bluuebunny/crossref_metadata_2025 huggingface dataset:
Abstract 6568: Extended support for model organisms: The next frontier for the molecular signatures database
Authors: Castanza Anthony S. , Recla Jill M. , Eby David , Wenzel Alexander T. , Thorvaldsdottir Helga , Bult Carol J. , Mesirov Jill P.
Published: April 2023

In 2005, we introduced the Gene Set Enrichment Analysis (GSEA) method to enable the identification and estimation of significance of activated biological pathways and processes in molecular data. Serving a community of over 300,000 registered users, and contributing scientific analysis to more than 30,000 publications, GSEA has become ubiquitous in gene expression analysis and particularly in cancer research. The power of GSEA relies, in a large part, on the Molecular Signatures Database (MSigDB) that provides tens of thousands of expertly curated and annotated gene sets representing cellular processes, canonical pathways, response signatures, etc., derived from prior studies, public data, and curated pathway databases. Here we describe an important recent addition to the GSEA/MSigDB resource.

Historically, the GSEA-MSigDB resource has focused specifically on human data, offering guidance and support for analysis of model organism data through limited provision of orthology mapping files. In recognition of the importance of the mouse as a model organism for cancer research, we recently significantly expanded our support for mouse data in two ways.

(1) We introduced Mouse MSigDB with a total of about 15,000 sets that are provided in the native mouse gene symbol space and are derived from published mouse datasets and mouse-focused resources. This allows GSEA analysis of mouse datasets without the need for orthology conversion.

(2) For investigators who wish to use MSigDB’s human gene sets to analyze mouse data, or vice versa, we also implemented a new procedure for orthology mapping gene identifiers in an input dataset to match the identifiers of the gene sets. The new mapping considers the particular requirements of gene set enrichment analysis, and incorporates high confidence gene ortholog data from the Alliance of Genome Resources and ortholog-match refinement utilizing Ensembl’s ortholog datasets.

Together, these new additions offer a substantial step forward for making mouse a first-class citizen of the GSEA-MSigDB ecosystem. The new Mouse MSigDB, and the full GSEA-MSigDB resource, is available at gsea-msigdb.org.

Citation Format: Anthony S. Castanza, Jill M. Recla, David Eby, Alexander T. Wenzel, Helga Thorvaldsdottir, Carol J. Bult, Jill P. Mesirov. Extended support for model organisms: The next frontier for the molecular signatures database [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 6568.
Abstract 6571: Mammonc-DB: A web based user-friendly tool for comprehensive multi-omics data analysis in breast cancer
Authors: Karthikeyan Santhosh Kumar , Chandrashekar Darshan S. , Manne Upender , Creighton Chad , Qin Zhaohui S. , Kumar Sidharth , Varambally Sooryanaraya
Published: April 2023

Breast cancer (BC) accounted for 15% cancer related death among women, in the United States last year. It is a highly heterogeneous and complex diseases with multiple molecular events occurring during cancer initiation and progression. It is important to unravel the heterogeneity of breast cancer and the molecular events to develop diagnostic biomarkers and targeted therapies. There is need for comprehensive and user-friendly tool for the utilization of available breast cancer data including metastatic and treatment response data. We have earlier created a highly used pan-cancer proteogenomic portal called UALCAN (ualcan.path.uab.edu). Based on the current unmet need for comprehensive BC data analysis and visualization resource, we developed an integrated proteo-genomicbreast cancer data analysis portal, called Mammonc-DB (http://resource.path.uab.edu/MammOnc-ge.html). For Mammonc-DB, we collected data from public repositories like NCBI Gene Expression Omnibus (GEO), The Cancer Genome Atlas (TCGA) for collecting and analysis of genomics and epigenetics data, and, PRIDE, and, ProteomeXchange for proteomics data. We procured and processed multi-omics studies related to normal, primary, and metastatic human breast cancer data with other clinical information available, for different clinical models. We also collected and analyzed different therapy, and treatment studies that are currently employed in treating BC patients. Mammonc-DB has user friendly interface that aid breast cancer researchers and clinicians in, a) allows users to identify potential biomarkers in breast cancer, b) accessing publicly available breast cancer multi-omics data, c) Visualizing the expression pattern of gene or protein of interest with clinical feature stratification in each dataset among others This resource serves as a one-stop resource to study gene expression (protein-coding and non-coding) analysis along with epigenetic regulation, and protein expression patterns in BC. With this platform, we tend to create global user base that will accelerate discovery of biomarkers in BC that might be involved in diagnosis, therapeutic target identification and treatments of breast cancer.

Citation Format: Santhosh Kumar Karthikeyan, Darshan S. Chandrashekar, Upender Manne, Chad Creighton, Zhaohui S. Qin, Sidharth Kumar, Sooryanaraya Varambally. Mammonc-DB: A web based user-friendly tool for comprehensive multi-omics data analysis 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 6571.
Abstract 672: A genetic defect in phenylalanine hydroxylase (PAH) affects the immune system in kidney
Authors: Kim Seojeong , Kang Chaelin , Park Jihyun , Han Seung Seok , Koh Youngil , Yoon Sung-Soo
Published: April 2023

PAH, one of the genes associated with inborn error of metabolism (IEM), codes for phenylalanine hydroxylase and is specifically expressed in the liver and kidney. When PAH is dysfunctional, phenylalanine (Phe) cannot be converted to tyrosine (Tyr), and it produces toxic metabolites such as phenylpyruvate by a metabolic shift. We previously analyzed germline variants of IEM-related genes using public cancer multi-omics data. As a result, there was a high frequency of mutations in the PAH gene, and germline variants were particularly high in renal cell carcinoma (RCC). Based on this data, we suggest that kidney-specific expressed PAH mutations could change the kidney tissue microenvironment, which makes them more vulnerable to chronic kidney disease (CKD) and affects cancer development. We used the PAH enu2 mice model, which has a missense mutation in the PAH gene. PAH homozygous mutant mice display phenylketonuria (PKU) when not maintained on a Phe-free diet. PAH enu2 mice were maintained a normal diet. The concentration of phenylalanine in the mice's serum was measured each week. Then, the proportions of immune cells were analyzed in peripheral blood and kidney. Next, Jurkat cells, which are well-known as human T-cell lines, were applied to the in vitro experiment. Jurkat cells were cultured in a medium containing Phe or PPA and were activated by PHA/PMA or anti-CD3/CD28. Then after, the expression of immune-related markers was evaluated. Additionally, the expression of the PAH enzyme in human RCC and normal tissue was assessed by immunohistochemistry (IHC). The concentration of Phe in mice serum was higher when the PAH gene was defective; homozygous mutant, heterozygous mutant. As PAH-defective mice got older, the T cell population decreased in the blood and kidney immune cells. When Jurkat T cells were cultured with Phe or PPA, the expression of IL-2, a cytokine related to T cell expansion, decreased in the PPA-treated and activated group. There were more significant changes when treated with PPA rather than Phe. IHC data shows the expression of PAH was significantly decreased in RCC tissues compared to non-tumor tissue. These results suggest that the immune system could be changed by PAH dysfunction bearing a germline mutation. Moreover, the kidney tissue microenvironment with PAH defects is vulnerable to the development of kidney disease, which can lead to RCC. This is a novel discovery that can explain the importance of the role PAH gene in kidney disease.

