selective vulnerability of ARID1A-deficient organoids to inhibition of BIRC5/survivin, functionally implicating this pathway as an essential mediator of ARID1A KO-dependent early-stage gastric tumorigenesis. Overall, we define distinct pathways downstream of oncogenic ARID1A mutation, with nonessential WNT-inhibited mucinous differentiation in parallel with essential transcriptional FOXM1/BIRC5-stimulated proliferation, illustrating the general utility of organoid-based forward genetic cancer analysis in human cells.
Significance:
We establish the first human forward genetic modeling of a commonly mutated tumor suppressor gene, ARID1A. Our study integrates diverse modalities including CRISPR/Cas9 genome editing, organoid culture, systems biology, and small-molecule screening to derive novel insights into early transformation mechanisms of ARID1A-deficient gastric cancers.

See related commentary by Zafra and Dow, p. 1327.

This article is highlighted in the In This Issue feature, p. 1307
Data from AKT Degradation Selectively Inhibits the Growth of PI3K/PTEN Pathway–Mutant Cancers with Wild-Type KRAS and BRAF by Destabilizing Aurora Kinase B
Authors: Xu Jia , Yu Xufen , Martin Tiphaine C. , Bansal Ankita , Cheung Kakit , Lubin Abigail , Stratikopoulos Elias , Cahuzac Kaitlyn M. , Wang Li , Xie Ling , Zhou Royce , Shen Yudao , Wu Xuewei , Yao Shen , Qiao Ruifang , Poulikakos Poulikos I. , Chen Xian , Liu Jing , Jin Jian , Parsons Ramon
Published: April 2023

Abstract
Using a panel of cancer cell lines, we characterized a novel degrader of AKT, MS21. In mutant PI3K–PTEN pathway cell lines, AKT degradation was superior to AKT kinase inhibition for reducing cell growth and sustaining lower signaling over many days. AKT degradation, but not kinase inhibition, profoundly lowered Aurora kinase B (AURKB) protein, which is known to be essential for cell division, and induced G2–M arrest and hyperploidy. PI3K activated AKT phosphorylation of AURKB on threonine 73, which protected it from proteasome degradation. A mutant of AURKB (T73E) that mimics phosphorylation and blocks degradation rescued cells from growth inhibition. Degrader-resistant lines were associated with low AKT phosphorylation, wild-type PI3K/PTEN status, and mutation of KRAS/BRAF. Pan-cancer analysis identified that 19% of cases have PI3K–PTEN pathway mutation without RAS pathway mutation, suggesting that these patients with cancer could benefit from AKT degrader therapy that leads to loss of AURKB.
Significance:
MS21 depletes cells of phosphorylated AKT (pAKT) and a newly identified AKT substrate, AURKB, to inhibit tumor growth in mice. MS21 is superior to prior agents that target PI3K and AKT due to its ability to selectively target active, pAKT and sustain repression of signaling to deplete AURKB.

This article is highlighted in the In This Issue feature, p. 2945
Data from Chemotherapy Induces Senescence-Like Resilient Cells Capable of Initiating AML Recurrence
Authors: Duy Cihangir , Li Meng , Teater Matt , Meydan Cem , Garrett-Bakelman Francine E. , Lee Tak C. , Chin Christopher R. , Durmaz Ceyda , Kawabata Kimihito C. , Dhimolea Eugen , Mitsiades Constantine S. , Doehner Hartmut , D'Andrea Richard J. , Becker Michael W. , Paietta Elisabeth M. , Mason Christopher E. , Carroll Martin , Melnick Ari M.
Published: April 2023

Abstract
Patients with acute myeloid leukemia (AML) frequently relapse after chemotherapy, yet the mechanism by which AML reemerges is not fully understood. Herein, we show that primary AML cells enter a senescence-like phenotype following chemotherapy in vitro and in vivo. This is accompanied by induction of senescence/inflammatory and embryonic diapause transcriptional programs, with downregulation of MYC and leukemia stem cell genes. Single-cell RNA sequencing suggested depletion of leukemia stem cells in vitro and in vivo, and enrichment for subpopulations with distinct senescence-like cells. This senescence effect was transient and conferred superior colony-forming and engraftment potential. Entry into this senescence-like phenotype was dependent on ATR, and persistence of AML cells was severely impaired by ATR inhibitors. Altogether, we propose that AML relapse is facilitated by a senescence-like resilience phenotype that occurs regardless of their stem cell status. Upon recovery, these post-senescence AML cells give rise to relapsed AMLs with increased stem cell potential.
Significance:
Despite entering complete remission after chemotherapy, relapse occurs in many patients with AML. Thus, there is an urgent need to understand the relapse mechanism in AML and the development of targeted treatments to improve outcome. Here, we identified a senescence-like resilience phenotype through which AML cells can survive and repopulate leukemia.

