bluuebunny/crossref_metadata_2025 huggingface dataset:
Numerical Simulation of Hetero Dielectric Trench Gate JAM Gate-All-Around FET (HDTG-JAM-GAAFET) for Label Free Biosensing Applications
Authors: Yadav Shivani , Rewari Sonam
Published: December 2023

The label free detection of various biomolecules associated with different diseases has been proposed in this manuscript using a novel biosensor design named as the Hetero Dielectric Trench Gate Junctionless Accumulation Mode Gate-All-Around FET (HDTG-JAM-GAAFET). This biosensor employs a silicon cylindrical Gate All Around FET which operates in Junctionless Accumulation Mode (JAM) and has a hetero dielectric layer comprised of SiO2 and HfO2. The cylindrical gate structure’s metal gate is trenched into the Hafnium oxide dielectric layer, which provides the gate with enhanced control over the surface characteristics of the channel. A Trench Gate architecture in a hetero dielectric Gate All Around FET is emulated for the biosensing for the first time. The HDTG-JAM-GAAFET has been compared to Normal Gate JAM Gate-All-Around FET (NG-JAM-GAAFET) biosensors immobilizing a variety of neutral biomolecules and biomolecules having a range of positive and negative charges. The effect of biomolecules on HDTG-JAM-GAAFET biosensor’s output properties, including surface potential, electron concentration, threshold voltage drift (ΔVTH), subthreshold leakage current (IOFF), subthreshold slope (SS), switching ratio (ION/IOFF), ION current sensitivity, transconductance (gm), output conductance (gd), channel resistance (Rch) and intrinsic gain (

A

V

int

) has been studied. For instance, HDTG-JAM-GAAFET biosensor has drain ON-current sensitivity

(
S

I

ON

)

which is 67.68% greater for gelatin biomolecules, 69.4% higher for positive biomolecules, and 8% higher for negative biomolecules bound in the nanogap cavity than that of a Normal Gate JAM Gate-All-Around FET. The proposed device exhibits exceptional performance characteristics and it can effectively identify specific biomolecules to diagnose many diseases, such as breast cancer, lung cancer, and numerous viral infections, using their respective biomarkers.
Utilization of Coffee Husk Ash on the Geotechnical Properties of Gypsum-Stabilized Expansive Clayey Soil
Authors: Tessema Amare Tilahun , Wolelaw Natnael Melsew , Abebe Awol Eyasu , Alene Getachew Asefa , Abeje Biruhi Tesfaye
Published: December 2023

Expansive clayey soils (CSs) expand and become softer as moisture content increases, but they get harder and stronger as they dry out. The earth’s swelling and shrinkage characteristics under varying moisture conditions make roads built on expansive CS, in particular, vulnerable to early degradation. In this investigation, coffee husk ash (CHA), gypsum, and a blend of the two additives (G-CHA) were used in experimental tests to treat expansive CS. This study aims to evaluate experimentally the potential of expansive soil stabilization using different additives: CHA, gypsum, and a combination of gypsum and CHA. Five different percentages of CHA (5%, 10%, 15%, 20%, and 25%), three percentages of gypsum (3%, 6%, and 9%), and variable percentages of their combinations were used to stabilize the soil for pavement subgrade application. Atterberg limits, compaction, linear shrinkage (LS), swelling, unconfined compressive strength (UCS), and California bearing ratio (CBR) tests were performed on treated and virgin soil specimens at 3, 7, 14, 28, and 56-day curing times. Results showed that CHA additives effectively reduced the plasticity, LS, and swell potential in addition to increasing the maximum dry unit weight, UCS, and CBR. It was determined that the UCS and CBR values for the 6% stabilized gypsum soil increased by 28.95% and 19.54%, respectively, and reduced by 41% of the plastic index parameter after the addition of 15% CHA. Based on the evaluation of the results, an optimum mixture of 6% gypsum and 15% CHA (SG6C15) stabilized soil can be used in pavement subgrade applications as it achieved the minimum strength target. The performance of CHA-treated samples as subgrade material is superior to that of untreated virgin soil. Because of the stronger subgrade, smaller pavement layers result in a thinner pavement structure.
Medication-Related Osteonecrosis of the Jaw: A Case Report of an Unusual Side Effect of Adalimumab
Authors: Sisalli Laura , Giordano Francesco , Chiacchio Andrea , Acerra Alfonso , Caggiano Mario
Published: December 2023

Background. Medication-related osteonecrosis of the jaw (MRONJ) is a serious adverse drug reaction characterized by progressive bone destruction and necrosis of mandibular and/or maxillary jaw bone that occurs in patients undergoing treatments with antiresorptive drugs such as bisphosphonates or denosumab, antiangiogenic agents such as bevacizumab, or other kinds of monoclonal antibodies such as rituximab and ipilimumab, for different oncologic and nononcologic diseases. The aim of this study was to report a case of MRONJ in a patient affected by rheumatoid arthritis disease in treatment with adalimumab. Case Presentation. A 70-year-old female patient affected by rheumatoid arthritis (RA), who had been undergoing adalimumab (40 mg subcutaneous injection) every two weeks for 5 years, with no history of antiresorptive or antiangiogenic agent administration, came to our attention for intraoral necrotic bone exposures of the anterior mandible. After drug withdrawal and antibiotic cycles, the patient underwent surgical treatment with bone resection and debridement of necrotic tissues. After an observation period of 8 months, a complete healing without signs of recurrence was detected.Conclusions. Based on this study, a correlation between adalimumab and MRONJ is possible. Therefore, we believe that an oral cavity examination should be done in every patients, before starting therapy with adalimumab, to possibly avoid MRONJ onset. Further studies are required to confirm the role of adalimumab in MRONJ.
Comparative Experimental Study on Strength Properties of Red Clay Modified by Cement and Industrial Solid Waste Powder
Authors: Lu Xianlong , Yu Qiang , Xu Jiayu , Yue Bing , Sheng Mingqiang
Published: December 2023

