bluuebunny/crossref_metadata_2025 huggingface dataset:
Supplementary figure 6 from Single-Cell Transcriptomic Analysis Identifies Senescent Osteocytes That Trigger Bone Destruction in Breast Cancer Metastasis
Authors: Kaur Japneet , Adhikari Manish , Sabol Hayley M. , Anloague Aric , Khan Sharmin , Kurihara Noriyoshi , Diaz-delCastillo Marta , Andreasen Christina Møller , Barnes Charles Lowry , Stambough Jeffrey B. , Palmieri Michela , Reyes-Castro Olivia , Zarrer Jennifer , Taipaleenmäki Hanna , Ambrogini Elena , Almeida Maria , O’Brien Charles A. , Nookaw Intawat , Delgado-Calle Jesus
Published: December 2024

Supplementary figure 6
Supplementary figure 15 from Single-Cell Transcriptomic Analysis Identifies Senescent Osteocytes That Trigger Bone Destruction in Breast Cancer Metastasis
Authors: Kaur Japneet , Adhikari Manish , Sabol Hayley M. , Anloague Aric , Khan Sharmin , Kurihara Noriyoshi , Diaz-delCastillo Marta , Andreasen Christina Møller , Barnes Charles Lowry , Stambough Jeffrey B. , Palmieri Michela , Reyes-Castro Olivia , Zarrer Jennifer , Taipaleenmäki Hanna , Ambrogini Elena , Almeida Maria , O’Brien Charles A. , Nookaw Intawat , Delgado-Calle Jesus
Published: December 2024

Supplementary figure 15
Supplementary figure 14 from Single-Cell Transcriptomic Analysis Identifies Senescent Osteocytes That Trigger Bone Destruction in Breast Cancer Metastasis
Authors: Kaur Japneet , Adhikari Manish , Sabol Hayley M. , Anloague Aric , Khan Sharmin , Kurihara Noriyoshi , Diaz-delCastillo Marta , Andreasen Christina Møller , Barnes Charles Lowry , Stambough Jeffrey B. , Palmieri Michela , Reyes-Castro Olivia , Zarrer Jennifer , Taipaleenmäki Hanna , Ambrogini Elena , Almeida Maria , O’Brien Charles A. , Nookaw Intawat , Delgado-Calle Jesus
Published: December 2024

Supplementary figure 14
Supplementary figure 1 from Single-Cell Transcriptomic Analysis Identifies Senescent Osteocytes That Trigger Bone Destruction in Breast Cancer Metastasis
Authors: Kaur Japneet , Adhikari Manish , Sabol Hayley M. , Anloague Aric , Khan Sharmin , Kurihara Noriyoshi , Diaz-delCastillo Marta , Andreasen Christina Møller , Barnes Charles Lowry , Stambough Jeffrey B. , Palmieri Michela , Reyes-Castro Olivia , Zarrer Jennifer , Taipaleenmäki Hanna , Ambrogini Elena , Almeida Maria , O’Brien Charles A. , Nookaw Intawat , Delgado-Calle Jesus
Published: December 2024

Supplementary figure 1
Supplemental Materials and Methods from Tumor-Associated Microglia Secrete Extracellular ATP to Support Glioblastoma Progression
Authors: Wu Caren Yu-Ju , Chen Yiyun , Lin Ya-Jui , Wei Kuo-Chen , Chang Kwang-Yu , Feng Li-Ying , Chen Ko-Ting , Li Gordon , Ren Alexander Liang , Nitta Ryan Takeo , Wu Janet Yuling , Cho Kwang Bog , Pant Ayush , Choi John , Mackall Crystal L. , Kim Lily H. , Wu An-Chih , Chuang Jian-Ying , Huang Chiung-Yin , Jackson Christopher M. , Chen Pin-Yuan , Lim Michael
Published: December 2024

Supp M&M
Figure S1 from LTβR Agonism Promotes Antitumor Immune Responses via Modulation of the Tumor Microenvironment
Authors: An Disi , Chen Guoying , Cheng Wei-Yi , Mohrs Katja , Adler Christina , Gupta Namita T. , Atwal Gurinder S. , DiLillo David J. , Daly Christopher , Lin John C. , Kuhnert Frank
Published: December 2024

Supplementary Figure S1
Data from Targeting NTRK1 Enhances Immune Checkpoint Inhibitor Efficacy in NTRK1 Wild-Type Non–Small Cell Lung Cancer
Authors: Smith Margaret R. , Dixon Caroline B. , Wang Yuezhu , Liu Yin , D’Agostino Ralph , Ruiz Jimmy , Oliver George , Miller Lance D. , Topaloglu Umit , Chan Michael D. , Farris Michael , Su Jing , Mileham Kathryn F. , Zhao Dawen , Li Wencheng , Sexton Tammy , Lycan Thomas , Haas Karen M. , Grayson Jason M. , Xing Fei
Published: December 2024

Abstract
Treatment of non–small cell lung cancer (NSCLC) has drastically changed in recent years owing to the robust anticancer effects of immune checkpoint inhibitors (ICI). However, only 20% of the patients with NSCLC benefit from ICIs, highlighting the need to uncover the mechanisms mediating resistance. By analyzing the overall survival (OS) and mutational profiles of 424 patients with NSCLC who received ICI treatments between 2015 and 2021, we determined that patients carrying a loss-of-function mutation in neurotrophic tyrosine kinase receptor 1 (NTRK1) had a prolonged OS when compared with patients with wild-type NTRK1. Notably, suppression of the NTRK1 pathway by knockdown or entrectinib treatment significantly enhanced ICI efficacy in mouse NSCLC models. Comprehensive T-cell population analyses demonstrated that stem-like CD4+ T cells and effector CD4+ and CD8+ T cells were highly enriched in anti–PD-1–treated mice bearing tumors with decreased NTRK1 signaling. RNA sequencing revealed that suppression of NTRK1 signaling in tumor cells increased complement C3 expression, which enhanced the recruitment of T cells and myeloid cells and stimulated M1-like macrophage polarization in the tumor. Together, this study demonstrates a role for NTRK1 signaling in regulating cross-talk between tumor cells and immune cells in the tumor microenvironment and provides a potential therapeutic approach to overcome immunotherapy resistance in patients with NSCLC with NTRK1 wild-type.

