bluuebunny/crossref_metadata_2025 huggingface dataset:
Data from Dianhydrogalactitol Overcomes Multiple Temozolomide Resistance Mechanisms in Glioblastoma
Authors: Jiménez-Alcázar Miguel , Curiel-García Álvaro , Nogales Paula , Perales-Patón Javier , Schuhmacher Alberto J. , Galán-Ganga Marcos , Zhu Lucía , Lowe Scott W. , Al-Shahrour Fátima , Squatrito Massimo
Published: April 2023

Abstract
Glioblastoma (GBM) is the most frequent and aggressive primary tumor type in the central nervous system in adults. Resistance to chemotherapy remains one of the major obstacles in GBM treatment. Identifying and overcoming the mechanisms of therapy resistance is instrumental to develop novel therapeutic approaches for patients with GBM. To determine the major drivers of temozolomide (TMZ) sensitivity, we performed shRNA screenings in GBM lines with different O6-methylguanine-DNA methyl-transferase (MGMT) status. We then evaluated dianhydrogalactitol (Val-083), a small alkylating molecule that induces interstrand DNA crosslinking, as a potential treatment to bypass TMZ-resistance mechanisms. We found that loss of mismatch repair (MMR) components and MGMT expression are mutually exclusive mechanisms driving TMZ resistance in vitro. Treatment of established GBM cells and tumorsphere lines with Val-083 induces DNA damage and cell-cycle arrest in G2–M phase, independently of MGMT or MMR status, thus circumventing conventional resistance mechanisms to TMZ. Combination of TMZ and Val-083 shows a synergic cytotoxic effect in tumor cells in vitro, ex vivo, and in vivo. We propose this combinatorial treatment as a potential approach for patients with GBM.
Data from Nonclinical Characterization of Bexmarilimab, a Clever-1–Targeting Antibody for Supporting Immune Defense Against Cancers
Authors: Hollmén Maija , Maksimow Mikael , Rannikko Jenna H. , Karvonen Matti K. , Vainio Marita , Jalkanen Sirpa , Jalkanen Markku , Mandelin Jami
Published: April 2023

Abstract
Common lymphatic endothelial and vascular endothelial receptor-1 (Clever-1) is a multifunctional type-1 transmembrane protein that plays an important role in immunosuppression against tumors. Clever-1 is highly expressed in a subset of human tumor-associated macrophages and associated with poor survival. In mice, Clever-1 supports tumor growth and metastasis formation, and its deficiency or blockage induces T-cell–dependent killing of cancer cells. Therefore, targeting Clever-1 could lead to T-cell activation and restoration of immune response also in patients with cancer. This is studied in an on-going clinical trial [Macrophage Antibody To INhibit immune Suppression (MATINS); NCT03733990] in patients with advanced solid tumors where bexmarilimab, a humanized IgG4 antibody against human Clever-1, shows promising safety and efficacy.

Here, we report the humanization and nonclinical characterization of physicochemical properties, biological potency, and safety profile of bexmarilimab.

Bexmarilimab showed high affinity to Clever-1 on KG-1 cells and bound to Clever-1 on the surface of classical and intermediate monocytes derived from healthy human blood. Bexmarilimab inhibited the internalization of its natural ligand acetylated low-density lipoprotein into KG-1 cells and increased TNFα secretion from macrophages but did not impair phagocytic clearance. Bexmarilimab did not induce significant cytokine release in human whole-blood cultures, did not contain nonsafe immunogenic glycans, or show any significant binding to human Fcγ receptors or complement pathway component C1q. In vivo, bexmarilimab showed dose-dependent duration of monocyte Clever-1 receptor occupancy in cynomolgus monkeys but did not induce a cytokine storm up to a dose of 100 mg/kg.

In conclusion, these data support the clinical development of bexmarilimab for the restoration of immune response in cancers.
Data from Predictive Value of MRP-1 in Localized High-Risk Soft Tissue Sarcomas: A Translational Research Associated to ISG-STS 1001 Randomized Phase III Trial
Authors: Martin-Broto Javier , Lopez-Alvarez Maria , Moura David S. , Ramos Rafael , Collini Paola , Romagosa Cleofe , Bagué Silvia , Renne Salvatore L. , Barisella Marta , Velasco Valerie , Coindre Jean-Michel , Lopez-Lopez Daniel , Dopazo Joaquin , Gambarotti Marco , Braglia Luca , Merlo Domenico Franco , Palmerini Emanuela , Stacchiotti Silvia , Quagliuolo Vittorio L. , Lopez-Pousa Antonio , Grignani Giovanni , Blay Jean-Yves , Brunello Antonella , Gutierrez Antonio , Valverde Claudia , Hindi Nadia , Dei Tos Angelo Paolo , Picci Piero , Casali Paolo G. , Gronchi Alessandro
Published: April 2023

Abstract
MRP-1 is implicated in multidrug resistance and was described as prognostic in high-risk patients with soft-tissue sarcoma (STS) in a previous study. The current research aimed to validate MRP-1 prognostic/predictive value in localized sarcomas treated with anthracyclines plus ifosfamide within the ISG-1001 phase III study. In addition, the inhibitory activity on MRP-1 was investigated in preclinical studies to identify new combinations able to increase the efficacy of standard chemotherapy in STS. MRP-1 expression was assessed by IHC in tissue microarrays from patients with STS and tested for correlation with disease-free survival (DFS) and overall survival (OS). In vitro studies tested the efficacy of MRP-1 inhibitors (nilotinib, ripretinib, selumetinib, and avapritinib) in sarcoma cell lines. The effect of combinations of the most active MRP-1 inhibitors and chemotherapy was measured on the basis of apoptosis. MRP-1 was evaluable in 231 of 264 cases who entered the study. MRP-1 expression (strong intensity) was independently associated with worse DFS [HR, 1.78; 95% confidence interval (CI), 1.11–2.83; P = 0.016], in the multivariate analysis, with a trend for a worse OS (HR, 1.78; 95% CI, 0.97–3.25; P = 0.062). In vitro studies showed that the addition of MRP-1 inhibitors (nilotinib or avapritinib) to doxorubicin plus palifosfamide, significantly increased cell death in SK-UT-1 and CP0024 cell lines. MRP-1 is an adverse predictive factor in localized high-risk patients with STS treated with neoadjuvant anthracyclines plus ifosfamide followed by surgery. In vitro findings support the clinical assessment of the combination of chemotherapy and MRP-1 inhibitors as a promising strategy to overcome the drug ceiling effect for chemotherapy.
Data from Overcoming Resistance to Anti–Nectin-4 Antibody-Drug Conjugate
Authors: Cabaud Olivier , Berger Ludovic , Crompot Emerence , Adélaide José , Finetti Pascal , Garnier Sèverine , Guille Arnaud , Carbuccia Nadine , Farina Anne , Agavnian Emilie , Chaffanet Max , Gonçalves Anthony , Charafe-Jauffret Emmanuelle , Mamessier Emilie , Birnbaum Daniel , Bertucci François , Lopez Marc
Published: April 2023

