bluuebunny/crossref_metadata_2025 huggingface dataset:
Duvelisib with Docetaxel for Patients with Anti–PD-1 Refractory, Recurrent, or Metastatic Head and Neck Squamous Cell Carcinoma
Authors: Hanna Glenn J. , Oakley L. B. , Shi R. , ONeill A. , Shin K. Y. , Scarfo N. , Sehgal K. , Dennis M. J. , Quinn N. , Jo V. Y. , Wong K. , Shvyrkova A. , Kushnarev V. , Shanthappa B. U. , Tkachuk A. , Kryukov K. , Sarachakov A. , Svekolkin V. , Lennerz J. , Waters S. , Haddad R. I.
Published: December 2024

Purpose:

Treatments after anti–PD-1 therapy for patients with recurrent, metastatic head and neck squamous cell carcinoma (HNSCC) are limited. Blocking PI3K signaling may lead to tumor immunomodulation and enhanced taxane sensitivity. This phase 2 trial evaluated dual, selective PI3Kδ/γ inhibition with docetaxel in patients with anti–PD-1 refractory recurrent, metastatic HNSCC.

Patients and Methods:

Patients received duvelisib (25 mg orally twice daily) with docetaxel (75 mg/m2 IV) every 21 days. The primary endpoint was overall response rate (RECIST v1.1), using a Simon two-stage design. Secondary endpoints were safety, progression-free survival, and overall survival, and exploratory endpoints were correlating immunologic and genomic parameters with outcomes.

Results:

From 11/1/21 to 10/10/23, 26 patients were enrolled (median age: 64, 96% men, 54% with human papillomavirus+ disease; primary site: 12 oropharynx, 11 oral cavity, and 3 larynx/hypopharynx. The best overall response rate was 19% [5/26; 95% confidence interval (CI), 6.8%–40.7%]. All were partial responses [median duration: 5.1 months (0.7–15.5)]; 46% (12/26) exhibited stable disease, and 32% (8/26) exhibited progression (1 unevaluable). Two patients remain on-treatment at data cutoff; 25% (6/24) came off for toxicity. Grade 3+ treatment-related adverse events were observed in 50% (13/26), most often elevated liver function tests (6, 23%). No deaths were treatment-related. At median follow-up of 6.5 months (0.7–26), median progression-free survival was 2.8 months (95% CI, 1.9–7.0); 17/26 patients had died. Median overall survival was 10.2 months (95% CI, 6.7–15.9), favoring human papillomavirus–negative patients. Greater tumor CD3+/CD8+ T-cell infiltration trended with improved outcomes.

Conclusions:

We report a favorable response rate when combining a selective PI3K pathway inhibitor and taxane in patients with anti–PD-1 refractory HNSCC.
Supplementary Figure 4 from Discovery of RGT-018: A Potent, Selective, and Orally Bioavailable SOS1 Inhibitor for KRAS-Driven Cancers
Authors: Xiao Fei , Wang Kailiang , Wang Xinjuan , Li Huijuan , Hu Zhilong , Ren Xiaoming , Huang Wei , Feng Teng , Yao Lili , Lin Jing , Li Chunlai , Zhang Zhuanzhuan , Mei Liufeng , Zhu Xiaotian , Zhong Wenge , Xie Zhi
Published: December 2024

Supplementary Figure 4
Supplementary Figure 2 from Discovery of RGT-018: A Potent, Selective, and Orally Bioavailable SOS1 Inhibitor for KRAS-Driven Cancers
Authors: Xiao Fei , Wang Kailiang , Wang Xinjuan , Li Huijuan , Hu Zhilong , Ren Xiaoming , Huang Wei , Feng Teng , Yao Lili , Lin Jing , Li Chunlai , Zhang Zhuanzhuan , Mei Liufeng , Zhu Xiaotian , Zhong Wenge , Xie Zhi
Published: December 2024

Supplementary Figure 2
Table S9 from Discovery and Characterization of Brigimadlin, a Novel and Highly Potent MDM2–p53 Antagonist Suitable for Intermittent Dose Schedules
Authors: Gollner Andreas , Rudolph Dorothea , Weyer-Czernilofsky Ulrike , Baumgartinger Rosa , Jung Peter , Weinstabl Harald , Ramharter Jürgen , Grempler Rolf , Quant Jens , Rinnenthal Jörg , Pérez Pitarch Alejandro , Golubovic Bojana , Gerlach Daniel , Bader Gerd , Wetzel Kristiane , Otto Sebastian , Mandl Christian , Boehmelt Guido , McConnell Darryl B. , Kraut Norbert , Sini Patrizia
Published: December 2024

Brigimadlin in vitro activity in normal cell lines.
Table S8 from Discovery and Characterization of Brigimadlin, a Novel and Highly Potent MDM2–p53 Antagonist Suitable for Intermittent Dose Schedules
Authors: Gollner Andreas , Rudolph Dorothea , Weyer-Czernilofsky Ulrike , Baumgartinger Rosa , Jung Peter , Weinstabl Harald , Ramharter Jürgen , Grempler Rolf , Quant Jens , Rinnenthal Jörg , Pérez Pitarch Alejandro , Golubovic Bojana , Gerlach Daniel , Bader Gerd , Wetzel Kristiane , Otto Sebastian , Mandl Christian , Boehmelt Guido , McConnell Darryl B. , Kraut Norbert , Sini Patrizia
Published: December 2024

In vitro activity of MDM2–p53 antagonists brigimadlin, alrizomadlin and milademetan in MDM2-amplified cell lines and MDM2 non-amplified cell lines.
Supplementary Table S1 from TR-107, an Agonist of Caseinolytic Peptidase Proteolytic Subunit, Disrupts Mitochondrial Metabolism and Inhibits the Growth of Human Colorectal Cancer Cells
Authors: Giarrizzo Michael , LaComb Joseph F. , Patel Hetvi R. , Reddy Rohan G. , Haley John D. , Graves Lee M. , Iwanowicz Edwin J. , Bialkowska Agnieszka B.
Published: December 2024

Supplementary Table S1. Proteomics data
Table S4 from Discovery and Characterization of Brigimadlin, a Novel and Highly Potent MDM2–p53 Antagonist Suitable for Intermittent Dose Schedules
Authors: Gollner Andreas , Rudolph Dorothea , Weyer-Czernilofsky Ulrike , Baumgartinger Rosa , Jung Peter , Weinstabl Harald , Ramharter Jürgen , Grempler Rolf , Quant Jens , Rinnenthal Jörg , Pérez Pitarch Alejandro , Golubovic Bojana , Gerlach Daniel , Bader Gerd , Wetzel Kristiane , Otto Sebastian , Mandl Christian , Boehmelt Guido , McConnell Darryl B. , Kraut Norbert , Sini Patrizia
Published: December 2024