Significance: Inhibition of NTRK1 signaling confers sensitivity to immunotherapy by enhancing complement C3-mediated T-cell and macrophage functions, leading to improved responses to immune checkpoint inhibitors in patients with lung cancer with NTRK1 mutations.
Supplementary Table S2 from Asymptomatic Incidence of Monoclonal Gammopathy of Undetermined Significance and Preclinical Duration to Myeloma Diagnosis: A Modeling Study
Authors: Ji Mengmeng , Shih Yi-Hsuan , Huber John H. , Wang Mei , Feuer Eric J. , Etzioni Ruth , Wang Shi-Yi , Chang Su-Hsin
Published: December 2024

Supplementary Table S2 shows the intermediate results of calculations used to estimate the age-specific incidence of asymptomatic MGUS for non-Hispanic black population aged 50 to 84.
Supplementary Figure S2 from Asymptomatic Incidence of Monoclonal Gammopathy of Undetermined Significance and Preclinical Duration to Myeloma Diagnosis: A Modeling Study
Authors: Ji Mengmeng , Shih Yi-Hsuan , Huber John H. , Wang Mei , Feuer Eric J. , Etzioni Ruth , Wang Shi-Yi , Chang Su-Hsin
Published: December 2024

Supplementary Figure S2 shows the modeling results using different years of NHANES datasets. The comparison is a part of the sensitivity analyses.
Supplementary Table S1 from Identification of High-Incidence Populations in the United States for Anti–Epstein-Barr Virus Serologic Screening for Nasopharyngeal Carcinoma
Authors: Clark Payton E. , Taparra Kekoa , Miller Jacob A.
Published: December 2024

Table S1. Age-Standardized Rates among U.S. Minoritized Populations and Matched National/Provincial Reference Populations from GLOBOCAN 2020
Supplementary Figure S3 from Identification of High-Incidence Populations in the United States for Anti–Epstein-Barr Virus Serologic Screening for Nasopharyngeal Carcinoma
Authors: Clark Payton E. , Taparra Kekoa , Miller Jacob A.
Published: December 2024

Figure S3. Prevalence of preclinical (undiagnosed) nasopharyngeal carcinoma per 100,000 subjects as a function of age, use of NPC screening, age at screening, and frequency of screening. Values are provided for reference case of Chinese American men and women screened with anti-BNLF2b + nasoendoscopy (strategy D). No screening is plotted in red, whereas once-lifetime screening is plotted in green. A) Once-lifetime screening, varied by age at screening. After once-lifetime screening, the prevalence of preclinical NPC decreases proportional to screening sensitivity, then rises over years as additional cases develop and prevalence returns to that of an unscreened population. B) Repeated screening starting at age 50, varied by interval of screening (once-lifetime versus every 1–5 years). After screening, the prevalence of preclinical NPC decreases proportional to screening sensitivity, then rises until the next screen. For frequent screening (every 1–2 years), the prevalence of preclinical NPC remains low until screening ceases at age 75. Prevalence approaches that of an unscreened population when screening interval exceeds five years. NPC, nasopharyngeal carcinoma.
Supplementary Table S6 from Associations of Prostate Tumor Immune Landscape with Vigorous Physical Activity and Prostate Cancer Progression
Authors: Huang Lanshan , Winter Sarah J. , Olsson Linnea T. , Hamilton Alina M. , Halliday Sophia R. , Kirk Erin L. , Farnan Laura , Gerstel Adrian , Craig Stephanie G. , Finn Stephen P. , LaBonte Wilson Melissa , Jain Suneil , Troester Melissa A. , Butler Eboneé N. , Bensen Jeannette T. , Wobker Sara E. , Allott Emma H.
Published: December 2024

Supplementary Table S6. Hazard ratios and 95% confidence intervals for associations between histologic inflammation and risk of prostate cancer progression in the pooled study, overall and stratified by ERG expression.
Supplementary Table S4 from Hepatocellular Carcinoma Etiology Drives Survival Outcomes: A Population-Based Analysis
Authors: Cranford Hannah M. , Jones Patricia D. , Wong Robert J. , Liu Qinran , Kobetz Erin N. , Reis Isildinha M. , Koru-Sengul Tulay , Pinheiro Paulo S.
Published: December 2024

4. Supplementary Table S4 shows multivariable Cox proportional hazards regression models in which HCC-specific survival is assessed based on period of diagnosis, prior or during 2013 and after 2013, for HCV only cases and for non-HCV related cases.
Supplementary Table S4 from Associations of Prostate Tumor Immune Landscape with Vigorous Physical Activity and Prostate Cancer Progression
Authors: Huang Lanshan , Winter Sarah J. , Olsson Linnea T. , Hamilton Alina M. , Halliday Sophia R. , Kirk Erin L. , Farnan Laura , Gerstel Adrian , Craig Stephanie G. , Finn Stephen P. , LaBonte Wilson Melissa , Jain Suneil , Troester Melissa A. , Butler Eboneé N. , Bensen Jeannette T. , Wobker Sara E. , Allott Emma H.
Published: December 2024

Supplementary Table S4. Associations between histologic inflammation and disease aggressiveness in the pooled study, overall and stratified by ERG expression.
Supplementary Table S1 from Hepatocellular Carcinoma Etiology Drives Survival Outcomes: A Population-Based Analysis
Authors: Cranford Hannah M. , Jones Patricia D. , Wong Robert J. , Liu Qinran , Kobetz Erin N. , Reis Isildinha M. , Koru-Sengul Tulay , Pinheiro Paulo S.
Published: December 2024

1. Supplementary Table S1 shows International Classification of Diseases discharge codes used to define the following hepatocellular carcinoma etiologies: chronic hepatitis C virus infection, chronic hepatitis B virus infection, alcohol-related liver conditions, metabolic/non-alcoholic fatty liver disease-related conditions, biliary conditions, autoimmune conditions, and genetic conditions.
Supplementary Table S1 from Associations of Prostate Tumor Immune Landscape with Vigorous Physical Activity and Prostate Cancer Progression
Authors: Huang Lanshan , Winter Sarah J. , Olsson Linnea T. , Hamilton Alina M. , Halliday Sophia R. , Kirk Erin L. , Farnan Laura , Gerstel Adrian , Craig Stephanie G. , Finn Stephen P. , LaBonte Wilson Melissa , Jain Suneil , Troester Melissa A. , Butler Eboneé N. , Bensen Jeannette T. , Wobker Sara E. , Allott Emma H.
Published: December 2024

Supplementary Table S1. Gene list of immune signature.
Supplementary Figure S3 from Associations of Prostate Tumor Immune Landscape with Vigorous Physical Activity and Prostate Cancer Progression
Authors: Huang Lanshan , Winter Sarah J. , Olsson Linnea T. , Hamilton Alina M. , Halliday Sophia R. , Kirk Erin L. , Farnan Laura , Gerstel Adrian , Craig Stephanie G. , Finn Stephen P. , LaBonte Wilson Melissa , Jain Suneil , Troester Melissa A. , Butler Eboneé N. , Bensen Jeannette T. , Wobker Sara E. , Allott Emma H.
Published: December 2024

Supplementary Figure S3. Boxplots comparing gene expression-based immune cell types in men with low tumor aggressiveness reporting any vs. no vigorous recreational activity. A. Gleason score ≤3 + 4. B. Clinical stage I-II.
Supplementary Materials 1 from Are Women’s Breast Cancer Risk Appraisals in Line with Updated Clinical Risk Estimates Communicated? Results from a UK Family History Risk and Prevention Clinic
Authors: Woof Victoria G. , Howell Anthony , Fox Lynne , McWilliams Lorna , Evans Dafydd Gareth R. , French David P.
Published: December 2024

