bluuebunny/crossref_metadata_2025 huggingface dataset:
Abstract 5693: Cancer cells subvert fibroblast function to promote a growth factor enriched tumor microenvironment in endocrine therapy resistant ER+ breast cancer
Authors: Griffiths Jason I. , Cosgrove Patrick A. , Castaneda Eric Medina , Nath Aritro , Chen Jinfeng , Adler Frederick R. , Chang Jeffrey T. , Khan Qamar J. , Bild Andrea H.
Published: April 2023

While endocrine therapy (ET) has considerably improved Stage II/III ER+ breast cancer survival rates, resistance emerges in 30-50% of patients. Recent advances have uncovered numerous cancer intrinsic and tumor-microenvironment mediated mechanisms contributing to ET resistance. However, the predominant mechanisms that prevent cure and ultimately lead to development of terminal metastatic cancer remain unknown. To reveal the leading causes of ET resistance in early-stage ER+ breast cancers, we used single-cell RNA sequencing to profile serial tumor biopsies from a larger cohort of patients. Patients received either endocrine therapy (letrozole) alone or in combination with a CDK4/6 cell cycle inhibitor (ribociclib). We examined the evolution of tumor composition, cellular communication, and the phenotypic diversity of tumor-associated cancer and non-cancer cells throughout treatment. Our analyses reveal that ET-resistant tumors are fibroblast- and endothelial-enriched and consistently exhibit broad upregulation of growth factor signaling to cancer cells, with consistent activation of ERBB communication across patient tumors. Fibroblasts emerged as the primary source of these additional growth factor signals. Upregulation of fibroblast growth factor signaling (via NRG1/2, EGF and IGF) was commensurate with differentiation to a mesenchymal cancer-associated-fibroblast (myCAF) phenotype, which was itself stimulated by cancer cells through EGF and TGF signaling. In response to growth factor enrichment, cancer cells of ET-resistant tumors showed activation of MAPK signal transduction and downstream transcription factors promoting proliferation including FOS, JUN and TRIB1. These results indicate that ET resistance emerges in patient tumors when cancer cells subvert fibroblast function to promote a growth factor enriched tumor microenvironment permitting estrogen independent cancer proliferation.

Citation Format: Jason I. Griffiths, Patrick A. Cosgrove, Eric Medina Castaneda, Aritro Nath, Jinfeng Chen, Frederick R. Adler, Jeffrey T. Chang, Qamar J. Khan, Andrea H. Bild. Cancer cells subvert fibroblast function to promote a growth factor enriched tumor microenvironment in endocrine therapy resistant ER+ 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 5693.
Abstract 5793: Met confers radioresistance-associated aggressiveness through enhancing PLXDC2-mediated cancer stem cell plasticity
Authors: Chen Fanghui , Lang Liwei , Shay Chloe , Chen Georgia , Saba Nabil , Teng Yong
Published: April 2023

The development of radioresistance in head and neck squamous cell carcinoma (HNSCC) remains a significant problem in cancer treatment, contributing to the lack of improvement in survival trends in the past decades. One of the clinical challenges is that radioresistance often promotes tumor aggressiveness. However, the underlying mechanisms and molecular determinants are largely unknown. We report here that radioresistance-associated HNSCC aggressiveness is effectively exacerbated by c-Met but can be suppressed by its genetic knockdown and pharmacological inactivation. Through unbiased RNAseq data, we further uncovered that the resulting upregulation of c-Met signaling increases the expression of PLXDC2. a critical gene associated with the tumor microenvironment. Mechanistically, PLXDC2 is upregulated in radioresistant HNSCC cells through c-Met mediated activation of ERK1/2-ELK1 signaling cascade. Most importantly, PLXDC2 modulates cancer cell plasticity by inducing epithelial-mesenchymal transition (EMT) and the emergence of cancer stem cell (CSC) subpopulation. Additionally, depletion of PLXDC2 overcomes c-Met-mediated radioresistance by reversing the EMT progress and blunting the self-renewal capacity of CSCs. Therapeutically, a combination of the c-Met selective inhibitor SU11274 with radiation remarkably induces tumor shrinkage and constrains tumor metastasis to lymph nodes in vivo. Our study is novel in being the first to explore the role and mechanism of the c-Met-PLXDC2 axis in radioresistance-associated HNSCC aggressiveness and the first to our knowledge to evaluate how to take advantage of blocking this signaling to overcome radioresistance in preclinical mouse models of HNSCC.

Citation Format: Fanghui Chen, Liwei Lang, Chloe Shay, Georgia Chen, Nabil Saba, Yong Teng. Met confers radioresistance-associated aggressiveness through enhancing PLXDC2-mediated cancer stem cell plasticity [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 5793.
Abstract 6703: Objective qualification of cell-free DNA by applying the cfDNA quality metric
Authors: Dorn Annika
Published: April 2023

Next Generation Sequencing (NGS) of cell-free DNA (cfDNA) has the potential to reveal new biomarkers for various conditions. Despite the establishment of low input library protocols, library preparation of cfDNA samples remains a challenge due to restricted amount of starting material and variable size distribution of cfDNA fragments. The yield and quality of cfDNA can vary and a lot of care is required to obtain appropriate cfDNA starting material for downstream applications. Further, cfDNA samples may contain high molecular weight (HMW) DNA that can negatively affect library yield and sequencing quality. Therefore, quality control of cfDNA starting material is essential to ensure the success of downstream experiments. The Agilent Tapestation system with the Cell-free DNA ScreenTape Assay is based on automated electrophoresis and thereby offers an objective and reliable qualification of cfDNA samples by applying the %cfDNA quality score. By comparing different samples with varying total DNA yield and HMW contamination, the additional level of information gained by the %cfDNA score is highlighted. While other QC methods might miss critical information on HMW DNA contamination, this could result in flawed yield estimations, ultimately threatening the successful outcome of downstream experiments. Therefore, accurate quantification of cfDNA starting material, taking also HMW DNA contamination into account is essential for NGS library preparation and generating reliable NGS results.