In vitro IC50 (AlphaScreen and CTG cell viability assay) of BI-0252, BI-0282, and brigimadlin
Table S13 from Discovery and Characterization of Brigimadlin, a Novel and Highly Potent MDM2–p53 Antagonist Suitable for Intermittent Dose Schedules
Authors: Gollner Andreas , Rudolph Dorothea , Weyer-Czernilofsky Ulrike , Baumgartinger Rosa , Jung Peter , Weinstabl Harald , Ramharter Jürgen , Grempler Rolf , Quant Jens , Rinnenthal Jörg , Pérez Pitarch Alejandro , Golubovic Bojana , Gerlach Daniel , Bader Gerd , Wetzel Kristiane , Otto Sebastian , Mandl Christian , Boehmelt Guido , McConnell Darryl B. , Kraut Norbert , Sini Patrizia
Published: December 2024

Total and unbound brigimadlin in humans and Crl:CD1(ICR) mice.
Supplementary Figure S6 from TR-107, an Agonist of Caseinolytic Peptidase Proteolytic Subunit, Disrupts Mitochondrial Metabolism and Inhibits the Growth of Human Colorectal Cancer Cells
Authors: Giarrizzo Michael , LaComb Joseph F. , Patel Hetvi R. , Reddy Rohan G. , Haley John D. , Graves Lee M. , Iwanowicz Edwin J. , Bialkowska Agnieszka B.
Published: December 2024

Supplementary Figure S6. Washout of TR-107 treatment suggests an irreversible inhibition of CRC cell viability. (A) HCT116 cells were treated in a 96-well plate format with vehicle control (0.1% DMSO) or indicated concentrations of TR-107 for 2, 4, 6, 8, 12, 24, and 72 hours. At each time point, wells were washed out twice with fresh media and replaced with fresh media lacking treatment up until 72 hours. Cell viability was assessed for all treatment durations after 72 hours. Data are presented as mean ± SD values (N=6). *, P < 0.05; **, P < 0.01; ***, P < 0.001; ****, P < 0.0001. (B) Western blot analysis of HCT116 cells after 24 hours of treatment with washout and 72 hours with no washout. HCT116 cells were treated with vehicle control (0.1% DMSO) or TR-107 10 nmol/L, 50 nmol/L, 1 μmol/L. Immunoblot was performed for ClpX, mtTFA, and β-actin as loading control.
Table S1 from Discovery and Characterization of Brigimadlin, a Novel and Highly Potent MDM2–p53 Antagonist Suitable for Intermittent Dose Schedules
Authors: Gollner Andreas , Rudolph Dorothea , Weyer-Czernilofsky Ulrike , Baumgartinger Rosa , Jung Peter , Weinstabl Harald , Ramharter Jürgen , Grempler Rolf , Quant Jens , Rinnenthal Jörg , Pérez Pitarch Alejandro , Golubovic Bojana , Gerlach Daniel , Bader Gerd , Wetzel Kristiane , Otto Sebastian , Mandl Christian , Boehmelt Guido , McConnell Darryl B. , Kraut Norbert , Sini Patrizia
Published: December 2024

Cell Lines.
Supplementary Methods from Discovery and Characterization of Brigimadlin, a Novel and Highly Potent MDM2–p53 Antagonist Suitable for Intermittent Dose Schedules
Authors: Gollner Andreas , Rudolph Dorothea , Weyer-Czernilofsky Ulrike , Baumgartinger Rosa , Jung Peter , Weinstabl Harald , Ramharter Jürgen , Grempler Rolf , Quant Jens , Rinnenthal Jörg , Pérez Pitarch Alejandro , Golubovic Bojana , Gerlach Daniel , Bader Gerd , Wetzel Kristiane , Otto Sebastian , Mandl Christian , Boehmelt Guido , McConnell Darryl B. , Kraut Norbert , Sini Patrizia
Published: December 2024

Supplementary Methods and Appendix
Supplementary Figure S11 from TR-107, an Agonist of Caseinolytic Peptidase Proteolytic Subunit, Disrupts Mitochondrial Metabolism and Inhibits the Growth of Human Colorectal Cancer Cells
Authors: Giarrizzo Michael , LaComb Joseph F. , Patel Hetvi R. , Reddy Rohan G. , Haley John D. , Graves Lee M. , Iwanowicz Edwin J. , Bialkowska Agnieszka B.
Published: December 2024

Supplementary Figure S11. TR-107 treatment reduces integrated stress response and antioxidant protein expression in CRC cells. Immunoblotting of ATF3 and ATF4 and densitometry analysis of colorectal cancer cells (A) DLD-1, (B) LS 1034, (C) HT29, and (D) HCT116 cells treated with TR-107 (50 nmol/L) for 24 and 72 hours indicate a reduction in stress response. Data are presented as mean ± SD values (N=3). *, P < 0.05; **, P < 0.01; ***, P < 0.001; ****, P < 0.0001.
Figure S1 from Discovery and Characterization of Brigimadlin, a Novel and Highly Potent MDM2–p53 Antagonist Suitable for Intermittent Dose Schedules
Authors: Gollner Andreas , Rudolph Dorothea , Weyer-Czernilofsky Ulrike , Baumgartinger Rosa , Jung Peter , Weinstabl Harald , Ramharter Jürgen , Grempler Rolf , Quant Jens , Rinnenthal Jörg , Pérez Pitarch Alejandro , Golubovic Bojana , Gerlach Daniel , Bader Gerd , Wetzel Kristiane , Otto Sebastian , Mandl Christian , Boehmelt Guido , McConnell Darryl B. , Kraut Norbert , Sini Patrizia
Published: December 2024

Brigimadlin dose-dependent regulation of p53 target genes and apoptosis in MDM2-amplified and non-amplified solid tumor cell lines.
Supplementary Table S3 from Fatty Acid Derivatization and Cyclization of the Immunomodulatory Peptide RP-182 Targeting CD206high Macrophages Improve Antitumor Activity
Authors: Singh Sitanshu S. , Calvo Raul , Kumari Anju , Sable Rushikesh V. , Fang Yuhong , Tao Dingyin , Hu Xin , Castle Sarah Gray , Nahar Saifun , Li Dandan , Major Emily , Sanchez Tino W. , Kato Rintaro , Xu Xin , Zhou Jian , Liu Liang , LeClair Christopher A. , Simeonov Anton , Baljinnyam Bolormaa , Henderson Mark J. , Marugan Juan , Rudloff Udo
Published: December 2024

Supplementary Data_Drug Curves
Supplementary Table S2 from Fatty Acid Derivatization and Cyclization of the Immunomodulatory Peptide RP-182 Targeting CD206high Macrophages Improve Antitumor Activity
Authors: Singh Sitanshu S. , Calvo Raul , Kumari Anju , Sable Rushikesh V. , Fang Yuhong , Tao Dingyin , Hu Xin , Castle Sarah Gray , Nahar Saifun , Li Dandan , Major Emily , Sanchez Tino W. , Kato Rintaro , Xu Xin , Zhou Jian , Liu Liang , LeClair Christopher A. , Simeonov Anton , Baljinnyam Bolormaa , Henderson Mark J. , Marugan Juan , Rudloff Udo
Published: December 2024

