bluuebunny/crossref_metadata_2025 huggingface dataset:
Abstract 725: Prostate cancer risk disparities and sociocultural factors in men of African ancestry
Authors: Brown Joan M.
Published: April 2023

Introduction: The purpose of this research study was to quantify the prostate cancer (PCa) mortality rate in Men of African Ancestry (MAA) living in the State of Florida, the tri-county region of South Florida including Broward, Palm Beach, and Miami-Dade, and to explore the embodiment of sociocultural factors that contribute to the PCa disparity in the United State (U.S.).

Method: A quantitative, non-experimental, descriptive study design was used to identify differences in the resident PCa mortality rate in MAA stratified based on single race of Black and birth origin of Haiti (HA), Jamaica (JA), or the United States (U.S.). The intersection of health disparities and the embodiment of chronic exposure to sociocultural stressors was also explored.

Results: The Paired t-Test was used for statistical testing. The results indicated death from PCa is a health disparity in MAA in Florida when examined in aggregate by ancestry and disaggregate by birth origin. In the state of Florida, when the PCa death rate was viewed in aggregate by ancestry, a significant difference was found between MAA and Men of European Ancestry (MEA) (t(2)=4.303, p≤.01). There was a statistically significant relationship found between being MAA and death from PCa (r=.866, p≤.01). This suggests there are place based health disparities among MAA in the State of Florida. When the PCa mortality rate in MAA in the tri county region of South Florida was examined in aggregate by ancestry versus disaggregate by birth origin a significant difference was shown between MAA and HA born men (t(2)=4.30, p=0.05). No difference was shown between MAA and U.S., or JA born men. By county, the highest death rate was found in JA born men in Miami-Dade, and HA born men in Broward and Palm Beach. Overall, the lowest death rates in each county were found in U.S. born men. The results suggest that there are clear placed based and birth origin disparities in the South Florida region.

Conclusions: Examining differences in the PCa mortality rates in MAA in disaggregate by birth origin provides opportunity for the observation of sociocultural factors that affect health such as cultural beliefs and fears, chronic exposure to stressors such as structural and explicit racism and racialization in the U.S, immigration status and barriers to healthcare; all sociocultural factors that if examined may aid in explaining the increased rate of PCa death experienced by MAA and why the disparity exists.

Citation Format: Joan M. Brown. Prostate cancer risk disparities and sociocultural factors in men of African ancestry [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 725.
Abstract 975: Treatment prognostic signature of patients with non-small cell lung cancer: a retrospective single-institutional study
Authors: Smith Margaret R. , Wang Yuezhu , D' Agostino Ralph , Liu Yin , Ruiz Jimmy , Lycan Thomas , Oliver George , Topaloglu Umit , Pinkney Jireh , Abdulhaleem Mohammed N. , Chan Michael D. , Farris Michael , Su Jing , Xing Fei
Published: April 2023

Introduction: Currently, several types of treatment can be used to treat non-small cell lung cancer (NSCLC) depending on a potential druggable mutation or stage of cancer. However, a limited number of biomarkers are available to guide clinicians in selecting the most effective therapy for all patients.

Methods: The clinical characteristics of 642 NSCLC patients and tumor sequencing data were collected retrospectively at Atrium Health Wake Forest Baptist. Cox-proportional hazard regression models were fit to identify mutations that were “beneficial” (hazard ratio < 1) or “detrimental” (hazard ratio > 1) for patients on different treatment regimens, followed by the generation of mutation composite scores (MCS) for each treatment. The overall survival (OS) of patients receiving each treatment was plotted based on the patients’ MCS, and receiver operating characteristics (ROC) curves tested the predictive power of each MCS for each treatment group. We also identified novel co-occurring and mutually exclusive mutations in each treatment group by mutation interaction analysis.

Results: We identified treatment-specific mutations associated with either a better or worse OS. The MCS generated for each treatment group significantly enhanced the prediction power compared to a single mutation with limited application in patients with rare mutations. Mutation signatures to chemotherapy (NTRK1, FBXW7, BRAF, MPL, KRAS, and GATA3) and immunotherapy (MAP2K1, EGFR, CDK4, NTRK1, and NOTCH1) have a comparable prediction power with actual clinical response.

Conclusions: NSCLC patients’ responses to specific treatments are diverse because of tumor heterogeneity. Our work demonstrates how analyzing patients’ sequencing data facilitates the clinical selection of optimized treatment strategies.

Citation Format: Margaret R. Smith, Yuezhu Wang, Ralph D' Agostino, Yin Liu, Jimmy Ruiz, Thomas Lycan, George Oliver, Umit Topaloglu, Jireh Pinkney, Mohammed N. Abdulhaleem, Michael D. Chan, Michael Farris, Jing Su, Fei Xing. Treatment prognostic signature of patients with non-small cell lung cancer: a retrospective single-institutional study [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 975.
Abstract 985: An innovative spatial biology biomarker discovery approach to enable acceleration of drug development
Authors: Reeves Jason W. , Anguiano Esperanza , Devgan Vikram , Confuorto Nicholas , Schmid Joachim , Liang Yan , Beechem Joseph
Published: April 2023

Biomarker development in the clinical trial setting is frequently limited by the availability of small tissue specimens, such as core needle biopsies. To enable forward and reverse translational assays to best understand patient-specified biomarkers, high-plex assays which can be performed on individual slides are critical. We’ve developed the GeoMx® Digital Spatial Profiler (DSP) and CosMx™ Spatial Molecular Imager (SMI) to allow researchers to explore more hypotheses simultaneously from standard histopathology slides. We demonstrate on standard FFPE sections how the GeoMx and CosMx platforms integrate within the context of biomarker discovery. The GeoMx platform can resolve transcriptome-wide RNA expression profiles or 150+ protein targets from tissue structures selected by pathological review. The CosMx platform allows subcellular profiling of up to 1000 RNA transcripts or 64 proteins from a single slide. We demonstrate the integration of GeoMx and CosMx into a multi-modal approach to how high-plex spatial platforms can complement conventional diagnostic assays for translational research. This includes integration with downstream analytical tools such as digital pathology suites as well as machine learning approaches to model patient outcomes. Spatial technologies, such as GeoMx and CosMx, present groundbreaking opportunities for improving accuracy in biomarker discovery and for providing rich biological insight beyond low-plex profiling approaches.