Abstract
Antibody–drug conjugates (ADC) represent a fast-growing drug class in oncology. However, ADCs are associated with resistance, and therapies able to overcome it are of utmost importance. Recently, enfortumab vedotin-ejfv (EV) was approved in nectin-4+ metastatic urothelial cancer. We previously described PVRL4/nectin-4 as a new therapeutic target in breast cancer and produced an efficient EV-like ADC comprising a human anti–nectin-4 mAb conjugated to monomethyl auristatin-E (MMAE) named N41mab-vcMMAE. To study the consequence of the long-term treatment with this ADC, we developed a preclinical breast cancer model in mice, and report a mechanism of resistance to N41mab-vcMMAE after 9-month treatment and a way to reverse it. RNA-sequencing pointed to an upregulation in resistant tumors of ABCB1 expression, encoding the multidrug resistance protein MDR-1/P-glycoprotein (P-gp), associated with focal gene amplification and high protein expression. Sensitivity to N41mab-vcMMAE of the resistant model was restored in vitro by P-gp pharmacologic inhibitors, like tariquidar. P-gp is expressed in a variety of normal tissues. By delivering the drug to the tumor more specifically than classical chemotherapy, we hypothesized that the combined use of ADC with P-gp inhibitors might reverse resistance in vivo without toxicity. Indeed, we showed that the tariquidar/N41mab-vcMMAE combination was well tolerated and induced a rapid regression of ADC-resistant tumors in mice. In contrast, the tariquidar/docetaxel combination was toxic and poorly efficient. These results show that ABC transporter inhibitors can be safely used with ADC to reverse ADC-induced resistance and open new opportunities in the fight against multidrug resistance.
Data from Targeting the IGF-Axis Potentiates Immunotherapy for Pancreatic Ductal Adenocarcinoma Liver Metastases by Altering the Immunosuppressive Microenvironment
Authors: Hashimoto Masakazu , Konda John David , Perrino Stephanie , Celia Fernandez Maria , Lowy Andrew M. , Brodt Pnina
Published: April 2023

Abstract
Pancreatic ductal adenocarcinoma (PDAC) is a highly aggressive malignancy, resistant to chemotherapy and associated with high incidence of liver metastases and poor prognosis. Using murine models of aggressive PDAC, we show here that in mice bearing hepatic metastases, treatment with the IGF-Trap, an inhibitor of type I insulin-like growth factor receptor (IGF-IR) signaling, profoundly altered the local, immunosuppressive tumor microenvironment in the liver, curtailing the recruitment of myeloid-derived suppressor cells, reversing innate immune cell polarization and inhibiting metastatic expansion. Significantly, we found that immunotherapy with anti–PD-1 antibodies also reduced the growth of experimental PDAC liver metastases, and this effect was enhanced when combined with IGF-Trap treatment, resulting in further potentiation of a T-cell response. Our results show that a combinatorial immunotherapy based on dual targeting of the prometastatic immune microenvironment of the liver via IGF blockade, on one hand, and reversing T-cell exhaustion on the other, can provide a significant therapeutic benefit in the management of PDAC metastases.
Data from Discovery of JNJ-63576253, a Next-Generation Androgen Receptor Antagonist Active Against Wild-Type and Clinically Relevant Ligand Binding Domain Mutations in Metastatic Castration-Resistant Prostate Cancer
Authors: Branch Jonathan R. , Bush Tammy L. , Pande Vineet , Connolly Peter J. , Zhang Zhuming , Hickson Ian , Ondrus Janine , Jaensch Steffen , Bischoff James R. , Habineza Georges , Van Hecke Geert , Meerpoel Lieven , Packman Kathryn , Parrett Christopher J. , Chong Yolanda T. , Gottardis Marco M. , Bignan Gilles
Published: April 2023

Abstract
Numerous mechanisms of resistance arise in response to treatment with second-generation androgen receptor (AR) pathway inhibitors in metastatic castration-resistant prostate cancer (mCRPC). Among these, point mutations in the ligand binding domain can transform antagonists into agonists, driving the disease through activation of AR signaling. To address this unmet need, we report the discovery of JNJ-63576253, a next-generation AR pathway inhibitor that potently abrogates AR signaling in models of human prostate adenocarcinoma. JNJ-63576253 is advancing as a clinical candidate with potential effectiveness in the subset of patients who do not respond to or are progressing while on second-generation AR-targeted therapeutics.
Data from Functional Characterization of Brain Tumor-Initiating Cells and Establishment of GBM Preclinical Models that Incorporate Heterogeneity, Therapy, and Sex Differences
Authors: Garcia Cesar A. , Bhargav Adip G. , Brooks Mieu , Suárez-Meade Paola , Mondal Sujan K. , Zarco Natanael , ReFaey Karim , Jentoft Mark , Middlebrooks Erik H. , Snuderl Matija , Carrano Anna , Guerrero-Cazares Hugo , Schiapparelli Paula , Sarabia-Estrada Rachel , Quiñones-Hinojosa Alfredo
Published: April 2023

Abstract
Glioblastoma (GBM) is the most common primary brain cancer in adults where tumor cell heterogeneity and sex differences influence clinical outcomes. Here, we functionally characterize three male and three female patient-derived GBM cell lines, identify protumorigenic BTICs, and create novel male and female preclinical models of GBM. Cell lines were evaluated on the following features: proliferation, stemness, migration, tumorigenesis, clinical characteristics, and sensitivity to radiation, TMZ, rhTNFSF10 (rhTRAIL), and rhBMP4. All cell lines were classified as GBM according to epigenetic subtyping, were heterogenous and functionally distinct from one another, and re-capitulated features of the original patient tumor. In establishing male and female preclinical models, it was found that two male-derived GBM cell lines (QNS108 and QNS120) and one female-derived GBM cell line (QNS315) grew at a faster rate in female mice brains. One male-derived GBM cell line (QNS108) decreased survival in female mice in comparison with male mice. However, no survival differences were observed for mice injected with a female-derived cell line (QNS315). In summary, a panel of six GBM patient-derived cell lines were functionally characterized, and it was shown that BTIC lines can be used to construct sex-specific models with differential phenotypes for additional studies.
Data from SENTI-101, a Preparation of Mesenchymal Stromal Cells Engineered to Express IL12 and IL21, Induces Localized and Durable Antitumor Immunity in Preclinical Models of Peritoneal Solid Tumors
Authors: Gonzalez-Junca Alba , Liu Frances D. , Nagaraja Archana S. , Mullenix Alyssa , Lee Chen-Ting , Gordley Russell M. , Frimannsson Daniel O. , Maller Ori , Garrison Brian S. , Iyer Dharini , Benabbas Anissa , Truong Tiffany A. , Quach Allison , Tian Mengxi , Martinez Rowena , Savur Rishi , Perry-McNamara Alyssa , Nguyen Denny , Almudhfar Niran , Blanco Carmina , Huynh Christina , Nand Asish , Lay Yu-An E. , Magal Ashita , Mangalampalli Sravani , Lee Philip J. , Lu Timothy K. , Lee Gary
Published: April 2023

