bluuebunny/crossref_metadata_2025 huggingface dataset:
Supplementary Table 2 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 mortality rate differences and excess mortality rate for common individual cancers, stratified by time from cancer diagnosis
Data 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

AbstractBackground:
Vigorous physical activity has been associated with lower risk of fatal prostate cancer. However, mechanisms contributing to this relationship are not understood.
Methods:
We studied 117 men with prostate cancer in the University of North Carolina Cancer Survivorship Cohort (UNC CSC) who underwent radical prostatectomy and 101 radiation-treated patients with prostate cancer in FASTMAN. Structured questionnaires administered in UNC CSC assessed physical activity. In both studies, digital image analysis of hematoxylin and eosin–stained tissues was applied to quantify tumor-infiltrating lymphocytes in segmented regions. NanoString gene expression profiling in UNC CSC and microarray in FASTMAN were performed on tumor tissue, and a 50-gene signature utilized to predict immune cell types.
Results:
Vigorous recreational activity, reported by 34 (29.1%) UNC CSC men, was inversely associated with tumor-infiltrating lymphocyte abundance. Tumors of men reporting any vigorous activity versus none showed lower gene expression–predicted abundance of Th, exhausted CD4 T cells, and macrophages. T-cell subsets, including regulatory T cells, Th, Tfh, exhausted CD4 T cells, and macrophages, were associated with an increased risk of biochemical recurrence, only among men with ERG-positive tumors.
Conclusions:
Vigorous activity was associated with lower prostate tumor inflammation and immune microenvironment differences. Macrophages and T-cell subsets, including those with immunosuppressive roles and those with lower abundance in men reporting vigorous exercise, were associated with worse outcomes in ERG-positive prostate cancer.
Impact:
Our novel findings contribute to our understanding of the role of the tumor immune microenvironment in prostate cancer progression and may provide insights into how vigorous exercise could affect prostate tumor biology.
Data 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

AbstractBackground:
Previous survival studies on hepatocellular carcinoma (HCC) by etiology are limited to hospital-based series, restricted cohorts, and monolithic etiologic categories. We studied population-based survival by seven mutually exclusive HCC etiologic groups—standalone hepatitis-C virus (HCV), hepatitis-B virus (HBV), alcohol-related liver disease (ALD), nonalcoholic fatty liver disease (NAFLD), and dual etiology HCV–HBV, HCV–ALD, and HBV–ALD—accounting for clinical and sociodemographic characteristics.
Methods:
All HCC cases diagnosed during 2005 to 2018 from the Florida Cancer Registry were linked for etiology using statewide discharge and viral hepatitis data. We performed a cause-specific survival analysis including Cox regression for the matched 15,616 cases by HCC etiology.
Results:
The leading etiology was HCV only (n = 4,983; 31.9%); the leading dual etiology was HCV–ALD (n = 2,552; 16.3%). The five-year adjusted survival was low—17.6% overall and <22% across all HCC etiologies. ALD-related etiologies [ALD only (14.4%; 95% confidence interval (CI), 12.7–16.0), HCV–ALD (10.2%; 95% CI, 8.7–11.7), and HBV–ALD (8.2%; 95% CI, 2.2–14.1)] showed lower survival than non-ALD causes—HCV only, HBV only, and NAFLD only. After adjustment for clinical and sociodemographic covariates, ALD and HBV–ALD HCC had 1.20 (95% CI, 1.13–1.27) and 1.28 (95% CI, 1.06–1.54) times higher risk of death compared with those with HCV-only HCC.
Conclusions:
ALD only and dual etiologies involving ALD show worse prognosis for HCC compared with viral etiology alone. To increase survival, improved screening and treatment are needed for patients with multiple HCC risk factors.
Impact:
Understanding US disparities in HCC survival by etiology can help guide the identification of etiologically specific biomarkers and potential therapeutic targets and inform public health measures.
Data 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

