bluuebunny/crossref_metadata_2025 huggingface dataset:
Figure 6 from Multistate Gene Cluster Switches Determine the Adaptive Mitochondrial and Metabolic Landscape of Breast Cancer
Authors: Menegollo Michela , Bentham Robert B. , Henriques Tiago , Ng Seow Q. , Ren Ziyu , Esculier Clarinde , Agarwal Sia , Tong Emily T.Y. , Lo Clement , Ilangovan Sanjana , Szabadkai Zorka , Suman Matteo , Patani Neill , Ghanate Avinash , Bryson Kevin , Stein Robert C. , Yuneva Mariia , Szabadkai Gyorgy
Published: September 2024

Protein expression profiles match transcriptomic switches. A, Western blot analysis of 29 metabolic enzymes across five cell lines representing MB1_UF and MB1_LF switch positions and cell states. Representative blots from n ≥ 3 independent experiments, used for quantification of signals, normalizing density values to either grp75 or β-actin. B, D, and E, Clustering and quantitative analysis of enzyme expression levels obtained from A. Values were separately normalized to either mitochondrial (left) or cytosolic (right) markers, grp75 or β-actin. The comparison of mitochondrial abundance based on the grp75/β-actin ratio is shown at the bottom in B. Heatmaps are based on a pairwise, robust to outliers distance measure of the mean protein expression values. The k-means clustering. D and E, Two-way ANOVA with uncorrected Fisher LSD multiple comparison tests. C, Heatmap and k-means clustering of transcript CV values of the 29 enzymes from the METABRIC dataset (see Figs. 1 and 2, positive values predicting higher expression of genes in MB1_UF and negative values corresponding to higher expression in MB1_LF) and scaled protein expression levels (wCV) averaged across all cell lines, normalized to grp75 (wCV_mito) or β-actin (wCV_cyto). ns, nonsignificant, P > 0.05; *, P ≤ 0.05; **, P ≤ 0.01; ***, P ≤ 0.001; ****, P ≤ 0.0001).
Figure 1 from Multistate Gene Cluster Switches Determine the Adaptive Mitochondrial and Metabolic Landscape of Breast Cancer
Authors: Menegollo Michela , Bentham Robert B. , Henriques Tiago , Ng Seow Q. , Ren Ziyu , Esculier Clarinde , Agarwal Sia , Tong Emily T.Y. , Lo Clement , Ilangovan Sanjana , Szabadkai Zorka , Suman Matteo , Patani Neill , Ghanate Avinash , Bryson Kevin , Stein Robert C. , Yuneva Mariia , Szabadkai Gyorgy
Published: September 2024

Large-scale transcriptome switches identify breast cancer subtypes. A, Gene set switch identification in bicluster samples. MCbiclust starts with a random gene set in a random sample set and performs a greedy search aiming for the sample set, across which, the gene set has the highest correlation. As the absolute value of correlation is maximized during the search, the resulting top correlating samples display two gene sets with sharp anticorrelation (switch) between them. The gene sets and sample sets can be extended to the whole transcriptome and sample set by quantifying correlations (see main text), which provides the basis for gene set enrichment analysis. B, Visualization of individual switches (MB1, MB2, MB3 biclusters) in all METABRIC samples. Two-dimensional distribution by PC1 and ranking index are shown, overlaid with PAM50 classifiers. Dashed lines represent the thresholds to include samples in the forks, calculated as 0.04 × forkscale (see Materials and Methods). C, UpSet matrix and plots of sample intersections between top and bottom positions of each bicluster switch. Unique and overlapping (intersect) samples are shown separately. D, Scheme of switches. MB1 and MB2 share their LF, thus representing a multistate switch, while MB3 is an independent bistate switch, thus the MB1_2 and MB_3 biclusters represent different switch mechanisms. E and F, Interswitch relationships are shown in two-dimensional distribution plots of samples by two biclusters (switches). The axes represent the scale between the UF and LF of each bicluster. The distribution of samples according to their MB1 vs. MB2 forkscale value (see Materials and Methods) is shown in E, while the combinations of MB3 with MB1 or MB2 are shown in F. G, Heatmap of the correlation values (CVs, Pearson r) across the whole transcriptome in the MB1 bicluster; a small set of midrange values were hidden (see gaps in heatmap). Annotations show the locations of mitochondrial and metabolic genes (top), and bicluster genes (bottom). For comparison between the switches, bottom annotation plots show the CV values of each sample in the three biclusters (switches). H, Fold enrichment of mitochondrial and metabolic (with intersections) genes in the anticorrelated gene sets. Heatmap shows enrichment values of each gene set in each position of all switches. Gene set intersections are on the Venn diagram below the heatmap.
Supplementary Methods from WNK1 Interaction with KEAP1 Promotes NRF2 Stabilization to Enhance the Oxidative Stress Response in Hepatocellular Carcinoma
Authors: Li Li , Xie Dacheng , Yu Shijun , Ma Muyuan , Fan Kailing , Chen Jingde , Xiu Mengxi , Xie Keping , Li Yandong , Gao Yong
Published: September 2024

Supplementary Methods
Supplementary Figure S8 from WNK1 Interaction with KEAP1 Promotes NRF2 Stabilization to Enhance the Oxidative Stress Response in Hepatocellular Carcinoma
Authors: Li Li , Xie Dacheng , Yu Shijun , Ma Muyuan , Fan Kailing , Chen Jingde , Xiu Mengxi , Xie Keping , Li Yandong , Gao Yong
Published: September 2024

Supplementary Figure S8
Supplementary Figure S7 from WNK1 Interaction with KEAP1 Promotes NRF2 Stabilization to Enhance the Oxidative Stress Response in Hepatocellular Carcinoma
Authors: Li Li , Xie Dacheng , Yu Shijun , Ma Muyuan , Fan Kailing , Chen Jingde , Xiu Mengxi , Xie Keping , Li Yandong , Gao Yong
Published: September 2024

Supplementary Figure S7
Supplementary Figure S6 from WNK1 Interaction with KEAP1 Promotes NRF2 Stabilization to Enhance the Oxidative Stress Response in Hepatocellular Carcinoma
Authors: Li Li , Xie Dacheng , Yu Shijun , Ma Muyuan , Fan Kailing , Chen Jingde , Xiu Mengxi , Xie Keping , Li Yandong , Gao Yong
Published: September 2024

Supplementary Figure S6
Supplementary Figure S3 from WNK1 Interaction with KEAP1 Promotes NRF2 Stabilization to Enhance the Oxidative Stress Response in Hepatocellular Carcinoma
Authors: Li Li , Xie Dacheng , Yu Shijun , Ma Muyuan , Fan Kailing , Chen Jingde , Xiu Mengxi , Xie Keping , Li Yandong , Gao Yong
Published: September 2024

Supplementary Figure S3
Supplementary Figures from RUVBL1/2 Blockade Targets YTHDF1 Activity to Suppress m6A-Dependent Oncogenic Translation and Colorectal Tumorigenesis
Authors: Chen Danyu , Ji Fenfen , Zhou Qiming , Cheung Henley , Pan Yasi , Lau Harry C.-H. , Liang Cong , Yang Zhenjie , Huang Pingmei , Wei Qinyao , Cheung Alvin H.-K. , Kang Wei , Chen Huarong , Yu Jun , Wong Chi Chun
Published: September 2024

