bluuebunny/crossref_metadata_2025 huggingface dataset:
Data from Ablation of p57+ Quiescent Cancer Stem Cells Suppresses Recurrence After Chemotherapy of Intestinal Tumors
Authors: Oka Takeru , Higa Tsunaki , Sugahara Osamu , Koga Daisuke , Nakayama Shogo , Nakayama Keiichi I.
Published: September 2024

Abstract
Quiescent cancer stem cells (CSCs) are resistant to conventional anti-cancer treatments and have been shown to contribute to disease relapse after therapy in some cancer types. The identification and characterization of quiescent CSCs could facilitate the development of strategies to target this cell population and block recurrence. Here, we established a syngeneic orthotopic transplantation model in mice based on intestinal cancer organoids to profile quiescent CSCs. Single-cell transcriptomic analysis of the primary tumors formed in vivo revealed that conventional Lgr5high intestinal CSCs comprise both actively and slowly cycling subpopulations, the latter of which specifically expresses the cyclin-dependent kinase inhibitor p57. Tumorigenicity assays and lineage tracing experiments showed that the quiescent p57+ CSCs contribute in only a limited manner to steady-state tumor growth but they are chemotherapy resistant and drive post-therapeutic cancer recurrence. Ablation of p57+ CSCs suppressed intestinal tumor regrowth after chemotherapy. Together, these results shed light on the heterogeneity of intestinal CSCs and reveal p57+ CSCs as a promising therapeutic target for malignant intestinal cancer.
Data from FPR2 shapes an immune-excluded pancreatic tumor microenvironment and drives T-cell exhaustion in a sex-dependent manner
Authors: He Fei , Tay Apple H.M. , Calandigary Ahmed , Malki Enana , Suzuki Sayaka , Liu Tianjie , Wang Qi , Fernández-Moro Carlos , Kaisso Marina , Olofsson‐Sahl Peter , Melssen Marit , Sze Siu Kwan , Björnstedt Mikael , Löhr Matthias J. , Karlsson Mikael C.I. , Heuchel Rainer , Sarhan Dhifaf
Published: September 2024

Abstract
Sex-driven immune differences can affect tumor progression and the landscape of the tumor microenvironment. Deeper understanding of these differences in males and females can inform patient selection to improve sex-optimized immunotherapy treatments. In this study, single-cell RNA-sequencing and protein analyses uncovered a subpopulation of myeloid cells in pancreatic lesions associated with an immune‐excluded tumor phenotype and effector T-cell exhaustion exclusively in females. This myeloid subpopulation was positively correlated with poor survival and genetic signatures of M2-like macrophages and T-cell exhaustion in females. The G-protein coupled receptor formyl peptide receptor 2 (FPR2) mediated these immunosuppressive effects. In vitro, treatment of myeloid cells with a specific FPR2 antagonist prevented exhaustion and enhanced cytotoxicity of effector cells. Proteomic analysis revealed high expression of immunosuppressive secretory proteins PGE2 and galectin-9, enriched integrin pathway, and reduced pro-inflammatory signals like TNFα and IFNγ in female M2-like macrophages upon FPR2 agonist treatment. In addition, myeloid cells treated with FPR2 agonists induced TIM3 and PD-1 expression only in female T cells. Treatment with anti-TIM3 antibodies reversed T cell exhaustion and stimulated their ability to infiltrate and kill pancreatic spheroids. In vivo, progression of syngeneic pancreatic tumors was significantly suppressed in FPR2 knockout (KO) female mice compared to wild-type (WT) female mice and to WT and FPR2 KO male mice. In female mice, inoculation of tumors with FPR2 KO macrophages significantly reduced tumor growth compared to WT macrophages. Overall, this study identified an immunosuppressive function of FPR2 in females, highlighting a potential sex‐specific precision immunotherapy strategy.
Data from Terminally exhausted CD8+ T cells resistant to PD-1 blockade promote generation and maintenance of aggressive cancer stem cells
Authors: Chakravarti Mohona , Dhar Sukanya , Bera Saurav , Sinha Abhipsa , Roy Kamalika , Sarkar Anirban , Dasgupta Shayani , Bhuniya Avishek , Saha Akata , Das Juhina , Banerjee Saptak , Vernekar Manisha , Pal Chiranjib , Alam Neyaz , Datta Dipak , Baral Rathindranath , Bose Anamika
Published: September 2024

Abstract
Heterogeneity within the tumor infiltrating lymphocyte (TIL) population limits immunotherapeutic efficacy against cancer. Between two subpopulations of exhausted CD8+ TILs (progenitor-exhausted, TPEX; terminally-exhausted, TTEX), TTEX cells remain unresponsive to anti-PD1 therapy. Deciphering whether and how PD1-resistant TTEX cells engage in tumor promotion could improve the response to immunotherapy. Here, we report that TTEX cells actively participate in tumor progression by modulating cancer stem cells (CSC). TTEX cells strongly correlated with elevated CSC frequency in poorly immune-infiltrated (CD8+ TIL low) advanced human breast and ovarian carcinomas. TTEX directly upregulated CSC frequency in vitro, which was not affected by anti-PD1 treatment. The TTEX-influenced CSCs were highly clonogenic and exhibited a multi-drug resistant phenotype, overexpressing drug efflux pumps like ABCC1 and ABCB1. These CSCs were highly invasive, displaying increased invadopodia development and elevated cofilin, CXCR4, and MMP7 expression. The invasive properties along with epithelial-mesenchymal plasticity of TTEX-educated CSCs increased metastasis in vivo. TTEX increased cell surface levels and activation of VEGFR2 in CSCs, and silencing or inhibition of VEGFR2 reversed the CSC-stimulatory effects of TTEX. LAMP3 and NRP1 on the surface of TTEX stimulated VEGFR2 in CSCs to promote aggressiveness. Cumulatively, these findings suggest that screening carcinoma patients for both CD8+ TIL and TTEX frequency prior to anti-PD1-therapy could improve patient outcomes. Additionally, targeting the LAMP3/NRP1-VEGFR2 axis could be a therapeutic strategy in advanced carcinoma patients with limited CD8+ T cell infiltration and high TTEX frequency.
Data from An in vivo CRISPR screen identifies that SNRPC promotes triple-negative breast cancer progression
Authors: Lu Xun-Xi , Yang Wen-Xiao , Pei Yu-Chen , Luo Hong , Li Xiaoguang , Wang Yun-Jin , Zhang Guo-Liang , Ling Hong , Shao Zhiming , Hu Xin
Published: September 2024