Citation Format: Annika Dorn. Objective qualification of cell-free DNA by applying the cfDNA quality metric [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 6703.
Abstract 6721: β3-adrenergic receptor correlates with tumor growth and progression in neuroblastoma
Authors: Boaretto Alessia , Bruno Gennaro , Nastasi Nicoletta , Favre Claudio , Calvani Maura
Published: April 2023

Neuroblastoma (NB) is a heterogeneous, often aggressive, extracranial tumor and the most common malignancy to be diagnosed in the first year of life. It has been already demonstrated that the specific antagonism of the β3-adrenergic receptor (β3-AR) on NB tumor cells affects tumor growth. To confirm the results obtained with the pharmacological approach on the crucial role played by the β3-AR receptor in influencing different pro-tumoral signaling pathways, here we investigated the effect of CRISPR/Cas9-mediated knock-out of β3-AR gene (ADRB3) on human NB cell line BE(2)-C in vitro and in vivo. Inoculation of BE(2)-C β3-AR−/- cells in athymic nude mice (NU(N-Cr)-Foxn1nu) showed a strong reduction of NB tumor growth compared to wild type cells, and in some cases β3-AR knock-out tumor cells failed in producing a tumor mass. RNA Sequencing on these tumor masses showed alterations of signaling pathways related to various tumor mechanisms, such as proliferation, cell motility and cell differentiation. Furthermore, we evaluated by flow cytometry the expression of β3-AR in circulating tumor cells (CTCs) from NB patients with different degrees of disease. Following depletion with anti-CD45 magnetic beads, tumor cells were identified through the expression of specific tumor markers, CD56 and GD2. Results showed that a high expression of β3-AR correlates with poor prognosis, characterized by metastatic or recurrent tumors, compared to patients with a favorable clinical outcome that instead show a low expression of β3-AR. Overall, our results demonstrate the β3-AR involvement in supporting NB tumor growth and suggest a possible role in regulating the metastatic potential of this tumor.

Citation Format: Alessia Boaretto, Gennaro Bruno, Nicoletta Nastasi, Claudio Favre, Maura Calvani. β3-adrenergic receptor correlates with tumor growth and progression in neuroblastoma. [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 6721.
Abstract 674: CRISPR and drug screens identify ERK as the mediator of IFNg-induced melanoma growth inhibition
Authors: Champhekar Ameya S. , Heymans Rachel , Gonzalez Cynthia , Font Guillem Turon , Karin Daniel , Lee June , Damoiseaux Robert , Ribas Antoni
Published: April 2023

Interferon-gamma (IFNg) is critical for the success of immune checkpoint blockade therapy. Disruption of IFNg signaling makes tumors resistant to anti-PD-1/L1 treatment primarily by evasion of the growth inhibition (GI) induced by this cytokine. However, the pathways mediating IFNg-induced GI are largely unknown. We used two independent approaches to delineate the IFNg GI pathway, a chemical genomics screen and a whole genome targeting CRISPR/Cas9 screen in an IFNg GI-sensitive patient-derived melanoma (PDM) cell line. Drug screening revealed that treatment with RAF and ERK inhibitors disrupted IFNg GI in PDM cells. For the CRISPR screen, gene-level analysis showed that the magnitude of enrichment for guide RNAs targeting ERK2 in IFNg-treated cells was comparable to proximal IFNg signaling proteins like JAK1, STAT1, IFNGR2, and JAK2 (>26-fold enrichment for ERK2, p = 2.28e-07). Thus, results from both these experiments converged upon ERK as the primary downstream target of IFNg essential for GI induction. We validated the involvement of ERK by detecting a sustained increase in phospho-ERK1/2 levels following IFNg treatment. In live imaging experiments, we found that blocking ERK activity with the ERK inhibitor Ulixertinib blocks the induction of cell death after IFNg treatment in 17 of 23 (~74%) IFNg-sensitive PDM lines covering all the MAPK mutant and triple wildtype molecular subtypes of melanoma. Decreasing and increasing ERK activity levels using shRNA and overexpression approaches also led to a decrease and increase in IFNg-mediated GI, respectively. We have identified NOXA and DR5 as likely mediators of cell death through the IFNg-ERK GI pathway by comparing gene expression profiles of control and IFNg-treated PDM cells. Finally, phorbol 12-myristate 13-acetate (PMA), a known ERK activator, synergizes with IFNg treatment to induce increased GI in PDM cells (Bliss synergy score 16.87, p = 1.83e-123). In summary, the IFNg-ERK signaling axis mediates cell death downstream of IFNg treatment in melanoma cells. This pathway is active in all melanoma subtypes, making it an attractive target to enhance IFNg GI in tumor cells. Our results provide a new understanding of the IFNg GI pathway that will also be crucial to define mechanisms of GI resistance in tumor cells.