Supplementary Materials 1: the summary letter women received, the analogy used to explain a PRS and the questionnaire women completed.
Table S2 from Plasma Ghrelin and Risks of Sex-Specific, Site-Specific, and Early-Onset Colorectal Cancer: A Mendelian Randomization Analysis
Authors: Hazelwood Emma , Lopez Manzano Catalina , Vincent Emma E. , Albanes Demetrius , Bishop David Timothy , Le Marchand Loïc , Ulrich Cornelia M. , Peters Ulrike , Murphy Gwen , Samadder Niloy Jewel , Anderson Laura , Gunter Marc J. , Murphy Neil , Van Guelpen Bethany , Papadimitriou Nikos
Published: December 2024

Cancer betas for the SNPs associated with plasma ghrelin
Supplementary Table S1 from Racial, Ethnic, and Socioeconomic Disparities in Meeting Physical Activity Guidelines among Female Breast Cancer Survivors in the United States
Authors: Wojcik Kaitlyn M. , Wilson Oliver W.A. , Shiels Meredith S. , Sheppard Vanessa B. , Jayasekera Jinani
Published: December 2024

Supplementary Table S1: National-level (weighted) Estimates and Absolute Differences among Female Breast Cancer Survivors and Adult Women without Cancer Who Met Both Aerobic and Muscle Strengthening Physical Activity Guidelines
Supplementary Table 1 from The University of North Carolina Cancer Survivorship Cohort: A Resource for Collaborative Survivorship Research
Authors: Anderson Chelsea , Bensen Jeannette T. , Allott Emma H. , Basta Patricia V. , Irwin Debra E. , Gerstel Adrian , Farnan Laura , Tan Hung-Jui , Kent Erin E. , Kuo Tzy-Mey , Baggett Christopher D. , Olshan Andrew F. , Earp H. Shelton , Nichols Hazel B.
Published: December 2024

Supplemental Table 1. UNC Cancer Survivorship Cohort cancer-specific questionnaires
Supplemental Table 4 from Lifecourse Growth and Development Determinants of Mammographic Density in Black Women
Authors: Bigham Zahna , Holder Etienne X. , Rodday Angie Mae , Breeze Janis L. , Nelson Kerrie P. , Palmer Julie R. , Freund Karen M. , Bertrand Kimberly A.
Published: December 2024

Supplemental Table 4 shows path analysis coefficients for the effect of factors related to growth and development on log-transformed absolute dense area
Supplemental Table 1 from Lifecourse Growth and Development Determinants of Mammographic Density in Black Women
Authors: Bigham Zahna , Holder Etienne X. , Rodday Angie Mae , Breeze Janis L. , Nelson Kerrie P. , Palmer Julie R. , Freund Karen M. , Bertrand Kimberly A.
Published: December 2024

Supplemental Table 1 shows baseline (1995) characteristics of invited, included, and excluded participants.
Supplementary Table 3 from Excess Mortality in Persons with Concurrent HIV and Cancer Diagnoses: A Retrospective Cohort Study
Authors: Lee Kamaria L. , Sarovar Varada , Lam Jennifer O. , Leyden Wendy A. , Alexeeff Stacey E. , Lea Alexandra N. , Hechter Rulin C. , Hu Haihong , Marcus Julia L. , Yuan Qing , Kramer Jennifer R. , Lin Lilie L. , Chiao Elizabeth Y. , Towner William J. , Horberg Michael A. , Silverberg Michael J.
Published: December 2024

Unadjusted and adjusted mortality rate differences and excess mortality rate for cancer groups and common individual cancers, stratified by calendar era
Data from Are Women’s Breast Cancer Risk Appraisals in Line with Updated Clinical Risk Estimates Communicated? Results from a UK Family History Risk and Prevention Clinic
Authors: Woof Victoria G. , Howell Anthony , Fox Lynne , McWilliams Lorna , Evans Dafydd Gareth R. , French David P.
Published: December 2024

AbstractBackground:
The incorporation of breast density and a polygenic risk score (PRS) into breast cancer risk prediction models can alter previously communicated risk estimates. Previous research finds that risk communication does not usually change personal risk appraisals. This study aimed to examine how women from the family history risk study appraise their breast cancer risk following communication of an updated risk estimate.
Methods:
In the family history risk study, 323 women attended a consultation to receive an updated breast cancer risk estimate. A subset (n = 190) completed a questionnaire, assessing their subjective breast cancer risk appraisals, satisfaction with the information provided, and cancer-related worry. One hundred and three were notified of a decreased risk, 34 an increased risk, and 53 an unchanged risk.
Results:
Women’s subjective risk appraisals were in line with the updated risk estimates provided, with age, a PRS, and breast density explaining most of the variance in these appraisals. Those notified of an increased risk demonstrated higher subjective risk perceptions compared with those whose risk remained unchanged or decreased.
Conclusions:
Women’s subjective breast cancer risk appraisals are amenable to change following updated risk feedback, with new information breast density and a PRS accepted and integrated into existing risk appraisals. Trust in the service, the analogies, and visual communication strategies used may have positively influenced the integration of this new information.
Impact:
Further research is warranted to assess whether similar patterns emerge for other illnesses and in different clinical contexts to determine the best strategies for communicating updated risk estimates.
Supplementary Table S2 from Neoadjuvant Intratumoral Plasmid IL-12 Electro-Gene-Transfer and Nivolumab in Patients with Operable, Locoregionally Advanced Melanoma
Authors: Tarhini Ahmad A. , Eroglu Zeynep , Eljilany Islam , Zager Jonathan S. , Gonzalez Ricardo J. , Sarnaik Amod A. , Cruse Carl Wayne , Khushalani Nikhil I. , De Aquino Deanryan B. , Abraham Edith , Acevedo Diana M. , Richards Allison , Schell Michael J. , Kalos Denise , Chen Pei-Ling , Messina Jane L. , Canton David A. , Sondak Vernon K.
Published: December 2024

Possibly, probably, or definitely TRAEs
Supplementary Table S1 from Neoadjuvant Intratumoral Plasmid IL-12 Electro-Gene-Transfer and Nivolumab in Patients with Operable, Locoregionally Advanced Melanoma
Authors: Tarhini Ahmad A. , Eroglu Zeynep , Eljilany Islam , Zager Jonathan S. , Gonzalez Ricardo J. , Sarnaik Amod A. , Cruse Carl Wayne , Khushalani Nikhil I. , De Aquino Deanryan B. , Abraham Edith , Acevedo Diana M. , Richards Allison , Schell Michael J. , Kalos Denise , Chen Pei-Ling , Messina Jane L. , Canton David A. , Sondak Vernon K.
Published: December 2024