Abstract
Dysregulation of RNA-binding proteins (RBPs) is one of the characteristics of cancer. Investigating the biological functions and molecular mechanisms of abnormal RBPs can help uncover new cancer biomarkers and treatment strategies. To identify oncogenic RBPs in triple-negative breast cancer (TNBC), we employed an in vivo CRISPR screen and a TNBC progression model, which revealed small nuclear ribonucleoprotein polypeptide C (SNRPC), a subunit of the U1 small nuclear ribonucleoprotein particle (U1 snRNP), as a key modulator of TNBC progression. SNRPC was frequently upregulated, which corresponded to poor prognosis in TNBC patients. SNRPC ablation significantly impaired the proliferation, migration and invasion of TNBC cells in vitro and in vivo. In addition, SNRPC was essential for the stability of U1 snRNP and contributed to the RNA Pol II-controlled transcriptional program. Knockdown of SNRPC decreased RNA Pol II enrichment on a subset of oncogenes (TNFAIP2, E2F2 and CDK4) and reduced their expression levels. Furthermore, SNRPC deletion was confirmed to inhibit TNBC progression partially through regulation of the TNFAIP2-Rac1-β-catenin signaling pathway. Taken together, this data suggests that SNRPC plays an oncogenic role in TNBC, is a marker of poor prognosis, and may be a valuable therapeutic target for patients with intractable TNBC.
Data from N6-methyladenosine promotes translation of VEGFA to accelerate angiogenesis in lung cancer
Authors: Zhang Haisheng , Zhou Jiawang , Li Jiexin , Wang Zhaotong , Chen Zhuojia , Lv Ziyan , Ge Lichen , Xie Guoyou , Deng Guoming , Rui Yalan , Huang Hongbing , Chen Likun , Wang Hongsheng
Published: September 2024

Abstract
Angiogenesis is hijacked by cancer to support tumor growth. RNA modifications such as N6-methyladenosine (m6A) can regulate several aspects of cancer, including angiogenesis. Here, we find that m6A triggers angiogenesis in lung cancer by upregulating vascular endothelial growth factor-A (VEGFA), a central regulator of neovasculature and blood vessel growth. m6A-sequencing and functional studies confirmed that m6A modification of the 5’UTR of VEGFA positively regulates its translation. Specifically, methylation of a 5’UTR internal ribosome entry site (IRES) recruited the YTHDC2/eIF4GI complex to trigger cap-independent translation initiation. Intriguingly, the m6A methylation site A856 of the 5’UTR was located within the conserved upstream open reading frame (uORF) of VEGFA IRES-A, which overcomes uORF-mediated translation suppression while facilitating G-quadruplex-induced translation of VEGFA. Targeted specific demethylation of VEGFA m6A significantly decreased expression of VEGFA and reduced lung cancer cell-driven angiogenesis. In vivo and clinical data confirmed the positive effects of m6A modification of VEGFA on angiogenesis and tumor growth of lung cancer. This study not only reveals that the m6A/VEGFA axis is a potential target for lung cancer therapy but also expands our understanding of the impact of m6A modification of IRES in the 5’UTR of mRNA on translation regulation.
Data from Genetic Modulation of BET1L Confers Colorectal Cancer Susceptibility by Reducing miRNA Binding and m6A Modification
Authors: Li Shuwei , Du Mulong , Xu Kaili , Ben Shuai , Zhu Tianru , Guo Mengfan , Xin Junyi , Zhu Lingjun , Gu Dongying , Zhang Zhengdong , Wang Meilin
Published: September 2024

Abstract
Genetic variants in regions encoding 3′ untranslated regions (UTR) of mRNA potentially alter miRNA binding affinity and N6-methyladenosine (m6A) levels to affect gene expression. A better understanding of the association of these variants with colorectal cancer susceptibility could facilitate development of cancer prevention and treatment approaches. Here, we analyzed miRNA expression profiles and integrated genetic analyses from 8,533 individuals to evaluate the effects of altered miRNA-binding sites on colorectal cancer risk. The single-nucleotide polymorphism rs11245997 in the BET1L 3′UTR was significantly associated with colorectal cancer risk. The rs11245997 A allele facilitated BET1L expression by disrupting miR-140–3p binding. It also reduced BET1L m6A modification, which upregulated BET1L expression levels through a mechanism mediated by the m6A methyltransferases (METTL14 and WTAP) and the m6A demethylase ALKBH5. Moreover, higher expression of BET1L was associated with advanced tumor stages and poor patient prognosis. Increased BET1L expression promoted growth of colorectal cancer cells in vitro and in vivo, which could be partially rescued with miR-140–3p overexpression. RNA sequencing and pathway analyses indicated that BET1L is associated with the steroid biosynthesis pathway through regulation of HSD17B7, CYP27B1, and COMT. These findings provide insights into the involvement of genetic variants of BET1L in the development and progression of colorectal cancer.
Significance:
The integration of miRNA expression profiles and genetic variants identified rs11245997 as a colorectal cancer risk-related variant that reduces miR-140–3p binding and m6A modification, leading to BET1L upregulation to promote colorectal tumorigenesis.
Data from β-catenin-driven differentiation is a tissue-specific epigenetic vulnerability in adrenal cancer
Authors: Mohan Dipika R. , Borges Kleiton S. , Finco Isabella , LaPensee Christopher R. , Rege Juilee , Solon April L. , Little Donald W. , Else Tobias , Almeida Madson Q. , Dang Derek , Haggerty-Skeans James , Apfelbaum April A. , Vinco Michelle , Wakamatsu Alda , Mariani Beatriz M. P. , Amorim Larissa Costa. , Latronico Ana Claudia. , Mendonca Berenice B. , Zerbini Maria Claudia N. , Lawlor Elizabeth R. , Ohi Ryoma , Auchus Richard J. , Rainey William E. , Marie Suely K.N. , Giordano Thomas J. , Venneti Sriram , Fragoso Maria Candida Barisson Villares , Breault David T. , Lerario Antonio Marcondes. , Hammer Gary D.
Published: September 2024

Abstract
Adrenocortical carcinoma (ACC) is a rare cancer in which tissue-specific differentiation is paradoxically associated with dismal outcomes. The differentiated ACC subtype CIMP-high is prevalent, incurable, and routinely fatal. CIMP-high ACC possess abnormal DNA methylation and frequent β-catenin activating mutations. Here, we demonstrated that ACC differentiation is maintained by a balance between nuclear, tissue-specific β-catenin-containing complexes and the epigenome. On chromatin, β-catenin bound master adrenal transcription factor SF1 and hijacked the adrenocortical super-enhancer landscape to maintain differentiation in CIMP-high ACC; off chromatin, β-catenin bound histone methyltransferase EZH2. SF1/β-catenin and EZH2/β-catenin complexes present in normal adrenals persisted through all phases of ACC evolution. Pharmacologic EZH2 inhibition in CIMP-high ACC expelled SF1/β-catenin from chromatin and favored EZH2/β-catenin assembly, erasing differentiation and restraining cancer growth in vitro and in vivo. These studies illustrate how tissue-specific programs shape oncogene selection, surreptitiously encoding targetable therapeutic vulnerabilities.
Data from Inter- and intra-metastatic heterogeneity shapes adaptive therapy cycling dynamics
Authors: Gallaher Jill , Strobl Maximilian , West Jeffrey , Gatenby Robert , Zhang Jingsong , Robertson-Tessi Mark , Anderson Alexander R.A.
Published: September 2024