Abstract
Advanced peritoneal carcinomatosis including high-grade ovarian cancer has poor prognoses and a poor response rate to current checkpoint inhibitor immunotherapies; thus, there is an unmet need for effective therapeutics that would provide benefit to these patients. Here we present the preclinical development of SENTI-101, a cell preparation of bone marrow-derived mesenchymal stromal (also known as stem) cells (MSC), which are engineered to express two potent immune-modulatory cytokines, IL12 and IL21. Intraperitoneal administration of SENTI-101 results in selective tumor-homing and localized and sustained cytokine production in murine models of peritoneal cancer. SENTI-101 has extended half-life, reduced systemic distribution, and improved antitumor activity when compared with recombinant cytokines, suggesting that it is more effective and has lower risk of systemic immunotoxicities. Treatment of tumor-bearing immune-competent mice with a murine surrogate of SENTI-101 (mSENTI-101) results in a potent and localized immune response consistent with increased number and activation of antigen presenting cells, T cells and B cells, which leads to antitumor response and memory-induced long-term immunity. Consistent with this mechanism of action, co-administration of mSENTI-101 with checkpoint inhibitors leads to synergistic improvement in antitumor response. Collectively, these data warrant potential clinical development of SENTI-101 for patients with peritoneal carcinomatosis and high-grade ovarian cancer.

Graphical abstract: SENTI-101 schematic and mechanism of action

SENTI-101 is a novel cell-based immunotherapeutic consisting of bone marrow–derived mesenchymal stromal cells (BM-MSC) engineered to express IL12 and IL21 intended for the treatment of peritoneal carcinomatosis including high-grade serous ovarian cancer. Upon intraperitoneal administration, SENTI-101 homes to peritoneal solid tumors and secretes IL12 and IL21 in a localized and sustained fashion. The expression of these two potent cytokines drives tumor infiltration and engagement of multiple components of the immune system: antigen-presenting cells, T cells, and B cells, resulting in durable antitumor immunity in preclinical models of cancer.
Data from Cytotoxic Engineered Induced Neural Stem Cells as an Intravenous Therapy for Primary Non–Small Cell Lung Cancer and Triple-Negative Breast Cancer
Authors: Mercer-Smith Alison R. , Jiang Wulin , Bago Juli R. , Valdivia Alain , Thang Morrent , Woodell Alex S. , Montgomery Stephanie A. , Sheets Kevin T. , Anders Carey K. , Hingtgen Shawn D.
Published: April 2023

Abstract
Converting human fibroblasts into personalized induced neural stem cells (hiNSC) that actively seek out tumors and deliver cytotoxic agents is a promising approach for treating cancer. Herein, we provide the first evidence that intravenously-infused hiNSCs secreting cytotoxic agent home to and suppress the growth of non–small cell lung cancer (NSCLC) and triple-negative breast cancer (TNBC). Migration of hiNSCs to NSCLC and TNBC in vitro was investigated using time-lapse motion analysis, which showed directional movement of hiNSCs to both tumor cell lines. In vivo, migration of intravenous hiNSCs to orthotopic NSCLC or TNBC tumors was determined using bioluminescent imaging (BLI) and immunofluorescent post-mortem tissue analysis, which indicated that hiNSCs colocalized with tumors within 3 days of intravenous administration and persisted through 14 days. In vitro, efficacy of hiNSCs releasing cytotoxic TRAIL (hiNSC-TRAIL) was monitored using kinetic imaging of co-cultures, in which hiNSC-TRAIL therapy induced rapid killing of both NSCLC and TNBC. Efficacy was determined in vivo by infusing hiNSC-TRAIL or control cells intravenously into mice bearing orthotopic NSCLC or TNBC and tracking changes in tumor volume using BLI. Mice treated with intravenous hiNSC-TRAIL showed a 70% or 72% reduction in NSCLC or TNBC tumor volume compared with controls within 14 or 21 days, respectively. Safety was assessed by hematology, blood chemistry, and histology, and no significant changes in these safety parameters was observed through 28 days. These results indicate that intravenous hiNSCs-TRAIL seek out and kill NSCLC and TNBC tumors, suggesting a potential new strategy for treating aggressive peripheral cancers.
Data from Comparison of Pyrrolobenzodiazepine Dimer Bis-imine versus Mono-imine: DNA Interstrand Cross-linking, Cytotoxicity, Antibody–Drug Conjugate Efficacy and Toxicity
Authors: Tiberghien Arnaud C. , Vijayakrishnan Balakumar , Esfandiari Arman , Ahmed Mahammad , Pardo Raul , Bingham John , Adams Lauren , Santos Kathleen , Kang Gyoung-Dong , Pugh Kathryn M. , Afif-Rider Shameen , Vashisht Kapil , Haque Kemal , Tammali Ravinder , Rosfjord Edward , Savoca Adriana , Hartley John A. , Howard Philip W.
Published: April 2023

Abstract
Antibody–drug conjugates (ADC) delivering pyrrolobenzodiazepine (PBD) DNA cross-linkers are currently being evaluated in clinical trials, with encouraging results in Hodgkin and non–Hodgkin lymphomas. The first example of an ADC delivering a PBD DNA cross-linker (loncastuximab tesirine) has been recently approved by the FDA for the treatment of relapsed and refractory diffuse large B-cell lymphoma. There has also been considerable interest in mono-alkylating PBD analogs. We conducted a head-to-head comparison of a conventional PBD bis-imine and a novel PBD mono-imine. Key Mitsunobu chemistry allowed clean and convenient access to the mono-imine class. Extensive DNA-binding studies revealed that the mono-imine mediated a type of DNA interaction that is described as “pseudo cross-linking,” as well as alkylation. The PBD mono-imine ADC demonstrated robust antitumor activity in mice bearing human tumor xenografts at doses 3-fold higher than those that were efficacious for the PBD bis-imine ADC. A single-dose toxicology study in rats demonstrated that the MTD of the PBD mono-alkylator ADC was approximately 3-fold higher than that of the ADC bearing a bis-imine payload, suggesting a comparable therapeutic index for this molecule. However, although both ADCs caused myelosuppression, renal toxicity was observed only for the bis-imine, indicating possible differences in toxicologic profiles that could influence tolerability and therapeutic index. These data show that mono-amine PBDs have physicochemical and pharmacotoxicologic properties distinct from their cross-linking analogs and support their potential utility as a novel class of ADC payload.
Data from Targeting DUSP Activity as a Treatment for High-Grade Serous Ovarian Carcinoma
Authors: Sanders Brooke E. , Yamamoto Tomomi M. , McMellen Alexandra , Woodruff Elizabeth R. , Berning Amber , Post Miriam D. , Bitler Benjamin G.
Published: April 2023