Citation Format: Seojeong Kim, Chaelin Kang, Jihyun Park, Seung Seok Han, Youngil Koh, Sung-Soo Yoon. A genetic defect in phenylalanine hydroxylase (PAH) affects the immune system in kidney [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 672.
Abstract 755: The impact of cancer treatment on cognitive function and quality of life in patients undergoing treatment at a tertiary care hospital in New Delhi, India
Authors: Francis Delfin Lovelina
Published: April 2023

Background: Cognitive dysfunction is becoming a more well-known complication of cancer and its treatment. Cancer-related cognitive changes and impairment have also been documented in non-central nervous system (non-CNS) cancer patients. The majority of research in this area has discovered that a subset of patients appear to be vulnerable to this complication even after treatment has ended, and they frequently struggle with multitasking, short-term memory, word-finding, attention, or concentration. It is critical to investigate the possible link between cancer and cognitive impairment because it can have a serious impact on quality of life.

Methods: This cross-sectional study between May 2022 and October 2022, included patients who were referred to the dental outpatient department as part of a preventive/prophylactic evaluation at the tertiary care centre in New Delhi, India. After receiving informed consent, the oral health impact profile-14 instrument to assess participants' oral health-related quality of life (OHRQoL) and the Montreal Cognitive Assessment (MOCA) for cognitive evaluation were used.

Results: Out of 283 patients 77% males and 23% females and vast majority had Stage III cancer. All patients' OHRQoL was hampered, but it was higher in those who developed visible oral changes during treatment versus those who did not (P =.001). Taking painkillers, losing sexual interest, difficulty in social contact, loss of taste and smell senses were the main factors affecting oral health related QoL (OHRQoL). A significant relationship was discovered between pain, speech, social eating, dry mouth, sticky saliva, and weight loss in relation to various treatment modalities. Those who were treated surgically alone had better QoL than others, according to the OHRQoL scores. In terms of delayed recall, 55% were found to be cognitively impaired, which was associated with lower OHRQoL.

Conclusion: Cognitive impairment is common in cancer patients, which may be caused by the cancer itself. It is also linked to OHRQoL and psychosocial variables. There has been little research into the relationships between cognitive function and quality of life (OHRQoL) in cancer patients. Together with previous research indicating that cognitive function and OHRQoL can influence treatment adherence and outcomes, the findings support the inclusion of cognitive screening and OHRQoL assessment as part of patient pretreatment assessment.

Citation Format: Delfin Lovelina Francis. The impact of cancer treatment on cognitive function and quality of life in patients undergoing treatment at a tertiary care hospital in New Delhi, India [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 755.
Abstract 767: Genomics and transcriptomics profiling of BRCA mutation carriers revealed the landscape of early pathogenesis of BRCA1/2-associated breast cancer
Authors: Ren Zuen , Lin Po-Han , Koh Siang Boon , Stewart Kai , Haradhvala Nick , Dedeoglu Aylin S , Smidt Ilze , Suzuki Akiko , Li David , Thant Win , Mueller Sarah , Joseph Taisha , Bossuyt Veerle , Lawrence Michael , Getz Gad , Ellisen Leif W.
Published: April 2023

Women who harbor germline heterozygous mutations of BRCA1 or BRCA2 have a high risk of breast cancer. Our previous study showed that patient-derived, ostensibly normal BRCA2mut/+ luminal progenitor (LP) cells are more prone to exhibit sub-chromosomal copy number variations and associated DNA damage relative to non-carriers potentially reflecting early breast tumorigenesis. The clinically assessable biomarkers for early pathological changes of BRCA1/2 mutation in LP cells remain unknown. Single-cell RNA sequencing (scRNAseq) of LP cells of BRCA1/2 mutation carriers revealed enrichment of KIT expression (KIT+) and subsequent transcriptional factor activations were observed in LP cells of BRCA1/2 mutation carriers relative to non-carriers. Moreover, overrepresented pathway analysis uncovered that KIT+ BRCA-mutated LP cells were enriched in pathways involving DNA binding transcription activator activity and oxidative phosphorylation. These gene signature profiles were recapitulated in bulk RNA-seq of BRCA2 mutation carrier LP cells. Collectively, our preliminary data suggest such analyses may identify potential biomarkers of the risk prediction for early pathogenesis of BRCA1/2 mutation carriers. Following validation of our findings via tissue microassay analysis and clinical trials, we hope to eventually assist clinicians in their decision making of prophylactic surgeries for BRCA1/2 mutation carriers.

Citation Format: Zuen Ren, Po-Han Lin, Siang Boon Koh, Kai Stewart, Nick Haradhvala, Aylin S Dedeoglu, Ilze Smidt, Akiko Suzuki, David Li, Win Thant, Sarah Mueller, Taisha Joseph, Veerle Bossuyt, Michael Lawrence, Gad Getz, Leif W. Ellisen. Genomics and transcriptomics profiling of BRCA mutation carriers revealed the landscape of early pathogenesis of BRCA1/2-associated 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 767.
Abstract 907: Evaluation of the anti-GPC1 scFv-Fc fusion protein as a detection tool of GPC1 expression in human cancers
Authors: Sawada Takeshi , Yaguchi Tomonori , Sakai Yuko , Suzuki Chinatsu , Morii Kenji , Aoki Masahiko , Fukahori Masaru , Serada Satoshi , Naka Tetsuji , Yamashita Jun K. , Kawakami Yutaka , Nakajima Takako E.
Published: April 2023

Background: We have developed a glypican-1 (GPC1) targeted CAR-T cell with strong anti-tumor effects against solid tumors in vivo (Kato et al 2020 eLife). In general, an antibody is used for detection of target protein expression in the tumor to identify appropriate targets for the CAR-T cell therapy in solid tumors. However, the local conjunction between CAR-T cells and the target is not exactly the same in the antibody and the target because CAR-T cell recognizes the target by single-chain variable fragment (scFv). In this study, we evaluated the anti-GPC1 scFv-Fc fusion protein as a detection tool of GPC1 expression in human cancer cell lines.