This article is highlighted in the In This Issue feature, p. 1307
Data from AACR Project GENIE: 100,000 Cases and Beyond
Authors: Pugh Trevor J. , Bell Jonathan L. , Bruce Jeff P. , Doherty Gary J. , Galvin Matthew , Green Michelle F. , Hunter-Zinck Haley , Kumari Priti , Lenoue-Newton Michele L. , Li Marilyn M. , Lindsay James , Mazor Tali , Ovalle Andrea , Sammut Stephen-John , Schultz Nikolaus , Yu Thomas V. , Sweeney Shawn M. , Bernard Brady
Published: April 2023

Abstract
The American Association for Cancer Research (AACR) Project Genomics Evidence Neoplasia Information Exchange (GENIE) is an international pan-cancer registry with the goal to inform cancer research and clinical care worldwide. Founded in late 2015, the milestone GENIE 9.1-public release contains data from >110,000 tumors from >100,000 people treated at 19 cancer centers from the United States, Canada, the United Kingdom, France, the Netherlands, and Spain. Here, we demonstrate the use of these real-world data, harmonized through a centralized data resource, to accurately predict enrollment on genome-guided trials, discover driver alterations in rare tumors, and identify cancer types without actionable mutations that could benefit from comprehensive genomic analysis. The extensible data infrastructure and governance framework support additional deep patient phenotyping through biopharmaceutical collaborations and expansion to include new data types such as cell-free DNA sequencing. AACR Project GENIE continues to serve a global precision medicine knowledge base of increasing impact to inform clinical decision-making and bring together cancer researchers internationally.
Significance:
AACR Project GENIE has now accrued data from >110,000 tumors, placing it among the largest repository of publicly available, clinically annotated genomic data in the world. GENIE has emerged as a powerful resource to evaluate genome-guided clinical trial design, uncover drivers of cancer subtypes, and inform real-world use of genomic data.

This article is highlighted in the In This Issue feature, p. 2007
Data from Transcription Elongation Machinery Is a Druggable Dependency and Potentiates Immunotherapy in Glioblastoma Stem Cells
Authors: Qiu Zhixin , Zhao Linjie , Shen Jia Z. , Liang Zhengyu , Wu Qiulian , Yang Kailin , Min Lihua , Gimple Ryan C. , Yang Qiyuan , Bhargava Shruti , Jin Chunyu , Kim Cheryl , Hinz Denise , Dixit Deobrat , Bernatchez Jean A. , Prager Briana C. , Zhang Guoxin , Dong Zhen , Lv Deguan , Wang Xujun , Kim Leo J.Y. , Zhu Zhe , Jones Katherine A. , Zheng Ye , Wang Xiuxing , Siqueira-Neto Jair L. , Chavez Lukas , Fu Xiang-Dong , Spruck Charles , Rich Jeremy N.
Published: April 2023

Abstract
Glioblastoma (GBM) is the most lethal primary brain cancer characterized by therapeutic resistance, which is promoted by GBM stem cells (GSC). Here, we interrogated gene expression and whole-genome CRISPR/Cas9 screening in a large panel of patient-derived GSCs, differentiated GBM cells (DGC), and neural stem cells (NSC) to identify master regulators of GSC stemness, revealing an essential transcription state with increased RNA polymerase II–mediated transcription. The YY1 and transcriptional CDK9 complex was essential for GSC survival and maintenance in vitro and in vivo. YY1 interacted with CDK9 to regulate transcription elongation in GSCs. Genetic or pharmacologic targeting of the YY1–CDK9 complex elicited RNA m6A modification–dependent interferon responses, reduced regulatory T-cell infiltration, and augmented efficacy of immune checkpoint therapy in GBM. Collectively, these results suggest that YY1–CDK9 transcription elongation complex defines a targetable cell state with active transcription, suppressed interferon responses, and immunotherapy resistance in GBM.
Significance:
Effective strategies to rewire immunosuppressive microenvironment and enhance immunotherapy response are still lacking in GBM. YY1-driven transcriptional elongation machinery represents a druggable target to activate interferon response and enhance anti–PD-1 response through regulating the m6A modification program, linking epigenetic regulation to immunomodulatory function in GBM.

This article is highlighted in the In This Issue feature, p. 275
Data from Reverse Transcriptase Inhibition Disrupts Repeat Element Life Cycle in Colorectal Cancer
Authors: Rajurkar Mihir , Parikh Aparna R. , Solovyov Alexander , You Eunae , Kulkarni Anupriya S. , Chu Chong , Xu Katherine H. , Jaicks Christopher , Taylor Martin S. , Wu Connie , Alexander Katherine A. , Good Charly R. , Szabolcs Annamaria , Gerstberger Stefanie , Tran Antuan V. , Xu Nova , Ebright Richard Y. , Van Seventer Emily E. , Vo Kevin D. , Tai Eric C. , Lu Chenyue , Joseph-Chazan Jasmin , Raabe Michael J. , Nieman Linda T. , Desai Niyati , Arora Kshitij S. , Ligorio Matteo , Thapar Vishal , Cohen Limor , Garden Padric M. , Senussi Yasmeen , Zheng Hui , Allen Jill N. , Blaszkowsky Lawrence S. , Clark Jeffrey W. , Goyal Lipika , Wo Jennifer Y. , Ryan David P. , Corcoran Ryan B. , Deshpande Vikram , Rivera Miguel N. , Aryee Martin J. , Hong Theodore S. , Berger Shelley L. , Walt David R. , Burns Kathleen H. , Park Peter J. , Greenbaum Benjamin D. , Ting David T.
Published: April 2023

Abstract
Altered RNA expression of repetitive sequences and retrotransposition are frequently seen in colorectal cancer, implicating a functional importance of repeat activity in cancer progression. We show the nucleoside reverse transcriptase inhibitor 3TC targets activities of these repeat elements in colorectal cancer preclinical models with a preferential effect in p53-mutant cell lines linked with direct binding of p53 to repeat elements. We translate these findings to a human phase II trial of single-agent 3TC treatment in metastatic colorectal cancer with demonstration of clinical benefit in 9 of 32 patients. Analysis of 3TC effects on colorectal cancer tumorspheres demonstrates accumulation of immunogenic RNA:DNA hybrids linked with induction of interferon response genes and DNA damage response. Epigenetic and DNA-damaging agents induce repeat RNAs and have enhanced cytotoxicity with 3TC. These findings identify a vulnerability in colorectal cancer by targeting the viral mimicry of repeat elements.
Significance:
Colorectal cancers express abundant repeat elements that have a viral-like life cycle that can be therapeutically targeted with nucleoside reverse transcriptase inhibitors (NRTI) commonly used for viral diseases. NRTIs induce DNA damage and interferon response that provide a new anticancer therapeutic strategy.