Cytotoxicity study of peptide analogs
Suppl Fig 6 from Fatty Acid Derivatization and Cyclization of the Immunomodulatory Peptide RP-182 Targeting CD206high Macrophages Improve Antitumor Activity
Authors: Singh Sitanshu S. , Calvo Raul , Kumari Anju , Sable Rushikesh V. , Fang Yuhong , Tao Dingyin , Hu Xin , Castle Sarah Gray , Nahar Saifun , Li Dandan , Major Emily , Sanchez Tino W. , Kato Rintaro , Xu Xin , Zhou Jian , Liu Liang , LeClair Christopher A. , Simeonov Anton , Baljinnyam Bolormaa , Henderson Mark J. , Marugan Juan , Rudloff Udo
Published: December 2024

Suppl Fig 6
Suppl Fig 4 from Fatty Acid Derivatization and Cyclization of the Immunomodulatory Peptide RP-182 Targeting CD206high Macrophages Improve Antitumor Activity
Authors: Singh Sitanshu S. , Calvo Raul , Kumari Anju , Sable Rushikesh V. , Fang Yuhong , Tao Dingyin , Hu Xin , Castle Sarah Gray , Nahar Saifun , Li Dandan , Major Emily , Sanchez Tino W. , Kato Rintaro , Xu Xin , Zhou Jian , Liu Liang , LeClair Christopher A. , Simeonov Anton , Baljinnyam Bolormaa , Henderson Mark J. , Marugan Juan , Rudloff Udo
Published: December 2024

Suppl Fig 4
Figure S2 from Targeting PDHK1 by DCA to Restore NK Cell Function in Hepatocellular Carcinoma
Authors: Yang Xinyi , Liu Yuanyuan , Wang Peng , Li Min , Xiang Tong , Xie Songzuo , Li Minxing , Wang Yan , Weng Desheng , Zhao Jingjing
Published: December 2024

Fig. S2 DCA increase activation receptors and reduced inhibitory receptors of huh7 tumor cell-infiltrating exhausted NK (A) The positive levels of PD-1, CD314 and TIGIT in NK cells were detected by flow cytometry. (B) Statistical analysis of PD-1, CD314 and TIGIT expressed by NK cells. Results represent the mean ± SEM, from three to four independent experiments. **P < 0.01; ***P < 0.001; ****P < 0.0001. Abbreviations: NK, natural killer; DCA, dichloroacetate.
Figure S5 from Immunoproteasome Activation Expands the MHC Class I Immunopeptidome, Unmasks Neoantigens, and Enhances T-cell Anti-Myeloma Activity
Authors: Rana Priyanka S. , Ignatz-Hoover James J. , Guo Chunna , Mosley Amber L. , Malek Ehsan , Federov Yuriy , Adams Drew J. , Driscoll James J.
Published: December 2024

Figure S5. Effect of Compound A on pan-MHC-I expression. a. ARH77 and U266 cells were treated with Compound A and probed with pan-MHC-I or MHC-I subtype allele-specific antibodies after which the samples were analyzed by flow cytometry. Pretreatment with Compound A significantly increased pan-MHC class-I HLA-ABC and HLA-B surface presentation in all MMCLs assayed. b. ARH77 and U266 cells were pre-treated with Compound A for 48 h after which they were washed and co-cultured with healthy CD8+ cytotoxic T-cells for 18 h at the E:T ratios of 1:1, 2:1and 3:1. Compound A increased CTL-mediated cytotoxicity of tumor cells which was measured by gating for CD138, Annexin-V and PI positive cells at E:T 2:1 and 3:1. Pretreatment of MMCLs and T-cells alone with Compound A resulted in ∼5-10% cell death which was enhanced further when MM cells were co-cultured at E:T ratios of 2:1 and 3:1. T-cells alone also did not show significant cell death when pre-treated with Compound A. There was <5% MM cell death detected with or without Compound A treatment. Similar results were observed with CD8+ T-cells alone. c. Effect of Compound A on the viability of ARH77 and U266 cells alone or combined with ICIs and CD8+ T-cells. MM cells and CD8+ T-cells were separately treated with or without Compound A and the indicated agents. Following co-culture, the relative percent of indicated viable cells was quantitated by annexin-V and propidium iodide staining and flow cytometry. c. Effect of Compound A on T-cell exhaustion markers. CD8+ T-cells were treated with compound A for 24 h after which they were assessed for surface expression of PD-1, TIM-3, CTLA-4, and LAG-3. Compound A induced a marked decrease in PD-1 surface expression, while no significant change was observed in TIM-3, CTLA-4, and LAG-3.
Figure S3 from Immunoproteasome Activation Expands the MHC Class I Immunopeptidome, Unmasks Neoantigens, and Enhances T-cell Anti-Myeloma Activity
Authors: Rana Priyanka S. , Ignatz-Hoover James J. , Guo Chunna , Mosley Amber L. , Malek Ehsan , Federov Yuriy , Adams Drew J. , Driscoll James J.
Published: December 2024

Figure S3. Time and dose-dependent effect of the top eights compounds (A-H) identified in the HTS on (a.) proteasome ChT-like activity and (b.) cell viability.
Supplementary Table S2 from Separable Cell Cycle Arrest and Immune Response Elicited through Pharmacological CDK4/6 and MEK Inhibition in RASmut Disease Models
Authors: Wu Jin , Wang Jianxin , O’Connor Thomas N. , Tzetzo Stephanie L. , Gurova Katerina V. , Knudsen Erik S. , Witkiewicz Agnieszka K.
Published: December 2024

Supplementary Table S2. In vitro and in vivo application of MEK inhibitors from the customized drug library used in the present study.
Supplementary Figure S6 from Separable Cell Cycle Arrest and Immune Response Elicited through Pharmacological CDK4/6 and MEK Inhibition in RASmut Disease Models
Authors: Wu Jin , Wang Jianxin , O’Connor Thomas N. , Tzetzo Stephanie L. , Gurova Katerina V. , Knudsen Erik S. , Witkiewicz Agnieszka K.
Published: December 2024

Supplementary Figure S6. A. Immunoblot analysis for TBK1 and cell cycle-related proteins in HT1080 and 519 cells treated with CDK4/6i (palbociclib, 100 nmol/L) and MEKi (trametinib, 25 nmol/L) with and without siTBK1 for 48 h. B. qPCR analysis of STAT2 and IRF9 IFN-related gene expression in HT1080 and 519 cells treated with DMSO or CDK4/6i (palbociclib, 100 nmol/L) and MEKi (trametinib, 25 nmol/L) with and without siTBK1. Data displayed as mean ± SD in triplicate. ****p < 0.0001 as determined by one-way ANOVA. C. Heatmap displaying expression as log2 fold change of immune-related genes independent of TBK1 pathway in 519 cells treated with CDK4/6i (palbociclib, 100 nmol/L) and MEKi (trametinib, 25 nmol/L) ± TBK1i (GSK8612, 5 μmol/L). D. Schematic representation of potential working model for IFN pathway activation mediated by CDK4/6 and MEK inhibitor treatment.
Supplementary Figure S4 from Separable Cell Cycle Arrest and Immune Response Elicited through Pharmacological CDK4/6 and MEK Inhibition in RASmut Disease Models
Authors: Wu Jin , Wang Jianxin , O’Connor Thomas N. , Tzetzo Stephanie L. , Gurova Katerina V. , Knudsen Erik S. , Witkiewicz Agnieszka K.
Published: December 2024