Abstract
Identifying novel, durable treatments for high-grade serous ovarian cancer (HGSOC) is paramount to extend both progression-free survival (PFS) and overall survival (OS) in patients afflicted with this disease. Dual-specificity phosphatase 1 (DUSP1) was identified as one of seven genes that may significantly affect prognosis in patients with HGSOC; however, the role of DUSP inhibition (DUSPi) in the treatment of HGSOC remains largely unknown. In this study, we show that DUSP1 is highly expressed in HGSOC and confers worse PFS and OS. Further, we corroborate data that show DUSP1 expression is directly associated with therapy resistance. Using a tissue microarray of 137 different serous ovarian carcinomas, we demonstrate the high expression of DUSP1 in primary and recurrent serous ovarian cancer. In both acquired and de novo therapy HGSOC-resistant models, DUSPi both inhibited cellular proliferation and promoted cell death. RPPA analysis of HGSOC cells revealed DUSPi led to the differential regulation of several pathways, including AMPK and mTORC. Further, in a patient-derived xenograft HGSOC model, DUSPi significantly inhibited tumor progression.
Supplementary Figures 1-6 from Multi-substrate Metabolic Tracing Reveals Marked Heterogeneity and Dependency on Fatty Acid Metabolism in Human Prostate Cancer
Authors: Fidelito Gio , De Souza David P. , Niranjan Birunthi , De Nardo William , Keerthikumar Shivakumar , Brown Kristin , Taylor Renea A. , Watt Matthew J.
Published: April 2023

Supplementary Figure 1. Metabolic profiles of prostate cancer PDX across different pathology. Supplementary Figure 2. Percent labeling of glycolysis end products and TCA cycle intermediates following 4 hours ex vivo labelling of 13C substrates. Supplementary Figure 3. Mass isotopologue distribution of malate following glucose, glutamine, palmitate, and lactate tracing. Supplementary Figure 4. PDXOs responses following metabolic inhibitors treatment. Supplementary Figure 5. Organoids viability following 7 days treatments of metabolic inhibitors. Supplementary Figure 6. Dose responses of metabolic inhibitors treatment in PDXOs.
Table S1 from Evolutionary Characteristics and Immunologic Divergence of Lung and Brain Metastasis Lesions in NSCLC
Authors: Xie Tongji , Liu Zhenghao , Li Yan , Wang Shouzheng , Zhai Yixin , Teng Fei , Hao Xuezhi , Wang Yan , Wang Hongyu , Zhang Xin , Wu Xi , Ying Jianming , Li Junling , Zhang Ye , Deng Yuefei , Xing Puyuan
Published: April 2023

The basic clinical information of all patients.
Supplementary Figure S4 from A Human Genome-Wide RNAi Screen Reveals Diverse Modulators that Mediate IRE1α–XBP1 Activation
Authors: Yang Zhifen , Zhang Jing , Jiang Dadi , Khatri Purvesh , Solow-Cordero David E. , Toesca Diego A.S. , Koumenis Constantinos , Denko Nicholas C. , Giaccia Amato J. , Le Quynh-Thu , Koong Albert C.
Published: April 2023

Validation of the screen hits (continued).
Supplementary Figure 4 from Circular RNA ciRS-7 Maintains Metastatic Phenotypes as a ceRNA of miR-1299 to Target MMPs
Authors: Sang Meixiang , Meng Lingjiao , Liu Sihua , Ding Pingan , Chang Sheng , Ju Yingchao , Liu Fei , Gu Lina , Lian Yishui , Geng Cuizhi
Published: April 2023

The expression of miR-1299 in TNBC, Luminal, Her-2 overexpression breast cancer and NATs.
Supplementary Figure 3 from Circular RNA ciRS-7 Maintains Metastatic Phenotypes as a ceRNA of miR-1299 to Target MMPs
Authors: Sang Meixiang , Meng Lingjiao , Liu Sihua , Ding Pingan , Chang Sheng , Ju Yingchao , Liu Fei , Gu Lina , Lian Yishui , Geng Cuizhi
Published: April 2023

The knock-down efficiency of three siRNAs in vivo.
Supplementary Table 1 from The Pioneering Role of GATA2 in Androgen Receptor Variant Regulation Is Controlled by Bromodomain and Extraterminal Proteins in Castrate-Resistant Prostate Cancer
Authors: Chaytor Lewis , Simcock Matthew , Nakjang Sirintra , Heath Richard , Walker Laura , Robson Craig , Jones Dominic , Gaughan Luke
Published: April 2023

siRNA sequences
Figure S3 from Multifunctional APJ Pathway Promotes Ovarian Cancer Progression and Metastasis
Authors: Neelakantan Deepika , Dogra Samrita , Devapatla Bharat , Jaiprasart Pharavee , Mukashyaka Marie Claire , Janknecht Ralf , Dwivedi Shailendra Kumar Dhar , Bhattacharya Resham , Husain Sanam , Ding Kai , Woo Sukyung
Published: April 2023

ML221 dose-response curves in OvCa cell lines.
Figure S2 from Dual Targeting of EGFR and IGF1R in the TNFAIP8 Knockdown Non–Small Cell Lung Cancer Cells
Authors: Day Timothy F. , Kallakury Bhaskar V.S. , Ross Jeffrey S. , Voronel Olga , Vaidya Shantashri , Sheehan Christine E. , Kasid Usha N.
Published: April 2023

qRT-PCR assay
Supplemental Figure 5 from Centriole Overduplication is the Predominant Mechanism Leading to Centrosome Amplification in Melanoma
Authors: Denu Ryan A. , Shabbir Maria , Nihal Minakshi , Singh Chandra K. , Longley B. Jack , Burkard Mark E. , Ahmad Nihal
Published: April 2023

Melanoma patient survival based on PLK4 expression.
Supplementary Figures 1-10 from Suppression of Breast Cancer Stem Cells and Tumor Growth by the RUNX1 Transcription Factor
Authors: Hong Deli , Fritz Andrew J. , Finstad Kristiaan H. , Fitzgerald Mark P. , Weinheimer Adam , Viens Adam L. , Ramsey Jon , Stein Janet L. , Lian Jane B. , Stein Gary S.
Published: April 2023