Supplementary Figures
Supplementary Figure 7 from Comprehensive Proteogenomic Profiling Reveals the Molecular Characteristics of Colorectal Cancer at Distinct Stages of Progression
Authors: Li Lingling , Jiang Dongxian , Liu Hui , Guo Chunmei , Zhang Qiao , Li Xuedong , Chen Xiaojian , Chen Zheqi , Feng Jinwen , Tan Subei , Huang Wen , Huang Jie , Xu Chen , Liu Chen-Ying , Yu Wei , Hou Yingyong , Ding Chen
Published: September 2024

Supplementary Figure 7 and related legend of the revised manuscript.
Supplementary Figure 3 from Comprehensive Proteogenomic Profiling Reveals the Molecular Characteristics of Colorectal Cancer at Distinct Stages of Progression
Authors: Li Lingling , Jiang Dongxian , Liu Hui , Guo Chunmei , Zhang Qiao , Li Xuedong , Chen Xiaojian , Chen Zheqi , Feng Jinwen , Tan Subei , Huang Wen , Huang Jie , Xu Chen , Liu Chen-Ying , Yu Wei , Hou Yingyong , Ding Chen
Published: September 2024

Supplementary Figure 3 and related legend of the revised manuscript.
Supplementary Data from Targeting the TRIM14/USP14 Axis Enhances Immunotherapy Efficacy by Inducing Autophagic Degradation of PD-L1
Authors: Liu Di , Li Mengqiu , Zhao Zhiyao , Zhou Liang , Zhi Feng , Guo Zhiyong , Cui Jun
Published: September 2024

Fig.S1-S8
Data from ARID1A-Deficient Tumors Acquire Immunogenic Neoantigens during the Development of Resistance to Targeted Therapy
Authors: Okada Masahiro , Yamasaki Satoru , Nakazato Hiroshi , Hirahara Yuhya , Ishibashi Takuya , Kawamura Masami , Shimizu Kanako , Fujii Shin-ichiro
Published: September 2024

Abstract
Neoantigen-based immunotherapy is an attractive potential treatment for previously intractable tumors. To effectively broaden the application of this approach, stringent biomarkers are crucial to identify responsive patients. ARID1A, a frequently mutated subunit of SWI/SNF chromatin remodeling complex, has been reported to determine tumor immunogenicity in some cohorts; however, mutations and deletions of ARID1A are not always linked to clinical responses to immunotherapy. In this study, we investigated immunotherapeutic responses based on ARID1A status in targeted therapy-resistant cancers. Mouse and human BRAFV600E melanomas with or without ARID1A expression were transformed into resistant to vemurafenib, an FDA-approved specific BRAFV600E inhibitor. Anti-PD-1 antibody treatment enhanced antitumor immune responses in vemurafenib-resistant ARID1A-deficient tumors but not in ARID1A-intact tumors or vemurafenib-sensitive ARID1A-deficient tumors. Neoantigens derived from accumulated somatic mutations during vemurafenib resistance were highly expressed in ARID1A-deficient tumors and promoted tumor immunogenicity. Furthermore, the newly generated neoantigens could be utilized as immunotherapeutic targets by vaccines. Finally, targeted therapy resistance–specific neoantigen in experimental human melanoma cells lacking ARID1A were validated to elicit T-cell receptor responses. Collectively, the classification of ARID1A-mutated tumors based on vemurafenib resistance as an additional indicator of immunotherapy response will enable a more accurate prediction to guide cancer treatment. Furthermore, the neoantigens that emerge with therapy resistance can be promising therapeutic targets for refractory tumors.

Significance: Chemotherapy resistance promotes the acquisition of immunogenic neoantigens in ARID1A-deficient tumors that confer sensitivity to immune checkpoint blockade and can be utilized for developing antitumor vaccines, providing strategies to improve immunotherapy efficacy.
Data from Comprehensive Proteogenomic Profiling Reveals the Molecular Characteristics of Colorectal Cancer at Distinct Stages of Progression
Authors: Li Lingling , Jiang Dongxian , Liu Hui , Guo Chunmei , Zhang Qiao , Li Xuedong , Chen Xiaojian , Chen Zheqi , Feng Jinwen , Tan Subei , Huang Wen , Huang Jie , Xu Chen , Liu Chen-Ying , Yu Wei , Hou Yingyong , Ding Chen
Published: September 2024

Abstract
Colorectal cancer is the second most common malignant tumor worldwide. Analysis of the changes that occur during colorectal cancer progression could provide insights into the molecular mechanisms driving colorectal cancer development and identify improved treatment strategies. In this study, we performed an integrated multiomic analysis of 435 trace tumor samples from 148 patients with colorectal cancer, covering nontumor, intraepithelial neoplasia (IEN), infiltration, and advanced stage colorectal cancer phases. Proteogenomic analyses demonstrated that KRAS and BRAF mutations were mutually exclusive and elevated oxidative phosphorylation in the IEN phase. Chr17q loss and chr20q gain were also mutually exclusive, which occurred predominantly in the IEN and infiltration phases, respectively, and impacted the cell cycle. Mutations in TP53 were frequent in the advanced stage colorectal cancer phase and associated with the tumor microenvironment, including increased extracellular matrix rigidity and stromal infiltration. Analysis of the profiles of colorectal cancer based on consensus molecular subtype and colorectal cancer intrinsic subtype classifications revealed the progression paths of each subtype and indicated that microsatellite instability was associated with specific subtype classifications. Additional comparison of molecular characteristics of colorectal cancer based on location showed that ANKRD22 amplification by chr10q23.31 gain enhanced glycolysis in the right-sided colorectal cancer. The AOM/DSS-induced colorectal cancer carcinogenesis mouse model indicated that DDX5 deletion due to chr17q loss promoted colorectal cancer development, consistent with the findings from the patient samples. Collectively, this study provides an informative resource for understanding the driving events of different stages of colorectal cancer and identifying the potential therapeutic targets.

Significance: Characterization of the proteogenomic landscape of colorectal cancer during progression provides a multiomic map detailing the alterations in each stage of carcinogenesis and suggesting potential diagnostic and therapeutic approaches for patients.
Data from PRKDC Induces Chemoresistance in Osteosarcoma by Recruiting GDE2 to Stabilize GNAS and Activate AKT
Authors: Zhang Wenchao , Li Wei , Yin Chi , Feng Chengyao , Liu Binfeng , Xu Haodong , Jin Xin , Tu Chao , Li Zhihong
Published: September 2024

Abstract
Chemoresistance is one of the major causes of poor prognosis in osteosarcoma. Alternative therapeutic strategies for osteosarcoma are limited, indicating that increasing sensitivity to currently used chemotherapies could be an effective approach to improve patient outcomes. Using a kinome-wide CRISPR screen, we identified PRKDC as a critical determinant of doxorubicin (DOX) sensitivity in osteosarcoma. The analysis of clinical samples demonstrated that PRKDC was hyperactivated in osteosarcoma, and functional experiments showed that the loss of PRKDC significantly increased sensitivity of osteosarcoma to DOX. Mechanistically, PRKDC recruited and bound GDE2 to enhance the stability of protein GNAS. The elevated GNAS protein levels subsequently activated AKT phosphorylation and conferred resistance to DOX. The PRKDC inhibitor AZD7648 and DOX synergized and strongly suppressed the growth of osteosarcoma in mouse xenograft models and human organoids. In conclusion, the PRKDC-GDE2-GNAS-AKT regulatory axis suppresses DOX sensitivity and comprises targetable candidates for improving the efficacy of chemotherapy in osteosarcoma.