Citation Format: Jason W. Reeves, Esperanza Anguiano, Vikram Devgan, Nicholas Confuorto, Joachim Schmid, Yan Liang, Joseph Beechem. An innovative spatial biology biomarker discovery approach to enable acceleration of drug development [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 985.
Abstract 991: Leveraging sequences missing from the human genome to detect cancer
Authors: Barnea Ofer Yizhar , Georgakopoulos-Soares Ilias , Ahituv Nadav , Chapman Jocelyn , Hemberg Martin , Mouratidis Ioannis , Syrigos Konstantinos , Syrigos Nikolaos , Vathiotis Ioannis , Mahajan Mayank , Panagiotou Emmanouil , Charpidou Andriani , Kvale Mark , Chan Candace S. , Easterlin Ryder
Published: April 2023

Introduction: Cancer diagnosis using cell-free DNA (cfDNA) has the potential to improve treatment and survival but has several technical limitations.

Methods: Here, we used neomers, short DNA sequences (13-17bp in length) that are largely absent from the healthy human genome, but appear in the tumor genome due to somatic mutations, to detect cancer at early stages from cfDNA. cfDNA was extracted from 1mL of plasma, and utilized from Whole Genome Sequencing at 5X coverage.

Results: First, we analyzed over 2,500 cancer whole-genome sequences (WGS), to show that a neomer-based classifier can distinguish twenty-one different tumor types with higher accuracy than state-of-the-art methods. Refinement of this classifier via manually selected neomer sets, identified additional cancer features with greater precision. We next generated cfDNA WGS data from >600 patients and non-cancerous controls across four different types of cancers (prostate, lung, ovarian, colorectal), and demonstrated that neomers can precisely identify cancer from a limited amount of plasma for all four cancer types, with exampled sensitivities of 93.73% and 73.47% for lung and ovarian cancers, respectively. Additionally, using both luciferase and massively parallel reporter assays (MPRAs), we show that our neomer-driven approach can detect cancer-associated non-coding mutations that affect gene regulatory activity.

Conclusions: Our results show that neomers provide a novel, sensitive, specific and potentially broadly applicable cancer detection tool. This approach has several advantages over existing strategies for liquid biopsies: 1) it is based on standard next-generation sequencing which is already widely available in the clinic; 2) it requires low amounts of starting material and is completely tumor agnostic; 3) it searches the entire genome and is not restricted to known driver mutations. 4) it allows the detection of early-stage disease.

Citation Format: Ofer Yizhar Barnea, Ilias Georgakopoulos-Soares, Nadav Ahituv, Jocelyn Chapman, Martin Hemberg, Ioannis Mouratidis, Konstantinos Syrigos, Nikolaos Syrigos, Ioannis Vathiotis, Mayank Mahajan, Emmanouil Panagiotou, Andriani Charpidou, Mark Kvale, Candace S. Chan, Ryder Easterlin. Leveraging sequences missing from the human genome to detect cancer [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 991.
Abstract PL04-05: LAG3: The third checkpoint inhibitor
Authors: Vignali Dario A.
Published: April 2023

Immunotherapies targeting the PD1/PDL1 pathway have had a major impact on cancer treatment. However, only a proportion of patients respond, and an even smaller proportion exhibit a long-term, durable cure. Several mechanisms of resistance and potential combinatorial approaches will be discussed. Lack of response to inhibitory receptor (IR) blockade therapy and increased disease burden has been associated with circulating, peripheral CD8+ T cell exhaustion, which is defined by poor T cell function linked to increased IR expression (eg: PD1, LAG3, neuropilin-1 [NRP1]). LAG3 is the third IR to be targeted in the clinic, consequently garnering considerable interest and scrutiny. However, persistent antigen exposure in the tumor microenvironment results in sustained PD1/LAG3 expression, contributing to a state of exhaustion manifest in impaired proliferation and cytokine production. This presentation will include a brief introduction LAG3, discussion of the signaling mechanism used by LAG3, and assessment of new insight in to the function of LAG3, alone and in combination with PD1, from mouse models of cancer and analysis of samples from patients treated with LAG3/PD1 therapeutics.

Citation Format: Dario A. Vignali. LAG3: The third checkpoint inhibitor. [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 PL04-05.
Abstract SY04-01: Understanding and targeting RNA splicing in breast cancer
Authors: Anczukow Olga A.
Published: April 2023

Upregulation of SR proteins, a family of 14 essential splicing factors (SFs), often occurs in solid tumors, including in breast, and promotes mammary cell transformation and metastasis in breast cancer models. SR protein alterations often occur without genomic copy number changes, suggesting misregulation at the transcriptional or post-transcriptional levels; however the underlying molecular mechanisms are incompletely understood. Here we investigate the transcriptional and post-transcriptional regulatory mechanisms that control SF-levels in normal mammary cells and their misregulation in cancer cells. We demonstrate the MYC oncogene directly regulates a network of splicing factors that are co-expressed in tumors and act together to regulate their downstream targets and promote cell invasion. In parallel, our work reveals the role of non-coding ‘poison exon’ in regulating SR proteins levels during cell differentiation and in tumors. We uncover an extensive cross-regulatory network used by the SR protein family to control their expression. Finally, we develop splice-switching antisense oligonucleotides to reverse the increased skipping of TRA2β poison exon detected in tumors, leading to selective anti-proliferative effects across a variety of cancer models. In summary, our work provides new insights into the regulatory mechanisms of SR proteins and identifies novel oncogenic spliced isoforms that represent potential biomarkers and targets for therapeutics development.

