bluuebunny/crossref_metadata_2025 huggingface dataset:
Data from Transcriptomes and shRNA Suppressors in a TP53 Allele–Specific Model of Early-Onset Colon Cancer in African Americans
Authors: Weige Charles C. , Birtwistle Marc R. , Mallick Himel , Yi Nengjun , Berrong Zuzana , Cloessner Emily , Duff Keely , Tidwell Josephine , Clendenning Megan , Wilkerson Brent , Farrell Christopher , Bunz Fred , Ji Hao , Shtutman Michael , Creek Kim E. , Banister Carolyn E. , Buckhaults Phillip J.
Published: April 2023

Abstract
African Americans are disproportionately affected by early-onset, high-grade malignancies. A fraction of this cancer health disparity can be explained by genetic differences between individuals of African or European descent. Here the wild-type Pro/Pro genotype at the TP53Pro72Arg (P72R) polymorphism (SNP: rs1042522) is more frequent in African Americans with cancer than in African Americans without cancer (51% vs. 37%), and is associated with a significant increase in the rates of cancer diagnosis in African Americans. To test the hypothesis that Tp53 allele–specific gene expression may contribute to African American cancer disparities, TP53 hemizygous knockout variants were generated and characterized in the RKO colon carcinoma cell line, which is wild type for TP53 and heterozygous at the TP53Pro72Arg locus. Transcriptome profiling, using RNAseq, in response to the DNA-damaging agent etoposide revealed a large number of Tp53-regulated transcripts, but also a subset of transcripts that were TP53Pro72Arg allele specific. In addition, a shRNA-library suppressor screen for Tp53 allele–specific escape from Tp53-induced arrest was performed. Several novel RNAi suppressors of Tp53 were identified, one of which, PRDM1β (BLIMP-1), was confirmed to be an Arg-specific transcript. Prdm1β silences target genes by recruiting H3K9 trimethyl (H3K9me3) repressive chromatin marks, and is necessary for stem cell differentiation. These results reveal a novel model for African American cancer disparity, in which the TP53 codon 72 allele influences lifetime cancer risk by driving damaged cells to differentiation through an epigenetic mechanism involving gene silencing.

Implications:TP53 P72R polymorphism significantly contributes to increased African American cancer disparity. Mol Cancer Res; 12(7); 1029–41. ©2014 AACR.
Data 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

Abstract
MED1 is a key coactivator of the androgen receptor (AR) and other signal-activated transcription factors. Whereas MED1 is overexpressed in prostate cancer cell lines and is thought to coactivate distinct target genes involved in cell-cycle progression and castration-resistant growth, the underlying mechanisms by which MED1 becomes overexpressed and its oncogenic role in clinical prostate cancer have remained unclear. Here, we report that MED1 is overexpressed in the epithelium of clinically localized human prostate cancer patients, which correlated with elevated cellular proliferation. In a Nkx3.1:Pten mutant mouse model of prostate cancer that recapitulates the human disease, MED1 protein levels were markedly elevated in the epithelium of both invasive and castration-resistant adenocarcinoma prostate tissues. Mechanistic evidence showed that hyperactivated ERK and/or AKT signaling pathways promoted MED1 overexpression in prostate cancer cells. Notably, ectopic MED1 overexpression in prostate cancer xenografts significantly promoted tumor growth in nude mice. Furthermore, MED1 expression in prostate cancer cells promoted the expression of a number of novel genes involved in inflammation, cell proliferation, and survival. Together, these findings suggest that elevated MED1 is a critical molecular event associated with prostate oncogenesis.

Visual Overview: http://mcr.aacrjournals.org/content/11/7/736/F1.large.jpg.

Mol Cancer Res; 11(7); 736–47. ©2013 AACR.
Data from Epithelial-Specific Deletion of 11β-HSD2 Hinders Apcmin/+ Mouse Tumorigenesis
Authors: Jiang Li , Yang Shilin , Yin Huiyong , Fan Xiaofeng , Wang Suwan , Yao Bing , Pozzi Ambra , Chen Xiaoping , Harris Raymond C. , Zhang Ming-Zhi
Published: April 2023

Abstract
Cyclooxygenase-2 (COX-2)–derived prostaglandin E2 (PGE2) promotes colorectal tumorigenesis. Glucocorticoids are endogenous and potent COX-2 inhibitors, and their local actions are downregulated by 11β-hydroxysteroid dehydrogenase type II (11β-HSD2)-mediated metabolism. Previously, it was reported that 11β-HSD2 is increased in human colonic and Apcmin/+ mouse intestinal adenomas and correlated with increased COX-2, and 11β-HSD2 inhibition suppressed the COX-2 pathway and decreased tumorigenesis. Because 11β-HSD2 is expressed in Apcmin/+ mouse intestinal adenoma stromal and epithelial cells, Apcmin/+ mice were generated with selective deletion of 11β-HSD2 in intestinal epithelial cells (Vil-Cre-HSD2−/− Apcmin/+). Deletion of 11β-HSD2 in intestinal epithelia led to marked inhibition of Apcmin/+ mouse intestinal tumorigenesis. Immunostaining indicated decreased 11β-HSD2 and COX-2 expression in adenoma epithelia, whereas stromal COX-2 expression was intact in Vil-Cre-HSD2−/− Apcmin/+ mice. In Vil-Cre-HSD2−/− Apcmin/+ mouse intestinal adenomas, both p53 and p21 mRNA and protein were increased, with a concomitant decrease in pRb, indicating glucocorticoid-mediated G1-arrest. Further study revealed that REDD1 (regulated in development and DNA damage responses 1), a novel stress-induced gene that inhibits mTOR signaling, was increased, whereas the mTOR signaling pathway was inhibited. Therefore, in Vil-Cre-HSD2−/− Apcmin/+ mice, epithelial cell 11β-HSD2 deficiency leads to inhibition of adenoma initiation and growth by attenuation of COX-2 expression, increased cell-cycle arrest, and inhibition of mTOR signaling as a result of increased tumor intracellular active glucocorticoids.