Methods: The sequences encoding the anti-GPC1 scFv are based on the sequence of anti-GPC1 mAb (clone: 1-12) that recognizes human and mouse GPC1 (Harada et al., 2017). The sequences of anti GPC-1 scFv were cloned into pCAG-Neo mIgG2a-Fc plasmid for the generation of anti GPC1_scFv-mIgG2a_Fc fusion proteins. The plasmids were transfected into 293 T cells and the fusion proteins were purified from their culture supernatants using Antibody TCS Purification Kit. LK2-GPC1 (a GPC1 overexpressing lung carcinoma cell line), TE8 (an esophageal carcinoma cell line with endogenous GPC1) and LK2-mock (a GPC1-negative lung carcinoma cell line) were used for the evaluation of the anti-GPC1 scFv-Fc fusion protein.

Results: In FACS assays, fluorescence microscopy analysis and immunohistochemistry staining, GPC1 expression was successfully detected by both anti-GPC1 scFv of VL-VH and VH-VL in LK2-GPC1 and TE-8, and not detected in LK2-mock. Localization of GPC1 expression on the cell membrane was confirmed by fluorescence microscopy.

Perspective: Further comparative evaluation between anti-GPC1 antibody and anti-GPC1 scFv-Fc fusion proteins are needed especially in human tumor tissues. We plan to evaluate a relationship between GPC1 positivity in various human tumor tissues detected by anti-GPC1 scFv-Fc fusion protein and CAR-T cell cytotoxicity against the tissue.

Citation Format: Takeshi Sawada, Tomonori Yaguchi, Yuko Sakai, Chinatsu Suzuki, Kenji Morii, Masahiko Aoki, Masaru Fukahori, Satoshi Serada, Tetsuji Naka, Jun K. Yamashita, Yutaka Kawakami, Takako E. Nakajima. Evaluation of the anti-GPC1 scFv-Fc fusion protein as a detection tool of GPC1 expression in human cancers [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 907.
Supplementary Table 1 from Hypoxia-Independent Gene Expression Mediated by SOX9 Promotes Aggressive Pancreatic Tumor Biology
Authors: Camaj Peter , Jäckel Carsten , Krebs Stefan , DeToni Enrico N. , Blum Helmut , Jauch Karl-Walter , Nelson Peter J. , Bruns Christiane J.
Published: April 2023

PDF file - 130K, Supplemental Table 1. Differential expression of the genes associated to cancer relevant pathways.
Supplementary Results, Figure Legend from Hypoxia-Independent Gene Expression Mediated by SOX9 Promotes Aggressive Pancreatic Tumor Biology
Authors: Camaj Peter , Jäckel Carsten , Krebs Stefan , DeToni Enrico N. , Blum Helmut , Jauch Karl-Walter , Nelson Peter J. , Bruns Christiane J.
Published: April 2023

PDF file - 163K
Supplementary Figure 5 from Hypoxia-Independent Gene Expression Mediated by SOX9 Promotes Aggressive Pancreatic Tumor Biology
Authors: Camaj Peter , Jäckel Carsten , Krebs Stefan , DeToni Enrico N. , Blum Helmut , Jauch Karl-Walter , Nelson Peter J. , Bruns Christiane J.
Published: April 2023

PDF file - 68K, S5. Methylation of Sox9-promoter, Sox9 and VEGF expression in patient samples.
Supplementary Figure 3 from Hypoxia-Independent Gene Expression Mediated by SOX9 Promotes Aggressive Pancreatic Tumor Biology
Authors: Camaj Peter , Jäckel Carsten , Krebs Stefan , DeToni Enrico N. , Blum Helmut , Jauch Karl-Walter , Nelson Peter J. , Bruns Christiane J.
Published: April 2023

PDF file - 190K, S3. Effect of genetics or epigenetics.
Supplementary Figure 2 from Hypoxia-Independent Gene Expression Mediated by SOX9 Promotes Aggressive Pancreatic Tumor Biology
Authors: Camaj Peter , Jäckel Carsten , Krebs Stefan , DeToni Enrico N. , Blum Helmut , Jauch Karl-Walter , Nelson Peter J. , Bruns Christiane J.
Published: April 2023

PDF file - 70K, S2. A) Differential methylation of the Sox9-promoter in NMET and HMET cells. B) Methylation and hypoxia. NMET and HMET cells were cultivated under hypoxia or normoxia, respectively. (C) Effect of methylation inhibition on VEGF expression. Relative transcription of VEGF in LMET and HMET cells is demonstrated. D) Effect of methylation inhibition on Sox9 expression.
Supplementary Figure 1 from Hypoxia-Independent Gene Expression Mediated by SOX9 Promotes Aggressive Pancreatic Tumor Biology
Authors: Camaj Peter , Jäckel Carsten , Krebs Stefan , DeToni Enrico N. , Blum Helmut , Jauch Karl-Walter , Nelson Peter J. , Bruns Christiane J.
Published: April 2023

PDF file - 253K, S1. (A) Clustering of the differentially expressed genes in NMET vs. HMET cells. B) Interaction between Sox9 and promoters of tumor relevant genes. (C) Immunopreciptates obtained via ChIP (Figure 4) were subjected to real time PCR. (D) Function of Sox9-shRNA. E) Expression of the differentially expressed Sox9-target genes. (F) TUNEL (terminal deoxynucleotidyl transferase dUTP nick end labelling) staining.
Supplementary Table 1 from Breast Cancer Metastasis Suppressor-1 Promoter Methylation in Primary Breast Tumors and Corresponding Circulating Tumor Cells
Authors: Chimonidou Maria , Kallergi Galatea , Georgoulias Vassilis , Welch Danny R. , Lianidou Evi S.
Published: April 2023

PDF 111KB, Oligonucleotide sequences of BRMS1 primers used in this study.
Supplementary Figure Legend from Neurotransmitter Substance P Mediates Pancreatic Cancer Perineural Invasion via NK-1R in Cancer Cells
Authors: Li Xuqi , Ma Guodong , Ma Qingyong , Li Wei , Liu Jiangbo , Han Liang , Duan Wanxing , Xu Qinhong , Liu Han , Wang Zheng , Sun Qing , Wang Fengfei , Wu Erxi
Published: April 2023