Abstract
Adaptive therapies that alternate between drug applications and drug-free vacations can exploit competition between sensitive and resistant cells to maximize the time to progression. However, optimal dosing schedules depend on the properties of metastases, which are often not directly measurable in clinical practice. Here, we proposed a framework for estimating features of metastases through tumor response dynamics during the first adaptive therapy treatment cycle. Longitudinal PSA levels in sixteen metastatic castration resistant prostate cancer patients undergoing adaptive androgen deprivation treatment were analyzed to investigate relationships between cycle dynamics and clinical variables such as Gleason score, the change in the number of metastases over a cycle, and the total number of cycles over the course of treatment. The first cycle of adaptive therapy, which consists of a response period (applying therapy until 50% PSA reduction), and a regrowth period (removing treatment until reaching initial PSA levels), delineated several features of the computational metastatic system: larger metastases had longer cycles; a higher proportion of drug resistant cells slowed the cycles; and a faster cell turnover rate sped up drug response time and slowed regrowth time. The number of metastases did not affect cycle times, as response dynamics were dominated by the largest tumors rather than the aggregate. In addition, systems with higher inter-metastasis heterogeneity responded better to continuous therapy and correlated with dynamics from patients with high or low Gleason scores. Conversely, systems with higher intra-metastasis heterogeneity responded better to adaptive therapy and correlated with dynamics from patients with intermediate Gleason scores.
Data from Kinome reprogramming is a targetable vulnerability in ESR1 fusion-driven breast cancer
Authors: Gou Xuxu , Kim Beom-Jun , Anurag Meenakshi , Lei Jonathan T. , Young Meggie N. , Holt Matthew V. , Fandino Diana , Vollert Craig T. , Singh Purba , Alzubi Mohammad A. , Malovannaya Anna , Dobrolecki Lacey E. , Lewis Michael T. , Li Shunqiang , Foulds Charles E. , Ellis Matthew J.
Published: September 2024

Abstract
Transcriptionally active ESR1 gene fusions (ESR1-TAF) are a potent cause of breast cancer endocrine therapy (ET) resistance. ESR1-TAFs are not directly druggable because the C-terminal estrogen/anti-estrogen binding domain is replaced with translocated in-frame partner gene sequences that confer constitutive transactivation. To discover alternative treatments, a mass spectrometry (MS)-based kinase inhibitor pulldown assay (KIPA) was deployed to identify druggable kinases that are upregulated by diverse ESR1-TAFs. Subsequent explorations of drug sensitivity validated RET kinase as a common therapeutic vulnerability despite remarkable ESR1-TAF C-terminal sequence and structural diversity. Organoids and xenografts from a pan-ET resistant patient-derived xenograft (PDX) model that harbors the ESR1-e6>YAP1 TAF were concordantly inhibited by the selective RET inhibitor pralsetinib to a similar extent as the CDK4/6 inhibitor palbociclib. Together, these findings provide preclinical rationale for clinical evaluation of RET inhibition for the treatment of ESR1-TAF-driven ET resistant breast cancer.
Data from Arginine Methylation of DDX3 by PRMT1 Mediates Mitochondrial Homeostasis to Promote Breast Cancer Metastasis
Authors: Hsu Wen-Jing , Chiang Ming-Chen , Chao Yi-Chun , Chang Yu-Chu , Hsu Ming-Chien , Chung Chu-Hung , Tsai I-Lin , Chu Cheng-Ying , Wu Han-Chung , Yang Ching-Chieh , Lee Chi-Ching , Lin Cheng-Wei
Published: September 2024

Abstract
Dysregulated mitochondrial dynamics and metabolism play important roles in tumorigenesis. Metastasizing tumor cells predominantly utilize mitochondrial metabolism, and regulators of metabolic reprogramming may provide reliable biomarkers for diagnosing cancer metastasis. Here, we identified a type I arginine methyltransferase–DEAD-box polypeptide 3, X-linked (PRMT1-DDX3) axis that promotes breast cancer metastasis by coordinating mitochondrial biogenesis and mitophagy to ensure mitochondrial quality control. Mechanistically, PRMT1 induces arginine methylation of DDX3, which enhances its protein stability and prevents proteasomal degradation. DDX3 mediates mitochondrial homeostasis by translocating to mitochondria where it facilitates phosphatase and tensin homology-induced kinase 1 translation in response to mitochondrial stress. Inhibition of DDX3 suppresses mitochondrial biogenesis and mitophagy, resulting in diminished cancer stemness and metastatic properties. Overall, this study uncovers a mechanism by which the PRMT1-DDX3 axis regulates mitochondrial homeostasis to support breast cancer metastasis, suggesting strategies for targeting metabolic vulnerabilities to treat metastatic breast cancer.

Significance: DDX3 is stabilized by PRMT1–mediated arginine methylation and coordinates mitophagy and mitochondrial biogenesis by upregulating PINK1 to facilitate breast cancer progression.
Data from IDH1 Inhibition Potentiates Chemotherapy Efficacy in Pancreatic Cancer
Authors: Zarei Mehrdad , Hajihassani Omid , Hue Jonathan J. , Loftus Alexander W. , Graor Hallie J. , Nakazzi Faith , Naji Parnian , Boutros Christina S. , Uppin Vinayak , Vaziri-Gohar Ali , Shalaby Akram S. , Asara John M. , Rothermel Luke D. , Brody Jonathan R. , Winter Jordan M.
Published: September 2024

Abstract
Pancreatic ductal adenocarcinoma (PDAC) is associated with a 5-year overall survival rate of just 13%, and development of chemotherapy resistance is nearly universal. PDAC cells overexpress wild-type isocitrate dehydrogenase 1 (IDH1) that can enable them to overcome metabolic stress, suggesting it could represent a therapeutic target in PDAC. Here, we found that anti-IDH1 therapy enhanced the efficacy of conventional chemotherapeutics. Chemotherapy treatment induced reactive oxygen species (ROS) and increased tricarboxylic acid cycle activity in PDAC cells, along with the induction of wild-type IDH1 expression as a key resistance factor. IDH1 facilitated PDAC survival following chemotherapy treatment by supporting mitochondrial function and antioxidant defense to neutralize ROS through the generation of α-ketoglutarate and NADPH, respectively. Pharmacologic inhibition of wild-type IDH1 with ivosidenib synergized with conventional chemotherapeutics in vitro and potentiated the efficacy of subtherapeutic doses of these drugs in vivo in murine PDAC models. This promising treatment approach is translatable through available and safe oral inhibitors and provides the basis of an open and accruing clinical trial testing this combination (NCT05209074).