Implications:Inhibition of 11β-HSD2 may represent a novel approach for colorectal cancer chemoprevention by increasing tumor glucocorticoid activity, which in turn inhibits tumor growth by multiple pathways. Mol Cancer Res; 11(9); 1040–50. ©2013 AACR.
Data from Bone Microenvironment Changes in Latexin Expression Promote Chemoresistance
Authors: Zhang Mi , Osisami Mary , Dai Jinlu , Keller Jill M. , Escara-Wilke June , Mizokami Atsushi , Keller Evan T.
Published: April 2023

Abstract
Although docetaxel is the standard of care for advanced prostate cancer, most patients develop resistance to docetaxel. Therefore, elucidating the mechanism that underlies resistance to docetaxel is critical to enhance therapeutic intervention. Mining cDNA microarray from the PC-3 prostate cancer cell line and its docetaxel-resistant derivative (PC3-TxR) revealed decreased latexin (LXN) expression in the resistant cells. LXN expression was inversely correlated with taxane resistance in a panel of prostate cancer cell lines. LXN knockdown conferred docetaxel resistance to prostate cancer cells in vitro and in vivo, whereas LXN overexpression reduced docetaxel resistance in several prostate cancer cell lines. A mouse model of prostate cancer demonstrated that prostate cancer cells developed resistance to docetaxel in the bone microenvironment, but not the soft tissue microenvironment. This was associated with decreased LXN expression in prostate cancer cells in the bone microenvironment compared with the soft tissue microenvironment. It was identified that bone stromal cells decreased LXN expression through methylation and induced chemoresistance in prostate cancer in vitro. These findings reveal that a subset of prostate cancer develops docetaxel resistance through loss of LXN expression associated with methylation and that the bone microenvironment promotes this drug resistance phenotype.

Implications: This study suggests that the LXN pathway should be further explored as a viable target for preventing or reversing taxane resistance in prostate cancer. Mol Cancer Res; 15(4); 457–66. ©2017 AACR.
Data from Synergistic Activity with NOTCH Inhibition and Androgen Ablation in ERG-Positive Prostate Cancer Cells
Authors: Mohamed Ahmed A. , Tan Shyh-Han , Xavier Charles P. , Katta Shilpa , Huang Wei , Ravindranath Lakshmi , Jamal Muhammad , Li Hua , Srivastava Meera , Srivatsan Eri S. , Sreenath Taduru L. , McLeod David G. , Srinivasan Alagarsamy , Petrovics Gyorgy , Dobi Albert , Srivastava Shiv
Published: April 2023

Abstract
The oncogenic activation of the ETS-related gene (ERG) due to gene fusions is present in over half of prostate cancers in Western countries. Because of its high incidence and oncogenic role, ERG and components of ERG network have emerged as potential drug targets for prostate cancer. Utilizing gene expression datasets, from matched normal and prostate tumor epithelial cells, an association of NOTCH transcription factors with ERG expression status was identified, confirming that NOTCH factors are direct transcriptional targets of ERG. Inhibition of ERG in TMPRSS2-ERG–positive VCaP cells led to decreased levels of NOTCH1 and 2 proteins and downstream transcriptional targets and partially recapitulated the phenotypes associated with ERG inhibition. Regulation of NOTCH1 and 2 genes by ERG were also noted with ectopic ERG expression in LNCaP (ERG-negative prostate cancer) and RWPE-1 (benign prostate–derived immortalized) cells. Furthermore, inhibition of NOTCH by the small-molecule γ-secretase inhibitor 1, GSI-1, conferred an increased sensitivity to androgen receptor (AR) inhibitors (bicalutamide and enzalutamide) or the androgen biosynthesis inhibitor (abiraterone) in VCaP cells. Combined treatment with bicalutamide and GSI-1 showed strongest inhibition of AR, ERG, NOTCH1, NOTCH2, and PSA protein levels along with decreased cell growth, cell survival, and enhanced apoptosis. Intriguingly, this effect was not observed in ERG-negative prostate cancer cells or immortalized benign/normal prostate epithelial cells. These data underscore the synergy of AR and NOTCH inhibitors in reducing the growth of ERG-positive prostate cancer cells.

Implications: Combinational targeting of NOTCH and AR signaling has therapeutic potential in advanced ERG-driven prostate cancers. Mol Cancer Res; 15(10); 1308–17. ©2017 AACR.
Data from Nucleoside Diphosphate Kinase-3 (NME3) Enhances TLR5-Induced NFκB Activation
Authors: Flentie Kelly , Gonzalez Caleb , Kocher Brandon , Wang Yue , Zhu Hongtu , Marasa Jayne , Piwnica-Worms David
Published: April 2023

Abstract
Bacterial flagellin is a potent activator of NFκB signaling, inflammation, and host innate immunity, and recent data indicate that flagellin represents a novel antitumor ligand acting through toll-like receptor 5 (TLR5) and the NFκB pathway to induce host immunity and aid in the clearance of tumor xenografts. To identify innate signaling components of TLR5 responsible for these antitumor effects, a loss-of-function high-throughput screen was employed utilizing carcinoma cells expressing a dynamic NFκB bioluminescent reporter stimulated by Salmonella typhimurium expressing flagellin. A live cell screen of a siRNA library targeting 691 known and predicted human kinases to identify novel tumor cell modulators of TLR5-induced NFκB activation uncovered several interesting positive and negative candidate regulators not previously recognized, including nucleoside diphosphate kinase 3 (NME3), characterized as an enhancer of signaling responses to flagellin. Targeted knockdown and overexpression assays confirmed the regulatory contribution of NME3 to TLR5-mediated NFκB signaling, mechanistically downstream of MyD88. Furthermore, Kaplan–Meier survival analysis showed that NME3 expression correlated highly with TLR5 expression in breast, lung, ovarian, and gastric cancers, and furthermore, high-level expression of NME3 increased overall survival for patients with breast, lung, and ovarian cancer, but the opposite in gastric cancer. Together, these data identify a previously unrecognized proinflammatory role for NME3 in signaling downstream of TLR5 that may potentiate cancer immunotherapies.

Implications: Proinflammatory signaling mediated by innate immunity engagement of flagellin-activated TLR5 in tumor cells results in antitumor effects through NME3 kinase, a positive downstream regulator of flagellin-mediated NFκB signaling, enhancing survival for several human cancers. Mol Cancer Res; 16(6); 986–99. ©2018 AACR.
Data from Therapeutic Effect of Y-27632 on Tumorigenesis and Cisplatin-Induced Peripheral Sensory Loss through RhoA–NF-κB
Authors: Zhu Yi , Howard George A. , Pittman Keith , Boykin Christi , Herring Laura E. , Wilkerson Emily M. , Verbanac Kathryn , Lu Qun
Published: April 2023