Citation Format: Olga A. Anczukow. Understanding and targeting RNA splicing in breast cancer. [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 SY04-01.
Abstract SY17-03: Age-related changes in the tumor microenvironment drive tumor progression
Authors: Stewart Sheila A.
Published: April 2023

Cancer is a disease of the aged. While the accumulation of cell autonomous mutations contributes to tumorigenesis, the central role age-related changes in the tumor microenvironment play in the transformation process is becoming more fully appreciated. Underscoring the importance of an aged microenvironment in cancer development are findings that senescent fibroblasts, which accumulate with age, directly stimulate preneoplastic and neoplastic cell growth and tumor progression. Investigations into how senescent fibroblasts promote tumorigenesis revealed that they express a plethora of growth factors, extracellular matrix remodeling enzymes, chemokines, and cytokines collectively referred to as the senescence associated secretory phenotype (SASP). To identify a role for senescent stromal cells in a spontaneous model of breast cancer, we used single cell RNA-Sequencing (scRNA-Seq) to interrogate the cell types and their functional status in the MMTV-PyMT breast tumor model. This analysis revealed the presence of senescent cancer associated fibroblasts (senCAFs) that we also identified in a human triple negative breast cancer scRNA-Seq database. To establish a role for senCAFs in breast cancer, we mated the PyMT model to the INKATTAC (INK) mouse that allowed us to inducibly eliminate senescent cells. We found that the elimination of senCAFs reduced tumor growth and unleashed the killing power of NK cells. We will discuss the mechanism by which senCAFs impact NK cell killing.

Citation Format: Sheila A. Stewart. Age-related changes in the tumor microenvironment drive tumor progression. [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 SY17-03.
Abstract SY19-02: Engineering a potent T-cell response against solid tumors
Authors: Saus Cristina Puig
Published: April 2023

The success of T cell therapies for solid tumors has been limited by the scarcity of tumor-specific targets, the T cell exhaustion and immunosuppressive tumor microenvironment, and the limited persistence and T cell trafficking to the tumor, among others. To better understand how successful T cell responses induced by immune checkpoint blockade (ICB) eliminate metastatic tumors, we conducted a longitudinal landscape analysis of the neoepitope-specific T cells during treatment in patients with melanoma, with and without response to ICB. Using newly developed technologies to isolate neoepitope-specific T cells, we characterized the target of the T cell responses and their evolution over time in the peripheral blood and the tumor. Briefly, after computational prediction of patient-specific putative neoantigens, hundreds of capture reagents were made consisting of the patient HLA class I subtypes loaded with the corresponding predicted neoantigens; neoepitope-specific T cells were then isolated, and the TCR alpha and beta sequenced. Tumor reactivity of the neoantigen-specific TCRs was assessed upon co-culture of autologous melanoma cell lines from each patient with T cells gene-edited to replace their endogenous TCR with the isolated neoantigen-specific TCRs. In these studies, we showed that all patients presented neoantigen-specific T cell responses that were tumor-reactive and targeted a limited number of immunodominant epitopes. Interestingly, in patients with clinical benefit from ICB, these responses were polyclonal, with multiple TCR clonotypes specific for the same mutations, and recurrently detected over time. Our results show that even in patients without response to ICB, we could isolate neoantigen-specific TCRs that could potentially be used to engineer large numbers of T cells for adoptive T cell therapy.

Another alternative for patients that do not respond to ICB is adoptive T cell therapy with T cells genetically modified to target shared antigens. We propose targeting the surface expression of TYRP1 for the treatment of cutaneous and rare subtypes of melanoma. TYRP1 is mainly expressed intracellularly in the melanosomes, with a small fraction of the total protein localized on the cell surface. Using a fine-tuning engineering approach, we developed a highly-sensitive CAR-T cell therapy that detects the low amounts of TYRP1 localized on the cell surface of tumor cells with high TYRP1 intracellular overexpression. The TYRP1 CAR-T cell therapy presents robust antitumor activity without toxicity in murine and patient-derived cutaneous, acral, and uveal melanoma models. Based on the efficacy and safety profile of this therapy, we are currently planning the phase I clinical trial.

Citation Format: Cristina Puig Saus. Engineering a potent T-cell response against solid 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 SY19-02.
Supplementary Table 1 from 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 S4 from Activation of the FGF2-FGFR1 Autocrine Pathway: A Novel Mechanism of Acquired Resistance to Gefitinib in NSCLC
Authors: Terai Hideki , Soejima Kenzo , Yasuda Hiroyuki , Nakayama Sohei , Hamamoto Junko , Arai Daisuke , Ishioka Kota , Ohgino Keiko , Ikemura Shinnosuke , Sato Takashi , Yoda Satoshi , Satomi Ryosuke , Naoki Katsuhiko , Betsuyaku Tomoko
Published: April 2023

Supplementary Figure S4 - PDF file 107K, DNA quantification for FGFR1 by quantitative-PCR. DNA copy number was not increased in PC9 GR and PC9 gr1 cells
Supplementary Figure Legend from A Modified HSP70 Inhibitor Shows Broad Activity as an Anticancer Agent
Authors: Balaburski Gregor M. , Leu Julia I.-Ju , Beeharry Neil , Hayik Seth , Andrake Mark D. , Zhang Gao , Herlyn Meenhard , Villanueva Jessie , Dunbrack Roland L. , Yen Tim , George Donna L. , Murphy Maureen E.
Published: April 2023

PDF file - 45K
Supplementary Figure 3 from A Modified HSP70 Inhibitor Shows Broad Activity as an Anticancer Agent
Authors: Balaburski Gregor M. , Leu Julia I.-Ju , Beeharry Neil , Hayik Seth , Andrake Mark D. , Zhang Gao , Herlyn Meenhard , Villanueva Jessie , Dunbrack Roland L. , Yen Tim , George Donna L. , Murphy Maureen E.
Published: April 2023

