bluuebunny/crossref_metadata_2025 huggingface dataset:
Supplementary Table 8 from Clinical and Genomic Features of Classical and Basal Transcriptional Subtypes in Pancreatic Cancer
Authors: Singh Harshabad , Xiu Joanne , Kapner Kevin S. , Yuan Chen , Narayan Raja R. , Oberley Matthew , Farrell Alex , Surana Rishi , Huffman Brandon M. , Perez Kimberly , Cleary James M. , Jordan Alexander C. , Dias Costa Andressa , Williams Hannah L. , Raghavan Srivatsan , Weinberg Benjamin , Pishvaian Michael J. , Shroff Rachna T. , Goel Sanjay , Dougan Stephanie K. , Nowak Jonathan A. , Spetzler David , Sledge George , Wolpin Brian M. , Aguirre Andrew J.
Published: November 2024

Supplementary Table 8
Supplementary Table 7 from Clinical and Genomic Features of Classical and Basal Transcriptional Subtypes in Pancreatic Cancer
Authors: Singh Harshabad , Xiu Joanne , Kapner Kevin S. , Yuan Chen , Narayan Raja R. , Oberley Matthew , Farrell Alex , Surana Rishi , Huffman Brandon M. , Perez Kimberly , Cleary James M. , Jordan Alexander C. , Dias Costa Andressa , Williams Hannah L. , Raghavan Srivatsan , Weinberg Benjamin , Pishvaian Michael J. , Shroff Rachna T. , Goel Sanjay , Dougan Stephanie K. , Nowak Jonathan A. , Spetzler David , Sledge George , Wolpin Brian M. , Aguirre Andrew J.
Published: November 2024

Supplementary Table 7
Supplementary Figures 1 from Clinical and Genomic Features of Classical and Basal Transcriptional Subtypes in Pancreatic Cancer
Authors: Singh Harshabad , Xiu Joanne , Kapner Kevin S. , Yuan Chen , Narayan Raja R. , Oberley Matthew , Farrell Alex , Surana Rishi , Huffman Brandon M. , Perez Kimberly , Cleary James M. , Jordan Alexander C. , Dias Costa Andressa , Williams Hannah L. , Raghavan Srivatsan , Weinberg Benjamin , Pishvaian Michael J. , Shroff Rachna T. , Goel Sanjay , Dougan Stephanie K. , Nowak Jonathan A. , Spetzler David , Sledge George , Wolpin Brian M. , Aguirre Andrew J.
Published: November 2024

Supplementary Figures
Supplementary Table S7 from Exploiting WEE1 Kinase Activity as FUS::DDIT3-Dependent Therapeutic Vulnerability in Myxoid Liposarcoma
Authors: Heinst Lorena , Lee Kwang Seok , Berthold Ruth , Isfort Ilka , Wosnig Svenja , Kuntze Anna , Hafner Susanne , Altvater Bianca , Rossig Claudia , Åman Pierre , Wardelmann Eva , Scholl Claudia , Hartmann Wolfgang , Fröhling Stefan , Trautmann Marcel
Published: November 2024

Supplementary Table S7. Densitometric analysis of western blot results (Supplementary figure S2). Dose-dependent sensitivity of MLS cells to pharmacologic inhibition of WEE1 activity and cellular localization.
Supplementary Table S3 from Exploiting WEE1 Kinase Activity as FUS::DDIT3-Dependent Therapeutic Vulnerability in Myxoid Liposarcoma
Authors: Heinst Lorena , Lee Kwang Seok , Berthold Ruth , Isfort Ilka , Wosnig Svenja , Kuntze Anna , Hafner Susanne , Altvater Bianca , Rossig Claudia , Åman Pierre , Wardelmann Eva , Scholl Claudia , Hartmann Wolfgang , Fröhling Stefan , Trautmann Marcel
Published: November 2024

Supplementary Table S3. Individual clinicopathological characteristics and semi-quantitative immunohistochemistry results of MLS patients (n=49).
Supplementary Figure S5 from Exploiting WEE1 Kinase Activity as FUS::DDIT3-Dependent Therapeutic Vulnerability in Myxoid Liposarcoma
Authors: Heinst Lorena , Lee Kwang Seok , Berthold Ruth , Isfort Ilka , Wosnig Svenja , Kuntze Anna , Hafner Susanne , Altvater Bianca , Rossig Claudia , Åman Pierre , Wardelmann Eva , Scholl Claudia , Hartmann Wolfgang , Fröhling Stefan , Trautmann Marcel
Published: November 2024

Supplementary Figure S5. Causal relationship between FUS::DDIT3-modulated G1/S cell cycle checkpoint regulation and requirement for WEE1 activity.
Supplementary Figure S1 from Exploiting WEE1 Kinase Activity as FUS::DDIT3-Dependent Therapeutic Vulnerability in Myxoid Liposarcoma
Authors: Heinst Lorena , Lee Kwang Seok , Berthold Ruth , Isfort Ilka , Wosnig Svenja , Kuntze Anna , Hafner Susanne , Altvater Bianca , Rossig Claudia , Åman Pierre , Wardelmann Eva , Scholl Claudia , Hartmann Wolfgang , Fröhling Stefan , Trautmann Marcel
Published: November 2024

Supplementary Figure S1. WEE 1 expression correlates with histological grade of MLS.
Supplementary Table S1 from A Histopathologic Correlation Study Evaluating Glymphatic Function in Brain Tumors by Multiparametric MRI
Authors: Gao Min , Liu Zhengliang , Zang Hongjing , Wu Xiong , Yan Yizhong , Lin Hai , Yuan Jianmin , Liu Tianming , Zhou Yu , Liu Jun
Published: November 2024

Supplementary Table S1. Representativeness of Study Participants: Brain tumor (HGG/Metastasis/Meningioma).
Supplementary Materials S1 from A Histopathologic Correlation Study Evaluating Glymphatic Function in Brain Tumors by Multiparametric MRI
Authors: Gao Min , Liu Zhengliang , Zang Hongjing , Wu Xiong , Yan Yizhong , Lin Hai , Yuan Jianmin , Liu Tianming , Zhou Yu , Liu Jun
Published: November 2024

Supplementary Materials S1. The details of MR scanning protocols.
Supplementary Table S4 from FDA Approval Summary: Enfortumab Vedotin plus Pembrolizumab for Locally Advanced or Metastatic Urothelial Carcinoma
Authors: Brave Michael H. , Maguire William F. , Weinstock Chana , Zhang Hui , Gao Xin , Li Fang , Yu Jingyu , Fu Wentao , Zhao Hong , Pierce William F. , Chang Elaine , Dinin Jeannette , Fiero Mallorie H. , Rahman Nam Atiqur , Tang Shenghui , Pazdur Richard , Kluetz Paul G. , Amiri-Kordestani Laleh , Suzman Daniel L.
Published: November 2024

PFS and OS by Availability of Post-Protocol Avelumab and EV
Supplementary Figure S2 from FDA Approval Summary: Enfortumab Vedotin plus Pembrolizumab for Locally Advanced or Metastatic Urothelial Carcinoma
Authors: Brave Michael H. , Maguire William F. , Weinstock Chana , Zhang Hui , Gao Xin , Li Fang , Yu Jingyu , Fu Wentao , Zhao Hong , Pierce William F. , Chang Elaine , Dinin Jeannette , Fiero Mallorie H. , Rahman Nam Atiqur , Tang Shenghui , Pazdur Richard , Kluetz Paul G. , Amiri-Kordestani Laleh , Suzman Daniel L.
Published: November 2024