Because of the existence of clay minerals such as montmorillonite in red clay, the strength of red clay decreases significantly as water content increases. This study aims to improve the strength of red clay by using three different kinds of industrial solid waste powder, i.e., steel slag (SS) powder, fly ash (FA), and ground-granulated blast furnace slag (GGBS). At the same time, the ordinary Portland cement (OPC) was selected as a comparison of the improvement effect on the strength of red clay modified by the aforementioned industrial solid waste powder. The properties of the red clay and the industrial solid waste powder were documented comprehensively. The unconfined compressive strength (UCS) tests were conducted on the specimens of the red clay and the red clay modified by the OPC, SS, FA, and GGBS, which had been cured for 3, 7, and 21 days at a temperature of 25°C, respectively. The results showed that the strength of red clay can be significantly improved by the three kinds of industrial solid waste powder. After a 21-day curing period, the experimental results showed that the UCS of the red clay modified by 7% SS, 5% FA, and 5% GGBS increased by 252%, 131%, and 140% compared to that of the red clay without modification. However, the modification effects of the SS, FA, and GGBS on the red clay were generally inferior to that of the OPC. By observing the microstructures of the modified clay, the mechanism of industrial solid waste powder and cement improving the strength of the red clay was analyzed. The findings in this study can provide a reference for improving subgrade strength by a soil-modification method in road constructions.
Fixed-Bed Adsorption of an Azo Dye (Methyl Orange) onto Chemically and Thermally Regenerated Activated Carbons
Authors: Taquieteu Idriss Kamdem , Dzoujo Hermann Tamaguelon , Shikuku Victor Odhiambo , Banenzoué Charles , Joh Dina Daniel David
Published: December 2023

In this study, the effectiveness of the recovery method for spent granular activated carbon (SGAC) for application in dye removal was evaluated. A comparative study of the textural (porosity), compositional, surface functionality, and adsorption performance of chemically (CAR400) and thermally regenerated activated carbons (CAR700 and CAR900) was conducted for the elimination of methyl orange (MO) dye by using a fixed-bed system. The results were compared with those of commercial activated carbon (CA). The influence of parameters such as the initial dye concentration, the flow rate, the internal diameter of the column, and the bed height was evaluated. Adsorption data were modelled by using the Thomas, Adams–Bohart, and Yoon–Nelson equations. The CAR400 activated carbon had a microporosity (1045 mg/g) comparable to that of the reference commercial (CA) activated carbon (1052 mg/g) but exhibited the least adsorption capacity. The breakthrough curves were best described by the Thomas model more than the Bohart–Adams and Yoon–Nelson’s models. Thomas’s model depicted that an increase in column diameter resulted in a decrease in the maximum adsorption capacity (qo). The CAR900 material exhibited the highest adsorption capacity (15.72 mg/g) comparable to that of commercial activated carbon, CA (16.90 mg/g). These results show that the physical/thermal regeneration of spent granular activated carbons (SGAC) is more suitable for the valorization of these waste materials for water purification applications.
Supplementary Figure 6 from RETRACTED: Physical and Functional Interaction of DNA Methyltransferase 3A with Mbd3 and Brg1 in Mouse Lymphosarcoma Cells
Authors: Datta Jhrana , Majumder Sarmila , Bai Shoumei , Ghoshal Kalpana , Kutay Huban , Smith David Spencer , Crabb John W. , Jacob Samson T.
Published: December 2023

Supplementary Figure 6 from RETRACTED: Physical and Functional Interaction of DNA Methyltransferase 3A with Mbd3 and Brg1 in Mouse Lymphosarcoma Cells
Supplementary Figure 1 from RETRACTED: Physical and Functional Interaction of DNA Methyltransferase 3A with Mbd3 and Brg1 in Mouse Lymphosarcoma Cells
Authors: Datta Jhrana , Majumder Sarmila , Bai Shoumei , Ghoshal Kalpana , Kutay Huban , Smith David Spencer , Crabb John W. , Jacob Samson T.
Published: December 2023

Supplementary Figure 1 from RETRACTED: Physical and Functional Interaction of DNA Methyltransferase 3A with Mbd3 and Brg1 in Mouse Lymphosarcoma Cells
Supplementary Figure Legends 1-4 from RETRACTED: Methylation Mediated Silencing of MicroRNA-1 Gene and Its Role in Hepatocellular Carcinogenesis
Authors: Datta Jharna , Kutay Huban , Nasser Mohd W. , Nuovo Gerard J. , Wang Bo , Majumder Sarmila , Liu Chang-Gong , Volinia Stefano , Croce Carlo M. , Schmittgen Thomas D. , Ghoshal Kalpana , Jacob Samson T.
Published: December 2023

Supplementary Figure Legends 1-4 from RETRACTED: Methylation Mediated Silencing of MicroRNA-1 Gene and Its Role in Hepatocellular Carcinogenesis
Supplementary Figures 1-2 from RETRACTED: A New Class of Quinoline-Based DNA Hypomethylating Agents Reactivates Tumor Suppressor Genes by Blocking DNA Methyltransferase 1 Activity and Inducing Its Degradation
Authors: Datta Jharna , Ghoshal Kalpana , Denny William A. , Gamage Swarna A. , Brooke Darby G. , Phiasivongsa Pasit , Redkar Sanjeev , Jacob Samson T.
Published: December 2023

Supplementary Figures 1-2 from RETRACTED: A New Class of Quinoline-Based DNA Hypomethylating Agents Reactivates Tumor Suppressor Genes by Blocking DNA Methyltransferase 1 Activity and Inducing Its Degradation
Supplementary Tables from Super Enhancer–Regulated LncRNA LINC01089 Induces Alternative Splicing of DIAPH3 to Drive Hepatocellular Carcinoma Metastasis
Authors: Su Tao , Zhang Nasha , Wang Teng , Zeng Jiajia , Li Wenwen , Han Linyu , Yang Ming
Published: December 2023

Supplementary Table S1-Table S6
Table S7 from TEAD Inhibition Overcomes YAP1/TAZ-Driven Primary and Acquired Resistance to KRASG12C Inhibitors
Authors: Edwards A. Cole , Stalnecker Clint A. , Jean Morales Alexis , Taylor Khalilah E. , Klomp Jennifer E. , Klomp Jeffrey A. , Waters Andrew M. , Sudhakar Niranjan , Hallin Jill , Tang Tracy T. , Olson Peter , Post Leonard , Christensen James G. , Cox Adrienne D. , Der Channing J.
Published: December 2023

PCR primers utilized in this study
Table S5 from TEAD Inhibition Overcomes YAP1/TAZ-Driven Primary and Acquired Resistance to KRASG12C Inhibitors
Authors: Edwards A. Cole , Stalnecker Clint A. , Jean Morales Alexis , Taylor Khalilah E. , Klomp Jennifer E. , Klomp Jeffrey A. , Waters Andrew M. , Sudhakar Niranjan , Hallin Jill , Tang Tracy T. , Olson Peter , Post Leonard , Christensen James G. , Cox Adrienne D. , Der Channing J.
Published: December 2023

siRNA oligonucleotides utilized in this study
supplementary data from Fructose-Induced mTORC1 Activation Promotes Pancreatic Cancer Progression through Inhibition of Autophagy
Authors: Cui Yanfen , Tian Jianfei , Wang Zhaosong , Guo Hui , Zhang He , Wang Zhiyong , Liu Hui , Song Weijie , Liu Liming , Tian Ruinan , Zuo Xiaoyan , Ren Sixin , Niu Ruifang , Zhang Fei
Published: December 2023