Representativeness of Study Participants
Supplementary Table S2 from Phase II Trial of Gemcitabine and Nab-Paclitaxel for Recurrent Osteosarcoma with Serial Monitoring Using Liquid Biopsy: A Report from the National Pediatric Cancer Foundation
Authors: Dhir Aditi , Hayashi Masanori , Bodlak Avery , Oesterheld Javier , Loeb David M. , Mascarenhas Leo , Isakoff Michael S. , Sandler Eric S. , Borinstein Scott C. , Trucco Matteo , Lagmay Joanne P. , Setty Bhuvana A. , Pratilas Christine A. , Caywood Emi , Metts Jonathan , Yin Hong , Fridley Brooke , Yin Jun , Laborde Jose , Reed Damon R. , Adams Daniel L. , Wagner Lars M.
Published: December 2024

Supplemental Table S2. Immunohistochemistry Results and Clinical Benefit
Supplementary Table S1 from Phase II Trial of Gemcitabine and Nab-Paclitaxel for Recurrent Osteosarcoma with Serial Monitoring Using Liquid Biopsy: A Report from the National Pediatric Cancer Foundation
Authors: Dhir Aditi , Hayashi Masanori , Bodlak Avery , Oesterheld Javier , Loeb David M. , Mascarenhas Leo , Isakoff Michael S. , Sandler Eric S. , Borinstein Scott C. , Trucco Matteo , Lagmay Joanne P. , Setty Bhuvana A. , Pratilas Christine A. , Caywood Emi , Metts Jonathan , Yin Hong , Fridley Brooke , Yin Jun , Laborde Jose , Reed Damon R. , Adams Daniel L. , Wagner Lars M.
Published: December 2024

Supplementary Table S1. Representativeness of Study Participants
Figure 3 from Preclinical Evaluation of AZD6422, an Armored Chimeric Antigen Receptor T Cell Targeting CLDN18.2 in Gastric, Pancreatic, and Esophageal Cancers
Authors: Barrett Allison M. , Britton Zachary T. , Carrasco Rosa A. , Breen Shannon , Broggi Maria A.S. , Hatke Amanda L. , Clark Benjamin , Yang Chunning , Phipps Sandrina , Ortiz Lorenzo , Janocha Brianna , Zanvit Peter , Giraldo Nicolas A. , Martin Philip L. , Lapointe Jean-Martin , Harder Nathalie , Cornish Georgina H. , Attili Bala N.N.R. , Mazor Yariv , Damschroder Melissa , Cobbold Mark , Moody Gordon , Bosco Emily E.
Published: December 2024

Evaluation of CLDN18.2-targeting CAR-T cells in vivo. A, NSG mice bearing PaTu8988s HS xenografts (CLDN18.2 H-score = 268) were dosed by tail vein with 9e6 CAR+ CLDN18.2 Bz CAR-T cells; total T-cell infusion number was matched across groups. Tumor volume and body weight were measured biweekly (n = 9). Serum levels of IFNγ were measured at 4, 7, and 14 days after infusion (n = 3). B, Schematic representation of a second-generation CAR-T design modified to replace 4-1BB with a CD28 costimulatory domain (28z). The average transduction efficiency (CAR+, day 9) of multiple healthy donors for clone 9 28z is shown. Representative FC plots of CAR surface expression at day 9 after lentivirus transduction were compared with UT control for a single donor. C, NSG mice bearing PaTu8988s HS xenografts were dosed as described in A with clone 9 CD28z or Bz CAR-T (n = 6) at indicated doses. Serum levels of IFNγ were measured at 4, 7, and 14 days after infusion (n = 3). D, Representative images of CLDN18.2 (top row) and CD3 (bottom row) staining in the stomachs of mice dosed with clone 9 CAR-T cells from C at indicated time points. All data represent mean ± SEM of replicate experiments or animals.
Figure 2 from Preclinical Evaluation of AZD6422, an Armored Chimeric Antigen Receptor T Cell Targeting CLDN18.2 in Gastric, Pancreatic, and Esophageal Cancers
Authors: Barrett Allison M. , Britton Zachary T. , Carrasco Rosa A. , Breen Shannon , Broggi Maria A.S. , Hatke Amanda L. , Clark Benjamin , Yang Chunning , Phipps Sandrina , Ortiz Lorenzo , Janocha Brianna , Zanvit Peter , Giraldo Nicolas A. , Martin Philip L. , Lapointe Jean-Martin , Harder Nathalie , Cornish Georgina H. , Attili Bala N.N.R. , Mazor Yariv , Damschroder Melissa , Cobbold Mark , Moody Gordon , Bosco Emily E.
Published: December 2024

Development and evaluation of CLDN18.2-targeting CAR-T cells in vitro. A, Schematic representation of second-generation CAR-T lentivirus design, which includes a 4-1BB costimulatory domain (Bz). The table shows for each CLDN18.2-reactive clone the relative binding affinity (human and mouse), reactivity to mutant CLDN18.2 (M149L), and average transduction efficiency (CAR+, day 9) of multiple healthy donors. Representative FC plots of CAR surface expression at day 9 after lentivirus transduction were compared with UT control for a single donor. B, CLDN18.2 cell surface expression of various cell lines as determined by FC with 5 μg/mL CLDN18.2-reactive clones compared with nonspecific isotype antibody (R347). C, Epitope characterization of CLDN18.2-reactive clones. The AlphaFold structure on the far left (red) represents all sites of point mutation in HEK293 cells that vary between CLDN18.1 and CLDN18.2 in the first extracellular loop; the color-coded diagrams represent sites that influence respective clone binding. D, Percent cytolysis of HEK293 + huCLDN18.1, HEK293 + huCLDN18.2, HEK293 + muCLDN18.1, HEK293 + muCLDN18.2, and PaTu8988s HS cells determined by xCELLigence RTCA assay after 48 hours of co-culture with CLDN18.2 CAR-T cells at a 1:1 E:T ratio. The supernatants from the xCELLigence assay were collected at 24 hours for cytokine assessment (Meso Scale Discovery) assay. All data represent mean ± SEM of replicate experiments.
Figure 1 from Preclinical Evaluation of AZD6422, an Armored Chimeric Antigen Receptor T Cell Targeting CLDN18.2 in Gastric, Pancreatic, and Esophageal Cancers
Authors: Barrett Allison M. , Britton Zachary T. , Carrasco Rosa A. , Breen Shannon , Broggi Maria A.S. , Hatke Amanda L. , Clark Benjamin , Yang Chunning , Phipps Sandrina , Ortiz Lorenzo , Janocha Brianna , Zanvit Peter , Giraldo Nicolas A. , Martin Philip L. , Lapointe Jean-Martin , Harder Nathalie , Cornish Georgina H. , Attili Bala N.N.R. , Mazor Yariv , Damschroder Melissa , Cobbold Mark , Moody Gordon , Bosco Emily E.
Published: December 2024