Kaplan-Meier curves of overall survival in EV-302
Supplementary Table S4 from Understanding and Overcoming Resistance to Selective FGFR Inhibitors across FGFR2-Driven Malignancies
Authors: Facchinetti Francesco , Loriot Yohann , Brayé Floriane , Vasseur Damien , Bahleda Rastislav , Bigot Ludovic , Barbé Rémy , Nobre Catline , Combarel David , Michiels Stefan , Italiano Antoine , Smolenschi Cristina , Tselikas Lambros , Scoazec Jean-Yves , Ponce-Aix Santiago , Besse Benjamin , André Fabrice , Olaussen Ken A. , Hollebecque Antoine , Friboulet Luc
Published: November 2024

Outcomes among patients suffering from intrahepatic cholangiocarcinoma, treated with either reversible FGFR inhibitors or the irreversible agent futibatinib.
Supplementary Table S3 from The Immune-Related 27-Gene Signature DetermaIO Predicts Response to Neoadjuvant Atezolizumab plus Chemotherapy in Triple-Negative Breast Cancer
Authors: Dugo Matteo , Huang Chiun-Sheng , Egle Daniel , Bermejo Begoña , Zamagni Claudio , Seitz Robert S. , Nielsen Tyler J. , Thill Marc , Antón-Torres Antonio , Russo Stefania , Ciruelos Eva Maria , Schweitzer Brock L. , Ross Douglas T. , Galbardi Barbara , Greil Richard , Semiglazov Vladimir , Gyorffy Balázs , Colleoni Marco , Kelly Catherine M. , Mariani Gabriella , Del Mastro Lucia , Blasi Olivia , Callari Maurizio , Pusztai Lajos , Valagussa Pinuccia , Viale Giuseppe , Gianni Luca , Bianchini Giampaolo
Published: November 2024

Supplementary Table 3. Univariate and multivariable regression of pCR according to NGS-based IO score in the RNA-Seq cohort.
Supplementary Figure S5 from The Immune-Related 27-Gene Signature DetermaIO Predicts Response to Neoadjuvant Atezolizumab plus Chemotherapy in Triple-Negative Breast Cancer
Authors: Dugo Matteo , Huang Chiun-Sheng , Egle Daniel , Bermejo Begoña , Zamagni Claudio , Seitz Robert S. , Nielsen Tyler J. , Thill Marc , Antón-Torres Antonio , Russo Stefania , Ciruelos Eva Maria , Schweitzer Brock L. , Ross Douglas T. , Galbardi Barbara , Greil Richard , Semiglazov Vladimir , Gyorffy Balázs , Colleoni Marco , Kelly Catherine M. , Mariani Gabriella , Del Mastro Lucia , Blasi Olivia , Callari Maurizio , Pusztai Lajos , Valagussa Pinuccia , Viale Giuseppe , Gianni Luca , Bianchini Giampaolo
Published: November 2024

Supplementary Figure 5. Comparison of IO score with additional immune signatures. A) Correlation of RT-qPCR and RNA-Seq continuous IO score in the respective NeoTRIP cohorts with previously published immune signatures; B) Comparison of univariate logistic regression models for IO score and additional immune signatures evaluated in the NeoTRIP RT-qPCR and RNA-Seq cohorts. Odds ratio (OR) and 95% confidence intervals are shown. P-values for the interaction test with treatment arm are reported. Asterisks highlight a p-value < 0.05 for the univariate logistic regression model in the specific arm.
Supplementary Figure S7 from Genetic Screen in a Preclinical Model of Sarcoma Development Defines Drivers and Therapeutic Vulnerabilities
Authors: Freeland Jack , Muñoz Maria , O’Donnell Edmond , Langerman Justin , Darrow Morgan , Bergonio Jessica , Suarez-Navarro Julissa , Thorpe Steven , Canter Robert , Randall Robert Lor , Plath Kathrin , Carraway Kermit L. , Witte Owen N. , Graeber Thomas G. , Carr-Ascher Janai R.
Published: November 2024

Additional Analysis of TCGA Data.
Supplementary figure 3 from Incorporating Supramaximal Resection into Survival Stratification of IDH-wildtype Glioblastoma: A Refined Multi-institutional Recursive Partitioning Analysis
Authors: Park Yae Won , Choi Kyu Sung , Foltyn-Dumitru Martha , Brugnara Gianluca , Banan Rouzbeh , Kim Sooyon , Han Kyunghwa , Park Ji Eun , Kessler Tobias , Bendszus Martin , Krieg Sandro , Wick Wolfgang , Sahm Felix , Choi Seung Hong , Kim Ho Sung , Chang Jong Hee , Kim Se Hoon , Wongsawaeng Doonyaporn , Pollock Jeffrey Michael , Lee Seung-Koo , Barajas Ramon Francisco , Vollmuth Philipp , Ahn Sung Soo
Published: November 2024

Supplementary figure 3
Supplementary figure 1 from Incorporating Supramaximal Resection into Survival Stratification of IDH-wildtype Glioblastoma: A Refined Multi-institutional Recursive Partitioning Analysis
Authors: Park Yae Won , Choi Kyu Sung , Foltyn-Dumitru Martha , Brugnara Gianluca , Banan Rouzbeh , Kim Sooyon , Han Kyunghwa , Park Ji Eun , Kessler Tobias , Bendszus Martin , Krieg Sandro , Wick Wolfgang , Sahm Felix , Choi Seung Hong , Kim Ho Sung , Chang Jong Hee , Kim Se Hoon , Wongsawaeng Doonyaporn , Pollock Jeffrey Michael , Lee Seung-Koo , Barajas Ramon Francisco , Vollmuth Philipp , Ahn Sung Soo
Published: November 2024

Supplementary figure 1
Supplementary Figure S4 from Genetic Screen in a Preclinical Model of Sarcoma Development Defines Drivers and Therapeutic Vulnerabilities
Authors: Freeland Jack , Muñoz Maria , O’Donnell Edmond , Langerman Justin , Darrow Morgan , Bergonio Jessica , Suarez-Navarro Julissa , Thorpe Steven , Canter Robert , Randall Robert Lor , Plath Kathrin , Carraway Kermit L. , Witte Owen N. , Graeber Thomas G. , Carr-Ascher Janai R.
Published: November 2024

Chromosome Specific CNV
Supplementary Figure S1 from Genetic Screen in a Preclinical Model of Sarcoma Development Defines Drivers and Therapeutic Vulnerabilities
Authors: Freeland Jack , Muñoz Maria , O’Donnell Edmond , Langerman Justin , Darrow Morgan , Bergonio Jessica , Suarez-Navarro Julissa , Thorpe Steven , Canter Robert , Randall Robert Lor , Plath Kathrin , Carraway Kermit L. , Witte Owen N. , Graeber Thomas G. , Carr-Ascher Janai R.
Published: November 2024