Supplementary data
Figure S2 from Fructose-Induced mTORC1 Activation Promotes Pancreatic Cancer Progression through Inhibition of Autophagy
Authors: Cui Yanfen , Tian Jianfei , Wang Zhaosong , Guo Hui , Zhang He , Wang Zhiyong , Liu Hui , Song Weijie , Liu Liming , Tian Ruinan , Zuo Xiaoyan , Ren Sixin , Niu Ruifang , Zhang Fei
Published: December 2023

Figure S2
Figure S1 from Fructose-Induced mTORC1 Activation Promotes Pancreatic Cancer Progression through Inhibition of Autophagy
Authors: Cui Yanfen , Tian Jianfei , Wang Zhaosong , Guo Hui , Zhang He , Wang Zhiyong , Liu Hui , Song Weijie , Liu Liming , Tian Ruinan , Zuo Xiaoyan , Ren Sixin , Niu Ruifang , Zhang Fei
Published: December 2023

Figure S1
Figure S1 from TEAD Inhibition Overcomes YAP1/TAZ-Driven Primary and Acquired Resistance to KRASG12C Inhibitors
Authors: Edwards A. Cole , Stalnecker Clint A. , Jean Morales Alexis , Taylor Khalilah E. , Klomp Jennifer E. , Klomp Jeffrey A. , Waters Andrew M. , Sudhakar Niranjan , Hallin Jill , Tang Tracy T. , Olson Peter , Post Leonard , Christensen James G. , Cox Adrienne D. , Der Channing J.
Published: December 2023

Supplementary Figure 1
Supplementary Information from Prostate Cancer Progression Relies on the Mitotic Kinase Citron Kinase
Authors: Rawat Chitra , Ben-Salem Salma , Singh Nidhi , Chauhan Gaurav , Rabljenovic Anja , Vaghela Vishwa , Venkadakrishnan Varadha Balaji , Macdonald Jonathan D. , Dahiya Ujjwal R. , Ghanem Yara , Bachour Salam , Su Yixue , DePriest Adam D. , Lee Sanghee , Muldong Michelle , Kim Hyun-Tae , Kumari Sangeeta , Valenzuela Malyn May , Zhang Dingxiao , Hu Qiang , Cortes Gomez Eduardo , Dehm Scott M. , Zoubeidi Amina , Jamieson Christina A.M. , Nicolas Marlo , McKenney Jesse , Willard Belinda , Klein Eric A. , Magi-Galluzzi Cristina , Stauffer Shaun R. , Liu Song , Heemers Hannelore V.
Published: December 2023

Supplementary Information file
Supplementary Figure 4 from Prostate Cancer Progression Relies on the Mitotic Kinase Citron Kinase
Authors: Rawat Chitra , Ben-Salem Salma , Singh Nidhi , Chauhan Gaurav , Rabljenovic Anja , Vaghela Vishwa , Venkadakrishnan Varadha Balaji , Macdonald Jonathan D. , Dahiya Ujjwal R. , Ghanem Yara , Bachour Salam , Su Yixue , DePriest Adam D. , Lee Sanghee , Muldong Michelle , Kim Hyun-Tae , Kumari Sangeeta , Valenzuela Malyn May , Zhang Dingxiao , Hu Qiang , Cortes Gomez Eduardo , Dehm Scott M. , Zoubeidi Amina , Jamieson Christina A.M. , Nicolas Marlo , McKenney Jesse , Willard Belinda , Klein Eric A. , Magi-Galluzzi Cristina , Stauffer Shaun R. , Liu Song , Heemers Hannelore V.
Published: December 2023

Supplementary Figure 4
Table S1 from Combining the Tyrosine Kinase Inhibitor Cabozantinib and the mTORC1/2 Inhibitor Sapanisertib Blocks ERK Pathway Activity and Suppresses Tumor Growth in Renal Cell Carcinoma
Authors: Wu Yige , Chen Siqi , Yang Xiaolu , Sato Kazuhito , Lal Preet , Wang Yuefan , Shinkle Andrew T. , Wendl Michael C. , Primeau Tina M. , Zhao Yanyan , Gould Alanna , Sun Hua , Mudd Jacqueline L. , Hoog Jeremy , Mashl R. Jay , Wyczalkowski Matthew A. , Mo Chia-Kuei , Liu Ruiyang , Herndon John M. , Davies Sherri R. , Liu Di , Ding Xi , Evrard Yvonne A. , Welm Bryan E. , Lum David , Koh Mei Yee , Welm Alana L. , Chuang Jeffrey H. , Moscow Jeffrey A. , Meric-Bernstam Funda , Govindan Ramaswamy , Li Shunqiang , Hsieh James , Fields Ryan C. , Lim Kian-Huat , Ma Cynthia X. , Zhang Hui , Ding Li , Chen Feng
Published: December 2023

Clinical information for the patients and corresponding tumors
Supplementary Figure 3 from Prostate Cancer Progression Relies on the Mitotic Kinase Citron Kinase
Authors: Rawat Chitra , Ben-Salem Salma , Singh Nidhi , Chauhan Gaurav , Rabljenovic Anja , Vaghela Vishwa , Venkadakrishnan Varadha Balaji , Macdonald Jonathan D. , Dahiya Ujjwal R. , Ghanem Yara , Bachour Salam , Su Yixue , DePriest Adam D. , Lee Sanghee , Muldong Michelle , Kim Hyun-Tae , Kumari Sangeeta , Valenzuela Malyn May , Zhang Dingxiao , Hu Qiang , Cortes Gomez Eduardo , Dehm Scott M. , Zoubeidi Amina , Jamieson Christina A.M. , Nicolas Marlo , McKenney Jesse , Willard Belinda , Klein Eric A. , Magi-Galluzzi Cristina , Stauffer Shaun R. , Liu Song , Heemers Hannelore V.
Published: December 2023

Supplementary Figure 3
Supplementary Figure 1 from Prostate Cancer Progression Relies on the Mitotic Kinase Citron Kinase
Authors: Rawat Chitra , Ben-Salem Salma , Singh Nidhi , Chauhan Gaurav , Rabljenovic Anja , Vaghela Vishwa , Venkadakrishnan Varadha Balaji , Macdonald Jonathan D. , Dahiya Ujjwal R. , Ghanem Yara , Bachour Salam , Su Yixue , DePriest Adam D. , Lee Sanghee , Muldong Michelle , Kim Hyun-Tae , Kumari Sangeeta , Valenzuela Malyn May , Zhang Dingxiao , Hu Qiang , Cortes Gomez Eduardo , Dehm Scott M. , Zoubeidi Amina , Jamieson Christina A.M. , Nicolas Marlo , McKenney Jesse , Willard Belinda , Klein Eric A. , Magi-Galluzzi Cristina , Stauffer Shaun R. , Liu Song , Heemers Hannelore V.
Published: December 2023