Significance: Targeting IDH1 improves sensitivity to chemotherapy by suppressing mitochondrial function and inducing oxidative stress, supporting the potential of the combination as an effective strategy for treating pancreatic cancer.
Supplementary Table S1 from Granulocyte colony stimulating factor is a novel mediator of T cell suppression and an immunotherapeutic target for women with colon cancer
Authors: Ray Anita L. , Saunders Apryl S. , Nofchissey Robert A. , Reidy Megan A. , Kamal Maria , Lerner Megan R. , Fung Kar-Ming , Lang Mark L. , Hanson Joshua A. , Guo Shaoxuan , Urdaneta-Perez Maria G. , Lewis Samara E. , Cloyde Michael , Morris Katherine T.
Published: September 2024

Supplementary Table 1: CyTOF antibody panel and source
Supplemental Figure 5 from Myosin light chain kinase inhibition potentiates the anti-tumor effects of avapritinib in PDGFRA D842V-mutant gastrointestinal stromal tumor
Authors: Rossi Ferdinand , Liu Mengyuan , Tieniber Andrew , Etherington Mark S. , Hanna Andrew , Vitiello Gerardo A. , Param Nesteene J. , Do Kevin , Wang Laura , Antonescu Cristina R. , Zeng Shan , Zhang Jennifer Q. , DeMatteo Ronald P.
Published: September 2024

Supplemental Figure 5.
Short term culture of cells derived from PDGFRA D842V PDXs are tumor cells.
Supplementary Figure 2 from Co-clinical study of [fam-] trastuzumab deruxtecan (DS8201a) in patient-derived xenograft models of uterine carcinosarcoma and its association with clinical efficacy
Authors: Yagishita Shigehiro , Nishikawa Tadaaki , Yoshida Hiroshi , Shintani Daisuke , Sato Sho , Miwa Maiko , Suzuki Mikiko , Yasuda Masanori , Ogitani Yusuke , Jikoh Takahiro , Yonemori Kan , Hasegawa Kosei , Hamada Akinobu
Published: September 2024

ER and p53 immunohistochemistry of original and patient-derived xenograft (PDX) tumors
Supplementary Table S1-S2 from Cytochrome P450 oxidoreductase, POR, associated with severe paclitaxel-induced peripheral neuropathy in patients of European ancestry from ECOG-ACRIN E5103
Authors: Shen Fei , Jiang Guanglong , Philips Santosh , Gardner Laura , Xue Gloria , Cantor Erica , Ly Reynold C. , Osei Wilberforce , Wu Xi , Dang Chau , Northfelt Donald , Skaar Todd , Miller Kathy D. , Sledge George W. , Schneider Bryan P.
Published: September 2024

Supplemental table 1-Covariates analyses;
Supplemental Table 2-Genotype frequency, variant allele frequency and Hardy-Weinberg Equilibrium (HWE) of variants in CYPs
Supplementary Table S2 from Integrative single-cell and bulk transcriptomes analyses identify intrinsic HNSCC subtypes with distinct prognoses and therapeutic vulnerabilities
Authors: Dai Yibin , Wang Ziyu , Xia Yingcao , Li Jin , Wu Yaping , Wang Yanling , Jiang Hongbing , Cheng Jie
Published: September 2024

iCMS classifier (marker genes) & biological enrichment
Supplementary Data 1 from MEK inhibition sensitizes pancreatic cancer to STING agonism by tumor-cell intrinsic amplification of type I interferon signaling
Authors: Ghukasyan Razmik , Liang Keke , Chau Kevin , Li Luyi , Chan Charlotte , Abt Evan R. , Le Thuc , Park Joon Y. , Wu Nanping , Premji Alykhan , Damoiseaux Robert , Luu Tony , Labora Amanda , Rashid Khalid , Link Jason M. , Radu Caius G. , Donahue Timothy R.
Published: September 2024

Supplementary Resources and Table
Supplementary Figure S5 from Patient Specific Targeting of the T-cell Receptor Variable Region as a Therapeutic Strategy in Clonal T-Cell Diseases
Authors: Lucero Olivia M. , Lee Ji-Ann , Bowman Jenna , Johnson Kara , Sapparapu Gopal , Thomas John K. , Fan Guang , Chang Bill H. , Thiel-Klare Karina , Eide Christopher A. , Okada Craig , Palazzolo Mike , Lind Evan , Kosaka Yoko , Druker Brian J. , Lydon Nicholas , Bowers Peter M.
Published: September 2024

Supplementary Figure 5. αVβ monoclonal antibodies induce target T-cell activation,
characterized by down modulation of the TCR complex
Supplementary Figure S3 from Patient Specific Targeting of the T-cell Receptor Variable Region as a Therapeutic Strategy in Clonal T-Cell Diseases
Authors: Lucero Olivia M. , Lee Ji-Ann , Bowman Jenna , Johnson Kara , Sapparapu Gopal , Thomas John K. , Fan Guang , Chang Bill H. , Thiel-Klare Karina , Eide Christopher A. , Okada Craig , Palazzolo Mike , Lind Evan , Kosaka Yoko , Druker Brian J. , Lydon Nicholas , Bowers Peter M.
Published: September 2024

Supplementary Figure 3: Vβ monoclonal antibodies induce antibody dependent
cellular cytotoxicity of target cells.
Supplementary Table S3 from The impact of germline alterations in appendiceal adenocarcinoma
Authors: Foote Michael B. , Walch Henry , Kemel Yelena , Vakiani Efsevia , Johannet Paul , Sheehan Margaret , Chatila Walid , Chung Sebastian , NASH Garrett , Maio Anna , Shia Jinru , Mandelker Diana , Berger Michael , Schultz Nikolaus , Diaz Luis A. , Cercek Andrea , Stadler Zsofia K.
Published: September 2024

Clinicopathologic Features of the Appendix-Specific Survival Analysis Cohort
Supplementary Figure S2 from The impact of germline alterations in appendiceal adenocarcinoma
Authors: Foote Michael B. , Walch Henry , Kemel Yelena , Vakiani Efsevia , Johannet Paul , Sheehan Margaret , Chatila Walid , Chung Sebastian , NASH Garrett , Maio Anna , Shia Jinru , Mandelker Diana , Berger Michael , Schultz Nikolaus , Diaz Luis A. , Cercek Andrea , Stadler Zsofia K.
Published: September 2024

Appendix cancer specific survival in patients with stage IV appendiceal adenocarcinoma stratified by presence of a germline variant in CHEK2 (n=3) or BRCA1(n=1) associated with homologous recombination deficiency (HRD). Patients with germline variants in non-HRD-associated genes were not included in the analysis. Highlighted Kaplan Meier curve areas display the 95% confidence interval for the respective survival curves.
Supplementary Figure S1 from The impact of germline alterations in appendiceal adenocarcinoma
Authors: Foote Michael B. , Walch Henry , Kemel Yelena , Vakiani Efsevia , Johannet Paul , Sheehan Margaret , Chatila Walid , Chung Sebastian , NASH Garrett , Maio Anna , Shia Jinru , Mandelker Diana , Berger Michael , Schultz Nikolaus , Diaz Luis A. , Cercek Andrea , Stadler Zsofia K.
Published: September 2024