Creation of Cell Lines Targeting RB1 and TP53
Supplementary Table S5 from Multiomics Profiling Distinguishes Sebaceous Carcinoma from Benign Sebaceous Neoplasms and Provides Insight into the Genetic Evolution of Sebaceous Carcinogenesis
Authors: Starrett Gabriel J. , Baikie Brittany C. , Stoff Benjamin K. , Grossniklaus Hans E. , Van Buren Inga , Berry Elizabeth G. , Novoa Roberto A. , Rieger Kerri E. , Sarin Kavita Y. , Lynch Charles F. , Royer Michael C. , Piaskowski Mary L. , Brownell Isaac , Chu Emily Y. , Godse Rama , Chen Suephy C. , Yu Kelly J. , Goldstein Alisa M. , Engels Eric A. , Sargen Michael R.
Published: November 2024

Output of dndscv.
Supplementary Table S4 from Multiomics Profiling Distinguishes Sebaceous Carcinoma from Benign Sebaceous Neoplasms and Provides Insight into the Genetic Evolution of Sebaceous Carcinogenesis
Authors: Starrett Gabriel J. , Baikie Brittany C. , Stoff Benjamin K. , Grossniklaus Hans E. , Van Buren Inga , Berry Elizabeth G. , Novoa Roberto A. , Rieger Kerri E. , Sarin Kavita Y. , Lynch Charles F. , Royer Michael C. , Piaskowski Mary L. , Brownell Isaac , Chu Emily Y. , Godse Rama , Chen Suephy C. , Yu Kelly J. , Goldstein Alisa M. , Engels Eric A. , Sargen Michael R.
Published: November 2024

Differentially expressed genes between periocular carcinomas and extraocular head and neck carcinomas.
Supplementary Figure S8 from Multiomics Profiling Distinguishes Sebaceous Carcinoma from Benign Sebaceous Neoplasms and Provides Insight into the Genetic Evolution of Sebaceous Carcinogenesis
Authors: Starrett Gabriel J. , Baikie Brittany C. , Stoff Benjamin K. , Grossniklaus Hans E. , Van Buren Inga , Berry Elizabeth G. , Novoa Roberto A. , Rieger Kerri E. , Sarin Kavita Y. , Lynch Charles F. , Royer Michael C. , Piaskowski Mary L. , Brownell Isaac , Chu Emily Y. , Godse Rama , Chen Suephy C. , Yu Kelly J. , Goldstein Alisa M. , Engels Eric A. , Sargen Michael R.
Published: November 2024

Fraction of mutation signatures of mutants with a variant allele frequency less than 20% versus those with an allele frequency between 30% and 45%.
Supplementary Figure S6 from Multiomics Profiling Distinguishes Sebaceous Carcinoma from Benign Sebaceous Neoplasms and Provides Insight into the Genetic Evolution of Sebaceous Carcinogenesis
Authors: Starrett Gabriel J. , Baikie Brittany C. , Stoff Benjamin K. , Grossniklaus Hans E. , Van Buren Inga , Berry Elizabeth G. , Novoa Roberto A. , Rieger Kerri E. , Sarin Kavita Y. , Lynch Charles F. , Royer Michael C. , Piaskowski Mary L. , Brownell Isaac , Chu Emily Y. , Godse Rama , Chen Suephy C. , Yu Kelly J. , Goldstein Alisa M. , Engels Eric A. , Sargen Michael R.
Published: November 2024

TERT expression in each histological category.
Supplementary Table S6 from A Phase II Study of Atezolizumab, Pertuzumab, and High-Dose Trastuzumab for Central Nervous System Metastases in Patients with HER2-Positive Breast Cancer
Authors: Giordano Antonio , Kumthekar Priya U. , Jin Qingchun , Binboga Kurt Busem , Ren Siyang , Li Tianyu , Leone Jose Pablo , Mittendorf Elizabeth A. , Pereslete Alyssa M. , Sharp Laura , Davis Raechel , DiLullo Molly , Tayob Nabihah , Mayer Erica L. , Winer Eric P. , Tolaney Sara M. , Lin Nancy U.
Published: November 2024

Supplementary Table S6. TMB data for all patients.
Supplementary Table S5 from A Phase II Study of Atezolizumab, Pertuzumab, and High-Dose Trastuzumab for Central Nervous System Metastases in Patients with HER2-Positive Breast Cancer
Authors: Giordano Antonio , Kumthekar Priya U. , Jin Qingchun , Binboga Kurt Busem , Ren Siyang , Li Tianyu , Leone Jose Pablo , Mittendorf Elizabeth A. , Pereslete Alyssa M. , Sharp Laura , Davis Raechel , DiLullo Molly , Tayob Nabihah , Mayer Erica L. , Winer Eric P. , Tolaney Sara M. , Lin Nancy U.
Published: November 2024

Supplementary Table S5. Complete details on treatment administered during study including dose delays, modifications, and holds.
Supplementary Figure S1 from A Phase II Study of Atezolizumab, Pertuzumab, and High-Dose Trastuzumab for Central Nervous System Metastases in Patients with HER2-Positive Breast Cancer
Authors: Giordano Antonio , Kumthekar Priya U. , Jin Qingchun , Binboga Kurt Busem , Ren Siyang , Li Tianyu , Leone Jose Pablo , Mittendorf Elizabeth A. , Pereslete Alyssa M. , Sharp Laura , Davis Raechel , DiLullo Molly , Tayob Nabihah , Mayer Erica L. , Winer Eric P. , Tolaney Sara M. , Lin Nancy U.
Published: November 2024

Supplementary Figure S1. Data on response rates in patients evaluated by RECIST 1.1.
Supplementary Table S1-S10 from Genomic Profiling and Immune Phenotyping of Neuroendocrine Bladder Cancer
Authors: Zang Jingyu , Shahatiaili Akezhouli , Cai Mei-Chun , Jin Di , Shen Peiye , Qian Lei , Zhang Lu , Zhang Tianxiang , Wu Yuchen , Yang Fan , Wu Zheng , Hou Yanli , Bai Yongrui , Xia Jun , Cheng Liang , Zhang Ruiyun , Zhuang Guanglei , Chen Haige
Published: November 2024

Table S1. Quality control of sequencing data. Table S2. Representativeness of study participants. Table S3. Clinicopathological characteristics of 35 patients diagnosed with NEBC. Table S4. Summary of clinicopathological characteristics for the NEBC cohort. Table S5. Comparing clinical characteristics of patients in the NEBC and UBC cohort before and after PSM. Table S6. Whole genome sequencing statistics of 19 patients in NEBC cohort. Table S7. Density of immune cells in CT and IM region and immunotypes of patients in NEBC cohort. Table S8. Cell density and Ki-67 expresion in NEBC region and UBC region of patients diagnosed with mixed-UBC. Table S9. Clinical characteristics of metastatic NEBC patients receiving systemic treatment. Table S10. Clinical characteristics and density of immune cells of patients receiving neoadjuvant treatment.
Supplementary Figure S7 from Genomic Profiling and Immune Phenotyping of Neuroendocrine Bladder Cancer
Authors: Zang Jingyu , Shahatiaili Akezhouli , Cai Mei-Chun , Jin Di , Shen Peiye , Qian Lei , Zhang Lu , Zhang Tianxiang , Wu Yuchen , Yang Fan , Wu Zheng , Hou Yanli , Bai Yongrui , Xia Jun , Cheng Liang , Zhang Ruiyun , Zhuang Guanglei , Chen Haige
Published: November 2024