Expression and prevalence of CLDN18.2 in normal tissues and GI adenocarcinomas. A, Normal tissue RNA expression of CLDN18 [represented as normalized transcripts per million (TPM); Human Protein Atlas, GTEx dataset]. HC, hippocampal formation. CLDN18.2 expression on representative images of the human stomach, NSG mouse stomach, and human lung are shown. B, CLDN18.2 expression on representative samples of gastric cancer (H-score = 249), PDAC (H-score = 175), and esophageal adenocarcinoma (H-score = 175). C, Prevalence and intensity of CLDN18.2 expression on tumor samples derived from patients with gastric cancer (n = 185), PDAC (n = 61), and esophageal adenocarcinoma (n = 32). Data are shown as H-scores and as the percentages of tumor cells at each level of intensity (1+, 2+, and 3+). EAc, esophageal adenocarcinoma; GC, gastric cancer.
Supplementary Table S1 from Association of Tumor Mutational Burden and PD-L1 with the Efficacy of Pembrolizumab with or without Chemotherapy versus Chemotherapy in Advanced Urothelial Carcinoma
Authors: Fléchon Aude , Morales-Barrera Rafael , Powles Thomas , Alva Ajjai , Özgüroğlu Mustafa , Csöszi Tibor , Loriot Yohann , Rodriguez-Vida Alejo , Géczi Lajos , Cheng Susanna Y. , Fradet Yves , Oudard Stéphane , Vulsteke Christof , Gunduz Seyda , Mamtani Ronac , Yu Evan Y. , Montesa Pino Alvaro , Anido Urbano , Sendur Mehmet A.N. , Gravis Gwenaelle , Révész János , Kostorov Vladimir , Huillard Olivier , Ma Junshui , Rajasagi Mohini , Vajdi Amir , Lunceford Jared , Cristescu Razvan , Imai Kentaro , Homet Moreno Blanca , Matsubara Nobuaki
Published: December 2024

Supplementary Table 1. Representativeness of study participants.
Supplementary Methods 1 from Characterization of FGFR Alterations and Activation in Patients with High-Risk Non–Muscle-Invasive Bladder Cancer
Authors: Eisner Joel R. , de Jong Florus C. , Shibata Yoichiro , Mayhew Gregory M. , Davison James M. , Carcione Jenna , Pappan Kirk L. , Thomas Shibu , Triantos Spyros , Santiago-Walker Ademi , Baig Mahadi , Milburn Michael V. , Beebe Kirk D. , Zuiverloon Tahlita C.M.
Published: December 2024

Supplementary Methods
Supplementary Table S2 from Determination of MYD88 and CXCR4 Mutations for Clinical Detection and Their Significance in Waldenström Macroglobulinemia
Authors: Yan Yuting , Yu Ying , Xiong Wenjie , Wang Jun , Yao Yao , Jia Yujiao , Huang Yanshan , Li Yuxi , Wang Tingyu , Lyu Rui , Sun Hao , Wang Haoxu , Wang Qi , Liu Wei , An Gang , Sui Weiwei , Xu Yan , Huang Wenyang , Yu Zhen , Zou Dehui , Hao Mu , Xiao Zhijian , Wang Jianxiang , Qiu Lugui , Yi Shuhua
Published: December 2024

Supplementary Table 2. Clinical characteristics and first-line treatment options for the entire symptomatic Waldenstrom macroglobulinemia (WM) cohort (n = 385) and for patients available for analysis of treatment response and outcome (n = 336).
Supplementary Table S1 from Determination of MYD88 and CXCR4 Mutations for Clinical Detection and Their Significance in Waldenström Macroglobulinemia
Authors: Yan Yuting , Yu Ying , Xiong Wenjie , Wang Jun , Yao Yao , Jia Yujiao , Huang Yanshan , Li Yuxi , Wang Tingyu , Lyu Rui , Sun Hao , Wang Haoxu , Wang Qi , Liu Wei , An Gang , Sui Weiwei , Xu Yan , Huang Wenyang , Yu Zhen , Zou Dehui , Hao Mu , Xiao Zhijian , Wang Jianxiang , Qiu Lugui , Yi Shuhua
Published: December 2024

Supplementary Table 1. Summary of the regimens for this cohort.
Supplemental Figure 4 from A Novel Human SDHA-Knockout Cell Line Model for the Functional Analysis of Clinically Relevant SDHA Variants
Authors: Kent Jason D. , Klug Lillian R. , Heinrich Michael C.
Published: December 2024

Supplemental Figure 4. Use of Abundance Scores characterization of SDHA VUS provides classification evidence with moderate clinical utility.
Supplemental Figure 3 from A Novel Human SDHA-Knockout Cell Line Model for the Functional Analysis of Clinically Relevant SDHA Variants
Authors: Kent Jason D. , Klug Lillian R. , Heinrich Michael C.
Published: December 2024

Supplemental Figure 3. Abundance score data versus computational prediction in providing evidence for clinical variant interpretation.
Supplemental Figure 2 from A Novel Human SDHA-Knockout Cell Line Model for the Functional Analysis of Clinically Relevant SDHA Variants
Authors: Kent Jason D. , Klug Lillian R. , Heinrich Michael C.
Published: December 2024

Supplemental Figure 2. Hypomorphic PMD variants have similar levels of SDHA protein expression as benign variants.
Supplementary Figure S4 from Determination of MYD88 and CXCR4 Mutations for Clinical Detection and Their Significance in Waldenström Macroglobulinemia
Authors: Yan Yuting , Yu Ying , Xiong Wenjie , Wang Jun , Yao Yao , Jia Yujiao , Huang Yanshan , Li Yuxi , Wang Tingyu , Lyu Rui , Sun Hao , Wang Haoxu , Wang Qi , Liu Wei , An Gang , Sui Weiwei , Xu Yan , Huang Wenyang , Yu Zhen , Zou Dehui , Hao Mu , Xiao Zhijian , Wang Jianxiang , Qiu Lugui , Yi Shuhua
Published: December 2024

Supplementary Figure 4. The IGHV-D-J repertoire in patients with mutated and wild-type CXCR4. Distribution of major VH family gene segments in CXCR4 wild-type group (A) and CXCR4 mutated group (B); Distribution of major DH family gene segments in CXCR4 wildtype group (C) and CXCR4 mutated group (D); Distribution of major JH family gene segments in CXCR4 wild-type group (E) and CXCR4 mutated group (F)
Supplementary Tables1 from Multidimensional Immunotyping of Human NF1-Associated Peripheral Nerve Sheath Tumors Uncovers Tumor-Associated Macrophages as Key Drivers of Immune Evasion in the Tumor Microenvironment
Authors: Zhang Lindy , Maalouf Alexandre , Makri Stavriani C. , Banerjee Jineta , Suru Aditya , Tam Ada J. , Calizo Ana , Pollard Kai , Wang Jiawan , Danilova Ludmila , Ioannou Maria , Levin Adam S. , Morris Carol D. , Rhee Daniel S. , Belzberg Allan J. , Blakeley Jaishri O. , Ladle Brian H. , Pardoll Drew M. , Lucas Calixto-Hope G. , Rodriguez Fausto J. , Gross John M. , Anders Robert A. , Pratilas Christine A. , Llosa Nicolas J.
Published: December 2024