Supplementary Figure S4. A. Volcano plots displaying differentially expressed genes in CDK4/6i (palbociclib, 0.5 μmol/L) and MEKi (trametinib, 25 nmol/L)-treated PDAC cell models (MIA PaCa-2, left; PANC-1, middle; and PA-TU 8988T, right). The RNAseq data was downloaded from the GEO database (GSE110397). B. Volcano plots displaying differentially expressed genes in CDK4/6i (palbociclib, 0.5 μmol/L) and MEKi (trametinib, 25 nmol/L)-treated lung cancer cell models (A549, left; H460, middle; and H2030, right). The RNAseq data was downloaded from the GEO database (GSE110397). C. Heatmap displaying log2 fold change of select cell cycle and IFN regulatory genes from three PDAC cell models (MIA PaCa-2, left; PANC-1, middle; and PA-TU 8988T, right) treated with CDK4/6i (palbociclib, 0.5 μmol/L) and MEKi (trametinib, 25 nmol/L). D. Heatmap displaying log2 fold change of select cell cycle and IFN regulatory genes from three lung cancer cell models (A549, left; H2030, middle; and H460, right) treated with CDK4/6i (palbociclib, 0.5 μmol/L) and MEKi (trametinib, 25 nmol/L).
Supplementary Figure S1 from Separable Cell Cycle Arrest and Immune Response Elicited through Pharmacological CDK4/6 and MEK Inhibition in RASmut Disease Models
Authors: Wu Jin , Wang Jianxin , O’Connor Thomas N. , Tzetzo Stephanie L. , Gurova Katerina V. , Knudsen Erik S. , Witkiewicz Agnieszka K.
Published: December 2024

Supplementary Figure S1. A. Synergistic inhibition of various MEK inhibitors with CDK4/6 inhibitor palbociclib on HT1080 cell growth rate. B. BrdU incorporation in HT1080 cells treated with DMSO, CDK4/6i (palbociclib, 100 nmol/L), MEKi (pimasertib, 250 nmol/L), or in combination for 72 h. C. Heatmap illustrating relative BrdU incorporation in HT1080 cells after 72 h of CDK4/6i/MEKi (palbociclib/pimasertib) treatment (left) and synergy plot of CDK4/6i and MEKi treatment (right), determined using the BLISS method. D. BrdU incorporation in MIA PaCa-2 cells treated with DMSO, CDK4/6i (palbociclib, 100 nmol/L), MEKi (pimasertib, 250 nmol/L), or in combination, for 72 h. E. Heatmap illustrating relative BrdU incorporation in MIA PaCa-2 cells after 72 h of CDK4/6i/MEKi (palbociclib/pimasertib) treatment (left) and synergy plot of CDK4/6i and MEKi treatment (right), determined using the BLISS method. Data displayed as mean ± SD in triplicate. **p < 0.01, ****p < 0.0001 as determined by one-way ANOVA.
Supplementary Materials and Methods from Targeting the Synthetic Lethal Relationship between FOCAD and TUT7 Represents a Potential Therapeutic Opportunity for TUT4/7 Small-Molecule Inhibitors in Cancer
Authors: Triboulet Robinson , Sadykov Khikmet , Harvey Darren M. , Wilson David M. , Steinbaugh Michael J. , Mayo Christopher B. , Hawley Dillon , Madanjian Andrew , Fyfe Corey , Bracken Christina , Rivera-Rivera Izarys , Ericsson Anna , Snyder Andrew R. , Knutson Sarah K. , Stein Ross L. , Gibaja Veronica , Ghosh Shomir , Campbell Robert M.
Published: December 2024

Supplementary Materials and Methods
Supplementary Data from Trametinib Potentiates Anti-PD-1 Efficacy in Tumors Established from Chemotherapy-Primed Pancreatic Cancer Cells
Authors: Pham Thao D. , Metropulos Anastasia E. , Mubin Nida , Becker Jeffrey H. , Shah Dhavan , Spaulding Christina , Shields Mario A. , Bentrem David J. , Munshi Hidayatullah G.
Published: December 2024

Supplemental Figure Legends
Figure S2 from Targeting the Synthetic Lethal Relationship between FOCAD and TUT7 Represents a Potential Therapeutic Opportunity for TUT4/7 Small-Molecule Inhibitors in Cancer
Authors: Triboulet Robinson , Sadykov Khikmet , Harvey Darren M. , Wilson David M. , Steinbaugh Michael J. , Mayo Christopher B. , Hawley Dillon , Madanjian Andrew , Fyfe Corey , Bracken Christina , Rivera-Rivera Izarys , Ericsson Anna , Snyder Andrew R. , Knutson Sarah K. , Stein Ross L. , Gibaja Veronica , Ghosh Shomir , Campbell Robert M.
Published: December 2024

Related to Figure 4 and Discussion
Supplemental Fig. S9 from Trametinib Potentiates Anti-PD-1 Efficacy in Tumors Established from Chemotherapy-Primed Pancreatic Cancer Cells
Authors: Pham Thao D. , Metropulos Anastasia E. , Mubin Nida , Becker Jeffrey H. , Shah Dhavan , Spaulding Christina , Shields Mario A. , Bentrem David J. , Munshi Hidayatullah G.
Published: December 2024

Supplemental Fig. S9. Trametinib reprograms the KPC-FIO tumors toward a less immunosuppressive tumor immune microenvironment (TiME). A-D. Mice with established 2138-FIO (A, B) and 2138 (C, D) tumors were treated with either DMSO as vehicle control or Trametinib (1 mg/kg, daily). At study endpoint, tumors were processed and analyzed by flow cytometry for the frequency of monocytic myeloid derived suppressive cells (M-MDSCs; CD45+CD11b+Ly6G−Ly6C+), granulocytic myeloid derived suppressive cells (G-MDSCs; CD45+CD11b+Ly6G+Ly6C−), and tumor-associated macrophages (TAMs; CD45+CD11b+F4/80+) (A, C), and their immunosuppressive markers (CD206, PD-L1, Arginase1 (Arg1)) (B, D). Error bars ± SEM. Unpaired t-test. *, p<0.05 **, p<0.01 ***, p<0.001 ns, non-significant. E. Slice cultures from neoadjuvant FOLFIRINOX-treated human tumors (n=3) were treated with either DMSO or Trametinib (5 µM). After 96 hours, slices were collected and analyzed for CD206 and Arginase1 (Arg1) expression by immunohistochemistry staining. Scale bar 100 μm. The number of positive cells were quantified by ImageJ and analyzed by GraphPad. Paired t-test. *, p<0.05.
Data from Targeting the Synthetic Lethal Relationship between FOCAD and TUT7 Represents a Potential Therapeutic Opportunity for TUT4/7 Small-Molecule Inhibitors in Cancer
Authors: Triboulet Robinson , Sadykov Khikmet , Harvey Darren M. , Wilson David M. , Steinbaugh Michael J. , Mayo Christopher B. , Hawley Dillon , Madanjian Andrew , Fyfe Corey , Bracken Christina , Rivera-Rivera Izarys , Ericsson Anna , Snyder Andrew R. , Knutson Sarah K. , Stein Ross L. , Gibaja Veronica , Ghosh Shomir , Campbell Robert M.
Published: December 2024