Gene expression and immune repertoire in NEBC.
Supplementary Figure S5 from Genomic Profiling and Immune Phenotyping of Neuroendocrine Bladder Cancer
Authors: Zang Jingyu , Shahatiaili Akezhouli , Cai Mei-Chun , Jin Di , Shen Peiye , Qian Lei , Zhang Lu , Zhang Tianxiang , Wu Yuchen , Yang Fan , Wu Zheng , Hou Yanli , Bai Yongrui , Xia Jun , Cheng Liang , Zhang Ruiyun , Zhuang Guanglei , Chen Haige
Published: November 2024

Chromoplexy events in NEBC.
Supplementary Figure S3 from Genomic Profiling and Immune Phenotyping of Neuroendocrine Bladder Cancer
Authors: Zang Jingyu , Shahatiaili Akezhouli , Cai Mei-Chun , Jin Di , Shen Peiye , Qian Lei , Zhang Lu , Zhang Tianxiang , Wu Yuchen , Yang Fan , Wu Zheng , Hou Yanli , Bai Yongrui , Xia Jun , Cheng Liang , Zhang Ruiyun , Zhuang Guanglei , Chen Haige
Published: November 2024

NMF analysis of NEBC mutational signatures.
Supplementary Figure S10 from Genomic Profiling and Immune Phenotyping of Neuroendocrine Bladder Cancer
Authors: Zang Jingyu , Shahatiaili Akezhouli , Cai Mei-Chun , Jin Di , Shen Peiye , Qian Lei , Zhang Lu , Zhang Tianxiang , Wu Yuchen , Yang Fan , Wu Zheng , Hou Yanli , Bai Yongrui , Xia Jun , Cheng Liang , Zhang Ruiyun , Zhuang Guanglei , Chen Haige
Published: November 2024

Radiographic evaluation and survival analysis in NEBC and UBC.
Supplementary Figure S1 from Genomic Profiling and Immune Phenotyping of Neuroendocrine Bladder Cancer
Authors: Zang Jingyu , Shahatiaili Akezhouli , Cai Mei-Chun , Jin Di , Shen Peiye , Qian Lei , Zhang Lu , Zhang Tianxiang , Wu Yuchen , Yang Fan , Wu Zheng , Hou Yanli , Bai Yongrui , Xia Jun , Cheng Liang , Zhang Ruiyun , Zhuang Guanglei , Chen Haige
Published: November 2024

Histopathological characteristics of NEBC and survival analysis in NEBC and UBC.
Data from Targeted Therapies, Novel Antibodies, and Immunotherapies in Advanced Non–Small Cell Lung Cancer: Clinical Evidence and Drug Approval Patterns
Authors: Koban Marén U. , Hartmann Markus , Amexis Georgios , Franco Pedro , Huggins Laura , Shah Imran , Karachaliou Niki
Published: November 2024

Abstract
Since 2011, the US FDA has approved 30 new drugs for use in advanced non–small cell lung cancer (NSCLC), mainly comprising tyrosine kinase inhibitors and immune checkpoint inhibitors. NSCLC with oncogene driver alterations is amenable to treatment with targeted drugs, usually small-molecule inhibitors. In these cases, the demonstration of high overall response rates, coupled with a lasting duration of response, has allowed for accelerated approval in the United States, based on single-cohort or multicohort trials. Confirmatory clinical evidence was subsequently provided through postmarketing trials. In NSCLC without such driver alterations, regulatory agencies in both the United States and the European Union set clinical evidence expectations that foster the conduct of studies primarily focused on determining survival or event-free survival, based on randomized controlled trial designs. This review analyzes the approval patterns of novel therapeutics for NSCLC with a focus on small-molecule inhibitors that target driver alterations, as well as biologics. The latter include mAbs inhibiting immune checkpoints like PD-(L)1 or cell surface receptors and antibody–drug conjugates, highly potent biologics linked to a cytotoxic compound. The differentiation of NSCLC into oncogene- and non–oncogene-addicted subtypes determines drug development strategies, the extent of the clinical development program, access to orphan drug development incentives, and regulatory approval strategies.
Data from Tumor-Infiltrating Lymphocytes in Necrotic Tumors after Melanoma Neoadjuvant Anti–PD-1 Therapy Correlate with Pathologic Response and Recurrence-Free Survival
Authors: Ma Kevin L. , Mitchell Tara C. , Dougher Meaghan , Sharon Cimarron E. , Tortorello Gabriella N. , Elder David E. , Morgan Eric E. , Gimotty Phyllis A. , Huang Alexander C. , Amaravadi Ravi K. , Schuchter Lynn M. , Flowers Ahron , Miura John T. , Karakousis Giorgos C. , Xu Xiaowei
Published: November 2024

AbstractPurpose:
Neoadjuvant anti–PD-1 therapy in melanoma may increase tumor-infiltrating lymphocytes (TIL), and more TIL are associated with better treatment response. A major pathologic response (MPR) in melanoma after neoadjuvant anti–PD-1 therapy usually comprises tumor necrosis and fibrosis. The role of TIL in necrotic tumor necrosis (nTIL) has not been explored.
Experimental Design:
We performed CD3 and CD8 IHC stains on 41 melanomas with geographic necrosis. Of the 41, 14 were immunotherapy-naïve, and 27 had been treated with one dose of neoadjuvant anti–PD-1 in two clinical trials. CD3+ and CD8+ nTIL were graded as absent/minimal or moderate/brisk. The percentage of necrotic areas in the tumor bed before and after treatment was quantified. The endpoints were MPR and 5-year recurrence-free survival (RFS).
Results:
In the immunotherapy-naïve cohort, 3/14 (21%) specimens had moderate/brisk CD3+, and 2/14 (14%) had moderate/brisk CD8+ nTIL. In the treated cohort, 16/27 (59%) specimens had moderate/brisk CD3+, and 15/27 (56%) had moderate/brisk CD8+ nTIL, higher than those of the naïve cohort (CD3, P = 0.046; CD8, P = 0.018). Tumor necrosis was significantly increased after anti–PD-1 therapy (P = 0.007). In the treated cohort, moderate/brisk CD3+ and CD8+ nTIL correlated with MPR (P = 0.042; P = 0.019, respectively). Treated patients with moderate/brisk CD3+ nTIL had higher 5-year RFS than those with absent/minimal nTIL (69% vs. 0%; P = 0.006). This persisted on multivariate analysis (HR, 0.16; 95% confidence interval, 0.03–0.84; P = 0.03), adjusted for pathologic response, which was borderline significant (HR, 0.26; 95% confidence interval, 0.07–1.01; P = 0.051).
Conclusions:
CD3+ and CD8+ nTIL are associated with pathologic response and 5-year RFS in patients with melanoma after neoadjuvant anti–PD-1 therapy.
Data from A Phase 1 First-in-Human Study of the MCL-1 Inhibitor AZD5991 in Patients with Relapsed/Refractory Hematologic Malignancies
Authors: Desai Pinkal , Lonial Sagar , Cashen Amanda , Kamdar Manali , Flinn Ian , O’Brien Susan , Garcia Jacqueline S. , Korde Neha , Moslehi Javid , Wey Margaret , Cheung Patricia , Sharma Shringi , Olabode Damilola , Chen Hong , Ali Syed Firasath , Liu Mary , Saeh Jamal , Andrade-Campos Marcio , Kadia Tapan M. , Blachly James S.
Published: November 2024