PDF file - 64K
Supplementary Figure 1 from Neurotransmitter Substance P Mediates Pancreatic Cancer Perineural Invasion via NK-1R in Cancer Cells
Authors: Li Xuqi , Ma Guodong , Ma Qingyong , Li Wei , Liu Jiangbo , Han Liang , Duan Wanxing , Xu Qinhong , Liu Han , Wang Zheng , Sun Qing , Wang Fengfei , Wu Erxi
Published: April 2023

PDF file - 5384K, S1. The effects of SP on neurites and BxPC-3cells.
Supplementary Tables 1 and 2 from FBXW7 Mediates Chemotherapeutic Sensitivity and Prognosis in NSCLCs
Authors: Yokobori Takehiko , Yokoyama Yozo , Mogi Akira , Endoh Hideki , Altan Bolag , Kosaka Takayuki , Yamaki Ei , Yajima Toshiki , Tomizawa Kenji , Azuma Yoko , Onozato Ryoichi , Miyazaki Tatsuya , Tanaka Shigebumi , Kuwano Hiroyuki
Published: April 2023

PDF - 88KB, Supplementary Table 1. Relationships between FBXW7 expression and clinicopathological factors in 103 patients with NSCLC. Supplementary Table 2. Univariate and multivariate analysis of clinicopathological factors affecting the overall survival rate of patients with NSCLC following surgery.
Supplementary Figure 1 from FBXW7 Mediates Chemotherapeutic Sensitivity and Prognosis in NSCLCs
Authors: Yokobori Takehiko , Yokoyama Yozo , Mogi Akira , Endoh Hideki , Altan Bolag , Kosaka Takayuki , Yamaki Ei , Yajima Toshiki , Tomizawa Kenji , Azuma Yoko , Onozato Ryoichi , Miyazaki Tatsuya , Tanaka Shigebumi , Kuwano Hiroyuki
Published: April 2023

PDF - 103KB, Supplementary Figure 1. Water-soluble tetrazolium (WST) assay in FBXW7 siRNA-treated cells. The proliferation rate of FBXW7 siRNA-treated cells was compared to that of control siRNA-treated and parent NSCLC cells.
Supplementary Figure 8 from Inhibition of mTOR Pathway Sensitizes Acute Myeloid Leukemia Cells to Aurora Inhibitors by Suppression of Glycolytic Metabolism
Authors: Liu Ling-Ling , Long Zi-Jie , Wang Le-Xun , Zheng Fei-Meng , Fang Zhi-Gang , Yan Min , Xu Dong-Fan , Chen Jia-Jie , Wang Shao-Wu , Lin Dong-Jun , Liu Quentin
Published: April 2023

PDF file - 376K, P62 expression in p62 knockdown-U937 cells.
Supplementary Figure 2 from Inhibition of mTOR Pathway Sensitizes Acute Myeloid Leukemia Cells to Aurora Inhibitors by Suppression of Glycolytic Metabolism
Authors: Liu Ling-Ling , Long Zi-Jie , Wang Le-Xun , Zheng Fei-Meng , Fang Zhi-Gang , Yan Min , Xu Dong-Fan , Chen Jia-Jie , Wang Shao-Wu , Lin Dong-Jun , Liu Quentin
Published: April 2023

PDF file - 1081K, Cell viability detection in Aurora kinase A knockdown-U937 cells.
Supplementary Tables 1 - 7 from Genomic Analysis of Head and Neck Squamous Cell Carcinoma Cell Lines and Human Tumors: A Rational Approach to Preclinical Model Selection
Authors: Li Hua , Wawrose John S. , Gooding William E. , Garraway Levi A. , Lui Vivian Wai Yan , Peyser Noah D. , Grandis Jennifer R.
Published: April 2023

PDF file - 108K, Supplemental Table 1: Source, Clinical, and Pathological Features of Sequenced HNSCC Cell Lines Supplemental Table 2: Genes Mutated in >50% in HNSCC Cell Lines Supplemental Table 3: TP53 Mutations in HNSCC Cell Lines Supplemental Table 4: The Numbers of HNSCC Cell Lines and Tumors Derived from Larynx, Oral Cavity and Pharynx Supplemental Table 5: Mutation Frequency Comparison by Gene. This table lists the results of the tests of significance for each of 23 genes ranked in order of p value. The unadjusted (raw) p value is listed along with the value after adjustment for false discovery. Supplemental Table 6: Genes Mutated in >10% of HNSCC Tumors But Not Mutated in Human HNSCC Cell Lines Supplemental Table 7: EGFR Pathway Mutations in HNSCC Cell Lines and Tumors Note: HNSCC tumor samples marked with * are from the Agrawal et al database. All of the other tumor samples are from the Stransky et al database.
Supplementary Figure 5 from Activation of the Wnt Pathway through AR79, a GSK3β Inhibitor, Promotes Prostate Cancer Growth in Soft Tissue and Bone
Authors: Jiang Yuan , Dai Jinlu , Zhang Honglai , Sottnik Joe L. , Keller Jill M. , Escott Katherine J. , Sanganee Hitesh J. , Yao Zhi , McCauley Laurie K. , Keller Evan T.
Published: April 2023

PDF file - 391K, Figure S5. Knockdown of β-catenin abrogates the ability of AR79 to increase nuclear B-catenin expression in DU145 and C4-2B cell lines
Supplementary Figure 3 from Activation of the Wnt Pathway through AR79, a GSK3β Inhibitor, Promotes Prostate Cancer Growth in Soft Tissue and Bone
Authors: Jiang Yuan , Dai Jinlu , Zhang Honglai , Sottnik Joe L. , Keller Jill M. , Escott Katherine J. , Sanganee Hitesh J. , Yao Zhi , McCauley Laurie K. , Keller Evan T.
Published: April 2023

PDF file - 294K, Figure S3. AR79 increases bone formation in normal mouse tibiae.
Supplementary Figure 2 from Activation of the Wnt Pathway through AR79, a GSK3β Inhibitor, Promotes Prostate Cancer Growth in Soft Tissue and Bone
Authors: Jiang Yuan , Dai Jinlu , Zhang Honglai , Sottnik Joe L. , Keller Jill M. , Escott Katherine J. , Sanganee Hitesh J. , Yao Zhi , McCauley Laurie K. , Keller Evan T.
Published: April 2023

PDF file - 290K, Figure S2. AR79 has no impact on p-HIPK2 expression in prostate cancer cell lines.
Supplementary Figure 1 from Activation of the Wnt Pathway through AR79, a GSK3β Inhibitor, Promotes Prostate Cancer Growth in Soft Tissue and Bone
Authors: Jiang Yuan , Dai Jinlu , Zhang Honglai , Sottnik Joe L. , Keller Jill M. , Escott Katherine J. , Sanganee Hitesh J. , Yao Zhi , McCauley Laurie K. , Keller Evan T.
Published: April 2023