Abstract
Targeting synthetic lethal interactions among genes has emerged as a promising strategy for cancer therapy. This study explores the intricate interplay among terminal uridylyltransferase 4 (TUT4) and terminal uridylyltransferase 7 (TUT7), the 3′-5′ exoribonuclease DIS3L2, and the superkiller (SKI) complex–interacting factor focadhesin (FOCAD) in the context of cancer vulnerability. Using CRISPR and public functional genomics data, we show impairment of cell proliferation upon knockout of TUT7 or DIS3L2, but not TUT4, on cancer cells with FOCAD loss. Moreover, we report the characterization of the first potent and selective TUT4/7 inhibitors that substantially reduce uridylation and demonstrate in vitro and in vivo antiproliferative activity specifically in FOCAD-deleted cancer. FOCAD deficiency posttranscriptionally disrupts the stability of the SKI complex, whose role is to safeguard cells against aberrant RNA. Reintroduction of FOCAD restores the SKI complex and makes these cells less sensitive to TUT4/7 inhibitors, indicating that TUT7 dependency is driven by FOCAD loss. We propose a model in which, in the absence of FOCAD, TUT7 and DIS3L2 function as a salvage mechanism that degrades aberrant RNA, and genetic or pharmacologic inhibition of this pathway leads to cell death. Our findings underscore the significance of FOCAD loss as a genetic driver of TUT7 vulnerability and provide insights into the potential utility of TUT4/7 inhibitors for cancer treatment.
Data from Integrated Imaging Probe and Bispecific Antibody Development Enables In Vivo Targeting of Glypican-3–Expressing Hepatocellular Carcinoma
Authors: Habibollahi Peiman , Gurevich Alexey , Hui James Z. , Weinfurtner Kelly , McClung George , Adler Justin , Soulen Michael C. , Kaplan David E. , Nadolski Gregory J. , Hunt Stephen J. , Tsourkas Andrew , Gade Terence P.
Published: December 2024

Abstract
Glypican-3 (GPC3) is a proteoglycan with high sensitivity and specificity for hepatocellular carcinoma (HCC). We describe the integrated development and validation of a GPC3-targeting optical imaging probe and T cell–redirecting antibody (TRAB) as a theranostic strategy for the detection and treatment of HCC. A novel TRAB targeting GPC3 on HCC tumor cells and the CD3 T-cell receptor as well as a distinct GPC3-specific optical imaging probe were developed from a short peptide. The efficacy of GPC3/CD3 TRAB was evaluated in vitro using IFNγ release and calcein-AM assays. Patient-derived xenografts were used to assess the in vivo efficacy of GPC3/CD3 TRAB and the GPC3 imaging probe for the detection of GPC3+ HCC. GPC3/CD3 TRAB caused a dose-dependent escalation in IFNγ release from inactive peripheral blood T cells (P = 0.001) and higher tumor-cell lysis (P = 0.01) compared with controls in vitro. Intratumorally injected GPC3/CD3 TRAB resulted in significant prolongation of tumor doubling time in the GPC3+ tumors, with an associated reduction of tumor fluorescent signal from the HiLyte 488–conjugated GPC3-specific peptide on optical imaging. These data demonstrate that HCC cell targeting using a GPC3/CD3 TRAB derived from a small peptide enabled effective T-cell activation and induction of a cytotoxic response toward GPC3+ HCC tumor cells both in vitro and in vivo. GPC3-specific optical imaging enabled the detection of the GPC3+ HCC cells and noninvasive monitoring of tumor response to adoptive immunotherapy. The integrated development of a targeted therapeutic and molecular imaging probe provides a promising paradigm for the development of cancer theranostics.
Table S1 from Ruthenium Drug BOLD-100 Regulates BRAFMT Colorectal Cancer Cell Apoptosis through AhR/ROS/ATR Signaling Axis Modulation
Authors: Griffin Daryl , Carson Robbie , Moss Debbie , Sessler Tamas , Lavin Deborah , Tiwari Vijay K. , Karelia Shivaali , Kennedy Richard , Savage Kienan I. , McDade Simon , Carie Adam , Pankovich Jim , Bazett Mark , Van Schaeybroeck Sandra
Published: December 2024

Table S1: Antibodies
Supplementary Figure 5 from Ruthenium Drug BOLD-100 Regulates BRAFMT Colorectal Cancer Cell Apoptosis through AhR/ROS/ATR Signaling Axis Modulation
Authors: Griffin Daryl , Carson Robbie , Moss Debbie , Sessler Tamas , Lavin Deborah , Tiwari Vijay K. , Karelia Shivaali , Kennedy Richard , Savage Kienan I. , McDade Simon , Carie Adam , Pankovich Jim , Bazett Mark , Van Schaeybroeck Sandra
Published: December 2024

BOLD-100 regulates apoptosis through BRAFMT-dependent AhR/CYP1A1/ROS/ATR axis activation.
Supplementary Figure 2 from Ruthenium Drug BOLD-100 Regulates BRAFMT Colorectal Cancer Cell Apoptosis through AhR/ROS/ATR Signaling Axis Modulation
Authors: Griffin Daryl , Carson Robbie , Moss Debbie , Sessler Tamas , Lavin Deborah , Tiwari Vijay K. , Karelia Shivaali , Kennedy Richard , Savage Kienan I. , McDade Simon , Carie Adam , Pankovich Jim , Bazett Mark , Van Schaeybroeck Sandra
Published: December 2024

Validation of the hits identified in the tumour suppressor genes (TSG) siRNA screen.
Figure 2 from Ruthenium Drug BOLD-100 Regulates BRAFMT Colorectal Cancer Cell Apoptosis through AhR/ROS/ATR Signaling Axis Modulation
Authors: Griffin Daryl , Carson Robbie , Moss Debbie , Sessler Tamas , Lavin Deborah , Tiwari Vijay K. , Karelia Shivaali , Kennedy Richard , Savage Kienan I. , McDade Simon , Carie Adam , Pankovich Jim , Bazett Mark , Van Schaeybroeck Sandra
Published: December 2024