AbstractBackground:
Epidemiological and laboratory-based studies have provided conflicting evidence for a role of ghrelin in colorectal cancer development. We conducted two-sample Mendelian randomization (MR) analyses to evaluate evidence for an association of circulating ghrelin and colorectal cancer risk overall and by sex, cancer subsite, and age at diagnosis.
Methods:
Genetic instruments proxying plasma total ghrelin levels were obtained from a recent genome-wide association study of 54,219 participants. Summary data for colorectal cancer risk were obtained from a recent meta-analysis of several genetic consortia (up to 73,673 cases and 86,854 controls). A two-sample MR approach and several sensitivity analyses were applied.
Results:
We found no evidence for an association of genetically predicted plasma total ghrelin levels and colorectal cancer risk (0.95, 95% confidence interval, 0.81–1.12; R2 of ghrelin genetic instruments: 4.6%), with similarly null results observed when stratified by sex, anatomical subsite, and for early-onset colorectal cancer.
Conclusions:
Our study suggests that plasma ghrelin levels are unlikely to have a causal relationship with overall, early-onset, and sex- and cancer subsite–stratified colorectal cancer risk.
Impact:
This large-scale analysis adds to the growing body of evidence that plasma total ghrelin levels are not associated with colorectal cancer risk.
Data from High Gastric Cancer Mortality and Years of Life Lost in Nicaragua: A Population-Based Study 1997 to 2012
Authors: Peña-Galo Edgar M. , Palacios-Navarro Guillermo , Pastora-Membreño Javier , Torres-Herman Tatiana , Norwood Dalton A. , Montalvan-Sanchez Eleazar E. , Beasley Timothy , Bravo Luis E. , Morgan Douglas R.
Published: December 2024

AbstractBackground:
Gastric adenocarcinoma is the fourth leading cause of cancer-related mortality and leading infection-associated cancer. Gastric adenocarcinoma has striking geographic variability, with high incidence in East Asia and mountainous Latin America. Reliable cancer data and population-based cancer registries are lacking for the majority of low- and middle-income countries, including the Central American Four region (CA-4, Nicaragua, El Salvador, Honduras, and Guatemala).
Methods:
Mortality data for Nicaragua were obtained from the highly rated Ministry of Health death registry. All the patients were diagnosed with gastric cancer between 1997 and 2012 (ICD-10 codes, C16.0–C16.9) and death due to any cause were included in the study. Data on variables such as sex, age (stratified by 5-year age groups), municipality, urban/rural, altitude, and year of death were analyzed.
Results:
A total of 3,886 stomach cancer deaths were reported in Nicaragua between 1997 and 2012, of which 2,214 (56.9%) were male. The age-standardized mortality rates were 13.1 and 8.7 per 100,000 habitants for males and females, respectively, and without significant change during the study period (annual percentage change = −0.7, P = 0.2). An average of 17.9 years were lost per death, accounting for 67,964 years of life lost (YLL).
Conclusions:
The burden of gastric cancer mortality is high in Nicaragua with a significantly elevated age-standardized mortality rate, YYL, and average YLL.
Impact:
The projected increase in mortality portends the double cancer burden in northern Central America, with persistent infection-associated cancers and growing transition cancers (e.g., breast and colon cancers), which has implications for cancer control in Mesoamerica and US Latino populations.

See related commentary by Riquelme and Abnet, p. 1550
Data from Adiposity throughout Adulthood and Risk of Young-Onset Breast Cancer Tumor Subtypes in the Young Women’s Health History Study
Authors: Marcus Post Lydia , Pathak Dorothy R. , Hamilton Ann S. , Hirko Kelly A. , Houang Richard T. , Guseman Emily H. , Sanfelippo Dan , Bohme Carnegie Nicole , Olson L. Karl , Rui Hallgeir , Schwartz Ann G. , Velie Ellen M.
Published: December 2024