Supplementary Figure 1
Supplementary Table S5 from Genome-Wide CRISPR Screens Identify Multiple Synthetic Lethal Targets That Enhance KRASG12C Inhibitor Efficacy
Authors: Mukhopadhyay Suman , Huang Hsin-Yi , Lin Ziyan , Ranieri Michela , Li Shuai , Sahu Soumyadip , Liu Yingzhuo , Ban Yi , Guidry Kayla , Hu Hai , Lopez Alfonso , Sherman Fiona , Tan Yi Jer , Lee Yeuan Ting , Armstrong Amanda P. , Dolgalev Igor , Sahu Priyanka , Zhang Tinghu , Lu Wenchao , Gray Nathanael S. , Christensen James G. , Tang Tracy T. , Velcheti Vamsidhar , Khodadadi-Jamayran Alireza , Wong Kwok-Kin , Neel Benjamin G.
Published: December 2023

Supplementary Table S5
MaGeCK analysis of TNO155 CRISPR/Cas9 screens of NSCLC cell lines
Supplementary Table S2 from Genome-Wide CRISPR Screens Identify Multiple Synthetic Lethal Targets That Enhance KRASG12C Inhibitor Efficacy
Authors: Mukhopadhyay Suman , Huang Hsin-Yi , Lin Ziyan , Ranieri Michela , Li Shuai , Sahu Soumyadip , Liu Yingzhuo , Ban Yi , Guidry Kayla , Hu Hai , Lopez Alfonso , Sherman Fiona , Tan Yi Jer , Lee Yeuan Ting , Armstrong Amanda P. , Dolgalev Igor , Sahu Priyanka , Zhang Tinghu , Lu Wenchao , Gray Nathanael S. , Christensen James G. , Tang Tracy T. , Velcheti Vamsidhar , Khodadadi-Jamayran Alireza , Wong Kwok-Kin , Neel Benjamin G.
Published: December 2023

Supplementary Table S2
Overlapping dropouts (FDR <0.1) from MRTX-849 CRISPR/Cas9 screens in NSCLC cell lines
Supplementary Table S10 from Genome-Wide CRISPR Screens Identify Multiple Synthetic Lethal Targets That Enhance KRASG12C Inhibitor Efficacy
Authors: Mukhopadhyay Suman , Huang Hsin-Yi , Lin Ziyan , Ranieri Michela , Li Shuai , Sahu Soumyadip , Liu Yingzhuo , Ban Yi , Guidry Kayla , Hu Hai , Lopez Alfonso , Sherman Fiona , Tan Yi Jer , Lee Yeuan Ting , Armstrong Amanda P. , Dolgalev Igor , Sahu Priyanka , Zhang Tinghu , Lu Wenchao , Gray Nathanael S. , Christensen James G. , Tang Tracy T. , Velcheti Vamsidhar , Khodadadi-Jamayran Alireza , Wong Kwok-Kin , Neel Benjamin G.
Published: December 2023

Supplementary Table S10
Differential gene expression analysis of scRNA-seq data from tumor cluster in patient #1778 (AMG-510-resistant tumor) vs patient #1566 (control, KRASG12V tumor)
Data from A New Class of Quinoline-Based DNA Hypomethylating Agents Reactivates Tumor Suppressor Genes by Blocking DNA Methyltransferase 1 Activity and Inducing Its Degradation
Authors: Datta Jharna , Ghoshal Kalpana , Denny William A. , Gamage Swarna A. , Brooke Darby G. , Phiasivongsa Pasit , Redkar Sanjeev , Jacob Samson T.
Published: December 2023

Abstract
Reactivation of silenced tumor suppressor genes by 5-azacytidine (Vidaza) and its congener 5-aza-2′-deoxycytidine (decitabine) has provided an alternate approach to cancer therapy. We have shown previously that these drugs selectively and rapidly induce degradation of the maintenance DNA methyltransferase (DNMT) 1 by a proteasomal pathway. Because the toxicity of these compounds is largely due to their incorporation into DNA, it is critical to explore novel, nonnucleoside compounds that can effectively reactivate the silenced genes. Here, we report that a quinoline-based compound, designated SGI-1027, inhibits the activity of DNMT1, DNMT3A, and DNMT3B as well M. SssI with comparable IC50 (6-13 μmol/L) by competing with S-adenosylmethionine in the methylation reaction. Treatment of different cancer cell lines with SGI-1027 resulted in selective degradation of DNMT1 with minimal or no effects on DNMT3A and DNMT3B. At a concentration of 2.5 to 5 μmol/L (similar to that of decitabine), complete degradation of DNMT1 protein was achieved within 24 h without significantly affecting its mRNA level. MG132 blocked SGI-1027–induced depletion of DNMT1, indicating the involvement of proteasomal pathway. Prolonged treatment of RKO cells with SGI-1027 led to demethylation and reexpression of the silenced tumor suppressor genes P16, MLH1, and TIMP3. Further, this compound did not exhibit significant toxicity in a rat hepatoma (H4IIE) cell line. This study provides a novel class of DNA hypomethylating agents that have the potential for use in epigenetic cancer therapy. [Cancer Res 2009;69(10):4277–85]
Data from LILRB3 Modulates Acute Myeloid Leukemia Progression and Acts as an Effective Target for CAR T-cell Therapy
Authors: Mai Sunny , Hodges Alan , Chen Hui-Ming , Zhang Jilu , Wang Yi-Ling , Liu Yongbin , Nakatsu Fumiko , Wang Xiaoxuan , Fang Jing , Xu Yitian , Davidov Vitaliy , Kang Kyeongah , Pingali Sai Ravi , Ganguly Siddhartha , Suzuki Masataka , Konopleva Marina , Prinzing Brooke , Zu Youli , Gottschalk Stephen , Lu Yong , Chen Shu-Hsia , Pan Ping-Ying
Published: December 2023