PDF file - 66K, Figure S1. Mouse body weights were not impacted by AR79 treatment.
Supplementary Table 2 from DNA Damage-Inducible Gene, Reprimo Functions as a Tumor Suppressor and Is Suppressed by Promoter Methylation in Gastric Cancer
Authors: Ooki Akira , Yamashita Keishi , Yamaguchi Kensei , Mondal Anupom , Nishimiya Hiroshi , Watanabe Masahiko
Published: April 2023

XLS file - 17K, Supplementary Table 2. Mutation sites of p53 in 83 patients with advanced gastirc cancer.
Supplementary Table 1 from DNA Damage-Inducible Gene, Reprimo Functions as a Tumor Suppressor and Is Suppressed by Promoter Methylation in Gastric Cancer
Authors: Ooki Akira , Yamashita Keishi , Yamaguchi Kensei , Mondal Anupom , Nishimiya Hiroshi , Watanabe Masahiko
Published: April 2023

XLS file - 80K, Supplementary Table 1. PCR condition and sequences of primer and fluorescent probe used in the present study.
Supplementary Figure 3 from DNA Damage-Inducible Gene, Reprimo Functions as a Tumor Suppressor and Is Suppressed by Promoter Methylation in Gastric Cancer
Authors: Ooki Akira , Yamashita Keishi , Yamaguchi Kensei , Mondal Anupom , Nishimiya Hiroshi , Watanabe Masahiko
Published: April 2023

PDF file - 127K, Supplementary Figure. 3. Anticancer effect of treatment combined with CDDP and 5-FU in mice injected with Reprimo-transfected cells (AZ-r10 or AZ-r16 cells) when compared to AZ-p or AZ-m cells. Mice with tumors approximately 5 mm in diameter received intraperitoneal administration of CDDP (0.1 mg/kg) and 5-FU (10 mg/kg) once daily for 7 days. The relative tumor volume was defined by the ratio of tumor volume in mice with combined CDDP and 5-FU treatment divided by that with mock treatment. The relative tumor volume 7days from start of treatment was compared in tumor in mice injected with AZ-r10 or AZ-r16 cells versus AZ-m or AZ-p cells. *, P<0.05; Error bars, SD; NS, not significant.
Supplementary Figure 2 from DNA Damage-Inducible Gene, Reprimo Functions as a Tumor Suppressor and Is Suppressed by Promoter Methylation in Gastric Cancer
Authors: Ooki Akira , Yamashita Keishi , Yamaguchi Kensei , Mondal Anupom , Nishimiya Hiroshi , Watanabe Masahiko
Published: April 2023

PDF file - 216K, Supplementary Figure. 2. Invasion assay and cell cycle assay. (A) Invasion assay. With AZ-m cells as 1.0, the relative invasive rates were shown. Bars, 200 �m; *, P<0.05; Error bars; SD; NS, not significant. (B) Cells without Reprimo methylation (AZ521 or H111 cells) were transfected with pcDNATM3.1-mock or pcDNATM3.1-Reprimo, and the stable cells were established by G418 selection. For cell cycle assay, after cells were synchronized for 48 hours in serum free medium, the cells were then cultured in complete medium for 24 hours. The percentage and SD of cell cycle phases are shown in each panel. *, P<0.05; Error bars; SD.
Supplementary Figure 1 from DNA Damage-Inducible Gene, Reprimo Functions as a Tumor Suppressor and Is Suppressed by Promoter Methylation in Gastric Cancer
Authors: Ooki Akira , Yamashita Keishi , Yamaguchi Kensei , Mondal Anupom , Nishimiya Hiroshi , Watanabe Masahiko
Published: April 2023

PDF file - 174K, Supplementary Figure. 1. Representative p53 gene status. Analysis of p53 mutation was performed by sequence using primer for exons 4 to 9 of p53 gene.
Supplementary Methods and Supplementary Figure 1 from The SmgGDS Splice Variant SmgGDS-558 Is a Key Promoter of Tumor Growth and RhoA Signaling in Breast Cancer
Authors: Hauser Andrew D. , Bergom Carmen , Schuld Nathan J. , Chen Xiuxu , Lorimer Ellen L. , Huang Jian , Mackinnon Alexander C. , Williams Carol L.
Published: April 2023

PDF - 139KB, Supplementary Materials and Methods; Supplementary Figure S1: MDA-MB-231 cells have more detergent soluble prenylated RhoA than RhoC.
Supplementary Table 4 from RAS/MEK–Independent Gene Expression Reveals BMP2-Related Malignant Phenotypes in the Nf1-Deficient MPNST
Authors: Sun Daochun , Haddad Ramsi , Kraniak Janice M. , Horne Steven D. , Tainsky Michael A.
Published: April 2023

XLSX file - 10K, Literature supports for EDN1
Supplementary Table 3 from RAS/MEK–Independent Gene Expression Reveals BMP2-Related Malignant Phenotypes in the Nf1-Deficient MPNST
Authors: Sun Daochun , Haddad Ramsi , Kraniak Janice M. , Horne Steven D. , Tainsky Michael A.
Published: April 2023

XLSX file - 464K, Data Set Annotations
Supplementary Figure 1 from Fer Protein-Tyrosine Kinase Promotes Lung Adenocarcinoma Cell Invasion and Tumor Metastasis
Authors: Ahn Joseph , Truesdell Peter , Meens Jalna , Kadish Carli , Yang Xiaolong , Boag Alexander H. , Craig Andrew W.B.
Published: April 2023

PDF file - 267K, Specificity of Fer IHC staining in NSCLC.
Supplementary Table 1 from Interleukin-6 and Oncostatin-M Synergize with the PI3K/AKT Pathway to Promote Aggressive Prostate Malignancy in Mouse and Human Tissues
Authors: Smith Daniel A. , Kiba Atsushi , Zong Yang , Witte Owen N.
Published: April 2023

XLSX file - 13K, Quantification of phenotypes observed across five histological sections from independent biological replicates.
Supplementary Figure Legend from Crizotinib-Resistant NPM-ALK Mutants Confer Differential Sensitivity to Unrelated Alk Inhibitors
Authors: Ceccon Monica , Mologni Luca , Bisson William , Scapozza Leonardo , Gambacorti-Passerini Carlo
Published: April 2023