AbstractBackground:
The role of adult adiposity in young-onset breast cancer (YOBC) subtype risk is not well understood.
Methods:
In this population-based case (n = 1812)–control (n = 1,381) study of invasive YOBC (ages <50 years), cases were identified from the Los Angeles County and Metropolitan Detroit Surveillance, Epidemiology, and End Results registries, 2010 to 2015. Area-based, frequency-matched controls were sampled from the 2010 Census. General adiposity [body mass index (BMI)] and central adiposity (waist circumference and waist-to-height ratio) across adulthood and covariates were collected from in-person interviews and measurements. ORs and 95% confidence intervals (CI) for adiposity and YOBC tumor subtypes [i.e., luminal A, luminal B, HER2+, and triple negative (TN)] were calculated, overall and by parity, using multivariable weighted logistic regression.
Results:
Obese young adult BMI was inversely associated with luminal A YOBC (OR = 0.35, 95% CI, 0.16–0.79); other subtype associations were nonsignificant. Similarly, adult overweight and obese BMIs were inversely associated with luminal A (OR = 0.66, 95% CI, 0.48–0.91 and OR = 0.59, 95% CI, 0.46–0.87, respectively), but not other subtypes. Conversely, larger waist circumference was associated with higher odds of luminal B and TN YOBC (OR = 1.48, 95% CI, 1.01–2.15 and OR = 2.48, 95% CI, 1.52–3.88, respectively), but not other subtypes (with similar results for weight-to-height ratio); highest odds were among parous women.
Conclusions:
Findings show greater general adult adiposity is associated with reduced odds of luminal A YOBC, whereas greater central adiposity is associated with increased odds of luminal B and TN YOBC, particularly among parous women.
Impact:
Additional studies of central adiposity and YOBC subtype risk, especially incorporating pregnancy history, are warranted.
Data from Population-Based Study of Gastric Cancer Survival and Associations in Rural Western Honduras
Authors: Dominguez Ricardo L. , Montalvan-Sanchez Eleazar E. , Norwood Dalton A. , Rodriguez-Murillo Aida , Dominguez Lucia , Estevez Ordoñez Dagoberto , Beasley Timothy , Bravo Luis E. , Morgan Douglas R.
Published: December 2024

AbstractBackground:
Two-thirds of global cancers occur in low/middle income countries (LMIC). Northern Central America is the largest LMIC region in the Western Hemisphere and lack cancer registries to guide cancer control. We conducted a gastric cancer survival study in rural Western Honduras, characterized as having among the highest gastric cancer incidence rates in Latin America.
Methods:
The cohort of incident gastric cancer diagnosed between 2002 and 2015 was studied with active follow-up with household visits. The regional gastric cancer registry was primary for case identification, with completeness examination with hospital data and national death certificates. Cox regression models were used for survival calculations.
Results:
Survival follow-up was achieved in 741/774 patients (95.7%). Household interviews were conducted in 74.1% (n = 549); 65.7% were male, median age at diagnosis was 64 years, 24.5% were <55 years; 43.9% of tumors had pyloric obstruction; 45.2%, 43.2%, and 7.3% of histology was intestinal, diffuse, and mixed, respectively. A total of 24.7% patients received treatment. The 5-year survival rates were 9.9% for both males and females, 7.7% for age <45, and 7.9% for diffuse gastric cancer. Median survival time was 4.8 months [95% confidence interval (CI), 4.2–5.6]. In the final Cox regression model including age, sex, Lauren subtype, and poverty index, only treatment was significantly associated with survival (hazard ratio = 2.43, 95% CI, 1.8–3.2).
Conclusions:
Markedly low gastric cancer 5-year survival rates are observed in rural Central America. The majority of patients present with advanced disease and a minority have access to therapy.
Impact:
The findings have implications for cancer control in the Central America LMICs and for US Latino populations.

See related commentary by Riquelme and Abnet, p. 1550
Supplementary Data1 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

Final supplementary data.
Supplementary Data1 from Efficacy and Safety of the Anti-IL1RAP Antibody Nadunolimab (CAN04) in Combination with Gemcitabine and Nab-Paclitaxel in Patients with Advanced/Metastatic Pancreatic Cancer
Authors: Van Cutsem Eric , Collignon Joelle , Eefsen Rikke L. , Ochsenreither Sebastian , Zvirbule Zanete , Ivanauskas Audrius , Arnold Dirk , Baltruskeviciene Edita , Pfeiffer Per , Yachnin Jeffrey , Magnusson Susanne , Rydberg Millrud Camilla , Sanfridson Annika , Losic Nedjad , Garcia-Ribas Ignacio , Tersago Dominique , Awada Ahmad
Published: December 2024

