bluuebunny/crossref_metadata_2025 huggingface dataset:
Abstract 3674: The polyamine acetylation enzyme SAT1 drives mesenchymal features and therapeutic resistance in glioblastoma
Authors: Rana Ayush B. , Horton Timothy M. , Thakur Vijay S. , Welford Scott M.
Published: April 2023

Background:

Glioblastoma multiforme (GBM) is the most common and lethal brain tumor in adults. Characterization of GBM heterogeneity has identified four molecular subtypes based on transcriptomic profile: classical, neural, proneural and mesenchymal. Tumors harboring the mesenchymal gene signature are considered the most aggressive, invasive, and multitherapy-resistant. We identify the polyamine acetylation enzyme, SAT1 (spermidine/spermine N1-acetyltransferase 1) as a component of the mesenchymal gene signature and mesenchymal-associated gene sets including (1) Hallmark EMT and (2) Hallmark TNFa signaling via NF-κB.

Design/Methods:

To validate the role of SAT1 in driving mesenchymal features in vivo, we utilized a genetically flexible, CRISPR-based model of GBM. Tumor bearing mice were generated through in utero electroporation, resulting in ablation of PTEN, P53 and NF1 in developing cortical cells. SAT1 knockout was achieved through cloning of additional guide RNA’s against SAT1 into the tumor initiating plasmid.

Results:

In our model, we found increased levels of both SAT1 and acetylated polyamines in tumors compared to normal brain. Ablation of SAT1 was insufficient to prolong overall survival in mice but rendered the otherwise treatment resistant tumors highly sensitive to chemoRT. Bulk RNA sequencing of murine tumors revealed that SAT1 knockout resulted in reduced expression of the mesenchymal gene signature as well as genes implicated in EMT and TNFa/NFKb signaling.

Conclusions:

Collectively, these results reveal that SAT1 not only identifies mesenchymal GBM but also drives expression of the mesenchymal gene signature and mesenchymal features including multi-therapy resistance.

Citation Format: Ayush B. Rana, Timothy M. Horton, Vijay S. Thakur, Scott M. Welford. The polyamine acetylation enzyme SAT1 drives mesenchymal features and therapeutic resistance in glioblastoma. [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2023; Part 1 (Regular and Invited Abstracts); 2023 Apr 14-19; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2023;83(7_Suppl):Abstract nr 3674.
Abstract 368: Neutralizing antibody against GDF-15 restores cachexia
Authors: He Feng , Peng Hao , Li Jianhui , Ding Li , Hao Feng , Ning Jinying , Wu Guojin
Published: April 2023

Growth and differentiation factor 15 (GDF-15) is an attractive target for the treatment of cachexia. Ponsegnomab is such a therapeutical antibody in the clinical trial. Here, we developed a humanized GDF-15 neutralizing antibody (KA1641-ZY1) with better efficacy than ponsegnomab in the pre-clinical experiments. KA1641-ZY1 had high affinity to GDF-15 (KD=0.05nM), with cross-reacting to monkey GDF15. KA1641-ZY1 neutralized GDF-15 in the culture medium and disrupted GDF-15-induced GFRAL signaling more efficiently than Ponsegnomab in reporter cell assay (IC50=0.13nM vs. 0.21nM). In a mouse model with exogenous GDF15 protein-induced body decrease, KA1641-ZY1 restored body weight by giving as low as 5ug/kg while ponsegnomab failed. In the HT1080, Colo 205, and LS513 xenograft tumor-induced cachexia mouse models, KA1641-ZY1 restored the body weight decrease with 0.3mg/kg while ponsegnomab restored the weight with higher than 1mg/kg. In addition, KA1641-ZY1 also restored cisplatin-induced body decrease in GDF15 humanized mice. It has no detectable non-specific binding to red blood cells, neutrophils, PBMCs, and HUVEC cells, with a half-life of about nine days in the mouse. These results suggest that KA1641-ZY1 is a potential candidate drug for cachexia.

Citation Format: Feng He, Hao Peng, Jianhui Li, Li Ding, Feng Hao, Jinying Ning, Guojin Wu. Neutralizing antibody against GDF-15 restores cachexia [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2023; Part 1 (Regular and Invited Abstracts); 2023 Apr 14-19; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2023;83(7_Suppl):Abstract nr 368.
Abstract 3875: Evaluation of resistance mechanisms to ARV471, an ER-targeted PROTAC
Authors: Friel Delia Margaret , Sandusky Zachary , Jiang Yijia , Qiu Xintao , Li Rong , Long Henry , Jeselsohn Rinath , Brown Myles
Published: April 2023

Estrogen receptor alpha (ER) is a ligand activated transcription factor and a driver of ER+ breast cancer. The discovery of activating mutations in ER (gene name ESR1), in patients with advanced endocrine-resistant ER+ breast cancer, has ignited a large pharmaceutical effort to develop next-generation ER antagonists that also target the mutant protein. Here, we profiled the potency and selectivity of many next-generation ER antagonists currently in clinical trials, including ER-targeted proteolysis-targeting chimeras (PROTACs), selective ER modulators (SERMs), and selective ER degraders (SERDs). To contextualize these antagonists, we evaluated their activity against the only FDA-approved SERD, Fulvestrant, at the level of chromatin, transcriptome, proteome, and cell viability, using cells expressing wild-type ER as well as activating mutant ER (ERY537S and ERD538G). Overall, we find that many of the novel oral SERDs are potent ER antagonists, including against mutant ER. To anticipate resistance mechanisms to these next-generation ER antagonists, we developed a strategy initially focused on ARV471 (the most clinically advanced ER PROTAC), with two approaches. First, we performed whole-genome CRISPR/Cas9-knockout screening in ER+ breast cancer cell lines treated with ARV471. Among the enriched gRNAs were PTEN, NF2, and CRBN. Loss of PTEN and NF2 results in activation of the PI3K and MAPK pathways, respectively, and CRBN is the ubiquitin E3 ligase required for ER protein degradation by ARV471. PTEN and NF2 are known mechanisms of endocrine resistance but it is not yet known if CRBN loss in response to PROTACs is a predominant clinical resistance mechanism. Therefore, in a second approach we generated ARV471 resistant breast cancer cell lines through long term exposure (LTE-ARV471). These cells developed an ER-independent resistance mechanism, with decreased ER expression and increased expression of pathways associated with Ras/MAPK and EMT. Therefore, as more potent ER degraders enter the clinic, such as PROTACs and oral SERDs, it may be important to monitor resistance mechanisms that involve loss of ER. Currently, we are following up our findings with LTE-ARV471 cells and performing CRISPR screening to identify targetable dependencies and combination therapies for endocrine resistant breast cancer.