Abstract
Chemotherapy-induced peripheral neuropathy (CIPN) is a major side effect of cancer therapy that frequently requires a reduction or cessation of treatments and negatively impacts the patient's quality of life. There is currently no effective means to prevent or treat CIPN. In this study, we developed and applied CIPN in an immunocompetent, syngeneic murine Lewis Lung Carcinoma (LLCab) model that enabled the elucidation of both tumor and host responses to cisplatin and treatments of Y-27632, a selective inhibitor of Rho kinase/p160ROCK. Y-27632 not only preserved cisplatin's efficacy toward tumor suppression but also the combination treatment inhibited tumor cell proliferation and increased cellular apoptosis. By alleviating the cisplatin-induced loss of epidermal nerve fibers (ENFs), Y-27632 protected tumor-bearing mice from cisplatin-induced reduction of touch sensation. Furthermore, quantitative proteomic analysis revealed the striking cisplatin-induced dysregulation in cellular stress (inflammation, mitochondrial deficiency, DNA repair, etc.)–associated proteins. Y-27632 was able to reverse the changes of these proteins that are associated with Rho GTPase and NF-κB signaling network, and also decreased cisplatin-induced NF-κB hyperactivation in both footpad tissues and tumor. Therefore, Y-27632 is an effective adjuvant in tumor suppression and peripheral neuroprotection. These studies highlight the potential of targeting the RhoA–NF-κB axis as a combination therapy to treat CIPN.
Implications:
This study, for the first time, demonstrated the dual antineoplastic and neuroprotective effects of Rho kinase/p160ROCK inhibition in a syngeneic immunocompetent tumor-bearing mouse model, opening the door for further clinical adjuvant development of RhoA–NF-κB axis to improve chemotherapeutic outcomes.
Data from Genomic Analysis of Nasopharyngeal Carcinoma Reveals TME-Based Subtypes
Authors: Zhang Li , MacIsaac Kenzie D. , Zhou Ting , Huang Pei-Yu , Xin Chunlin , Dobson Jason R. , Yu Kun , Chiang Derek Y. , Fan Yue , Pelletier Marc , Wang Yan , Jaeger Savina , Krishnamurthy Radhakrishnan Viveksagar , JeBailey Lellean , Skewes-Cox Peter , Zhang Jing , Fang Wenfeng , Huang Yan , Zhao Hongyun , Zhao Yuanyuan , Li En , Peng Bin , Huang Alan , Dranoff Glenn , Hammerman Peter S. , Engelman Jeffrey , Bitter Hans , Zeng Yi-Xin , Yao Yao
Published: April 2023

Abstract
Nasopharyngeal carcinoma (NPC) is an Epstein–Barr virus (EBV) associated cancer characterized by a poor prognosis and a high level of lymphocyte infiltrate. Genetic hallmarks of NPC are not completely known but include deletion of the p16 (CDKN2A) locus and mutations in NF-κB pathway components, with a relatively low total mutational load. To better understand the genetic landscape, an integrated genomic analysis was performed using a large clinical cohort of treatment-naïve NPC tumor specimens. This genomic analysis was generally concordant with previous studies; however, three subtypes of NPC were identified by differences in immune cell gene expression, prognosis, tumor cell morphology, and genetic characteristics. A gene expression signature of proliferation was poorly prognostic and associated with either higher mutation load or specific EBV gene expression patterns in a subtype-specific manner. Finally, higher levels of stromal tumor-infiltrating lymphocytes associated with good prognosis and lower expression of a WNT and TGFβ pathway activation signature.

Implications: This study represents the first integrated analysis of mutation, copy number, and gene expression data in NPC and suggests how tumor genetics and EBV infection influence the tumor microenvironment in this disease. These insights should be considered for guiding immunotherapy treatment strategies in this disease. Mol Cancer Res; 15(12); 1722–32. ©2017 AACR.
Data from The Clonal Evolution of Metastatic Osteosarcoma as Shaped by Cisplatin Treatment
Authors: Brady Samuel W. , Ma Xiaotu , Bahrami Armita , Satas Gryte , Wu Gang , Newman Scott , Rusch Michael , Putnam Daniel K. , Mulder Heather L. , Yergeau Donald A. , Edmonson Michael N. , Easton John , Alexandrov Ludmil B. , Chen Xiang , Mardis Elaine R. , Wilson Richard K. , Downing James R. , Pappo Alberto S. , Raphael Benjamin J. , Dyer Michael A. , Zhang Jinghui
Published: April 2023

Abstract
To investigate the genomic evolution of metastatic pediatric osteosarcoma, we performed whole-genome and targeted deep sequencing on 14 osteosarcoma metastases and two primary tumors from four patients (two to eight samples per patient). All four patients harbored ancestral (truncal) somatic variants resulting in TP53 inactivation and cell-cycle aberrations, followed by divergence into relapse-specific lineages exhibiting a cisplatin-induced mutation signature. In three of the four patients, the cisplatin signature accounted for >40% of mutations detected in the metastatic samples. Mutations potentially acquired during cisplatin treatment included NF1 missense mutations of uncertain significance in two patients and a KIT G565R activating mutation in one patient. Three of four patients demonstrated widespread ploidy differences between samples from the sample patient. Single-cell seeding of metastasis was detected in most metastatic samples. Cross-seeding between metastatic sites was observed in one patient, whereas in another patient a minor clone from the primary tumor seeded both metastases analyzed. These results reveal extensive clonal heterogeneity in metastatic osteosarcoma, much of which is likely cisplatin-induced.
Implications:
The extent and consequences of chemotherapy-induced damage in pediatric cancers is unknown. We found that cisplatin treatment can potentially double the mutational burden in osteosarcoma, which has implications for optimizing therapy for recurrent, chemotherapy-resistant disease.
Data from NME1 Drives Expansion of Melanoma Cells with Enhanced Tumor Growth and Metastatic Properties
Authors: Wang Ying , Leonard M. Kathryn , Snyder Devin E. , Fisher Matthew L. , Eckert Richard L. , Kaetzel David M.
Published: April 2023

