bluuebunny/crossref_metadata_2025 huggingface dataset:
Supplementary Figure S3 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

Further Characterization of Primary and Secondary Screens
Supplementary Table S3 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 adenomas and carcinomas.
Supplementary Table S4 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 S4. Response rates in patients with extracranial disease.
Supplementary Table S2 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 S2. A complete list of prior chemotherapy regimens for each patient.
Supplementary Figure S9 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

Immunotype distribution and fibrotic barriers in NEBC.
Supplementary Figure S8 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

Survival outcomes by immunotype in NEBC.
Supplementary Figure S6 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

Tumor purity, ploidy, and CNVs in NEBC.
Supplementary Figure S2 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

p53 expression and mutational landscape in NEBC.
Data 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

Abstract
On December 15, 2023, the FDA granted traditional approval to enfortumab vedotin-ejfv plus pembrolizumab (EV + Pembro) for patients with locally advanced or metastatic urothelial carcinoma (la/mUC). Substantial evidence of effectiveness was obtained from EV-302/KEYNOTE-A39 (NCT04223856), an open-label, randomized trial evaluating EV + Pembro versus cisplatin or carboplatin plus gemcitabine (Plat + Gem) in patients with previously untreated la/mUC. A total of 886 patients were randomized (1:1) to receive EV 1.25 mg/kg intravenously on days 1 and 8 of each 21-day cycle until disease progression or unacceptable toxicity plus Pembro 200 mg intravenously on day 1 of each 21-day cycle for up to 35 cycles or Plat + Gem for up to 6 cycles. Dual primary endpoints were progression-free survival determined by blinded independent central review and overall survival. The median progression-free survival was 12.5 months [95% confidence interval (CI), 10.4–16.6] in the EV + Pembro arm and 6.3 months (95% CI, 6.2–6.5) in the Plat + Gem arm [HR, 0.450 (95% CI, 0.377–0.538); P value < 0.0001]. The median overall survival was 31.5 months (95% CI, 25.4–not estimable) in the EV + Pembro arm and 16.1 months (95% CI, 13.9–18.3) in the Plat + Gem arm [HR, 0.468 (95% CI, 0.376–0.582); P value < 0.0001]. The safety profile of EV + Pembro was similar to that observed in EV-103/KEYNOTE-869 in cisplatin-ineligible patients with la/mUC. This article summarizes the data and the FDA thought process supporting traditional approval of EV + Pembro, as well as additional exploratory analyses conducted by the FDA.
Data 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

AbstractPurpose:
Understanding resistance to selective FGFR inhibitors is crucial to improve the clinical outcomes of patients with FGFR2-driven malignancies.
Experimental Design:
We analyzed sequential ctDNA, ± whole-exome sequencing, or targeted next-generation sequencing on tissue biopsies from patients with tumors harboring activating FGFR2 alterations progressing on pan-FGFR–selective inhibitors, collected in the prospective UNLOCK program. FGFR2::BICC1 Ba/F3 and patient-derived xenograft models were used for functional studies.
Results:
Thirty-six patients were included. In cholangiocarcinoma, at resistance to both reversible inhibitors (e.g., pemigatinib and erdafitinib) and the irreversible inhibitor futibatinib, polyclonal FGFR2 kinase domain mutations were frequent (14/27 patients). Tumors other than cholangiocarcinoma shared the same mutated FGFR2 residues, but polyclonality was rare (1/9 patients). At resistance to reversible inhibitors, 14 residues in the FGFR2 kinase domain were mutated—after futibatinib, only the molecular brake N550 and the gatekeeper V565. Off-target alterations in PI3K/mTOR and MAPK pathways were found in 11 patients, often together with on-target mutations. At progression to a first FGFR inhibitor, 12 patients received futibatinib or lirafugratinib (irreversible inhibitors), with variable clinical outcomes depending on previous resistance mechanisms. Two patients with TSC1 or PIK3CA mutations benefited from everolimus. In cell viability assays on Ba/F3 and in pharmacologic studies on patient-derived xenografts, irreversible inhibitors retained better activity against FGFR2 kinase domain mutations, with lirafugratinib active against the recalcitrant V565L/F/Y.
Conclusions:
At progression to FGFR inhibitors, FGFR2-driven malignancies are characterized by high intra- and interpatient molecular heterogeneity, particularly in cholangiocarcinoma. Resistance to FGFR inhibitors can be overcome by sequential, molecularly oriented treatment strategies across FGFR2-driven tumors.
Data from Clonal Hematopoiesis and Clinical Outcomes in Metastatic Castration-Resistant Prostate Cancer Patients Given Androgen Receptor Pathway Inhibitors (Alliance A031201)
Authors: Jensen Jeffrey L. , Bobek Olivia , Chan Irenaeus C. C. , Miller Brian C. , Hillman David W. , Heller Glenn , Druley Todd , Armstrong Andrew J. , Morris Michael J. , Milowsky Matthew I. , Beltran Himisha , Bolton Kelly L. , Coombs Catherine C.
Published: November 2024