This article is highlighted in the In This Issue feature, p. 1397
Data from Mutant IDH Inhibits IFNγ–TET2 Signaling to Promote Immunoevasion and Tumor Maintenance in Cholangiocarcinoma
Authors: Wu Meng-Ju , Shi Lei , Dubrot Juan , Merritt Joshua , Vijay Vindhya , Wei Ting-Yu , Kessler Emily , Olander Kira E. , Adil Ramzi , Pankaj Amaya , Tummala Krishna Seshu , Weeresekara Vajira , Zhen Yuanli , Wu Qibiao , Luo Meiqi , Shen William , García-Beccaria María , Fernández-Vaquero Mirian , Hudson Christine , Ronseaux Sebastien , Sun Yi , Saad-Berreta Rodrigo , Jenkins Russell W. , Wang Tong , Heikenwälder Mathias , Ferrone Cristina R. , Goyal Lipika , Nicolay Brandon , Deshpande Vikram , Kohli Rahul M. , Zheng Hongwu , Manguso Robert T. , Bardeesy Nabeel
Published: April 2023

Abstract
Isocitrate dehydrogenase 1 mutations (mIDH1) are common in cholangiocarcinoma. (R)-2-hydroxyglutarate generated by the mIDH1 enzyme inhibits multiple α-ketoglutarate–dependent enzymes, altering epigenetics and metabolism. Here, by developing mIDH1-driven genetically engineered mouse models, we show that mIDH1 supports cholangiocarcinoma tumor maintenance through an immunoevasion program centered on dual (R)-2-hydroxyglutarate–mediated mechanisms: suppression of CD8+ T-cell activity and tumor cell–autonomous inactivation of TET2 DNA demethylase. Pharmacologic mIDH1 inhibition stimulates CD8+ T-cell recruitment and interferon γ (IFNγ) expression and promotes TET2-dependent induction of IFNγ response genes in tumor cells. CD8+ T-cell depletion or tumor cell–specific ablation of TET2 or IFNγ receptor 1 causes treatment resistance. Whereas immune-checkpoint activation limits mIDH1 inhibitor efficacy, CTLA4 blockade overcomes immunosuppression, providing therapeutic synergy. The findings in this mouse model of cholangiocarcinoma demonstrate that immune function and the IFNγ–TET2 axis are essential for response to mIDH1 inhibition and suggest a novel strategy for potentiating efficacy.
Significance:
Mutant IDH1 inhibition stimulates cytotoxic T-cell function and derepression of the DNA demethylating enzyme TET2, which is required for tumor cells to respond to IFNγ. The discovery of mechanisms of treatment efficacy and the identification of synergy by combined CTLA4 blockade provide the foundation for new therapeutic strategies.

See related commentary by Zhu and Kwong, p. 604.

This article is highlighted in the In This Issue feature, p. 587
Data from Synthetic Essentiality of Tryptophan 2,3-Dioxygenase 2 in APC-Mutated Colorectal Cancer
Authors: Lee Rumi , Li Jiexi , Li Jun , Wu Chang-Jiun , Jiang Shan , Hsu Wen-Hao , Chakravarti Deepavali , Chen Peiwen , LaBella Kyle A. , Li Jing , Spring Denise J. , Zhao Di , Wang Y. Alan , DePinho Ronald A.
Published: April 2023

Abstract
Inactivation of adenomatous polyposis coli (APC) is common across many cancer types and serves as a critical initiating event in most sporadic colorectal cancers. APC deficiency activates WNT signaling, which remains an elusive target for cancer therapy, prompting us to apply the synthetic essentiality framework to identify druggable vulnerabilities for APC-deficient cancers. Tryptophan 2,3-dioxygenase 2 (TDO2) was identified as a synthetic essential effector of APC-deficient colorectal cancer. Mechanistically, APC deficiency results in the TCF4/β-catenin–mediated upregulation of TDO2 gene transcription. TDO2 in turn activates the Kyn–AhR pathway, which increases glycolysis to drive anabolic cancer cell growth and CXCL5 secretion to recruit macrophages into the tumor microenvironment. Therapeutically, APC-deficient colorectal cancer models were susceptible to TDO2 depletion or pharmacologic inhibition, which impaired cancer cell proliferation and enhanced antitumor immune profiles. Thus, APC deficiency activates a TCF4–TDO2–AhR–CXCL5 circuit that affects multiple cancer hallmarks via autonomous and nonautonomous mechanisms and illuminates a genotype-specific vulnerability in colorectal cancer.
Significance:
This study identifies critical effectors in the maintenance of APC-deficient colorectal cancer and demonstrates the relationship between APC/WNT pathway and kynurenine pathway signaling. It further determines the tumor-associated macrophage biology in APC-deficient colorectal cancer, informing genotype-specific therapeutic targets and the use of TDO2 inhibitors.