Citation Format: Ameya S. Champhekar, Rachel Heymans, Cynthia Gonzalez, Guillem Turon Font, Daniel Karin, June Lee, Robert Damoiseaux, Antoni Ribas. CRISPR and drug screens identify ERK as the mediator of IFNg-induced melanoma growth inhibition [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 674.
Abstract 6764: Multi-parametric comparison of scRNA-seq with CITE-seq and ultrahigh-plex spatial phenotyping of proteins in FFPE head and neck tumor biopsies: An opportunity to generate uniquely comprehensive multi-omic single cell datasets to investigate the tumor microenvironment
Authors: Pratapa Aditya , Jensen Shawn M. , Jhaveri Niyati , Koguchi Yoshinobu , Rajamanickam Venkatesh , Bernard Brady , Christie Tanisha , Piening Brian , Leidner Rom S. , Braubach Oliver , Fox Bernard A.
Published: April 2023

Single cell RNA-seq (scRNA-seq) performed on cell suspensions isolated from tumor biopsies provides substantial insights into the transcriptional state of the cells in the tumor microenvironment (TME). Complementing this work with multi-omic Cellular Indexing of Transcriptomes and Epitopes (CITE-seq), which adds barcoded antibodies to label the surface of isolated cells, allows us to additionally characterize surface proteins. While information gleaned from these studies is dramatically expanding our understanding of the evolving immune response and tumor-immune interactions, it lacks an appreciation of the many spatial relationships that are present within the TME. Spatial phenotyping with the power of single cell resolution and whole slide imaging provides a valuable tool for identifying the cellular architecture and organization of spatial neighborhoods that perform critical roles in tumor progression, resistance, and clinical responses. Here, we explore bioinformatic strategies aimed at combining scRNA-seq and CITE-seq data with single-cell spatial protein data obtained with the PhenoCycler-Fusion (PCF) imaging platform. To this end, we performed whole-slide spatial phenotyping with an ultrahigh-plex PCF panel on FFPE human head and neck tumors. The same biopsies were also enzymatically digested and subjected to CITE-seq and scRNA-seq analysis. The combined multi-omic, single cell dataset provides a uniquely comprehensive account of the cellular states, functional significance and spatial neighborhoods that govern the TME. This study represents a novel approach to integrate high dimensional data from bulk tissue and single-cell spatial technologies to provide deeper insights into tumor biology and, in turn, to develop more informed strategies for combination immunotherapy trials and improved patient outcomes.

Citation Format: Aditya Pratapa, Shawn M. Jensen, Niyati Jhaveri, Yoshinobu Koguchi, Venkatesh Rajamanickam, Brady Bernard, Tanisha Christie, Brian Piening, Rom S. Leidner, Oliver Braubach, Bernard A. Fox. Multi-parametric comparison of scRNA-seq with CITE-seq and ultrahigh-plex spatial phenotyping of proteins in FFPE head and neck tumor biopsies: An opportunity to generate uniquely comprehensive multi-omic single cell datasets to investigate the tumor microenvironment [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 6764.
Abstract PL03-01: New insights into carcinogenesis from normal esophagus
Authors: Jones Phil H.
Published: April 2023

All normal tissues studied to date carry somatic mutant clones, the burden of which increases with age. This talk considers how insights into the biology of mutants in normal tissues can inform our understanding of the earliest stages of carcinogenesis. The esophagus becomes a patchwork of mutant clones. As they expand, these clones compete for the limited space available, resulting in selection of the fittest mutant genes. The ability to out compete other mutants in normal tissue does not correlate with carcinogenic potential. For example, NOTCH1 mutant clones colonize most of the esophagus by middle age but NOTCH1 mutations are comparatively rare in squamous cancers. In mouse models Notch pathway mutant clones eliminate microscopic intraepithelial neoplasms and loss of Notch1 markedly slows esophageal tumor growth. In contrast, mutant TP53 is less effective than NOTCH1 at driving clonal expansion but is found in almost all human squamous esophageal cancers and contributes to carcinogenesis in mice.

The normal tissue mutational landscape of the esophagus is shaped by environmental factors. For example, body metabolism alters the behavior of mutant PIK3CA which drives clonal expansions in the esophagus of overweight humans and mice. The mutation causes cells to switch their metabolism to aerobic glycolysis, giving the mutants a proliferative advantage. One way to reduce the competitive advantage of mutants is to increase the fitness of the neighboring cells. Treating cells or mice with metformin, a drug used to treat type 2 diabetes, induces aerobic glycolysis throughout the tissue. This eliminates the growth advantage of Pik3ca mutant clones, showing it may be possible to halt the expansion of oncogenic mutant populations.

Beyond the esophagus, these findings suggest the need to consider the relative prevalence of mutations in normal tissue and the corresponding cancer(s) before deciding if a mutant gene is a cancer driver or not. Variation in cancer risk between different human populations may depend on the proportion of pro- and anti-oncogenic mutants in normal tissue. Understanding how certain mutations can impede cancer development and how environmental factors alter selection of oncogenic mutants in normal tissue may guide new approaches to cancer prevention.

Citation Format: Phil H. Jones. New insights into carcinogenesis from normal esophagus. [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 PL03-01.
Abstract SY26-01: Mapping cellular plasticity in tumor progression and drug resistance
Authors: Yanai Itai
Published: April 2023

Cellular plasticity is emerging as an important driving force underlying cancer progression and drug resistance. In this talk, I will discuss the concept of cancer cell states present in the tumor prior to treatment, as well as those that accompany resistance to increasing drug doses. In particular, I will discuss work published in our recent manuscript 'Cancer cell states recur across tumor types and form specific interactions with the tumor microenvironment' and recent developments in this project. Second, I will discuss our new work of 'Drug-induced adaptation along a resistance continuum in cancer cells'.