Supplemental Figure 1: Appendix cancer specific survival in patients with stage IV appendiceal adenocarcinoma stratified by presence of a germline variant. Highlighted Kaplan Meier curve areas display the 95% confidence interval for the respective survival curves.
Supplementary Figure S6 from HLA class II loss and JAK1/2 deficiency coevolve in melanoma leading to CD4 T cell and IFNγ cross-resistance
Authors: Stupia Simone , Heeke Christina , Brüggemann Alicia , Zaremba Anne , Thier Beatrice , Kretz Julia , Sucker Antje , Philip Manuel , Zelinskyy Gennadiy , Ferrone Soldano , Roesch Alexander , Horn Susanne , Hadaschik Eva , Schadendorf Dirk , Trilling Mirko , Dittmer Ulf , Griewank Klaus , Zhao Fang , Paschen Annette
Published: September 2024

JAK inhibition downregulates HLA-II but not HLA-I or PD-L1 expression in melanoma cells
Figure S3 from The Immunogenomic Landscape of Neuroendocrine Prostate Cancer
Authors: Bhinder Bhavneet , Ferguson Alison , Sigouros Michael , Uppal Manik , Elsaeed Ahmed G. , Bareja Rohan , Alnajar Hussein , Eng Kenneth Wha. , Conteduca Vincenza , Sboner Andrea , Mosquera Juan Miguel , Elemento Olivier , Beltran Himisha
Published: September 2024

Suppl Figure 3. Identification of gene modules associated with NEPC T-cell immune classes.
Figure S2 from The Immunogenomic Landscape of Neuroendocrine Prostate Cancer
Authors: Bhinder Bhavneet , Ferguson Alison , Sigouros Michael , Uppal Manik , Elsaeed Ahmed G. , Bareja Rohan , Alnajar Hussein , Eng Kenneth Wha. , Conteduca Vincenza , Sboner Andrea , Mosquera Juan Miguel , Elemento Olivier , Beltran Himisha
Published: September 2024

Suppl Figure 2. T-cell signature-based classification of prostate cancer types and other independent cancer cohorts.
Supplementary Fig. 2 from A Phase 1/2 Multicenter Randomized Trial of Local Ablation Plus Toripalimab Versus Toripalimab Alone for Previously Treated Unresectable Hepatocellular Carcinoma
Authors: Zhou Chunhui , Li Yan , Li Jiaping , Song Botian , Li Hanfeng , Liang Bin , Gu Shanzhi , Li Haiping , Chen Changyong , Li Sai , Peng Changli , Liu Fei , Xiao Juxiong , Long Xueying , Li Ping , Xiong Zhengping , Yi Xiaoping , Liao Weihua , Shi Liangrong
Published: September 2024

Supplementary Fig. 2 The association of CD8+ TIL density and PD-L1 expression with tumor objective response.
Supplementary Data 1 from A Phase 1/2 Multicenter Randomized Trial of Local Ablation Plus Toripalimab Versus Toripalimab Alone for Previously Treated Unresectable Hepatocellular Carcinoma
Authors: Zhou Chunhui , Li Yan , Li Jiaping , Song Botian , Li Hanfeng , Liang Bin , Gu Shanzhi , Li Haiping , Chen Changyong , Li Sai , Peng Changli , Liu Fei , Xiao Juxiong , Long Xueying , Li Ping , Xiong Zhengping , Yi Xiaoping , Liao Weihua , Shi Liangrong
Published: September 2024

Supplementary Method, Table 1-9
Supplemental Table 4 from The GENIE BPC NSCLC cohort: a real-world repository integrating standardized clinical and genomic data for 1,846 patients with non-small cell lung cancer
Authors: Choudhury Noura J. , Lavery Jessica A. , Brown Samantha , de Bruijn Ino , Jee Justin , Tran Thinh Ngoc. , Rizvi Hira , Arbour Kathryn C. , Whiting Karissa , Shen Ronglai , Hellmann Matthew , Bedard Philippe L. , Yu Celeste , Leighl Natasha , LeNoue-Newton Michele , Micheel Christine , Warner Jeremy L. , Ginsberg Michelle S. , Plodkowski Andrew , Girshman Jeffrey , Sawan Peter , Pillai Shirin , Sweeney Shawn M. , Kehl Kenneth L. , Panageas Katherine S. , Schultz Nikolaus , Schrag Deb , Riely Gregory J.
Published: September 2024

Supplemental Table 4
Supplemental Table 1 from The GENIE BPC NSCLC cohort: a real-world repository integrating standardized clinical and genomic data for 1,846 patients with non-small cell lung cancer
Authors: Choudhury Noura J. , Lavery Jessica A. , Brown Samantha , de Bruijn Ino , Jee Justin , Tran Thinh Ngoc. , Rizvi Hira , Arbour Kathryn C. , Whiting Karissa , Shen Ronglai , Hellmann Matthew , Bedard Philippe L. , Yu Celeste , Leighl Natasha , LeNoue-Newton Michele , Micheel Christine , Warner Jeremy L. , Ginsberg Michelle S. , Plodkowski Andrew , Girshman Jeffrey , Sawan Peter , Pillai Shirin , Sweeney Shawn M. , Kehl Kenneth L. , Panageas Katherine S. , Schultz Nikolaus , Schrag Deb , Riely Gregory J.
Published: September 2024

Supplemental Table 1
Supplemental Fig. 3 from The GENIE BPC NSCLC cohort: a real-world repository integrating standardized clinical and genomic data for 1,846 patients with non-small cell lung cancer
Authors: Choudhury Noura J. , Lavery Jessica A. , Brown Samantha , de Bruijn Ino , Jee Justin , Tran Thinh Ngoc. , Rizvi Hira , Arbour Kathryn C. , Whiting Karissa , Shen Ronglai , Hellmann Matthew , Bedard Philippe L. , Yu Celeste , Leighl Natasha , LeNoue-Newton Michele , Micheel Christine , Warner Jeremy L. , Ginsberg Michelle S. , Plodkowski Andrew , Girshman Jeffrey , Sawan Peter , Pillai Shirin , Sweeney Shawn M. , Kehl Kenneth L. , Panageas Katherine S. , Schultz Nikolaus , Schrag Deb , Riely Gregory J.
Published: September 2024

Supplemental Figure 3: PFS estimates for patients with NSCLC treated with standard first- and second-line therapies.
Supplementary Table S2 from Patient-Reported Outcomes as Inter-Radiographic Predictors of Response in Non-Small Cell Lung Cancer
Authors: Bhatt Ambika , Schabath Matthew B. , Hoogland Aasha I. , Jim Heather S.L. , Brady-Nicholls Renee
Published: September 2024