Abstract
Identifying novel cell surface receptors that regulate leukemia cell differentiation and can be targeted to inhibit cellular proliferation is crucial to improve current treatment modalities in acute myeloid leukemia (AML), especially for relapsed or chemotherapy-refractory leukemia. Leukocyte immunoglobulin-like receptor type B (LILRB) is an immunomodulatory receptor originally found to be expressed in myeloid cells. In this study, we found that LILRB receptors can be induced under inflammatory stimuli and chemotherapy treatment conditions. Blockade of LILRB3 inhibited leukemia cell proliferation and leukemia progression. In addition, treatment with LILRB3 blocking antibodies upregulated myeloid lineage differentiation transcription factors, including PU.1, C/EBP family, and IRF, whereas phosphorylation of proliferation regulators, for example, AKT, cyclin D1, and retinoblastoma protein, was decreased. Conversely, transcriptomic analysis showed LILRB3 activation by agonist antibodies may enhance leukemia survival through upregulation of cholesterol metabolism, which has been shown to promote leukemia cell survival. Moreover, LILRB3-targeted CAR T cells exhibited potent antitumor effects both in vitro and in vivo. Taken together, our results suggest that LILRB3 is a potentially potent target for multiple treatment modalities in AML.
Significance:
LILRB3 regulates differentiation and proliferation in acute myeloid leukemia and can be targeted with monoclonal antibodies and CAR T cells to suppress leukemia growth.
Data from FGFR3 Alterations in Bladder Cancer Stimulate Serine Synthesis to Induce Immune-Inert Macrophages That Suppress T-cell Recruitment and Activation
Authors: Ouyang Yi , Ou Ziwei , Zhong Wenlong , Yang Jin , Fu Sha , Ouyang Nengtai , Chen Junyu , Xu Longhao , Wu Daqin , Qian Junan , Lin Yi , Lin Tianxin , Huang Jian
Published: December 2023

Abstract
FGFR3 alterations are common in patients with bladder cancer. While the FGFR tyrosine kinase inhibitor erdafitinib has been approved as a targeted therapy for patients with FGFR3-altered (aFGFR3) bladder cancer, the response rate remains suboptimal, prompting development of strategies to improve treatment response. Here, we observed an immune-desert tumor microenvironment (TME) phenotype in human aFGFR3 bladder cancer and demonstrated that mutant FGFR3 indirectly induces a “cold” TME in mouse bladder cancer models. Single-cell RNA sequencing revealed the central role of macrophages in inducing the cold TME of aFGFR3 tumors. Macrophages in aFGFR3 tumors exhibited reduced T-cell recruitment and antigen presentation capabilities. Increased serine synthesis in bladder cancer cells that was induced by mutant FGFR3 activated the PI3K/Akt pathway in macrophages, shifting them to an immune-inert phenotype. Targeting PI3K in aFGFR3 tumors with duvelisib achieved promising efficacy by reversing the macrophage phenotype, and combination therapy with duvelisib and erdafitinib demonstrated increased antitumor activity. Overall, these findings reveal the critical role of enhanced serine synthesis efflux from cancer cells with mutant FGFR3 in shifting macrophages to an immune-inert phenotype. Reversing the macrophage phenotype holds promise for enhancing erdafitinib efficacy.
Significance:
Metabolic reprogramming of bladder cancer cells driven by mutant FGFR3 increases serine synthesis that suppresses macrophage immunostimulatory functions to generate an immunosuppressive TME, which can be overcome by targeting PI3K.
Data from TEAD Inhibition Overcomes YAP1/TAZ-Driven Primary and Acquired Resistance to KRASG12C Inhibitors
Authors: Edwards A. Cole , Stalnecker Clint A. , Jean Morales Alexis , Taylor Khalilah E. , Klomp Jennifer E. , Klomp Jeffrey A. , Waters Andrew M. , Sudhakar Niranjan , Hallin Jill , Tang Tracy T. , Olson Peter , Post Leonard , Christensen James G. , Cox Adrienne D. , Der Channing J.
Published: December 2023

Abstract
Primary/intrinsic and treatment-induced acquired resistance limit the initial response rate to and long-term efficacy of direct inhibitors of the KRASG12C mutant in cancer. To identify potential mechanisms of resistance, we applied a CRISPR/Cas9 loss-of-function screen and observed loss of multiple components of the Hippo tumor suppressor pathway, which acts to suppress YAP1/TAZ-regulated gene transcription. YAP1/TAZ activation impaired the antiproliferative and proapoptotic effects of KRASG12C inhibitor (G12Ci) treatment in KRASG12C-mutant cancer cell lines. Conversely, genetic suppression of YAP1/WWTR1 (TAZ) enhanced G12Ci sensitivity. YAP1/TAZ activity overcame KRAS dependency through two distinct TEAD transcription factor–dependent mechanisms, which phenocopy KRAS effector signaling. First, TEAD stimulated ERK-independent transcription of genes normally regulated by ERK (BIRC5, CDC20, ECT2, FOSL1, and MYC) to promote progression through the cell cycle. Second, TEAD caused activation of PI3K–AKT–mTOR signaling to overcome apoptosis. G12Ci treatment-induced acquired resistance was also caused by YAP1/TAZ-TEAD activation. Accordingly, concurrent treatment with pharmacologic inhibitors of TEAD synergistically enhanced KRASG12C inhibitor antitumor activity in vitro and prolonged tumor suppression in vivo. In summary, these observations reveal YAP1/TAZ-TEAD signaling as a crucial driver of primary and acquired resistance to KRAS inhibition and support the use of TEAD inhibitors to enhance the antitumor efficacy of KRAS-targeted therapies.
Significance:
YAP1/TAZ-TEAD activation compensates for loss of KRAS effector signaling, establishing a mechanistic basis for concurrent inhibition of TEAD to enhance the efficacy of KRASG12C-selective inhibitor treatment of KRASG12C-mutant cancers.

See related commentary by Johnson and Haigis, p. 4005
Data from Prostate Cancer Progression Relies on the Mitotic Kinase Citron Kinase
Authors: Rawat Chitra , Ben-Salem Salma , Singh Nidhi , Chauhan Gaurav , Rabljenovic Anja , Vaghela Vishwa , Venkadakrishnan Varadha Balaji , Macdonald Jonathan D. , Dahiya Ujjwal R. , Ghanem Yara , Bachour Salam , Su Yixue , DePriest Adam D. , Lee Sanghee , Muldong Michelle , Kim Hyun-Tae , Kumari Sangeeta , Valenzuela Malyn May , Zhang Dingxiao , Hu Qiang , Cortes Gomez Eduardo , Dehm Scott M. , Zoubeidi Amina , Jamieson Christina A.M. , Nicolas Marlo , McKenney Jesse , Willard Belinda , Klein Eric A. , Magi-Galluzzi Cristina , Stauffer Shaun R. , Liu Song , Heemers Hannelore V.
Published: December 2023