Citation Format: Itai Yanai. Mapping cellular plasticity in tumor progression and drug resistance. [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 SY26-01.
Supplementary Figure 1 from Minocycline Targets the NF-κB Nexus through Suppression of TGF-β1-TAK1-IκB Signaling in Ovarian Cancer
Authors: Ataie-Kachoie Parvin , Badar Samina , Morris David L. , Pourgholami Mohammad H.
Published: April 2023

PDF file - 1416K, Minocycline ablated TAK-1-induced activation of NF-кB.
Supplementary Table 3 from Mutual Exclusivity Analysis of Genetic and Epigenetic Drivers in Melanoma Identifies a Link Between p14ARF and RARβ Signaling
Authors: Dahl Christina , Christensen Claus , Jönsson Göran , Lorentzen Anders , Skjødt Mette Louise , Borg Åke , Pawelec Graham , Guldberg Per
Published: April 2023

PDF file - 43K, Copy number gains.
Supplementary Figure S7 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 S7 - PDF file 110K, The relative expression profiles of mRNA of FGFRs by microarray analysis. The log2 of fold change to PC9 na was calculated for each sample by using Gene Spring GX software. Each group of columns represents the result from 1 microarray probe
Supplementary Figure 1 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 - 130K, A) Chemical structure of biotinylated PES B) Chemical structure of PES and derivatives NSC85560, NSC166772 and NSC303578 (nomenclature is from the National Cancer Institute Drug Repository). C) Cell viability of H1299 and PANC1 cells after 48 hour treatment with 10 uM PES, NSC85560 (855600), NSC166777 (16677) and NSC303578 (303578). Data are the averaged results from three independent experiments, and error bars mark standard deviations. D) 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.
Table S1 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

Sequence of primers
Figure S1 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 S1. Expression of CHCHD2 and EGFR in NSCLC cell lines
Supplementary Table 1 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 - 68K, Supplementary Table S1. Panel of human BRAF mutated melanoma-derived cell lines.
Supplementary Figure 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 - 92K, Supplementary Fig. S4. Quantification of Crystal Violet staining experiments.
Fig. S4 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

Fig.S4 with embedded videos in panel B
Supplementary Data from ZEB1 Collaborates with ELK3 to Repress E-Cadherin Expression in Triple-Negative Breast Cancer Cells
Authors: Cho Hyeon-Ju , Oh Nuri , Park Ji-Hoon , Kim Kwang-Soo , Kim Hyung-Keun , Lee Eunbyeol , Hwang Sohyun , Kim Seong-Jin , Park Kyung-Soon
Published: April 2023

Figure S1. (A) Quantified presentation of ZEB1, ELK3 and CDH1 expression with the dataset of 49 breast cancer cell lines obtained from the University of California Santa Cruz (UCSC) Xena Browser (http://xena.ucsc.edu/). (B) Correlation efficiency analysis of ZEB1/ELK3, CHD1/ELK3 and CDH1/ZEB1 expression in 49 breast cancer cell lines. The data of triple negative breast cancer cell lines are presented as grey color. Figure S2. Correlation analysis of ELK3 and ZEB1 protein expression in 6 breast cell lines of figure 1C. Immunoblot band intensity of ELK3 and ZEB1 is normalized to that of GAPDH. The data of basal type of breast cancer cell lines are presented as red dots. Figure S3. The effect of ELK3 suppression on the expression of EMT-related transcription factors. Figure S4. Survival analysis mediated by the expression of ELK3 and ZEB1. Figure S5. The transcriptional repressor activity of the ELK3 deletion mutant on the E-cadherin promoter. Figure S6. ZEB1-independent transcriptional repressor activity of ELK3 on the E-cadherin promoter. Figure S7. Correlation of ELK3 and other EMT related transcription factors in breast cancer patients. The Cancer Genome Atlas (TCGA) database was analyzed by GenExMiner 3.0. Table S1. Plasmids used in this study Table S2. siRNAs used in this study Table S3. Oligomers used in this study Table S4. Antibodies used in this study
Supplementary Figure 4 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 ADRB2 overexpression
Supplementary Figure 1 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

Supplementary Figure 1 from Reactive Oxygen Species (ROS)-Inducing Triterpenoid Inhibits Rhabdomyosarcoma Cell and Tumor Growth through Targeting Sp Transcription Factors
Figure S2 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

A, co-culture with fibroblasts isolated from normal gastric tissues (NAFs) could not upregulate the expression of DDR1. B, There was no difference in DDR1 gene expression levels between MKN74 cells co-cultured with cancer-associated fibroblasts (CAFs) and MKN74 cells cultured without CAFs.
Supplementary figure legends and supplementary methods from Efficacy of a Covalent ERK1/2 Inhibitor, CC-90003, in KRAS-Mutant Cancer Models Reveals Novel Mechanisms of Response and Resistance
Authors: Aronchik Ida , Dai Yumin , Labenski Matt , Barnes Carmen , Jones Terri , Qiao Lixin , Beebe Lisa , Malek Mehnaz , Elis Winfried , Shi Tao , Mavrommatis Konstantinos , Bray Gordon L. , Filvaroff Ellen H.
Published: April 2023

Supplementary figure legends and supplementary materials and methods
Figure 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

DEDD overexpression confers resistance to TNFα mediated apoptosis.
Figure S2 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 overexpression does not lead to resistance of the intrinsic pathway of apoptosis.
Figure S3 from Pattern-Specific Transcriptomics Identifies ASGR2 as a Predictor of Hematogenous Recurrence of Gastric Cancer
Authors: Tanaka Haruyoshi , Kanda Mitsuro , Miwa Takashi , Tanaka Chie , Kobayashi Daisuke , Umeda Shinichi , Shibata Masahiro , Suenaga Masaya , Hattori Norifumi , Hayashi Masamichi , Iwata Naoki , Yamada Suguru , Nakayama Goro , Fujiwara Michitaka , Kodera Yasuhiro
Published: April 2023

ASGR2 inhibitory assay of N87 cells.
Figure S2 from Pattern-Specific Transcriptomics Identifies ASGR2 as a Predictor of Hematogenous Recurrence of Gastric Cancer
Authors: Tanaka Haruyoshi , Kanda Mitsuro , Miwa Takashi , Tanaka Chie , Kobayashi Daisuke , Umeda Shinichi , Shibata Masahiro , Suenaga Masaya , Hattori Norifumi , Hayashi Masamichi , Iwata Naoki , Yamada Suguru , Nakayama Goro , Fujiwara Michitaka , Kodera Yasuhiro
Published: April 2023