AbstractPurpose:
Mutations in hematopoietic progenitor cells accumulate with age leading to clonal expansion, termed clonal hematopoiesis (CH). CH in the general population is associated with hematopoietic neoplasms and reduced overall survival (OS), predominantly through cardiovascular adverse events (CVAE). Because androgen receptor pathway inhibitors (ARPI) used in metastatic castration-resistant prostate cancer (mCRPC) are also associated with CVAEs and because CH negatively impacted survival in an advanced solid tumor cohort, we hypothesized that CH in mCRPC may be associated with increased CVAEs and inferior survival.
Experimental Design:
A targeted DNA sequencing panel captured common CH mutations in pretreatment blood samples from 957 patients enrolled in Alliance A031201: a randomized trial of enzalutamide ± abiraterone/prednisone in the first-line mCRPC setting. The primary outcome was the impact of CH on OS; the secondary outcomes were progression-free survival (PFS) and CVAEs.
Results:
Baseline comorbidities were similar by CH status. No differences in OS/progression-free survival were detected regardless of treatment arm or the variant allele frequency threshold used to define CH [primary: 2% (normal-CH, N-CH); exploratory: 0.5% (low-CH) and 10% (high-CH, H-CH)]. Patients with H-CH (7.2%) and TET2-mutated N-CH (6.0%) had greater odds of any CVAE (14.5% vs. 4.0%; P = 0.0004 and 12.3% vs. 4.2%; P = 0.010, respectively). More major CVAEs were observed in patients with H-CH (5.8% vs. 1.9%; P = 0.042) and N-CH (3.4% vs. 1.8%; P = 0.147).
Conclusions:
CH did not affect survival in patients with mCRPC treated with ARPIs in A031201. H-CH and TET2-mutated CH were associated with more CVAEs. These findings inform the risk/benefit discussion about ARPIs in mCRPC.
Data 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

AbstractPurpose:
To propose a novel recursive partitioning analysis (RPA) classification model in patients with IDH-wildtype glioblastomas that incorporates the recently expanded conception of the extent of resection (EOR) in terms of both supramaximal and total resections.
Experimental Design:
This multicenter cohort study included a developmental cohort of 622 patients with IDH-wildtype glioblastomas from a single institution (Severance Hospital) and validation cohorts of 536 patients from three institutions (Seoul National University Hospital, Asan Medical Center, and Heidelberg University Hospital). All patients completed standard treatment including concurrent chemoradiotherapy and underwent testing to determine their IDH mutation and MGMTp methylation status. EORs were categorized into either supramaximal, total, or non-total resections. A novel RPA model was then developed and compared with a previous Radiation Therapy Oncology Group (RTOG) RPA model.
Results:
In the developmental cohort, the RPA model included age, MGMTp methylation status, Karnofsky performance status, and EOR. Younger patients with MGMTp methylation and supramaximal resections showed a more favorable prognosis [class I: median overall survival (OS) 57.3 months], whereas low-performing patients with non-total resections and without MGMTp methylation showed the worst prognosis (class IV: median OS 14.3 months). The prognostic significance of the RPA was subsequently confirmed in the validation cohorts, which revealed a greater separation between prognostic classes for all cohorts compared with the previous RTOG RPA model.
Conclusions:
The proposed RPA model highlights the impact of supramaximal versus total resections and incorporates clinical and molecular factors into survival stratification. The RPA model may improve the accuracy of assessing prognostic groups.