Abstract
Prostate cancer remains the second leading cause of cancer death in men in Western cultures. A deeper understanding of the mechanisms by which prostate cancer cells divide to support tumor growth could help devise strategies to overcome treatment resistance and improve survival. Here, we identified that the mitotic AGC family protein kinase citron kinase (CIT) is a pivotal regulator of prostate cancer growth that mediates prostate cancer cell interphase progression. Increased CIT expression correlated with prostate cancer growth induction and aggressive prostate cancer progression, and CIT was overexpressed in prostate cancer compared with benign prostate tissue. CIT overexpression was controlled by an E2F2–Skp2–p27 signaling axis and conferred resistance to androgen-targeted treatment strategies. The effects of CIT relied entirely on its kinase activity. Conversely, CIT silencing inhibited the growth of cell lines and xenografts representing different stages of prostate cancer progression and treatment resistance but did not affect benign epithelial prostate cells or nonprostatic normal cells, indicating a potential therapeutic window for CIT inhibition. CIT kinase activity was identified as druggable and was potently inhibited by the multikinase inhibitor OTS-167, which decreased the proliferation of treatment-resistant prostate cancer cells and patient-derived organoids. Isolation of the in vivo CIT substrates identified proteins involved in diverse cellular functions ranging from proliferation to alternative splicing events that are enriched in treatment-resistant prostate cancer. These findings provide insights into the regulation of aggressive prostate cancer cell behavior by CIT and identify CIT as a functionally diverse and druggable driver of prostate cancer progression.
Significance:
The poorly characterized protein kinase citron kinase is a therapeutic target in prostate cancer that drives tumor growth by regulating diverse substrates, which control several hallmarks of aggressive prostate cancer progression.

See related commentary by Mishra et al., p. 4008
LILRB3 Modulates Acute Myeloid Leukemia Progression and Acts as an Effective Target for CAR T-cell Therapy
Authors: Mai Sunny , Hodges Alan , Chen Hui-Ming , Zhang Jilu , Wang Yi-Ling , Liu Yongbin , Nakatsu Fumiko , Wang Xiaoxuan , Fang Jing , Xu Yitian , Davidov Vitaliy , Kang Kyeongah , Pingali Sai Ravi , Ganguly Siddhartha , Suzuki Masataka , Konopleva Marina , Prinzing Brooke , Zu Youli , Gottschalk Stephen , Lu Yong , Chen Shu-Hsia , Pan Ping-Ying
Published: December 2023

Identifying novel cell surface receptors that regulate leukemia cell differentiation and can be targeted to inhibit cellular proliferation is crucial to improve current treatment modalities in acute myeloid leukemia (AML), especially for relapsed or chemotherapy-refractory leukemia. Leukocyte immunoglobulin-like receptor type B (LILRB) is an immunomodulatory receptor originally found to be expressed in myeloid cells. In this study, we found that LILRB receptors can be induced under inflammatory stimuli and chemotherapy treatment conditions. Blockade of LILRB3 inhibited leukemia cell proliferation and leukemia progression. In addition, treatment with LILRB3 blocking antibodies upregulated myeloid lineage differentiation transcription factors, including PU.1, C/EBP family, and IRF, whereas phosphorylation of proliferation regulators, for example, AKT, cyclin D1, and retinoblastoma protein, was decreased. Conversely, transcriptomic analysis showed LILRB3 activation by agonist antibodies may enhance leukemia survival through upregulation of cholesterol metabolism, which has been shown to promote leukemia cell survival. Moreover, LILRB3-targeted CAR T cells exhibited potent antitumor effects both in vitro and in vivo. Taken together, our results suggest that LILRB3 is a potentially potent target for multiple treatment modalities in AML.

Significance:

LILRB3 regulates differentiation and proliferation in acute myeloid leukemia and can be targeted with monoclonal antibodies and CAR T cells to suppress leukemia growth.
Citron Kinase Is a Druggable Target in Treatment-Resistant Prostate Cancer
Authors: Mishra Rashmi , Blinka Steven , Hsieh Andrew C.
Published: December 2023

Prolonged treatment with androgen deprivation therapy (ADT) inevitably leads to castration-resistant prostate cancer (CRPC). Development of novel androgen-targeting agents and chemo/radiotherapies has resulted in improved survival. However, metastatic CRPC remains incurable. New therapeutics are greatly needed, and exploration of novel pathways such as the mechanisms underlying prostate cancer cell proliferation could potentially augment the natural course of CRPC. In the latest issue of Cancer Research, Rawat and colleagues delved deeply into the mechanistic role of citron kinase (CIT) in orchestrating prostate cancer proliferation and revealed its catalytic activity as a druggable target for treatment-resistant prostate cancer. The researchers utilized in vitro and in vivo methodologies to elucidate the function of CIT in mediating uncontrolled interphase progression and prostate cancer growth. Furthermore, the authors employed both androgen receptor–dependent and independent models to validate the significance of CIT kinase activity as a crucial factor in driving treatment-resistant prostate cancer growth. At a mechanistic level they determined that the E2F2-Skp2-p27 axis regulates CIT expression. Finally, they defined the landscape of CIT substrates in prostate cancer that encompasses a spectrum of cellular functions that spans key proliferation regulators to alternative splicing events. This comprehensive work provides insights into CIT as a potential biomarker for prostate cancer treatment resistance and disease progression and establishes the CIT kinase domain as a druggable target in CRPC.

See related article by Rawat et al., p. 4142
Supplementary Table 1 from Phase I Trial of the Multi-kinase Inhibitor Cabozantinib, a CYP3A4 Substrate, plus CYP3A4-Interacting Antiretroviral Therapy in People Living with HIV and Cancer (AMC-087)
Authors: Haigentz Missak , Lee Jeannette Y. , Chiao Elizabeth Y. , Aboulafia David M. , Ratner Lee , Ambinder Richard F. , Baiocchi Robert A. , Mitsuyasu Ronald T. , Wachsman William , Sparano Joseph A. , Rudek Michelle A.
Published: December 2023

Supplementary Table 1. Representativeness of Study Participants
Supplementary Table S2 from Safety and Efficacy of Tucatinib, Letrozole, and Palbociclib in Patients with Previously Treated HR+/HER2+ Breast Cancer
Authors: Shagisultanova Elena , Gradishar William , Brown-Glaberman Ursa , Chalasani Pavani , Brenner Andrew J. , Stopeck Alison , Parris Hannah , Gao Dexiang , McSpadden Tessa , Mayordomo Jose , Diamond Jennifer R. , Kabos Peter , Borges Virginia F.
Published: December 2023

Serious adverse events
Supplementary Table S1 from Safety and Efficacy of Tucatinib, Letrozole, and Palbociclib in Patients with Previously Treated HR+/HER2+ Breast Cancer
Authors: Shagisultanova Elena , Gradishar William , Brown-Glaberman Ursa , Chalasani Pavani , Brenner Andrew J. , Stopeck Alison , Parris Hannah , Gao Dexiang , McSpadden Tessa , Mayordomo Jose , Diamond Jennifer R. , Kabos Peter , Borges Virginia F.
Published: December 2023

