bluuebunny/crossref_metadata_2025 huggingface dataset:
Supplementary Figure S1 from Molecular Subtypes of High-Grade Serous Ovarian Cancer across Racial Groups and Gene Expression Platforms
Authors: Davidson Natalie R. , Barnard Mollie E. , Hippen Ariel A. , Campbell Amy , Johnson Courtney E. , Way Gregory P. , Dalley Brian K. , Berchuck Andrew , Salas Lucas A. , Peres Lauren C. , Marks Jeffrey R. , Schildkraut Joellen M. , Greene Casey S. , Doherty Jennifer A.
Published: August 2024

Case selection for self-identified Black study participants
Supplementary Table 4. from Joint Associations of Diet and Device-Measured Physical Activity with Mortality and Incident CVD and Cancer: A Prospective Analysis of the UK Biobank Study
Authors: Inan-Eroglu Elif , Ahmadi Matthew , Biswas Raaj Kishore , Ding Ding , Rezende Leandro F.M. , Lee I-Min , Giovannucci Edward L. , Stamatakis Emmanuel
Published: August 2024

Supplementary Table 4 shows the independent association between physical activity and dietary measures with all-cause mortality, cardiovascular disease, total cancer, and physical activity, diet, and adiposity-related cancer incidence.
Supplementary Figure 9 from Joint Associations of Diet and Device-Measured Physical Activity with Mortality and Incident CVD and Cancer: A Prospective Analysis of the UK Biobank Study
Authors: Inan-Eroglu Elif , Ahmadi Matthew , Biswas Raaj Kishore , Ding Ding , Rezende Leandro F.M. , Lee I-Min , Giovannucci Edward L. , Stamatakis Emmanuel
Published: August 2024

Joint dose-response association between physical activity volume (minutes/day), diet quality score with cardiovascular disease incidence.Supplementary Figure 9 shows the joint dose-response association between physical activity volume (minutes/day) and diet quality score with respect to cardiovascular disease incidence.
Supplemental Table S1 from Rural–Urban Cancer Incidence and Trends in the United States, 2000 to 2019
Authors: Semprini Jason , Gadag Khyathi , Williams Gawain , Muldrow Aniyah , Zahnd Whitney E.
Published: August 2024

Supplemental Table S1: Risk Associated and Primary Cancer Site Cancer Definitions
Supplementary Figure 2. from Joint Associations of Diet and Device-Measured Physical Activity with Mortality and Incident CVD and Cancer: A Prospective Analysis of the UK Biobank Study
Authors: Inan-Eroglu Elif , Ahmadi Matthew , Biswas Raaj Kishore , Ding Ding , Rezende Leandro F.M. , Lee I-Min , Giovannucci Edward L. , Stamatakis Emmanuel
Published: August 2024

Kaplan-Meier curves for all-cause mortality and cardiovascular disease, total cancer and physical activity, diet and adiposity related cancer incidence survival.Supplementary Figure 2 shows Kaplan-Meier curves illustrating the survival rates for all-cause mortality, cardiovascular disease, total cancer, and the incidence of adiposity-related cancer survival in relation to physical activity and diet.
Data from Understanding Benign Breast Disease and Subsequent Breast Cancer in Hispanic White Females: A Step Closer to Evidence-Based Management
Authors: Lohani Kush R. , Nibbe Andrea M. , Vierkant Robert A. , Pacheco-Spann Laura M. , Seymour Lisa R. , Vachon Celine M. , Sherman Mark E. , Winham Stacey J. , Degnim Amy C. , Hill Deirdre A.
Published: August 2024

AbstractIntroduction:
Although Hispanic White (HW) females have a lower incidence of breast cancer than non-Hispanic White (NHW) females, breast cancer risk is unclear for HW females after benign breast disease (BBD).
Methods:
We compared BBD characteristics and subsequent breast cancer risk among HW and NHW females in New Mexico using a population-based collection of benign breast biopsies (1996–2007). BBD was categorized as nonproliferative disease (NPD), proliferative disease without atypia (PDWA), or atypical hyperplasia (AH). Breast cancer risk was assessed as absolute risk (AR) using cumulative incidence and RR by comparing the number of breast cancer events in BBDs to non-BBD.
Results:
This study included 3,684 HW and 6,587 NHW females with BBD. HW females had similar proportions of NPD (58.6% vs. 54.3%), PDWA (21.4% vs. 23.5%), and AH (3.6% vs. 3.3%) as NHW females. Breast cancer risk among all females with BBD was higher than population-based expected rates (RR, 1.87) and was similar for HW and NHW subgroups (RR = 1.99 vs. 1.84). As expected, breast cancer risk increased with increasing BBD severity, both overall [RR, 1.81 (NPD), 1.85 (PDWA), and 3.10 (AH)] and in the HW and NHW subgroups. Adjusted AR of breast cancer at 5 years also increased with the severity of BBD (HW vs. NHW; NPD: 1.4% vs. 2.1%; PDWA: 1.5% vs. 2.7%; AH: 6% vs. 4.8%).
Conclusions:
We found similar breast cancer RRs and ARs in HW and NHW. Risk counseling should ensure that HW females receive breast cancer clinical management warranted by their similar absolute risks.
Impact:
The present population-based provides evidence for the clinical management of HW females with BBD for the prevention of breast cancer.
Data from Disparities and Determinants of Testing for Early Detection of Cervical Cancer among Nepalese Women: Evidence from a Population-Based Survey
Authors: Rahman Md. Shafiur , Rahman Md. Mahfuzur , Acharya Kiran , Haruyama Rei , Shah Richa , Matsuda Tomohiro , Inoue Manami , Abe Sarah K.
Published: August 2024

AbstractBackground:
Cervical cancer presents a considerable challenge in South Asia, notably in Nepal, where screening remains limited. Past research in Nepal lacked national representation and a thorough exploration of factors influencing cervical cancer screening, such as educational and socioeconomic disparities. This study aims to measure these gaps and identify associated factors in testing for early detection of cervical cancer among Nepalese women.
Methods:
Data from the 2019 Nepal Noncommunicable Disease Risk Factors survey (World Health Organization STEPwise approach to noncommunicable risk factor surveillance), involving 2,332 women aged 30 to 69 years, were used. Respondents were asked if they had undergone cervical cancer testing through visual inspection with acetic acid, Pap smear, or human papillomavirus test ever or in the past 5 years. The slope index of inequality (SII) and relative concentration index were used to measure socioeconomic and education-based disparities in cervical cancer test uptake.
Results:
Only 7.1% [95% confidence interval (CI): 5.1–9.9] Nepalese women had ever undergone cervical cancer testing, whereas 5.1% (95% CI: 3.4–7.5) tested within the last 5 years. The ever uptake of cervical cancer testing was 5.1 percentage points higher (SII: 5.1, 95% CI: −0.1 to 10.2) among women from the richest compared with the poorest households. Education-based disparities were particularly pronounced, with a 13.9 percentage point difference between highly educated urban residents and their uneducated counterparts (SII: 13.9, 95% CI: 5.8–21.9).
Conclusions:
Less than one in ten women in Nepal had a cervical cancer testing, primarily favoring higher educated and wealthier individuals.
Impact:
Targeted early detection and cervical cancer screening interventions are necessary to address these disparities and improve access and uptake.
Supplementary Table S1 from A Proof-of-Concept Study of Sequential Treatment with the HDAC Inhibitor Vorinostat following BRAF and MEK Inhibitors in BRAFV600-Mutated Melanoma
Authors: Embaby Alaa , Huijberts Sanne C.F.A. , Wang Liqin , Leite de Oliveira Rodrigo , Rosing Hilde , Nuijen Bastiaan , Sanders Joyce , Hofland Ingrid , van Steenis Charlaine , Kluin Roelof J.C. , Lieftink Cor , Smith Christopher G. , Blank Christian U. , van Thienen Johannes V. , Haanen John B.A.G. , Steeghs Neeltje , Opdam Frans L. , Beijnen Jos H. , Huitema Alwin D.R. , Bernards Rene , Schellens Jan H.M. , Wilgenhof Sofie
Published: August 2024