PDF file - 395K, A) Binding assays of H1299 cells transfected with HA-tagged full-length and truncated HSP70 encoding the amino acids (aa) shown, treated with 20 uM biotinylated PES (B-PES) and 20 uM PES-Cl (PES-Cl). Biotinylated PES complexes were precipitated with avidin beads, eluted and detected with an anti-HA antibody following imunoblotting. Input is shown on the top panel, immunoprecipitation (IP) with avidin is depicted on the bottom panel. B) Cell viability of WI38 non-transformed fibroblasts after 48 hour treatment with 10 uM PES and PES-Cl. The values shown are the averaged results from three independent experiments, and error bars mark standard deviations. C) Western blot analysis of HSP90 client proteins in soluble cell extract following 48 hours of treatment with 10 uM PES-Cl. Actin is shown as a loading control. D) In silico docking of PES-Cl to the substrate binding domain of HSP70.
Supplementary Figure 2 from A Modified HSP70 Inhibitor Shows Broad Activity as an Anticancer Agent
Authors: Balaburski Gregor M. , Leu Julia I.-Ju , Beeharry Neil , Hayik Seth , Andrake Mark D. , Zhang Gao , Herlyn Meenhard , Villanueva Jessie , Dunbrack Roland L. , Yen Tim , George Donna L. , Murphy Maureen E.
Published: April 2023

PDF file - 280K, A) Chemical structures of PES and synthesized derivatives. P=pyrrolidine; CM= carboxymethyl; Cl=chloride. B) MTT cell viability analyses of H1299 and PANC1 cells after 48 hour treatment with 10 uM PES, PES-P, PES-PCM and PES-PCl. The values shown are the averaged results from three independent experiments, and error bars mark standard deviations. C) Immunoblot analysis of H1299 cells following treatment with 10 uM of the compounds indicated for the timepoints indicated, using antisera to the autophagy (p62SQSTM1 and LC3) and apoptosis (cleaved lamin A) markers indicated, as well as HSP70 and actin (control). The arrows mark monomeric and oligomeric forms of p62SQSTM1, as well as cleaved and lipidated forms of LC3 I and II.
Supplementary Table 3 from Comparative microRNA Profiling of Prostate Carcinomas with Increasing Tumor Stage by Deep Sequencing
Authors: Hart Martin , Nolte Elke , Wach Sven , Szczyrba Jaroslaw , Taubert Helge , Rau Tilman T. , Hartmann Arndt , Grässer Friedrich A. , Wullich Bernd
Published: April 2023

PDF file - 85K, Results of Illumina sequencing of small RNAs with corresponding relative expression of miRNAs. The miRNA expression in five RNA pools of normal, normal prostate, pT2, pT3 and lymph node metastasizing (pN1) PCa was analyzed by deep sequencing. The absolute number of all identified transcripts in the five cDNA libraries, as well as relative expression as a percentage of the total miRNA count, is given for every miRNA found.
Supplementary Figure 1 from Comparative microRNA Profiling of Prostate Carcinomas with Increasing Tumor Stage by Deep Sequencing
Authors: Hart Martin , Nolte Elke , Wach Sven , Szczyrba Jaroslaw , Taubert Helge , Rau Tilman T. , Hartmann Arndt , Grässer Friedrich A. , Wullich Bernd
Published: April 2023

PDF file - 205K, Validation of the microRNA expression profile by Northern blotting. For confirmation of the results obtained by the sequencing the relative expression levels of miR-375, -148a, -200b, -20a, -15a, -145, -143 and let-7c in the RNA pools used for sequencing were analyzed by northern blotting using specific radiolabeled probes. tRNA served as loading control. A PhosphoImager? was used for visualization of the hybridized probes.
Supplementary Figure Legends from Bioactive Lipids S1P and C1P Are Prometastatic Factors in Human Rhabdomyosarcoma, and Their Tissue Levels Increase in Response to Radio/Chemotherapy
Authors: Schneider Gabriela , Bryndza Ewa , Abdel-Latif Ahmed , Ratajczak Janina , Maj Magdalena , Tarnowski Maciej , Klyachkin Yuri M. , Houghton Peter , Morris Andrew J. , Vater Axel , Klussmann Sven , Kucia Magdalena , Ratajczak Mariusz Z.
Published: April 2023

Supplementary Figure Legends - PDF files 72K, Supplementary Figure Legends
Supplementary Figure 2 from Bioactive Lipids S1P and C1P Are Prometastatic Factors in Human Rhabdomyosarcoma, and Their Tissue Levels Increase in Response to Radio/Chemotherapy
Authors: Schneider Gabriela , Bryndza Ewa , Abdel-Latif Ahmed , Ratajczak Janina , Maj Magdalena , Tarnowski Maciej , Klyachkin Yuri M. , Houghton Peter , Morris Andrew J. , Vater Axel , Klussmann Sven , Kucia Magdalena , Ratajczak Mariusz Z.
Published: April 2023

Supplementary Figure 2 - PDF file 174KB, High levels of S1P and C1P in CM from irradiated organs create a pro-metastatic microenvironment
Supplementary Figure 1, Tables 1 - 3 from Loss of the Nucleosome-Binding Protein HMGN1 Affects the Rate of N-Nitrosodiethylamine-Induced Hepatocarcinogenesis in Mice
Authors: Postnikov Yuri V. , Furusawa Takashi , Haines Diana C. , Factor Valentina M. , Bustin Michael
Published: April 2023

PDF file - 390K, Supplementary Figure 1. Histopathology of early lesions in DEN-injected Hmgn1+/+ and Hmgn1 tm1/tm1 at 25 weeks of age. Supplementary Table S1. Primers used in the study. Supplementary Table S2. List of differentially expressed genes (FC>2, p?0.01) in livers of Hmgn1+/+ and Hmgn1tm1/tm1 mice in groups A, B, and C. Supplementary Table S3. GO analysis of the differentially expressed genes
Supplementary Table 2 from Alpha-CaMKII Plays a Critical Role in Determining the Aggressive Behavior of Human Osteosarcoma
Authors: Daft Paul G. , Yuan Kaiyu , Warram Jason M. , Klein Michael J. , Siegal Gene P. , Zayzafoon Majd
Published: April 2023

Supplementary Table 2 PDF file - 68K, Association of p-�-CaMKII IHC staining with osteosarcoma grade
Supplementary Figure 1 from Alpha-CaMKII Plays a Critical Role in Determining the Aggressive Behavior of Human Osteosarcoma
Authors: Daft Paul G. , Yuan Kaiyu , Warram Jason M. , Klein Michael J. , Siegal Gene P. , Zayzafoon Majd
Published: April 2023