Significance: Targeting PRKDC suppresses AKT activation and increases sensitivity to doxorubicin in osteosarcoma, which provides a therapeutic strategy for overcoming chemoresistance.
FDA Approval Summary: Enfortumab Vedotin plus Pembrolizumab for Locally Advanced or Metastatic Urothelial Carcinoma
Authors: Brave Michael H. , Maguire William F. , Weinstock Chana , Zhang Hui , Gao Xin , Li Fang , Yu Jingyu , Fu Wentao , Zhao Hong , Pierce William F. , Chang Elaine , Dinin Jeannette , Fiero Mallorie H. , Rahman Nam Atiqur , Tang Shenghui , Pazdur Richard , Kluetz Paul G. , Amiri-Kordestani Laleh , Suzman Daniel L.
Published: September 2024

On December 15, 2023, the FDA granted traditional approval to enfortumab vedotin-ejfv plus pembrolizumab (EV + Pembro) for patients with locally advanced or metastatic urothelial carcinoma (la/mUC). Substantial evidence of effectiveness was obtained from EV-302/KEYNOTE-A39 (NCT04223856), an open-label, randomized trial evaluating EV + Pembro versus cisplatin or carboplatin plus gemcitabine (Plat + Gem) in patients with previously untreated la/mUC. A total of 886 patients were randomized (1:1) to receive EV 1.25 mg/kg intravenously on days 1 and 8 of each 21-day cycle until disease progression or unacceptable toxicity plus Pembro 200 mg intravenously on day 1 of each 21-day cycle for up to 35 cycles or Plat + Gem for up to 6 cycles. Dual primary endpoints were progression-free survival determined by blinded independent central review and overall survival. The median progression-free survival was 12.5 months [95% confidence interval (CI), 10.4–16.6] in the EV + Pembro arm and 6.3 months (95% CI, 6.2–6.5) in the Plat + Gem arm [HR, 0.450 (95% CI, 0.377–0.538); P value < 0.0001]. The median overall survival was 31.5 months (95% CI, 25.4–not estimable) in the EV + Pembro arm and 16.1 months (95% CI, 13.9–18.3) in the Plat + Gem arm [HR, 0.468 (95% CI, 0.376–0.582); P value < 0.0001]. The safety profile of EV + Pembro was similar to that observed in EV-103/KEYNOTE-869 in cisplatin-ineligible patients with la/mUC. This article summarizes the data and the FDA thought process supporting traditional approval of EV + Pembro, as well as additional exploratory analyses conducted by the FDA.
Supplementary Figure S3 from MYTX-011: A pH-Dependent Anti–c-MET Antibody–Drug Conjugate Designed for Enhanced Payload Delivery to c-MET–Expressing Tumor Cells
Authors: Gera Nimish , Fitzgerald Kyle M. , Ramesh Vijay , Patel Purvi , Kanojia Deepak , Colombo Federico , Kien Lena , Aoyama Simon , Xu Lihui , Jean Jussekia , Deshpande Amit M. , Comb William C. , Chittenden Thomas , Fiske Brian P.
Published: September 2024

MMAE levels in cynomolgus monkeys following single dosing of MYTX-011, parent and benchmark ADCs.
Supplementary Figure S2 from MYTX-011: A pH-Dependent Anti–c-MET Antibody–Drug Conjugate Designed for Enhanced Payload Delivery to c-MET–Expressing Tumor Cells
Authors: Gera Nimish , Fitzgerald Kyle M. , Ramesh Vijay , Patel Purvi , Kanojia Deepak , Colombo Federico , Kien Lena , Aoyama Simon , Xu Lihui , Jean Jussekia , Deshpande Amit M. , Comb William C. , Chittenden Thomas , Fiske Brian P.
Published: September 2024

Species cross reactivity of MYTX-011.
Supplementary Data Figure 2 from Radiation and Chemo-Sensitizing Effects of DNA-PK Inhibitors Are Proportional in Tumors and Normal Tissues
Authors: Baker Jennifer H.E. , Kyle Alastair H. , Liu Nannan A. , Wang Taixiang , Liu Xinhe , Teymori Sevin , Banáth Judit P. , Minchinton Andrew I.
Published: September 2024

Radiosensitization of the gut and tongue with DNA-PK inhibitors
Supplementary Data Figure 1 from Radiation and Chemo-Sensitizing Effects of DNA-PK Inhibitors Are Proportional in Tumors and Normal Tissues
Authors: Baker Jennifer H.E. , Kyle Alastair H. , Liu Nannan A. , Wang Taixiang , Liu Xinhe , Teymori Sevin , Banáth Judit P. , Minchinton Andrew I.
Published: September 2024

Tumour-control activity of DNA-PK inhibitors
Table S6 from HPN328, a Trispecific T Cell–Activating Protein Construct Targeting DLL3-Expressing Solid Tumors
Authors: Molloy Mary E. , Aaron Wade H. , Barath Manasi , Bush Mabel C. , Callihan Evan C. , Carlin Kevin , Cremin Michael , Evans Thomas , Guerrero Maria G. , Hemmati Golzar , Hundal Avneel S. , Lao Llewelyn , Laurie Payton , Lemon Bryan D. , Lin S.J. , O’Rear Jessica , Patnaik Purbasa , Sotelo Rocha Sony , Santiago Linda , Strobel Kathryn L. , Valenzuela Laura B. , Wu Chi-Heng , Yu Stephen , Yu Timothy Z. , Anand Banmeet S. , Law Che-Leung , Sun Liping L. , Wesche Holger , Austin Richard J.
Published: September 2024

EC50 Values for HPN328 mediated induction of CD69.
Table S4 from HPN328, a Trispecific T Cell–Activating Protein Construct Targeting DLL3-Expressing Solid Tumors
Authors: Molloy Mary E. , Aaron Wade H. , Barath Manasi , Bush Mabel C. , Callihan Evan C. , Carlin Kevin , Cremin Michael , Evans Thomas , Guerrero Maria G. , Hemmati Golzar , Hundal Avneel S. , Lao Llewelyn , Laurie Payton , Lemon Bryan D. , Lin S.J. , O’Rear Jessica , Patnaik Purbasa , Sotelo Rocha Sony , Santiago Linda , Strobel Kathryn L. , Valenzuela Laura B. , Wu Chi-Heng , Yu Stephen , Yu Timothy Z. , Anand Banmeet S. , Law Che-Leung , Sun Liping L. , Wesche Holger , Austin Richard J.
Published: September 2024