This article is highlighted in the In This Issue feature, p. 1599
Data from Senescence Rewires Microenvironment Sensing to Facilitate Antitumor Immunity
Authors: Chen Hsuan-An , Ho Yu-Jui , Mezzadra Riccardo , Adrover Jose M. , Smolkin Ryan , Zhu Changyu , Woess Katharina , Bernstein Nicholas , Schmitt Georgia , Fong Linda , Luan Wei , Wuest Alexandra , Tian Sha , Li Xiang , Broderick Caroline , Hendrickson Ronald C. , Egeblad Mikala , Chen Zhenghao , Alonso-Curbelo Direna , Lowe Scott W.
Published: April 2023

Abstract
Cellular senescence involves a stable cell-cycle arrest coupled to a secretory program that, in some instances, stimulates the immune clearance of senescent cells. Using an immune-competent liver cancer model in which senescence triggers CD8 T cell–mediated tumor rejection, we show that senescence also remodels the cell-surface proteome to alter how tumor cells sense environmental factors, as exemplified by type II interferon (IFNγ). Compared with proliferating cells, senescent cells upregulate the IFNγ receptor, become hypersensitized to microenvironmental IFNγ, and more robustly induce the antigen-presenting machinery—effects also recapitulated in human tumor cells undergoing therapy-induced senescence. Disruption of IFNγ sensing in senescent cells blunts their immune-mediated clearance without disabling the senescence state or its characteristic secretory program. Our results demonstrate that senescent cells have an enhanced ability to both send and receive environmental signals and imply that each process is required for their effective immune surveillance.
Significance:
Our work uncovers an interplay between tissue remodeling and tissue-sensing programs that can be engaged by senescence in advanced cancers to render tumor cells more visible to the adaptive immune system. This new facet of senescence establishes reciprocal heterotypic signaling interactions that can be induced therapeutically to enhance antitumor immunity.

See related article by Marin et al., p. 410.

This article is highlighted in the In This Issue feature, p. 247
Supplementary Figure Legend from IL4 Limits the Efficacy of Tumor-Targeted Antibody Therapy in a Murine Model
Authors: Surana Rishi , Wang Shangzi , Xu Wei , Jablonski Sandra A. , Weiner Louis M.
Published: April 2023

Supplementary Figure Legend
Supplemental Figure 1 from IL4 Limits the Efficacy of Tumor-Targeted Antibody Therapy in a Murine Model
Authors: Surana Rishi , Wang Shangzi , Xu Wei , Jablonski Sandra A. , Weiner Louis M.
Published: April 2023

IL-4 neutralization alters the composition of the tumor microenvironment.
Figure S1 from PARP1 Suppresses the Transcription of PD-L1 by Poly(ADP-Ribosyl)ating STAT3
Authors: Ding Ling , Chen Xi , Xu Xiaqing , Qian Yuli , Liang Guikai , Yao Fengqi , Yao Zhangting , Wu Honghai , Zhang Jieqiong , He Qiaojun , Yang Bo
Published: April 2023

PARP1 suppresses the transcription of PD-L1 in various cancer cells.
Table S1 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

Primer sequences were used in our study.
Figure S4 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

TGF-b,secreted by MDSCs,could regulate MAEL through Smad2/Smad3.
Supplementary Table 1 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 - 88K, Supplemental Table 1: Primers used for qRT-PCR.
Figure S3 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 effect of MAEL,Reparixin and MDSCs on tumor growth.
Figure 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

IL-8 played a role in tumor microenvironment.
Supplementary Figure 1 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 - 180K, Supplemental Figure 1: Complete deletion of Dlg1 in three independent Cre-expression systems permits development of mature, peripheral B cell subsets.
Supplementary Figures 1 - 3 from Antigen-Specific Bacterial Vaccine Combined with Anti-PD-L1 Rescues Dysfunctional Endogenous T Cells to Reject Long-Established Cancer
Authors: Binder David C. , Engels Boris , Arina Ainhoa , Yu Ping , Slauch James M. , Fu Yang-Xin , Karrison Theodore , Burnette Byron , Idel Christian , Zhao Ming , Hoffman Robert M. , Munn David H. , Rowley Donald A. , Schreiber Hans
Published: April 2023

PDF file - 291K, Figure S1. A1-R SIINF preferentially accumulates in established B16-OVA tumors. Figure S2. A1-R SIINF induces systemic SIINF-specific CD8+ T cell proliferation. Figure S3. Weekly A1-R SIINF treatment leads to rejection of established B16-OVA tumors. Figure S4. The majority of intratumoral SIINF-specific CD8+ T cells still express a high level of PD-1 following A1-R OVA treatment.
Supplementary Figure 4 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 - 27K, Figure S4. Activation of Mekk2/Erk5 pathway is required for tumor cells to escape NK cell-mediated immunosurveillance.
Supplementary Table 3 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

Cox Proportional Hazard table of the Estimated TIL content and patient survival
Supplementary Figure 1 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 - 36K, Figure S1: Generation and characterization of monoclonal cell lines with different expression levels of miR-17~92 cluster miRNAs.
Supplementary Figure 3 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

Supplementary Figure 3 has the top 25 TCR clones from tumor biopsies at pre-treatment and the frequency of these clones in the blood.
Supplementary Figure 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