Supplementary Figure 1 PDF file - 151K, Deletion of �-CaMKII in 143B osteosarcoma cells decreases in vivo tumor formation
Supplemental Table 14 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

Multivariate COX analysis of MFS for EZH2 and CBX7 combined expression levels in the series of 456 breast tumors.
Supplemental Table 12 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 P15 transcripts levels and classical clinical biological parameters in a series of 456 breast cancers.
Supplemental Figure 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

Dendrogram of the 10 ANRIL pathway genes constructed using hierarchical clustering, according to the gene profiling of the 456 breast tumors.
Supplemental Figure 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

Immunohistochemical staining for H3K27me3 and H3K27ac.
Supplementary Figure 1 from miR-200c Targets CDK2 and Suppresses Tumorigenesis in Renal Cell Carcinoma
Authors: Wang Xuegang , Chen Xuanyu , Han Weiwei , Ruan Anming , Chen Li , Wang Rong , Xu Zhenghong , Xiao Pei , Lu Xing , Zhao Yan , Zhou Jia , Chen Shaoyong , Du Quansheng , Yang Hongmei , Zhang Xiaoping
Published: April 2023

Supplementary Figure 1. Quantification of miR200c overexpression in stable lines SN12-PM6 miR-200c and 786-O miR-200c.
Legends of Supplemental Figures 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

Legends of Supplemental Figures S1, S2, S3 and S4
Supplementary Table 1 from FGFR3 Translocations in Bladder Cancer: Differential Sensitivity to HSP90 Inhibition Based on Drug Metabolism
Authors: Acquaviva Jaime , He Suqin , Zhang Chaohua , Jimenez John-Paul , Nagai Masazumi , Sang Jim , Sequeira Manuel , Smith Donald L. , Ogawa Luisa Shin , Inoue Takayo , Tatsuta Noriaki , Knowles Margaret A. , Bates Richard C. , Proia David A.
Published: April 2023

PDF - 67K, FGFR3 fusion-positive bladder cell line sensitivity and metabolism profiles of targeted anticancer compounds.
Supplementary Figure Legends from FGFR3 Translocations in Bladder Cancer: Differential Sensitivity to HSP90 Inhibition Based on Drug Metabolism
Authors: Acquaviva Jaime , He Suqin , Zhang Chaohua , Jimenez John-Paul , Nagai Masazumi , Sang Jim , Sequeira Manuel , Smith Donald L. , Ogawa Luisa Shin , Inoue Takayo , Tatsuta Noriaki , Knowles Margaret A. , Bates Richard C. , Proia David A.
Published: April 2023

PDF - 59K, Supplementary Figure Legends.
Supplementary Figure 1 from FGFR3 Translocations in Bladder Cancer: Differential Sensitivity to HSP90 Inhibition Based on Drug Metabolism
Authors: Acquaviva Jaime , He Suqin , Zhang Chaohua , Jimenez John-Paul , Nagai Masazumi , Sang Jim , Sequeira Manuel , Smith Donald L. , Ogawa Luisa Shin , Inoue Takayo , Tatsuta Noriaki , Knowles Margaret A. , Bates Richard C. , Proia David A.
Published: April 2023

PDF - 667K, Ganetespib treatment overcomes the FGFR inhibitor resistant phenotype in FGFR3 mutant bladder cancer cell lines.
Figure S3 from miR-652 Promotes Tumor Proliferation and Metastasis by Targeting RORA in Endometrial Cancer
Authors: Sun Xiaomei , Dongol Samina , Qiu Chunping , Xu Ying , Sun Chenggong , Zhang Zhiwei , Yang Xingsheng , Zhang Qing , Kong Beihua
Published: April 2023

Up-regulation of miR-652 could not affect the apoptosis of EC cells
Figure S2 from CHCHD2 Is Coamplified with EGFR in NSCLC and Regulates Mitochondrial Function and Cell Migration
Authors: Wei Yuhong , Vellanki Ravi N. , Coyaud Étienne , Ignatchenko Vladimir , Li Lei , Krieger Jonathan R. , Taylor Paul , Tong Jiefei , Pham Nhu-An , Liu Geoffrey , Raught Brian , Wouters Bradly G. , Kislinger Thomas , Tsao Ming Sound , Moran Michael F.
Published: April 2023

Figure S2. Analysis of ECAR in NSCLC cell lines
Supplementary Figure S1 from E2F4 Program Is Predictive of Progression and Intravesical Immunotherapy Efficacy in Bladder Cancer
Authors: Cheng Chao , Varn Frederick S. , Marsit Carmen J.
Published: April 2023

(A) The distribution of E2F4 scores in primary bladder tumor samples. (B) Stratification of patients into E2F4>0 and E2F4<0 groups, and then compare their cancer specific survival (CSS) curves. (C) Stratification of patients into high, intermediate and low groups based on their E2F4 scores, and then comparing their cancer specific survival (CSS) curves. The scores at the two dashed lines in (A) are used as cut-off values for defining groups. (D) Comparison of the overall survival (OS) curves between the E2F4>0 and E2F4<0 groups. (E) Comparison of the recurrence-free survival (RFS) curves between the E2F4>0 and E2F4<0 groups. Only NMIBC samples are used in this analysis. (F) Comparison of the progression-free survival (PFS) curves between the E2F4>0 and E2F4<0 groups. This figure is similar to Figure 3, but all patients with or without systemic chemotherapy treatment are included.
Supplementary Table 4 from BRAFV600E Cooperates with PI3K Signaling, Independent of AKT, to Regulate Melanoma Cell Proliferation
Authors: Silva Jillian M. , Bulman Christina , McMahon Martin
Published: April 2023

PDF file - 66K, Supplementary Table S4. Pathway significance of the phosphorylation site(s) for each phosphoprotein.
Supplementary Figure Legends from Sonic Hedgehog Signaling Drives Mitochondrial Fragmentation by Suppressing Mitofusins in Cerebellar Granule Neuron Precursors and Medulloblastoma
Authors: Malhotra Anshu , Dey Abhinav , Prasad Niyathi , Kenney Anna Marie
Published: April 2023