Supplementary Tables S1, S2, S3 and S4
Supplementary Figure 4 from Multidimensional Immunotyping of Human NF1-Associated Peripheral Nerve Sheath Tumors Uncovers Tumor-Associated Macrophages as Key Drivers of Immune Evasion in the Tumor Microenvironment
Authors: Zhang Lindy , Maalouf Alexandre , Makri Stavriani C. , Banerjee Jineta , Suru Aditya , Tam Ada J. , Calizo Ana , Pollard Kai , Wang Jiawan , Danilova Ludmila , Ioannou Maria , Levin Adam S. , Morris Carol D. , Rhee Daniel S. , Belzberg Allan J. , Blakeley Jaishri O. , Ladle Brian H. , Pardoll Drew M. , Lucas Calixto-Hope G. , Rodriguez Fausto J. , Gross John M. , Anders Robert A. , Pratilas Christine A. , Llosa Nicolas J.
Published: December 2024

Supplementary Figure 4
Table S2. First progression sites2 from Safety, Efficacy, and Biomarker Analysis of Crizotinib in MET-Mutated Non–Small Cell Lung Cancer—Results from the Drug Rediscovery Protocol
Authors: Verkerk Karlijn , van der Wel Tijmen J.W.T. , Zeverijn Laurien J. , Geurts Birgit S. , Spiekman Ilse A.C. , de Wit Gijs F. , Roepman Paul , Jansen Anne M.L. , van der Noort Vincent , Smit Egbert F. , Hoeben Ann , Hendriks Lizza E.L. , van den Heuvel Michel M. , Piet Berber , Herder Gerarda J.M. , Hashemi Sayed M.S. , Gelderblom Hans , Verheul Henk M.W. , Voest Emile E. , de Langen Adrianus J.
Published: December 2024

Site or type of first progression of all patients that started crizotinib treatment. * Multiple sites include: bone and lymph node; bone, heart and lung; bone, lung and pleura; brain and lung; lung and bone; lung and thyroid gland.
Table S1. Response associations1 from Safety, Efficacy, and Biomarker Analysis of Crizotinib in MET-Mutated Non–Small Cell Lung Cancer—Results from the Drug Rediscovery Protocol
Authors: Verkerk Karlijn , van der Wel Tijmen J.W.T. , Zeverijn Laurien J. , Geurts Birgit S. , Spiekman Ilse A.C. , de Wit Gijs F. , Roepman Paul , Jansen Anne M.L. , van der Noort Vincent , Smit Egbert F. , Hoeben Ann , Hendriks Lizza E.L. , van den Heuvel Michel M. , Piet Berber , Herder Gerarda J.M. , Hashemi Sayed M.S. , Gelderblom Hans , Verheul Henk M.W. , Voest Emile E. , de Langen Adrianus J.
Published: December 2024

Baseline characteristics of all patients that completed at least one treatment cycle, stratified by objective response. Percentages may not total 100 due to rounding. Annotations: * Two patients with non-small cell lung cancer not otherwise specified (no objective response) and one patient with undifferentiated non-small cell lung cancer (objective response). ® Missing for one patient with objective response. Abbreviations: IQR, Interquartile range; ECOG, Eastern Cooperative Oncology Group; PD-L1, Programmed death-ligand 1.
Data from Nivolumab in Patients with Metastatic Castration-Resistant Prostate Cancer with and without DNA Repair Defects
Authors: Isaacsson Velho Pedro , Bastos Diogo Assed , Saint’ana Pedro Tofani , Rigatti Brenda , da Costa Emily Tonin , Muniz David Q.B. , Andreis Felipe , Ferreira Rafael Dal Ponte , Giongo Pedrotti Luana , Maistro Simone , Katayama Maria Lucia Hirata , Folgueira Maria Aparecida Azevedo Koike , Morelle Alessandra , Leal Alessandro , de Castro Gilberto
Published: December 2024

AbstractPurpose:
Despite the success of immune checkpoint inhibitors (ICI) across various cancers, their efficacy in metastatic castration-resistant prostate cancer (mCRPC) is modest, except for a subset of patients who experience significant, yet unpredictable, benefits. DNA repair defects (DRD) are associated with higher neoantigen load, which may predict response. Our study explored the potential of DRD for enhanced responsiveness to the ICI nivolumab.
Patients and Methods:
We conducted a phase II, multicenter, single-arm trial evaluating nivolumab in patients with mCRPC with prior docetaxel therapy. The DRD were assessed using ctDNA. The primary endpoint was PSA50 response. Secondary endpoints included the objective response rate, radiographic progression-free survival (rPFS), and overall survival. Also, exploratory comprehensive genomic profiling was performed via whole-exome sequencing of tumor samples and matched normal tissues, alongside PD-L1 expression evaluation.
Results:
Among the 38 enrolled patients, DRD was identifiable in 30.5% (11/36) through ctDNA and/or whole-exome sequencing analyses. The overall PSA50 response rate was 10.5% (4/38). The PSA50 and objective response rates did not significantly differ between patients with and without DRD (18.2% vs. 8%; P = 0.57 and 50% vs. 17.6%; P = 0.27, respectively). The median PSA-PFS (1.9 vs. 2.8 months; P = 0.52) and rPFS (3.4 vs. 5.5 months; P = 0.7) were not statistically different between patients with and without DRD. Grade ≥ 3 adverse events were reported in 47.3% of participants.
Conclusions:
Nivolumab has clinical activity in a subset of patients with mCRPC; however, DRD does not predict response. These results highlight the necessity of identifying new biomarkers to more accurately determine patients with mCRPC who might respond to ICIs.
Data from Determination of MYD88 and CXCR4 Mutations for Clinical Detection and Their Significance in Waldenström Macroglobulinemia
Authors: Yan Yuting , Yu Ying , Xiong Wenjie , Wang Jun , Yao Yao , Jia Yujiao , Huang Yanshan , Li Yuxi , Wang Tingyu , Lyu Rui , Sun Hao , Wang Haoxu , Wang Qi , Liu Wei , An Gang , Sui Weiwei , Xu Yan , Huang Wenyang , Yu Zhen , Zou Dehui , Hao Mu , Xiao Zhijian , Wang Jianxiang , Qiu Lugui , Yi Shuhua
Published: December 2024