Citation Format: Delia Margaret Friel, Zachary Sandusky, Yijia Jiang, Xintao Qiu, Rong Li, Henry Long, Rinath Jeselsohn, Myles Brown. Evaluation of resistance mechanisms to ARV471, an ER-targeted PROTAC. [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2023; Part 1 (Regular and Invited Abstracts); 2023 Apr 14-19; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2023;83(7_Suppl):Abstract nr 3875.
Abstract 5442: SlideQC: An AI-based tool for automated quality control of whole-slide digital pathology images
Authors: Rodrigues Daniela , Reinhard Stefan , Waldburger Therese , Martin Daniel , Couto Suzana , Zlobec Inti , Caie Peter , Burlingame Erik
Published: April 2023

Introduction: Artifacts are often introduced during tissue collection and processing, slide preparation, and/or when generating whole slide images (WSI). The presence of artifacts has a negative impact on the digital pathology workflow as artifacts may hinder diagnostic reporting and can lead to false positive and false negative results when using image analysis algorithms or computer-aided diagnosis systems. Manual quality control of WSI is a time-consuming procedure and therefore automated quality control tools, which report and exclude artifacts, are highly desirable to streamline digital pathology workflows. To automate the quality control step, we developed SlideQC, an AI-based quality control tool that automatically detects, reports, and outlines artifacts such as air bubbles, dust/debris, folds, out-of-focus,and pen marks, in both research and clinical workflows. Methods: SlideQC was trained with a DenseNet-based network using 1984 annotations for artifacts including air bubbles, dust/debris, folds, out-of-focus, and pen markers, across 254 Haematoxylin and Eosin (H&E) stained WSI from more than 9 tissue types. A set of 2048 annotations from synthetically generated out-of-focus images was added to supplement the training data. The performance of the SlideQC was evaluated on an external test cohort of 49 WSI H&E images sourced from the open-source database ‘HistoQCRepo’, across 375 annotations (tissue and artifact), and compared with the performance of HistoQC, an open-source quality control tool for digital pathology slides. Results: On the external test cohort, SlideQC showed high sensitivity, specificity, and F1-score with average values of 0.93, 0.99, and 0.93, across the five artifact types. In the same cohort, HistoQC attained an average sensitivity, specificity, and F1-score of 0.65, 0.79, and 0.54, respectively. Conclusions: SlideQC achieved high sensitivity, specificity, and F1-score on an external test cohort. SlideQC can add efficiency gains to a workflow by performing quality control on 100% of slides rather than the currently manually performed on only a subset of the slides in clinical pathology departments. SlideQC can allowthe triaging and alerting of slides containing a high level of artifact within a digital pathology workflow. The tool can also be used to exclude the artifact region from downstream analysis by subsequent image analysis algorithms.

Citation Format: Daniela Rodrigues, Stefan Reinhard, Therese Waldburger, Daniel Martin, Suzana Couto, Inti Zlobec, Peter Caie, Erik Burlingame. SlideQC: An AI-based tool for automated quality control of whole-slide digital pathology images. [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2023; Part 1 (Regular and Invited Abstracts); 2023 Apr 14-19; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2023;83(7_Suppl):Abstract nr 5442.
Abstract 5722: The mutational signatures of 100,477 targeted sequenced tumors
Authors: Lee Donghyuk , Hua Min , Wang Difei , Song Lei , Zhang Tongwu , Yu Kai , Yang Xiaohong R. , Shi Jianxin , Chanock Stephen J. , Landi Maria Teresa , Zhu Bin
Published: April 2023

Mutational signatures, the footprints of somatic mutations, are associated with the causes of cancer and have been well-studied for tumors with whole exome or genome sequencing. However, due to the low number of detected mutations, mutational signatures were insufficiently explored for many tumors sequenced by targeted panels in clinics. It impedes the clinical application of mutational signatures. Here, we present a new method, SALMON (Signature Analyzer for Low Mutation cOuNts), to identify mutational signatures in targeted sequenced tumors based on tumor mutational burden. SALMON adjusts for panel size differences and uses a large number of targeted sequenced tumors rather than a large number of mutations per tumor (as with whole exome or genome sequencing) to overcome the challenges of mutational signature analysis for targeted sequencing. Extensive simulations and pseudo-targeted sequenced data show that SALMON can accurately detect spiky or common signatures. We applied SALMON to investigate the pan-cancer patterns of mutational signatures for 100,477 targeted sequenced tumors in AACR Project GENIE, including 14,428 lung and 11,389 breast tumors. We detected well-established signatures in tumor types that have not previously been associated with these signatures, such as the smoking signature in ovarian tumors. Interestingly, analysis of thousands of tumors per cancer type from diverse populations revealed gender discrepancies, self-described race differences, subtype heterogeneity, and metastatic enrichment of mutational signatures. For instance, most sex-biased signatures are more frequently present in males for non-gender-specific cancers. Thiopurine treatment-induced signature in glioma is enriched in Black patients. And endometrioid ovarian or uterine cancers have a higher prevalence of polymerase epsilon (POLE) deficiency-related signatures than non-endometrioid ovarian or uterine cancers, respectively. Our study demonstrates the feasibility and utility of mutational signature analysis for targeted sequenced tumors, enabling precision applications of mutational signatures in the clinical setting.

Citation Format: Donghyuk Lee, Min Hua, Difei Wang, Lei Song, Tongwu Zhang, Kai Yu, Xiaohong R. Yang, Jianxin Shi, Stephen J. Chanock, Maria Teresa Landi, Bin Zhu. The mutational signatures of 100,477 targeted sequenced tumors. [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2023; Part 1 (Regular and Invited Abstracts); 2023 Apr 14-19; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2023;83(7_Suppl):Abstract nr 5722.
Abstract 6129: The proapoptotic peptide PEP-010 is efficient on several models of different tumor origins and it can be monitored by pharmacodynamic biomarker candidates in clinical practice
Authors: Farhat Rayan , Dadon Laura , Nemati F , Rebollo A , Decaudin D , Wiels Joelle , Brenner Catherine , Germini Diego
Published: April 2023