Gene set enrichment analysis of ASGR2 expression in GSE62254
Supplementary Figure 3 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

Growth curves 2D BPECs cultures
Supplemental Figures 1-10 from Sleeping Beauty Screen Identifies RREB1 and Other Genetic Drivers in Human B-cell Lymphoma
Authors: Rahrmann Eric P. , Wolf Natalie K. , Otto George M. , Heltemes-Harris Lynn , Ramsey Laura B. , Shu Jingmin , LaRue Rebecca S. , Linden Michael A. , Rathe Susan K. , Starr Timothy K. , Farrar Michael A. , Moriarity Branden S. , Largaespada David A.
Published: April 2023

PDF with supplemental figures 1-10 with each containing a figure legend at the bottom fo the figure.
Supplemental text from BMP7 Signaling in TGFBR2-Deficient Stromal Cells Provokes Epithelial Carcinogenesis
Authors: Eikesdal Hans Petter , Becker Lisa M. , Teng Yingqi , Kizu Akane , Carstens Julienne L. , Kanasaki Keizo , Sugimoto Hikaru , LeBleu Valerie S. , Kalluri Raghu
Published: April 2023

Supplementary methods and figure legends
Figure S4 from Epigenetic Silencing of THY1 Tracks the Acquisition of the Notch1–EGFR Signaling in a Xenograft Model of CD44+/CD24low/CD90+ Myoepithelial Cells
Authors: Montanari Micaela , Carbone Maria Rita , Coppola Luigi , Giuliano Mario , Arpino Grazia , Lauria Rossella , Nardone Agostina , Leccia Felicia , Trivedi Meghana V. , Garbi Corrado , Bianco Roberto , Avvedimento Enrico V. , De Placido Sabino , Veneziani Bianca Maria
Published: April 2023

Uncropped blots
Table S2 from YAP Tyrosine Phosphorylation and Nuclear Localization in Cholangiocarcinoma Cells Are Regulated by LCK and Independent of LATS Activity
Authors: Sugihara Takaaki , Werneburg Nathan W. , Hernandez Matthew C. , Yang Lin , Kabashima Ayano , Hirsova Petra , Yohanathan Lavanya , Sosa Carlos , Truty Mark J. , Vasmatzis George , Gores Gregory J. , Smoot Rory L.
Published: April 2023

Table of ten most differentially regulated genes in RNAsequencing of Patient-Derived Intrahepatic Cholangiocarcinoma xenografts.
Supplemental Figure Legends from YAP Tyrosine Phosphorylation and Nuclear Localization in Cholangiocarcinoma Cells Are Regulated by LCK and Independent of LATS Activity
Authors: Sugihara Takaaki , Werneburg Nathan W. , Hernandez Matthew C. , Yang Lin , Kabashima Ayano , Hirsova Petra , Yohanathan Lavanya , Sosa Carlos , Truty Mark J. , Vasmatzis George , Gores Gregory J. , Smoot Rory L.
Published: April 2023

Supplemental Figure Legends
Figure S2 from Novel Regulation of Integrin Trafficking by Rab11-FIP5 in Aggressive Prostate Cancer
Authors: Das Lipsa , Gard Jaime M.C. , Prekeris Rytis , Nagle Raymond B. , Morrissey Colm , Knudsen Beatrice S. , Miranti Cindy K. , Cress Anne E.
Published: April 2023

Supplementary Figure 2. Distribution of α6 integrin in EEA1 vesicles. Surface integrin α6 was labelled with J1B5 in DU145 cells and allowed to internalize for 40 minutes. Cells were fixed, permeabilized, and immunostained for the early endosome marker EEA1. (A) Untreated DU145 cells and (B) siFIP5 treated cells stained for α6 integrin (red), EEA1 (green) and DAPI (blue) in merged images. Images acquired by deconvolution microscopy and single Z-plane is shown. (C) Magnified images of boxed sections for untreated and siFIP5 DU145 cells. White arrows indicate colocalization of α6 integrin in EEA1 vesicles. (D) Percent α6 integrin in EEA1 vesicles and mean Pearson coefficients of correlation of α6 integrin with EEA1 (Pr(α6/EEA1)) for untreated or siFIP5 cells are shown based on 10 different fields of view in 4 independent experiments (*p<0.05).
Figure S1 from Novel Regulation of Integrin Trafficking by Rab11-FIP5 in Aggressive Prostate Cancer
Authors: Das Lipsa , Gard Jaime M.C. , Prekeris Rytis , Nagle Raymond B. , Morrissey Colm , Knudsen Beatrice S. , Miranti Cindy K. , Cress Anne E.
Published: April 2023

Supplementary Figure 1. PC3N cells are negative for β4 integrin expression. DU145 and PC3N cells were labelled with an antibody against β4 integrin and cell surface levels of β4 integrin were measured using flow cytometry. Flow histograms of β4 integrin surface levels (top panel) in unlabeled PC3N cells (solid line), PC3N cells labelled with a non-specific fluorophore conjugated secondary antibody (2{degree sign} Ab only, dotted line) and DU145 (shaded solid line) and PC3N (dashed line) cells labeled with antibody against β4 integrin. The mean peak fluorescence values are reported for each condition (bottom panel).
Supplementary Figure 3 from Reversal of Triple-Negative Breast Cancer EMT by miR-200c Decreases Tryptophan Catabolism and a Program of Immunosuppression
Authors: Rogers Thomas J. , Christenson Jessica L. , Greene Lisa I. , O'Neill Kathleen I. , Williams Michelle M. , Gordon Michael A. , Nemkov Travis , D'Alessandro Angelo , Degala Greg D. , Shin Jimin , Tan Aik-Choon , Cittelly Diana M. , Lambert James R. , Richer Jennifer K.
Published: April 2023