AbstractPurpose:
AZD5991, a human MCL-1 inhibitor, was assessed for safety, tolerability, pharmacokinetics, and antitumor activity as monotherapy and in combination with venetoclax in patients with relapsed or refractory hematologic malignancies.
Patients and Methods:
In the monotherapy cohort (n = 61), patients with hematologic malignancies received AZD5991 intravenously in escalating doses either once or twice weekly, following intrapatient dose escalation, during a 3-week cycle. In the combination cohort (n = 17), patients with acute myeloid leukemia and myelodysplastic syndrome received escalating doses of AZD5991 and venetoclax during either a 3- or 4-week cycle. Primary objectives were safety and maximum tolerated dose; secondary objectives included plasma pharmacokinetics and antitumor activity.
Results:
The most common (≥30%) adverse events were diarrhea (59.0%), nausea (55.1%), and vomiting (47.4%). Four deaths occurred because of adverse events: cardiac arrest, sepsis, tumor lysis syndrome, and acute respiratory failure; only tumor lysis syndrome was related to AZD5991. Dose-limiting toxicities occurred in five patients. Three patients with myelodysplastic syndrome achieved an objective response: one marrow complete remission without hematologic improvement, one partial remission with AZD5991 monotherapy, and one marrow complete remission with AZD5991 + venetoclax. Asymptomatic elevations of troponin I or T were observed in eight (10.3%) patients. Post hoc retrospective analysis revealed elevated troponin T in 14/31 patients before any AZD5991 dose and in 54/65 patients after any AZD5991 dose at or after Cycle 1. No associations were found between elevated troponin and cardiovascular risk factors.
Conclusions:
Treatment with AZD5991 was associated with high incidence of laboratory troponin elevation and a low overall response rate.
Data from Genetic Screen in a Preclinical Model of Sarcoma Development Defines Drivers and Therapeutic Vulnerabilities
Authors: Freeland Jack , Muñoz Maria , O’Donnell Edmond , Langerman Justin , Darrow Morgan , Bergonio Jessica , Suarez-Navarro Julissa , Thorpe Steven , Canter Robert , Randall Robert Lor , Plath Kathrin , Carraway Kermit L. , Witte Owen N. , Graeber Thomas G. , Carr-Ascher Janai R.
Published: November 2024

AbstractPurpose:
High-grade complex karyotype sarcomas are a heterogeneous group of tumors with a uniformly poor prognosis. Within complex karyotype sarcomas, there are innumerable genetic changes but identifying those that are clinically relevant has been challenging.
Experimental Design:
To address this, we utilized a pooled genetic screening approach, informed by The Cancer Genome Atlas (TCGA) data, to identify key drivers and modifiers of sarcoma development that were validated in vivo.
Results:
YAP1 and wild-type KRAS were validated as drivers and transformed human mesenchymal stem cells into two distinct sarcoma subtypes, undifferentiated pleomorphic sarcoma and myxofibrosarcoma, respectively. A subset of tumors driven by CDK4 and PIK3CA reflected leiomyosarcoma and osteosarcoma demonstrating the plasticity of this approach and the potential to investigate sarcoma subtype heterogeneity. All generated tumors histologically reflected human sarcomas and had increased aneuploidy as compared to simple karyotype sarcomas. Comparing differential gene expression of TCGA samples to model data identified increased oxidative phosphorylation signaling in YAP1 tumors. Treatment of a panel of soft tissue sarcomas with a combination of YAP1 and oxidative phosphorylation inhibitors led to significantly decreased viability.
Conclusions:
Transcriptional co-analysis of TCGA patient samples to YAP1 and KRAS model tumors supports that these sarcoma subtypes lie along a spectrum of disease and adds guidance for further transcriptome-based refinement of sarcoma subtyping. This approach can be used to begin to understand pathways and mechanisms driving human sarcoma development, the relationship between sarcoma subtypes, and to identify and validate new therapeutic vulnerabilities for this aggressive and heterogeneous disease.
Data from A Phase II Study of Atezolizumab, Pertuzumab, and High-Dose Trastuzumab for Central Nervous System Metastases in Patients with HER2-Positive Breast Cancer
Authors: Giordano Antonio , Kumthekar Priya U. , Jin Qingchun , Binboga Kurt Busem , Ren Siyang , Li Tianyu , Leone Jose Pablo , Mittendorf Elizabeth A. , Pereslete Alyssa M. , Sharp Laura , Davis Raechel , DiLullo Molly , Tayob Nabihah , Mayer Erica L. , Winer Eric P. , Tolaney Sara M. , Lin Nancy U.
Published: November 2024

AbstractPurpose:
Patients with HER2-positive breast cancer brain metastases have few effective systemic therapy options. In a prior study, pertuzumab with high-dose trastuzumab demonstrated a high clinical benefit rate (CBR) in the central nervous system (CNS) in patients with brain metastases. The current trial evaluated whether the addition of atezolizumab to this regimen would produce further improvements in CNS response.
Patients and Methods:
This was a single-arm, multicenter, phase II trial of atezolizumab, pertuzumab, and high-dose trastuzumab for patients with HER2-positive breast cancer brain metastases. Participants received atezolizumab 1,200 mg i.v. every 3 weeks, pertuzumab (loading dosage 840 mg i.v., then 420 mg i.v. every 3 weeks), and high-dose trastuzumab (6 mg/kg i.v. weekly for 24 weeks, then 6 mg/kg i.v. every 3 weeks). The primary endpoint was CNS overall response rate per Response Assessment in Neuro-Oncology Brain Metastases criteria. Key secondary endpoints included CBR, overall survival, and safety and tolerability of the combination.
Results:
Among 19 enrolled participants, two had a confirmed intracranial partial response for a CNS overall response rate of 10.5% (90% confidence interval, 1.9%–29.6%). The study did not meet the prespecified efficacy threshold and was terminated early. The CBR was 42.1% at 18 weeks and 31.6% at 24 weeks. Seven patients (36.8%) required a dose delay or hold, and the most frequent any-grade adverse events were diarrhea (26.3%) and fatigue (26.3%).
Conclusions:
The addition of atezolizumab to pertuzumab plus high-dose trastuzumab does not result in improved CNS responses in patients with HER2-positive breast cancer brain metastases.
Supplementary Figure S7 from GRAIL1 Stabilizes Misfolded Mutant p53 through a Ubiquitin Ligase-Independent, Chaperone Regulatory Function
Authors: Ray Paramita , Jaiswal Sangeeta , Ferrer-Torres Daysha , Wang Zhuwen , Nancarrow Derek , Curtin Meghan , Martinho May San , Lacy Shannon M. , Kasturirangan Srimathi , Thomas Dafydd , Spence Jason R. , Truttmann Matthias C. , Lagisetty Kiran H. , Lawrence Theodore S. , Wang Thomas D. , Beer David G. , Ray Dipankar
Published: November 2024