S1. RUNX1 mRNA is decreased during breast cancer progression. S2. RUNX1 does not change cell proliferation. S3. RUNX1 represses tumor growth in mammary fat pad. S4. Gate for MCF10AT1 sorting. S5. CD24high Cells have high RUNX1 expression in MCF10AT1 cells. S6. Loss of RUNX1 promotes stemness in MCF10A and MCF7 cells. S7. Overexpression RUNX1 in MCF10CA1a cells does not change BCSC population. S8. Zeb1 is expressed at low level in MCF10CA1a cells. S9. Schematic diagram of ChIP qPCR primers and amplicons over Zeb1 for ChIP-qPCR. S10. Knockdown Zeb1 in MCF10AT1 ns cells does not change cancer stem cell phenotypes.
Supplementary Table 4 from Combined AURKA and H3K9 Methyltransferase Targeting Inhibits Cell Growth By Inducing Mitotic Catastrophe
Authors: Mathison Angela , Salmonson Ann , Missfeldt Mckenna , Bintz Jennifer , Williams Monique , Kossak Sarah , Nair Asha , de Assuncao Thiago M. , Christensen Trace , Buttar Navtej , Iovanna Juan , Huebert Robert , Lomberk Gwen
Published: April 2023

qPCR and RNA-seq expression values for cell cycle checkpoint gene.
Supplementary Table 3 from Combined AURKA and H3K9 Methyltransferase Targeting Inhibits Cell Growth By Inducing Mitotic Catastrophe
Authors: Mathison Angela , Salmonson Ann , Missfeldt Mckenna , Bintz Jennifer , Williams Monique , Kossak Sarah , Nair Asha , de Assuncao Thiago M. , Christensen Trace , Buttar Navtej , Iovanna Juan , Huebert Robert , Lomberk Gwen
Published: April 2023

Fold change values for expression of individual DEGs found in response to combination treatment.
Table S5 from Molecular Correlates of Metastasis by Systematic Pan-Cancer Analysis Across The Cancer Genome Atlas
Authors: Chen Fengju , Zhang Yiqun , Varambally Sooryanarayana , Creighton Chad J.
Published: April 2023

For each cancer type examined, the correlations with metastasis for RPPA (Reverse Phase Protein Array) and microRNA features represented in TCGA.
Supplementary Figure 1 from Combined AURKA and H3K9 Methyltransferase Targeting Inhibits Cell Growth By Inducing Mitotic Catastrophe
Authors: Mathison Angela , Salmonson Ann , Missfeldt Mckenna , Bintz Jennifer , Williams Monique , Kossak Sarah , Nair Asha , de Assuncao Thiago M. , Christensen Trace , Buttar Navtej , Iovanna Juan , Huebert Robert , Lomberk Gwen
Published: April 2023

Additional data on clonogenic cell survival assay, cell viability, apoptosis, quantification of mitotic catastrophe and global decrease of H3K9me3 upon combination treatment.
Table S3 from Molecular Correlates of Metastasis by Systematic Pan-Cancer Analysis Across The Cancer Genome Atlas
Authors: Chen Fengju , Zhang Yiqun , Varambally Sooryanarayana , Creighton Chad J.
Published: April 2023

For each cancer type, top metastasis-associated mRNA features, selected using Pearson's correlation on log-transformed data with Storey and Tibshirini estimate of False Discovery Rate (FDR) of <10%.
Table S2 from Molecular Correlates of Metastasis by Systematic Pan-Cancer Analysis Across The Cancer Genome Atlas
Authors: Chen Fengju , Zhang Yiqun , Varambally Sooryanarayana , Creighton Chad J.
Published: April 2023

For all genes represented in TCGA RNA-seq datasets, the mRNA-level correlations with metastasis for each cancer type.
Figure S3 from Satellite RNA Increases DNA Damage and Accelerates Tumor Formation in Mouse Models of Pancreatic Cancer
Authors: Kishikawa Takahiro , Otsuka Motoyuki , Suzuki Tatsunori , Seimiya Takahiro , Sekiba Kazuma , Ishibashi Rei , Tanaka Eri , Ohno Motoko , Yamagami Mari , Koike Kazuhiko
Published: April 2023

DNA damage by high-fat diet feeding.
Table S1 from Molecular Correlates of Metastasis by Systematic Pan-Cancer Analysis Across The Cancer Genome Atlas
Authors: Chen Fengju , Zhang Yiqun , Varambally Sooryanarayana , Creighton Chad J.
Published: April 2023

TCGA cancer cases and molecular profiles examined in this study.
Supplemental Table from Phosphatase 1 Nuclear Targeting Subunit (PNUTS) Regulates Aurora Kinases and Mitotic Progression
Authors: Wang Feifei , Wang Ling , Fisher Laura A. , Li Chunling , Wang Weidong , Peng Aimin
Published: April 2023

Table S1
Supplementary Figures S1 - S7 from Cholesterol Esterification Inhibition Suppresses Prostate Cancer Metastasis by Impairing the Wnt/β-catenin Pathway
Authors: Lee Hyeon Jeong , Li Jie , Vickman Renee E. , Li Junjie , Liu Rui , Durkes Abigail C. , Elzey Bennett D. , Yue Shuhua , Liu Xiaoqi , Ratliff Timothy L. , Cheng Ji-Xin
Published: April 2023

Supplementary figure S1 shows CE depletion by avasimibe treatment in prostate cancer cells. Supplementary figure S2 shows prostate cancer migration suppressed by ACAT inhibition. Supplementary figure S3 shows suppression of prostate cancer metastasis by targeting cholesterol esterification. Supplementary figure S4 shows expression profiling of prostate cancer-related genes after ACAT inhibition. Supplementary figure S5 shows inactivation of Wnt/beta-catenin pathway by ACAT-1 knockdown. Supplementary figure S6 shows inactivation of Wnt/beta-catenin pathway by cholesteryl ester depletion in multiple prostate cancer cell lines. Supplementary figure S7 shows inactivation of Wnt by ACAT-1 knockdown.
Table S4 from HPV Integration in HNSCC Correlates with Survival Outcomes, Immune Response Signatures, and Candidate Drivers
Authors: Koneva Lada A. , Zhang Yanxiao , Virani Shama , Hall Pelle B. , McHugh Jonathan B. , Chepeha Douglas B. , Wolf Gregory T. , Carey Thomas E. , Rozek Laura S. , Sartor Maureen A.
Published: April 2023