A targeted TSG siRNA screen identifies loss of C8 as a mechanism of resistance to BOLD-100. A, Primary siRNA screen (left): HCT116 colorectal cancer cells were reverse transfected with siRNAs targeting 177 TSGs and 24 hours later treated with either DMSO control or 50 μmol/L BOLD-100. Cell viability was recorded 48 hours later using the CTG assay. Scatter plot showing distribution of rZ-scores for TSG siRNA screen. Positive scores indicate potential mediators of resistance to BOLD-100, whereas negative scores indicate potential mediators of sensitivity to BOLD-100. Secondary siRNA screen (right): HCT116 cells were reverse transfected with two additional independent siRNAs targeting 46 TSGs and positive hits from the primary screen. Waterfall plot showing distribution of rZ-scores. Each siRNA targeting C8 is highlighted in black. B,BRAFMT HT-29 (left) and VACO432 (right) cells were treated with BOLD-100 and preincubated with DMSO or the pan-caspase inhibitor (20 μmol/L). Apoptosis was determined by PARP and caspase 3/7 activity assay. C, HT-29 cells were transfected with 10 nmol/L C8 or/and C9 siRNA for 24 hours and thereafter treated with BOLD-100 for 24 hours. Apoptosis was assessed by WB analysis for PARP (left) and caspase-3/7 activity (right). Expression of pro-caspase-8, pro-caspase-9, GRP78 are also shown. D, Paired CRISPR HCT116C8WT and HCT116C8null cells were treated with increasing concentrations of BOLD-100 for 48 hours. Apoptosis was determined by WB for PARP (left) and caspase-3/7 activity levels (right). Expression of pro-caspase-8, GRP78, and CHOP are also shown.
Figure 1 from Ruthenium Drug BOLD-100 Regulates BRAFMT Colorectal Cancer Cell Apoptosis through AhR/ROS/ATR Signaling Axis Modulation
Authors: Griffin Daryl , Carson Robbie , Moss Debbie , Sessler Tamas , Lavin Deborah , Tiwari Vijay K. , Karelia Shivaali , Kennedy Richard , Savage Kienan I. , McDade Simon , Carie Adam , Pankovich Jim , Bazett Mark , Van Schaeybroeck Sandra
Published: December 2024

Sensitivity of colorectal cancer cell lines to BOLD-100. A, Consort diagram showing the 155 colorectal cancer GSE59857 cell line dataset selected for analysis of genes/pathways differentially expressed in BRAFMT and KRAS/BRAFWT colorectal cancer cell lines. B, GSE59857 heatmap visualizing the “cancer hallmarks pathways” (22) comparing BRAFMT and BRAF/KRASWT colorectal cancer cells. Heatmap displays the mean Z-scores from single sample gene set enrichment analysis (red and blue rectangles). Top 20 pathways with largest mean Z-scores differences between BRAFMT and BRAF/KRASWT colorectal cancer cells are presented, ranked according to the highest Z-score for BRAFMT colorectal cancer. C, HT-29 cells were treated with BOLD-100 for the indicated times. Left: GRP78, CHOP and PARP levels were determined by Western blotting (WB). HSPA5 (middle) and DDIT3 (right) mRNA were quantified using RT-PCR. Raw values were normalized to the expression of housekeeping genes ACTB and GAPDH and were analyzed using the ΔΔCT method. mRNA levels presented are relative to untreated control. D, Colorectal cancer cells (left) were treated with increasing concentrations of BOLD-100 for 72 hours and cell viability determined using CTG assay. IC50 values were calculated using Prism software package. Mean IC50 value of three independent experiments is shown. Dashed lines indicates 75% and 25% cell viability. BRAFMT colorectal cancer cells (right) were treated with 100umol/l BOLD-100 for 48 hours. Apoptosis was assessed using annexin-V/PI staining by high content screening. The graph indicates the percentage of positive stained cells. E,BRAFMT VACO432 colorectal cancer cells, and its isogenic VT1 clone, were treated with increasing concentrations of BOLD-100. Cell viability was determined using CTG assays (top left) and PARP levels determined by WB (bottom left). WB analyses (middle) for PARP, cleaved caspase-3, caspase-8, BRAF, pMEK1/2S217/221 and MEK1/2 in VT1 cells transiently transfected with 1 µg of BRAFV600E expression construct for 12 hours followed by 48 hours treatment with BOLD-100. HT-29 cells (right) were preincubated with vemurafenib for 3 hours and thereafter treated with 50 μmol/L BOLD-100 for 48 hours and PARP, GRP78, CHOP, pMEK1/2S217/221, and MEK expression determined by WB (top). Apoptosis was assessed by caspase-3/7 activity assay (bottom). CONT, control; VEM, vemurafenib; B-100, BOLD-100.
Supplementary Figure 1 from LRRC75A-AS1 Drives the Epithelial–Mesenchymal Transition in Cervical Cancer by Binding IGF2BP1 and Inhibiting SYVN1-Mediated NLRP3 Ubiquitination
Authors: Sui Hongying , Shi Caixia , Yan Zhipeng , Chen Jinyang , Man Lin , Wang Fang
Published: December 2024

Supplementary Figure 1. LRRC75A-AS1 promoted EMT and activated NLRP3/IL-1β/Smad2/3 signaling in cervical cancer. HeLa cells were transfected with sh-NC or sh-LRRC75A-AS1, and CaSki cells were transfected with OE-NC or OE-LRRC75A-AS1 vector for 48 h. (A) MMP-9, E-cadherin, N-cadherin, and slug levels were detected via Western blotting. (B) qRT-PCR analysis of E-cadherin, N-cadherin, and NLRP3 levels in HeLa and CaSki cells. (C) NLRP3, ASC, cleaved caspase-1, IL-1β, p-Smad2, Smad2, p-Smad3, and Smad3 levels were detected via Western blotting. Cell experiments in this study were biologically repeated for at least three times. *P < 0.05, **P < 0.01 and ***P < 0.001.
Supplementary Table 5 from EHMT1/2 Inhibition Promotes Regression of Therapy-Resistant Ovarian Cancer Tumors in a CD8 T-cell–Dependent Manner
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 , Lin Shujian , Villagomez Fabian R. , Jeong Abigail D. , Guntupalli Saketh R. , Behbakht Kian , Gibaja Veronica , Arnoult Nausica , Chuong Edward B. , Bitler Benjamin G.
Published: December 2024

Hallmark pathways enriched in ID8-OR cells treated with combinatory UNC0642/Olaparib compared to DMSO control.
Supplementary Table 2 from EHMT1/2 Inhibition Promotes Regression of Therapy-Resistant Ovarian Cancer Tumors in a CD8 T-cell–Dependent Manner
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 , Lin Shujian , Villagomez Fabian R. , Jeong Abigail D. , Guntupalli Saketh R. , Behbakht Kian , Gibaja Veronica , Arnoult Nausica , Chuong Edward B. , Bitler Benjamin G.
Published: December 2024

Flow cytometry antibody list
Supplementary Table 16 from EHMT1/2 Inhibition Promotes Regression of Therapy-Resistant Ovarian Cancer Tumors in a CD8 T-cell–Dependent Manner
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 , Lin Shujian , Villagomez Fabian R. , Jeong Abigail D. , Guntupalli Saketh R. , Behbakht Kian , Gibaja Veronica , Arnoult Nausica , Chuong Edward B. , Bitler Benjamin G.
Published: December 2024

Hallmark pathways negatively enriched in ID8-R cells treated with combinatory EZM8266/Olaparib compared to Olaparib alone.
Supplementary Table 14 from EHMT1/2 Inhibition Promotes Regression of Therapy-Resistant Ovarian Cancer Tumors in a CD8 T-cell–Dependent Manner
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 , Lin Shujian , Villagomez Fabian R. , Jeong Abigail D. , Guntupalli Saketh R. , Behbakht Kian , Gibaja Veronica , Arnoult Nausica , Chuong Edward B. , Bitler Benjamin G.
Published: December 2024