Effects of TNF-a or IL-1B or the combination on HO-1 protein in BT549 cells.
Figure S6. from Novel Aberrations Uncovered in Barrett's Esophagus and Esophageal Adenocarcinoma Using Whole Transcriptome Sequencing
Authors: Maag Jesper L.V. , Fisher Oliver M. , Levert-Mignon Angelique , Kaczorowski Dominik C. , Thomas Melissa L. , Hussey Damian J. , Watson David I. , Wettstein Antony , Bobryshev Yuri V. , Edwards Melanie , Dinger Marcel E. , Lord Reginald V.
Published: April 2023

Supplementary figure 6. Differences between TP53mut vs TP53wt EAC gene expression. EAC patients were divided up into patients with no mutated TP53 transcripts (TP53-) and those with wild-type TP53 transcripts (e.g. no identification of SNPs in the TP53 consensus reads
Supplementary Table 1 from Serum CD95L Level Correlates with Tumor Immune Infiltration and Is a Positive Prognostic Marker for Advanced High-Grade Serous Ovarian Cancer
Authors: De La Motte Rouge Thibault , Corné Julien , Cauchois Aurélie , Le Boulch Marie , Poupon Clotilde , Henno Sébastien , Rioux-Leclercq Nathalie , Le Pabic Estelle , Laviolle Bruno , Catros Véronique , Levêque Jean , Fautrel Alain , Le Gallo Matthieu , Legembre Patrick , Lavoué Vincent
Published: April 2023

Table S1. Clinical characteristics of the patients
Supplementary Data, Figure 1 from Serum CD95L Level Correlates with Tumor Immune Infiltration and Is a Positive Prognostic Marker for Advanced High-Grade Serous Ovarian Cancer
Authors: De La Motte Rouge Thibault , Corné Julien , Cauchois Aurélie , Le Boulch Marie , Poupon Clotilde , Henno Sébastien , Rioux-Leclercq Nathalie , Le Pabic Estelle , Laviolle Bruno , Catros Véronique , Levêque Jean , Fautrel Alain , Le Gallo Matthieu , Legembre Patrick , Lavoué Vincent
Published: April 2023

Figure 1A: Membranous CD95 expression on ovarian cancer cell lines and primary cancer cells by cytometry Figure 1B: Evaluation of epithelial mesenchymal transition expression (EMT) profile using vimentin and E-cadherin expression on ovarian cancer cell line and primary cancer cells by Western Blot (A). Vimentin and E-cadherin expression ratio mean on ovarian cancer cells based on 3 experiments (B). Figure 1C: ALDH1 activity with or without s-CD95L (100 ng/mL) evaluated by cytometry. Figure 1D: Proliferation of OVCAR3 cell lines using cytometry and G1, G2 and S phase markers E: Proliferation of O170 primary cell lines using cytometry and G1, G2 and S phase markers F: Proliferation of various ovarian cancer cell lines or primary cell lines with or without s-CD95L (100 ng/mL) in medium using cytometry and G1, G2 and S phase markers
Table S2 from Diffuse Intrinsic Pontine Glioma Cells Are Vulnerable to Mitotic Abnormalities Associated with BMI-1 Modulation
Authors: Senthil Kumar Shiva , Sengupta Satarupa , Zhu Xiaoting , Mishra Deepak Kumar , Phoenix Timothy , Dyer Lisa , Fuller Christine , Stevenson Charles B. , DeWire Mariko , Fouladi Maryam , Drissi Rachid
Published: April 2023

IC50 (nM) of PTC596 in cell lines treated for 72hrs.
Figure S2, E from Diffuse Intrinsic Pontine Glioma Cells Are Vulnerable to Mitotic Abnormalities Associated with BMI-1 Modulation
Authors: Senthil Kumar Shiva , Sengupta Satarupa , Zhu Xiaoting , Mishra Deepak Kumar , Phoenix Timothy , Dyer Lisa , Fuller Christine , Stevenson Charles B. , DeWire Mariko , Fouladi Maryam , Drissi Rachid
Published: April 2023

E, Representative IF-FISH images of metaphase spreads with centromere probe (red) and γH2AX (green) in CCHMC-DIPG-1 and SU-DIPG-IV cells treated with PTC596 (60 nM and 30 nM respectively) for 48 hrs. DAPI (blue) indicates chromosomes. White arrowheads indicate chromosomes with PSCS.
Supplementary Figure 2 from Next-Generation Sequencing Analysis and Algorithms for PDX and CDX Models
Authors: Khandelwal Garima , Girotti María Romina , Smowton Christopher , Taylor Sam , Wirth Christopher , Dynowski Marek , Frese Kristopher K. , Brady Ged , Dive Caroline , Marais Richard , Miller Crispin
Published: April 2023

Variant Allele Frequencies for the CDXF1 model.
Supplementary Figure Legends from UNC-45A Is a Novel Microtubule-Associated Protein and Regulator of Paclitaxel Sensitivity in Ovarian Cancer Cells
Authors: Mooneyham Ashley , Iizuka Yoshie , Yang Qing , Coombes Courtney , McClellan Mark , Shridhar Vijayalakshmi , Emmings Edith , Shetty Mihir , Chen Liqiang , Ai Teng , Meints Joyce , Lee Michael K. , Gardner Melissa , Bazzaro Martina
Published: April 2023

Supplementary Figure Legends
Figure S9 from UNC-45A Is a Novel Microtubule-Associated Protein and Regulator of Paclitaxel Sensitivity in Ovarian Cancer Cells
Authors: Mooneyham Ashley , Iizuka Yoshie , Yang Qing , Coombes Courtney , McClellan Mark , Shridhar Vijayalakshmi , Emmings Edith , Shetty Mihir , Chen Liqiang , Ai Teng , Meints Joyce , Lee Michael K. , Gardner Melissa , Bazzaro Martina
Published: April 2023