Supplementary methods and results
Supplementary Table S2 from Reduced Platelet Activation in Triple-Negative Essential Thrombocythemia Compared with JAK2V617F-Mutated Essential Thrombocythemia
Authors: Dong Huan , Chen Jia , Zhang Jing , Xue Feng , Li Huiyuan , Zhang Donglei , Zhou Hu , Zhang Xian , Huang Yueting , Liu Xiaofan , Chen Yunfei , Liu Wei , Chi Ying , Wang Wentian , Sun Ting , Ju Mankai , Dai Xinyue , Gu Wenjing , Yang Renchi , Fu Rongfeng , Zhang Lei
Published: December 2024

Supplementary Table S2. Targeted 267-gene panel for next-generation sequencing.
Supplementary Figure S2 from Reduced Platelet Activation in Triple-Negative Essential Thrombocythemia Compared with JAK2V617F-Mutated Essential Thrombocythemia
Authors: Dong Huan , Chen Jia , Zhang Jing , Xue Feng , Li Huiyuan , Zhang Donglei , Zhou Hu , Zhang Xian , Huang Yueting , Liu Xiaofan , Chen Yunfei , Liu Wei , Chi Ying , Wang Wentian , Sun Ting , Ju Mankai , Dai Xinyue , Gu Wenjing , Yang Renchi , Fu Rongfeng , Zhang Lei
Published: December 2024

Supplementary Figure S2. Platelet CD62P expression and phosphatidylserine exposure of TN-ET platelets after ROS inhibition.
Supplementary Figure S3 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 Figure 3. Kaplan-Meier estimates of survival by dual TMB and PD-L1 CPS cutoffs for pembrolizumab monotherapy versus chemotherapy. A, PFS. B, OS.
Supplementary Table 2 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

Supplementary Table 2: Oncogenic or Likely Oncogenic DRD genomic alterations found in ctDNA and/or WES
Supplementary Figure 3C 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

Supplementary Figure 3C: KM curve of OS in patients with and without DRD.
Supplementary Figure 3B 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

Supplementary Figure 3B: KM curve of rPFS in patients with and without DRD.
Supplementary Figure 3A 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

Supplementary Figure 3A: KM curve of PSA-PFS in patients with and without DRD.
Supplementary Figure 2B 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

Supplementary Figure 2B: KM curve of rPFS by TMB
Supplementary Table S1 from Synthetic Lethal Targeting of CDK12-Deficient Prostate Cancer with PARP Inhibitors
Authors: Chou Jonathan , Robinson Troy M. , Egusa Emily A. , Lodha Roshan , Zhang Meng , Badura Michelle , Mikayelyan Mane , Delavan Henry M. , Swinderman Jason , Wilson Chris , Zhu Jun , Das Rajdeep , Nguyen Minh , Loehr Andrea , Golsorkhi Tony , Simmons Andrew , Abida Wassim , Chinnaiyan Arul M. , Arkin Michelle R. , Small Eric J. , Quigley David A. , Yang Lixing , Kim Minkyu , Ashworth Alan , Feng Felix Y.
Published: December 2024

Hit list summary from a chemical screen of approximately 1800 bioactive compounds in C42B and CDK12 KO cells at 72h and 168 h timepoints.
Supplementary Data 1 from Synthetic Lethal Targeting of CDK12-Deficient Prostate Cancer with PARP Inhibitors
Authors: Chou Jonathan , Robinson Troy M. , Egusa Emily A. , Lodha Roshan , Zhang Meng , Badura Michelle , Mikayelyan Mane , Delavan Henry M. , Swinderman Jason , Wilson Chris , Zhu Jun , Das Rajdeep , Nguyen Minh , Loehr Andrea , Golsorkhi Tony , Simmons Andrew , Abida Wassim , Chinnaiyan Arul M. , Arkin Michelle R. , Small Eric J. , Quigley David A. , Yang Lixing , Kim Minkyu , Ashworth Alan , Feng Felix Y.
Published: December 2024

Supplemental Figures S1-S7
Supplementary Table S1 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

Supplementary Table S1. Clinical characteristics of AML patients
Supplementary Table S8 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 8. The response rate by MYD88/CXCR4 genotype during first-line cytotoxic therapy.
Supplementary Figure S4 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