Supplementary Table S1. Representativeness of study participants.
Supplementary Table S7 from Plasma Proteomic Signature Predicts Myeloid Neoplasm Risk
Authors: Tran Duc , Beeler J. Scott , Liu Jie , Wiley Brian , Chan Irenaeus C.C. , Xin Zilan , Kramer Michael H. , Batchi-Bouyou Armel L. , Zong Xiaoyu , Walter Matthew J. , Petrone Giulia E.M. , Chlamydas Sarantis , Ferraro Francesca , Oh Stephen T. , Link Daniel C. , Busby Ben , Cao Yin , Bolton Kelly L.
Published: August 2024

Association between plasma protein levels and individual clonal hematopoiesis (CH) genes with frequency greater than 20 (N=13 genes).
Supplementary Figure S2 from Ultrasound-Guided Quantitative Fluorescence Molecular Endoscopy for Monitoring Response in Patients with Esophageal Cancer Following Neoadjuvant Chemoradiotherapy
Authors: Schmidt Iris , Zhao Xiaojuan , van der Waaij Anne M. , Meersma Gert Jan , Dijkstra Frederieke A. , Haveman Jan Willem , van Etten Boudewijn , Robinson Dominic J. , Kats-Ugurlu Gursah , Nagengast Wouter B.
Published: August 2024

Distribution of semi-quantitative VEGF expression
Supplementary Table 4 from Mapping the Single-Cell Differentiation Landscape of Osteosarcoma
Authors: Truong Danh D. , Weistuch Corey , Murgas Kevin A. , Admane Prasad , King Bridgette L. , Chauviere Lee Jes , Lamhamedi-Cherradi Salah-E. , Swaminathan Jyothishmathi , Daw Najat C. , Gordon Nancy , Gopalakrishnan Vidya , Gorlick Richard G. , Somaiah Neeta , Deasy Joseph O. , Mikos Antonios G. , Tannenbaum Allen , Ludwig Joseph
Published: August 2024

Gene Correlates
Supplementary Figure 5 from Mapping the Single-Cell Differentiation Landscape of Osteosarcoma
Authors: Truong Danh D. , Weistuch Corey , Murgas Kevin A. , Admane Prasad , King Bridgette L. , Chauviere Lee Jes , Lamhamedi-Cherradi Salah-E. , Swaminathan Jyothishmathi , Daw Najat C. , Gordon Nancy , Gopalakrishnan Vidya , Gorlick Richard G. , Somaiah Neeta , Deasy Joseph O. , Mikos Antonios G. , Tannenbaum Allen , Ludwig Joseph
Published: August 2024

Selection of rank for nNMF
Supplementary Figure 2 from Mapping the Single-Cell Differentiation Landscape of Osteosarcoma
Authors: Truong Danh D. , Weistuch Corey , Murgas Kevin A. , Admane Prasad , King Bridgette L. , Chauviere Lee Jes , Lamhamedi-Cherradi Salah-E. , Swaminathan Jyothishmathi , Daw Najat C. , Gordon Nancy , Gopalakrishnan Vidya , Gorlick Richard G. , Somaiah Neeta , Deasy Joseph O. , Mikos Antonios G. , Tannenbaum Allen , Ludwig Joseph
Published: August 2024

Expression of YAP/TAZ in the MTL
Supplemental Table 3 from Anastrozole Dose Escalation for Optimal Estrogen Suppression in Postmenopausal Early-Stage Breast Cancer: A Prospective Trial
Authors: Haddad Tufia C. , Suman Vera J. , Giridhar Karthik V. , Sideras Kostandinos , Northfelt Donald W. , Ernst Brenda J. , O’Sullivan Ciara C. , Singh Ravinder J. , Desta Zeruesenay , Peethambaram Prema P. , Hobday Timothy J. , Chumsri Saranya , Leon-Ferre Roberto A. , Ruddy Kathryn J. , Yadav Siddhartha , Taraba Jodi L. , Goodnature Barbara , Goetz Matthew P. , Wang Liewei , Ingle James N.
Published: August 2024

Supplemental Table 3: Representativeness of Study Participants.
Supplementary Table S4 from Bystander Effects, Pharmacokinetics, and Linker-Payload Stability of EGFR-Targeting Antibody-Drug Conjugates Losatuxizumab Vedotin and Depatux-M in Glioblastoma Models
Authors: Jain Sonia , Griffith Jessica I. , Porath Kendra A. , Rathi Sneha , Le Jiayan , Pasa Tugce I. , Decker Paul A. , Gupta Shiv K. , Hu Zeng , Carlson Brett L. , Bakken Katrina , Burgenske Danielle M. , Feldsien Thomas M. , Lefebvre Didier R. , Vaubel Rachael A. , Eckel-Passow Jeanette E. , Reilly Edward B. , Elmquist William F. , Sarkaria Jann N.
Published: August 2024

In vivo efficacy
Supplementary Table S2 from Bystander Effects, Pharmacokinetics, and Linker-Payload Stability of EGFR-Targeting Antibody-Drug Conjugates Losatuxizumab Vedotin and Depatux-M in Glioblastoma Models
Authors: Jain Sonia , Griffith Jessica I. , Porath Kendra A. , Rathi Sneha , Le Jiayan , Pasa Tugce I. , Decker Paul A. , Gupta Shiv K. , Hu Zeng , Carlson Brett L. , Bakken Katrina , Burgenske Danielle M. , Feldsien Thomas M. , Lefebvre Didier R. , Vaubel Rachael A. , Eckel-Passow Jeanette E. , Reilly Edward B. , Elmquist William F. , Sarkaria Jann N.
Published: August 2024