See related commentary by Karschnia et al., p. 4811
Supplementary Table 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 Table S1. Frag J-Jm Interactors
Supplementary Figure S2 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 S2. Full-length GRAIL1 does not interact with DNAJA1-GFP.
Supplementary Figure 6 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

S6. METTL14-mediated m6A methylation of Bim mRNA maintains its stability and increases Bim expression.
Supplementary Figure 1 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

S1. The validation of resistance to third-generation TKIs osimertinib, furmonertinib and almonertinib in osimertinib-resistant NSCLC cells.
Supplementary Table 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

Primer sequences for qRT-PCR
Table 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

Univariate and multivariate Cox proportional hazard analyses of OS in 189 patients with TNBC.
Figure S5 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 the interaction between PDAC cells and human umbilical vein endothelial cells, and predicted transcriptional regulation of CXCL8 by MYC
Figure S2 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 proliferation and apoptosis in PDAC cells in vitro.
Supplementary Figure S2 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

Unbiased discovery of PM cancer programs and association with patient survival
Supplementary Video 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

Live cell imaging of EML4-overexpressing H358 cells in wound healing assay.
Supplementary Video S4 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

Live cell imaging of EML4-overexpressing H358 cells in wound healing assay.
Supplementary Video 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

Live cell imaging of EML4-overexpressing A549 cells in wound healing assay.
Supplementary Table S4 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

BLVRA m6A and mRNA expression levels in the validation cohorts.
Supplementary Figure 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

The oncogenic function of EML4.
Supplementary Figure S6 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

Global m6A hypo-methylation in LUAD.
Supplementary Figure 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

The function of BLVRA m6A.
Supplementary Figure S11 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

Toxicity assessment of STM2457 treatment.
Supplementary Table 1 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

List of regulatory approvals for targeted therapies and associated clinical trials in SCRUM-Japan MONSTAR-SCREEN project
Supplementary Figure 7 from Rational Protein Engineering to Enhance MHC-Independent T-cell Receptors
Authors: Chang Ju-Fang , Landmann Jack H. , Chang Tien-Ching , Selli Mehmet Emrah , Tenzin Yangdon , Warrington John M. , Ritchey Julie , Hsu Yu-Sung , Slade Michael , Gupta Deepesh Kumar , DiPersio John F. , Holehouse Alex S. , Singh Nathan
Published: November 2024

Supplementary Figure 7 | a, Overlay of predicted mut031 α chain variable region and resolved FMC63 variable chain structure. Modeling performed using AlphaFold2. b, Memory lineages of human T cells engineered to express miTCR1 WT or mut035 at the conclusion of manufacturing cultures. c-d, Proportion of human T cells that were early lineage (naïve or central memory) c, throughout 6 day stimulation manufacturing cultures or d, one day after clearance of Nalm6. e, Expansion of human T cells expressing miTCR1 WT, mut035 or 19/BBζ CAR from two donors. b-d, data from one donor.
Supplementary Tables S5 and S6 from Clinical Validation of a Cell-Free DNA Fragmentome Assay for Augmentation of Lung Cancer Early Detection
Authors: Mazzone Peter J. , Bach Peter B. , Carey Jacob , Schonewolf Caitlin A. , Bognar Katalin , Ahluwalia Manmeet S. , Cruz-Correa Marcia , Gierada David , Kotagiri Sonali , Lloyd Kathryn , Maldonado Fabien , Ortendahl Jesse D. , Sequist Lecia V. , Silvestri Gerard A. , Tanner Nichole , Thompson Jeffrey C. , Vachani Anil , Wong Kwok-Kin , Zaidi Ali H. , Catallini Joseph , Gershman Ariel , Lumbard Keith , Millberg Laurel K. , Nawrocki Jeff , Portwood Carter , Rangnekar Aakanksha , Sheridan Carolina Campos , Trivedi Niti , Wu Tony , Zong Yuhua , Cotton Lindsey , Ryan Allison , Cisar Christopher , Leal Alessandro , Dracopoli Nicholas , Scharpf Robert B. , Velculescu Victor E. , Pike Luke R. G.
Published: November 2024