Supplementary Figure S4. (A) Heatmap of differentially expressed genes involved in ferroptosis in KG-1α cells after treatments with CS055 (4 μM) and chiglitazar (16 μM). (B) GSEA analysis for lipid metabolism pathway in KG-1α cells after treatments with CS055 (4 μM) and chiglitazar (16 μM). (C) Cell viability was counted in KG-1α and Kasumi-1 cells after treatments with erastin (1.875 μM, 3.75 μM, 7.5 μM, 15 μM, 30 μM) for 24h. (D) Erastin induced the death level of KG-1α and Kasumi-1 cells, and cell death was measured by PI staining and analyzed by flow cytometry. (E) KG-1α and Kasumi-1 cells treated with erastin (3.75 μM, 7.5 μM, 15 μM, 30 μM) for 24h and stained with C11-BODIPY and endogenous lipid peroxidation analysis by flow cytometry. (F-G) The glutamate release (F) and intracellular GSH (G) were detected in KG-1α and Kasumi-1 cells treated with erastin (3.75 μM, 7.5 μM, 15 μM, 30 μM) for 24h. (H) Cell viability was counted in KG-1α and Kasumi-1 cells after treatments with erastin (15 μM), Ferr-1 (2 μM), DFO (10 μM), Z-VAD (10 μM) and Nec-1 (10 μM) for 24 h. *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001.
Supplemental Table 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 Table 3. Consolidated SDHA functional data
Supplemental Table 1 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 Table 1. Interpretations used for variant selection and control classification.
Supplemental Figure 1 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 1. Validation of HAP1 SDHAKO clonal cell line.
Supplementary Figure 2 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 2
Table S4. Differential expression4 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

Results of the differential expression analysis.
Data 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

AbstractPurpose:
Claudin 18.2 (CLDN18.2) is a surface membrane protein that is crucial for maintaining tight junctions in gastric mucosal cells and is highly expressed in gastric, esophageal, and pancreatic cancers. Thus, CLDN18.2 is suited for exploration as a clinical target for chimeric antigen receptor T-cell (CAR-T) therapy in these indications. Although CAR-T therapies show promise, a challenge faced in their development for solid tumors is the immunosuppressive tumor microenvironment, which is often characterized by the presence of immune and stromal cells secreting high levels of TGFβ. The addition of TGFβ armoring can potentially expand CAR-T activity in solid tumors. We report on the preclinical development of a CLDN18.2-targeting CAR-T therapy showing effectiveness in patient models with CLDN18.2-positive gastric, esophageal, and pancreatic tumors.
Experimental Design:
The lead lentivirus product contains a unique single-chain variable fragment; CD28 and CD3z costimulatory and signaling domains; and dominant-negative TGF-β receptor armoring, enhancing targeting and safety and counteracting suppression. We developed a shortened cell manufacturing process to enhance the potency of the final product AZD6422.
Results:
AZD6422 exhibited significant antitumor activity and tolerability in multiple patient-derived tumor xenograft models with various CLDN18.2 and TGF-β levels, as determined by IHC. The efficacy of armored CAR-T cells in tumor models with elevated TGFβ was increased in vitro and in vivo. In vitro restimulation assays established greater persistence and cytolytic function of AZD6422 compared with a traditionally manufactured CAR-T.
Conclusions:
AZD6422 was safe and efficacious in patient-derived, CLDN18.2-positive murine models of gastrointestinal cancers. Our data support further clinical development of AZD6422 for patients with these cancers.
Data from Pilot Trial of Perampanel on Peritumoral Hyperexcitability in Newly Diagnosed High-grade Glioma
Authors: Tobochnik Steven , Regan Michael S. , Dorotan Maria K.C. , Reich Dustine , Lapinskas Emily , Hossain Md Amin , Stopka Sylwia , Meredith David M. , Santagata Sandro , Murphy Melissa M. , Arnaout Omar , Bi Wenya Linda , Chiocca E. Antonio , Golby Alexandra J. , Mooney Michael A. , Smith Timothy R. , Ligon Keith L. , Wen Patrick Y. , Agar Nathalie Y.R. , Lee Jong Woo
Published: December 2024