Abstract
Melanoma is a lethal skin cancer prone to progression and metastasis, and resistant to therapy. Metastasis and therapy resistance of melanoma and other cancers are driven by tumor cell plasticity, largely via acquisition/loss of stem-like characteristics and transitions between epithelial and mesenchymal phenotypes (EMT/MET). NME1 is a metastasis suppressor gene that inhibits metastatic potential when its expression is enforced in melanoma and other cancers. Herein, we have unmasked a novel role for NME1 as a driver of melanoma growth distinct from its canonical function as a metastasis suppressor. NME1 promotes expansion of stem-like melanoma cells that exhibit elevated expression of stem cell markers (e.g., Sox2, Sox10, Oct-4, KLF4, and Ccnb-1), enhanced growth as melanoma spheres in culture, and enhanced tumor growth and lung colonizing activities in vivo. In contrast, NME1 expression did not affect the proliferation of melanoma cell lines in monolayer culture conditions. Silencing of NME1 expression resulted in a dramatic reduction in melanoma sphere size, and impaired tumor growth and metastatic activities of melanoma sphere cells when xenografted in immunocompromised mice. Individual cells within melanoma sphere cultures displayed a wide range of NME1 expression across multiple melanoma cell lines. Cell subpopulations with elevated NME1 expression were fast cycling and displayed enhanced expression of stem cell markers.
Implications:
Our findings suggest the current model of NME1 as a metastasis-suppressing factor requires refinement, bringing into consideration its heterogeneous expression within melanoma sphere cultures and its novel role in promoting the expansion and tumorigenicity of stem-like cells.
Data from Inhibition of the Hedgehog Pathway Targets the Tumor-Associated Stroma in Pancreatic Cancer
Authors: Hwang Rosa F. , Moore Todd T. , Hattersley Maureen Mertens , Scarpitti Meghan , Yang Bin , Devereaux Erik , Ramachandran Vijaya , Arumugam Thiruvengadam , Ji Baoan , Logsdon Craig D. , Brown Jeffrey L. , Godin Robert
Published: April 2023

Abstract
Purpose: The Hedgehog (Hh) pathway has emerged as an important pathway in multiple tumor types and is thought to be dependent on a paracrine signaling mechanism. The purpose of this study was to determine the role of pancreatic cancer-associated fibroblasts (human pancreatic stellate cells, HPSCs) in Hh signaling. In addition, we evaluated the efficacy of a novel Hh antagonist, AZD8542, on tumor progression with an emphasis on the role of the stroma compartment.

Experimental Design: Expression of Hh pathway members and activation of the Hh pathway were analyzed in both HPSCs and pancreatic cancer cells. We tested the effects of Smoothened (SMO) inhibition with AZD8542 on tumor growth in vivo using an orthotopic model of pancreatic cancer containing varying amounts of stroma.

Results: HPSCs expressed high levels of SMO receptor and low levels of Hh ligands, whereas cancer cells showed the converse expression pattern. HPSC proliferation was stimulated by Sonic Hedgehog with upregulation of downstream GLI1 mRNA. These effects were abrogated by AZD8542 treatment. In an orthotopic model of pancreatic cancer, AZD8542 inhibited tumor growth only when HPSCs were present, implicating a paracrine signaling mechanism dependent on stroma. Further evidence of paracrine signaling of the Hh pathway in prostate and colon cancer models is provided, demonstrating the broader applicability of our findings.

Conclusion: Based on the use of our novel human-derived pancreatic cancer stellate cells, our results suggest that Hh-targeted therapies primarily affect the tumor-associated stroma, rather than the epithelial compartment. Mol Cancer Res; 10(9); 1147–57. ©2012 AACR.
Data from Membrane-Associated RING-CH 8 Functions as a Novel PD-L1 E3 Ligase to Mediate PD-L1 Degradation Induced by EGFR Inhibitors
Authors: Qian Guoqing , Guo Jianping , Vallega Karin A. , Hu Changjiang , Chen Zhen , Deng Yunfu , Wang Qiming , Fan Songqing , Ramalingam Suresh S. , Owonikoko Taofeek K. , Wei Wenyi , Sun Shi-Yong
Published: April 2023

Abstract
Expression of programmed death-ligand 1 (PD-L1) on cancer cells is a critical mechanism contributing to immunosuppression and immune escape. PD-L1 expression may also affect therapeutic outcomes of epidermal growth factor receptor (EGFR)-targeted therapy (e.g., with osimertinib/AZD9291) against EGFR-mutant non–small cell lung cancers (NSCLC) and can even be altered during the treatment albeit with largely undefined mechanisms. This study primarily focuses on elucidating the mechanism by which osimertinib induces PD-L1 degradation in addition to validating osimertinib's effect on decreasing PD-L1 expression in EGFR-mutant NSCLC cells and tumors. Osimertinib and other EGFR inhibitors effectively decreased PD-L1 levels primarily in EGFR-mutant NSCLCs and xenografted tumors. Osimertinib not only decreased PD-L1 mRNA expression, but also prompted proteasomal degradation of PD-L1 protein, indicating both transcriptional and posttranslational mechanisms accounting for osimertinib-induced reduction of PD-L1. Knockdown of β-TrCP or inhibition of GSK3 failed to prevent PD-L1 reduction induced by osimertinib. Rather, knockdown of membrane-associated RING-CH 8 (MARCH8) that encodes a membrane-bound E3 ubiquitin ligase rescued osimertinib-induced PD-L1 reduction. Furthermore, manipulation of MARCH8 expression accordingly altered PD-L1 degradation rate. Critically, MARCH8 interacted with PD-L1 through its N-terminal region and also ubiquitinated PD-L1 in cells. Collectively, these results strongly suggest that MARCH8 is a previously undiscovered E3 ubiquitin ligase responsible for PD-L1 degradation including osimertinib-induced PD-L1 degradation, establishing a novel connection between MARCH8 and PD-L1 regulation.
Implications:
This study has demonstrated a previously undiscovered function of MARCH8 in mediating PD-L1 degradation induced by EGFR inhibitors in EGFR-mutant NSCLC cells, establishing a novel connection between MARCH8 and PD-L1 regulation.
Data from Suppression of MET Signaling Mediated by Pitavastatin and Capmatinib Inhibits Oral and Esophageal Cancer Cell Growth
Authors: Xu Bo , Muramatsu Tomoki , Inazawa Johji
Published: April 2023

Abstract
Despite increasing knowledge on oral and esophageal squamous cell carcinoma (OSCC and ESCC), specific medicines against both have not yet been developed. Here, we aimed to find novel anticancer drugs through functional cell-based screening of an FDA-approved drug library against OSCC and ESCC. Pitavastatin, an HMGCR inhibitor, emerged as an anticancer drug that inhibits tumor growth by downregulating AKT and ERK signals in OSCC and ESCC cells. One of the mechanisms by which pitavastatin inhibits cell growth might be the suppression of MET signaling through immature MET due to dysfunction of the Golgi apparatus. Moreover, the sensitivity of tumor growth to pitavastatin might be correlated with GGPS1 expression levels. In vivo therapeutic models revealed that the combination of pitavastatin with capmatinib, a MET-specific inhibitor, dramatically reduced tumor growth. Our findings suggest that GGPS1 expression could be a biomarker in cancer therapy with pitavastatin, and the combination of pitavastatin with capmatinib might be a promising therapeutic strategy in OSCC and ESCC.
Implications:
This study provides new insight into the mechanism of pitavastatin as an anticancer drug and suggests that the combination of pitavastatin with capmatinib is a useful therapeutic strategy in OSCC and ESCC.
Data from An IFNγ/STAT1/JMJD3 Axis Induces ZEB1 Expression and Promotes Aggressiveness in Lung Adenocarcinoma
Authors: Yang Jianjian , Wang Xue , Huang Bing , Liu Rong , Xiong Hui , Ye Fan , Zeng Chenxi , Fu Xiangning , Li Lequn
Published: April 2023