Whole genome cfDNA analyses. Clinical and demographic characteristics of individuals analyzed.
Supplementary Figure 7 from ROR2 Regulates Cellular Plasticity in Pancreatic Neoplasia and Adenocarcinoma
Authors: Benitz Simone , Steep Alec , Nasser Malak M. , Preall Jonathan , Mahajan Ujjwal Mukund , McQuithey Holly , Loveless Ian , Davis Erick T. , Wen Hui-Ju , Long Daniel W. , Metzler Thomas , Zwernik Samuel , Louw Michaela , Rempinski Donald , Salas-Escabillas Daniel J. , Brender Sydney M. , Song Linghao , Huang Ling , Theisen Brian K. , Zhang Zhenyu , Steele Nina G. , Regel Ivonne , Bednar Filip , Crawford Howard C.
Published: November 2024

ROR2 regulates cell proliferation.
Supplementary Figure 2 from ROR2 Regulates Cellular Plasticity in Pancreatic Neoplasia and Adenocarcinoma
Authors: Benitz Simone , Steep Alec , Nasser Malak M. , Preall Jonathan , Mahajan Ujjwal Mukund , McQuithey Holly , Loveless Ian , Davis Erick T. , Wen Hui-Ju , Long Daniel W. , Metzler Thomas , Zwernik Samuel , Louw Michaela , Rempinski Donald , Salas-Escabillas Daniel J. , Brender Sydney M. , Song Linghao , Huang Ling , Theisen Brian K. , Zhang Zhenyu , Steele Nina G. , Regel Ivonne , Bednar Filip , Crawford Howard C.
Published: November 2024

ROR2 is associated with gastric identity.
Supplemental Table 3 from Mechanisms of Resistance to Oncogenic KRAS Inhibition in Pancreatic Cancer
Authors: Dilly Julien , Hoffman Megan T. , Abbassi Laleh , Li Ziyue , Paradiso Francesca , Parent Brendan D. , Hennessey Connor J. , Jordan Alexander C. , Morgado Micaela , Dasgupta Shatavisha , Uribe Giselle A. , Yang Annan , Kapner Kevin S. , Hambitzer Felix P. , Qiang Li , Feng Hanrong , Geisberg Jacob , Wang Junning , Evans Kyle E. , Lyu Hengyu , Schalck Aislyn , Feng Ningping , Lopez Anastasia M. , Bristow Christopher A. , Kim Michael P. , Rajapakshe Kimal I. , Bahrambeigi Vahid , Roth Jennifer A. , Garg Kavita , Guerrero Paola A. , Stanger Ben Z. , Cristea Simona , Lowe Scott W. , Baslan Timour , Van Allen Eliezer M. , Mancias Joseph D. , Chan Emily , Anderson Abraham , Katlinskaya Yuliya V. , Shalek Alex K. , Hong David S. , Pant Shubham , Hallin Jill , Anderes Kenna , Olson Peter , Heffernan Timothy P. , Chugh Seema , Christensen James G. , Maitra Anirban , Wolpin Brian M. , Raghavan Srivatsan , Nowak Jonathan A. , Winter Peter S. , Dougan Stephanie K. , Aguirre Andrew J.
Published: November 2024

MRTX1133 sensitivty across the PRISM cohort of cell lines.
Supplementary Figure S7 from Mechanisms of Response and Tolerance to Active RAS Inhibition in KRAS-Mutant Non–Small Cell Lung Cancer
Authors: Araujo Haniel A. , Pechuan-Jorge Ximo , Zhou Teng , Do Minh Truong , Hu Xin , Rojas Alvarez Frank R. , Salvatierra Maria E. , Ibarguen Heladio P. , Lee Richard , Raghulan Rashi , Shah Harshit , Moreno Ayala Mariela A. , Chen Kevin , Tovbis Shifrin Nataliya , Wu Shuhong , Solis Soto Luisa M. , Negrao Marcelo V. , Gibbons Don L. , Hong David S. , Roth Jack A. , Heymach John V. , Zhang Jianjun , Jiang Jingjing , Singh Mallika , Smith Jacqueline A.M. , Quintana Elsa , Skoulidis Ferdinandos
Published: November 2024