In cancer cells, the proapoptotic proteins caspase-9 and PP2A interaction prevents them to play their role in apoptosis. PEP-010, a drug candidate developed by PEP-Therapy, a French Biotech company, is a proapoptotic peptide targeting and disrupting this interaction leading to restoration of the apoptotic cascade. PEP-010 is an innovative bifunctional peptide. It penetrates into cells thanks to its cell penetrating part and specifically disrupts the caspase-9/PP2A interaction thanks to its interfering part. PEP-010 is currently in Phase I a/b multicenter clinical trial for the treatment of advanced solid tumors.To the aim of screening different potential therapeutic targets, to investigate the molecular mechanism-of-action of PEP-010 and to identify potential pharmacodynamic biomarkers, we have tested PEP-010 efficacy on several cell models of different tumor origins. By the Annexin V/Propidium Iodide staining and flow cytometry analysis, we found that PEP-010 induces apoptosis in most of the tested models. One possible mechanism-of-action is an involvement of the PP2A which, once released by PEP-010, could regulate expression and/or activity of different intracellular factors leading to caspases activation and cell death.The identification of the major molecular features involved in PEP-010 mechanism-of-action, were instrumental to identify different pharmacodynamic biomarker candidates (e.g. active caspase-3). Hence, such biomarkers could be useful in clinical practice to monitor the effect of PEP-010 at molecular level. We have compared specific features related to the mechanism-of-action of PEP-010 in sensitive (MDA-MB-231, IGROV1) and not sensitive cell models of different tumor origins and in tissue sections derived from Patient-Derived Xenografts models of breast cancer treated or not with PEP-010. Widely used techniques as immunofluorescent staining and immunohistochemistry were employed, making these results easily transferable in clinical routine.Taken together, our pre-clinical data showed the potential of PEP-010 as an anti-cancer peptide on a wide variety of malignancies and enabled the identification of pharmacodynamic biomarker candidates, important to ease the clinical development.

Citation Format: Rayan Farhat, Laura Dadon, F Nemati, A Rebollo, D Decaudin, Joelle Wiels, Catherine Brenner, Diego Germini. The proapoptotic peptide PEP-010 is efficient on several models of different tumor origins and it can be monitored by pharmacodynamic biomarker candidates in clinical practice. [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2023; Part 1 (Regular and Invited Abstracts); 2023 Apr 14-19; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2023;83(7_Suppl):Abstract nr 6129.
Abstract 6647: Dostarlimab shows dose-dependent immune activation of the tumor microenvironment in a patient-derived NSCLC explant model similar to pembrolizumab
Authors: Perrin Jessica , Wippich Frank , Sherina Valeriia , Dvornikov Dmytro , Lupar Katharina , Melhem Murad M. , Hanafin Patrick , Waight Jeremy , Yu Jong , Yadavilli Sapna , Poeckel Daniel , Bergamini Giovanna
Published: April 2023

The ability to more faithfully mimic the tumor microenvironment (TME) of cancer patients offers a wide range of possibilities for non-clinical evaluation of anti-cancer therapeutics, including guidance for patient selection, dose, and combinations. We have established a patient-derived tumor explant (PDE) model to monitor immune activation within a structurally preserved TME, following ex vivo incubation with immune check point inhibitors (ICI). When testing anti-PD-1 agents, such as dostarlimab and pembrolizumab, in a cohort of NSCLC explants from stage I-III treatment-naïve patients, we observed that approximately half demonstrate release of inflammatory cytokines after two days incubation. Interestingly, responsive tumors presented with a high level of PD-L1 expression (high TPS), had elevated TMB, and were highly infiltrated by CD8+ T cells at baseline, in line with tumor baseline characteristics predictive of clinical response to anti-PD-1. When testing a dose-range of dostarlimab and pembrolizumab comparable potencies were observed when measuring cytokine release after treatment of the NSCLC explants. In conclusion, we describe here an in vitro patient-derived NSCLC model that mirrors the heterogeneity of patients’ response for anti-PD-1 agents observed in clinical settings, representing a valuable tool for comparative analysis of novel ICI assets and combinations, such as the CD226 axis members. Importantly, this system is also amenable to extensive multi-omics and genetics-based analyses, providing the opportunity to better identify predictive or pharmacodynamic characteristics within patient tumors.

Citation Format: Jessica Perrin, Frank Wippich, Valeriia Sherina, Dmytro Dvornikov, Katharina Lupar, Murad M. Melhem, Patrick Hanafin, Jeremy Waight, Jong Yu, Sapna Yadavilli, Daniel Poeckel, Giovanna Bergamini. Dostarlimab shows dose-dependent immune activation of the tumor microenvironment in a patient-derived NSCLC explant model similar to pembrolizumab [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2023; Part 1 (Regular and Invited Abstracts); 2023 Apr 14-19; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2023;83(7_Suppl):Abstract nr 6647.
Supplementary Figure 5 from Interleukin-6 and Oncostatin-M Synergize with the PI3K/AKT Pathway to Promote Aggressive Prostate Malignancy in Mouse and Human Tissues
Authors: Smith Daniel A. , Kiba Atsushi , Zong Yang , Witte Owen N.
Published: April 2023

PDF file - 3842K, Loss of PTEN results in increased expression of total AKT, ERK1/2 and STAT3 in transformed epithelial tissues.
Supplementary Table 1 from RETRACTED: miRNA-302b Suppresses Human Hepatocellular Carcinoma by Targeting AKT2
Authors: Wang Lumin , Yao Jiayi , Zhang Xiaogang , Guo Bo , Le Xiaofeng , Cubberly Mark , Li Zongfang , Nan Kejun , Song Tusheng , Huang Chen
Published: April 2023

PDF file - 42K, The relationship between miR-302b levels and differentiated tumor.
Supplementary Figure 6 from Nullifying the CDKN2AB Locus Promotes Mutant K-ras Lung Tumorigenesis
Authors: Schuster Katja , Venkateswaran Niranjan , Rabellino Andrea , Girard Luc , Peña-Llopis Samuel , Scaglioni Pier Paolo
Published: April 2023

PDF file - 1036K, Progression-Free and overall survival of patients with CDKN2A or CDKN2AB mutant lung cancer.
Supplemental File 2 from Hypoxia Regulates Alternative Splicing of HIF and non-HIF Target Genes
Authors: Sena Johnny A. , Wang Liyi , Heasley Lynn E. , Hu Cheng-Jun
Published: April 2023

Supplemental File 2: genes in each pathway
Supplemental Table 6 from Expression of ANRIL–Polycomb Complexes–CDKN2A/B/ARF Genes in Breast Tumors: Identification of a Two-Gene (EZH2/CBX7) Signature with Independent Prognostic Value
Authors: Meseure Didier , Vacher Sophie , Alsibai Kinan Drak , Nicolas Andre , Chemlali Walid , Caly Martial , Lidereau Rosette , Pasmant Eric , Callens Celine , Bieche Ivan
Published: April 2023