Abstract
Active IFNγ signaling is a common feature of tumors responding to PD-1 checkpoint blockade. IFNγ exhibits both anti- and protumor activities. Here, we show that the treatment of lung adenocarcinoma cells with IFNγ led to a rapid increase of ZEB1 expression and a significant change in epithelial-to-mesenchymal transition (EMT)-associated gene expression pattern. Moreover, functional analyses show that IFNγ promoted cell migration in vitro and metastasis in vivo. We demonstrate that ZEB1 is required for IFNγ-promoted EMT, cell migration, and metastasis, as RNAi-mediated knockdown of ZEB1 abrogated EMT, cell migration, and metastasis induced by IFNγ. We show that IFNγ induced upregulation of JMJD3 significantly reduced H3K27 trimethylation in the promoter of the ZEB1 gene, which led to activation of ZEB1 gene transcription. IFNγ-induced JMJD3 expression was JAK1/2-STAT1 dependent. Inhibition of JMJD3 abrogated IFNγ-induced ZEB1 expression. IFNγ-induced ZEB1 also reduced miR-200 expression. Downregulation of ZEB1 increased miR-200 expression, which led to a reduction of PD-L1 expression induced by IFNγ. It is worth noting that knockdown of ZEB1 did not affect IFNγ-mediated antiproliferation and induction of CXCL9 and CXCL10. Thus, downregulation of ZEB1 may prevent the protumor activity of IFNγ while retaining its antitumor function. This study expands our understanding of IFNγ-mediated signaling and helps to identify therapeutic targets to improve current immunotherapies.
Implications:
IFNγ increases ZEB1 expression in a STAT1-JMJD3 dependent manner, and consequently promotes cancer cell aggressiveness. This study provides a potential target to minimize the procancer effect of IFNγ while preserving its antitumor function.
Data from O-GlcNAcylation of Blimp-1 in Lymphocytes Inhibits Its Transcriptional Function and Is Associated with Migration and Invasion of Breast Cancer Cells
Authors: Chen Yan-Fang , Shao Guang-Can , Li Jie , Yang An-Qi , Li Jing , Ye Xin-Shan
Published: April 2023

Abstract
Lymphocyte infiltration is an important feature of cancer. There is a complex network of chemokines that influence the degree and phenotype of lymphocyte infiltration, as well as the growth, survival, migration, and angiogenesis of tumor cells. High heterogeneity metastasis is a major obstacle to the treatment of breast cancer. Herein, we showed that O-GlcNAcylation of B lymphocyte–induced maturation protein-1 (Blimp-1) in lymphocytes inhibited the migration and invasion of breast cancer cells. It was found that Blimp-1 O-GlcNAcylation at Ser448 and Ser472 in lymphocytes promoted its nuclear localization, and blocked the bindings to three regions upstream of the ccl3l1 promoter to inhibit its expression. Decreased expression of CCL3L1 in lymphocytes not only decreased CCR5 expression in breast cancer cells, but also inhibited the membrane localization and activation of CCR5, thus blocking the migration and invasion of breast cancer cells in vitro. Therefore, O-GlcNAcylation of Blimp-1 in lymphocytes may serve as a new target for the treatment of metastatic breast cancer.
Implications:
This study reveals a new mechanism by which the lymphatic system promotes breast cancer cell metastasis.
Data from Dependence on the MUC1-C Oncoprotein in Classic, Variant, and Non–neuroendocrine Small Cell Lung Cancer
Authors: Fushimi Atsushi , Morimoto Yoshihiro , Ishikawa Satoshi , Yamashita Nami , Bhattacharya Atrayee , Daimon Tatsuaki , Rajabi Hasan , Jin Caining , Hagiwara Masayuki , Yasumizu Yota , Luan Zhou , Suo Wenhao , Wong Kwok-Kin , Withers Henry , Liu Song , Long Mark D. , Kufe Donald
Published: April 2023

Abstract
Small cell lung cancer (SCLC) is a recalcitrant malignancy defined by subtypes on the basis of differential expression of the ASCL1, NEUROD1, and POU2F3 transcription factors. The MUC1-C protein is activated in pulmonary epithelial cells by exposure to environmental carcinogens and promotes oncogenesis; however, there is no known association between MUC1-C and SCLC. We report that MUC1-C is expressed in classic neuroendocrine (NE) SCLC-A, variant NE SCLC-N and non-NE SCLC-P cells and activates the MYC pathway in these subtypes. In SCLC cells characterized by NE differentiation and DNA replication stress, we show that MUC1-C activates the MYC pathway in association with induction of E2F target genes and dysregulation of mitotic progression. Our studies further demonstrate that the MUC1-C→MYC pathway is necessary for induction of (i) NOTCH2, a marker of pulmonary NE stem cells that are the proposed cell of SCLC origin, and (ii) ASCL1 and NEUROD1. We also show that the MUC1-C→MYC→NOTCH2 network is necessary for self-renewal capacity and tumorigenicity of NE and non-NE SCLC cells. Analyses of datasets from SCLC tumors confirmed that MUC1 expression in single SCLC cells significantly associates with activation of the MYC pathway. These findings demonstrate that SCLC cells are addicted to MUC1-C and identify a potential new target for SCLC treatment.
Implications:
This work uncovers addiction of SCLC cells to MUC1-C, which is a druggable target that could provide new opportunities for advancing SCLC treatment.
Data from Concurrent Disruption of the Ras/MAPK and NF-κB Pathways Induces Circadian Deregulation and Hepatocarcinogenesis
Authors: Hanley Kaisa L. , Liang Yan , Wang Gaowei , Lin Xiaoxue , Yang Meixiang , Karin Michael , Fu Wenxian , Feng Gen-Sheng
Published: April 2023