Hallmark pathways negatively enriched in ID8-R cells treated with combinatory EZM8266/Olaparib compared to EZM8266 alone.
Data from Ruthenium Drug BOLD-100 Regulates BRAFMT Colorectal Cancer Cell Apoptosis through AhR/ROS/ATR Signaling Axis Modulation
Authors: Griffin Daryl , Carson Robbie , Moss Debbie , Sessler Tamas , Lavin Deborah , Tiwari Vijay K. , Karelia Shivaali , Kennedy Richard , Savage Kienan I. , McDade Simon , Carie Adam , Pankovich Jim , Bazett Mark , Van Schaeybroeck Sandra
Published: December 2024

Abstract
Patients with class I V600EBRAF-mutant (MT) colorectal cancer exhibit a poor prognosis, and their response to combined anti-BRAF/EGFR inhibition remains limited. An unmet need exits for further understanding the biology of V600EBRAFMT colorectal cancer. We used differential gene expression of BRAFWT and MT colorectal cancer cells to identify pathways underpinning BRAFMT colorectal cancer. We tested a panel of molecularly/genetically subtyped colorectal cancer cells for their sensitivity to the unfolded protein response (UPR) activator BOLD-100. To identify novel combination strategies for BOLD-100, we performed RNA sequencing and high-throughput drug screening. Pathway enrichment analysis identified significant enrichment of the UPR and DNA repair pathways in BRAFMT colorectal cancer. We found that oncogenic BRAF plays a crucial role in mediating the response to BOLD-100. Using a systems biology approach, we identified V600EBRAFMT-dependent activation of the replication stress response kinase ataxia telangiectasia and Rad3-related (ATR) as a key mediator of resistance to BOLD-100. Further analysis identified acute increases in BRAFMT-dependent-reactive oxygen species levels following treatment with BOLD-100, which promoted ATR/CHK1 activation and apoptosis. Furthermore, activation of reactive oxygen species/ATR/CHK1 following BOLD-100 was mediated through the AhR transcription factor and CYP1A1. Importantly, pharmacological blockade of this resistance pathway with ATR inhibitors synergistically increased BOLD-100-induced apoptosis and growth inhibition in BRAFMT models. These results highlight a possible novel therapeutic opportunity for BRAFMT colorectal cancer.

Implications: BOLD-100 induces BRAFMT-dependent replication stress, and targeted strategies against replication stress (e.g., by using ATR inhibitors) in combination with BOLD-100 may serve as a potential novel therapeutic strategy for clinically aggressive BRAFMT colorectal cancer.
Supplementary Table S1 from Construction and Validation of a Novel Forecasting Nomogram to the Risk of Colorectal Adenomas: Preventing Colorectal Cancer at Its Origin
Authors: Li Mao , Cui Mingyu , Zhou Xiaobin , Song Ying
Published: December 2024

Supplementary Table S1: Baseline clinical characteristics of subjects in the colorectal adenoma and no adenoma groups
Supplementary Figure 5 from Oncogenic HRAS Induces Metformin Resistance in Head and Neck Cancer by Promoting Glycolytic Metabolism
Authors: Wu Xingyu , Adame-Garcia Sendi Rafael , Koshizuka Keiichi , Vo Pham Thuy Tien , Hoang Thomas S. , Sato Kuniaki , Izumi Hiroki , Goto Yusuke , Allevato Michael M. , Wood Kris C. , Lippman Scott M. , Gutkind Jorge Silvio
Published: December 2024

Supplementary Figure 5: the orthotopic mouse model
Table S2 from CAR T Cells Engineered to Secrete IFNκ Induce Tumor Ferroptosis via an IFNAR/STAT1/ACSL4 Axis
Authors: Gao Yaoxin , Liu Shasha , Huang Yifan , Wang Hui , Zhao Yuyu , Cui Xuyang , Peng Yajing , Li Feng , Zhang Yi
Published: December 2024

Primers sequence
Table S1 from CAR T Cells Engineered to Secrete IFNκ Induce Tumor Ferroptosis via an IFNAR/STAT1/ACSL4 Axis
Authors: Gao Yaoxin , Liu Shasha , Huang Yifan , Wang Hui , Zhao Yuyu , Cui Xuyang , Peng Yajing , Li Feng , Zhang Yi
Published: December 2024

shRNA sequence
Supplementary Movie 3 from Targeting BTN2A1 Enhances Vγ9Vδ2 T-Cell Effector Functions and Triggers Tumor Cell Pyroptosis
Authors: Le Floch Anne-Charlotte , Imbert Caroline , Boucherit Nicolas , Gorvel Laurent , Fattori Stéphane , Orlanducci Florence , Le Roy Aude , Archetti Lorenzo , Crescence Lydie , Panicot-Dubois Laurence , Dubois Christophe , Vey Norbert , Briantais Antoine , Anastasio Amandine , Cano Carla , Guittard Geoffrey , Frechin Mathieu , Olive Daniel
Published: December 2024

Visualization of Vγ9Vδ2 T cells (E) and Ishikawa (T) coculture using a label-free method within 20 hours. Ratio T/E = 1/2. Cells treated with 10ug/ml of mIgG1 control antibody.
Figure S8 from CAR T Cells Engineered to Secrete IFNκ Induce Tumor Ferroptosis via an IFNAR/STAT1/ACSL4 Axis
Authors: Gao Yaoxin , Liu Shasha , Huang Yifan , Wang Hui , Zhao Yuyu , Cui Xuyang , Peng Yajing , Li Feng , Zhang Yi
Published: December 2024

IFN-κ-CD276-CAR-T cells had better persistence in vivo.
Figure S5 from CAR T Cells Engineered to Secrete IFNκ Induce Tumor Ferroptosis via an IFNAR/STAT1/ACSL4 Axis
Authors: Gao Yaoxin , Liu Shasha , Huang Yifan , Wang Hui , Zhao Yuyu , Cui Xuyang , Peng Yajing , Li Feng , Zhang Yi
Published: December 2024

Immune cell viability was detected using flow cytometry.
Figure S9 from Targeting BTN2A1 Enhances Vγ9Vδ2 T-Cell Effector Functions and Triggers Tumor Cell Pyroptosis
Authors: Le Floch Anne-Charlotte , Imbert Caroline , Boucherit Nicolas , Gorvel Laurent , Fattori Stéphane , Orlanducci Florence , Le Roy Aude , Archetti Lorenzo , Crescence Lydie , Panicot-Dubois Laurence , Dubois Christophe , Vey Norbert , Briantais Antoine , Anastasio Amandine , Cano Carla , Guittard Geoffrey , Frechin Mathieu , Olive Daniel
Published: December 2024

Supplementary Figure S9. Anti-BTN2A1 sensitizes Vɣ9Vδ2 T cell cytotoxicity against PC3 cell line.
Figure S8 from Targeting BTN2A1 Enhances Vγ9Vδ2 T-Cell Effector Functions and Triggers Tumor Cell Pyroptosis
Authors: Le Floch Anne-Charlotte , Imbert Caroline , Boucherit Nicolas , Gorvel Laurent , Fattori Stéphane , Orlanducci Florence , Le Roy Aude , Archetti Lorenzo , Crescence Lydie , Panicot-Dubois Laurence , Dubois Christophe , Vey Norbert , Briantais Antoine , Anastasio Amandine , Cano Carla , Guittard Geoffrey , Frechin Mathieu , Olive Daniel
Published: December 2024