Supplementary Figure S7. Single-cell atlas of tumor infiltrating lymphoid cells in response to RAS inhibition.
Supplementary Figure S5 from Mechanisms of Response and Tolerance to Active RAS Inhibition in KRAS-Mutant Non–Small Cell Lung Cancer
Authors: Araujo Haniel A. , Pechuan-Jorge Ximo , Zhou Teng , Do Minh Truong , Hu Xin , Rojas Alvarez Frank R. , Salvatierra Maria E. , Ibarguen Heladio P. , Lee Richard , Raghulan Rashi , Shah Harshit , Moreno Ayala Mariela A. , Chen Kevin , Tovbis Shifrin Nataliya , Wu Shuhong , Solis Soto Luisa M. , Negrao Marcelo V. , Gibbons Don L. , Hong David S. , Roth Jack A. , Heymach John V. , Zhang Jianjun , Jiang Jingjing , Singh Mallika , Smith Jacqueline A.M. , Quintana Elsa , Skoulidis Ferdinandos
Published: November 2024

Supplementary Figure S5. Active RAS inhibition in KrasG12C/+;Lkb1-/- GEMMs.
Supplementary Figure S2 from Mechanisms of Response and Tolerance to Active RAS Inhibition in KRAS-Mutant Non–Small Cell Lung Cancer
Authors: Araujo Haniel A. , Pechuan-Jorge Ximo , Zhou Teng , Do Minh Truong , Hu Xin , Rojas Alvarez Frank R. , Salvatierra Maria E. , Ibarguen Heladio P. , Lee Richard , Raghulan Rashi , Shah Harshit , Moreno Ayala Mariela A. , Chen Kevin , Tovbis Shifrin Nataliya , Wu Shuhong , Solis Soto Luisa M. , Negrao Marcelo V. , Gibbons Don L. , Hong David S. , Roth Jack A. , Heymach John V. , Zhang Jianjun , Jiang Jingjing , Singh Mallika , Smith Jacqueline A.M. , Quintana Elsa , Skoulidis Ferdinandos
Published: November 2024

Supplementary Figure S2. Models and mechanisms of acquired resistance to RAS inhibitors
Supplementary Table 2 from A Classical Epithelial State Drives Acute Resistance to KRAS Inhibition in Pancreatic Cancer
Authors: Singhal Anupriya , Styers Hannah C. , Rub Jonathan , Li Zhuxuan , Torborg Stefan R. , Kim Jung Yun , Grbovic-Huezo Olivera , Feng Huijin , Tarcan Zeynep Cagla , Sahin Ozkan Hulya , Hallin Jill , Basturk Olca , Yaeger Rona , Christensen James G. , Betel Doron , Yan Yan , Chio Iok In Christine , de Stanchina Elisa , Tammela Tuomas
Published: November 2024

Supplementary Table 2 includes primer sequences and antibodies used in this study.
Supplementary Table 5 from A Call for Innovative Translational and Clinical Research to Address China’s Unique Cancer Landscape
Authors: Zhang Chaoqi , Wu Peng , Li Dongyu , Gu Xuanyu , Lin Chuqi , Zhou Junhan , Shang Dexin , Liu Jingjing , Ma Ruijie , Zhao Bohui , Sun Nan , He Jie
Published: November 2024

Supplementary Table 5. The number of clinical trials evaluating Chinese domestic anti-cancer agents regarding different types of cancer from 2018-2023.
Supplementary Table 4 from A Call for Innovative Translational and Clinical Research to Address China’s Unique Cancer Landscape
Authors: Zhang Chaoqi , Wu Peng , Li Dongyu , Gu Xuanyu , Lin Chuqi , Zhou Junhan , Shang Dexin , Liu Jingjing , Ma Ruijie , Zhao Bohui , Sun Nan , He Jie
Published: November 2024

Supplementary Table 4. The incidence rates, in terms of age-standardized rates (ASRs), of the top 20 cancer types in China and globally from the 2022 edition of data of the GLOBOCAN database.
Data 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

Abstract
Immunotherapies have shown great promise in pleural mesothelioma (PM), yet most patients still do not achieve significant clinical response, highlighting the importance of improving the understanding of the tumor microenvironment (TME). Here, we utilized high-throughput, single-cell RNA sequencing (scRNA-seq) to de novo identify 54 expression programs and construct a comprehensive cellular catalog of the PM TME. We found four cancer-intrinsic programs associated with poor disease outcome and a novel fetal-like, endothelial cell population that likely responds to VEGF signaling and promotes angiogenesis. Across cellular compartments, we observe substantial difference in the TME associated with a cancer-intrinsic sarcomatoid signature, including enrichment in fetal-like endothelial cells, CXCL9+ macrophages, and cytotoxic, exhausted, and regulatory T cells, which we validated using imaging and bulk deconvolution analyses on independent cohorts. Finally, we show, both computationally and experimentally, that NKG2A:HLA-E interaction between NK and tumor cells represents an important new therapeutic axis in PM, especially for epithelioid cases.