Abstract
The Ras/Erk and NF-κB pathways play critical roles in cell proliferation and are known to drive oncogenesis when overactivated. Herein we report a gatekeeper function of the two pathways by working in synergy to suppress liver tumorigenesis. Hepatocyte-specific deletion of both Shp2/Ptpn11 and Ikkβ in mice, which promote Ras/Erk and NF-κB signaling, respectively, exacerbated chemical carcinogenesis and even triggered spontaneous development of hepatocellular carcinoma (HCC). We show that the unanticipated severe tumor phenotype was contributed collectively by severe cholestasis, metabolic changes, upregulated cell-cycle progression, and disruption of circadian rhythm in mutant hepatocytes. Remarkably, human HCCs with dysregulated circadian gene expression displayed downregulation of Ras/Erk and NF-κB signaling and poor prognosis. Together, these data indicate that at the ground state, the two central pathways, previously known as oncogenic, cooperate to sustain tumor-suppressive physiologic homeostasis and to prevent hepatic damage. Disruption of this intricate signaling network is carcinogenic in the liver.
Implications:
We demonstrate here that basal levels of the Ras/MAPK and NF-κB pathways, while promoting tumorigenesis if overactivated, are required to maintain physiologic homeostasis and regulate circadian rhythm in the liver, which are antitumorigenic.
Supplementary Table 1 from A Prospective Targeted Serum Metabolomics Study of Pancreatic Cancer in Postmenopausal Women
Authors: Jiao Li , Maity Suman , Coarfa Cristian , Rajapakshe Kimal , Chen Liang , Jin Feng , Putluri Vasanta , Tinker Lesley F. , Mo Qianxing , Chen Fengju , Sen Subrata , Sangi-Hyghpeykar Haleh , El-Serag Hashem B. , Putluri Nagireddy
Published: April 2023

180 chemicals in cases and controls in the discovery stage
Supplementary Material from A Prospective Targeted Serum Metabolomics Study of Pancreatic Cancer in Postmenopausal Women
Authors: Jiao Li , Maity Suman , Coarfa Cristian , Rajapakshe Kimal , Chen Liang , Jin Feng , Putluri Vasanta , Tinker Lesley F. , Mo Qianxing , Chen Fengju , Sen Subrata , Sangi-Hyghpeykar Haleh , El-Serag Hashem B. , Putluri Nagireddy
Published: April 2023

Supplemental material 1, chemical list
Supplementary Figure 2 from A Prospective Targeted Serum Metabolomics Study of Pancreatic Cancer in Postmenopausal Women
Authors: Jiao Li , Maity Suman , Coarfa Cristian , Rajapakshe Kimal , Chen Liang , Jin Feng , Putluri Vasanta , Tinker Lesley F. , Mo Qianxing , Chen Fengju , Sen Subrata , Sangi-Hyghpeykar Haleh , El-Serag Hashem B. , Putluri Nagireddy
Published: April 2023

Supplemental figure 2
Supplementary Table S1 from Fusobacterium Nucleatum Subspecies Animalis Influences Proinflammatory Cytokine Expression and Monocyte Activation in Human Colorectal Tumors
Authors: Ye Xiangcang , Wang Rui , Bhattacharya Rajat , Boulbes Delphine R. , Fan Fan , Xia Ling , Adoni Harish , Ajami Nadim J. , Wong Matthew C. , Smith Daniel P. , Petrosino Joseph F. , Venable Susan , Qiao Wei , Baladandayuthapani Veera , Maru Dipen , Ellis Lee M.
Published: April 2023

Clinical characteristics of the study patients with CRC.
Supplementary Figure S3 from Fusobacterium Nucleatum Subspecies Animalis Influences Proinflammatory Cytokine Expression and Monocyte Activation in Human Colorectal Tumors
Authors: Ye Xiangcang , Wang Rui , Bhattacharya Rajat , Boulbes Delphine R. , Fan Fan , Xia Ling , Adoni Harish , Ajami Nadim J. , Wong Matthew C. , Smith Daniel P. , Petrosino Joseph F. , Venable Susan , Qiao Wei , Baladandayuthapani Veera , Maru Dipen , Ellis Lee M.
Published: April 2023

CCL20-specific ELISA confirming differential expression of CCL20 in human colorectal tumors.
Supplemental Figure 3 from The Prolyl Isomerase Pin1 Is a Novel Target of 6,7,4′-Trihydroxyisoflavone for Suppressing Esophageal Cancer Growth
Authors: Lim Tae-Gyu , Lee Sung-Young , Duan Zhaoheng , Lee Mee-Hyun , Chen Hanyong , Liu Fangfang , Liu Kangdong , Jung Sung Keun , Kim Dong Joon , Bode Ann M. , Lee Ki Won , Dong Zigang
Published: April 2023

6,7,4'-THIF inhibits esophageal cancer cell growth more effectively than 7,8,4'-THIF. 6,7,4'-THIF shows a better inhibitory effect on (A) KYSE 30, (B) 450 or (C) 510 esophageal cancer cell growth compared to 7,8,4'-THIF. Cell growth was estimated by MTS assay after 72 h of treatment. Total experimental procedures are described in Materials and Methods.
Supplemental Figure S1 from STAT3 as a Chemoprevention Target in Carcinogen-Induced Head and Neck Squamous Cell Carcinoma
Authors: Peyser Noah D. , Wang Lin , Zeng Yan , Acquafondata Marie , Freilino Maria , Li Hua , Sen Malabika , Gooding William E. , Satake Masanobu , Wang Zhenghe , Johnson Daniel E. , Grandis Jennifer R.
Published: April 2023

Parallel slopes indicate identical response to Stattic in PTPRT WT and KO mice. Vertical distance indicates improved outcome of Stattic-treated mice compared to vehicle-treated.
Supplemental Figure 6 from Suppression of Colon Tumorigenesis in Mutant Apc Mice by a Novel PDE10 Inhibitor that Reduces Oncogenic β-Catenin
Authors: Lee Kevin J. , Chang Wen-Chi L. , Chen Xi , Valiyaveettil Jacob , Ramirez-Alcantara Veronica , Gavin Elaine , Musiyenko Alla , Madeira da Silva Luciana , Annamdevula Naga S. , Leavesley Silas J. , Ward Antonio , Mattox Tyler , Lindsey Ashley S. , Andrews Joel , Zhu Bing , Wood Charles , Neese Ashleigh , Nguyen Ashley , Berry Kristy , Maxuitenko Yulia , Moyer Mary Pat , Nurmemmedov Elmar , Gorman Greg , Coward Lori , Zhou Gang , Keeton Adam B. , Cooper Harry S. , Clapper Margie L. , Piazza Gary A.
Published: April 2023