EC50 Values from TDCC assays with anti-DLL3 TriTAC in the T:A:C Configuration.
Figure S7 from HPN328, a Trispecific T Cell–Activating Protein Construct Targeting DLL3-Expressing Solid Tumors
Authors: Molloy Mary E. , Aaron Wade H. , Barath Manasi , Bush Mabel C. , Callihan Evan C. , Carlin Kevin , Cremin Michael , Evans Thomas , Guerrero Maria G. , Hemmati Golzar , Hundal Avneel S. , Lao Llewelyn , Laurie Payton , Lemon Bryan D. , Lin S.J. , O’Rear Jessica , Patnaik Purbasa , Sotelo Rocha Sony , Santiago Linda , Strobel Kathryn L. , Valenzuela Laura B. , Wu Chi-Heng , Yu Stephen , Yu Timothy Z. , Anand Banmeet S. , Law Che-Leung , Sun Liping L. , Wesche Holger , Austin Richard J.
Published: September 2024

HPN328 binding selectivity to human DLL1 and human DLL4.
Figure S6 from HPN328, a Trispecific T Cell–Activating Protein Construct Targeting DLL3-Expressing Solid Tumors
Authors: Molloy Mary E. , Aaron Wade H. , Barath Manasi , Bush Mabel C. , Callihan Evan C. , Carlin Kevin , Cremin Michael , Evans Thomas , Guerrero Maria G. , Hemmati Golzar , Hundal Avneel S. , Lao Llewelyn , Laurie Payton , Lemon Bryan D. , Lin S.J. , O’Rear Jessica , Patnaik Purbasa , Sotelo Rocha Sony , Santiago Linda , Strobel Kathryn L. , Valenzuela Laura B. , Wu Chi-Heng , Yu Stephen , Yu Timothy Z. , Anand Banmeet S. , Law Che-Leung , Sun Liping L. , Wesche Holger , Austin Richard J.
Published: September 2024

HPN328 binding cross-reactivity to mouse targets.
Figure S2 from HPN328, a Trispecific T Cell–Activating Protein Construct Targeting DLL3-Expressing Solid Tumors
Authors: Molloy Mary E. , Aaron Wade H. , Barath Manasi , Bush Mabel C. , Callihan Evan C. , Carlin Kevin , Cremin Michael , Evans Thomas , Guerrero Maria G. , Hemmati Golzar , Hundal Avneel S. , Lao Llewelyn , Laurie Payton , Lemon Bryan D. , Lin S.J. , O’Rear Jessica , Patnaik Purbasa , Sotelo Rocha Sony , Santiago Linda , Strobel Kathryn L. , Valenzuela Laura B. , Wu Chi-Heng , Yu Stephen , Yu Timothy Z. , Anand Banmeet S. , Law Che-Leung , Sun Liping L. , Wesche Holger , Austin Richard J.
Published: September 2024

HPN328 purity and biophysical stability.
Figure S19 from HPN328, a Trispecific T Cell–Activating Protein Construct Targeting DLL3-Expressing Solid Tumors
Authors: Molloy Mary E. , Aaron Wade H. , Barath Manasi , Bush Mabel C. , Callihan Evan C. , Carlin Kevin , Cremin Michael , Evans Thomas , Guerrero Maria G. , Hemmati Golzar , Hundal Avneel S. , Lao Llewelyn , Laurie Payton , Lemon Bryan D. , Lin S.J. , O’Rear Jessica , Patnaik Purbasa , Sotelo Rocha Sony , Santiago Linda , Strobel Kathryn L. , Valenzuela Laura B. , Wu Chi-Heng , Yu Stephen , Yu Timothy Z. , Anand Banmeet S. , Law Che-Leung , Sun Liping L. , Wesche Holger , Austin Richard J.
Published: September 2024

Repeat doses of HPN328 treatment in female cynomolgus monkeys leads to transient and dose dependent increases cytokines.
Figure S16 from HPN328, a Trispecific T Cell–Activating Protein Construct Targeting DLL3-Expressing Solid Tumors
Authors: Molloy Mary E. , Aaron Wade H. , Barath Manasi , Bush Mabel C. , Callihan Evan C. , Carlin Kevin , Cremin Michael , Evans Thomas , Guerrero Maria G. , Hemmati Golzar , Hundal Avneel S. , Lao Llewelyn , Laurie Payton , Lemon Bryan D. , Lin S.J. , O’Rear Jessica , Patnaik Purbasa , Sotelo Rocha Sony , Santiago Linda , Strobel Kathryn L. , Valenzuela Laura B. , Wu Chi-Heng , Yu Stephen , Yu Timothy Z. , Anand Banmeet S. , Law Che-Leung , Sun Liping L. , Wesche Holger , Austin Richard J.
Published: September 2024

HPN328 binds to the MC38-hDLL3 cell line.
Figure S12 from HPN328, a Trispecific T Cell–Activating Protein Construct Targeting DLL3-Expressing Solid Tumors
Authors: Molloy Mary E. , Aaron Wade H. , Barath Manasi , Bush Mabel C. , Callihan Evan C. , Carlin Kevin , Cremin Michael , Evans Thomas , Guerrero Maria G. , Hemmati Golzar , Hundal Avneel S. , Lao Llewelyn , Laurie Payton , Lemon Bryan D. , Lin S.J. , O’Rear Jessica , Patnaik Purbasa , Sotelo Rocha Sony , Santiago Linda , Strobel Kathryn L. , Valenzuela Laura B. , Wu Chi-Heng , Yu Stephen , Yu Timothy Z. , Anand Banmeet S. , Law Che-Leung , Sun Liping L. , Wesche Holger , Austin Richard J.
Published: September 2024

IHC staining of NCI-H82 xenograft tumors.
Figure S11 from HPN328, a Trispecific T Cell–Activating Protein Construct Targeting DLL3-Expressing Solid Tumors
Authors: Molloy Mary E. , Aaron Wade H. , Barath Manasi , Bush Mabel C. , Callihan Evan C. , Carlin Kevin , Cremin Michael , Evans Thomas , Guerrero Maria G. , Hemmati Golzar , Hundal Avneel S. , Lao Llewelyn , Laurie Payton , Lemon Bryan D. , Lin S.J. , O’Rear Jessica , Patnaik Purbasa , Sotelo Rocha Sony , Santiago Linda , Strobel Kathryn L. , Valenzuela Laura B. , Wu Chi-Heng , Yu Stephen , Yu Timothy Z. , Anand Banmeet S. , Law Che-Leung , Sun Liping L. , Wesche Holger , Austin Richard J.
Published: September 2024

TDCC co-cultures show no secretion of cytokines in the presence DLL3 negative tumor cell line.
Supplementary Figures from Pretargeted Radioimmunotherapy with the Novel Anti-oxMIF/HSG Bispecific Antibody ON105 Results in Significant Tumor Regression in Murine Models of Cancer
Authors: Puchol Tarazona Alejandro A. , Schinagl Alexander , Mirkina Irina , Rossmueller Gregor , Kerschbaumer Randolf J. , Bachmann Friedmund , Thiele Michael
Published: September 2024