PDF file - 39K
Supplementary Figure Legend from NF-YA Underlies EZH2 Upregulation and Is Essential for Proliferation of Human Epithelial Ovarian Cancer Cells
Authors: Garipov Azat , Li Hua , Bitler Benjamin G. , Thapa Roshan J. , Balachandran Siddharth , Zhang Rugang
Published: April 2023

PDF file - 97K
Supplementary Figure 5 from Crizotinib-Resistant NPM-ALK Mutants Confer Differential Sensitivity to Unrelated Alk Inhibitors
Authors: Ceccon Monica , Mologni Luca , Bisson William , Scapozza Leonardo , Gambacorti-Passerini Carlo
Published: April 2023

PDF file - 2602K, SUPM2CR03 cell line is resistant even at higher doses of AP26113 and NVP-TAE684 (100nM).
Supplementary Figure 3 from Crizotinib-Resistant NPM-ALK Mutants Confer Differential Sensitivity to Unrelated Alk Inhibitors
Authors: Ceccon Monica , Mologni Luca , Bisson William , Scapozza Leonardo , Gambacorti-Passerini Carlo
Published: April 2023

PDF file - 590K, Chromatograms representative of the two major mutations found on KARPAS299 and SUP-M2 cell lines.
Supplementary Figure 3 from NF-YA Underlies EZH2 Upregulation and Is Essential for Proliferation of Human Epithelial Ovarian Cancer Cells
Authors: Garipov Azat , Li Hua , Bitler Benjamin G. , Thapa Roshan J. , Balachandran Siddharth , Zhang Rugang
Published: April 2023

PDF file - 177K, Cell transform does not upregualte NF-YA expression.
Supplementary Figure 2 from Crizotinib-Resistant NPM-ALK Mutants Confer Differential Sensitivity to Unrelated Alk Inhibitors
Authors: Ceccon Monica , Mologni Luca , Bisson William , Scapozza Leonardo , Gambacorti-Passerini Carlo
Published: April 2023

PDF file - 2629K, ALK phosphorylation status of Crizotinib resistant human cell lines.
Supplementary Figure 1 from Crizotinib-Resistant NPM-ALK Mutants Confer Differential Sensitivity to Unrelated Alk Inhibitors
Authors: Ceccon Monica , Mologni Luca , Bisson William , Scapozza Leonardo , Gambacorti-Passerini Carlo
Published: April 2023

PDF file - 2845K, Cell viability and absolute cell number during cell selection.
Supplementary Figure 1 from NF-YA Underlies EZH2 Upregulation and Is Essential for Proliferation of Human Epithelial Ovarian Cancer Cells
Authors: Garipov Azat , Li Hua , Bitler Benjamin G. , Thapa Roshan J. , Balachandran Siddharth , Zhang Rugang
Published: April 2023

PDF file - 446K, Two CCAAT sites in the proximal region of the human EZH2 gene promoter are critical for its transcriptional activity.
Supplementary Figures 1 - 4 from Suppression of Ser/Thr Phosphatase 4 (PP4C/PPP4C) Mimics a Novel Post-Mitotic Action of Fostriecin, Producing Mitotic Slippage Followed by Tetraploid Cell Death
Authors: Theobald Benjamin , Bonness Kathy , Musiyenko Alla , Andrews Joel F. , Urban Gudrun , Huang Xizhong , Dean Nicholas M. , Honkanen Richard E.
Published: April 2023

PDF file - 2199K, Figure 1S. Inhibition of PP4C mRNA and protein expression by treatment with antisense oligodeoxynucleotides. Figure 2S. Images selected from time-lapse live cell imaging of H2B-GFP expressing HeLa cells representing typical behavior of cell populations treated with antisense oligonucleotides targeting PP2ACα. Figure 3S. Comparison of the effects produced by fostriecin, mismatch controls, and antisense oligodeoxynucleotides targeting PP2ACα or PP4C. Figure 4S. Representative confocal microscopic images non-mitotic cells treated with antisense targeting PP4C.
Supplementary Table 2 from AKR1B10, a Transcriptional Target of p53, Is Downregulated in Colorectal Cancers Associated with Poor Prognosis
Authors: Ohashi Tomoko , Idogawa Masashi , Sasaki Yasushi , Suzuki Hiromu , Tokino Takashi
Published: April 2023

XLSX file - 54K, The gene cluster that was increased by adriamycin in control HCT116 cells and not in AKR1B10 knockdown cells.
Supplementary Table 1 from AKR1B10, a Transcriptional Target of p53, Is Downregulated in Colorectal Cancers Associated with Poor Prognosis
Authors: Ohashi Tomoko , Idogawa Masashi , Sasaki Yasushi , Suzuki Hiromu , Tokino Takashi
Published: April 2023

XLSX file - 108K, Genes which was increased by p53 more than 8-fold compared to LacZ.
Supplementary Figure 1 from AKR1B10, a Transcriptional Target of p53, Is Downregulated in Colorectal Cancers Associated with Poor Prognosis
Authors: Ohashi Tomoko , Idogawa Masashi , Sasaki Yasushi , Suzuki Hiromu , Tokino Takashi
Published: April 2023

PDF file - 31K, The effect of AKR1B10 knockdown on the activity of caspases and the amount of cellular NADPH.
Supplementary Procedures and Supplementary Figures 1 through 3 from C-C Chemokine Receptor 5 on Pulmonary Mesenchymal Cells Promotes Experimental Metastasis via the Induction of Erythroid Differentiation Regulator 1
Authors: Mango Robert L. , Wu Qing Ping , West Michelle , McCook Everett C. , Serody Jonathan S. , van Deventer Hendrik W.
Published: April 2023

PDF - 384KB, Supplementary Experimental Procedures; S1. Semi-quantitative RT-PCR for genes differentially regulated at 6, 24, and 48 hours after injection by B16 F10 injection. Figure S2. Sequence alignment comparing the coding sequence for Erdr1 from cDNA extracted from PMCs with the consensus published sequences. Figure S3. MEFs promote tumor metastasis.
Supplementary Figure 1 from Systems Analysis of the NCI-60 Cancer Cell Lines by Alignment of Protein Pathway Activation Modules with “-OMIC” Data Fields and Therapeutic Response Signatures
Authors: Federici Giulia , Gao Xi , Slawek Janusz , Arodz Tomasz , Shitaye Amanuel , Wulfkuhle Julia D. , De Maria Ruggero , Liotta Lance A. , Petricoin Emanuel F.
Published: April 2023