ADT 061 pharmacokinetics and tissue distribution. ADT 061 was detected in plasma at a concentration of 2.8 ÂµM 0.5 hr after a single oral administration of a dose of 100 mg/kg in 0.5% CMC/0.25% T80 in water to female C57BL/6 mice and reached plasma Cmax of 4.9 ÂµM 4 hr after administration, which is >10 times higher than human colon cancer cell growth inhibition IC50 values. ADT 061 reached a Cmax in colon mucosa within 2 hr after oral administration (62.6 nmol/g) and was still present at concentrations exceeding IC50 values 8 hr after administration (28.9 nmol/g). ADT 061 concentrations in lungs, ovaries, and uterus (1-2 nmol/g) were appreciably lower than colon mucosa levels, while the ADT 061 concentration in the brain was nearly undetectable 2 and 8 hr post treatment (0.1 and 0.2 nmol/g, respectively) (n=4, mean {plus minus} SD).
Supplemental Figure 4B from Suppression of Colon Tumorigenesis in Mutant Apc Mice by a Novel PDE10 Inhibitor that Reduces Oncogenic β-Catenin
Authors: Lee Kevin J. , Chang Wen-Chi L. , Chen Xi , Valiyaveettil Jacob , Ramirez-Alcantara Veronica , Gavin Elaine , Musiyenko Alla , Madeira da Silva Luciana , Annamdevula Naga S. , Leavesley Silas J. , Ward Antonio , Mattox Tyler , Lindsey Ashley S. , Andrews Joel , Zhu Bing , Wood Charles , Neese Ashleigh , Nguyen Ashley , Berry Kristy , Maxuitenko Yulia , Moyer Mary Pat , Nurmemmedov Elmar , Gorman Greg , Coward Lori , Zhou Gang , Keeton Adam B. , Cooper Harry S. , Clapper Margie L. , Piazza Gary A.
Published: April 2023

Mass spectroscopy of ADT 061
Supplemental Figure 3C from Suppression of Colon Tumorigenesis in Mutant Apc Mice by a Novel PDE10 Inhibitor that Reduces Oncogenic β-Catenin
Authors: Lee Kevin J. , Chang Wen-Chi L. , Chen Xi , Valiyaveettil Jacob , Ramirez-Alcantara Veronica , Gavin Elaine , Musiyenko Alla , Madeira da Silva Luciana , Annamdevula Naga S. , Leavesley Silas J. , Ward Antonio , Mattox Tyler , Lindsey Ashley S. , Andrews Joel , Zhu Bing , Wood Charles , Neese Ashleigh , Nguyen Ashley , Berry Kristy , Maxuitenko Yulia , Moyer Mary Pat , Nurmemmedov Elmar , Gorman Greg , Coward Lori , Zhou Gang , Keeton Adam B. , Cooper Harry S. , Clapper Margie L. , Piazza Gary A.
Published: April 2023

HPLC chromatogram of compound 5.
Supplementary Table from Plasma Growth Factor Gene Expression and Mammographic Breast Density in Postmenopausal Women
Authors: Akinjiyan Favour A. , Adams Andrea , Xu Shuai , Wang Mei , Toriola Adetunji T.
Published: April 2023

Supplementary Table from Plasma Growth Factor Gene Expression and Mammographic Breast Density in Postmenopausal Women
Table S3 from Multiparametric Detection of Antibodies against Different EBV Antigens to Predict Risk for Nasopharyngeal Carcinoma in a High-Risk Population of China
Authors: Chen Hao , Chen Shulin , Lu Jie , Wang Xueping , Li Jianpei , Li Linfang , Fu Jihuan , Scheper Thomas , Meyer Wolfgang , Peng Yu-Hui , Liu Wanli
Published: April 2023

Comparison of sensitivity between Anti-EBV EUROLINE and other methods in early NPC stage
Table S2 from Multiparametric Detection of Antibodies against Different EBV Antigens to Predict Risk for Nasopharyngeal Carcinoma in a High-Risk Population of China
Authors: Chen Hao , Chen Shulin , Lu Jie , Wang Xueping , Li Jianpei , Li Linfang , Fu Jihuan , Scheper Thomas , Meyer Wolfgang , Peng Yu-Hui , Liu Wanli
Published: April 2023

Test performance of different indexes
Table S1 from Losartan and Vitamin D Inhibit Colonic Tumor Development in a Conditional Apc-Deleted Mouse Model of Sporadic Colon Cancer
Authors: Dougherty Urszula , Mustafi Reba , Haider Haider I. , Khalil Abdurahman , Souris Jeffrey S. , Joseph Loren , Hart John , Konda Vani J. , Zhang Wei , Pekow Joel , Li Yan Chun , Bissonnette Marc
Published: April 2023

Transcripts of Notch signaling components
Supplementary Data from The Ashitaba (Angelica keiskei) Chalcones 4-hydroxyderricin and Xanthoangelol Suppress Melanomagenesis By Targeting BRAF and PI3K
Authors: Zhang Tianshun , Wang Qiushi , Fredimoses Mangaladoss , Gao Ge , Wang Keke , Chen Hanyong , Wang Ting , Oi Naomi , Zykova Tatyana A. , Reddy Kanamata , Yao Ke , Ma Weiya , Chang Xiaoyu , Lee Mee-Hyun , Rathore Moeez Ghani , Bode Ann M. , Ashida Hitoshi , Lippman Scott M. , Dong Zigang
Published: April 2023

Table S1, Supplementary Figure Legends, Figure S1-S7
Supplementary Figure Legends from Myeloid Differentiation Factor 88 Signaling in Bone Marrow–Derived Cells Promotes Gastric Tumorigenesis by Generation of Inflammatory Microenvironment
Authors: Maeda Yusuke , Echizen Kanae , Oshima Hiroko , Yu Liang , Sakulsak Natthiya , Hirose Osamu , Yamada Yoichi , Taniguchi Tadatsugu , Jenkins Brendan J. , Saya Hideyuki , Oshima Masanobu
Published: April 2023

Supplementary Figure Legends.
Supplementary Figure 5 from Myeloid Differentiation Factor 88 Signaling in Bone Marrow–Derived Cells Promotes Gastric Tumorigenesis by Generation of Inflammatory Microenvironment
Authors: Maeda Yusuke , Echizen Kanae , Oshima Hiroko , Yu Liang , Sakulsak Natthiya , Hirose Osamu , Yamada Yoichi , Taniguchi Tadatsugu , Jenkins Brendan J. , Saya Hideyuki , Oshima Masanobu
Published: April 2023