Representativeness of study participants table
Figure S8 from BBT-176, a Novel Fourth-Generation Tyrosine Kinase Inhibitor for Osimertinib-Resistant Epidermal Growth Factor Receptor Mutations in Non-Small Cell Lung Cancer
Authors: Lim Sun Min , Fujino Toshio , Kim Chulwon , Lee Gwanghee , Lee Yong-Hee , Kim Dong-Wan , Ahn Jin Seok , Mitsudomi Tetsuya , Jin Taiguang , Lee Sang-Yoon
Published: September 2024

Supplementary Figure 8. Circulating tumor DNA analysis data from Case 1. A, Allelic configuration analysis by liquid biopsy confirmed cis relationship between EGFR T790M and C797S mutations; no trans clones were detected. B, Serial changes in allelic frequency of all mutations detected in blood.
Supplementary Figure S1 from The DRD2 antagonist haloperidol mediates autophagy-induced ferroptosis to increase temozolomide sensitivity by promoting endoplasmic reticulum stress in glioblastoma
Authors: Shi Linyong , Chen Hanning , Chen Kunxiang , Zhong Chengzong , Song Chong , Huang Yifeng , Wang Tong , Chen Lei , Li Chiyang , Huang Annie , Li Hong , Lu Yuntao
Published: September 2024

Fig. S1. HP does not trigger apoptosis in GBM cells.
Supplementary Figures 1 from Spatial Immunoprofiling of Adenoid Cystic Carcinoma Reveals B7-H4 Is a Therapeutic Target for Aggressive Tumors
Authors: de Sousa Luana G. , McGrail Daniel J. , Lazar Neto Felippe , Li Kaiyi , Marques-Piubelli Mario L. , Ferri-Borgogno Sammy , Dai Hui , Mitani Yoshitsugu , Spardy Burr Nicole , Cooper Zachary A. , Kinneer Krista , Cortez Maria Angelica. , Lin Shiaw-Yih , Bell Diana , El-Naggar Adel , Burks Jared , Ferrarotto Renata
Published: September 2024

Supplementary Figures
Supplementary Fig. 1 from An open-label phase I study of GDC-0927 in postmenopausal women with locally advanced or metastatic estrogen receptor positive breast cancer
Authors: Chandarlapaty Sarat , Dickler Maura N. , Perez Fidalgo Jose Alejandro , Villanueva-Vázquez Rafael , Giltnane Jennifer , Gates Mary , Chang Ching-Wei , Cheeti Sravanthi , Fredrickson Jill , Wang Xiaojing , Collier Ann , Moore Heather M. , Metcalfe Ciara , Lauchle Jennifer , Humke Eric W. , Bardia Aditya
Published: September 2024

Supplementary Fig. S1. Study scheme.
Supplementary Figure S3 from A bi-functional PARP-HDAC inhibitor with activity in Ewing sarcoma
Authors: Ramos Louise , Truong Sarah , Zhai Beibei , Joshi Jay , Ghaidi Fariba , Lizardo Michael M. , Shyp Taras , Kung Sonia H.Y. , Rezakhanlou Alireza M. , Oo Htoo Zarni , Adomat Hans , Le Bihan Stephane , Collins Colin , Bacha Jeffrey , Brown Dennis , Langlands John , Shen Wang , Lallous Nada , Sorensen Poul H. , Daugaard Mads
Published: September 2024

Replicates of cell cycle assays and statistics
Supplementary Figure S6 from Autocrine 17-β-estradiol/estrogen receptor-α loop determines the response to immune-checkpoint inhibitors in non-small cell lung cancer
Authors: Anobile Dario P. , Salaroglio Iris C. , Tabbò Fabrizio , La Vecchia Sofia , Akman Muhlis , Napoli Francesca , Bungaro Maristella , Benso Federica , Aldieri Elisabetta , Bironzo Paolo , Kopecka Joanna , Passiglia Francesco , Righi Luisella , Novello Silvia , Scagliotti Giorgio V. , Riganti Chiara
Published: September 2024

Levels of ERβ and ERα target genes in non-small cell lung cancer cells
a. ERβ mRNA, measured by RT-PCR (technical triplicates), in female (F)-derived NCI-H1385 and NCI-H1975 cells, and in male (M)-derived A549 and NCI-H1650 cells. The relative expression of ERβ in NCI-H1385 cells was considered 1. Data are means+SD (n=3). ***p<0.001: NCI-H1975 cells versus NCI-H1385; °°p<0.01: M-derived cells versus mean of F-derived cells (ANOVA). b. Expression of ERβ mRNA, measured by RT-PCR (technical triplicates), plotted versus expression of surface PD-L1, measured by flow cytometry (technical triplicates), in 29 human NSCLC cell lines derived from F or M patients. c. Expression of ERα-target genes CXCL12, IGFBP4 and ABCA3, measured by RT-PCR (technical triplicates). The relative expression of each gene in NCI-H1385 cells was considered 1. Data are means+SD (n=3). *p<0.05, ***p<0.001: NCI-H1975 cells versus NCI-H1385; °p<0.05, °°p<0.01, °°°p<0.001: M-derived cells versus mean of F-derived cells (ANOVA).
Supplementary Figure S15 from Autocrine 17-β-estradiol/estrogen receptor-α loop determines the response to immune-checkpoint inhibitors in non-small cell lung cancer
Authors: Anobile Dario P. , Salaroglio Iris C. , Tabbò Fabrizio , La Vecchia Sofia , Akman Muhlis , Napoli Francesca , Bungaro Maristella , Benso Federica , Aldieri Elisabetta , Bironzo Paolo , Kopecka Joanna , Passiglia Francesco , Righi Luisella , Novello Silvia , Scagliotti Giorgio V. , Riganti Chiara
Published: September 2024