Representativeness of the study participants
Supplementary Fig. S1 from Safety and Efficacy of Tucatinib, Letrozole, and Palbociclib in Patients with Previously Treated HR+/HER2+ Breast Cancer
Authors: Shagisultanova Elena , Gradishar William , Brown-Glaberman Ursa , Chalasani Pavani , Brenner Andrew J. , Stopeck Alison , Parris Hannah , Gao Dexiang , McSpadden Tessa , Mayordomo Jose , Diamond Jennifer R. , Kabos Peter , Borges Virginia F.
Published: December 2023

PK analysis
Supplementary Table S6 from A PERK-Specific Inhibitor Blocks Metastatic Progression by Limiting Integrated Stress Response–Dependent Survival of Quiescent Cancer Cells
Authors: Calvo Veronica , Zheng Wei , Adam-Artigues Anna , Staschke Kirk A. , Huang Xin , Cheung Julie F. , Nobre Ana Rita , Fujisawa Sho , Liu David , Fumagalli Maria , Surguladze David , Stokes Michael E. , Nowacek Ari , Mulvihill Mark , Farias Eduardo F. , Aguirre-Ghiso Julio A.
Published: December 2023

Supplementary Table 6: KINOMEscan™ screening comparison of HC4, HC19, HC28 and GSK-157 at concentrations of 0.1, 1.0 and 10 mM versus select kinases in the HER family signaling pathway
Supplementary Table S1 from A PERK-Specific Inhibitor Blocks Metastatic Progression by Limiting Integrated Stress Response–Dependent Survival of Quiescent Cancer Cells
Authors: Calvo Veronica , Zheng Wei , Adam-Artigues Anna , Staschke Kirk A. , Huang Xin , Cheung Julie F. , Nobre Ana Rita , Fujisawa Sho , Liu David , Fumagalli Maria , Surguladze David , Stokes Michael E. , Nowacek Ari , Mulvihill Mark , Farias Eduardo F. , Aguirre-Ghiso Julio A.
Published: December 2023

Supplementary Table 1 Human breast cancer metastases samples
Supplementary Figure S5 from A PERK-Specific Inhibitor Blocks Metastatic Progression by Limiting Integrated Stress Response–Dependent Survival of Quiescent Cancer Cells
Authors: Calvo Veronica , Zheng Wei , Adam-Artigues Anna , Staschke Kirk A. , Huang Xin , Cheung Julie F. , Nobre Ana Rita , Fujisawa Sho , Liu David , Fumagalli Maria , Surguladze David , Stokes Michael E. , Nowacek Ari , Mulvihill Mark , Farias Eduardo F. , Aguirre-Ghiso Julio A.
Published: December 2023

Supplementary Figure S5. (a) Scoring system used for the quantification of P-HER2 levels in mammary gland tumor sections. The IHC P-HER2positive area was multiplied by its intensity score according to established score shown in these representative images. Scale bar, 100 µm. (b)MCF10A-HER2 cells were starved o/n and treated +/-HC4 (2 µM), after which +/-EGF (100 ng/ml) was added for 20 min before collection. The levelsof P-HER2/Y1112 and P-HER2/Y877 were assessed by Western blot. GAPDH and HSP90 were used as loading controls.
Supplementary Figure S4 from A PERK-Specific Inhibitor Blocks Metastatic Progression by Limiting Integrated Stress Response–Dependent Survival of Quiescent Cancer Cells
Authors: Calvo Veronica , Zheng Wei , Adam-Artigues Anna , Staschke Kirk A. , Huang Xin , Cheung Julie F. , Nobre Ana Rita , Fujisawa Sho , Liu David , Fumagalli Maria , Surguladze David , Stokes Michael E. , Nowacek Ari , Mulvihill Mark , Farias Eduardo F. , Aguirre-Ghiso Julio A.
Published: December 2023

Supplementary Figure S4. (a) Tumor volumes from vehicle- (left) and HC4-treated (right) MMTV-HER2 females. Each line represents a tumor(N=16 per group). (b) Percentage decrease in tumor size in HC4-treated females that showed tumor shrinkage. Each line represents a tumor andanimal (N=4). (c) IHC for P-histone H3 in mammary gland tumor sections in vehicle (N=5) and HC4-treated (N=6) MMTV-HER2 mice. Representativeimages (left) and quantification (right graph). P by Mann-Whitney test. Size bar 50 µm (d) HER2- overexpressing ZR-75-1 cells were seeded onMatrigel and after acinus establishment (day 4) wells were treated with vehicle (control) or HC4 (2 µM) for 10 days. Percentage of cleaved caspase-3positive cells per acini (N=25 per condition) ± s.d. P by Student’s t test. (e) MCF10A-HER2 cells were seeded on Matrigel and after acinusestablishment (day 4) wells were treated with vehicle (control) or HC4 (2 µM) for 10 days. Percentage of P-histone H3-positive cells per acini (N=20)± s.d. P by Student’s t test.
Supplementary Data 1 from Nuclear GRP78 Promotes Metabolic Reprogramming and Therapeutic Resistance in Pancreatic Ductal Adenocarcinoma
Authors: Zhao Tiansuo , Jiang Tingting , Li Xiaojia , Chang Shaofei , Sun Qihui , Kong Fanyang , Kong Xiangyu , Wei Fang , He Jie , Hao Jihui , Xie Keping
Published: December 2023

4 Supplementary Tables
7 Supplementary Figures
Supplementary Table S5 from OvaPrint—A Cell-free DNA Methylation Liquid Biopsy for the Risk Assessment of High-grade Serous Ovarian Cancer
Authors: Buckley David N. , Lewinger Juan Pablo , Gooden Gerald , Spillman Monique , Neuman Monica , Guo X. Mona , Tew Ben Yi , Miller Heather , Khetan Varun U. , Shulman Lee P. , Roman Lynda , Salhia Bodour
Published: December 2023

Table S5: OvaPrint™ risk scores for all cfDNA samples analyzed.
Table summarizes the OvaPrint™ risk classification of all cfDNA samples analyzed. Each row
represents a unique subtype and class, which denotes high-grade, low-grade, and borderline cases.
Totals are annotated in the final row and final column.
Supplementary Table S4 from OvaPrint—A Cell-free DNA Methylation Liquid Biopsy for the Risk Assessment of High-grade Serous Ovarian Cancer
Authors: Buckley David N. , Lewinger Juan Pablo , Gooden Gerald , Spillman Monique , Neuman Monica , Guo X. Mona , Tew Ben Yi , Miller Heather , Khetan Varun U. , Shulman Lee P. , Roman Lynda , Salhia Bodour
Published: December 2023