Suppression of NF-ÎºB and Wnt signaling by Myd88 disruption in BMDCs.
Supplementary Figure 4 from Myeloid Differentiation Factor 88 Signaling in Bone Marrow–Derived Cells Promotes Gastric Tumorigenesis by Generation of Inflammatory Microenvironment
Authors: Maeda Yusuke , Echizen Kanae , Oshima Hiroko , Yu Liang , Sakulsak Natthiya , Hirose Osamu , Yamada Yoichi , Taniguchi Tadatsugu , Jenkins Brendan J. , Saya Hideyuki , Oshima Masanobu
Published: April 2023

Induction of Tlr2 and Cd14 in regenerating gastric mucosa.
Supplementary Data from Mushroom Consumption and Risk of Total and Site-Specific Cancer in Two Large U.S. Prospective Cohorts
Authors: Lee Dong Hoon , Yang Meng , Keum NaNa , Giovannucci Edward L. , Sun Qi , Chavarro Jorge E.
Published: April 2023

Supplementary tables
Supplementary Data from Comprehensive Analysis of Multiple Cohort Datasets Deciphers the Utility of Germline Single-Nucleotide Polymorphisms in Prostate Cancer Diagnosis
Authors: Zhang Wensheng , Dong Yan , Sartor Oliver , Zhang Kun
Published: April 2023

Text S1, Text S2, Text S3, Text S4, Figure S1, Table S1, Table S2
supplemental Figure 4 from Unconjugated Bilirubin Is a Novel Prognostic Biomarker for Nasopharyngeal Carcinoma and Inhibits Its Metastasis via Antioxidation Activity
Authors: Deng Cheng-Cheng , Xu Miao , Li Jing , Luo Xiao-Lin , Zhu Yu-Jia , Jiang Rou , Zhang Meng-Xia , Lei Jin-Ju , Lian Yi-Fan , Zou Xiong , You Rui , Chen Li-Zhen , Feng Qi-Sheng , Bei Jin-Xin , Chen Ming-Yuan , Zeng Yi-Xin
Published: April 2023

Supplemental Figure 4.UCB does not inhibit growth or induce apoptosis at low concentrations.
Supplemental Tables and Figures from Interception Targets of Angelica Gigas Nakai Root Extract versus Pyranocoumarins in Prostate Early Lesions and Neuroendocrine Carcinomas in TRAMP Mice
Authors: Tang Su-Ni , Jiang Peixin , Kim Sangyub , Zhang Jinhui , Jiang Cheng , Lü Junxuan
Published: April 2023

Supplemental data
Figure S3 from Temporal Efficacy of a Sulforaphane-Based Broccoli Sprout Diet in Prevention of Breast Cancer through Modulation of Epigenetic Mechanisms
Authors: Li Yuanyuan , Buckhaults Phillip , Li Shizhao , Tollefsbol Trygve
Published: April 2023

Histological analysis by H&E staining.
Supplementary Data from Weight is More Informative than Body Mass Index for Predicting Postmenopausal Breast Cancer Risk: Prospective Family Study Cohort (ProF-SC)
Authors: Ye Zhoufeng , Li Shuai , Dite Gillian S. , Nguyen Tuong L. , MacInnis Robert J. , Andrulis Irene L. , Buys Saundra S. , Daly Mary B. , John Esther M. , Kurian Allison W. , Genkinger Jeanine M. , Chung Wendy K. , Phillips Kelly-Anne , Thorne Heather , Winship Ingrid M. , Milne Roger L. , Dugué Pierre-Antoine , Southey Melissa C. , Giles Graham G. , Terry Mary Beth , Hopper John L.
Published: April 2023

Supplementary Data from Weight is More Informative than Body Mass Index for Predicting Postmenopausal Breast Cancer Risk: Prospective Family Study Cohort (ProF-SC)
Supplementary Figure 1 from Targeting of CD40 and PD-L1 Pathways Inhibits Progression of Oral Premalignant Lesions in a Carcinogen-induced Model of Oral Squamous Cell Carcinoma
Authors: Monteiro de Oliveira Novaes Jose A. , Hirz Taghreed , Guijarro Irene , Nilsson Monique , Pisegna Marlese A. , Poteete Alissa , Barsoumian Hampartsoum B. , Fradette Jared J. , Chen Limo N. , Gibbons Don L. , Tian Xiangjun , Wang Jing , Myers Jeffrey N. , McArthur Mark J. , Bell Diana , William William N. , Heymach John V.
Published: April 2023

Percentage of CD4+CD44hi
Figure S1, Table S1-7 from Calcium Intake and Risk of Colorectal Cancer According to Tumor-infiltrating T Cells
Authors: Yang Wanshui , Liu Li , Keum NaNa , Qian Zhi Rong , Nowak Jonathan A. , Hamada Tsuyoshi , Song Mingyang , Cao Yin , Nosho Katsuhiko , Smith-Warner Stephanie A. , Zhang Sui , Masugi Yohei , Ng Kimmie , Kosumi Keisuke , Ma Yanan , Garrett Wendy S. , Wang Molin , Nan Hongmei , Giannakis Marios , Meyerhardt Jeffrey A. , Chan Andrew T. , Fuchs Charles S. , Nishihara Reiko , Wu Kana , Giovannucci Edward L. , Ogino Shuji , Zhang Xuehong
Published: April 2023

Figure S1, Table S1-7
Table S1 from Scutellarin Suppresses Patient-Derived Xenograft Tumor Growth by Directly Targeting AKT in Esophageal Squamous Cell Carcinoma
Authors: Liu Feifei , Zu Xueyin , Xie Xiaomeng , Zhang Yuanyuan , Liu Kangdong , Chen Hanyong , Wang Ting , Bode Ann M. , Dong Zigang , Kim Dong Joon
Published: April 2023

Clinical information of PDX tissue
Figure S4 from Scutellarin Suppresses Patient-Derived Xenograft Tumor Growth by Directly Targeting AKT in Esophageal Squamous Cell Carcinoma
Authors: Liu Feifei , Zu Xueyin , Xie Xiaomeng , Zhang Yuanyuan , Liu Kangdong , Chen Hanyong , Wang Ting , Bode Ann M. , Dong Zigang , Kim Dong Joon
Published: April 2023

Assessing the toxicity of scutellarin in vivo
Figure S1 from Scutellarin Suppresses Patient-Derived Xenograft Tumor Growth by Directly Targeting AKT in Esophageal Squamous Cell Carcinoma
Authors: Liu Feifei , Zu Xueyin , Xie Xiaomeng , Zhang Yuanyuan , Liu Kangdong , Chen Hanyong , Wang Ting , Bode Ann M. , Dong Zigang , Kim Dong Joon
Published: April 2023

Chemical structure of scutellarin