Supplementary Figure S8. Segmentation of live cells using Refractive Index (RI).
Figure S3 from CAR T Cells Engineered to Secrete IFNκ Induce Tumor Ferroptosis via an IFNAR/STAT1/ACSL4 Axis
Authors: Gao Yaoxin , Liu Shasha , Huang Yifan , Wang Hui , Zhao Yuyu , Cui Xuyang , Peng Yajing , Li Feng , Zhang Yi
Published: December 2024

Screening the potential fatty acids.
Figure S6 from Targeting BTN2A1 Enhances Vγ9Vδ2 T-Cell Effector Functions and Triggers Tumor Cell Pyroptosis
Authors: Le Floch Anne-Charlotte , Imbert Caroline , Boucherit Nicolas , Gorvel Laurent , Fattori Stéphane , Orlanducci Florence , Le Roy Aude , Archetti Lorenzo , Crescence Lydie , Panicot-Dubois Laurence , Dubois Christophe , Vey Norbert , Briantais Antoine , Anastasio Amandine , Cano Carla , Guittard Geoffrey , Frechin Mathieu , Olive Daniel
Published: December 2024

Supplementary Figure S6. Anti-BTN2A1 107G3B5 increases Vɣ9Vδ2 T cell effectors functions against hematological cell lines.
Figure S5 from Targeting BTN2A1 Enhances Vγ9Vδ2 T-Cell Effector Functions and Triggers Tumor Cell Pyroptosis
Authors: Le Floch Anne-Charlotte , Imbert Caroline , Boucherit Nicolas , Gorvel Laurent , Fattori Stéphane , Orlanducci Florence , Le Roy Aude , Archetti Lorenzo , Crescence Lydie , Panicot-Dubois Laurence , Dubois Christophe , Vey Norbert , Briantais Antoine , Anastasio Amandine , Cano Carla , Guittard Geoffrey , Frechin Mathieu , Olive Daniel
Published: December 2024

Supplementary Figure S5. Cytotoxicity assays of 4 cancer cell lines (PC3, KARPAS, 697 and SUP-T1) and primary ALL blasts (n=4) using Annexin and 7-AAD labelling.
Figure S4 from Targeting BTN2A1 Enhances Vγ9Vδ2 T-Cell Effector Functions and Triggers Tumor Cell Pyroptosis
Authors: Le Floch Anne-Charlotte , Imbert Caroline , Boucherit Nicolas , Gorvel Laurent , Fattori Stéphane , Orlanducci Florence , Le Roy Aude , Archetti Lorenzo , Crescence Lydie , Panicot-Dubois Laurence , Dubois Christophe , Vey Norbert , Briantais Antoine , Anastasio Amandine , Cano Carla , Guittard Geoffrey , Frechin Mathieu , Olive Daniel
Published: December 2024

Supplementary Figure S4. Anti-BTN2A1 107G3B5 mAb characterization.
Figure S12 from Targeting BTN2A1 Enhances Vγ9Vδ2 T-Cell Effector Functions and Triggers Tumor Cell Pyroptosis
Authors: Le Floch Anne-Charlotte , Imbert Caroline , Boucherit Nicolas , Gorvel Laurent , Fattori Stéphane , Orlanducci Florence , Le Roy Aude , Archetti Lorenzo , Crescence Lydie , Panicot-Dubois Laurence , Dubois Christophe , Vey Norbert , Briantais Antoine , Anastasio Amandine , Cano Carla , Guittard Geoffrey , Frechin Mathieu , Olive Daniel
Published: December 2024

Supplementary Figure 12. The caspase-3-specific inhibitor zDEVD-FMK inhibits the cleavage of GSDME.
Figure S11 from Targeting BTN2A1 Enhances Vγ9Vδ2 T-Cell Effector Functions and Triggers Tumor Cell Pyroptosis
Authors: Le Floch Anne-Charlotte , Imbert Caroline , Boucherit Nicolas , Gorvel Laurent , Fattori Stéphane , Orlanducci Florence , Le Roy Aude , Archetti Lorenzo , Crescence Lydie , Panicot-Dubois Laurence , Dubois Christophe , Vey Norbert , Briantais Antoine , Anastasio Amandine , Cano Carla , Guittard Geoffrey , Frechin Mathieu , Olive Daniel
Published: December 2024

Supplementary figure S11. Anti-BTN2A1 107G3B5 induces a colocalization of BTN3A1 and BTN2A1.
Supplementary Figure 3 from Cannabidiol Enhances Atezolizumab Efficacy by Upregulating PD-L1 Expression via the cGAS–STING Pathway in Triple-Negative Breast Cancer Cells
Authors: Kim Bu Gyeom , Kim Bo Ram , Kim Dae Yeong , Kim Woo Young , Kang Sanghee , Lee Sun Il , Oh Sang Cheul
Published: December 2024

CBD induced immunogenic cell death in TNBC cells
Figure S10 from Integrated Germline and Somatic Features Reveal Divergent Immune Pathways Driving Response to Immune Checkpoint Blockade
Authors: Sears Timothy J. , Pagadala Meghana S. , Castro Andrea , Lee Ko-han , Kong JungHo , Tanaka Kairi , Lippman Scott M. , Zanetti Maurizio , Carter Hannah
Published: December 2024

Fig S10. A. Univariate analysis of potential checkpoint inhibitors in the discovery samples. B. Proportion of patients responding in each MHC reliance group when discovery samples are partitioned according to low versus high expression of 7 different checkpoint genes. C. Univariate analysis of potential checkpoint inhibitors in the validation samples. D. Proportion of patients responding in each MHC reliance group when validation samples are partitioned according to low versus high expression of 7 different checkpoint genes
Table S6 from Inflammation Mediated by Gut Microbiome Alterations Promotes Lung Cancer Development and an Immunosuppressed Tumor Microenvironment
Authors: Rahal Zahraa , Liu Yuejiang , Peng Fuduan , Yang Sujuan , Jamal Mohamed A. , Sharma Manvi , Moreno Hannah , Damania Ashish V. , Wong Matthew C. , Ross Matthew C. , Sinjab Ansam , Zhou Tieling , Chen Minyue , Tarifa Reischle Inti , Feng Jiping , Chukwuocha Chidera , Tang Elizabeth , Abaya Camille , Lim Jamie K. , Leung Cheuk Hong , Lin Heather Y. , Deboever Nathaniel , Lee Jack J. , Sepesi Boris , Gibbons Don L. , Wargo Jennifer A. , Fujimoto Junya , Wang Linghua , Petrosino Joseph F. , Ajami Nadim J. , Jenq Robert R. , Moghaddam Seyed Javad , Cascone Tina , Hoffman Kristi , Kadara Humam
Published: December 2024

Differentially expressed genes in the tumor microenvironment.