Letrozole sensitizes xenografts to a second cycle of pembrolizumab by modulating the tumor-associated immune-environment.
60 Hu-CD34+NSG mice bearing female-derived ERα lowNCI-H11385 and ERα highNCI-H1975 tumors, male-derived ERα lowA549 and ERα highNCI-H1650 tumors (15/tumor type) were treated for 5 weeks with pembrolizumab+letrozole with 10 mg/kg i.p. of 100 µL saline solution of pembrolizumab (day 1) followed by 5 mg/kg i.p. (days 7, 14, 21, 28, 35), and 1 mg/kg per os of 100 µL saline solution of letrozole daily (days 1-35), and then divided into three cohorts of 20 animals (n=5 mice/tumor type within each cohort). The first cohort of animals (left panel) was left untreated until week 15 (-Pemb-Letr); the second cohort (middle panel) was treated with 1 mg/kg per os of 100 µL saline solution of letrozole daily until week 15 (+Letr); the third cohort (right panel) was treated with 1 mg/kg per os of 100 µL saline solution of letrozole daily from week 6 to week 10, and then with pembrolizumab+letrozole from week 11 to week 15 (+Pemb+Letr). a. Tumor growth was monitored daily using calipers. Data are presented as mean volumes+ SD. **p<0.01, ***p<0.001: volume of female ERα lowNCI-H1385 and ERα highNCI-H1975 tumors (left panel), or ERα highNCI-H1975 tumors (middle-right panels) versus mean volume of male ERα lowA549 and ERα highNCI-H1650 tumors. b. PD-L1 expression was measured using flow cytometry on dissociated tumor cells after explants at week 15 (n=5/group). *p<0.05: +Pemb+Letr versus -Pemb-Letr (NCI-H1650 tumors), +Letr versus -Pemb-Letr (NCI-H1385 tumors); **p<0.01: +Pemb+Letr versus -Pemb-Letr (NCI-H1385 tumors); ***p<0.001: +Letr/+Pemb+Letr versus -Pemb-Letr (NCI-H1975 tumors) (ANOVA). c-e. On TILs isolated from tumor extracts (week 15), the percentage of CD8+Ki67+IFNγ+cells (panel c), CD56+Ki67+IFNγ+cells (panel d), and Vγ9+Ki67+IFNγ+cells (panel e) was measured by flow cytometry (n=5/group). CD8+Ki67+IFNγ+cells: *p<0.05: +Pemb+Letr versus -Pemb-Letr (NCI-H1975 and NCI-H1650 tumors), ***p<0.001: +Pemb+Letr versus -Pemb-Letr (NCI-H1385 tumors). CD56+Ki67+IFNγ+cells: *p<0.05: +Pemb+Letr versus -Pemb-Letr (NCI-H1385, NCI-H1975 and NCI-H1650 tumors). Vγ9+Ki67+IFNγ+cells: *p<0.05: +Pemb+Letr versus -Pemb-Letr (NCI-H1385, NCI-H1975 and NCI-H1650 tumors) (ANOVA).
Supplementary Table S2 from Thyroid cancers exhibit oncogene-enhanced macropinocytosis that is restrained by IGF1R and promotes albumin-drug-conjugate response
Authors: Hu Huiyu , Ng Thomas S.C. , Kang Mikyung , Scott Ella , Li Ran , Quintana Jeremy M. , Matvey Dylan , Vantaku Venkata R. , Weissleder Ralph , Parangi Sareh , Miller Miles A.
Published: September 2024

Pharmacologic screening, over-representation analysis, and gene expression of macropinocytosis screen hits
Supplementary Figure S5 from Thyroid cancers exhibit oncogene-enhanced macropinocytosis that is restrained by IGF1R and promotes albumin-drug-conjugate response
Authors: Hu Huiyu , Ng Thomas S.C. , Kang Mikyung , Scott Ella , Li Ran , Quintana Jeremy M. , Matvey Dylan , Vantaku Venkata R. , Weissleder Ralph , Parangi Sareh , Miller Miles A.
Published: September 2024

IGF1R inhibition augments macropinocytosis and is blocked by IGF1
Supplementary Table S4 from Activin A-mediated polarization of cancer-associated fibroblasts and macrophages confers resistance to checkpoint immunotherapy in skin cancer
Authors: Pich-Bavastro Christine , Yerly Laura , Di Domizio Jeremy , Tissot-Renaud Stéphanie , Gilliet Michel , Kuonen François
Published: September 2024

Supplementary Table S4. Cluster marker genes of the Myeloid cell populations.
Supplementary Figure S2 from Activin A-mediated polarization of cancer-associated fibroblasts and macrophages confers resistance to checkpoint immunotherapy in skin cancer
Authors: Pich-Bavastro Christine , Yerly Laura , Di Domizio Jeremy , Tissot-Renaud Stéphanie , Gilliet Michel , Kuonen François
Published: September 2024

Supplementary Figure S2: Establishment of spatial transcriptional signatures for TMEs with distinct immune profiles.
Supplementary Figure S10 from Activin A-mediated polarization of cancer-associated fibroblasts and macrophages confers resistance to checkpoint immunotherapy in skin cancer
Authors: Pich-Bavastro Christine , Yerly Laura , Di Domizio Jeremy , Tissot-Renaud Stéphanie , Gilliet Michel , Kuonen François
Published: September 2024

Supplementary Figure S10: Unsupervised clustering of secretome gene expression reflects Macrophage subpopulations.
Supplementary Figure S1 from Genomic profiling of metastatic castration-resistant prostate cancer samples resistant to androgen-receptor pathway inhibitors
Authors: Menssouri Naoual , Poiraudeau Loic , Helissey Carole , Bigot Ludovic , Sabio Jonathan , Ibrahim Tony , Pobel Cedric , Nicotra Claudio , Ngo-Camus Maud , Lacroix Ludovic , Rouleau Etienne , Tselikas Lambros , CHAUCHEREAU Anne , Blanc-Durand Félix , Bernard-Tessier Alice , Patrikidou Anna , Naoun Natacha , Flippot Ronan , Colomba Emeline , Fuerea Alina , Albiges Laurence , Lavaud Pernelle , van de Wiel Paul , den Biezen-Timmermans Eveline , Wesseling-Rozendaal Yvonne , Ponce-Aix Santiago , Michiels Stefan , Massard Christophe , Gautheret Daniel , Barlesi Fabrice , Andre Fabrice , Besse Benjamin , Scoazec Jean-Yves , Friboulet Luc , Fizazi Karim , Loriot Yohann
Published: September 2024

CONSORT flow diagram of patients enrolled in the study
Supplementary Figure S9 from Dissecting the mechanisms underlying the Cytokine Release Syndrome (CRS) mediated by T Cell Bispecific Antibodies
Authors: Leclercq-Cohen Gabrielle , Steinhoff Nathalie , Albertí-Servera Llucia , Nassiri Sina , Danilin Sabrina , Piccione Emily , Yángüez Emilio , Hüsser Tamara , Herter Sylvia , Schmeing Stephan , Gerber Petra , Schwalie Petra , Sam Johannes , Briner Stefanie , Jenni Sylvia , Bianchi Roberta , Biehl Marlene , Cremasco Floriana , Apostolopoulou Katerina , Haegel Hélène , Klein Christian , Umana Pablo , Bacac Marina
Published: September 2024

Supplementary Figure S9. Single cell RNA-sequencing of whole blood treated with 0.2 μg/mL CD20-TCB was performed using the BD Rhapsody platform
Supplementary Figure S8 from Dissecting the mechanisms underlying the Cytokine Release Syndrome (CRS) mediated by T Cell Bispecific Antibodies
Authors: Leclercq-Cohen Gabrielle , Steinhoff Nathalie , Albertí-Servera Llucia , Nassiri Sina , Danilin Sabrina , Piccione Emily , Yángüez Emilio , Hüsser Tamara , Herter Sylvia , Schmeing Stephan , Gerber Petra , Schwalie Petra , Sam Johannes , Briner Stefanie , Jenni Sylvia , Bianchi Roberta , Biehl Marlene , Cremasco Floriana , Apostolopoulou Katerina , Haegel Hélène , Klein Christian , Umana Pablo , Bacac Marina
Published: September 2024