In vivo treatment doses
Supplementary Table S4 from A 5-Hydroxymethylcytosine-Based Noninvasive Model for Early Detection of Colorectal Carcinomas and Advanced Adenomas: The METHOD-2 Study
Authors: Chang Wenju , Zhang Zhou , Jia Baoqing , Ding Kefeng , Pan Zhizhong , Su Guoqiang , Zhang Wei , Liu Tianyu , Zhong Yunshi , He Guodong , Ren Li , Wei Ye , Li Dongdong , Cui Xiaolong , Yang Jun , Shi Yixiang , Bissonnette Marc , He Chuan , Zhang Wei , Fan Jia , Xu Jianmin
Published: August 2024

Differetially modified gene bodies between CRC/AA and controls.
Supplementary Table S3 from A 5-Hydroxymethylcytosine-Based Noninvasive Model for Early Detection of Colorectal Carcinomas and Advanced Adenomas: The METHOD-2 Study
Authors: Chang Wenju , Zhang Zhou , Jia Baoqing , Ding Kefeng , Pan Zhizhong , Su Guoqiang , Zhang Wei , Liu Tianyu , Zhong Yunshi , He Guodong , Ren Li , Wei Ye , Li Dongdong , Cui Xiaolong , Yang Jun , Shi Yixiang , Bissonnette Marc , He Chuan , Zhang Wei , Fan Jia , Xu Jianmin
Published: August 2024

Participant characteristics of 80 patients with other cancers.
Supplementary Figure S9 from A 5-Hydroxymethylcytosine-Based Noninvasive Model for Early Detection of Colorectal Carcinomas and Advanced Adenomas: The METHOD-2 Study
Authors: Chang Wenju , Zhang Zhou , Jia Baoqing , Ding Kefeng , Pan Zhizhong , Su Guoqiang , Zhang Wei , Liu Tianyu , Zhong Yunshi , He Guodong , Ren Li , Wei Ye , Li Dongdong , Cui Xiaolong , Yang Jun , Shi Yixiang , Bissonnette Marc , He Chuan , Zhang Wei , Fan Jia , Xu Jianmin
Published: August 2024

The 5hmC diagnostic model for CRC/AA detects patients with stage IV CRC in the validation sets.
Supplementary Figure S4 from A 5-Hydroxymethylcytosine-Based Noninvasive Model for Early Detection of Colorectal Carcinomas and Advanced Adenomas: The METHOD-2 Study
Authors: Chang Wenju , Zhang Zhou , Jia Baoqing , Ding Kefeng , Pan Zhizhong , Su Guoqiang , Zhang Wei , Liu Tianyu , Zhong Yunshi , He Guodong , Ren Li , Wei Ye , Li Dongdong , Cui Xiaolong , Yang Jun , Shi Yixiang , Bissonnette Marc , He Chuan , Zhang Wei , Fan Jia , Xu Jianmin
Published: August 2024

Performance of single marker genes for distinguishing CRC/AA from controls.
Figure 6 from Anti-EGFR Antibody–Drug Conjugate Carrying an Inhibitor Targeting CDK Restricts Triple-Negative Breast Cancer Growth
Authors: Cheung Anthony , Chenoweth Alicia M. , Johansson Annelie , Laddach Roman , Guppy Naomi , Trendell Jennifer , Esapa Benjamina , Mavousian Antranik , Navarro-Llinas Blanca , Haider Syed , Romero-Clavijo Pablo , Hoffmann Ricarda M. , Andriollo Paolo , Rahman Khondaker M. , Jackson Paul , Tsoka Sophia , Irshad Sheeba , Roxanis Ioannis , Grigoriadis Anita , Thurston David E. , Lord Christopher J. , Tutt Andrew N. J. , Karagiannis Sophia N.
Published: August 2024

ADC growth inhibition of orthotopic TNBC xenografts in vivo.A, Staining for EGFR was confirmed using FFPE blocks of cell line xenografts of known EGFR expression pattern (see Fig. 3A; EGFR-high/positive: MDA-MB-468, HCC1143, MDA-MB-231, SUM149; EGFR-low: CAL51, MCF7), compared with human normal breast glandular epithelium and normal tonsil. Scale bar, 100 μm. B, Effects of ADC treatment on tumor growth in vivo. (i) Orthotopic tumor growth of MDA-MB-468 and CAL51 xenografts (n = 4) treated with vehicle, SNS-032 (5 mg/kg), cetuximab, isotype ADC, or ADC (7.5 mg/kg, weekly injection for 4 weeks). P values determined by one-way ANOVA. (ii) Body weight measurement. C, IHC evaluation of EGFR in a TMA of 38 PDX samples established from 35 patients (28 TNBC, five ER+, and two HER2+; disease characteristics: Supplementary Table S2). Representative images showing various staining intensities across samples (scale bar, 100 μm). Pathologists scored the TMA spots for EGFR positivity: score 0, no membrane staining; score 1, weak incomplete membrane staining in >10% cells; score 2, moderate complete membrane staining in >10% cells or strong complete membrane staining in ≤10% cells; score 3, strong (intense and uniform) complete membrane staining in >10% cells. D, Pie chart showing out of 38 PDX samples: 47.4% (n = 18, gray) were negative for membrane EGFR expression; 39.5% (n = 15, yellow) were score 1; 10.5% (n = 4, orange) were score 2; 2.6% (n = 1, red) is highly positive (score 3). E, Microarray-based EGFR mRNA expression was compared with membrane EGFR staining positivity tested by IHC. P value determined by two-tailed unpaired t test. F, Effects of ADC treatment on KCL004 PDX tumor growth in vivo. Left, representative tumor images after two doses of isotype ADC or ADC, where no visible residual tumor was found in any mice treated with ADC during the experimental timeframe. (i) KCL004 PDX orthotopic tumor growth (n = 5) with isotype-ADC or ADC treatment (two doses, 10 mg/kg). (ii) Body weight measurements. P values determined by one-way ANOVA.
Figure 5 from Anti-EGFR Antibody–Drug Conjugate Carrying an Inhibitor Targeting CDK Restricts Triple-Negative Breast Cancer Growth
Authors: Cheung Anthony , Chenoweth Alicia M. , Johansson Annelie , Laddach Roman , Guppy Naomi , Trendell Jennifer , Esapa Benjamina , Mavousian Antranik , Navarro-Llinas Blanca , Haider Syed , Romero-Clavijo Pablo , Hoffmann Ricarda M. , Andriollo Paolo , Rahman Khondaker M. , Jackson Paul , Tsoka Sophia , Irshad Sheeba , Roxanis Ioannis , Grigoriadis Anita , Thurston David E. , Lord Christopher J. , Tutt Andrew N. J. , Karagiannis Sophia N.
Published: August 2024