Significance: This manuscript presents the first single-cell RNA sequencing atlas of PM tumor microenvironment. Findings of translational relevance, validated experimentally and using independent bulk cohorts, include identification of gene programs predictive of survival, a fetal-like endothelial cell population, and NKG2A blockade as a promising new immunotherapeutic intervention in PM.
Data 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

Abstract
Comprehensive N6-methyladenosine (m6A) epitranscriptomic profiling of primary tumors remains largely uncharted. Here, we profiled the m6A epitranscriptome of 10 nonneoplastic lung tissues and 51 lung adenocarcinoma (LUAD) tumors, integrating the corresponding transcriptomic, proteomic, and extensive clinical annotations. We identified distinct clusters and genes that were exclusively linked to disease progression through m6A modifications. In comparison with nonneoplastic lung tissues, we identified 430 transcripts to be hypo-methylated and 222 to be hyper-methylated in tumors. Among these genes, EML4 emerged as a novel metastatic driver, displaying significant hypermethylation in tumors. m6A modification promoted the translation of EML4, leading to its widespread overexpression in primary tumors. Functionally, EML4 modulated cytoskeleton dynamics by interacting with ARPC1A, enhancing lamellipodia formation, cellular motility, local invasion, and metastasis. Clinically, high EML4 protein abundance correlated with features of metastasis. METTL3 small-molecule inhibitor markedly diminished both EML4 m6A and protein abundance and efficiently suppressed lung metastases in vivo.

Significance: Our study reveals a dynamic and functional epitranscriptomic landscape in LUAD, offering a valuable resource for further research in the field. We identified EML4 hypermethylation as a key driver of tumor metastasis, highlighting a novel therapeutic strategy of targeting EML4 to prevent LUAD metastasis.
Data from ROR2 Regulates Cellular Plasticity in Pancreatic Neoplasia and Adenocarcinoma
Authors: Benitz Simone , Steep Alec , Nasser Malak M. , Preall Jonathan , Mahajan Ujjwal Mukund , McQuithey Holly , Loveless Ian , Davis Erick T. , Wen Hui-Ju , Long Daniel W. , Metzler Thomas , Zwernik Samuel , Louw Michaela , Rempinski Donald , Salas-Escabillas Daniel J. , Brender Sydney M. , Song Linghao , Huang Ling , Theisen Brian K. , Zhang Zhenyu , Steele Nina G. , Regel Ivonne , Bednar Filip , Crawford Howard C.
Published: November 2024

Abstract
Cellular plasticity is a hallmark of pancreatic ductal adenocarcinoma (PDAC) starting from the conversion of normal cells into precancerous lesions, to the progression of carcinoma subtypes associated with aggressiveness and therapeutic response. We discovered that normal acinar cell differentiation, maintained by the transcription factor PDX1, suppresses a broad gastric cell identity that is maintained in metaplasia, neoplasia, and the classical subtype of PDAC in a mouse and human. We identified the receptor tyrosine kinase ROR2 as marker of a gastric metaplasia-like identity in pancreas neoplasms. Ablation of Ror2 in a mouse model of pancreatic tumorigenesis promoted a switch to a gastric pit cell identity that largely persisted through progression to the classical subtype of PDAC. In both human and mouse pancreatic cancer, ROR2 activity continued to antagonize the gastric pit cell identity, strongly promoting an epithelial to mesenchymal transition, conferring resistance to KRAS inhibition, and vulnerability to AKT inhibition.

Significance: We discovered the receptor tyrosine kinase ROR2 as an important regulator of cellular identity in pancreatic precancerous lesions and pancreatic cancer. ROR2 drives an aggressive PDAC phenotype and confers resistance to KRAS inhibitors, suggesting that targeting ROR2 will enhance sensitivity to this new generation of targeted therapies.