Relationship between EED transcripts levels and classical clinical biological parameters in a series of 446 breast cancers.
Supplemental Table 4 from Expression of ANRIL–Polycomb Complexes–CDKN2A/B/ARF Genes in Breast Tumors: Identification of a Two-Gene (EZH2/CBX7) Signature with Independent Prognostic Value
Authors: Meseure Didier , Vacher Sophie , Alsibai Kinan Drak , Nicolas Andre , Chemlali Walid , Caly Martial , Lidereau Rosette , Pasmant Eric , Callens Celine , Bieche Ivan
Published: April 2023

Relationship between EZH2 transcripts levels and classical clinical biological parameters in a series of 456 breast cancers.
Supplemental Table 3 from Expression of ANRIL–Polycomb Complexes–CDKN2A/B/ARF Genes in Breast Tumors: Identification of a Two-Gene (EZH2/CBX7) Signature with Independent Prognostic Value
Authors: Meseure Didier , Vacher Sophie , Alsibai Kinan Drak , Nicolas Andre , Chemlali Walid , Caly Martial , Lidereau Rosette , Pasmant Eric , Callens Celine , Bieche Ivan
Published: April 2023

Relationship between ANRIL transcripts levels and classical clinical biological parameters in a series of 456 breast cancers.
Characteristics of human breast tumor tissues used in this study from Increased Expression of Beige/Brown Adipose Markers from Host and Breast Cancer Cells Influence Xenograft Formation in Mice
Authors: Singh Rajan , Parveen Meher , Basgen John M. , Fazel Sayeda , Meshesha Meron F. , Thames Easter C. , Moore Brandis , Martinez Luis , Howard Carolyn B. , Vergnes Laurent , Reue Karen , Pervin Shehla
Published: April 2023

Human breast tumor tissues were characterized based on ethnicity and age
Supplementary Table 2 from Prognostic Relevance of Tumor Purity and Interaction with MGMT Methylation in Glioblastoma
Authors: Schulze Heuling Eva , Knab Felix , Radke Josefine , Eskilsson Eskil , Martinez-Ledesma Emmanuel , Koch Arend , Czabanka Marcus , Dieterich Christoph , Verhaak Roel G. , Harms Christoph , Euskirchen Philipp
Published: April 2023

Primers and annealing temperatures used in quantitative allele-specific real-time PCR.
Supplementary Figure S1 from Sulfiredoxin Promotes Colorectal Cancer Cell Invasion and Metastasis through a Novel Mechanism of Enhancing EGFR Signaling
Authors: Jiang Hong , Wu Lisha , Chen Jing , Mishra Murli , Chawsheen Hedy A. , Zhu Haining , Wei Qiou
Published: April 2023

Orthotopical implantation of human HCT116 cells into mouse cecum. (A) Injection of human CRC cells into the cecal wall. Arrows indicate before and after of a successful injection. (B) Macroscopic tumor metastasis found in the mouse liver and lung as visualized by naked eye. Arrows indicate tumor nodules.
Table S3 from Metabolic Profiling in Formalin-Fixed and Paraffin-Embedded Prostate Cancer Tissues
Authors: Cacciatore Stefano , Zadra Giorgia , Bango Clyde , Penney Kathryn L. , Tyekucheva Svitlana , Yanes Oscar , Loda Massimo
Published: April 2023

Analysis of the metabolites present in the frozen cell samples and missed in the supernatant and FF cell samples categorized by superclass, class, subclass, substituent, physical/chemical properties, and pathways.
Supplemental material from Metabolic Profiling in Formalin-Fixed and Paraffin-Embedded Prostate Cancer Tissues
Authors: Cacciatore Stefano , Zadra Giorgia , Bango Clyde , Penney Kathryn L. , Tyekucheva Svitlana , Yanes Oscar , Loda Massimo
Published: April 2023

Supplemental material
Supplementary Table 3 from Gene Silencing Associated with SWI/SNF Complex Loss during NSCLC Development
Authors: Song Shujie , Walter Vonn , Karaca Mehmet , Li Ying , Bartlett Christopher S. , Smiraglia Dominic J. , Serber Daniel , Sproul Christopher D. , Plass Christoph , Zhang Jiren , Hayes D. Neil , Zheng Yanfang , Weissman Bernard E.
Published: April 2023

XLSX file - 67K, Genes upregulated by TSA only.
Supplementary Figure 6 from SGEF Is Regulated via TWEAK/Fn14/NF-κB Signaling and Promotes Survival by Modulation of the DNA Repair Response to Temozolomide
Authors: Ensign Shannon P. Fortin , Roos Alison , Mathews Ian T. , Dhruv Harshil D. , Tuncali Serdar , Sarkaria Jann N. , Symons Marc H. , Loftus Joseph C. , Berens Michael E. , Tran Nhan L.
Published: April 2023

Supplementary Figure 6. SGEF protein levels across a panel of primary parental versus TMZ-R xenografts.
Supplementary Figure 4 from SGEF Is Regulated via TWEAK/Fn14/NF-κB Signaling and Promotes Survival by Modulation of the DNA Repair Response to Temozolomide
Authors: Ensign Shannon P. Fortin , Roos Alison , Mathews Ian T. , Dhruv Harshil D. , Tuncali Serdar , Sarkaria Jann N. , Symons Marc H. , Loftus Joseph C. , Berens Michael E. , Tran Nhan L.
Published: April 2023

Supplementary Figure 4. TMZ treatment induces nuclear RhoG activity.
Comparison of the biochemical response to erlotinib between the EGFRvIII+ and EGFRÎ"768+ BE2C clones from A Novel EGFR Extracellular Domain Mutant, EGFRΔ768, Possesses Distinct Biological and Biochemical Properties in Neuroblastoma
Authors: Keller James , Nimnual Anjaruwee S. , Varghese Mathew S. , VanHeyst Kristen A. , Hayman Michael J. , Chan Edward L.
Published: April 2023

S5. Concentrations of erlotinib ranged from 0.025 - 2.5 uM. MW: molecular weight; Tx: treatment.
Data Supplement from Targeted Deletion and Lipidomic Analysis Identify Epithelial Cell COX-2 as a Major Driver of Chemically Induced Skin Cancer
Authors: Jiao Jing , Ishikawa Tomo-O , Dumlao Darren S. , Norris Paul C. , Magyar Clara E. , Mikulec Carol , Catapang Art , Dennis Edward A. , Fischer Susan M. , Herschman Harvey R.
Published: April 2023

Antibodies used for Immunohistochemistry analyses.
Supplementary Methods from Actin-Binding Protein, Espin: A Novel Metastatic Regulator for Melanoma
Authors: Yanagishita Takeshi , Yajima Ichiro , Kumasaka Mayuko , Kawamoto Yoshiyuki , Tsuzuki Toyonori , Matsumoto Yoshinari , Watanabe Daisuke , Kato Masashi
Published: April 2023