Supplementary Figure 2 has the statistical analysis of TCR sequencing from new samples of control patients (no immunotherapy) compared with DC vaccine patients.
Supplementary Methods from Rescue of Notch-1 Signaling in Antigen-Specific CD8+ T Cells Overcomes Tumor-Induced T-cell Suppression and Enhances Immunotherapy in Cancer
Authors: Sierra Rosa A. , Thevenot Paul , Raber Patrick L. , Cui Yan , Parsons Chris , Ochoa Augusto C. , Trillo-Tinoco Jimena , Valle Luis Del , Rodriguez Paulo C.
Published: April 2023

PDF file - 97KB
Supplementary Figure 3 from Prolonged Benefit from Ipilimumab Correlates with Improved Outcomes from Subsequent Pembrolizumab
Authors: Shreders Amanda , Joseph Richard , Peng Chengwei , Ye Fei , Zhao Shilin , Puzanov Igor , Sosman Jeffrey A. , Johnson Douglas B.
Published: April 2023

Progression free survival and overall survival to pembrolizumab in ipilimumab responders vs. non-responders. (1=ipilimumab responders, 0=ipilimumab non-responders)
Supplementary Figure 5 from In Vitro Characterization of the Anti-PD-1 Antibody Nivolumab, BMS-936558, and In Vivo Toxicology in Non-Human Primates
Authors: Wang Changyu , Thudium Kent B. , Han Minhua , Wang Xi-Tao , Huang Haichun , Feingersh Diane , Garcia Candy , Wu Yi , Kuhne Michelle , Srinivasan Mohan , Singh Sujata , Wong Susan , Garner Neysa , Leblanc Heidi , Bunch R. Todd , Blanset Diann , Selby Mark J. , Korman Alan J.
Published: April 2023

PDF file - 25K, Figure S5. Effect of nivolumab on CD8+ T-cell subsets and DCs in PBMCs from nivolumab-treated cynomolgus monkeys.
Supplementary Figure 1 from In Vitro Characterization of the Anti-PD-1 Antibody Nivolumab, BMS-936558, and In Vivo Toxicology in Non-Human Primates
Authors: Wang Changyu , Thudium Kent B. , Han Minhua , Wang Xi-Tao , Huang Haichun , Feingersh Diane , Garcia Candy , Wu Yi , Kuhne Michelle , Srinivasan Mohan , Singh Sujata , Wong Susan , Garner Neysa , Leblanc Heidi , Bunch R. Todd , Blanset Diann , Selby Mark J. , Korman Alan J.
Published: April 2023

PDF file - 72K, Figure S1. Binding of nivolumab to human T cells.
Supplementary Figure S4 from A Paracrine Role for IL6 in Prostate Cancer Patients: Lack of Production by Primary or Metastatic Tumor Cells
Authors: Yu Shu-Han , Zheng Qizhi , Esopi David , Macgregor-Das Anne , Luo Jun , Antonarakis Emmanuel S. , Drake Charles G. , Vessella Robert , Morrissey Colm , De Marzo Angelo M. , Sfanos Karen S.
Published: April 2023

IL-6 CISH assay is more sensitive than IL-6 IHC. (A) Standard curve generated using estimated copies of IL-6 cDNA clone expression vector (Origene, SC125236) used to determine IL-6 mRNA copy number in DU145 and PC3 cells. (B) IL-6 CISH on corresponding DU145 and PC3 cells. Note DU145 cells with many copies of IL-6 mRNA (arrow) and cells where lower copy numbers (5-10 dots per cell, arrowhead) can be visualized. Side-by-side IL-6 IHC is negative.
Supplementary Figures 1 through 6 from Angiopoietin-2 as a Biomarker and Target for Immune Checkpoint Therapy
Authors: Wu Xinqi , Giobbie-Hurder Anita , Liao Xiaoyun , Connelly Courtney , Connolly Erin M. , Li Jingjing , Manos Michael P. , Lawrence Donald , McDermott David , Severgnini Mariano , Zhou Jun , Gjini Evisa , Lako Ana , Lipschitz Mikel , Pak Christine J. , Abdelrahman Sara , Rodig Scott , Hodi F. Stephen
Published: April 2023

Fig. S1. Kaplan-Meier survival curves of patients receiving ipilimumab or ipilimumab plus bevacizumab. Fig. S2. Clinical responses and survival of PD-1 blockade-treated patients based on serum ANGPT2 fold changes. Fig. S3. Hypoxia upregulated ANGPT2 expression in melanoma cells. Fig. S4. ANGPT2 enhanced PD-L1 expression on CSF1-activated MDM from healthy donors. Fig. S5. Antibody responses to ANGPT2 and clinical responses of melanoma patients receiving immune checkpoint therapy. Fig. S6. Enriched endogenous anti-ANGPT2 antibodies inhibited ANGPT2-mediated Erk1/2 phosphorylation.
Supplementary Figure S1 from A Paracrine Role for IL6 in Prostate Cancer Patients: Lack of Production by Primary or Metastatic Tumor Cells
Authors: Yu Shu-Han , Zheng Qizhi , Esopi David , Macgregor-Das Anne , Luo Jun , Antonarakis Emmanuel S. , Drake Charles G. , Vessella Robert , Morrissey Colm , De Marzo Angelo M. , Sfanos Karen S.
Published: April 2023