Anti-EGFR ADC reduces breast cancer cell activities and demonstrated bystander killing effects. A, MTT viability assay following 96-hour treatment with SNS-032, cetuximab, isotype ADC or ADC. Top, EGFR-high breast cancer models. Bottom, EGFR-low breast cancer and immune cell models. B, Cell viability assessment of MDA-MB-468 showed that the addition of SNS-032 did not re-sensitize cells to EGFR inhibition by cetuximab alone, whereas reduced cancer cell viability was detected only when SNS-032 was conjugated to cetuximab as an ADC, suggesting that inhibition of cancer cell viability was induced by ADC internalization and subsequent drug release within cancer cells. SNS-032 efficacy improved by conjugating in the ADC instead of treating it as a free drug. C, Reduction of surface EGFR expression using siRNA, and cell viability comparisons between parental and knockdown cells after 96 hours of ADC treatment (10 nmol/L). D, Time-lapse measurement of cell confluency for cells treated with isotype control (10 nmol/L), cetuximab, and ADC (1 or 10 nmol/L) using Incucyte live-cell microscopy (representative phase images of EGFR-high MDA-MB-468). Scale bar, 0.2 mm. E, TNBC spheroids in Matrigel were treated with 10 nmol/L cetuximab, ADC, or isotype controls, and confluence measured for 7 days using Incucyte. ADC-treated MDA-MB-231 and MDA-MB-468 showed reduced spheroid growth, whereas the ADC showed less potent effects on CAL51. Scale bar, 0.5 mm. F, MDA-MB-468 were transduced with a lentiviral expression vector encoding a mCherry fluorescent protein tag (mChery-MDA-MB-468). Bystander killing effects of the ADC were accessed in co-cultures of high and low EGFR-expressing cells in a one-to-one ratio. High EGFR-expressing mCherry-MDA-MB-468 and either low EGFR-expressing MCF7 or CAL51 cells were plated alone as mono-culture or co-culture, and treated with 1 nmol/L ADC or unconjugated-isotype control antibody. Cell count was measured by Incucyte after washing at 120 hours. Scale bar, 0.5 mm. P values determined by two-tailed unpaired t test of three independent experiments.
Figure 4 from Anti-EGFR Antibody–Drug Conjugate Carrying an Inhibitor Targeting CDK Restricts Triple-Negative Breast Cancer Growth
Authors: Cheung Anthony , Chenoweth Alicia M. , Johansson Annelie , Laddach Roman , Guppy Naomi , Trendell Jennifer , Esapa Benjamina , Mavousian Antranik , Navarro-Llinas Blanca , Haider Syed , Romero-Clavijo Pablo , Hoffmann Ricarda M. , Andriollo Paolo , Rahman Khondaker M. , Jackson Paul , Tsoka Sophia , Irshad Sheeba , Roxanis Ioannis , Grigoriadis Anita , Thurston David E. , Lord Christopher J. , Tutt Andrew N. J. , Karagiannis Sophia N.
Published: August 2024

Spatiotemporal analysis of ADC internalization in lysosomal clusters and inhibition of cell cycle progression. A, Images represent monitoring treatment of MDA-MB-468 with 10 nmol/L Alexa-Fluor-647-labeled ADC (magenta) for 0, 3, and 24 hours and the colocalization with lysosomes. Following incubation, live cells were stained with low pH lysosome dye (orange) followed by Hoechst 3,342 (blue). Scale bar, 5 μm. Very little cell surface binding and uptake of ADC were shown by EGFR-low CAL51 cells at any time point (Supplementary Fig. S4B). Image J colocalization analysis demonstrated moderate colocalization with low pH lysosomes after 3 hours in MDA-MB-468 (cetuximab vs. lysosome, Pearson’s correlation r = 0.342, n = 45 cells; ADC vs. lysosome, r = 0.281, n = 34 cells), whereas correlation was strong at 24 hours (cetuximab vs. lysosome, r = 0.630, n = 64 cells; ADC vs. lysosome, r = 0.600, n = 28 cells). Right, white box: zoom-in images showing individual channels of a representative area of colocalization between ADC and lysosomal staining. B, 3D reconstruction image of a live MDA-MB-468 cell. The Z-stack images showed spatial information of ADC colocalization within lysosome clusters at 24 hours. Top, merged Z-stack 3D image; bottom, 2D images of individual channels. Scale bar, 10 μm. 3D reconstruction of the Z-stack images demonstrating internalized ADC-lysosome clusters can be found in Supplementary Video S1. C, Confocal images showing a high level of colocalization of internalized ADC in lysosome clusters within the ER in close proximity to the nucleus. Scale bar, 5 μm. D, Quantitative analyses on the distribution of cell cycle phases by flow cytometry after 72 hours of cetuximab-ADC treatment, compared with SNS-032, isotype-ADC, and unconjugated-cetuximab controls. Significant cell cycle inhibition (G1 arrest) was observed with SNS-032 (at 10, 100, 1,000 nmol/L) in both TNBC models, whereas only high EGFR-expressing MDA-MB-468 demonstrated significant inhibition by the ADC (10 nmol/L), but not in EGFR-low CAL51. P values determined via the χ2 test against untreated control in three independent experiments.
Supplementary Table S2 from Chimeric Antigen Receptor T Cell with an Inducible Caspase-9 Suicide Gene Eradicates Uveal Melanoma Liver Metastases via B7-H3 Targeting
Authors: Ventin Marco , Cattaneo Giulia , Arya Shahrzad , Jia Jingyu , Gelmi Maria C. , Sun Yi , Maggs Luke , Ksander Bruce R. , Verdijk Robert M. , Boland Genevieve M. , Jenkins Russell W. , Haq Rizwan , Jager Martine J. , Wang Xinhui , Ryeom Sandra , Ferrone Cristina R.
Published: August 2024

Supplementary Table S2. Score of B7-H3 expression and clinical information of metastatic UM tissue samples.
SupplemetaryFigure1-5 from Sequential Analysis of cfDNA Reveals Clonal Evolution in Patients with Neuroblastoma Receiving ALK-Targeted Therapy
Authors: Bobin Charles , Iddir Yasmine , Butterworth Charlotte , Masliah-Planchon Julien , Saint-Charles Alexandra , Bellini Angela , Bhalshankar Jaydutt , Pierron Gaelle , Combaret Valérie , Attignon Valéry , André Nicolas , Corradini Nadège , Dumont Benoit , Mansuy Ludovic , Khanfar Camille , Klein Sebastien , Briandet Claire , Plantaz Dominique , Millot Frederic , Thouvenin Sandrine , Aerts Isabelle , Ndounga-Diakou Lee Aymar , Laghouati Salim , Abbou Samuel , Jehanno Nina , Tissot Hubert , Renault Shufang , Baulande Sylvain , Raynal Virginie , Bozec Laurence , Bieche Ivan , Delattre Olivier , Berlanga Pablo , Schleiermacher Gudrun
Published: August 2024