PDF file - 115K
Data Supplement from Cyclosporin A Promotes Tumor Angiogenesis in a Calcineurin-Independent Manner by Increasing Mitochondrial Reactive Oxygen Species
Authors: Zhou Alice Yao , Ryeom Sandra
Published: April 2023

Supplemental Figure 2: Adenovirus Cre infection in Calcineurin Bf/f (CnBf/f) endothelial cells results in the loss of calcineurin A protein.
Supplementary Table 1 from RNA-seq Reveals Aurora Kinase–Driven mTOR Pathway Activation in Patients with Sarcomatoid Metastatic Renal Cell Carcinoma
Authors: Pal Sumanta K. , He Miaoling , Tong Tommy , Wu Huiqing , Liu Xueli , Lau Clayton , Wang Jin-Hui , Warden Charles , Wu Xiwei , Signoretti Sabina , Choueiri Toni K. , Karam Jose A. , Jones Jeremy O.
Published: April 2023

RNA-seq QC data (C=clear cell, S=sarcomatoid, B=benign).
Video 2 from Therapeutic Targeting of Nuclear γ-Tubulin in RB1-Negative Tumors
Authors: Lindström Lisa , Villoutreix Bruno O. , Lehn Sophie , Hellsten Rebecka , Nilsson Elise , Crneta Enisa , Olsson Roger , Alvarado-Kristensson Maria
Published: April 2023

Video 2. Fluorescence images from a time-lapse confocal microscopy using a laser-scanning confocal microscope of a mitotic U2OS cell transiently expressing pmTurquoise2-tagged- ÃŽÂ±-tubulin (red) treated with 100 ÃŽÂ¼M CDA. Images were collected every 30 s.
Supplementary figure S6 from Therapeutic Targeting of Nuclear γ-Tubulin in RB1-Negative Tumors
Authors: Lindström Lisa , Villoutreix Bruno O. , Lehn Sophie , Hellsten Rebecka , Nilsson Elise , Crneta Enisa , Olsson Roger , Alvarado-Kristensson Maria
Published: April 2023

Supplementary figure S6. The body weight changes of treated mice xenografted with U1690RB1 cells.
Supplementary Methods from Differential Response of Glioma Stem Cells to Arsenic Trioxide Therapy Is Regulated by MNK1 and mRNA Translation
Authors: Bell Jonathan B. , Eckerdt Frank , Dhruv Harshil D. , Finlay Darren , Peng Sen , Kim Seungchan , Kroczynska Barbara , Beauchamp Elspeth M. , Alley Kristen , Clymer Jessica , Goldman Stewart , Cheng Shi-Yuan , James C. David , Nakano Ichiro , Horbinski Craig , Mazar Andrew P. , Vuori Kristiina , Kumthekar Priya , Raizer Jeffrey , Berens Michael E. , Platanias Leonidas C.
Published: April 2023

Relates to materials & methods.
Video S4 from Dual Targeting of Mesenchymal and Amoeboid Motility Hinders Metastatic Behavior
Authors: Jones Brandon C. , Kelley Laura C. , Loskutov Yuriy V. , Marinak Kristina M. , Kozyreva Varvara K. , Smolkin Matthew B. , Pugacheva Elena N.
Published: April 2023

Ibidi chemotactic invasion of MDA-MB-231 cells with NEDD9 and RhoA depletion
Supplementary Figure Legends from Dual Promoter Usage as Regulatory Mechanism of let-7c Expression in Leukemic and Solid Tumors
Authors: Pelosi Andrea , Careccia Silvia , Sagrestani Giulia , Nanni Simona , Manni Isabella , Schinzari Valeria , Martens Joost H.A. , Farsetti Antonella , Stunnenberg Hendrik G. , Gentileschi Maria Pia , Del Bufalo Donatella , De Maria Ruggero , Piaggio Giulia , Rizzo Maria Giulia
Published: April 2023

PDF file - 77KB
Supplementary Figures 1 - 6 from miR-21 Targets 15-PGDH and Promotes Cholangiocarcinoma Growth
Authors: Lu Lu , Byrnes Kathleen , Han Chang , Wang Ying , Wu Tong
Published: April 2023

PDF file - 964K, S1. Soft-agar colony formation assay. S2. Overexpression of miR-21 promotes cell invasion. S3. SG231 cells were transfected miR-21 inhibitor. S4. H69 cells were transfected with the control and COX-2 expression plasmids. S5. CCLP1 cells were transfected with miR-21 promoter reporter plasmid. S6. HuCCT1 cells were treated with the COX-2 inhibitor, NS-398, at indicated concentrations.
SUPPLEMENTARY FILE 8 - Imunnohistochemistry staining pattern of adjacente normal tissue for PLXDC2 and GNB3 from An Integrative Approach Uncovers Biomarkers that Associate with Clinically Relevant Disease Outcomes in Vulvar Carcinoma
Authors: Lavorato-Rocha Andre M. , Akagi Erica M. , de Melo Maia Beatriz , Rodrigues Iara S. , Botelho Mayara Caroline Silva , Marchi Fabio A. , Fernandes Gabriel , Baiocchi Glauco , Soares Fernando A. , Rogatto Silvia Regina , Sato-Kuwabara Yukie , Rocha Rafael M.
Published: April 2023

A - GNB3 immunohistochemistry staining; B - PLXDC2 immunohistochemistry staining
Supplemental Excel File 11 from A New Role for ERα: Silencing via DNA Methylation of Basal, Stem Cell, and EMT Genes
Authors: Ariazi Eric A. , Taylor John C. , Black Michael A. , Nicolas Emmanuelle , Slifker Michael J. , Azzam Diana J. , Boyd Jeff
Published: April 2023

Supplemental Excel File 11 - Low and high expression DMFS metagenes
S1. Tam induced IGFBP-1 transcription in MCF-7 cells from IGF-1 Receptor Modulates FoxO1-Mediated Tamoxifen Response in Breast Cancer Cells
Authors: Vaziri-Gohar Ali , Zheng Yan , Houston Kevin D.
Published: April 2023

qPCR analysis of IGFBP-1 transcription after 24h treatment with vehicle or 1 µM Tam in absence and presence of actinomycin D (2 μg/ml) pretreatment in MCF-7 cells in serum-free condition. * = p < 0.05 and results are representative of two independent experiments. Error bars are SEM.
Data Supplement from SMAD4 Suppresses AURKA-Induced Metastatic Phenotypes via Degradation of AURKA in a TGFβ-Independent Manner
Authors: Jia Lina , Lee Hun Seok , Wu Chun Fu , Kundu Juthika , Park Sang Gyu , Kim Ryong Nam , Wang Li-Hui , Erkin Özgür Cem , Choi Jong-Sun , Chae Seoung Wan , Yang Ho Bin , Choi Yoon-La , Shin Young Kee
Published: April 2023