IL-6 mRNA expression in macrophages and endothelial cells. RNAscope 2-plex assay for IL-6 (red) and CD68 (green) (A) or IL-6 (red) and CD31 (green) (B) indicated that some IL-6 positive cells in the stroma are macrophages or endothelial cells, respectively (arrows).
Supplementary Figure Legends from A Paracrine Role for IL6 in Prostate Cancer Patients: Lack of Production by Primary or Metastatic Tumor Cells
Authors: Yu Shu-Han , Zheng Qizhi , Esopi David , Macgregor-Das Anne , Luo Jun , Antonarakis Emmanuel S. , Drake Charles G. , Vessella Robert , Morrissey Colm , De Marzo Angelo M. , Sfanos Karen S.
Published: April 2023

Supplementary Figure Legends
Supplementary Figure Legends from STING Ligand c-di-GMP Improves Cancer Vaccination against Metastatic Breast Cancer
Authors: Chandra Dinesh , Quispe-Tintaya Wilber , Jahangir Arthee , Asafu-Adjei Denise , Ramos Ilyssa , Sintim Herman O. , Zhou Jie , Hayakawa Yoshihiro , Karaolis David K.R. , Gravekamp Claudia
Published: April 2023

PDF file - 114K
Supplementary Figure 7 from STING Ligand c-di-GMP Improves Cancer Vaccination against Metastatic Breast Cancer
Authors: Chandra Dinesh , Quispe-Tintaya Wilber , Jahangir Arthee , Asafu-Adjei Denise , Ramos Ilyssa , Sintim Herman O. , Zhou Jie , Hayakawa Yoshihiro , Karaolis David K.R. , Gravekamp Claudia
Published: April 2023

PDF file - 287K, Figure S7: Maturation of DC and MDSC in spleens of 4T1 tumor-bearing mice by c-di-GMP in vitro.
Supplementary Figure 6 from STING Ligand c-di-GMP Improves Cancer Vaccination against Metastatic Breast Cancer
Authors: Chandra Dinesh , Quispe-Tintaya Wilber , Jahangir Arthee , Asafu-Adjei Denise , Ramos Ilyssa , Sintim Herman O. , Zhou Jie , Hayakawa Yoshihiro , Karaolis David K.R. , Gravekamp Claudia
Published: April 2023

PDF file - 36K, Figure S6: Kinetic curve of 4T1 primary tumors in c-di-GMP-treated and saline mice.
Supplementary Figures 1 through 10 and Supplementary Tables 1 through 4 from Immunotherapy Converts Nonimmunogenic Pancreatic Tumors into Immunogenic Foci of Immune Regulation
Authors: Lutz Eric R. , Wu Annie A. , Bigelow Elaine , Sharma Rajni , Mo Guanglan , Soares Kevin , Solt Sara , Dorman Alvin , Wamwea Anthony , Yager Allison , Laheru Daniel , Wolfgang Christopher L. , Wang Jiang , Hruban Ralph H. , Anders Robert A. , Jaffee Elizabeth M. , Zheng Lei
Published: April 2023

Figure S1 Schema of the Neoadjuvant and Adjuvant Study of Panc GVAX. Figure S2 Pre- and post-vaccination mesothelin peptide-specific T cell levels in responders versus nonresponders. Figure S3 Intratumoral tertiary lymphoid aggregate in PDACs from patients treated with GVAX and lymphocyte cluster in PDACs from patients not treated with GVAX. Figure S4 The development of post-vaccination intratumoral lymphoid aggregates is associated with survival. Figure S5 Relatively more Granzyme B expressing cells observed outside of the lymphoid aggregates. Figure S6 Microdissection of Lymphoid Aggregates for Microarray Analysis. Figure S7 Microarray analysis of lymphoid aggregates revealed gene signatures in four pathways involved in regulating immune cell trafficking and function. Figure S8 Decreased Treg and increased TH17 pathway gene expression signatures are associated with improved post-vaccination responses. Figure S9 Downregulation of Treg pathway gene expression in TIL following treatment with PDAC GVAX is associated with longer survival. Figure S10 IL17A-producing T cells are present in low levels in TIL from PDAC GVAX treated patients. Figure S11 Treatment with low dose Cy increases post-vaccination densities of intratumoral lymphoid aggregates and reduces Treg levels in the PDAC TME. Figure S12 T cell infiltration in PDACs with low versus high CD8/Foxp3 ratio. Table S1 Immunohistochemistry protocols. Table S2 Quantitative real-time RT-PCR primers. Table S3 Scores of TH1, TH2, Treg, and TH17 pathway gene expression in PDAC TIL analyzed by quantitative real-time RT-PCR. Table S4 Numbers of TIL specimens with detectable expression of immune related genes.
Supplemental Figure S6 from Extracellular Vesicles Present in Human Ovarian Tumor Microenvironments Induce a Phosphatidylserine-Dependent Arrest in the T-cell Signaling Cascade
Authors: Kelleher Raymond J. , Balu-Iyer Sathy , Loyall Jenni , Sacca Anthony J. , Shenoy Gautam N. , Peng Peng , Iyer Vandana , Fathallah Anas M. , Berenson Charles S. , Wallace Paul K. , Tario Joseph , Odunsi Kunle , Bankert Richard B.
Published: April 2023

Fig S6. EVs directly inhibit CD4+ and CD8+ T cell activation
Supplemental Figure S5 from Extracellular Vesicles Present in Human Ovarian Tumor Microenvironments Induce a Phosphatidylserine-Dependent Arrest in the T-cell Signaling Cascade
Authors: Kelleher Raymond J. , Balu-Iyer Sathy , Loyall Jenni , Sacca Anthony J. , Shenoy Gautam N. , Peng Peng , Iyer Vandana , Fathallah Anas M. , Berenson Charles S. , Wallace Paul K. , Tario Joseph , Odunsi Kunle , Bankert Richard B.
Published: April 2023