Supplementary Figure S7. Design and testing of scrambled peptides as negative controls.
Supplementary Figure S6 from GRAIL1 Stabilizes Misfolded Mutant p53 through a Ubiquitin Ligase-Independent, Chaperone Regulatory Function
Authors: Ray Paramita , Jaiswal Sangeeta , Ferrer-Torres Daysha , Wang Zhuwen , Nancarrow Derek , Curtin Meghan , Martinho May San , Lacy Shannon M. , Kasturirangan Srimathi , Thomas Dafydd , Spence Jason R. , Truttmann Matthias C. , Lagisetty Kiran H. , Lawrence Theodore S. , Wang Thomas D. , Beer David G. , Ray Dipankar
Published: November 2024

Supplementary Figure S6. Metabolic stability of Pep J.
Supplementary Figure S5 from GRAIL1 Stabilizes Misfolded Mutant p53 through a Ubiquitin Ligase-Independent, Chaperone Regulatory Function
Authors: Ray Paramita , Jaiswal Sangeeta , Ferrer-Torres Daysha , Wang Zhuwen , Nancarrow Derek , Curtin Meghan , Martinho May San , Lacy Shannon M. , Kasturirangan Srimathi , Thomas Dafydd , Spence Jason R. , Truttmann Matthias C. , Lagisetty Kiran H. , Lawrence Theodore S. , Wang Thomas D. , Beer David G. , Ray Dipankar
Published: November 2024

Supplementary Figure S5. Intracellular localization of Frag J and Frag J-Δ.
Supplementary Figure S3 from GRAIL1 Stabilizes Misfolded Mutant p53 through a Ubiquitin Ligase-Independent, Chaperone Regulatory Function
Authors: Ray Paramita , Jaiswal Sangeeta , Ferrer-Torres Daysha , Wang Zhuwen , Nancarrow Derek , Curtin Meghan , Martinho May San , Lacy Shannon M. , Kasturirangan Srimathi , Thomas Dafydd , Spence Jason R. , Truttmann Matthias C. , Lagisetty Kiran H. , Lawrence Theodore S. , Wang Thomas D. , Beer David G. , Ray Dipankar
Published: November 2024

Supplementary Figure S3. GRAIL1 is a glycosylated protein that undergoes processing.
Supplementary Figure S1 from GRAIL1 Stabilizes Misfolded Mutant p53 through a Ubiquitin Ligase-Independent, Chaperone Regulatory Function
Authors: Ray Paramita , Jaiswal Sangeeta , Ferrer-Torres Daysha , Wang Zhuwen , Nancarrow Derek , Curtin Meghan , Martinho May San , Lacy Shannon M. , Kasturirangan Srimathi , Thomas Dafydd , Spence Jason R. , Truttmann Matthias C. , Lagisetty Kiran H. , Lawrence Theodore S. , Wang Thomas D. , Beer David G. , Ray Dipankar
Published: November 2024

Supplementary Figure S1. Purification of GRAIL1 C-terminal fragment.
Supplementary Table 3 from NAP1L1 Promotes Endometrial Cancer Progression via EP300-Mediated DDX5 Promoter Acetylation
Authors: Zhu Xiangfei , Li Yishan , Shao Zhiying , Lu Xiaoyuan , Chen Youguo
Published: November 2024

Target sequences of siRNAs
Supplementary Figure 1 from NAP1L1 Promotes Endometrial Cancer Progression via EP300-Mediated DDX5 Promoter Acetylation
Authors: Zhu Xiangfei , Li Yishan , Shao Zhiying , Lu Xiaoyuan , Chen Youguo
Published: November 2024

The mRNA level of NAP1L1 was correlated with tumor size (A), grade (B), and stage (C).
Table S4 from lncRNA-WAL Promotes Triple-Negative Breast Cancer Aggression by Inducing β-Catenin Nuclear Translocation
Authors: Huang Hongyan , Jin Haiyun , Lei Rong , He Zhanghai , He Shishi , Chen Jiewen , Saw Phei E. , Qiu Zhu , Ren Guosheng , Nie Yan
Published: November 2024

Correlation of lnc-WAL expression with clinicopathologic status of 189 patients with TNBC.
Table S1 from lncRNA-WAL Promotes Triple-Negative Breast Cancer Aggression by Inducing β-Catenin Nuclear Translocation
Authors: Huang Hongyan , Jin Haiyun , Lei Rong , He Zhanghai , He Shishi , Chen Jiewen , Saw Phei E. , Qiu Zhu , Ren Guosheng , Nie Yan
Published: November 2024

Primer sequences for qRT–PCR.
Figure S5 from lncRNA-WAL Promotes Triple-Negative Breast Cancer Aggression by Inducing β-Catenin Nuclear Translocation
Authors: Huang Hongyan , Jin Haiyun , Lei Rong , He Zhanghai , He Shishi , Chen Jiewen , Saw Phei E. , Qiu Zhu , Ren Guosheng , Nie Yan
Published: November 2024

lnc-WAL inhibits β-catenin phosphorylation by physically obstructing AXIN.
Figure S4 from lncRNA-WAL Promotes Triple-Negative Breast Cancer Aggression by Inducing β-Catenin Nuclear Translocation
Authors: Huang Hongyan , Jin Haiyun , Lei Rong , He Zhanghai , He Shishi , Chen Jiewen , Saw Phei E. , Qiu Zhu , Ren Guosheng , Nie Yan
Published: November 2024

Lnc-WAL promotes malignant progression of TNBC cells.
Figure S3 from lncRNA-WAL Promotes Triple-Negative Breast Cancer Aggression by Inducing β-Catenin Nuclear Translocation
Authors: Huang Hongyan , Jin Haiyun , Lei Rong , He Zhanghai , He Shishi , Chen Jiewen , Saw Phei E. , Qiu Zhu , Ren Guosheng , Nie Yan
Published: November 2024

lnc-WAL promotes malignant progression of TNBC cells.
Figure S1 from lncRNA-WAL Promotes Triple-Negative Breast Cancer Aggression by Inducing β-Catenin Nuclear Translocation
Authors: Huang Hongyan , Jin Haiyun , Lei Rong , He Zhanghai , He Shishi , Chen Jiewen , Saw Phei E. , Qiu Zhu , Ren Guosheng , Nie Yan
Published: November 2024

Identification of Wnt/β-catenin pathway-associated lncRNAs.
Figure S3 from hnRNPAB Promotes Pancreatic Ductal Adenocarcinoma Extravasation and Liver Metastasis by Stabilizing MYC mRNA
Authors: Lei Ke , Sun Mingyue , Chen Xianghan , Wang Jia , Liu Xiaolan , Ning Ying , Ping Shuai , Gong Ruining , Zhang Yu , Qing Gong , Zhao Chenyang , Ren He
Published: November 2024

Effects of hnRNPAB on epithelial-mesenchymal transition (EMT), MYC transcription in PDAC cells
Figure S1 from hnRNPAB Promotes Pancreatic Ductal Adenocarcinoma Extravasation and Liver Metastasis by Stabilizing MYC mRNA
Authors: Lei Ke , Sun Mingyue , Chen Xianghan , Wang Jia , Liu Xiaolan , Ning Ying , Ping Shuai , Gong Ruining , Zhang Yu , Qing Gong , Zhao Chenyang , Ren He
Published: November 2024