PDF file - 160K, Unsupervised hierarchical clustering representing the NCI-60 cell lines (horizontal axis) and the RTKs (vertical axis) analyzed. The NCI-60 sample names have been colorized according to their tissue origin: orange - kidney, blue - lung, pink - breast, red - blood, green - colon, brown - prostate, purple - ovary, black - skin and gray - central nervous system.
Supplementary Tables 1 - 4 from Epigenetic Control of NF-κB-Dependent FAS Gene Transcription during Progression of Myelodysplastic Syndromes
Authors: Ettou Sandrine , Humbrecht Catherine , Benet Blandine , Billot Katy , d'Allard Diane , Mariot Virginie , Goodhardt Michele , Kosmider Olivier , Mayeux Patrick , Solary Eric , Fontenay Michaela
Published: April 2023

PDF file - 143K, Table S1: Clinical and biological characteristics of 53 patients with MDS/sAML. Table S2: Primers and experimental conditions for FAS and BCL2L1 quantification by RT-qPCR. Table S3: Biotinylated oligonucleotide sequences for in vitro p65 pull-down and primers for DNA methylation assay. Table S4: Primers for chromatin immunoprecipitation at FAS, B2M, RAG1 and PAX6 promoters.
Supplementary Table 1 from Nullifying the CDKN2AB Locus Promotes Mutant K-ras Lung Tumorigenesis
Authors: Schuster Katja , Venkateswaran Niranjan , Rabellino Andrea , Girard Luc , Peña-Llopis Samuel , Scaglioni Pier Paolo
Published: April 2023

PDF file - 102K, Metastatic disease in LSL Kras mice.
Supplementary Figure 4 from Nullifying the CDKN2AB Locus Promotes Mutant K-ras Lung Tumorigenesis
Authors: Schuster Katja , Venkateswaran Niranjan , Rabellino Andrea , Girard Luc , Peña-Llopis Samuel , Scaglioni Pier Paolo
Published: April 2023

PDF file - 2336K, Analysis of tumors and survival in Kras-GFP mice.
Supplementary Figure 3 from Nullifying the CDKN2AB Locus Promotes Mutant K-ras Lung Tumorigenesis
Authors: Schuster Katja , Venkateswaran Niranjan , Rabellino Andrea , Girard Luc , Peña-Llopis Samuel , Scaglioni Pier Paolo
Published: April 2023

PDF file - 1846K, Lung specific expression of Kras and GFP in the mouse.
Supplementary Fig. 4 from Transcription Factor Interactions Mediate EGF-Dependent COX-2 Expression
Authors: Xu Kaiming , Shu Hui-Kuo G.
Published: April 2023

Supplementary Fig. 4 - PDF file 96K, EGF-dependent signaling to p38-MAPK requires Src activity
Supplementary Tables from TDP1 and PARP1 Deficiency Are Cytotoxic to Rhabdomyosarcoma Cells
Authors: Fam Hok Khim , Walton Cheryl , Mitra Sheetal A. , Chowdhury Miraj , Osborne Nichola , Choi Kunho , Sun Guobin , Wong Patrick C.W. , O'Sullivan Maureen J. , Turashvili Gulisa , Aparicio Samuel , Triche Timothy J. , Bond Mason , Pallen Catherine J. , Boerkoel Cornelius F.
Published: April 2023

Supplementary Tables - PDF file 330K, Supplementary Table 1. Nucleotide sequences for oligonucleotides, TDP1 siRNAs and TDP1 shRNAs used. Supplementary Table 2. Comparison of Tdp1 expression between noncancerous skeletal muscle and RMS subtypes. Supplementary Table 3. Effect of 96 - hour PARP inhibitor treatment on the proliferation of RMS cell lines. Supplementary Table 4. Summary of BRCA1 mutations in RMS cell lines. Supplementary Table 5. Summary of BRCA2 mutations in RMS cell lines
Supplementary Figure and Table Legends from TDP1 and PARP1 Deficiency Are Cytotoxic to Rhabdomyosarcoma Cells
Authors: Fam Hok Khim , Walton Cheryl , Mitra Sheetal A. , Chowdhury Miraj , Osborne Nichola , Choi Kunho , Sun Guobin , Wong Patrick C.W. , O'Sullivan Maureen J. , Turashvili Gulisa , Aparicio Samuel , Triche Timothy J. , Bond Mason , Pallen Catherine J. , Boerkoel Cornelius F.
Published: April 2023

Supplementary Figure and Table Legends - PDF file 96K, Supplementary Figure and Table Legends
Supplementary Figure 2 from Oncogenic MUC1-C Promotes Tamoxifen Resistance in Human Breast Cancer
Authors: Kharbanda Akriti , Rajabi Hasan , Jin Caining , Raina Deepak , Kufe Donald
Published: April 2023

PDF file - 542K, A. MCF-7/MUC1-C cells were treated with 10 μM LY294002 (LY) for the indicated times. Lysates were immunoblotted with the indicated antibodies. B. MCF-7/MUC1-C cells were left untreated (Control) or treated with 10 μM LY294002 for 48 h. Aliquots of control and LY294002-treated cells were then incubated in the presence of 5 μM tamoxifen for an additional 48 h. Cell viability at 96 h was determined by trypan blue staining. The results (mean+SD of three determinations) are expressed as percentage cell death.
Supplementary Figure 1 from B56γ Tumor-Associated Mutations Provide New Mechanisms for B56γ-PP2A Tumor Suppressor Activity
Authors: Nobumori Yumiko , Shouse Geoffrey P. , Wu Yong , Lee Kyu Joon , Shen Binghui , Liu Xuan
Published: April 2023

PDF file - 76K, Supplementary Figure 1. Cell proliferation assay was carried out using a tetracycline-inducible U2OS stable cell line that overexpresses wild type B56γ upon induction.
Supplementary Figure 2 from Resveratrol and P-glycoprotein Inhibitors Enhance the Anti-Skin Cancer Effects of Ursolic Acid
Authors: Junco Jacob J. , Mancha Anna , Malik Gunjan , Wei Sung-Jen , Kim Dae Joon , Liang Huiyun , Slaga Thomas J.
Published: April 2023

PDF file - 814K, Figure S2: 200 microM RES strongly sensitized Ca3/7 cells to UA-mediated growth suppression (average of 3 independent experiments, n=3/exp, * p<0.05, ** p<0.01, *** p<0.005, and **** p<0.001).
Supplementary Figure 3 from Autophagy-Dependent Metabolic Reprogramming Sensitizes TSC2-Deficient Cells to the Antimetabolite 6-Aminonicotinamide
Authors: Parkhitko Andrey A. , Priolo Carmen , Coloff Jonathan L. , Yun Jihye , Wu Julia J. , Mizumura Kenji , Xu Wenping , Malinowska Izabela A. , Yu Jane , Kwiatkowski David J. , Locasale Jason W. , Asara John M. , Choi Augustine M.K. , Finkel Toren , Henske Elizabeth P.
Published: April 2023