GO terms and KEGG pathways enriched for genes differentially expressed between integration-positive and integration-negative HNC tumors.
Supplementary Data from PTPN11 Plays Oncogenic Roles and Is a Therapeutic Target for BRAF Wild-Type Melanomas
Authors: Hill Kristen S. , Roberts Evan R. , Wang Xue , Marin Ellen , Park Taeeun D. , Son Sorany , Ren Yuan , Fang Bin , Yoder Sean , Kim Sungjune , Wan Lixin , Sarnaik Amod A. , Koomen John M. , Messina Jane L. , Teer Jamie K. , Kim Youngchul , Wu Jie , Chalfant Charles E. , Kim Minjung
Published: April 2023

Supplementary Table 1
Supplementary Data from PTPN11 Plays Oncogenic Roles and Is a Therapeutic Target for BRAF Wild-Type Melanomas
Authors: Hill Kristen S. , Roberts Evan R. , Wang Xue , Marin Ellen , Park Taeeun D. , Son Sorany , Ren Yuan , Fang Bin , Yoder Sean , Kim Sungjune , Wan Lixin , Sarnaik Amod A. , Koomen John M. , Messina Jane L. , Teer Jamie K. , Kim Youngchul , Wu Jie , Chalfant Charles E. , Kim Minjung
Published: April 2023

Supplementary Table 2
Supplementary Figure S2 from Loss of Uracil DNA Glycosylase Selectively Resensitizes p53-Mutant and -Deficient Cells to 5-FdU
Authors: Yan Yan , Qing Yulan , Pink John J. , Gerson Stanton L.
Published: April 2023

Figure S2 shows UDG depletion by two other different shRNAs selectively sensitizes p53 KO cells to 5-FdU.
Supplementary Figure 2 from The Proto-oncogene PKCι Regulates the Alternative Splicing of Bcl-x Pre-mRNA
Authors: Shultz Jacqueline C. , Vu Ngoc , Shultz Michael D. , Mba Mba-Uzoma U. , Shapiro Brian A. , Chalfant Charles E.
Published: April 2023

PDF file - 188K
Supplementary Figure 1 from The Proto-oncogene PKCι Regulates the Alternative Splicing of Bcl-x Pre-mRNA
Authors: Shultz Jacqueline C. , Vu Ngoc , Shultz Michael D. , Mba Mba-Uzoma U. , Shapiro Brian A. , Chalfant Charles E.
Published: April 2023

PDF file - 195K
Supplementary Figure 2 from In Situ Analysis of Mutant EGFRs Prevalent in Glioblastoma Multiforme Reveals Aberrant Dimerization, Activation, and Differential Response to Anti-EGFR Targeted Therapy
Authors: Gajadhar Aaron S. , Bogdanovic Elena , Muñoz Diana Marcela , Guha Abhijit
Published: April 2023

PDF file - 202K
Supplementary Tables 1-8 from Targeting RET Kinase in Neuroendocrine Prostate Cancer
Authors: VanDeusen Halena R. , Ramroop Johnny R. , Morel Katherine L. , Bae Song Yi , Sheahan Anjali V. , Sychev Zoi , Lau Nathan A. , Cheng Larry C. , Tan Victor M. , Li Zhen , Petersen Ashley , Lee John K. , Park Jung Wook , Yang Rendong , Hwang Justin H. , Coleman Ilsa , Witte Owen N. , Morrissey Colm , Corey Eva , Nelson Peter S. , Ellis Leigh , Drake Justin M.
Published: April 2023

Supplemental Table 1: Known genetic mutations of genes commonly mutated in mCRPC in cell lines used in phosphoproteome analysis Supplemental Table 2: Phospho-Serine/Threonine proteome of Prostate Cancer Adenocarcinoma and Aggressive Variant Prostate Cancer Cell Lines Supplemental Table 3: Phospho-Tyrosine proteome of Prostate Cancer Adenocarcinoma and Aggressive Variant Prostate Cancer Cell Lines Supplemental Table 4: Kinase Substrate Enrichment Analysis results from phospho-serine/threonine proteome dataset Supplemental Table 5: Kinase Substrate Enrichment Analysis results from phospho-tyrosine proteome dataset Supplemental Table 6: Phospho-Serine/Threonine proteome of Adenocarcinoma or Small cell/Mixed phenotype mCRPC patient samples Supplemental Table 7. Spearman's Correlation Between the Dependency Ranks of RET and Other Genes in Prostate Cancer Cell Lines Supplemental Table 8. RET Dependency Scores of Cancer Cell Lines
Supplementary Figure 2 from MYC-Driven Tumorigenesis Is Inhibited by WRN Syndrome Gene Deficiency
Authors: Moser Russell , Toyoshima Masafumi , Robinson Kristin , Gurley Kay E. , Howie Heather L. , Davison Jerry , Morgan Martin , Kemp Christopher J. , Grandori Carla
Published: April 2023

PDF file - 164K
Supplementary Figures 1-6 from Phosphoinositide 3-kinase/AKT/mTORC1/2 Signaling Determines Sensitivity of Burkitt's Lymphoma Cells to BH3 mimetics
Authors: Spender Lindsay C. , Inman Gareth J.
Published: April 2023

PDF file - 355K
Table S3 from Inactivation of NF1 Promotes Resistance to EGFR Inhibition in KRAS/NRAS/BRAFV600-Wild-Type Colorectal Cancer
Authors: Georgiou Alexandros , Stewart Adam , Cunningham David , Banerji Udai , Whittaker Steven R.
Published: April 2023

Table S3. GI50 values for cell lines treated with agents for 4 d. Results are calculated from at least 3 independent experiments carried out in quadruplicate.
Table S2 from Inactivation of NF1 Promotes Resistance to EGFR Inhibition in KRAS/NRAS/BRAFV600-Wild-Type Colorectal Cancer
Authors: Georgiou Alexandros , Stewart Adam , Cunningham David , Banerji Udai , Whittaker Steven R.
Published: April 2023

Table S2. Details of sgRNAs used in this study.
Supplementary Table 1B from Capping Protein Regulator and Myosin 1 Linker 3 Is Required for Tumor Metastasis
Authors: Wang Huan , Wang Chao , Peng Guang , Yu Doudou , Cui Xin-Gang , Sun Ying-Hao , Ma Xiaojing
Published: April 2023

Supplementary Table 1B shows multivariate Cox regression analysis of prognostic factors of breast cancer patients (cohort GSE42568, N=104)
Figure S4 from Inactivation of NF1 Promotes Resistance to EGFR Inhibition in KRAS/NRAS/BRAFV600-Wild-Type Colorectal Cancer
Authors: Georgiou Alexandros , Stewart Adam , Cunningham David , Banerji Udai , Whittaker Steven R.
Published: April 2023

Figure S4. Quantification of colony assays from Figure 2B.
Figure S5 from Capping Protein Regulator and Myosin 1 Linker 3 Is Required for Tumor Metastasis
Authors: Wang Huan , Wang Chao , Peng Guang , Yu Doudou , Cui Xin-Gang , Sun Ying-Hao , Ma Xiaojing
Published: April 2023