SupplemetaryFigure12345
Supplementary Table S1 from Evaluating Immune Checkpoint Blockade in Metastatic Castration-Resistant Prostate Cancers with Deleterious CDK12 Alterations in the Phase 2 IMPACT Trial
Authors: Nguyen Charles B. , Reimers Melissa A. , Perera Chamila , Abida Wassim , Chou Jonathan , Feng Felix Y. , Antonarakis Emmanuel S. , McKay Rana R. , Pachynski Russell K. , Zhang Jingsong , Reichert Zachery R. , Palmbos Phillip L. , Caram Megan E.V. , Vaishampayan Ulka N. , Heath Elisabeth I. , Hopkins Alexander C. , Cieslik Marcin P. , Wu Yi-Mi , Robinson Dan R. , Baladandayuthapani Veerabhadran , Chinnaiyan Arul M. , Alva Ajjai S.
Published: August 2024

Supplementary Table S1. Study representativeness.
Supplementary Figure S2 from Evaluating Immune Checkpoint Blockade in Metastatic Castration-Resistant Prostate Cancers with Deleterious CDK12 Alterations in the Phase 2 IMPACT Trial
Authors: Nguyen Charles B. , Reimers Melissa A. , Perera Chamila , Abida Wassim , Chou Jonathan , Feng Felix Y. , Antonarakis Emmanuel S. , McKay Rana R. , Pachynski Russell K. , Zhang Jingsong , Reichert Zachery R. , Palmbos Phillip L. , Caram Megan E.V. , Vaishampayan Ulka N. , Heath Elisabeth I. , Hopkins Alexander C. , Cieslik Marcin P. , Wu Yi-Mi , Robinson Dan R. , Baladandayuthapani Veerabhadran , Chinnaiyan Arul M. , Alva Ajjai S.
Published: August 2024

Supplementary Figure S2. Cohort flow diagram for patients enrolled in cohorts A and C and those included in the analyses.
Data from Bystander Effects, Pharmacokinetics, and Linker-Payload Stability of EGFR-Targeting Antibody-Drug Conjugates Losatuxizumab Vedotin and Depatux-M in Glioblastoma Models
Authors: Jain Sonia , Griffith Jessica I. , Porath Kendra A. , Rathi Sneha , Le Jiayan , Pasa Tugce I. , Decker Paul A. , Gupta Shiv K. , Hu Zeng , Carlson Brett L. , Bakken Katrina , Burgenske Danielle M. , Feldsien Thomas M. , Lefebvre Didier R. , Vaubel Rachael A. , Eckel-Passow Jeanette E. , Reilly Edward B. , Elmquist William F. , Sarkaria Jann N.
Published: August 2024

AbstractPurpose:
Antibody-drug conjugates (ADC) are targeted therapies with robust efficacy in solid cancers, and there is intense interest in using EGFR-specific ADCs to target EGFR-amplified glioblastoma (GBM). Given GBM’s molecular heterogeneity, the bystander activity of ADCs may be important for determining treatment efficacy. In this study, the activity and toxicity of two EGFR-targeted ADCs with similar auristatin toxins, Losatuxizumab vedotin (ABBV-221) and Depatuxizumab mafodotin (Depatux-M), were compared in GBM patient-derived xenografts (PDX) and normal murine brain following direct infusion by convection-enhanced delivery (CED).
Experimental Design:
EGFRviii-amplified and non-amplified GBM PDXs were used to determine in vitro cytotoxicity, in vivo efficacy, and bystander activities of ABBV-221 and Depatux-M. Nontumor-bearing mice were used to evaluate the pharmacokinetics (PK) and toxicity of ADCs using LC-MS/MS and immunohistochemistry.
Results:
CED improved intracranial efficacy of Depatux-M and ABBV-221 in three EGFRviii-amplified GBM PDX models (Median survival: 125 to >300 days vs. 20–49 days with isotype control AB095). Both ADCs had comparable in vitro and in vivo efficacy. However, neuronal toxicity and CD68+ microglia/macrophage infiltration were significantly higher in brains infused with ABBV-221 with the cell-permeable monomethyl auristatin E (MMAE), compared with Depatux-M with the cell-impermeant monomethyl auristatin F. CED infusion of ABBV-221 into the brain or incubation of ABBV-221 with normal brain homogenate resulted in a significant release of MMAE, consistent with linker instability in the brain microenvironment.
Conclusions:
EGFR-targeting ADCs are promising therapeutic options for GBM when delivered intratumorally by CED. However, the linker and payload for the ADC must be carefully considered to maximize the therapeutic window.
Data from Anti-EGFR Antibody–Drug Conjugate Carrying an Inhibitor Targeting CDK Restricts Triple-Negative Breast Cancer Growth
Authors: Cheung Anthony , Chenoweth Alicia M. , Johansson Annelie , Laddach Roman , Guppy Naomi , Trendell Jennifer , Esapa Benjamina , Mavousian Antranik , Navarro-Llinas Blanca , Haider Syed , Romero-Clavijo Pablo , Hoffmann Ricarda M. , Andriollo Paolo , Rahman Khondaker M. , Jackson Paul , Tsoka Sophia , Irshad Sheeba , Roxanis Ioannis , Grigoriadis Anita , Thurston David E. , Lord Christopher J. , Tutt Andrew N. J. , Karagiannis Sophia N.
Published: August 2024

AbstractPurpose:
Anti-EGFR antibodies show limited response in breast cancer, partly due to activation of compensatory pathways. Furthermore, despite the clinical success of cyclin-dependent kinase (CDK) 4/6 inhibitors in hormone receptor–positive tumors, aggressive triple-negative breast cancers (TNBC) are largely resistant due to CDK2/cyclin E expression, whereas free CDK2 inhibitors display normal tissue toxicity, limiting their therapeutic application. A cetuximab-based antibody drug conjugate (ADC) carrying a CDK inhibitor selected based on oncogene dysregulation, alongside patient subgroup stratification, may provide EGFR-targeted delivery.
Experimental Design:
Expressions of G1/S-phase cell cycle regulators were evaluated alongside EGFR in breast cancer. We conjugated cetuximab with CDK inhibitor SNS-032, for specific delivery to EGFR-expressing cells. We assessed ADC internalization and its antitumor functions in vitro and in orthotopically grown basal-like/TNBC xenografts.
Results:
Transcriptomic (6,173 primary, 27 baseline, and matched post-chemotherapy residual tumors), single-cell RNA sequencing (150,290 cells, 27 treatment-naïve tumors), and spatial transcriptomic (43 tumor sections, 22 TNBCs) analyses confirmed expression of CDK2 and its cyclin partners in basal-like/TNBCs, associated with EGFR. Spatiotemporal live-cell imaging and super-resolution confocal microscopy demonstrated ADC colocalization with late lysosomal clusters. The ADC inhibited cell cycle progression, induced cytotoxicity against high EGFR-expressing tumor cells, and bystander killing of neighboring EGFR-low tumor cells, but minimal effects on immune cells. Despite carrying a small molar fraction (1.65%) of the SNS-032 inhibitor, the ADC restricted EGFR-expressing spheroid and cell line/patient-derived xenograft tumor growth.
Conclusions:
Exploiting EGFR overexpression, and dysregulated cell cycle in aggressive and treatment-refractory tumors, a cetuximab–CDK inhibitor ADC may provide selective and efficacious delivery of cell cycle–targeted agents to basal-like/TNBCs, including chemotherapy-resistant residual disease.
Data from Plasma versus Tissue Tumor Mutational Burden as Biomarkers of Durvalumab plus Tremelimumab Response in Patients with Metastatic Colorectal Cancer in the CO.26 Trial
Authors: Loree Jonathan M. , Titmuss Emma , Topham James T. , Kennecke Hagen F. , Feilotter Harriet , Virk Shakeel , Lee Young S. , Banks Kimberly , Quinn Katie , Karsan Aly , Renouf Daniel J. , Jonker Derek J. , Tu Dongsheng , O’Callaghan Chris J. , Chen Eric X.
Published: August 2024