Supplementary Figure S8. Single cell RNA-sequencing of whole blood treated with 0.2 μg/mL CD20-TCB was performed using the BD Rhapsody platform.
Supplementary Figure S4 from Dissecting the mechanisms underlying the Cytokine Release Syndrome (CRS) mediated by T Cell Bispecific Antibodies
Authors: Leclercq-Cohen Gabrielle , Steinhoff Nathalie , Albertí-Servera Llucia , Nassiri Sina , Danilin Sabrina , Piccione Emily , Yángüez Emilio , Hüsser Tamara , Herter Sylvia , Schmeing Stephan , Gerber Petra , Schwalie Petra , Sam Johannes , Briner Stefanie , Jenni Sylvia , Bianchi Roberta , Biehl Marlene , Cremasco Floriana , Apostolopoulou Katerina , Haegel Hélène , Klein Christian , Umana Pablo , Bacac Marina
Published: September 2024

Supplementary Figure S4. Multidimensional scaling plot of gene expression distances between pseudobulks
Supplementary Figure S12 from Dissecting the mechanisms underlying the Cytokine Release Syndrome (CRS) mediated by T Cell Bispecific Antibodies
Authors: Leclercq-Cohen Gabrielle , Steinhoff Nathalie , Albertí-Servera Llucia , Nassiri Sina , Danilin Sabrina , Piccione Emily , Yángüez Emilio , Hüsser Tamara , Herter Sylvia , Schmeing Stephan , Gerber Petra , Schwalie Petra , Sam Johannes , Briner Stefanie , Jenni Sylvia , Bianchi Roberta , Biehl Marlene , Cremasco Floriana , Apostolopoulou Katerina , Haegel Hélène , Klein Christian , Umana Pablo , Bacac Marina
Published: September 2024

Supplementary Figure S12. Individual tumor growth curves for each treatment group. OCI-Ly18 (DLBCL)-bearing humanized NSG mice were pre-treated with 30 mg/kg Gazyva (Gpt, grey arrow) and treated weekly with escalating doses of CD20-TCB (0.5 mg/kg, 1 mg/kg, 2 mg/kg, red arrows). Adalimumab (25 mg/kg, orange arrow, TNF-α blockade) and tocilizumab (10 mg/kg, green arrow, IL-6R blockade) were given 1 day and 1 hour before the first CD20-TCB infusion. Dexamethasone (1 mg/kg, blue arrow) was given 1 hour prior each therapy. Anakinra (10 mg/kg, purple arrow, IL-1R blockade) and the NLRP3 inhibitor (20 mg/kg, light blue arrow) were administered 1 hour before, 4 hrs and 24 hrs after the first CD20-TCB infusion as well as 1 hr before and 4 hrs after the second CD20-TCB treatment. Individual tumor growth curves for each treatment group.
Supplementary Figure S11 from Dissecting the mechanisms underlying the Cytokine Release Syndrome (CRS) mediated by T Cell Bispecific Antibodies
Authors: Leclercq-Cohen Gabrielle , Steinhoff Nathalie , Albertí-Servera Llucia , Nassiri Sina , Danilin Sabrina , Piccione Emily , Yángüez Emilio , Hüsser Tamara , Herter Sylvia , Schmeing Stephan , Gerber Petra , Schwalie Petra , Sam Johannes , Briner Stefanie , Jenni Sylvia , Bianchi Roberta , Biehl Marlene , Cremasco Floriana , Apostolopoulou Katerina , Haegel Hélène , Klein Christian , Umana Pablo , Bacac Marina
Published: September 2024

Supplementary Figure S11. Single cell RNA-sequencing of whole blood treated with 0.2 μg/mL CD20-TCB was performed using the BD Rhapsody platform. A. UMAP plots of neutrophils colored by treatment. B. UMAP plots showing IL-1β (IL1B), IL-1Ra (IL1RN), IL-6 (IL6), IP-10 (CXCL10), IL-8 (CXCL8), TNF-α (TNF), MCP-1 (CCL2), MIP-1α (CCL3), MIP-1β (CCL4) gene expression within neutrophil clusters identified above. C. Violin plots showing the kinetics of gene expression distribution in neutrophils. The cytokine and cytokine receptor genes are listed on the y axis. The color code on the right side of the violin plots represents the median gene expression. The untreated condition corresponds to the pooled baseline and untreated samples. N= 4 donors (baseline, and 20 hrs) and n=2 donors (2 hrs, 4 hrs and 6 hrs).
Supplementary Tables 1-3 from De novo and histologically transformed small cell lung cancer is sensitive to lurbinectedin treatment through the modulation of EMT and NOTCH signaling pathways.
Authors: Chakraborty Subhamoy , Coleman Charles , Manoj Parvathy , Demircioglu Deniz , Shah Nisargbhai , de Stanchina Elisa , Rudin Charles M. , Hasson Dan , Sen Triparna
Published: September 2024

Supplementary Tables 1-3
Supplementary Table 2 from Impact of Frontline Ivosidenib on Volumetric Growth Patterns in Isocitrate Dehydrogenase (IDH) mutant Astrocytic and Oligodendroglial Tumors
Authors: Kamson David Olayinka. , Puri Sushant , Sang Yingying , Shi Meihui Jessica. , Blair Lindsay , Blakeley Jaishri O. , Laterra John
Published: September 2024

Supplementary Table 2 - Raw data for growth modeling.
Figure S1 from Results of an Open-label, Phase 1a/b Study of Pembrolizumab plus Olaratumab in Patients with Unresectable, Locally Advanced or Metastatic Soft Tissue Sarcoma
Authors: Schöffski Patrick , Bahleda Rastislav , Wagner Andrew J. , Burgess Melissa A. , Junker Niels , Chisamore Michael , Peterson Patrick , Szpurka Anna M. , Ceccarelli Matteo , Tap William D.
Published: September 2024

Figure S1: Study design.
Supplementary Figure S18 from Trackable Intratumor Microdosing and Spatial Profiling Provide Early Insights into Activity of Investigational Agents in the Intact Tumor Microenvironment
Authors: Derry Jonathan M.J. , Burns Connor , Frazier Jason P. , Beirne Emily , Grenley Marc , DuFort Christopher C. , Killingbeck Emily , Leon Michael , Williams Claire , Gregory Mark , Houlton Jeffrey , Clayburgh Daniel , Swiecicki Paul , Huszar Dennis , Berger Allison , Klinghoffer Richard A.
Published: September 2024

Correlation of MKI67 gene expression levels to Percent MIL113 Positivity for Tumors 7 and 8