Fig S5. EVs inhibit CD69 upregulation of CD4+ and CD8+ T cells.
Supplementary Figure 5 from Using Quantitative Seroproteomics to Identify Antibody Biomarkers in Pancreatic Cancer
Authors: Jhaveri Darshil T. , Kim Min-Sik , Thompson Elizabeth D. , Huang Lanqing , Sharma Rajni , Klein Alison P. , Zheng Lei , Le Dung T. , Laheru Daniel A. , Pandey Akhilesh , Jaffee Elizabeth M. , Anders Robert A.
Published: April 2023

MYPT1 and PSMC5 expression in 3 different subtypes (basal, HER-2 positive and ER positive) of breast cancer.
Supplementary Figures 1 - 5 from Combination of 4-1BB Agonist and PD-1 Antagonist Promotes Antitumor Effector/Memory CD8 T Cells in a Poorly Immunogenic Tumor Model
Authors: Chen Shihao , Lee Li-Fen , Fisher Timothy S. , Jessen Bart , Elliott Mark , Evering Winston , Logronio Kathryn , Tu Guang Huan , Tsaparikos Konstantinos , Li Xiaoai , Wang Hui , Ying Chi , Xiong Mengli , VanArsdale Todd , Lin John C.
Published: April 2023

Supplementary Figure S1. Anti-4-1BB and anti-PD-1 synergized to suppress B16F10 tumor growth. Supplementary Figure S2. The flow cytometric gating strategy to analyze immune cells. Supplementary Figure S3. Elevated expression of genes associated with anti-tumor immune response in MC38 colon carcinomas. Supplementary Figure S4. Accumulation of CD8+ T cell and memory phenotype differentiation in MC38 model. Supplementary Figure S5. Serum liver enzyme levels and hematology alterations in response to 4-1BB activation therapy in B16F10 tumor-bearing mice.
Supplementary Table S1 from Decitabine Enhances Lymphocyte Migration and Function and Synergizes with CTLA-4 Blockade in a Murine Ovarian Cancer Model
Authors: Wang Lei , Amoozgar Zohreh , Huang Jing , Saleh Mohammad H. , Xing Deyin , Orsulic Sandra , Goldberg Michael S.
Published: April 2023

Supplementary Table 1: A list of genes regulated by decitabine treatment in BR5FVB1-Akt cells.
Supplementary Figure S3 from Decitabine Enhances Lymphocyte Migration and Function and Synergizes with CTLA-4 Blockade in a Murine Ovarian Cancer Model
Authors: Wang Lei , Amoozgar Zohreh , Huang Jing , Saleh Mohammad H. , Xing Deyin , Orsulic Sandra , Goldberg Michael S.
Published: April 2023

Supplementary Figure 3: Decitabine promotes CD80 expression and apoptosis in BR5FVB1-Akt ovarian cancer cells when administered at high concentrations.
Supplementary Figure S1 from Decitabine Enhances Lymphocyte Migration and Function and Synergizes with CTLA-4 Blockade in a Murine Ovarian Cancer Model
Authors: Wang Lei , Amoozgar Zohreh , Huang Jing , Saleh Mohammad H. , Xing Deyin , Orsulic Sandra , Goldberg Michael S.
Published: April 2023

Supplementary Figure 1: Decitabine upregulates major histocompatibility complex I on BR5FVB1-Akt cells in a dose-dependent manner.
Supplemental Figure 2 from CALGB 150905 (Alliance): Rituximab Broadens the Antilymphoma Response by Activating Unlicensed NK Cells
Authors: Du Juan , Lopez-Verges Sandra , Pitcher Brandelyn N. , Johnson Jeffrey , Jung Sin-Ho , Zhou Lili , Hsu Katharine , Czuczman Myron S. , Cheson Bruce , Kaplan Lawrence , Lanier Lewis L. , Venstrom Jeffrey M.
Published: April 2023

NK cell licensing endows a "missing self" response to HLA class I-deficient K562 myeloid cell line.
Supplemental Figure 1 from CALGB 150905 (Alliance): Rituximab Broadens the Antilymphoma Response by Activating Unlicensed NK Cells
Authors: Du Juan , Lopez-Verges Sandra , Pitcher Brandelyn N. , Johnson Jeffrey , Jung Sin-Ho , Zhou Lili , Hsu Katharine , Czuczman Myron S. , Cheson Bruce , Kaplan Lawrence , Lanier Lewis L. , Venstrom Jeffrey M.
Published: April 2023

Exclusion gating technique and NK cell flow cytometric analysis to determine the effector potency of individual NK cell populations.
Supplementary Table 5 from Identification of Anti-CA125 Antibody Responses in Ovarian Cancer Patients by a Novel Deep Sequence–Coupled Biopanning Platform
Authors: Frietze Kathryn M. , Roden Richard B.S. , Lee Ji-Hyun , Shi Yang , Peabody David S. , Chackerian Bryce
Published: April 2023

Supplemental Table 5. 2X2 table for CA125 and Anti-CA125.
Supplemental Figure 1 from Identification of Anti-CA125 Antibody Responses in Ovarian Cancer Patients by a Novel Deep Sequence–Coupled Biopanning Platform
Authors: Frietze Kathryn M. , Roden Richard B.S. , Lee Ji-Hyun , Shi Yang , Peabody David S. , Chackerian Bryce
Published: April 2023