AbstractPurpose:
Tissue-derived tumor mutation burden (TMB) of ≥10 mutations/Mb is a histology-agnostic biomarker for the immune checkpoint inhibitor (ICI) pembrolizumab. However, the dataset in which this was validated lacked colorectal cancers (CRC), and there is limited evidence for immunotherapy benefits in CRC using this threshold.
Patients and Methods:
CO.26 was a randomized phase II study of 180 patients, comparing durvalumab and tremelimumab (D + T, n = 119 patients) versus best supportive care (BSC; n = 61 patients). ctDNA sequencing was available for 168 patients (n = 118 D + T; n = 50), of whom 165 had evaluable plasma TMB (pTMB). Tissue sequencing was available for 108 patients. Optimal thresholds for stratifying patients based on OS were determined using a minimal P value approach. This report includes the final OS analysis.
Results:
Tissue TMB ≥10 mutations/Mb was not predictive of benefit from D + T compared with BSC in microsatellite stable (MSS) metastatic CRC [HR, 0.71 (95% CI, 0.28–1.80); P = 0.47]. No tissue TMB threshold could identify a high TMB group that benefited from ICI. By contrast, plasma TMB (pTMB) ≥28 mutations/Mb was predictive of benefit from D + T [HR, 0.34 (95% CI, 0.13–0.85); P = 0.022], as was clonal pTMB ≥10.6 mutations/Mb [HR, 0.10 (95% CI, 0.014–0.79); P = 0.029] and subclonal pTMB ≥25.9/Mb [HR, 0.20 (95% CI, 0.061–0.69); P = 0.010]. Higher pTMB was associated with length of time on cytotoxic agents (P = 0.021) and prior anti-EGFR exposure (P = 2.44 × 10−06).
Conclusions:
pTMB derived from either clonal or subclonal mutations may identify a group likely to benefit from immunotherapy, although validation is required. Tissue TMB provided no predictive utility for immunotherapy in this trial.
Table S2 from A Selective FGFR1/2 PROTAC Degrader with Antitumor Activity
Authors: Kong Ying , Zhao Xinyue , Wang Zhaofu , Yuan Siqi , Chen Sheng , Lou Shidi , Ma Shichao , Li Yunfeng , Wang Xinghao , Ge Yangfeng , Li Guobin , Yang Hongbing , Zhao Mengxi , Li Dandan , Zhang Hailong , Tan Wenfu , Wang Juan
Published: August 2024

Anti-proliferative activity of BR-cpd7 and BGJ398 in multiple human cancer cell lines. Human cancer cells were subjected to different concentrations of BR-cpd7 or BGJ398, and IC50 at 4 or 5 days was calculated (n=3 replicates).
Supplementary Figure S3 from INA03: A Potent Transferrin-Competitive Antibody–Drug Conjugate against CD71 for Safer Acute Leukemia Treatment
Authors: Bratti Manuela , Stubbs Elisa , Kolodych Sergii , Souchet Herve , Kelly Lois , Merlin Johanna , Marchal Michelle , Castellano Remy , Josselin Emmanuelle , Pasquer Hélène , Benajiba Lina , Puissant Alexandre , Koniev Oleksandr , Collette Yves , Belanger Coralie , Hermine Olivier , Monteiro Renato C. , Launay Pierre
Published: August 2024

Figure S3
Supplemental Figure S5 from Enhancing Standard of Care Chemotherapy Efficacy Using DNA-Dependent Protein Kinase (DNA-PK) Inhibition in Preclinical Models of Ewing Sarcoma
Authors: Collins Victor J. , Ludwig Katelyn R. , Nelson Ariana E. , Sundara Rajan Soumya , Yeung Choh , Vulikh Ksenia , Isanogle Kristine A. , Mendoza Arnulfo , Difilippantonio Simone , Karim Baktiar O. , Caplen Natasha J. , Heske Christine M.
Published: August 2024

TOP2 poisons synergize with DNA-PK inhibition in EWS
Supplemental Figure S10 from Enhancing Standard of Care Chemotherapy Efficacy Using DNA-Dependent Protein Kinase (DNA-PK) Inhibition in Preclinical Models of Ewing Sarcoma
Authors: Collins Victor J. , Ludwig Katelyn R. , Nelson Ariana E. , Sundara Rajan Soumya , Yeung Choh , Vulikh Ksenia , Isanogle Kristine A. , Mendoza Arnulfo , Difilippantonio Simone , Karim Baktiar O. , Caplen Natasha J. , Heske Christine M.
Published: August 2024

Concomitant AZD-7648 and etoposide treatments impair tumor growth
Table S4 from Antitumor Activity of a Novel LAIR1 Antagonist in Combination with Anti-PD1 to Treat Collagen-Rich Solid Tumors
Authors: Rodriguez Bertha L. , Huang Jiawei , Gibson Laura , Fradette Jared J. , Chen Hung-I.H. , Koyano Kikuye , Cortez Czrina , Li Betty , Ho Carmence , Ashique Amir M. , Lin Vicky Y. , Crawley Suzanne , Roda Julie M. , Chen Peirong , Fan Bin , Kim Jeong , Sissons James , Sitrin Jonathan , Kaplan Daniel D. , Gibbons Don L. , Rivera Lee B.
Published: August 2024

NGM438 binding to recombinant LAIR proteins.
Supplementary Data from M3258 Is a Selective Inhibitor of the Immunoproteasome Subunit LMP7 (β5i) Delivering Efficacy in Multiple Myeloma Models
Authors: Sanderson Michael P. , Friese-Hamim Manja , Walter-Bausch Gina , Busch Michael , Gaus Stefanie , Musil Djordje , Rohdich Felix , Zanelli Ugo , Downey-Kopyscinski Sondra L. , Mitsiades Constantine S. , Schadt Oliver , Klein Markus , Esdar Christina
Published: August 2024