Supplementary Figure 5, Molecular pathway enrichment of CARMIL3. Related to Fig. 5. A. KEGG pathway enrichment plots of Gene Set Enrichment Analysis (GSEA) with gene ex-pression profiles of 4T1 WT and Carmil3 KO cells. B. Biological Process (BP) analysis result of DAVID with genes whose readout counts>100 and the fold change >=4 of RNA-seq. C. Western blot result of WT and Carmil3 KO 4T1 cells, together with WT and Carmil3 KO cells re-expressing FLAG-CARMIL3 with indicated antibodies. D. Enrichment analysis of CARMIL3 in TCGA-BRCA. CARMIL3 high group was defined by Z-score >1 (RNA-seq). Statistic meth-od: Student's t test.
Supplementary Data from Transforming Growth Factor-β Signaling–Deficient Fibroblasts Enhance Hepatocyte Growth Factor Signaling in Mammary Carcinoma Cells to Promote Scattering and Invasion
Authors: Cheng Nikki , Chytil Anna , Shyr Yu , Joly Alison , Moses Harold L.
Published: April 2023

Supplementary Data from Transforming Growth Factor-β Signaling–Deficient Fibroblasts Enhance Hepatocyte Growth Factor Signaling in Mammary Carcinoma Cells to Promote Scattering and Invasion
Figure S3 from Capping Protein Regulator and Myosin 1 Linker 3 Is Required for Tumor Metastasis
Authors: Wang Huan , Wang Chao , Peng Guang , Yu Doudou , Cui Xin-Gang , Sun Ying-Hao , Ma Xiaojing
Published: April 2023

Supplementary Figure 3, Carmil3 KO in tumor cells reduces metastasis. Related to Fig. 3. A. Analysis of tumor cells migration with scratch assay. B. Result of transwell assay measur-ing tumor cell migratory capacity. Cells which migrated down through the membrane to the lower chamber of the plate were determined with MTS assay. C. WT or Carmil3 KO 4T1 tu-mor cells were injected subcutaneously to the mammary fat pad of BALB/c mice. The mice were sacrificed at day 28 and the lung metastasis of 4T1 tumor cells was determined by 6-thioguanine assay. Representative images of metastatic cell colonies in cell culture plate were shown. Statistic method: student's t test, *** p < 0.001. The experiments were repeated three times independently.
Figure S1 from Capping Protein Regulator and Myosin 1 Linker 3 Is Required for Tumor Metastasis
Authors: Wang Huan , Wang Chao , Peng Guang , Yu Doudou , Cui Xin-Gang , Sun Ying-Hao , Ma Xiaojing
Published: April 2023

Supplementary Figure 1, CARIML3 expression is upregulated among various types of cancer. Related to Figure 1. A. CARMIL3 copy number variance (CNV) level across various types of cancer in TCGA. B. CARMIL3 mRNA (RNA-Seq) expression among different types of cancer samples compared with their normal counterpart in TCGA. C. Analysis of CARMIL3 mRNA (RNA-seq) expression in TCGA-BRCA cohort grouped by major subclasses (with TNBC). D. Immunohistochemistry (IHC) staining image of CARMIL3 with breast cancer patient sample (ID: 2565). The image was from The Human Protein Atlas (HPA) database. E. CARMIL3 mRNA expression analysis in prostate cancer patients, dataset from GEO GSE3325. (F-I). Analysis of CARMIL3 mRNA expression in prostate cancer samples, in cBioPortal dataset (Beltran, 2016, Nature medicine) (F); in dataset GSE21034 (G); in dataset GSE35988 (H); in the cBioPortal dataset (Broad/Cornell,Nat Genet 2012) (I). J. Kaplan-Meier curve showing PRAD patient survival of the cBioPortal cohort (MSKCC, Caner Cell, 2010). Statistic methods: C and E-I Student's t-test; J Log-rank test.
Supplementary Figure 1 from Loss of TGF-β Responsiveness in Prostate Stromal Cells Alters Chemokine Levels and Facilitates the Development of Mixed Osteoblastic/Osteolytic Bone Lesions
Authors: Li Xiaohong , Sterling Julie A. , Fan Kang-Hsien , Vessella Robert L. , Shyr Yu , Hayward Simon W. , Matrisian Lynn M. , Bhowmick Neil A.
Published: April 2023

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Supplementary Figure 5 from RBM38 Is a Direct Transcriptional Target of E2F1 that Limits E2F1-Induced Proliferation
Authors: Feldstein Orit , Ben-Hamo Rotem , Bashari Dana , Efroni Sol , Ginsberg Doron
Published: April 2023

PDF file - 118K, Correlated expression of E2F1 and RBM38 is associated with increased survival in glioblastoma patients
Supplementary Table 1 from Autocrine Leukemia Inhibitory Factor Promotes Esophageal Squamous Cell Carcinoma Progression via Src Family Kinase-Dependent Yes-Associated Protein Activation
Authors: Kawazoe Tetsuro , Saeki Hiroshi , Oki Eiji , Oda Yoshinao , Maehara Yoshihiko , Mori Masaki , Taniguchi Koji
Published: April 2023

Primer sequences used for quantitative real-time PCR in this study
Supplementary Figure 3 from RBM38 Is a Direct Transcriptional Target of E2F1 that Limits E2F1-Induced Proliferation
Authors: Feldstein Orit , Ben-Hamo Rotem , Bashari Dana , Efroni Sol , Ginsberg Doron
Published: April 2023

PDF file - 132K, RBM38 restricts E2F1- induced G1-exit
Supplementary Figure 5 from Autocrine Leukemia Inhibitory Factor Promotes Esophageal Squamous Cell Carcinoma Progression via Src Family Kinase-Dependent Yes-Associated Protein Activation
Authors: Kawazoe Tetsuro , Saeki Hiroshi , Oki Eiji , Oda Yoshinao , Maehara Yoshihiko , Mori Masaki , Taniguchi Koji
Published: April 2023

The effects of YAP knockdown and YAP inhibitors on cell proliferation and sphere formation in human ESCC
Supplementary Figure 3 from Autocrine Leukemia Inhibitory Factor Promotes Esophageal Squamous Cell Carcinoma Progression via Src Family Kinase-Dependent Yes-Associated Protein Activation
Authors: Kawazoe Tetsuro , Saeki Hiroshi , Oki Eiji , Oda Yoshinao , Maehara Yoshihiko , Mori Masaki , Taniguchi Koji
Published: April 2023