Table S4: Source of plasma for EOC tumors.
Table summarizes the source of each malignant cfDNA sample with totals annotated in the final row
and final column.
Supplementary Table S2 from The Clinical Implications of Reversions in Patients with Advanced Pancreatic Cancer and Pathogenic Variants in BRCA1, BRCA2, or PALB2 after Progression on Rucaparib
Authors: Brown Timothy J. , Yablonovitch Arielle , Till Jacob E. , Yen Jennifer , Kiedrowski Lesli A. , Hood Ryan , O'Hara Mark H. , Teitelbaum Ursina , Karasic Thomas B. , Schneider Charles , Carpenter Erica L. , Nathanson Katherine , Domchek Susan M. , Reiss Kim A.
Published: December 2023

Patient-level data
Supplementary Table S3 from OvaPrint—A Cell-free DNA Methylation Liquid Biopsy for the Risk Assessment of High-grade Serous Ovarian Cancer
Authors: Buckley David N. , Lewinger Juan Pablo , Gooden Gerald , Spillman Monique , Neuman Monica , Guo X. Mona , Tew Ben Yi , Miller Heather , Khetan Varun U. , Shulman Lee P. , Roman Lynda , Salhia Bodour
Published: December 2023

Table S3: Source of plasma for benign tumors and normal samples.
Table summarizes the source of each benign cfDNA sample with totals annotated in the final row and
final column.
Supplementary Figure S5 from OvaPrint—A Cell-free DNA Methylation Liquid Biopsy for the Risk Assessment of High-grade Serous Ovarian Cancer
Authors: Buckley David N. , Lewinger Juan Pablo , Gooden Gerald , Spillman Monique , Neuman Monica , Guo X. Mona , Tew Ben Yi , Miller Heather , Khetan Varun U. , Shulman Lee P. , Roman Lynda , Salhia Bodour
Published: December 2023

Figure S5: OvaPrint™ analysis of stage IV HGSOC plasma samples
Supplementary Table 6 from Cancer-Associated Fibroblast-Like Tumor Cells Remodel the Ewing Sarcoma Tumor Microenvironment
Authors: Wrenn Emma D. , Apfelbaum April A. , Rudzinski Erin R. , Deng Xuemei , Jiang Wei , Sud Sudha , Van Noord Raelene A. , Newman Erika A. , Garcia Nicolas M. , Miyaki Aya , Hoglund Virginia J. , Bhise Shruti S. , Kanaan Sami B. , Waltner Olivia G. , Furlan Scott N. , Lawlor Elizabeth R.
Published: December 2023

Supplemental Table 6. List of genes that positively correlate with NT5E expression in 3 independent patient tumor cohorts.
Supplementary Table 1 from Cancer-Associated Fibroblast-Like Tumor Cells Remodel the Ewing Sarcoma Tumor Microenvironment
Authors: Wrenn Emma D. , Apfelbaum April A. , Rudzinski Erin R. , Deng Xuemei , Jiang Wei , Sud Sudha , Van Noord Raelene A. , Newman Erika A. , Garcia Nicolas M. , Miyaki Aya , Hoglund Virginia J. , Bhise Shruti S. , Kanaan Sami B. , Waltner Olivia G. , Furlan Scott N. , Lawlor Elizabeth R.
Published: December 2023

Supplemental Table 1. Table of selected reagents and resources used.
Supplemental Figure S5 from Cancer-Associated Fibroblast-Like Tumor Cells Remodel the Ewing Sarcoma Tumor Microenvironment
Authors: Wrenn Emma D. , Apfelbaum April A. , Rudzinski Erin R. , Deng Xuemei , Jiang Wei , Sud Sudha , Van Noord Raelene A. , Newman Erika A. , Garcia Nicolas M. , Miyaki Aya , Hoglund Virginia J. , Bhise Shruti S. , Kanaan Sami B. , Waltner Olivia G. , Furlan Scott N. , Lawlor Elizabeth R.
Published: December 2023

Supplemental Figure S5. Patient tumor gene expression microarrays display heterogeneity of expression of NT5E and associated mesenchymal gene signature. Related to Figure 5.
Supplementary Table S3 from Genomic Tumor Correlates of Clinical Outcomes Following Organ-Sparing Chemoradiation Therapy for Bladder Cancer
Authors: Kamran Sophia C. , Zhou Yuzhen , Otani Keisuke , Drumm Michael , Otani Yukako , Wu Shulin , Wu Chin-Lee , Feldman Adam S. , Wszolek Matthew , Lee Richard J. , Saylor Philip J. , Lennerz Jochen , Van Allen Eliezer , Willers Henning , Hong Theodore S. , Liu Yang , Davicioni Elai , Gibb Ewan A. , Shipley William U. , Mouw Kent W. , Efstathiou Jason A. , Miyamoto David T.
Published: December 2023

Association of Alliance/RETAIN Trial DDR Genes with Loss-of-function as per OncoKB with Clinical Outcomes following TMT
Supplemental Figure S4 from Cancer-Associated Fibroblast-Like Tumor Cells Remodel the Ewing Sarcoma Tumor Microenvironment
Authors: Wrenn Emma D. , Apfelbaum April A. , Rudzinski Erin R. , Deng Xuemei , Jiang Wei , Sud Sudha , Van Noord Raelene A. , Newman Erika A. , Garcia Nicolas M. , Miyaki Aya , Hoglund Virginia J. , Bhise Shruti S. , Kanaan Sami B. , Waltner Olivia G. , Furlan Scott N. , Lawlor Elizabeth R.
Published: December 2023

Supplemental Figure S4. RNA vs. protein concordance in DSP ROIs. Related to Figure 4.
Supplemental Figure S1 from Cancer-Associated Fibroblast-Like Tumor Cells Remodel the Ewing Sarcoma Tumor Microenvironment
Authors: Wrenn Emma D. , Apfelbaum April A. , Rudzinski Erin R. , Deng Xuemei , Jiang Wei , Sud Sudha , Van Noord Raelene A. , Newman Erika A. , Garcia Nicolas M. , Miyaki Aya , Hoglund Virginia J. , Bhise Shruti S. , Kanaan Sami B. , Waltner Olivia G. , Furlan Scott N. , Lawlor Elizabeth R.
Published: December 2023

Supplemental Figure S1. CD73+ EwS cells retain proliferative and tumorigenic capacity. Related to Figure 1.
Supplementary Figure S7 from Genomic Tumor Correlates of Clinical Outcomes Following Organ-Sparing Chemoradiation Therapy for Bladder Cancer
Authors: Kamran Sophia C. , Zhou Yuzhen , Otani Keisuke , Drumm Michael , Otani Yukako , Wu Shulin , Wu Chin-Lee , Feldman Adam S. , Wszolek Matthew , Lee Richard J. , Saylor Philip J. , Lennerz Jochen , Van Allen Eliezer , Willers Henning , Hong Theodore S. , Liu Yang , Davicioni Elai , Gibb Ewan A. , Shipley William U. , Mouw Kent W. , Efstathiou Jason A. , Miyamoto David T.
Published: December 2023

Clinical outcomes of the entire cohort.