Supplemental Data and Methods
Data from TNIK Inhibition Sensitizes TNIK-Overexpressing Lung Squamous Cell Carcinoma to Radiotherapy
Authors: Nguyen Triet , Carrieri Francesca A. , Connis Nick , Lafargue Audrey , Chang Jinhee , Chan Aaron , Shetty Amol C. , Song Yang , Hoang Tung , Jagtap Shreya , Chowdhury Dipanwita D. , Khan Muhammad A. , Gabrielson Kathleen L. , Rezaee Mohammad , Torres-Ayuso Pedro , Brognard John , Hann Christine L. , Tran Phuoc T.
Published: August 2024

Abstract
Most patients with lung squamous cell carcinoma (LSCC) undergo chemotherapy, radiotherapy, and adjuvant immunotherapy for locally advanced disease. The efficacy of these treatments is still limited because of dose-limiting toxicity or locoregional recurrence. New combination approaches and targets such as actionable oncogenic drivers are needed to advance treatment options for patients with LSCC. Moreover, other options for chemotherapy-ineligible patients are limited. As such, there is a critical need for the development of selective and potent chemoradiosensitizers for locally advanced LSCC. In this study, we investigated inhibiting TRAF2- and NCK-interacting protein kinase (TNIK), which is amplified in 40% of patients with LSCC, as a strategy to sensitize LSCC tumors to chemotherapy and radiotherapy. Employing a range of human LSCC cell lines and the TNIK inhibitor NCB-0846, we investigated the potential of TNIK as a chemo- and radiosensitizing target with in vitro and in vivo preclinical models. The combination of NCB-0846 with cisplatin or etoposide was at best additive. Interestingly, pre-treating LSCC cells with NCB-0846 prior to ionizing radiation (IR) potentiated the cytotoxicity of IR in a TNIK-specific fashion. Characterization of the radiosensitization mechanism suggested that TNIK inhibition may impair the DNA damage response and promote mitotic catastrophe in irradiated cells. In a subcutaneous xenograft in vivo model, pretreatment with NCB-0846 significantly enhanced the efficacy of IR and caused elevated necrosis in TNIKhigh LK2 tumors but not TNIKlow KNS62 tumors. Overall, these results indicate that TNIK inhibition may be a promising strategy to increase the efficacy of radiotherapy in patients with LSCC with high TNIK expression.
Supplementary Table 2 from A Linear Relationship between the Number of Cancers among First-Degree Relatives and the Risk of Multiple Primary Cancers
Authors: He Shisi , Barry Kathryn H. , Mitchell Braxton D. , Chen Shuo , Zhang Yuji , Beane Freeman Laura E. , Berndt Sonja I.
Published: August 2024

Supplementary Table 2 shows the risk of multiple primary cancers and family history of cancer stratified by other baseline characteristics in the PLCO Cancer Screening Trial
Data from Stool Protein Mass Spectrometry Identifies Biomarkers for Early Detection of Diffuse-type Gastric Cancer
Authors: Ho Chi-Lee C. , Gilbert Michael B. , Urtecho Guillaume , Lee Hyoungjoo , Drew David A. , Klempner Samuel J. , Cho Jin S. , Ryan Thomas J. , Rustgi Naryan , Lee Hyuk , Lee Jeeyun , Caraballo Alexander , Magicheva-Gupta Marina V. , Rios Carmen , Shin Alice E. , Tseng Yuen-Yi , Davis Jeremy L. , Chung Daniel C. , Chan Andrew T. , Wang Harris H. , Ryeom Sandra
Published: August 2024

Abstract
There is a high unmet need for early detection approaches for diffuse gastric cancer (DGC). We examined whether the stool proteome of mouse models of gastric cancer (GC) and individuals with hereditary diffuse gastric cancer (HDGC) have utility as biomarkers for early detection. Proteomic mass spectrometry of the stool of a genetically engineered mouse model driven by oncogenic KrasG12D and loss of p53 and Cdh1 in gastric parietal cells [known as Triple Conditional (TCON) mice] identified differentially abundant proteins compared with littermate controls. Immunoblot assays validated a panel of proteins, including actinin alpha 4 (ACTN4), N-acylsphingosine amidohydrolase 2 (ASAH2), dipeptidyl peptidase 4 (DPP4), and valosin-containing protein (VCP), as enriched in TCON stool compared with littermate control stool. Immunofluorescence analysis of these proteins in TCON stomach sections revealed increased protein expression compared with littermate controls. Proteomic mass spectrometry of stool obtained from patients with HDGC with CDH1 mutations identified increased expression of ASAH2, DPP4, VCP, lactotransferrin (LTF), and tropomyosin-2 relative to stool from healthy sex- and age-matched donors. Chemical inhibition of ASAH2 using C6 urea ceramide was toxic to GC cell lines and GC patient-derived organoids. This toxicity was reversed by adding downstream products of the S1P synthesis pathway, which suggested a dependency on ASAH2 activity in GC. An exploratory analysis of the HDGC stool microbiome identified features that correlated with patient tumors. Herein, we provide evidence supporting the potential of analyzing stool biomarkers for the early detection of DGC.

Prevention Relevance: This study highlights a novel panel of stool protein biomarkers that correlate with the presence of DGC and has potential use as early detection to improve clinical outcomes.
Supplementary Figure S8 from CLN-617 Retains IL2 and IL12 in Injected Tumors to Drive Robust and Systemic Immune-Mediated Antitumor Activity
Authors: Mehta Naveen K. , Rakhra Kavya , Meetze Kristan A. , Li Bochong , Momin Noor , Chang Jason Y.H. , Wittrup K. Dane , Baeuerle Patrick A. , Michaelson Jennifer S.
Published: August 2024

Minimal effects on Treg and NK cells
Supplementary Figure S7 from CLN-617 Retains IL2 and IL12 in Injected Tumors to Drive Robust and Systemic Immune-Mediated Antitumor Activity
Authors: Mehta Naveen K. , Rakhra Kavya , Meetze Kristan A. , Li Bochong , Momin Noor , Chang Jason Y.H. , Wittrup K. Dane , Baeuerle Patrick A. , Michaelson Jennifer S.
Published: August 2024

IFNγ release
Supplementary Figure S6 from CLN-617 Retains IL2 and IL12 in Injected Tumors to Drive Robust and Systemic Immune-Mediated Antitumor Activity
Authors: Mehta Naveen K. , Rakhra Kavya , Meetze Kristan A. , Li Bochong , Momin Noor , Chang Jason Y.H. , Wittrup K. Dane , Baeuerle Patrick A. , Michaelson Jennifer S.
Published: August 2024

No correlation between injection volume or systemic mCLN-617 levels and abscopal effect
Supplementary Figure S14 from CLN-617 Retains IL2 and IL12 in Injected Tumors to Drive Robust and Systemic Immune-Mediated Antitumor Activity
Authors: Mehta Naveen K. , Rakhra Kavya , Meetze Kristan A. , Li Bochong , Momin Noor , Chang Jason Y.H. , Wittrup K. Dane , Baeuerle Patrick A. , Michaelson Jennifer S.
Published: August 2024