The effects of LIF knockdown by shRNAs on cell proliferation and apoptosis in human ESCC
Supplementary Data from Metallothionein Induction by Hypoxia Involves Cooperative Interactions between Metal-Responsive Transcription Factor-1 and Hypoxia-Inducible Transcription Factor-1α
Authors: Murphy Brian J. , Kimura Tomoki , Sato Barbara G. , Shi Yihui , Andrews Glen K.
Published: April 2023

Supplementary Data from Metallothionein Induction by Hypoxia Involves Cooperative Interactions between Metal-Responsive Transcription Factor-1 and Hypoxia-Inducible Transcription Factor-1α
Supplementary Data from High-Throughput Hacking of the Methylation Patterns in Breast Cancer by In vitro Transcription and Thymidine-Specific Cleavage Mass Array on MALDI-TOF Silico-Chip
Authors: Radpour Ramin , Haghighi Mahdi Montazer , Fan Alex Xiu-Cheng , Torbati Peyman Mohammadi , Hahn Sinuhe , Holzgreve Wolfgang , Zhong Xiao Yan
Published: April 2023

Supplementary Data from High-Throughput Hacking of the Methylation Patterns in Breast Cancer by In vitro Transcription and Thymidine-Specific Cleavage Mass Array on MALDI-TOF Silico-Chip
Supplementary Table 1, Figure 1, Methods from Somatic Mutations in CCK2R Alter Receptor Activity that Promote Oncogenic Phenotypes
Authors: Willard Melinda D. , Lajiness Mary E. , Wulur Isabella H. , Feng Bo , Swearingen Michelle L. , Uhlik Mark T. , Kinzler Kenneth W. , Velculescu Victor E. , Sjöblom Tobias , Markowitz Sanford D. , Powell Steven M. , Vogelstein Bert , Barber Thomas D.
Published: April 2023

PDF file - 211K
Supplementary figures and figure legends from Ku80-Targeted pH-Sensitive Peptide–PNA Conjugates Are Tumor Selective and Sensitize Cancer Cells to Ionizing Radiation
Authors: Kaplan Alanna R. , Pham Ha , Liu Yanfeng , Oyaghire Stanley , Bahal Raman , Engelman Donald M. , Glazer Peter M.
Published: April 2023

Fig. S1: pHLIP-αKu80(γ) binds to the mouse Ku80 sequence. Fig. S2: Validation of tumor vs. stromal cell sorting in EMT6-GFP cells. Fig. S3: Partial suppression of Ku80 expression induces radiosensitivity in cultured cancer cells. Fig. S4: pHLIP-αKu80(γ) causes tumor radiosensitization. Fig. S5: pHLIP-αKu80(γ) causes in vitro radiosensitization. Fig. S6: pHLIP-αKu80(γ) does not induce electrolyte abnormalities. Fig. S7: pHLIP-αKu80(γ) does not cause bone marrow suppression.
Supplementary Methods from Copper Modulates Zinc Metalloproteinase-Dependent Ectodomain Shedding of Key Signaling and Adhesion Proteins and Promotes the Invasion of Prostate Cancer Epithelial Cells
Authors: Parr-Sturgess Catherine A. , Tinker Claire L. , Hart Claire A. , Brown Michael D. , Clarke Noel W. , Parkin Edward T.
Published: April 2023

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Supplementary Figure 1 from The p38 MAPK–MK2 Axis Regulates E2F1 and FOXM1 Expression after Epirubicin Treatment
Authors: de Olano Natalia , Koo Chuay-Yeng , Monteiro Lara J. , Pinto Paola H. , Gomes Ana R. , Aligue Rosa , Lam Eric W.-F.
Published: April 2023

PDF file, 525K, Effects of the p38 inhibitor SB203580 on P-E2F1, E2F1 and FOXM1 induction in response to epirubicin in U2OS cells.
Supplementary Figure Legends 1-4 from α-Catulin Marks the Invasion Front of Squamous Cell Carcinoma and Is Important for Tumor Cell Metastasis
Authors: Cao Christine , Chen Yibu , Masood Rizwan , Sinha Uttam K. , Kobielak Agnieszka
Published: April 2023

PDF file - 67K
Supplementary Table 2 from Reduced DICER1 Elicits an Interferon Response in Endometrial Cancer Cells
Authors: Chiappinelli Katherine B. , Haynes Brian C. , Brent Michael R. , Goodfellow Paul J.
Published: April 2023

XLS file - 3.1K
Supplementary Figure 4 from α-Catulin Marks the Invasion Front of Squamous Cell Carcinoma and Is Important for Tumor Cell Metastasis
Authors: Cao Christine , Chen Yibu , Masood Rizwan , Sinha Uttam K. , Kobielak Agnieszka
Published: April 2023

PDF file - 4.7MB, We further analyzed the tumors that formed from the injection of control and �-catulin-deficient USC-HN1 cell lines. We can observe and track injected cells by the tGFP reporter. A and B, checking for proliferation rate, we do not see a considerable difference between the two tumors, as assessed by the proliferative marker, Ki67. C and D, when analyzing the tumors for human-specific lymphatic vessel marker, lyve-1, the control tumor (C) had collective groups of cells that were able to invade the surrounding stroma and form their own lymphatic vessels, whereas �-catulin-deficient tumors (D) were unable to do so. E-F, IHC staining using phospho-JNK antibody show an increase in activated phospho-JNK in control tumor (E) compared to �-catulin-deficient tumor (F). Arrows indicate invasive tumor fronts in control tumors, whereas dashed lines indicate a less invasive tumor margin in �-catulin-deficient tumors
Supplementary Table 1 from Reduced DICER1 Elicits an Interferon Response in Endometrial Cancer Cells
Authors: Chiappinelli Katherine B. , Haynes Brian C. , Brent Michael R. , Goodfellow Paul J.
Published: April 2023

XLS file - 131K
Supplementary Figure 4 from Reduced DICER1 Elicits an Interferon Response in Endometrial Cancer Cells
Authors: Chiappinelli Katherine B. , Haynes Brian C. , Brent Michael R. , Goodfellow Paul J.
Published: April 2023

PDF file - 81K
Supplementary Figure 1 from α-Catulin Marks the Invasion Front of Squamous Cell Carcinoma and Is Important for Tumor Cell Metastasis
Authors: Cao Christine , Chen Yibu , Masood Rizwan , Sinha Uttam K. , Kobielak Agnieszka
Published: April 2023

PDF file - 1MB, 3 days after isolation, metastatic hSCC USC-HN1 GFP-labeled cells from the lymphatic vessels (A) show a mesenchymal morphology, compared to USC-HN1 cells from the primary SCC tumor (C). 10 days after isolation, the metastatic cells from the lymphatic vessels (B) revert to an epithelial morphology, typical of USC-HN1 cells, as compared to the cells from the primary SCC tumor (D)