Supplementary Figure S1: (a) mRNA expression analysis of Mfn1, Mfn2 and Drp1 genes was carried out in CGNPs. No significant changes were observed between the expression levels of vehicle and Shh treated CGNPs. (b) Automated quantification, using ImageJ software, of CGNPs {plus minus}Shh, stained with Tom20. Supplementary Figure S2: (a,c) Automated quantification, using ImageJ software, of CGNPs over-expressing Mfn1 or 2, stained with mitotracker Red. (b,d) Quantification of proliferating cell numbers after BrdU incorporation in CGNPs over-expressing Mfn1 or 2. Supplementary Figure S3: (a) Automated quantification, using ImageJ software, of CGNPs over-expressing Drp1, stained with mitotracker Red. (b) Quantification of proliferating cell numbers after BrdU incorporation in CGNPs over-expressing Drp1. Supplementary Figure S4: (a,b) Automated quantification, using ImageJ software, of CGNPs over-expressing Mfn1, 2 or Drp1, stained with mitotracker Red.
Supplementary Fig. S9 from Tumor Cell-Derived Periostin Regulates Cytokines That Maintain Breast Cancer Stem Cells
Authors: Lambert Arthur W. , Wong Chen Khuan , Ozturk Sait , Papageorgis Panagiotis , Raghunathan Rekha , Alekseyev Yuriy , Gower Adam C. , Reinhard Björn M. , Abdolmaleky Hamid M. , Thiagalingam Sam
Published: April 2023

POSTN expression in breast tumors
Supplementary Figure 5 from Contribution of Tumor Heterogeneity in a New Animal Model of CNS Tumors
Authors: Chen Fuyi , Becker Albert J. , LoTurco Joseph J.
Published: April 2023

PDF file - 1195K, Additional immunohistopathological features of ATRT like tumor induced by PBCAG-NeuroD1 and PBCAG-HRasV12/AKT.
Supplementary Figure 2 from Contribution of Tumor Heterogeneity in a New Animal Model of CNS Tumors
Authors: Chen Fuyi , Becker Albert J. , LoTurco Joseph J.
Published: April 2023

PDF file - 7152K, Tumor cells can form tumor spheres in vitro.
Supplementary Figures from Interaction Between MUC1 and STAT1 Drives IFITM1 Overexpression in Aromatase Inhibitor–Resistant Breast Cancer Cells and Mediates Estrogen-Induced Apoptosis
Authors: Escher Taylor E. , Lui Asona J. , Geanes Eric S. , Walter Katherine R. , Tawfik Ossama , Hagan Christy R. , Lewis-Wambi Joan
Published: April 2023

S1. E2 and GO-201 decrease IFITM1 expression. S2. Combination treatment with JAK/STAT inhibitor. S3. Alterations to IFITM1 expression upon MUC1 knockdown and Rux treatment. S4. Estrogen treatment reduces tumor size in Nude mice injected with MCF-7:5C AI-resistant cells in vivo. S5.Estrogen treatment reduces MUC 1, P-STAT1, and FITM 1 levels in Nude mice injected injected with MCF-7:5C AI-resistant cells in vivo. S6. TUNEL staining from AI-sensitive tumors. S7. MUC 1 staining intensities for ER+ breast cancer patients.
Supplementary Figures 1-6 from O-GlcNAcylation Enhances Double-Strand Break Repair, Promotes Cancer Cell Proliferation, and Prevents Therapy-Induced Senescence in Irradiated Tumors
Authors: Efimova Elena V. , Appelbe Oliver K. , Ricco Natalia , Lee Steve S.-Y. , Liu Yue , Wolfgeher Donald J. , Collins Tamica N. , Flor Amy C. , Ramamurthy Aishwarya , Warrington Sara , Bindokas Vytautas P. , Kron Stephen J.
Published: April 2023

S1. Validation of TagRFP-IBD as IRIF reporter in vitro. S2. Effects of radiation on MCF7 cells with altered O-GlcNAcylation. S3. Targeting O-GlcNAc modification by small molecule inhibitors affects kinetics of IRIF resolution in different cell lines. S4. Cellular apoptosis assays using fluorescent dyes and a caspase substrate probe. S5. Alloxan potentiates senescence in Panc02 cells in a radiation dose-dependent manner. S6. Blocking O-GlcNAcylation in vivo by inducing shOGT or alloxan treatment qualitatively reduces EZH2 immunoreactivity after irradiation.
Fig S7 from Therapeutic Implications of p53 Status on Cancer Cell Fate Following Exposure to Ionizing Radiation and the DNA-PK Inhibitor M3814
Authors: Sun Qing , Guo Yige , Liu Xiaohong , Czauderna Frank , Carr Michael I. , Zenke Frank T. , Blaukat Andree , Vassilev Lyubomir T.
Published: April 2023

SI Fig. 7 with 4 embedded videos. Please click on arrow to see videos
Supplementary Table 1 from Identification of Cdk1–LATS–Pin1 as a Novel Signaling Axis in Anti-tubulin Drug Response of Cancer Cells
Authors: Yeung Benjamin , Khanal Prem , Mehta Virja , Trinkle-Mulcahy Laura , Yang Xiaolong
Published: April 2023

Supplementary Table 1. Cellular proteins with enhanced interaction with LATS2 after TX and NOC treatments.
Supplementary Figure 1 from Whole-Genome and Transcriptional Analysis of Treatment-Emergent Small-Cell Neuroendocrine Prostate Cancer Demonstrates Intraclass Heterogeneity
Authors: Aggarwal Rahul R. , Quigley David A. , Huang Jiaoti , Zhang Li , Beer Tomasz M. , Rettig Matthew B. , Reiter Rob E. , Gleave Martin E. , Thomas George V. , Foye Adam , Playdle Denise , Lloyd Paul , Chi Kim N. , Evans Christopher P. , Lara Primo N. , Feng Felix Y. , Alumkal Joshi J. , Small Eric J.
Published: April 2023