Contains supplementary figures S1 to S6
Figure S4 from Pretargeted Radioimmunotherapy with the Novel Anti-oxMIF/HSG Bispecific Antibody ON105 Results in Significant Tumor Regression in Murine Models of Cancer
Authors: Puchol Tarazona Alejandro A. , Schinagl Alexander , Mirkina Irina , Rossmueller Gregor , Kerschbaumer Randolf J. , Bachmann Friedmund , Thiele Michael
Published: September 2024

Figure S4
Supplementary Table S3 from A Senescence-Mimicking (Senomimetic) VEGFR TKI Side Effect Primes Tumor Immune Responses via IFN/STING Signaling
Authors: Dolan Melissa , Shi Yuhao , Mastri Michalis , Long Mark D. , McKenery Amber , Hill James W. , Vaghi Cristina , Benzekry Sebastien , Barbi Joseph , Ebos John M.L.
Published: September 2024

Supplementary Table S3: Primer sequences used in qRT-PCR.
Supplementary Table S2 from A Senescence-Mimicking (Senomimetic) VEGFR TKI Side Effect Primes Tumor Immune Responses via IFN/STING Signaling
Authors: Dolan Melissa , Shi Yuhao , Mastri Michalis , Long Mark D. , McKenery Amber , Hill James W. , Vaghi Cristina , Benzekry Sebastien , Barbi Joseph , Ebos John M.L.
Published: September 2024

Supplementary Table S2: List of SM+ and SM- signature genes.
Supplementary Figure S5 from A Senescence-Mimicking (Senomimetic) VEGFR TKI Side Effect Primes Tumor Immune Responses via IFN/STING Signaling
Authors: Dolan Melissa , Shi Yuhao , Mastri Michalis , Long Mark D. , McKenery Amber , Hill James W. , Vaghi Cristina , Benzekry Sebastien , Barbi Joseph , Ebos John M.L.
Published: September 2024

Supplementary Figure S5: Extended data from Fig 5 - CD8 T-cell stimulating effects of SM+ cells off-set the immune-suppressive secretory effects. (A-B) Log2FC of %Divided, %GRMB+, or %IFNγ+ gated CD8+ stimulated splenocytes following treatment with (A) CM derived from EMT6CaR tumor cells or (B) co-cultured with EMT6CaR compared to respective parental controls evaluated by flow cytometry (n=3-4). (C-D) %Divided, %GRMB+, or %IFNγ+ gated CD8+ stimulated splenocytes following treatment with (C) CM derived from 4T1AxR tumor cells or (D) co-cultured with 4T1AxR compared to respective parental controls evaluated by flow cytometry (n=3). (E-F) %Divided, %GRMB+, or %IFNγ + gated CD8+ stimulated splenocytes following treatment with (E) CM derived from EMT6CaR tumor cells or (F) co-cultured with EMT6CaR compared to parental controls evaluated by flow cytometry (n=3-4). (G-H) Log2FC of %Divided, %GRMB+, or % IFNγ + gated CD8+ stimulated splenocytes following treatment with (G) CM derived from EMT6CaR SM+ tumor cells or (H) co-cultured with EMT6CaR SM+ compared to SM- controls evaluated by flow cytometry (n=3-4). (I-J) %Divided, %GRMB+, or %IFNγ+ gated CD8+ stimulated splenocytes following treatment with (I) CM derived from 4T1AxR SM+ tumor cells or (J) co-cultured with 4T1AxR SM+ compared to SM- controls evaluated by flow cytometry (n=3-9). (K-L) %Divided, %GRMB+, or %IFNy+ gated CD8+ stimulated splenocytes following treatment with (K) CM derived from EMT6CaR SM+ tumor cells or (L) co-cultured with EMT6CaR SM+ compared to SM- controls evaluated by flow cytometry (n=3-4). Parental (P); Metastatic parental control for EMT6CaR (M); Axitinib-resistant (AxR); Cabozantinib-resistant (CaR); Senescence-marker (SM); Granzyme B (GRMB); Interferon gamma (IFNγ); Conditioned media (CM); Fold Change (FC); Standard Deviation (SD); Normalized (Norm.); Quantitative data shown as mean ± SD. * p<0.05; ** p<0.01; ***n p<0.001; **** p<0.0001.
Supplementary Figure S2 from A Senescence-Mimicking (Senomimetic) VEGFR TKI Side Effect Primes Tumor Immune Responses via IFN/STING Signaling
Authors: Dolan Melissa , Shi Yuhao , Mastri Michalis , Long Mark D. , McKenery Amber , Hill James W. , Vaghi Cristina , Benzekry Sebastien , Barbi Joseph , Ebos John M.L.
Published: September 2024

Figure S2: SM+ and SM- signature genes in 4T1 variants used to generate the SM+ T score. (A) SM+ signature gene expression using log2CPMs in 4T1P, 4T1AxR, 4T1AxR SM+ and 4T1AxR SM- cells. (B) SM- cell signature gene expression using log2CPMs in 4T1P, 4T1AxR, 4T1AxR SM+ and 4T1AxR SM- cells. Parental (P); Axitinib-resistant (AxR); Senescence-marker (SM); Counts per million (CPM)
Figure S3 from IL-15/IL-15Rα-Fc-Fusion Protein XmAb24306 Potentiates Activity of CD3 Bispecific Antibodies through Enhancing T-Cell Expansion
Authors: Li Ji , Clark Robyn , Slaga Dionysos , Avery Kendra , Liu Ke , Schubbert Suzanne , Varma Rajat , Chiang Eugene , Totpal Klara , Bernett Matthew J. , Holder Patrick G. , Junttila Teemu T.
Published: September 2024

Supplementary figure S2 shows extended data on the effects of XmAb24306 on TDB-induced T-cell proliferation
Supplementary Table S4 from Combining EHMT and PARP Inhibition: A Strategy to Diminish Therapy-Resistant Ovarian Cancer Tumor Growth while Stimulating Immune Activation
Authors: Nguyen Lily L. , Watson Zachary L. , Ortega Raquel , Woodruff Elizabeth R. , Jordan Kimberly R. , Iwanaga Ritsuko , Yamamoto Tomomi M. , Bailey Courtney A. , To Francis , Jeong Abigail D. , Guntupalli Saketh R. , Behbakht Kian , Gibaja Veronica , Arnoult Nausica , Cocozaki Alexis , Chuong Edward B. , Bitler Benjamin G.
Published: September 2024

Supplementary Table S4 shows the quantitative PCR primer sequences.
Supplementary Table S1 from Combining EHMT and PARP Inhibition: A Strategy to Diminish Therapy-Resistant Ovarian Cancer Tumor Growth while Stimulating Immune Activation
Authors: Nguyen Lily L. , Watson Zachary L. , Ortega Raquel , Woodruff Elizabeth R. , Jordan Kimberly R. , Iwanaga Ritsuko , Yamamoto Tomomi M. , Bailey Courtney A. , To Francis , Jeong Abigail D. , Guntupalli Saketh R. , Behbakht Kian , Gibaja Veronica , Arnoult Nausica , Cocozaki Alexis , Chuong Edward B. , Bitler Benjamin G.
Published: September 2024