Supplementary Figure 1A. HeLa cells were transfected with indicated plasmids as negative controls. Fluorescence images indicated in each panel were captured under fluorescence microscopy (Ã¯?'40) at 18 h after transfection. Scale bar, 5 ÃŽÂ¼m.
Legends for supplemental figure from Cyclin A2 and CDK2 as Novel Targets of Aspirin and Salicylic Acid: A Potential Role in Cancer Prevention
Authors: Dachineni Rakesh , Ai Guoqiang , Kumar D. Ramesh , Sadhu Satya S. , Tummala Hemachand , Bhat G. Jayarama
Published: April 2023

Supplemental Figure 1: Dose-dependent effect of aspirin and salicylic acid on the growth rates in HT-29, SK-MEL-28, and MDA-MB-231cells. Supplemental Figure 2: Dose-dependent effect of aspirin and salicylic acid on cyclins B1, D3 and E1 in HT-29 cells. Supplemental Figure 3: Dose-dependent effect of aspirin and salicylic acid on CDKs 1, 4 and 6. Supplemental Figure 4: Dose-dependent effect of aspirin and salicylic acid on CDK inhibitors p-21 and p-27. Supplemental Figure 5: Schematic representation of the steps involved in immunoprecipitation described for Fig. 5A and B. Supplemental Figure 6: Molecular docking studies on aspirin and salicylic acid with CDK2, cyclin A2, and CDK2/cyclin A2 complex.
Supplemental Information from Intrinsic Resistance to Cixutumumab Is Conferred by Distinct Isoforms of the Insulin Receptor
Authors: Forest Amelie , Amatulli Michael , Ludwig Dale L. , Damoci Christopher B. , Wang Ying , Burns Colleen A. , Donoho Gregory P. , Zanella Nina , Fiebig Heinz H. , Prewett Marie C. , Surguladze David , DeLigio James T. , Houghton Peter J. , Smith Malcolm A. , Novosiadly Ruslan
Published: April 2023

Supplemental Information. This file contains Supplemental Materials and Methods, Tables and Figure Legends
Supplementary Table S1 from Let-7 Status Is Crucial for PARP1 Expression in HER2-Overexpressing Breast Tumors
Authors: Wielgos Monica E. , Rajbhandari Rajani , Cooper Tiffiny S. , Wei Shi , Nozell Susan , Yang Eddy S.
Published: April 2023

Expression of miR-223 is not significantly altered between HER2- and HER2+ breast cancer cells.
Supplementary Figure S2 from Let-7 Status Is Crucial for PARP1 Expression in HER2-Overexpressing Breast Tumors
Authors: Wielgos Monica E. , Rajbhandari Rajani , Cooper Tiffiny S. , Wei Shi , Nozell Susan , Yang Eddy S.
Published: April 2023

Let-7a regulates c-myc and PARP1 protein expression levels.
Supplemental Figure S4 from MYC Mediates mRNA Cap Methylation of Canonical Wnt/β-Catenin Signaling Transcripts By Recruiting CDK7 and RNA Methyltransferase
Authors: Posternak Valeriya , Ung Matthew H. , Cheng Chao , Cole Michael D.
Published: April 2023

MYC promotes Wnt signaling activity in part by enhancing mRNA cap methylation.
Supplemental Figure S3 from MYC Mediates mRNA Cap Methylation of Canonical Wnt/β-Catenin Signaling Transcripts By Recruiting CDK7 and RNA Methyltransferase
Authors: Posternak Valeriya , Ung Matthew H. , Cheng Chao , Cole Michael D.
Published: April 2023

MYC-mediated mRNA cap methylation of MAX transcripts.
Supplemental Figure S2 from MYC Mediates mRNA Cap Methylation of Canonical Wnt/β-Catenin Signaling Transcripts By Recruiting CDK7 and RNA Methyltransferase
Authors: Posternak Valeriya , Ung Matthew H. , Cheng Chao , Cole Michael D.
Published: April 2023

Global total mRNA expression in P493-6 cells with varying MYC levels and validation in HO rat fibroblasts and IMEC cells.
Supplemental Figure 6 from AMPKα2 Regulates Bladder Cancer Growth through SKP2-Mediated Degradation of p27
Authors: Kopsiaftis Stavros , Sullivan Katie L. , Garg Isha , Taylor John A. , Claffey Kevin P.
Published: April 2023

Knockdown of SKP2 negates the effects of AMPKï�¡2 mediated control of p27 and cell proliferation.
Supplemental Figure S1 from MYC Mediates mRNA Cap Methylation of Canonical Wnt/β-Catenin Signaling Transcripts By Recruiting CDK7 and RNA Methyltransferase
Authors: Posternak Valeriya , Ung Matthew H. , Cheng Chao , Cole Michael D.
Published: April 2023

Schematic and validation of methyl-capped (m7G) mRNA pulldown.
Supplemental Figure 4 from AMPKα2 Regulates Bladder Cancer Growth through SKP2-Mediated Degradation of p27
Authors: Kopsiaftis Stavros , Sullivan Katie L. , Garg Isha , Taylor John A. , Claffey Kevin P.
Published: April 2023

AMPKï�¡2 knockdown alters cell cycle regulators.
Data Supplement from Extrinsic Apoptosis Is Impeded by Direct Binding of the APL Fusion Protein NPM-RAR to TRADD
Authors: Chattopadhyay Anuja , Hood Brian L. , Conrads Thomas P. , Redner Robert L.
Published: April 2023

Legend for Supplementary Figure
Supplemental Figure 2 from AMPKα2 Regulates Bladder Cancer Growth through SKP2-Mediated Degradation of p27
Authors: Kopsiaftis Stavros , Sullivan Katie L. , Garg Isha , Taylor John A. , Claffey Kevin P.
Published: April 2023

AMPK activation in bladder cancer alters cell cycle regulators.
Supplemental Figure 1 from AMPKα2 Regulates Bladder Cancer Growth through SKP2-Mediated Degradation of p27
Authors: Kopsiaftis Stavros , Sullivan Katie L. , Garg Isha , Taylor John A. , Claffey Kevin P.
Published: April 2023

AMPK activation reduces p27 through mTOR dependent mechanism.
Data Supplement from SNF5/INI1 Deficiency Redefines Chromatin Remodeling Complex Composition during Tumor Development
Authors: Wei Darmood , Goldfarb Dennis , Song Shujie , Cannon Courtney , Yan Feng , Sakellariou-Thompson Donastas , Emanuele Michael , Major Michael B. , Weissman Bernard E. , Kuwahara Yasumichi
Published: April 2023