AbstractPurpose:
Glutamatergic neuron–glioma synaptogenesis and peritumoral hyperexcitability promote glioma growth in a positive feedback loop. The objective of this study was to evaluate the feasibility and estimated effect sizes of the targeted AMPA receptor antagonist perampanel on peritumoral hyperexcitability.
Experimental Design:
An open-label trial was performed comparing perampanel with standard of care (SOC) in patients undergoing resection of newly diagnosed radiologic high-grade glioma. Perampanel was administered as a preoperative loading dose followed by maintenance therapy until progressive disease or up to 12 months. SOC treatment involved levetiracetam for 7 days or as clinically indicated. The primary outcome of hyperexcitability was defined by intraoperative electrocorticography high-frequency oscillation (HFO) rates. Seizure freedom and overall survival were estimated by the Kaplan–Meier method. Tissue concentrations of perampanel, levetiracetam, and correlative biomarkers were measured by mass spectrometry.
Results:
HFO rates were similar between patients treated with perampanel and levetiracetam. The trial was terminated early after a planned interim analysis, and outcomes assessed in 11 patients (seven perampanel treated; four treated with SOC). Over a median 281 days of postenrollment follow-up, 27% of patients had seizures, including 14% maintained on perampanel and 50% treated with SOC. Overall survival in perampanel-treated patients was similar to that in a glioblastoma reference cohort. Glutamate concentrations in surface biopsies were positively correlated with HFO rates in adjacent electrode contacts and were not significantly associated with treatment assignment or drug concentrations.
Conclusions:
Glioma peritumoral glutamate concentrations correlated with high-gamma oscillation rates. Targeting glutamatergic activity with perampanel achieved similar electrocorticographic hyperexcitability levels as in levetiracetam-treated patients.
Data 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

AbstractPurpose:
The three-arm, phase III KEYNOTE-361 study did not meet its dual primary endpoints of progression-free survival (PFS) or overall survival (OS) with first-line pembrolizumab plus chemotherapy versus chemotherapy in advanced urothelial carcinoma. This prespecified exploratory analysis assessed the association of tumor mutational burden (TMB) and PD-L1 combined positive score (CPS) with clinical outcomes.
Patients and Methods:
TMB and PD-L1 CPS were determined via whole-exome sequencing and PD-L1 IHC 22C3 pharmDx, respectively. The association was evaluated in each treatment arm using logistic regression [objective response rate (ORR)] and Cox proportional hazards regression models (PFS and OS); one-sided (pembrolizumab monotherapy; pembrolizumab plus chemotherapy) and two-sided (chemotherapy) nominal P values were calculated. Significance was prespecified at α = 0.05 without multiplicity adjustment. Efficacy was evaluated by prespecified cutoffs of 175 mutations/exome (TMB) and CPS 10 (PD-L1).
Results:
Of the 993 treated patients, 820 (82.6%) and 993 (100%) had evaluable TMB and CPS data, respectively. Continuous TMB was positively associated with ORR, PFS, and OS for pembrolizumab monotherapy (one-sided P < 0.001, P < 0.001, and P = 0.007, respectively); PFS and OS for pembrolizumab plus chemotherapy (one-sided P = 0.007 and P = 0.010, respectively); and OS for chemotherapy alone (two-sided P = 0.040). Continuous PD-L1 CPS showed evidence of anticipated association with ORR and PFS for pembrolizumab monotherapy. The subgroup with TMB ≥175 mutations/exome and PD-L1 CPS ≥10 had the highest PFS and OS improvements with pembrolizumab alone or with chemotherapy versus chemotherapy alone.
Conclusions:
These data suggest that TMB may be predictive of the response to pembrolizumab alone or with chemotherapy in advanced urothelial carcinoma.
Data from Phase 2 Trial of Regorafenib in Recurrent/Metastatic Adenoid Cystic Carcinoma
Authors: Desilets Antoine , Vos Joris L. , Katabi Nora , Kuo Fengshen , Nadeem Zaineb , Linxweiler Maximilian , Ostrovnaya Irina , Baxi Shrujal , Dunn Lara A. , Sherman Eric J. , Pfister David G. , Morris Luc G.T. , Ho Alan L.
Published: December 2024