Effects on UNC-45A loss on SKOV-3 ovarian cancer cells
Figure S7 from UNC-45A Is a Novel Microtubule-Associated Protein and Regulator of Paclitaxel Sensitivity in Ovarian Cancer Cells
Authors: Mooneyham Ashley , Iizuka Yoshie , Yang Qing , Coombes Courtney , McClellan Mark , Shridhar Vijayalakshmi , Emmings Edith , Shetty Mihir , Chen Liqiang , Ai Teng , Meints Joyce , Lee Michael K. , Gardner Melissa , Bazzaro Martina
Published: April 2023

Loss of UNC-45A results in decrease in proliferation rate
Table S1 from Genomic Alterations Associated with Recurrence and TNBC Subtype in High-Risk Early Breast Cancers
Authors: Wilson Timothy R. , Udyavar Akshata R. , Chang Ching-Wei , Spoerke Jill M. , Aimi Junko , Savage Heidi M. , Daemen Anneleen , O'Shaughnessy Joyce A. , Bourgon Richard , Lackner Mark R.
Published: April 2023

Comparison of demographics between the cohort of patients that experienced a disease-free survival event, to patients that did not experience a disease-free survival event, the additional biomarker samples used to increase the statistical precision of prevalence estimates and the entire study population.
Supplemental Methods from Genomic Alterations Associated with Recurrence and TNBC Subtype in High-Risk Early Breast Cancers
Authors: Wilson Timothy R. , Udyavar Akshata R. , Chang Ching-Wei , Spoerke Jill M. , Aimi Junko , Savage Heidi M. , Daemen Anneleen , O'Shaughnessy Joyce A. , Bourgon Richard , Lackner Mark R.
Published: April 2023

Supplemental Methods describing NGS and gene expression studies.
Figure S5 from UNC-45A Is a Novel Microtubule-Associated Protein and Regulator of Paclitaxel Sensitivity in Ovarian Cancer Cells
Authors: Mooneyham Ashley , Iizuka Yoshie , Yang Qing , Coombes Courtney , McClellan Mark , Shridhar Vijayalakshmi , Emmings Edith , Shetty Mihir , Chen Liqiang , Ai Teng , Meints Joyce , Lee Michael K. , Gardner Melissa , Bazzaro Martina
Published: April 2023

UNC-45A overexpression results with decrease in MT stability
Supplementary Figure 2. Classification of the VUS as a function of the impact of the corresponding missense variations on BRCT domain expression in E. coli. from Combining Homologous Recombination and Phosphopeptide-binding Data to Predict the Impact of BRCA1 BRCT Variants on Cancer Risk
Authors: Petitalot Ambre , Dardillac Elodie , Jacquet Eric , Nhiri Naima , Guirouilh-Barbat Josée , Julien Patrick , Bouazzaoui Isslam , Bonte Dorine , Feunteun Jean , Schnell Jeff A. , Lafitte Philippe , Aude Jean-Christophe , Noguès Catherine , Rouleau Etienne , Lidereau Rosette , Lopez Bernard S. , Zinn-Justin Sophie , Caputo Sandrine M.
Published: April 2023

Mutated BRCT domains fused to GST were expressed in E. coli and purified by affinity chromatography using glutathione beads. This figure shows a SDS-PAGE gel with samples from the bacterial pellet (P), supernatant (S) and the glutathione beads (G) after incubation with the supernatant and washing. VUS were classified into 3 groups as a function of the amount of (1) soluble and (2) purified protein obtained from bacterial cultures. Lanes corresponding to a typical insoluble fusion protein, a typical poorly soluble fusion protein and a typical fusion protein as soluble as the WT fusion protein are boxed in orange, grey and black, respectively (colors are as in Figure 4 excepted for mutations that cause aggregation during purification, which are in yellow on Figure 4 even if they displayed a "grey-like" profile at the expression and first affinity purification stages).
Figure S2 from The Tissue-Reconstructing Ability of Colon CSCs Is Enhanced by FK506 and Suppressed by GSK3 Inhibition
Authors: Ishida Ryo , Koyanagi-Aoi Michiyo , Oshima Nobu , Kakeji Yoshihiro , Aoi Takashi
Published: April 2023

Co-culture of cancer cells, human umbilical vascular endothelial cells (HUVECs) and mesenchymal stem cells (MSCs).
Supplemental Figure Legends. from A Role for Tryptophan-2,3-dioxygenase in CD8 T-cell Suppression and Evidence of Tryptophan Catabolism in Breast Cancer Patient Plasma
Authors: Greene Lisa I. , Bruno Tullia C. , Christenson Jessica L. , D'Alessandro Angelo , Culp-Hill Rachel , Torkko Kathleen , Borges Virginia F. , Slansky Jill E. , Richer Jennifer K.
Published: April 2023

Figure legends for Supplemental Figures 1-4
Supplementary Video 1 from Adaptive Resistance to EGFR-Targeted Therapy by Calcium Signaling in NSCLC Cells
Authors: Mulder Celine , Prust Nadine , van Doorn Sander , Reinecke Maria , Kuster Bernhard , van Bergen en Henegouwen Paul , Lemeer Simone
Published: April 2023

Supplementary Video 1
Supplemental Figure 4 from A Role for Tryptophan-2,3-dioxygenase in CD8 T-cell Suppression and Evidence of Tryptophan Catabolism in Breast Cancer Patient Plasma
Authors: Greene Lisa I. , Bruno Tullia C. , Christenson Jessica L. , D'Alessandro Angelo , Culp-Hill Rachel , Torkko Kathleen , Borges Virginia F. , Slansky Jill E. , Richer Jennifer K.
Published: April 2023