AbstractPurpose:
This study aims to explore the incidence and clinical features of MYD88 and CXCR4 mutations in patients with Waldenström macroglobulinemia (WM) and determine the optimal method for routine clinical practice. Additionally, we seek to evaluate the prognostic significance of these features across various therapeutic backgrounds [the cytotoxic group, the rituximab/bortezomib-based group, and the Bruton tyrosine kinase inhibitor (BTKi) group].
Experimental Design:
A total of 385 symptomatic patients with WM were analyzed for MYD88 and CXCR4 mutations using Sanger sequencing, next-generation sequencing, allele-specific qPCR (AS-PCR), and/or droplet digital PCR (ddPCR).
Results:
The overall MYD88 mutation rate was 87.8%, relatively lower than that in the Western cohort. Both AS-PCR and ddPCR demonstrated high sensitivity in unsorted samples, detecting 98.5% and 97.7% of mutations, respectively, including those with low tumor burdens. The total CXCR4 mutation rate was 30.9%, with next-generation sequencing exhibiting the highest sensitivity of 78.0%. CXCR4 mutation was significantly linked to shorter OS only within the BTKi treatment group. The multivariate analysis indicated that MYD88 and CXCR4 mutations were not independent prognostic factors in the non-BTKi group when considering the International Prognostic Scoring System for Waldenström macroglobulinemia (IPSSWM) clinical staging. However, in the BTKi treatment group, these mutations emerged as independent adverse prognostic factors, overshadowing the prognostic significance of the IPSSWM classification (MYD88: HR, 0.229; P = 0.030; CXCR4: HR, 3.349; P = 0.012).
Conclusions:
Testing for MYD88 mutations using AS-PCR or ddPCR in unsorted samples is viable for routine clinical practice. Under BTKi treatment, MYD88 and CXCR4 mutations hold greater prognostic importance than IPSSWM staging in WM.
Data from Combinations of HDAC Inhibitor and PPAR Agonist Induce Ferroptosis of Leukemic Stem Cell–like Cells in Acute Myeloid Leukemia
Authors: Zhou Hui , Qin Dongmei , Xie Chendi , Zhou Jie , Jia Shuman , Zhou Ziwei , Qiu Yi , Xu Bing , Zha Jie
Published: December 2024

AbstractPurpose:
Leukemic stem cells (LSC) are responsible for leukemia initiation, relapse, and therapeutic resistance. Therefore, the development of novel therapeutic approaches targeting LSCs is urgently needed for patients with acute myeloid leukemia (AML).
Experimental Design:
The LSC-like cell lines (KG-1α and Kasumi-1) and CD34+ primary AML cells purified from patients with AML (n = 23) treated with CS055 and/or chiglitazar and were analyzed for viability, death, and colony formation assay. We performed RNA sequencing, glutamate release, intracellular glutathione, lipid reactive oxygen species, transmission electron microscopy, and Western blotting assay and confirmed ferroptosis in LSC-like cells. The luciferase reporter, co-immunoprecipitation, histone deacetylase 3 (HDAC3)-shRNA/HDAC3/deacetylase-deficient LSC-like cell lines, histidine pull-down, and chromatin immunoprecipitation assays performed to clarify the molecular mechanism of CS055/chiglitazar in LSC-like cells. We also established cell-derived xenograft and patient-derived xenograft mouse models to evaluate the therapeutic efficacy of CS055/chiglitazar against AML in vivo.
Results:
We report that the HDAC inhibitor CS055, in combination with peroxisome proliferator–activated receptor pan-agonist (chiglitazar), synergistically targets leukemic stem-like cells from leukemia cell lines and patient samples while sparing normal hematopoietic progenitor cells. Mechanistically, chiglitazar enhances the inhibitory effect of CS055 on HDAC3 and induces ferroptosis in LSC-like cells by downregulating the expression of ferroptosis suppressor SLC7A11. In fact, the inhibition of HDAC3 increases H3K27AC levels in the promoter region of activating transcription factor 3 (ATF3), a transcriptional repressor of the SLC7A11 gene, and upregulates the expression of ATF3. In contrast, ATF4, a SLC7A11 activator, is suppressed by HDAC3 inhibition.
Conclusions:
Our findings suggest that treatment with CS055 combined with chiglitazar will target LSCs by inducing ferroptosis and may confer an effective approach for the treatment of AML.
Data from Safety, Efficacy, and Biomarker Analysis of Crizotinib in MET-Mutated Non–Small Cell Lung Cancer—Results from the Drug Rediscovery Protocol
Authors: Verkerk Karlijn , van der Wel Tijmen J.W.T. , Zeverijn Laurien J. , Geurts Birgit S. , Spiekman Ilse A.C. , de Wit Gijs F. , Roepman Paul , Jansen Anne M.L. , van der Noort Vincent , Smit Egbert F. , Hoeben Ann , Hendriks Lizza E.L. , van den Heuvel Michel M. , Piet Berber , Herder Gerarda J.M. , Hashemi Sayed M.S. , Gelderblom Hans , Verheul Henk M.W. , Voest Emile E. , de Langen Adrianus J.
Published: December 2024

AbstractPurpose:
 To provide patients with MET-mutated advanced non–small cell lung cancer (METmut aNSCLC) access to crizotinib, further substantiate evidence of its efficacy and safety in this setting, and find potential biomarkers for nonresponse.
Patients and Methods:
In the Drug Rediscovery Protocol (NCT0295234), patients with an actionable molecular profile are treated with off-label registered drugs. Both treated and untreated patients with aNSCLC harboring MET exon 14 skipping or other MET mutations received crizotinib 250 mg BID until disease progression or intolerable toxicity. Primary endpoints were clinical benefit [CB: RECIST v1.1 confirmed partial response, complete response (CR), or stable disease ≥16 weeks] and safety. Patients were enrolled using a Simon-like two-stage design, with eight patients in stage I and if ≥1/8 patients had CB, 24 patients in stage II. Whole-genome sequencing and RNA sequencing were performed on baseline biopsies.
Results:
Between September 2018 and October 2022, 30 patients started treatment, and 24 were response-evaluable after completing ≥1 full treatment cycle. Two patients (8.3%) achieved CR, 13 (54.2%) partial response, and two (8.3%) stable disease. The CB rate was 70.8% [95% confidence interval (CI), 48.9–87.4], and the objective response rate was 62.5% (95% CI, 40.6–81.2). After 21.2-month median follow-up, median duration of response, progression-free survival, and overall survival were 9.3 (95% CI, 6.5–not available), 10.2 (95% CI, 6.0–20.1), and 13.0 months (95% CI, 9.0–not available), respectively. Twenty-three treatment-related grade ≥ 3 adverse events occurred in 12/30 patients (40%), causing treatment discontinuation in three (10%). One patient (achieving CR) had a tyrosine kinase domain mutation (p.H1094Y), and all other patients had MET exon 14 skipping mutations.
Conclusions:
Crizotinib is a valuable treatment option in METmut aNSCLC.
Supplementary Table S9 from Botensilimab, an Fc-Enhanced Anti–CTLA-4 Antibody, Is Effective against Tumors Poorly Responsive to Conventional Immunotherapy
Authors: Chand Dhan , Savitsky David A. , Krishnan Shanmugarajan , Mednick Gabriel , Delepine Chloe , Garcia-Broncano Pilar , Soh Kah Teong , Wu Wei , Wilkens Margaret K. , Udartseva Olga , Vincent Sylvia , Joshi Bishnu , Keith Justin G. , Manrique Mariana , Marques Marilyn , Tanne Antoine , Levey Daniel L. , Han Haiyong , Ng Serina , Ridpath Jackson , Huber Olivia , Morin Benjamin , Galand Claire , Bourdelais Sean , Gombos Randi B. , Ward Rebecca , Qin Yu , Waight Jeremy D. , Costa Matthew R. , Sebastian-Yague Alvaro , Rudqvist Nils-Petter , Pupecka-Swider Malgorzata , Venkatraman Vignesh , Slee Andrew , Patel Jaymin M. , Grossman Joseph E. , Wilson Nicholas S. , Von Hoff Daniel D. , Stebbing Justin , Curiel Tyler J. , Buell Jennifer S. , O’Day Steven J. , Stein Robert B.
Published: December 2024