OvCa and normal plasma reactivity to DISGTNTSRA by ELISA.
Supplementary Methods from Glioblastoma Eradication Following Immune Checkpoint Blockade in an Orthotopic, Immunocompetent Model
Authors: Reardon David A. , Gokhale Prafulla C. , Klein Sarah R. , Ligon Keith L. , Rodig Scott J. , Ramkissoon Shakti H. , Jones Kristen L. , Conway Amy Saur , Liao Xiaoyun , Zhou Jun , Wen Patrick Y. , Van Den Abbeele Annick D. , Hodi F. Stephen , Qin Lei , Kohl Nancy E. , Sharpe Arlene H. , Dranoff Glenn , Freeman Gordon J.
Published: April 2023

Supplementary Methods
Supplementary Figures 1 through 7 and Supplementary Table 1 from Glioblastoma Eradication Following Immune Checkpoint Blockade in an Orthotopic, Immunocompetent Model
Authors: Reardon David A. , Gokhale Prafulla C. , Klein Sarah R. , Ligon Keith L. , Rodig Scott J. , Ramkissoon Shakti H. , Jones Kristen L. , Conway Amy Saur , Liao Xiaoyun , Zhou Jun , Wen Patrick Y. , Van Den Abbeele Annick D. , Hodi F. Stephen , Qin Lei , Kohl Nancy E. , Sharpe Arlene H. , Dranoff Glenn , Freeman Gordon J.
Published: April 2023

Supplemental Figure 1. Bioluminescence plots of individual animals following treatment with immune checkpoint blocking mAbs. Supplemental Figure 2. Immune cell infiltrates within intracranial GL261-luc2 tumor following treatment with isotype control IgG or combination therapy with CTLA-4 plus PD-1 mAb therapy. Supplemental Figure 3: Treatment antibody and detection antibody for PD-1 do not share same the epitope. Supplemental Figure 4. Representative immunohistochemistry results of intratumoral CD3+, CD4+ and CD8+ T cell infiltrates following immune checkpoint therapy with mAbs against CTLA-4, PD-1 and both CTLA-4 and PD-1. Supplemental Figure 5. Immune cell infiltration within the draining cervical lymph node (cLN) of GL261-luc2 tumor-bearing mice following treatment with isotype control IgG or combination therapy with mAbs against CTLA-4 plus PD-1. Supplemental Figure 6. Comparisons of chemokine expression levels in sera of mice treated with checkpoint blockade. Supplemental Figure 7: Expression of checkpoint ligands and receptors on GL261-Luc cells in vitro. Supplementary Table 1. Arrangement of chemokines on the Mouse Chemokine Antibody Array.
Supplementary Table 1 from Durable Complete Response from Metastatic Melanoma after Transfer of Autologous T Cells Recognizing 10 Mutated Tumor Antigens
Authors: Prickett Todd D. , Crystal Jessica S. , Cohen Cyrille J. , Pasetto Anna , Parkhurst Maria R. , Gartner Jared J. , Yao Xin , Wang Rong , Gros Alena , Li Yong F. , El-Gamil Mona , Trebska-McGowan Kasia , Rosenberg Steven A. , Robbins Paul F.
Published: April 2023

A list of genes that were found to be somatically mutated in pt3713 and all of the major information needed for our genomic study
Supplementary Figure 1 from Durable Complete Response from Metastatic Melanoma after Transfer of Autologous T Cells Recognizing 10 Mutated Tumor Antigens
Authors: Prickett Todd D. , Crystal Jessica S. , Cohen Cyrille J. , Pasetto Anna , Parkhurst Maria R. , Gartner Jared J. , Yao Xin , Wang Rong , Gros Alena , Li Yong F. , El-Gamil Mona , Trebska-McGowan Kasia , Rosenberg Steven A. , Robbins Paul F.
Published: April 2023

The number of each of the six classes of base substitutions resulting in non-synonymous changes in the whole exome screen is shown.
Supplementary Figure Legends from CD4+ T Lymphocyte Ablation Prevents Pancreatic Carcinogenesis in Mice
Authors: Zhang Yaqing , Yan Wei , Mathew Esha , Bednar Filip , Wan Shanshan , Collins Meredith A. , Evans Rebecca A. , Welling Theodore H. , Vonderheide Robert H. , di Magliano Marina Pasca
Published: April 2023

PDF file - 68K
Supplementary Figure 4 from CD4+ T Lymphocyte Ablation Prevents Pancreatic Carcinogenesis in Mice
Authors: Zhang Yaqing , Yan Wei , Mathew Esha , Bednar Filip , Wan Shanshan , Collins Meredith A. , Evans Rebecca A. , Welling Theodore H. , Vonderheide Robert H. , di Magliano Marina Pasca
Published: April 2023

PDF file - 358K, Cytokine expression is altered in CD4-deficient iKras* mice.
Supplementary Figure 3 from CD4+ T Lymphocyte Ablation Prevents Pancreatic Carcinogenesis in Mice
Authors: Zhang Yaqing , Yan Wei , Mathew Esha , Bednar Filip , Wan Shanshan , Collins Meredith A. , Evans Rebecca A. , Welling Theodore H. , Vonderheide Robert H. , di Magliano Marina Pasca
Published: April 2023

PDF file - 949K, The process of tissue repair following pancreatitis induction is delayed in CD4-/- mice.