Alterations in tryptophan catabolites by breast cancer stage.
Supplementary Methods and Materials from S-Nitrosylation of EGFR and Src Activates an Oncogenic Signaling Network in Human Basal-Like Breast Cancer
Authors: Switzer Christopher H. , Glynn Sharon A. , Cheng Robert Y.-S. , Ridnour Lisa A. , Green Jeffrey E. , Ambs Stefan , Wink David A.
Published: April 2023

PDF file - 93K
Supplemental Tables from Senescent Carcinoma-Associated Fibroblasts Upregulate IL8 to Enhance Prometastatic Phenotypes
Authors: Wang Tao , Notta Faiyaz , Navab Roya , Joseph Joella , Ibrahimov Emin , Xu Jing , Zhu Chang-Qi , Borgida Ayelet , Gallinger Steven , Tsao Ming-Sound
Published: April 2023

Table S1. Antibodies used in immunofluorescence and immunohistochemistry Table S2. qPCR primer sequences
Supplemental Figures from Senescent Carcinoma-Associated Fibroblasts Upregulate IL8 to Enhance Prometastatic Phenotypes
Authors: Wang Tao , Notta Faiyaz , Navab Roya , Joseph Joella , Ibrahimov Emin , Xu Jing , Zhu Chang-Qi , Borgida Ayelet , Gallinger Steven , Tsao Ming-Sound
Published: April 2023

Figure S1. MiaPaca2-YFP flow sort parameters. Figure S2. Immunofluorescence of primary CAF cell lines. Figure S3. Immunohistochemistry of Thy-1 and PDGFR-Î² on frozen pancreatic cancer tissues. Figure S4. Flow cytometry of CAF5 cells and cell cycle analysis. Figure S5. Î²-galactosidase staining of five CAF lines. Figure S6. Liver (A) and lung (E) metastasis from orthotopically implanted PDAC cells. Figure S7. Effect of IL8 on pancreatic cancer cell growth rates. Figure S8. Cell count and toxicity assays for SB225002. Figure S9. Effect of reparixin on transwell cancer migration. Figure S10. p16 and Ki67 immunohistochemistry in human PDAC. Figure S11. IHC of human PDAC showing low (A) vs. high (B) IL8 staining.
Supplementary Figure 1 from The Hedgehog Receptor Patched Functions in Multidrug Transport and Chemotherapy Resistance
Authors: Bidet Michel , Tomico Amandine , Martin Patrick , Guizouarn Hélène , Mollat Patrick , Mus-Veteau Isabelle
Published: April 2023

PDF file - 1.1MB, Structure of the different drugs used
Supplementary Figure 2 from The Activation of MEK/ERK Signaling Pathway by Bone Morphogenetic Protein 4 to Increase Hepatocellular Carcinoma Cell Proliferation and Migration
Authors: Chiu Chiang-Yen , Kuo Kung-Kai , Kuo Tzu-Lei , Lee King-The , Cheng Kuang-Hung
Published: April 2023

PDF file - 126K
Supplementary Figures 1-3 from Notch Signaling Modulates Hypoxia-Induced Neuroendocrine Differentiation of Human Prostate Cancer Cells
Authors: Danza Giovanna , Di Serio Claudia , Rosati Fabiana , Lonetto Giuseppe , Sturli Niccolò , Kacer Doreen , Pennella Antonio , Ventimiglia Giuseppina , Barucci Riccardo , Piscazzi Annamaria , Prudovsky Igor , Landriscina Matteo , Marchionni Niccolò , Tarantini Francesca
Published: April 2023

PDF file - 67K
Supplementary Table 1 from MicroRNAs Associated with Mitogen-Activated Protein Kinase in Human Pancreatic Cancer
Authors: Ikeda Yushi , Tanji Etsuko , Makino Naohiko , Kawata Sumio , Furukawa Toru
Published: April 2023

XLS file - 158K
Supplementary Table 1 from Cancer-Associated Fibroblasts Induce Matrix Metalloproteinase–Mediated Cetuximab Resistance in Head and Neck Squamous Cell Carcinoma Cells
Authors: Johansson Ann-Charlotte , Ansell Anna , Jerhammar Fredrik , Lindh Maja Bradic , Grénman Reidar , Munck-Wikland Eva , Östman Arne , Roberg Karin
Published: April 2023

PDF file - 91K, PCR array gene list
Supplementary Figure 1 from Cancer-Associated Fibroblasts Induce Matrix Metalloproteinase–Mediated Cetuximab Resistance in Head and Neck Squamous Cell Carcinoma Cells
Authors: Johansson Ann-Charlotte , Ansell Anna , Jerhammar Fredrik , Lindh Maja Bradic , Grénman Reidar , Munck-Wikland Eva , Östman Arne , Roberg Karin
Published: April 2023

PDF file - 156K, Cancer-associated fibroblasts induce cetuximab resistance in head and neck squamous cell carcinoma cell lines
Supplementary Table 2 from Diverse BRAF Gene Fusions Confer Resistance to EGFR-Targeted Therapy via Differential Modulation of BRAF Activity
Authors: Stangl Christina , Post Jasmin B. , van Roosmalen Markus J. , Hami Nizar , Verlaan-Klink Ingrid , Vos Harmjan R. , van Es Robert M. , Koudijs Marco J. , Voest Emile E. , Snippert Hugo J.G. , Kloosterman W.P.
Published: April 2023

Supplementary Table 2. Differential Gene Expression Analysis on BRAF (fusion) gene expressing organoid lines (provided separately due to size)
Supplementary Table 2 from Analysis of mRNA Profiles after MEK1/2 Inhibition in Human Pancreatic Cancer Cell Lines Reveals Pathways Involved in Drug Sensitivity
Authors: Gysin Stephan , Paquette Jesse , McMahon Martin
Published: April 2023

PDF file, 46K, Top 50 regulated mRNAs in most MEK inhibitor sensitive cell lines.