Supplementary Table S1 shows the patient information from the ex vivo primary tumors.
Supplementary Figure S5 from Combining EHMT and PARP Inhibition: A Strategy to Diminish Therapy-Resistant Ovarian Cancer Tumor Growth while Stimulating Immune Activation
Authors: Nguyen Lily L. , Watson Zachary L. , Ortega Raquel , Woodruff Elizabeth R. , Jordan Kimberly R. , Iwanaga Ritsuko , Yamamoto Tomomi M. , Bailey Courtney A. , To Francis , Jeong Abigail D. , Guntupalli Saketh R. , Behbakht Kian , Gibaja Veronica , Arnoult Nausica , Cocozaki Alexis , Chuong Edward B. , Bitler Benjamin G.
Published: September 2024

Supplementary Figure S5 shows the transcriptional changes of genes and transposable elements via volcano plot and pathway analysis due to the treatment of primary ex vivo tumors following single treatments.
Supplementary Figure S4 from Combining EHMT and PARP Inhibition: A Strategy to Diminish Therapy-Resistant Ovarian Cancer Tumor Growth while Stimulating Immune Activation
Authors: Nguyen Lily L. , Watson Zachary L. , Ortega Raquel , Woodruff Elizabeth R. , Jordan Kimberly R. , Iwanaga Ritsuko , Yamamoto Tomomi M. , Bailey Courtney A. , To Francis , Jeong Abigail D. , Guntupalli Saketh R. , Behbakht Kian , Gibaja Veronica , Arnoult Nausica , Cocozaki Alexis , Chuong Edward B. , Bitler Benjamin G.
Published: September 2024

Supplementary Figure S4 shows the in vivo model of HGS2 olaparib-resistant cells at day 0 and day 14 of treatment. It also shows mouse weight over the course of the treatment.
Supplementary Table 1 from Enhancing Neutrophil Cytotoxicity of a Panel of Clinical EGFR Antibodies by Fc Engineering to IgA3.0
Authors: Chan Chilam , Jansen J.H. Marco , Hendriks Ilona S.T. , van der Peet Ida C. , Verdonschot Meggy E.L. , Passchier Elsemieke M. , Tsioumpekou Maria , Nederend Maaike , Klomp Sharon A. , Valerius Thomas , Peipp Matthias , Leusen Jeanette H.W. , Olofsen Patricia A.
Published: September 2024

Supplementary Table 1: Antibody sequences
Supplementary Figure 2 from Enhancing Neutrophil Cytotoxicity of a Panel of Clinical EGFR Antibodies by Fc Engineering to IgA3.0
Authors: Chan Chilam , Jansen J.H. Marco , Hendriks Ilona S.T. , van der Peet Ida C. , Verdonschot Meggy E.L. , Passchier Elsemieke M. , Tsioumpekou Maria , Nederend Maaike , Klomp Sharon A. , Valerius Thomas , Peipp Matthias , Leusen Jeanette H.W. , Olofsen Patricia A.
Published: September 2024

Supplementary Figure 2: Binding characteristics of clinical IgG EGFR antibodies.
Data from Pretargeted Radioimmunotherapy with the Novel Anti-oxMIF/HSG Bispecific Antibody ON105 Results in Significant Tumor Regression in Murine Models of Cancer
Authors: Puchol Tarazona Alejandro A. , Schinagl Alexander , Mirkina Irina , Rossmueller Gregor , Kerschbaumer Randolf J. , Bachmann Friedmund , Thiele Michael
Published: September 2024

Abstract
Radioimmunotherapy (RIT) uses monoclonal antibodies to deliver radionuclides to cancer cells or the tumor microenvironment and has shown promise in treating localized and diffuse tumors. Although RIT agents have gained FDA/EMA approval for certain hematologic malignancies, effectiveness of RIT in treating solid tumors remains limited. In this study, we present PreTarg-it, a novel approach for pretargeted RIT, providing optimized delivery of payloads in a two-step regimen. The effectiveness of PreTarg-it is demonstrated by a powerful combination of ON105, a novel bispecific antibody against both oxidized macrophage migration inhibitory factor (oxMIF) and the histamine-succinyl-glycyl (HSG) hapten, as the first component and the radioactively labeled DOTA-di-HSG peptide as the second component in murine models of cancer. Mice bearing either subcutaneous mouse colorectal CT26 or human pancreatic CFPAC-1 tumors received an i.v. injection of ON105. After ON105 had accumulated in the tumor and cleared from circulation to approximately 1% to 3% of its peak concentration, 177Lu-DOTA-di-HSG peptide was administered. A single PreTarg-it treatment cycle resulted in tumor regression when mice bearing CT26 tumors were given the highest treatment dose with a pretargeting delay of 3 days. Administered with a 5-day interval, the highest dose arrested tumor growth in both CT26 syngrafts and CFPAC-1 xenografts. In all cases, the highest treatment dose resulted in 100% survival at the study endpoint, whereas the control cohorts showed 0% and 60% survival in the CT26 and CFPAC-1 models, respectively. Therefore, PreTarg-it holds potential as a novel and potent therapy for patients with hard-to-treat solid tumors, such as pancreatic cancer, as well as those with late-stage malignancies.
Data from Enhancing Neutrophil Cytotoxicity of a Panel of Clinical EGFR Antibodies by Fc Engineering to IgA3.0
Authors: Chan Chilam , Jansen J.H. Marco , Hendriks Ilona S.T. , van der Peet Ida C. , Verdonschot Meggy E.L. , Passchier Elsemieke M. , Tsioumpekou Maria , Nederend Maaike , Klomp Sharon A. , Valerius Thomas , Peipp Matthias , Leusen Jeanette H.W. , Olofsen Patricia A.
Published: September 2024

Abstract
EGFR plays an essential role in cellular signaling pathways that regulate cell growth, proliferation, and survival and is often dysregulated in cancer. Several monoclonal IgG antibodies have been clinically tested over the years, which exert their function via blocking the ligand binding domain (thereby inhibiting downstream signaling) and inducing Fc-related effector functions, such as antibody-dependent cellular cytotoxicity (ADCC) and antibody-dependent cellular phagocytosis (ADCP). However, these IgG antibodies do not optimally recruit neutrophils, which are the most abundant white blood cell population in humans. Therefore, we reformatted six therapeutic EGFR antibodies (cetuximab, panitumumab, nimotuzumab, necitumumab, zalutumumab, and matuzumab) into the IgA3.0 format, which is an IgA2 isotype adapted for clinical application. Reformatting these antibodies preserved Fab-mediated functions such as EGFR binding, growth inhibition, and ligand blockade. In addition, whole leukocyte ADCC was significantly increased when using this panel of IgA3.0 antibodies compared with their respective IgG counterparts, with no major differences between IgA3.0 antibodies. In vivo, IgA3.0 matuzumab outperformed the other antibodies, resulting in the strongest suppression of tumor outgrowth in a long intraperitoneal model. We showed that neutrophils are important for the suppression of tumor outgrowth. IgA3.0 matuzumab exhibited reduced receptor internalization compared with the other antibodies, possibly accounting for its superior in vivo Fc-mediated tumor cell killing efficacy. In conclusion, reformatting EGFR antibodies into an IgA3.0 format increased Fc-mediated killing while retaining Fab-mediated functions and could therefore be a good alternative for the currently available antibody therapies.
Supplementary Figure S7 from Crizotinib Enhances PARP Inhibitor Efficacy in Ovarian Cancer Cells and Xenograft Models by Inducing Autophagy
Authors: Santiago-O’Farrill Janice M. , Blessing Bollu Alicia , Yang Hailing , Orellana Vivian , Pina Marc , Zhang Xudong , Liu Jinsong , Bast Robert C. , Lu Zhen
Published: September 2024