AbstractPurpose:
There is a significant need for effective therapies to treat recurrent/metastatic (R/M) adenoid cystic carcinoma (ACC). This study evaluated the multitargeted VEGFR tyrosine kinase inhibitor (TKI) regorafenib in patients with R/M ACC.
Patients and Methods:
Patients with progressive R/M ACC were treated with regorafenib until disease progression, consent withdrawal, or excessive toxicity. The co-primary endpoints were best overall response and 6-month progression-free survival (PFS). Genomic and transcriptomic biomarker analyses were performed in tumors from trial participants.
Results:
Thirty-eight patients were enrolled, including 7 (18%) patients with prior VEGFR TKIs. No objective responses were observed. The 6-month PFS was 45%, and the median PFS was 7.2 months (95% confidence interval, 5.2–11.9 months). The presence of either activating NOTCH1 (22%) or KDM6A alterations (24%) was associated with decreased PFS [HR 2.6; 95% confidence interval (CI), 1.1–6.1; P = 0.03]. Bulk RNA sequencing of pretreatment tumors revealed that regorafenib clinical benefit (CB; PFS ≥ 6 months; n = 11) was associated with the native enrichment of immune-related signatures. Immune deconvolution revealed a greater degree of macrophage and T-cell infiltration in CB tumors. Tumors from patients with no clinical benefit (NCB; PFS < 6 months; n = 9) had greater expression of signatures related to cell-cycle progression (E2F targets, G2–M checkpoint).
Conclusions:
The trial failed to meet the prespecified 6-month PFS and best overall response targets. We hypothesize that TKI efficacy may be reliant upon an interplay between kinase inhibition and the ACC immune microenvironment, whereas programs promoting cell-cycle progression may contribute to TKI resistance. These observations suggest that trials evaluating CDK4/6 inhibition plus a VEGFR TKI should be considered.
Data 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

AbstractPurpose:
SDHA mutations are the most common cause of succinate dehydrogenase (SDH)–deficient GIST. Enhanced cancer surveillance of individuals carrying a known pathogenic germline SDHA mutation has the potential to detect early-stage tumors, allowing for improved patient outcomes. However, more than 95% of the >1,000 SDHA missense variants listed in ClinVar are variants of uncertain significance. Our ability to interpret the significance of SDHA variants must improve before genetic sequencing can be utilized to its full potential.
Experimental Design:
SDHA variants were introduced into a clonal SDHA-knockout cell line via Bxb1-mediated recombination. SDH activity and SDHA abundance were determined for each variant, and logistic regression analysis was used to derive functional evidence for clinical variant interpretation.
Results:
Our analysis revealed that cancer-associated SDHA missense variants can be clearly distinguished from noncancer variants according to the extent of SDH dysfunction caused. As such, SDH activity data can be used to predict cancer pathogenicity with strong performance metrics, exceeding those of computational prediction tools. From these data, we obtained functional evidence for clinical variant interpretation from 21 of 22 assayed variants of uncertain significance, with 19 in favor of cancer pathogenicity and two against pathogenicity. Lastly, simulating the addition of our functional evidence with limited preexisting evidence allowed for 18 of 22 variants to be reclassified.
Conclusions:
We describe a novel pipeline for investigating the functional consequences of SDHA missense variants. In total, we characterized 72 variants, developed criteria for obtaining functional evidence, and demonstrated the potential of this evidence for clinical variant interpretation.
Supplementary Table 3 from Increased RNA and Protein Degradation Is Required for Counteracting Transcriptional Burden and Proteotoxic Stress in Human Aneuploid Cells
Authors: Ippolito Marica Rosaria , Zerbib Johanna , Eliezer Yonatan , Reuveni Eli , Viganò Sonia , De Feudis Giuseppina , Shulman Eldad D. , Savir Kadmon Anouk , Slutsky Rachel , Chang Tiangen , Campagnolo Emma M. , Taglietti Silvia , Scorzoni Simone , Gianotti Sara , Martin Sara , Muenzner Julia , Mülleder Michael , Rozenblum Nir , Rubolino Carmela , Ben-Yishay Tal , Laue Kathrin , Cohen-Sharir Yael , Vigorito Ilaria , Nicassio Francesco , Ruppin Eytan , Ralser Markus , Vazquez Francisca , Santaguida Stefano , Ben-David Uri
Published: December 2024