This dataset summarizes the grade 3 or higher treatment-related adverse events (TRAEs) observed in patients with advanced solid tumors treated in the ongoing phase 1 trial of botensilimab. This safety information is crucial for assessing the risk-benefit profile of botensilimab alone and in combination with balstilimab.
Figure S4 from RNA Shielding of p65 Is Required to Potentiate Oncogenic Inflammation in TET2-Mutated Clonal Hematopoiesis
Authors: Ben-Crentsil Nana Adjoa , Mohammed Ismail Wazim , Balasis Maria E. , Newman Hannah , Quintana Ariel , Binder Moritz , Kruer Traci , Neupane Surendra , Ferrall-Fairbanks Meghan C. , Fernandez Jenna , Lasho Terra L. , Finke Christy M. , Ibrahim Mohammed L. , McGraw Kathy L. , Wysota Michael , Aldrich Amy L. , Ryder Christopher B. , Letson Christopher T. , Traina Joshua , McLemore Amy F. , Droin Nathalie , Shastri Aditi , Yun Seongseok , Solary Eric , Sallman David A. , Beg Amer A. , Ma Li , Gaspar-Maia Alexandre , Patnaik Mrinal M. , Padron Eric
Published: December 2024

Contains data related to Figure 4 but which was not included in the main figure
Supplementary Figure S17 from Botensilimab, an Fc-Enhanced Anti–CTLA-4 Antibody, Is Effective against Tumors Poorly Responsive to Conventional Immunotherapy
Authors: Chand Dhan , Savitsky David A. , Krishnan Shanmugarajan , Mednick Gabriel , Delepine Chloe , Garcia-Broncano Pilar , Soh Kah Teong , Wu Wei , Wilkens Margaret K. , Udartseva Olga , Vincent Sylvia , Joshi Bishnu , Keith Justin G. , Manrique Mariana , Marques Marilyn , Tanne Antoine , Levey Daniel L. , Han Haiyong , Ng Serina , Ridpath Jackson , Huber Olivia , Morin Benjamin , Galand Claire , Bourdelais Sean , Gombos Randi B. , Ward Rebecca , Qin Yu , Waight Jeremy D. , Costa Matthew R. , Sebastian-Yague Alvaro , Rudqvist Nils-Petter , Pupecka-Swider Malgorzata , Venkatraman Vignesh , Slee Andrew , Patel Jaymin M. , Grossman Joseph E. , Wilson Nicholas S. , Von Hoff Daniel D. , Stebbing Justin , Curiel Tyler J. , Buell Jennifer S. , O’Day Steven J. , Stein Robert B.
Published: December 2024

This dataset analyzes the relationship between FCGR2A and FCGR3A gene expression and immune cell type enrichment in tumor biopsies from patients treated with botensilimab alone or in combination with balstilimab. The analysis provides insights into the immune landscape associated with FCGR2A and FCGR3A expression in the tumor microenvironment, suggesting potential cellular mechanisms underlying botensilimab's efficacy. This data supports the role of FCGR2A and FCGR3A as potential biomarkers and helps elucidate how their expression may relate to specific immune cell infiltration patterns relevant to botensilimab's unique Fc-dependent mechanism of action.
Supplementary Figure S10 from Botensilimab, an Fc-Enhanced Anti–CTLA-4 Antibody, Is Effective against Tumors Poorly Responsive to Conventional Immunotherapy
Authors: Chand Dhan , Savitsky David A. , Krishnan Shanmugarajan , Mednick Gabriel , Delepine Chloe , Garcia-Broncano Pilar , Soh Kah Teong , Wu Wei , Wilkens Margaret K. , Udartseva Olga , Vincent Sylvia , Joshi Bishnu , Keith Justin G. , Manrique Mariana , Marques Marilyn , Tanne Antoine , Levey Daniel L. , Han Haiyong , Ng Serina , Ridpath Jackson , Huber Olivia , Morin Benjamin , Galand Claire , Bourdelais Sean , Gombos Randi B. , Ward Rebecca , Qin Yu , Waight Jeremy D. , Costa Matthew R. , Sebastian-Yague Alvaro , Rudqvist Nils-Petter , Pupecka-Swider Malgorzata , Venkatraman Vignesh , Slee Andrew , Patel Jaymin M. , Grossman Joseph E. , Wilson Nicholas S. , Von Hoff Daniel D. , Stebbing Justin , Curiel Tyler J. , Buell Jennifer S. , O’Day Steven J. , Stein Robert B.
Published: December 2024

This dataset provides important insights into botensilimab's effects on the myeloid compartment of the immune system. The increase in CD11c+ HLA-DR+ myeloid cells, which likely represent antigen-presenting cells, suggests that botensilimab may enhance antigen presentation and T cell activation. The lack of effect on CD16- myeloid cells indicates a selective impact on specific myeloid subsets. These findings contribute to understanding botensilimab's unique mechanism of action, suggesting it may enhance anti-tumor immunity not only through effects on T cells but also by modulating myeloid cell populations.
Supplementary Table S10A from MARK2/MARK3 Kinases Are Catalytic Codependencies of YAP/TAZ in Human Cancer
Authors: Klingbeil Olaf , Skopelitis Damianos , Tonelli Claudia , Yoshimoto Toyoki , Alpsoy Aktan , Panepinto Maria C. , Minicozzi Francesca , Merrill Joseph R. , Cafiero Amanda M. , Aggarwal Disha , Russo Suzanne , Ha Taehoon , Demerdash Osama E. , Wee Tse-Luen , Spector David L. , Lyons Scott K. , Tuveson David A. , Cifani Paolo , Vakoc Christopher R.
Published: December 2024

RNA-seq results. Combined tables for DESeq2 output of Ctrl, MARK2/3, YAP/TAZ double knockout in 20 cancer cell lines.