Bioactivity of CLN-617
Supplementary Figure S11 from CLN-617 Retains IL2 and IL12 in Injected Tumors to Drive Robust and Systemic Immune-Mediated Antitumor Activity
Authors: Mehta Naveen K. , Rakhra Kavya , Meetze Kristan A. , Li Bochong , Momin Noor , Chang Jason Y.H. , Wittrup K. Dane , Baeuerle Patrick A. , Michaelson Jennifer S.
Published: August 2024

T-cell gating scheme for flow cytometry data analysis
Supplementary Table 3 from Multifunctional Bispecific Nanovesicles Targeting SLAMF7 Trigger Potent Antitumor Immunity
Authors: Zhu Manman , Wu Yongjian , Zhu Tianchuan , Chen Jian , Chen Zhenxing , Ding Hanxi , Tan Siyi , He Jianzhong , Zeng Qi , Huang Xi
Published: August 2024

Supplementary Table 3
Supplementary Table 1 from Multifunctional Bispecific Nanovesicles Targeting SLAMF7 Trigger Potent Antitumor Immunity
Authors: Zhu Manman , Wu Yongjian , Zhu Tianchuan , Chen Jian , Chen Zhenxing , Ding Hanxi , Tan Siyi , He Jianzhong , Zeng Qi , Huang Xi
Published: August 2024

Supplementary Table 1
Supplementary Table S1 from Venetoclax Induces BCL-2–Dependent Treg to TH17 Plasticity to Enhance the Antitumor Efficacy of Anti–PD-1 Checkpoint Blockade
Authors: Liao Rosy , Hsu Jocelyn Y. , Aboelella Nada S. , McKeever Joshua A. , Thomas-Toth Anika T. , Koh Andrew S. , LaBelle James L.
Published: August 2024

Supplementary Table S1
Figure S2 from Venetoclax Induces BCL-2–Dependent Treg to TH17 Plasticity to Enhance the Antitumor Efficacy of Anti–PD-1 Checkpoint Blockade
Authors: Liao Rosy , Hsu Jocelyn Y. , Aboelella Nada S. , McKeever Joshua A. , Thomas-Toth Anika T. , Koh Andrew S. , LaBelle James L.
Published: August 2024

Supplementary Figure S2. Venetoclax results in significant lymphodepletion in (A) lymph node and (B) spleen.
Supplementary Figure S7 from Overexpression of an Engineered SERPINB9 Enhances Allogeneic T-cell Persistence and Efficacy
Authors: Teo Pei Y. , Jung Youngrock , Quach David H. , Koh Joanna , Ong Richard W. , Goh Angeline , Tan Alrina , Ng Chee H. , Seh Cheah C. , Tan Kar W. , Horak Ivan D. , Low Lionel
Published: August 2024

Supplementary Figure S7. Manufacturing of Allo-T cells which are pre-primed alloreactive ‘recipient’ cells that recognize and kill ‘donor’ cells. A, Manufacturing timeline for the generation of Allo-T. B, CD30 expression of CD30KO Allo-T cells determined by the staining of CD30 with two different antibody clones, BY88 and BerH8, and flow cytometry analysis.
Supplementary Figure S3 from Overexpression of an Engineered SERPINB9 Enhances Allogeneic T-cell Persistence and Efficacy
Authors: Teo Pei Y. , Jung Youngrock , Quach David H. , Koh Joanna , Ong Richard W. , Goh Angeline , Tan Alrina , Ng Chee H. , Seh Cheah C. , Tan Kar W. , Horak Ivan D. , Low Lionel
Published: August 2024

Supplementary Figure S3. CD30.CAR with IgG1 spacer (CD30.Ig) TCRαβKO ATCs expressing different variants of SB9 had similar CD30.Ig expression and cytotoxicity. A, Expression of TCRαβ on CD3 wildtype (WT) T cells or T cells after TCRαβKO gene modification using Crispr gene editing measured by flow cytometry analysis. B, Expression of different variants of SB9 on CD30.Ig TCRαβKO ATCs measured by intracellular flow cytometry analysis of one representative donor. C, Relative median fluorescence intensity (MFI) of different variants of SB9, normalized to SB9 expression in CD30.Ig sample. The bars denote median ± SD (n = 3 donors). D, CD30.Ig expression on TCRαβKO ATCs expressing different variants of SB9, measured by flow cytometry analysis of a representative donor. E and F, Pooled data of CD30.Ig expression (%; E) and CD30.Ig expression (geometric mean fluorescence intensity, MFI; F) on CD30.Ig TCRαβKO ATCs, measured by flow cytometry analysis of n = 3 donors, where bars denote median ± SD. G, CD30.Ig TCRαβKO ATC-mediated cytolysis of KM-H2 cells, of a representative donor, measured using the xCELLigence system. CD30.Ig TCRαβKO ATCs manufactured from three donors were tested and found to have similar results.
Supplementary Figure S14 from Overexpression of an Engineered SERPINB9 Enhances Allogeneic T-cell Persistence and Efficacy
Authors: Teo Pei Y. , Jung Youngrock , Quach David H. , Koh Joanna , Ong Richard W. , Goh Angeline , Tan Alrina , Ng Chee H. , Seh Cheah C. , Tan Kar W. , Horak Ivan D. , Low Lionel
Published: August 2024

Supplementary Figure S14. Overexpression of SB9(CAS) in ‘donor’ CD30.CAR with 4-1BB spacer (CD30.bb) EBVSTs increases resistance to allorejection in a B-ALL allorejection model in which ‘donor’ CAR T cell and ‘recipient’ cell levels were quantified via IVIS imaging and flow cytometry, respectively. A, Manufacturing timeline for the generation of CD30.bb EBVSTs expressing eGFP-ffLuc. B, Schematic of in-vivo allorejection model for (C-D), where 2.5 x 106 HLADKO NALM6-CD30 tumor cells were injected intravenously into NSG (MHCKO) mice. 18 days later, 5 x 106 ‘donor’ eGFP-ffLuc-expressing CD30.bb EBVSTs with or without 5 x 106 ‘recipient’ CD30KO Allo-T cells were co-infused intravenously. C, Bioluminescent images of CD30.bb EBVST FFluc+ in NSG (MHCKO) mice bearing HLADKO NALM6-CD30 tumors, with or without the presence of Allo-T cells, at specified time points. D, Quantified bioluminescence of unmodified CD30.bb EBVSTs in the presence (black lines) or absence (grey lines) of Allo-T cells in individual mice at specified time points, (n = 11 for CD30.bb-treated group and n = 12 for CD30.bb + Allo-T treated group). The same data for unmodified ‘donor’ CD30.bb EBVSTs in the presence of ‘recipient’ Allo-T is represented in both (D) and (Fig. 3I). The graphs denote mean + SD.