Supplementary Table 2. A table of qPCR primers used for these studies.
Supplemental Data from Astrocyte Elevated Gene-1 Regulates β-Catenin Signaling to Maintain Glioma Stem-like Stemness and Self-Renewal
Authors: Hu Bin , Emdad Luni , Kegelman Timothy P. , Shen Xue-Ning , Das Swadesh K. , Sarkar Devanand , Fisher Paul B.
Published: April 2023

Legends for supplemental figures, table and antibody list
Supplementary Figure Legends from ERβ Regulates NSCLC Phenotypes by Controlling Oncogenic RAS Signaling
Authors: Nikolos Fotis , Thomas Christoforos , Rajapaksa Gayani , Bado Igor , Gustafsson Jan-Åke
Published: April 2023

PDF file - 110K
Supplementary Tables 1 - 15 from Whole Transcriptome Sequencing Reveals Extensive Unspliced mRNA in Metastatic Castration-Resistant Prostate Cancer
Authors: Sowalsky Adam G. , Xia Zheng , Wang Liguo , Zhao Hao , Chen Shaoyong , Bubley Glenn J. , Balk Steven P. , Li Wei
Published: April 2023

Supplementary Table 1. Normalized RPKM expression values and normalized Affymetrix microarray intensity values for each CRPC sample used for correlation analysis. Supplementary Table 2. Complete listing of high probability, protein-coding somatic mutations detected by RNA-seq in CRPC samples. Mutations are classified as either a nonsense or missense single nucleotide variant (SNV) or as a >1 base insertion (INS) or deletion (DEL). The gene symbol and Genbank ID is provided for each predicted amino acid change given. Supplementary Table 3. High confidence putative fusions detected by ChimeraScan (at least one breakpoint-spanning read) and deFuse (greater than 50% probability score) for each CRPC sample. Supplementary Table 4. RPKM values for approximately 45,500 transcripts for all 8 CRPC samples. Supplementary Table 5. Top 100 expressed genes as measured by the mean RPKM across all 8 CRPC samples. Supplementary Table 6. Top 100 expressed genes as measured by the median RPKM across all 8 CRPC samples. Supplementary Table 7. Novel candidate lncRNAs observed CRPC. List is sorted by average FPKM for expression of the lncRNA. Supplementary Table 8. Transcripts, gene names, and gene description for the 1,465 transcripts with the widest range of expression used for unsupervised clustering of TCGA and CRPC samples. The average RPKM difference between CRPC and TCGA primary prostate cancers is shown. Supplementary Table 9. RNA-SeQC mapping statistics for 8 CRPC RNA-seq samples. For each sample, the Illumina instrument model, RIN score, type of run, and the number of total and uniquely-mapping reads is shown. In addition, it is indicated which percentage of quality-filtered reads mapped to exon, intron or intergenic coordinates, the number of Ensembl genes determined as expressed, and the percentage of reads mapping to ribosomal RNA. Supplementary Tables 10-11. Intronic RPB values for genes in CRPC 49 and 66. Supplementary Table 12. Global analysis of splicing in CRPC. For each CRPC sample, the number of sequence reads uniquely mapping to an exon-exon splice junction or overlapping an exon-intron splice boundary is shown. The percentage of unspliced out of the total is indicated. Supplementary Table 13. Primer sequences for the detection of correctly or incorrectly spliced portions of AR, KLK2, KLK3, STEAP2, CPSF6, and CDK19. Supplementary Table 14. Complete results for ChimeraScan on CRPC samples. Supplementary Table 15. Complete results for deFuse on CRPC samples.
Supplementary Table Legends from Whole Transcriptome Sequencing Reveals Extensive Unspliced mRNA in Metastatic Castration-Resistant Prostate Cancer
Authors: Sowalsky Adam G. , Xia Zheng , Wang Liguo , Zhao Hao , Chen Shaoyong , Bubley Glenn J. , Balk Steven P. , Li Wei
Published: April 2023

Supplementary Table Legends
Supplementary Table 5 from Mutational Landscape of the Essential Autophagy Gene BECN1 in Human Cancers
Authors: Laddha Saurabh V. , Ganesan Shridar , Chan Chang S. , White Eileen
Published: April 2023

PDF file - 1483KB, Table S5. Gene expression levels of BECN1 across different cancer types.
Supplementary Table 3 from Mutational Landscape of the Essential Autophagy Gene BECN1 in Human Cancers
Authors: Laddha Saurabh V. , Ganesan Shridar , Chan Chang S. , White Eileen
Published: April 2023

PDF file - 1462KB, Table S3. The types of somatic mutations found for BECN1.
Supplementary Figure 5 from Whole Transcriptome Sequencing Reveals Extensive Unspliced mRNA in Metastatic Castration-Resistant Prostate Cancer
Authors: Sowalsky Adam G. , Xia Zheng , Wang Liguo , Zhao Hao , Chen Shaoyong , Bubley Glenn J. , Balk Steven P. , Li Wei
Published: April 2023

Clustering and pathway analysis of CRPC samples.
Supplementary Figure 3 from Whole Transcriptome Sequencing Reveals Extensive Unspliced mRNA in Metastatic Castration-Resistant Prostate Cancer
Authors: Sowalsky Adam G. , Xia Zheng , Wang Liguo , Zhao Hao , Chen Shaoyong , Bubley Glenn J. , Balk Steven P. , Li Wei
Published: April 2023

PHF20L1:LRRC6 fusion transcript detected in CRPC 66.
Supplemental Figures from Targeting AR Variant–Coactivator Interactions to Exploit Prostate Cancer Vulnerabilities
Authors: Magani Fiorella , Peacock Stephanie O. , Rice Meghan A. , Martinez Maria J. , Greene Ann M. , Magani Pablo S. , Lyles Rolando , Weitz Jonathan R. , Burnstein Kerry L.
Published: April 2023

Supplemental Figure 1: Expression of Vav3 DH domain inhibits the growth of AR-expressing cells only, and does not decrease total levels of FL-AR, AR-V7, Vav3 or Vav2. Supplemental Figure 2: Disruption of coactivator interactions with FL-AR or AR-V7 increases cell death through apoptosis.
Supplementary Table 1 from High-Throughput Drug Screen Identifies Chelerythrine as a Selective Inducer of Death in a TSC2-null Setting
Authors: Medvetz Doug , Sun Yang , Li Chenggang , Khabibullin Damir , Balan Murugabaskar , Parkhitko Andrey , Priolo Carmen , Asara John M. , Pal Soumitro , Yu Jane , Henske Elizabeth P.
Published: April 2023