PDF file - 34K, Effect of chloroquine on the metabolome of Tsc2+/+ MEFs.
Supplementary Figure Legends from Integrin α3β1 Can Function to Promote Spontaneous Metastasis and Lung Colonization of Invasive Breast Carcinoma
Authors: Zhou Bo , Gibson-Corley Katherine N. , Herndon Mary E. , Sun Yihan , Gustafson-Wagner Elisabeth , Teoh-Fitzgerald Melissa , Domann Frederick E. , Henry Michael D. , Stipp Christopher S.
Published: April 2023

PDF file, 88K.
Supplementary Methods from NEDD9 Depletion Leads to MMP14 Inactivation by TIMP2 and Prevents Invasion and Metastasis
Authors: McLaughlin Sarah L. , Ice Ryan J. , Rajulapati Anuradha , Kozyulina Polina Y. , Livengood Ryan H. , Kozyreva Varvara K. , Loskutov Yuriy V. , Culp Mark V. , Weed Scott A. , Ivanov Alexey V. , Pugacheva Elena N.
Published: April 2023

PDF file - 85K
Supplementary Figure 2 from NEDD9 Depletion Leads to MMP14 Inactivation by TIMP2 and Prevents Invasion and Metastasis
Authors: McLaughlin Sarah L. , Ice Ryan J. , Rajulapati Anuradha , Kozyulina Polina Y. , Livengood Ryan H. , Kozyreva Varvara K. , Loskutov Yuriy V. , Culp Mark V. , Weed Scott A. , Ivanov Alexey V. , Pugacheva Elena N.
Published: April 2023

PDF file - 2433K, Supplementary Fig. 2 (A). Representative images of live microscopy of BT549-shCon, - shNEDD9 (N4) cells embedded in DQ-Collagen IV 48h post plating. DNA (blue), shRNA expressing cells (RFP, red) and degradation of DQ-Collagen (green). (B). Quantification of DQCollagen IV degradation as shown in (A). Statistical analysis by one-way ANOVA based on 3 independent experiments in 100-200 cells in each group. *p<0.005 (shCon/shN1 or N4), ns (shN1/N4). (C). IF analysis of MDA-MB-231-shCon, -shNEDD9 cells with anti-cortactin (blue), anti-F-actin (red) and MMP14 (green) antibodies. Scale bar is 20μm. White arrows indicate membrane area with increase in MMP14.
Supplementary Table 1 from A Proangiogenic Signature Is Revealed in FGF-Mediated Bevacizumab-Resistant Head and Neck Squamous Cell Carcinoma
Authors: Gyanchandani Rekha , Ortega Alves Marcus V. , Myers Jeffrey N. , Kim Seungwon
Published: April 2023

PDF file - 132K, Differentially expressed genes between resistant/bevacizumab tumors compared to parental/bevacizumab tumors.
Supplementary Table 5 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 - 128K, Primer sequences.
Supplementary Figures 1 - 4 from ERK and AKT Signaling Drive MED1 Overexpression in Prostate Cancer in Association with Elevated Proliferation and Tumorigenicity
Authors: Jin Feng , Irshad Shazia , Yu Wei , Belakavadi Madesh , Chekmareva Marina , Ittmann Michael M. , Abate-Shen Cory , Fondell Joseph D.
Published: April 2023

PDF file - 529K, Fig. S1. MED1 antibody specificity. Fig. S2. Anti-phospho-MED1 antibody specificity. Fig. S3. Inhibition of ERK or AKT signaling decreases MED1 phosphorylation and expression in prostate cancer cells. Fig. S4. Phospho-MED1 binds to the androgen receptor in prostate cancer cells.
Supplementary Data from Transcriptional Regulation of CXCR4 in Prostate Cancer: Significance of TMPRSS2-ERG Fusions
Authors: Singareddy Rajareddy , Semaan Louie , Conley-LaComb M. Katie , St. John Jason , Powell Katelyn , Iyer Matthew , Smith Daryn , Heilbrun Lance K. , Shi Dongping , Sakr Wael , Cher Michael L. , Chinni Sreenivasa R.
Published: April 2023

Supplementary Data - PDF file 589K, S1. Mutations in putative Ets/ERG binding sites in CXCR4 promoter oigos diminishes oligo binding with either VCaP cell nuclear extracts or in vitro translated ERG protein. S2. ERG ChIP seq analysis of VCaP cells. S3. N-terminus deletion of ERG regulates CXCR4 promoter activation similar to full length ERG protein. S4. LNCaP cells were transfected with ARR2Pb-LUC as a vector control and ARR2Pb-ERG-LUC plasmid. S5. MS3 spectrum of trypsin-digested, TiO2 eluted ERG peptides from VCaP cells
Supplementary Figure Legend from Dual Inhibition of PI3K and mTOR Mitigates Compensatory AKT Activation and Improves Tamoxifen Response in Breast Cancer
Authors: Chen Xiaosong , Zhao Meizhong , Hao Mingang , Sun Xueqing , Wang Jinglong , Mao Yan , Zu Lidong , Liu Junjun , Shen Yandong , Wang Jianhua , Shen Kunwei
Published: April 2023

PDF file - 81K
Supplementary Figure 3 from Dual Inhibition of PI3K and mTOR Mitigates Compensatory AKT Activation and Improves Tamoxifen Response in Breast Cancer
Authors: Chen Xiaosong , Zhao Meizhong , Hao Mingang , Sun Xueqing , Wang Jinglong , Mao Yan , Zu Lidong , Liu Junjun , Shen Yandong , Wang Jianhua , Shen Kunwei
Published: April 2023

PDF file - 436K, Efficacy of PI3K inhibitors on pAkt cross-talk activation on the basis of tamoxifen and everolimus treatment in MCF-7 (left) and BT474 (right) cell lines.
Supplementary Figure 2 from Dual Inhibition of PI3K and mTOR Mitigates Compensatory AKT Activation and Improves Tamoxifen Response in Breast Cancer
Authors: Chen Xiaosong , Zhao Meizhong , Hao Mingang , Sun Xueqing , Wang Jinglong , Mao Yan , Zu Lidong , Liu Junjun , Shen Yandong , Wang Jianhua , Shen Kunwei
Published: April 2023

PDF file - 471K, Growth-inhibitory effects of tamoxifen, everolimus, and various PI3K inhibitors on breast cancer cell lines.