Supplementary Figure 1. A gene set reported by Beltran and colleagues to distinguish adenocarcinoma and neuroendocrine tumors separated WGS t-SCNC and neuroendocrine samples, confirming the neuroendocrine phenotype of the t-SCNC samples.
Supplementary Figure 5 from The β2-Adrenergic Receptor Is a Molecular Switch for Neuroendocrine Transdifferentiation of Prostate Cancer Cells
Authors: Braadland Peder R. , Ramberg Håkon , Grytli Helene Hartvedt , Urbanucci Alfonso , Nielsen Heidi Kristin , Guldvik Ingrid Jenny , Engedal Andreas , Ketola Kirsi , Wang Wanzhong , Svindland Aud , Mills Ian G. , Bjartell Anders , Taskén Kristin Austlid
Published: April 2023

Canonical WNT signalling
Supplementary Figure 2 from The β2-Adrenergic Receptor Is a Molecular Switch for Neuroendocrine Transdifferentiation of Prostate Cancer Cells
Authors: Braadland Peder R. , Ramberg Håkon , Grytli Helene Hartvedt , Urbanucci Alfonso , Nielsen Heidi Kristin , Guldvik Ingrid Jenny , Engedal Andreas , Ketola Kirsi , Wang Wanzhong , Svindland Aud , Mills Ian G. , Bjartell Anders , Taskén Kristin Austlid
Published: April 2023

NEtD characterization shADRB2 and shCtrl cell lines
Supplementary Figure 1 from The β2-Adrenergic Receptor Is a Molecular Switch for Neuroendocrine Transdifferentiation of Prostate Cancer Cells
Authors: Braadland Peder R. , Ramberg Håkon , Grytli Helene Hartvedt , Urbanucci Alfonso , Nielsen Heidi Kristin , Guldvik Ingrid Jenny , Engedal Andreas , Ketola Kirsi , Wang Wanzhong , Svindland Aud , Mills Ian G. , Bjartell Anders , Taskén Kristin Austlid
Published: April 2023

Correlation ADRB2 and NXK3-1
Supplementary Figures S1-S8, Supplementary Table S1, Supplementary Materials and Methods, Supplementary References from Distinct Roles for BET Family Members in Estrogen Receptor α Enhancer Function and Gene Regulation in Breast Cancer Cells
Authors: Murakami Shino , Li Rui , Nagari Anusha , Chae Minho , Camacho Cristel V. , Kraus W. Lee
Published: April 2023

Figure S1. The activity of BET family members is required for the growth of T-47D cells. Figure S2. BET proteins are required for E2-dependent gene expression in T-47D cells. Figure S3. JQ1 does not affect the expression of ERα, SRC2, and SRC3 in MCF-7 cells. Figure S4. JQ1 inhibits the E2-dependent expression of enhancer RNAs (eRNAs) in MCF-7 cells. Figure S5. E2-dependent Myc upregulation is not affected by JQ1. Figure S6. BET proteins are critical regulators of E2-dependent gene expression in T-47D cells. Figure S7. BRD3 is enriched at a subset of ERBSs. Figure S8. E2-induced genes affected by JQ1 are associated with ERα binding sites enriched with BRD3. Table S1. Gene ontologies associated with E2 up-regulated genes repressed by JQ1.
Supplementary Figure 4 from Inhibition of the ATR–CHK1 Pathway in Ewing Sarcoma Cells Causes DNA Damage and Apoptosis via the CDK2-Mediated Degradation of RRM2
Authors: Koppenhafer Stacia L. , Goss Kelli L. , Terry William W. , Gordon David J.
Published: April 2023

Supplementary Figure 4 shows the effect of LY2603618 and AZD1775 on cell cycle and the impact of AZD1775 and AZD6738 on cell growth.
Supplementary Figure 2 from Inhibition of the ATR–CHK1 Pathway in Ewing Sarcoma Cells Causes DNA Damage and Apoptosis via the CDK2-Mediated Degradation of RRM2
Authors: Koppenhafer Stacia L. , Goss Kelli L. , Terry William W. , Gordon David J.
Published: April 2023

Supplementary Figure 2 shows the effects RO-3306 on apoptosis and DNA damage.
Supplementary Table 2 from Reactive Oxygen Species (ROS)-Inducing Triterpenoid Inhibits Rhabdomyosarcoma Cell and Tumor Growth through Targeting Sp Transcription Factors
Authors: Kasiappan Ravi , Jutooru Indira , Mohankumar Kumaravel , Karki Keshav , Lacey Alexandra , Safe Stephen
Published: April 2023

Primers for ChIP assay.
Figure S3 from Inhibition of Discoidin Domain Receptor 1 Prevents Stroma-Induced Peritoneal Metastasis in Gastric Carcinoma
Authors: Jin Hyejin , Ham In-Hye , Oh Hye Jeong , Bae Cheong A , Lee Dakeun , Kim Young-Bae , Son Sang-Yong , Chwae Yong-Joon , Han Sang-Uk , Brekken Rolf A. , Hur Hoon
Published: April 2023

Secretome analysis of conditioned media and transcriptome and western blotting analysis.
Supplementary Figure S2 from ABCC1-Exported Sphingosine-1-phosphate, Produced by Sphingosine Kinase 1, Shortens Survival of Mice and Patients with Breast Cancer
Authors: Yamada Akimitsu , Nagahashi Masayuki , Aoyagi Tomoyoshi , Huang Wei-Ching , Lima Santiago , Hait Nitai C. , Maiti Aparna , Kida Kumiko , Terracina Krista P. , Miyazaki Hiroshi , Ishikawa Takashi , Endo Itaru , Waters Michael R. , Qi Qianya , Yan Li , Milstien Sheldon , Spiegel Sarah , Takabe Kazuaki
Published: April 2023