HnRNPAB promotes the liver metastasis of PDAC cells
Data from GRAIL1 Stabilizes Misfolded Mutant p53 through a Ubiquitin Ligase-Independent, Chaperone Regulatory Function
Authors: Ray Paramita , Jaiswal Sangeeta , Ferrer-Torres Daysha , Wang Zhuwen , Nancarrow Derek , Curtin Meghan , Martinho May San , Lacy Shannon M. , Kasturirangan Srimathi , Thomas Dafydd , Spence Jason R. , Truttmann Matthias C. , Lagisetty Kiran H. , Lawrence Theodore S. , Wang Thomas D. , Beer David G. , Ray Dipankar
Published: November 2024

Abstract
Frequent (>70%) TP53 mutations often promote its protein stabilization, driving esophageal adenocarcinoma (EAC) development linked to poor survival and therapy resistance. We previously reported that during Barrett’s esophagus progression to EAC, an isoform switch occurs in the E3 ubiquitin ligase RNF128 (aka GRAIL—gene related to anergy in lymphocytes), enriching isoform 1 (hereby GRAIL1) and stabilizing the mutant p53 protein. Consequently, GRAIL1 knockdown degrades mutant p53. But, how GRAIL1 stabilizes the mutant p53 protein remains unclear. In search for a mechanism, here, we performed biochemical and cell biology studies to identify that GRAIL has a binding domain (315-PMCKCDILKA-325) for heat shock protein 40/DNAJ. This interaction can influence DNAJ chaperone activity to modulate misfolded mutant p53 stability. As predicted, either the overexpression of a GRAIL fragment (Frag-J) encompassing the DNAJ binding domain or a cell-permeable peptide (Pep-J) encoding the above 10 amino acids can bind and inhibit DNAJ-Hsp70 co-chaperone activity, thus degrading misfolded mutant p53. Consequently, either Frag-J or Pep-J can reduce the survival of mutant p53 containing dysplastic Barrett’s esophagus and EAC cells and inhibit the growth of patient-derived organoids of dysplastic Barrett’s esophagus in 3D cultures. The misfolded mutant p53 targeting and growth inhibitory effects of Pep-J are comparable with simvastatin, a cholesterol-lowering drug that can degrade misfolded mutant p53 also via inhibiting DNAJA1, although by a distinct mechanism.

Implications: We identified a novel ubiquitin ligase-independent, chaperone-regulating domain in GRAIL and further synthesized a first-in-class novel misfolded mutant p53 degrading peptide having future translational potential.
Data from METTL14-Mediated Bim mRNA m6A Modification Augments Osimertinib Sensitivity in EGFR-Mutant NSCLC Cells
Authors: Fan Siwen , Lv Xinwu , Zhang Chuantao , Zeng Bingbing , Liang Yanqing , Chen Danyang , Xu Zumin , Li Pan , Wu Shanshan , Liu Hao , Luo Kai , Liu Zongcai , Yi Yanmei
Published: November 2024

Abstract
Resistance to osimertinib represents a significant challenge for the successful treatment of non–small cell lung cancer (NSCLC) harboring activating mutations in EGFR. N6-methyladenosine (m6A) on mRNAs is critical for various biological processes, yet whether m6A regulates osimertinib resistance of NSCLC remains unknown. In this study, we demonstrated that developing osimertinib-resistant phenotypes depends on m6A reduction resulting from downexpression of m6A methyltransferase METTL14 in EGFR-mutant NSCLCs. Both in vitro and in vivo assays showed that specific knockdown of METTL14 was sufficient to confer osimertinib resistance and that elevated expression of METTL14 rescued the efficacy of osimertinib in the resistant NSCLC cells. Mechanistically, METTL14 promoted m6A methylation of pro-apoptotic Bim mRNA and increased Bim mRNA stability and expression, resulting in activating the Bim-dependent pro-apoptotic signaling and thereby promoting osimertinib-induced cell apoptosis. Analysis of clinical samples revealed that decreased expression of METTL14 was observed in osimertinib-resistant NSCLC tissues and significantly associated with a poor prognosis. In conclusion, our study reveals a novel regulatory mechanism by which METTL14-mediated m6A methylation of Bim mRNA inhibited osimertinib resistance of NSCLC cells. It offers more evidences for the involvement of m6A modification in regulation of osimertinib resistance and provides potential therapeutic targets for novel approaches to overcome the tolerance of osimertinib and other EGFR tyrosine kinase inhibitors.

Implications: This study offers more evidences for the involvement of METTL14-mediated N6-methyladenosine modification in regulation of osimertinib resistance and provides potential therapeutic targets for novel approaches to overcome the tolerance of osimertinib and other EGFR tyrosine kinase inhibitors.
Data from hnRNPAB Promotes Pancreatic Ductal Adenocarcinoma Extravasation and Liver Metastasis by Stabilizing MYC mRNA
Authors: Lei Ke , Sun Mingyue , Chen Xianghan , Wang Jia , Liu Xiaolan , Ning Ying , Ping Shuai , Gong Ruining , Zhang Yu , Qing Gong , Zhao Chenyang , Ren He
Published: November 2024

Abstract
Heterogeneous nuclear ribonucleoprotein AB (hnRNPAB) is considered a cancer-promoting heterogeneous nuclear ribonucleoprotein in many cancers, but its function in pancreatic ductal adenocarcinoma (PDAC) is poorly understood. hnRNPAB was highly expressed in PDAC tissues compared with normal pancreatic tissues, and high expression of hnRNPAB was associated with poor overall survival and recurrence-free survival in patients with PDAC. hnRNPAB promotes migration and invasion of PDAC cells in vitro. In xenograft tumor mouse models, hnRNPAB deprivation significantly attenuated liver metastasis. hnRNPAB mRNA and protein levels are positively associated with MYC in PDAC cells. Mechanistically, hnRNPAB bound to MYC mRNA and prolonged its half-life. hnRNPAB induced PDAC cells to secrete CXCL8 via MYC, which promoted neutrophil recruitment and facilitated tumor cells entrancing into the hepatic parenchyma. These findings point to a novel regulatory mechanism via which hnRNPAB promotes PDAC metastasis.

Implications: hnRNPAB participates in the posttranscriptional regulation of the oncogene MYC by binding and stabilizing MYC mRNA, thereby promoting liver metastasis in PDAC.
Supplementary Table S5 from Single-Cell View of Tumor Microenvironment Gradients in Pleural Mesothelioma
Authors: Giotti Bruno , Dolasia Komal , Zhao William , Cai Peiwen , Sweeney Robert , Merritt Elliot , Kiner Evgeny , Kim Grace S. , Bhagwat Atharva , Nguyen Thinh , Hegde Samarth , Fitzgerald Bailey G. , Shroff Sanjana , Dawson Travis , Garcia-Barros Monica , Abdul-Ghafar Jamshid , Chen Rachel , Gnjatic Sacha , Soto Alan , Brody Rachel , Kim-Schulze Seunghee , Chen Zhihong , Beaumont Kristin G. , Merad Miriam , Flores Raja M. , Sebra Robert P. , Horowitz Amir , Marron Thomas U. , Tocheva Anna , Wolf Andrea , Tsankov Alexander M.
Published: November 2024