List of hits from HTS.
Supplementary Figure 2 from High-Throughput Drug Screen Identifies Chelerythrine as a Selective Inducer of Death in a TSC2-null Setting
Authors: Medvetz Doug , Sun Yang , Li Chenggang , Khabibullin Damir , Balan Murugabaskar , Parkhitko Andrey , Priolo Carmen , Asara John M. , Pal Soumitro , Yu Jane , Henske Elizabeth P.
Published: April 2023

CI-1040 and PD8059 inhibited phosphorylation of Erk1/2 in Tsc2+/+ and Tsc2-/- MEFs.
Supplementary Figure 1 from High-Throughput Drug Screen Identifies Chelerythrine as a Selective Inducer of Death in a TSC2-null Setting
Authors: Medvetz Doug , Sun Yang , Li Chenggang , Khabibullin Damir , Balan Murugabaskar , Parkhitko Andrey , Priolo Carmen , Asara John M. , Pal Soumitro , Yu Jane , Henske Elizabeth P.
Published: April 2023

Paroxetine inhibits the growth of Tsc2-null ELT3-V3 cells.
Supplemental Figure Legends from EWS/FLI is a Master Regulator of Metabolic Reprogramming in Ewing Sarcoma
Authors: Tanner Jason M. , Bensard Claire , Wei Peng , Krah Nathan M. , Schell John C. , Gardiner Jamie , Schiffman Joshua , Lessnick Stephen L. , Rutter Jared
Published: April 2023

Figure legends for Supplemental Figures S1, S2 and S3.
Figure S2 from EWS/FLI is a Master Regulator of Metabolic Reprogramming in Ewing Sarcoma
Authors: Tanner Jason M. , Bensard Claire , Wei Peng , Krah Nathan M. , Schell John C. , Gardiner Jamie , Schiffman Joshua , Lessnick Stephen L. , Rutter Jared
Published: April 2023

MetaboAnalyst plot, western blots confirmation of EF, SHMT2, and PHGDH.
Supplemental Methods, Table 1 from CD44 Regulates Pancreatic Cancer Invasion through MT1-MMP
Authors: Jiang Wei , Zhang Yaqing , Kane Kevin T. , Collins Meredith A. , Simeone Diane M. , di Magliano Marina Pasca , Nguyen Kevin Tri
Published: April 2023

Detailed methods, list of primers and antibodies.
Supplemental Figure legends from CD44 Regulates Pancreatic Cancer Invasion through MT1-MMP
Authors: Jiang Wei , Zhang Yaqing , Kane Kevin T. , Collins Meredith A. , Simeone Diane M. , di Magliano Marina Pasca , Nguyen Kevin Tri
Published: April 2023

Legends for figures S1-S3
Supplementary Table 1 from HDAC Inhibition for the Treatment of Epithelioid Sarcoma: Novel Cross Talk Between Epigenetic Components
Authors: Lopez Gonzalo , Song Yechun , Lam Ryan , Ruder Dennis , Creighton Chad J. , Bid Hemant Kumar , Bill Kate Lynn , Bolshakov Svetlana , Zhang Xiaoli , Lev Dina , Pollock Raphael E.
Published: April 2023

The Molecular Signatures Database (MSigDB) analysis associates EZH2 transcriptional targets with HDACi-induced differential expression (NUYTTEN_EZH2_TARGETS_UP, genes up-regulated in prostate cancer cell line PC3 after EZH2 siRNA knockdown.
Supplemental Figure S2 from CD44 Regulates Pancreatic Cancer Invasion through MT1-MMP
Authors: Jiang Wei , Zhang Yaqing , Kane Kevin T. , Collins Meredith A. , Simeone Diane M. , di Magliano Marina Pasca , Nguyen Kevin Tri
Published: April 2023

CD44 regulates EMT genes.
Supplemental Figure S1 from CD44 Regulates Pancreatic Cancer Invasion through MT1-MMP
Authors: Jiang Wei , Zhang Yaqing , Kane Kevin T. , Collins Meredith A. , Simeone Diane M. , di Magliano Marina Pasca , Nguyen Kevin Tri
Published: April 2023

CD44 regulates pancreatic cancer invasion and metastasis.
Supplemental Figure Legends from HDAC Inhibition for the Treatment of Epithelioid Sarcoma: Novel Cross Talk Between Epigenetic Components
Authors: Lopez Gonzalo , Song Yechun , Lam Ryan , Ruder Dennis , Creighton Chad J. , Bid Hemant Kumar , Bill Kate Lynn , Bolshakov Svetlana , Zhang Xiaoli , Lev Dina , Pollock Raphael E.
Published: April 2023

Supplemental Data Figure Legends 1-3, Supplemental Table 1
Supplementary Figure 5 from Active FOXO1 Is a Key Determinant of Isoform-Specific Progesterone Receptor Transactivation and Senescence Programming
Authors: Diep Caroline H. , Knutson Todd P. , Lange Carol A.
Published: April 2023

FOXO1 enhances PR Ser294 phosphorylation in PR-B+ cells.
Supplementary Figure 5 from The Nuclear Pool of Tetraspanin CD9 Contributes to Mitotic Processes in Human Breast Carcinoma
Authors: Rappa Germana , Green Toni M. , Lorico Aurelio
Published: April 2023

Nuclear expression of CD9 in breast cancer patients employing an anti-CD9 mAb against a different epitope.
Legends of Supplemental Figures from Nuclear Receptor CAR Suppresses GADD45B-p38 MAPK Signaling to Promote Phenobarbital-induced Proliferation in Mouse Liver
Authors: Hori Takeshi , Saito Kosuke , Moore Rick , Flake Gordon P. , Negishi Masahiko
Published: April 2023

Legends of Supplemental Figures
Supplementary Figure S5 from IL8 Expression Is Associated with Prostate Cancer Aggressiveness and Androgen Receptor Loss in Primary and Metastatic Prostate Cancer
Authors: Maynard Janielle P. , Ertunc Onur , Kulac Ibrahim , Baena-Del Valle Javier A. , De Marzo Angelo M. , Sfanos Karen S.
Published: April 2023

Supplementary Figure S5 shows CCLE data on IL-8 and AR mRNA co-expression as well as examples of IL-8 expression in AR null metastases.
Supplementary Table S3 from Runx2 Suppression by miR-342 and miR-363 Inhibits Multiple Myeloma Progression
Authors: Gowda Pramod S. , Wildman Benjamin J. , Trotter Timothy N. , Xu Xiaoxuan , Hao Xiaoxiao , Hassan Mohammad Q. , Yang Yang
Published: April 2023

Target UTR fragment sequences cloned in pMIR-REPORT-Luc vector (Addgene Cambridge, MA).