Effects of overexpression of ABCC1 in MCF7 cells on levels of extracellular and intracellular sphingolipids.
Table S3 from MCL1 and DEDD Promote Urothelial Carcinoma Progression
Authors: Hong Andrew L. , Guerriero Jennifer L. , Doshi Mihir B. , Kynnap Bryan D. , Kim Won Jun , Schinzel Anna C. , Modiste Rebecca , Schlauch Amy J. , Adam Rosalyn M. , Kwiatkowski David J. , Beroukhim Rameen , Letai Anthony , Rosenberg Jonathan E. , Hahn William C.
Published: April 2023

Cell lines used in this study
Table S1 from MCL1 and DEDD Promote Urothelial Carcinoma Progression
Authors: Hong Andrew L. , Guerriero Jennifer L. , Doshi Mihir B. , Kynnap Bryan D. , Kim Won Jun , Schinzel Anna C. , Modiste Rebecca , Schlauch Amy J. , Adam Rosalyn M. , Kwiatkowski David J. , Beroukhim Rameen , Letai Anthony , Rosenberg Jonathan E. , Hahn William C.
Published: April 2023

Copy number variation (CNV) of samples in TCGA
Figure S1 from MCL1 and DEDD Promote Urothelial Carcinoma Progression
Authors: Hong Andrew L. , Guerriero Jennifer L. , Doshi Mihir B. , Kynnap Bryan D. , Kim Won Jun , Schinzel Anna C. , Modiste Rebecca , Schlauch Amy J. , Adam Rosalyn M. , Kwiatkowski David J. , Beroukhim Rameen , Letai Anthony , Rosenberg Jonathan E. , Hahn William C.
Published: April 2023

DEDD and MCL1 overexpression are not necessary for initiation of tumorigenesis.
Supplementary Data all from CCL2 Is a Vascular Permeability Factor Inducing CCR2-Dependent Endothelial Retraction during Lung Metastasis
Authors: Roblek Marko , Protsyuk Darya , Becker Paul F. , Stefanescu Cristina , Gorzelanny Christian , Glaus Garzon Jesus F. , Knopfova Lucia , Heikenwalder Mathias , Luckow Bruno , Schneider Stefan W. , Borsig Lubor
Published: April 2023

Supplementary Figure 1. Characterization of Ccr2ecKO mice and analysis of primary tumors. Supplementary Figure 2. Endothelial CCR2 is required for generation of spontaneous and experimental lung metastasis. Supplementary Figure 3. Formation of the metastasis niche in the lungs is unaffected in Ccr2ecKO mice. Supplementary Figure 4. Inhibition of CCL2-induced endothelial retraction attenuates tumor cell migration.
Suppl. Figures 1-5, Suppl. Table 1 from PARP1 Trapping and DNA Replication Stress Enhance Radiosensitization with Combined WEE1 and PARP Inhibitors
Authors: Parsels Leslie A. , Karnak David , Parsels Joshua D. , Zhang Qiang , Vélez-Padilla Jonathan , Reichert Zachery R. , Wahl Daniel R. , Maybaum Jonathan , O'Connor Mark J. , Lawrence Theodore S. , Morgan Meredith A.
Published: April 2023

Supplemental Figure 1: Cytotoxicity by combined WEE1 and PARP inhibition. Supplemental Figure 2: The effects of AZD1775 and olaparib on the radiation-induced G2 checkpoint. Supplemental Figure 3: The effects of AZD1775 and olaparib on RT-mediated γH2AX-staining in lung cancer cells. Supplemental Figure 4: Exogenous nucleosides attenuate AZD1775-induced high-intensity γH2AX staining but do not rescue AZD1775-mediated inhibition of RAD51 focus formation. Supplemental Figure 5: Relative levels of chromatin-bound PARP1 in Calu-6 cells treated with radiation (6 Gy), AZD1775 and either olaparib or veliparib. Supplemental Table 1: The effects of AZD1775 and olaparib on radiosensitization of Calu-6-derived tumor xenografts.
Supplementary Figure 4 from Radiation-Induced Malignant Transformation of Preneoplastic and Normal Breast Primary Epithelial Cells
Authors: Repullés Joan , Anglada Teresa , Soler David , Ramírez Juan Carlos , Genescà Anna , Terradas Mariona
Published: April 2023

Anchorage assay results
Supplementary Table S4 from Pooled Genomic Screens Identify Anti-apoptotic Genes as Targetable Mediators of Chemotherapy Resistance in Ovarian Cancer
Authors: Stover Elizabeth H. , Baco Maria B. , Cohen Ofir , Li Yvonne Y. , Christie Elizabeth L. , Bagul Mukta , Goodale Amy , Lee Yenarae , Pantel Sasha , Rees Matthew G. , Wei Guo , Presser Adam G. , Gelbard Maya K. , Zhang Weiqun , Zervantonakis Ioannis K. , Bhola Patrick D. , Ryan Jeremy , Guerriero Jennifer L. , Montero Joan , Liang Felice J. , Cherniack Andrew D. , Piccioni Federica , Matulonis Ursula A. , Bowtell David D.L. , Sarosiek Kristopher A. , Letai Anthony , Garraway Levi A. , Johannessen Cory M. , Meyerson Matthew
Published: April 2023

Secondary mini-pool overexpression screen data
Supplementary Table S2 from Pooled Genomic Screens Identify Anti-apoptotic Genes as Targetable Mediators of Chemotherapy Resistance in Ovarian Cancer
Authors: Stover Elizabeth H. , Baco Maria B. , Cohen Ofir , Li Yvonne Y. , Christie Elizabeth L. , Bagul Mukta , Goodale Amy , Lee Yenarae , Pantel Sasha , Rees Matthew G. , Wei Guo , Presser Adam G. , Gelbard Maya K. , Zhang Weiqun , Zervantonakis Ioannis K. , Bhola Patrick D. , Ryan Jeremy , Guerriero Jennifer L. , Montero Joan , Liang Felice J. , Cherniack Andrew D. , Piccioni Federica , Matulonis Ursula A. , Bowtell David D.L. , Sarosiek Kristopher A. , Letai Anthony , Garraway Levi A. , Johannessen Cory M. , Meyerson Matthew
Published: April 2023

ORF overexpression screen enrichment analysis