Gene signatures for all 54 de novo discovered PM cNMF modules
Supplementary Figure S5 from Single-Cell View of Tumor Microenvironment Gradients in Pleural Mesothelioma
Authors: Giotti Bruno , Dolasia Komal , Zhao William , Cai Peiwen , Sweeney Robert , Merritt Elliot , Kiner Evgeny , Kim Grace S. , Bhagwat Atharva , Nguyen Thinh , Hegde Samarth , Fitzgerald Bailey G. , Shroff Sanjana , Dawson Travis , Garcia-Barros Monica , Abdul-Ghafar Jamshid , Chen Rachel , Gnjatic Sacha , Soto Alan , Brody Rachel , Kim-Schulze Seunghee , Chen Zhihong , Beaumont Kristin G. , Merad Miriam , Flores Raja M. , Sebra Robert P. , Horowitz Amir , Marron Thomas U. , Tocheva Anna , Wolf Andrea , Tsankov Alexander M.
Published: November 2024

Molecular dissection of T cell programs and IC molecules shows association with scS-score
Supplementary Table S9 from The N6-methyladenosine Epitranscriptomic Landscape of Lung Adenocarcinoma
Authors: Wang Shiyan , Zeng Yong , Zhu Lin , Zhang Min , Zhou Lei , Yang Weixiong , Luo Weishan , Wang Lina , Liu Yanming , Zhu Helen , Xu Xin , Su Peiran , Zhang Xinyue , Ahmed Musaddeque , Chen Wei , Chen Moliang , Chen Sujun , Slobodyanyuk Mykhaylo , Xie Zhongpeng , Guan Jiansheng , Zhang Wen , Khan Aafaque Ahmad , Sakashita Shingo , Liu Ni , Pham Nhu-An , Boutros Paul C. , Ke Zunfu , Moran Michael F. , Cai Zongwei , Cheng Chao , Yu Jun , Tsao Ming S. , He Housheng H.
Published: November 2024

Sequence information of primers, siRNAs, shRNAs and sgRNAs.
Supplementary Table S8 from The N6-methyladenosine Epitranscriptomic Landscape of Lung Adenocarcinoma
Authors: Wang Shiyan , Zeng Yong , Zhu Lin , Zhang Min , Zhou Lei , Yang Weixiong , Luo Weishan , Wang Lina , Liu Yanming , Zhu Helen , Xu Xin , Su Peiran , Zhang Xinyue , Ahmed Musaddeque , Chen Wei , Chen Moliang , Chen Sujun , Slobodyanyuk Mykhaylo , Xie Zhongpeng , Guan Jiansheng , Zhang Wen , Khan Aafaque Ahmad , Sakashita Shingo , Liu Ni , Pham Nhu-An , Boutros Paul C. , Ke Zunfu , Moran Michael F. , Cai Zongwei , Cheng Chao , Yu Jun , Tsao Ming S. , He Housheng H.
Published: November 2024

Information of EML4 and IgG control antibody precipitated proteins identified by Co-IP/MS.
Supplementary Table S5 from The N6-methyladenosine Epitranscriptomic Landscape of Lung Adenocarcinoma
Authors: Wang Shiyan , Zeng Yong , Zhu Lin , Zhang Min , Zhou Lei , Yang Weixiong , Luo Weishan , Wang Lina , Liu Yanming , Zhu Helen , Xu Xin , Su Peiran , Zhang Xinyue , Ahmed Musaddeque , Chen Wei , Chen Moliang , Chen Sujun , Slobodyanyuk Mykhaylo , Xie Zhongpeng , Guan Jiansheng , Zhang Wen , Khan Aafaque Ahmad , Sakashita Shingo , Liu Ni , Pham Nhu-An , Boutros Paul C. , Ke Zunfu , Moran Michael F. , Cai Zongwei , Cheng Chao , Yu Jun , Tsao Ming S. , He Housheng H.
Published: November 2024

Summary and gene enrichment of hyper-, hypo-, NL-specific and tumor-specific methylated genes.
Supplementary Table S1 from The N6-methyladenosine Epitranscriptomic Landscape of Lung Adenocarcinoma
Authors: Wang Shiyan , Zeng Yong , Zhu Lin , Zhang Min , Zhou Lei , Yang Weixiong , Luo Weishan , Wang Lina , Liu Yanming , Zhu Helen , Xu Xin , Su Peiran , Zhang Xinyue , Ahmed Musaddeque , Chen Wei , Chen Moliang , Chen Sujun , Slobodyanyuk Mykhaylo , Xie Zhongpeng , Guan Jiansheng , Zhang Wen , Khan Aafaque Ahmad , Sakashita Shingo , Liu Ni , Pham Nhu-An , Boutros Paul C. , Ke Zunfu , Moran Michael F. , Cai Zongwei , Cheng Chao , Yu Jun , Tsao Ming S. , He Housheng H.
Published: November 2024

Sample information and gene list of NL-specific, tumor-specific and common methylated genes.
Supplementary Figure S2 from The N6-methyladenosine Epitranscriptomic Landscape of Lung Adenocarcinoma
Authors: Wang Shiyan , Zeng Yong , Zhu Lin , Zhang Min , Zhou Lei , Yang Weixiong , Luo Weishan , Wang Lina , Liu Yanming , Zhu Helen , Xu Xin , Su Peiran , Zhang Xinyue , Ahmed Musaddeque , Chen Wei , Chen Moliang , Chen Sujun , Slobodyanyuk Mykhaylo , Xie Zhongpeng , Guan Jiansheng , Zhang Wen , Khan Aafaque Ahmad , Sakashita Shingo , Liu Ni , Pham Nhu-An , Boutros Paul C. , Ke Zunfu , Moran Michael F. , Cai Zongwei , Cheng Chao , Yu Jun , Tsao Ming S. , He Housheng H.
Published: November 2024

mRNA abundance of m6A regulators in lung tissues and genomic characteristics of G1, G2 and G3 gene groups.
Supplementary Table 4 from The SCRUM-MONSTAR Cancer-Omics Ecosystem: Striving for a Quantum Leap in Precision Medicine
Authors: Hashimoto Tadayoshi , Nakamura Yoshiaki , Fujisawa Takao , Imai Mitsuho , Shibuki Taro , Iida Naoko , Ozaki Hiroshi , Nonomura Norio , Morizane Chigusa , Iwata Hiroji , Okano Susumu , Yamagami Wataru , Yamazaki Naoya , Kadowaki Shigenori , Taniguchi Hiroya , Ueno Makoto , Boku Shogen , Oki Eiji , Komatsu Yoshito , Yuki Satoshi , Makiyama Akitaka , Otsuka Tomoyuki , Hara Hiroki , Okano Naohiro , Nishina Tomohiro , Sakamoto Yasutoshi , Miki Izumi , Kobayashi Shin , Yuda Junichiro , Kageyama Shun-Ichiro , Nagamine Michiko , Sakashita Shingo , Sakamoto Naoya , Yamashita Riu , Koga Yoshikatsu , Bando Hideaki , Ishii Genichiro , Kuwata Takeshi , Park Woong-Yang , Ohtsu Atsushi , Yoshino Takayuki
Published: November 2024

Summary of umbrella and basket trials evaluating the efficacy of targeted biomarker-driven therapies