Pre-ranked gene set enrichment analysis of differential mRNA expression between all aneuploid clones (SS6, SS119, SS51, SS111) and the pseudo-diploid clone (SS48)
Supplementary Figures 1-8 from Increased RNA and Protein Degradation Is Required for Counteracting Transcriptional Burden and Proteotoxic Stress in Human Aneuploid Cells
Authors: Ippolito Marica Rosaria , Zerbib Johanna , Eliezer Yonatan , Reuveni Eli , Viganò Sonia , De Feudis Giuseppina , Shulman Eldad D. , Savir Kadmon Anouk , Slutsky Rachel , Chang Tiangen , Campagnolo Emma M. , Taglietti Silvia , Scorzoni Simone , Gianotti Sara , Martin Sara , Muenzner Julia , Mülleder Michael , Rozenblum Nir , Rubolino Carmela , Ben-Yishay Tal , Laue Kathrin , Cohen-Sharir Yael , Vigorito Ilaria , Nicassio Francesco , Ruppin Eytan , Ralser Markus , Vazquez Francisca , Santaguida Stefano , Ben-David Uri
Published: December 2024

Supplementary Figure 1: Dosage compensation in trisomic cells occurs at both mRNA and protein levels (related to Fig. 1). Supplementary Figure 2: RNA degradation does not confound the results of the differential gene expression analyses (related to Fig. 2). Supplementary Figure 3: Aneuploid clones activate the nonsense-mediated decay (NMD) pathway, and depend on it for downregulating their gene expression (related to Fig. 3). Supplementary Figure 4: Increased dependency on the nonsense-mediated decay pathway is a general feature of aneuploid cells (related to Fig. 3). Supplementary Figure 5: Trisomic clones activate the miRNA-mediated RNA degradation pathway, and depend on it for downregulating their gene expression (related to Fig. 4). Supplementary Figure 6: Aneuploid cells depend on miRNA machinery cofactors PRKRA and TARBP2 (related to Fig. 4). Supplementary Figure 7: Multiple models of aneuploid cells experience proteotoxic stress and attenuate protein translation (related to Fig. 5). Supplementary Figure 8: Multiple models of aneuploid cells activate the proteasome, and depend on its activity for downregulating their protein expression (related to Fig. 6).
Supplementary Table S8 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 best overall response of each patient reported in the manuscript. It offers insights into clinical responses to botensilimab alone and in combination with balstilimab across various advanced solid tumor types. Importantly, it includes data on patients who progressed on prior conventional immune checkpoint therapy or have tumor types historically non-responsive to immunotherapy. By providing a patient-level view of treatment efficacy, this dataset allows for a nuanced understanding of how different tumor types and individual patients respond to botensilimab.
Supplementary Table S4 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 toxicology findings from a 13-week repeat-dose study of botensilimab in cynomolgus monkeys. This comprehensive toxicology profile is crucial for assessing the safety of botensilimab, and is particularly relevant for predicting potential human toxicity.
Supplementary Table S2 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 contains the binding affinity measurements of the botensilimab and the corresponding parental IgG1 anti-CTLA-4 antibody to human Fc gamma receptors as determined by surface plasmon resonance. It also includes calculated activating to inhibitory (A/I) ratios for each antibody.
Supplementary Figure 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 presents results showing the effect of botensilimab on CD4+ non-regulatory T cells (non-Tregs) in stimulated human peripheral blood mononuclear cell (PBMC) cultures. It demonstrates that unlike conventional anti-CTLA-4, botensilimab treatment does not lead to a decrease in CD4+ non-Treg populations in stimulated human PBMC cultures. This information is crucial for understanding botensilimab's unique mechanism of action and its potential advantages over conventional IgG1 anti-CTLA-4 antibodies. Importantly, these results further support the hypothesis that under context of antigen-stimulation, botensilimab decreases the generation of Tregs rather than promoting depletion via antibody-dependent cellular cytotoxicity. This mechanism distinguishes botensilimab from conventional anti-CTLA-4 antibodies and may account for its superior T cell responsiveness and activation.
Figure S7 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 6 but which were not included in the main figure
Supplementary Figure S8 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 a comprehensive analysis of the Fcγ receptor binding kinetics and Fc-mediated functions of botensilimab compared to other approved anti-CTLA-4 antibodies. These results highlight the unique Fc-mediated properties of botensilimab, particularly its enhanced engagement of activating Fcγ receptors without inducing complement-dependent cytotoxicity. This data further provides mechanistic insights into botensilimab's potential for enhanced immune modulation and anti-tumor efficacy.