Supplementary Figure S7 shows the effect of knocking down ALK on the sensitivity of ovarian cancer cells to Olaparib/crizotinib combination
Supplementary Figure S5 from Crizotinib Enhances PARP Inhibitor Efficacy in Ovarian Cancer Cells and Xenograft Models by Inducing Autophagy
Authors: Santiago-O’Farrill Janice M. , Blessing Bollu Alicia , Yang Hailing , Orellana Vivian , Pina Marc , Zhang Xudong , Liu Jinsong , Bast Robert C. , Lu Zhen
Published: September 2024

Supplementary Figure S5 shows induction of ROS, DNA damage and apoptosis after treatment with Olaparib and crizotinib
Supplementary Figure S3 from Crizotinib Enhances PARP Inhibitor Efficacy in Ovarian Cancer Cells and Xenograft Models by Inducing Autophagy
Authors: Santiago-O’Farrill Janice M. , Blessing Bollu Alicia , Yang Hailing , Orellana Vivian , Pina Marc , Zhang Xudong , Liu Jinsong , Bast Robert C. , Lu Zhen
Published: September 2024

Supplementary Figure S3 shows the viability of ovarian cancer cells treated with other PARPi in combination with Olaparib
Supplementary Table 4 from Hepatitis B Virus X Protein Represses Expression of Tumor Suppressor PTPN18 in Hepatocellular Carcinoma
Authors: Zhou Zhenyu , Yu Wei , Li Huoming , Shi Juanyi , Meng Shiyu , Yan Yongcong , Chen Ruibin , Liu Haohan , Wang Jie , Sun Jian , Xiao Zhiyu , Zhang Jianlong
Published: September 2024

The data of phospho-protein microarray.
Supplementary Figure 6 from Hepatitis B Virus X Protein Represses Expression of Tumor Suppressor PTPN18 in Hepatocellular Carcinoma
Authors: Zhou Zhenyu , Yu Wei , Li Huoming , Shi Juanyi , Meng Shiyu , Yan Yongcong , Chen Ruibin , Liu Haohan , Wang Jie , Sun Jian , Xiao Zhiyu , Zhang Jianlong
Published: September 2024

HBx inhibits PTPN18 expression through miR-128-3p.
Supplementary Data from Hepatitis B Virus X Protein Represses Expression of Tumor Suppressor PTPN18 in Hepatocellular Carcinoma
Authors: Zhou Zhenyu , Yu Wei , Li Huoming , Shi Juanyi , Meng Shiyu , Yan Yongcong , Chen Ruibin , Liu Haohan , Wang Jie , Sun Jian , Xiao Zhiyu , Zhang Jianlong
Published: September 2024

Supplementary materials and methods
Table 3 from Intrinsic Epigenetic State of Primary Osteosarcoma Drives Metastasis
Authors: Singh Irtisha , Rainusso Nino , Kurenbekova Lyazat , Nirala Bikesh K. , Dou Juan , Muruganandham Abhinaya , Yustein Jason T.
Published: September 2024

Supplementary Table 3
Table 2 from Intrinsic Epigenetic State of Primary Osteosarcoma Drives Metastasis
Authors: Singh Irtisha , Rainusso Nino , Kurenbekova Lyazat , Nirala Bikesh K. , Dou Juan , Muruganandham Abhinaya , Yustein Jason T.
Published: September 2024

Supplementary Table 2
Table 1 from Intrinsic Epigenetic State of Primary Osteosarcoma Drives Metastasis
Authors: Singh Irtisha , Rainusso Nino , Kurenbekova Lyazat , Nirala Bikesh K. , Dou Juan , Muruganandham Abhinaya , Yustein Jason T.
Published: September 2024

Clinical and Histological Characteristics of Patient Specimens
Figure S4 from Intrinsic Epigenetic State of Primary Osteosarcoma Drives Metastasis
Authors: Singh Irtisha , Rainusso Nino , Kurenbekova Lyazat , Nirala Bikesh K. , Dou Juan , Muruganandham Abhinaya , Yustein Jason T.
Published: September 2024

Effects of PREX1 knockdown on localized PDX-derived TCCC-OS94 cells.
Figure S1 from Intrinsic Epigenetic State of Primary Osteosarcoma Drives Metastasis
Authors: Singh Irtisha , Rainusso Nino , Kurenbekova Lyazat , Nirala Bikesh K. , Dou Juan , Muruganandham Abhinaya , Yustein Jason T.
Published: September 2024

Hierarchical clustering of signal intensity (tags per million) of top 20% most variable regions by median absolute deviation (n = 31,690) of all H3K27ac enriched peaks.
Supplementary Video 8 from Mechanisms of Glioblastoma Replication: Ca2+ Flares and Cl− Currents
Authors: Li Yunzhen , Sanchez Triviño Cesar Adolfo , Hernandez Andres , Mortal Simone , Spada Federica , Krivosheia Ilona , Franco Nicoletta , Spelat Renza , Cesselli Daniela , Manini Ivana , Skrap Miran , Menini Anna , Cesca Fabrizia , Torre Vincent
Published: September 2024

Cl–dependent cell volume changes.
Supplementary Video 6 from Mechanisms of Glioblastoma Replication: Ca2+ Flares and Cl− Currents
Authors: Li Yunzhen , Sanchez Triviño Cesar Adolfo , Hernandez Andres , Mortal Simone , Spada Federica , Krivosheia Ilona , Franco Nicoletta , Spelat Renza , Cesselli Daniela , Manini Ivana , Skrap Miran , Menini Anna , Cesca Fabrizia , Torre Vincent
Published: September 2024

Live imaging of Cl- and Ca2+transients during a complete mitotic cycle.
Supplementary Video 4 from Mechanisms of Glioblastoma Replication: Ca2+ Flares and Cl− Currents
Authors: Li Yunzhen , Sanchez Triviño Cesar Adolfo , Hernandez Andres , Mortal Simone , Spada Federica , Krivosheia Ilona , Franco Nicoletta , Spelat Renza , Cesselli Daniela , Manini Ivana , Skrap Miran , Menini Anna , Cesca Fabrizia , Torre Vincent
Published: September 2024

Calcium flares in patient-derived GSCs.
Supplementary Video 3 from Mechanisms of Glioblastoma Replication: Ca2+ Flares and Cl− Currents
Authors: Li Yunzhen , Sanchez Triviño Cesar Adolfo , Hernandez Andres , Mortal Simone , Spada Federica , Krivosheia Ilona , Franco Nicoletta , Spelat Renza , Cesselli Daniela , Manini Ivana , Skrap Miran , Menini Anna , Cesca Fabrizia , Torre Vincent
Published: September 2024

Ca2+ flares are evident during the late phase of mitosis.
Supplementary Figure S6 from USP44 Overexpression Drives a MYC-Like Gene Expression Program in Neuroblastoma through Epigenetic Reprogramming
Authors: Ekstrom Thomas L. , Hussain Sajjad , Bedekovics Tibor , Ali Asma , Paolini Lucia , Mahmood Hina , Rosok Raya M. , Koster Jan , Johnsen Steven A. , Galardy Paul J.
Published: September 2024

USP44 expression declines with development.
Supplementary Figure S4 from USP44 Overexpression Drives a MYC-Like Gene Expression Program in Neuroblastoma through Epigenetic Reprogramming
Authors: Ekstrom Thomas L. , Hussain Sajjad , Bedekovics Tibor , Ali Asma , Paolini Lucia , Mahmood Hina , Rosok Raya M. , Koster Jan , Johnsen Steven A. , Galardy Paul J.
Published: September 2024

Cell lines used in this study.
Figure S2 from Mechanisms of Glioblastoma Replication: Ca2+ Flares and Cl− Currents
Authors: Li Yunzhen , Sanchez Triviño Cesar Adolfo , Hernandez Andres , Mortal Simone , Spada Federica , Krivosheia Ilona , Franco Nicoletta , Spelat Renza , Cesselli Daniela , Manini Ivana , Skrap Miran , Menini Anna , Cesca Fabrizia , Torre Vincent
Published: September 2024

Change of volume during the transition from metaphase to telophase.
Figure S14 from Mechanisms of Glioblastoma Replication: Ca2+ Flares and Cl− Currents
Authors: Li Yunzhen , Sanchez Triviño Cesar Adolfo , Hernandez Andres , Mortal Simone , Spada Federica , Krivosheia Ilona , Franco Nicoletta , Spelat Renza , Cesselli Daniela , Manini Ivana , Skrap Miran , Menini Anna , Cesca Fabrizia , Torre Vincent
Published: September 2024

Toxicity analysis of NFA and CBX on U87 cells.
Figure S13 from Mechanisms of Glioblastoma Replication: Ca2+ Flares and Cl− Currents
Authors: Li Yunzhen , Sanchez Triviño Cesar Adolfo , Hernandez Andres , Mortal Simone , Spada Federica , Krivosheia Ilona , Franco Nicoletta , Spelat Renza , Cesselli Daniela , Manini Ivana , Skrap Miran , Menini Anna , Cesca Fabrizia , Torre Vincent
Published: September 2024

Toxicity and functional assays on mouse cortical neurons upon treatment with increasing concentrations of NFA and CBX.
Supplementary Figure S12 from USP44 Overexpression Drives a MYC-Like Gene Expression Program in Neuroblastoma through Epigenetic Reprogramming
Authors: Ekstrom Thomas L. , Hussain Sajjad , Bedekovics Tibor , Ali Asma , Paolini Lucia , Mahmood Hina , Rosok Raya M. , Koster Jan , Johnsen Steven A. , Galardy Paul J.
Published: September 2024

USP44 alters the epigenome and regulates gene expression.
Figure S12 from Mechanisms of Glioblastoma Replication: Ca2+ Flares and Cl− Currents
Authors: Li Yunzhen , Sanchez Triviño Cesar Adolfo , Hernandez Andres , Mortal Simone , Spada Federica , Krivosheia Ilona , Franco Nicoletta , Spelat Renza , Cesselli Daniela , Manini Ivana , Skrap Miran , Menini Anna , Cesca Fabrizia , Torre Vincent
Published: September 2024

Expression of p53 in U87 cells increases after treatment with NFA and CBX.
Supplementary Figure S11 from USP44 Overexpression Drives a MYC-Like Gene Expression Program in Neuroblastoma through Epigenetic Reprogramming
Authors: Ekstrom Thomas L. , Hussain Sajjad , Bedekovics Tibor , Ali Asma , Paolini Lucia , Mahmood Hina , Rosok Raya M. , Koster Jan , Johnsen Steven A. , Galardy Paul J.
Published: September 2024

Processes altered by USP44.
Supplementary Table S8 from miR-497 Target Gene Regulatory Network in Angiosarcoma
Authors: Benton Annaleigh , Moriarty Noah M. , Terwilliger Emma , Liu Bozhi , Murphy Ant , Maluvac Hannah , Shu Mae , Gartenhaus Lauren E. , Janson Nimod D. , Pfeffer Claire M. , Utturkar Sagar M. , Parkinson Elizabeth I. , Lanman Nadia A. , Hanna Jason A.
Published: September 2024

Gene ontology analysis of common miR-497 mimic downregulated genes and upregulated genes in ADcKO tumors.
Figure S9 from Clinically Relevant Humanized Mouse Models of Metastatic Prostate Cancer Facilitate Therapeutic Evaluation
Authors: Kostlan Raymond J. , Phoenix John T. , Budreika Audris , Ferrari Marina G. , Khurana Neetika , Choi Jae E. , Juckette Kristin , Mahapatra Somnath , McCollum Brooke L. , Moskal Russell , Mannan Rahul , Qiao Yuanyuan , Vander Griend Donald J. , Chinnaiyan Arul M. , Kregel Steven
Published: September 2024

Immune-profile in huNOG-EXL 22Rv1 xenograft spleen.
Figure S8 from Clinically Relevant Humanized Mouse Models of Metastatic Prostate Cancer Facilitate Therapeutic Evaluation
Authors: Kostlan Raymond J. , Phoenix John T. , Budreika Audris , Ferrari Marina G. , Khurana Neetika , Choi Jae E. , Juckette Kristin , Mahapatra Somnath , McCollum Brooke L. , Moskal Russell , Mannan Rahul , Qiao Yuanyuan , Vander Griend Donald J. , Chinnaiyan Arul M. , Kregel Steven
Published: September 2024

22Rv1 growth in huNOG-EXL and NOG mice.
Supplementary Figure S6 from miR-497 Target Gene Regulatory Network in Angiosarcoma
Authors: Benton Annaleigh , Moriarty Noah M. , Terwilliger Emma , Liu Bozhi , Murphy Ant , Maluvac Hannah , Shu Mae , Gartenhaus Lauren E. , Janson Nimod D. , Pfeffer Claire M. , Utturkar Sagar M. , Parkinson Elizabeth I. , Lanman Nadia A. , Hanna Jason A.
Published: September 2024

Promoter methylation and Kaplan-Meier survival plot of miR-497 expression in sarcomas.