See related commentary by Marasco and Misale, p. 2018
Data from Mechanisms of Resistance to Oncogenic KRAS Inhibition in Pancreatic Cancer
Authors: Dilly Julien , Hoffman Megan T. , Abbassi Laleh , Li Ziyue , Paradiso Francesca , Parent Brendan D. , Hennessey Connor J. , Jordan Alexander C. , Morgado Micaela , Dasgupta Shatavisha , Uribe Giselle A. , Yang Annan , Kapner Kevin S. , Hambitzer Felix P. , Qiang Li , Feng Hanrong , Geisberg Jacob , Wang Junning , Evans Kyle E. , Lyu Hengyu , Schalck Aislyn , Feng Ningping , Lopez Anastasia M. , Bristow Christopher A. , Kim Michael P. , Rajapakshe Kimal I. , Bahrambeigi Vahid , Roth Jennifer A. , Garg Kavita , Guerrero Paola A. , Stanger Ben Z. , Cristea Simona , Lowe Scott W. , Baslan Timour , Van Allen Eliezer M. , Mancias Joseph D. , Chan Emily , Anderson Abraham , Katlinskaya Yuliya V. , Shalek Alex K. , Hong David S. , Pant Shubham , Hallin Jill , Anderes Kenna , Olson Peter , Heffernan Timothy P. , Chugh Seema , Christensen James G. , Maitra Anirban , Wolpin Brian M. , Raghavan Srivatsan , Nowak Jonathan A. , Winter Peter S. , Dougan Stephanie K. , Aguirre Andrew J.
Published: November 2024

Abstract
KRAS inhibitors demonstrate clinical efficacy in pancreatic ductal adenocarcinoma (PDAC); however, resistance is common. Among patients with KRASG12C-mutant PDAC treated with adagrasib or sotorasib, mutations in PIK3CA and KRAS, and amplifications of KRASG12C, MYC, MET, EGFR, and CDK6 emerged at acquired resistance. In PDAC cell lines and organoid models treated with the KRASG12D inhibitor MRTX1133, epithelial-to-mesenchymal transition and PI3K-AKT-mTOR signaling associate with resistance to therapy. MRTX1133 treatment of the KrasLSL-G12D/+; Trp53LSL-R172H/+; p48-Cre (KPC) mouse model yielded deep tumor regressions, but drug resistance ultimately emerged, accompanied by amplifications of Kras, Yap1, Myc, Cdk6, and Abcb1a/b, and co-evolution of drug-resistant transcriptional programs. Moreover, in KPC and PDX models, mesenchymal and basal-like cell states displayed increased response to KRAS inhibition compared to the classical state. Combination treatment with KRASG12D inhibition and chemotherapy significantly improved tumor control in PDAC mouse models. Collectively, these data elucidate co-evolving resistance mechanisms to KRAS inhibition and support multiple combination therapy strategies.

Significance: Acquired resistance may limit the impact of KRAS inhibition in patients with PDAC. Using clinical samples and multiple preclinical models, we define heterogeneous genetic and non-genetic mechanisms of resistance to KRAS inhibition that may guide combination therapy approaches to improve the efficacy and durability of these promising therapies for patients.

See related commentary by Marasco and Misale, p. 2018
Data from A Classical Epithelial State Drives Acute Resistance to KRAS Inhibition in Pancreatic Cancer
Authors: Singhal Anupriya , Styers Hannah C. , Rub Jonathan , Li Zhuxuan , Torborg Stefan R. , Kim Jung Yun , Grbovic-Huezo Olivera , Feng Huijin , Tarcan Zeynep Cagla , Sahin Ozkan Hulya , Hallin Jill , Basturk Olca , Yaeger Rona , Christensen James G. , Betel Doron , Yan Yan , Chio Iok In Christine , de Stanchina Elisa , Tammela Tuomas
Published: November 2024

Abstract
Intratumoral heterogeneity in pancreatic ductal adenocarcinoma (PDAC) is characterized by a balance between basal and classical epithelial cancer cell states, with basal dominance associating with chemoresistance and a dismal prognosis. Targeting oncogenic KRAS, the primary driver of pancreatic cancer, shows early promise in clinical trials, but efficacy is limited by acquired resistance. Using genetically engineered mouse models and patient-derived xenografts, we find that basal PDAC cells are highly sensitive to KRAS inhibitors. Employing fluorescent and bioluminescent reporter systems, we longitudinally track cell-state dynamics in vivo and reveal a rapid, KRAS inhibitor–induced enrichment of the classical state. Lineage tracing uncovers that these enriched classical PDAC cells are a reservoir for disease relapse. Genetic or chemotherapy-mediated ablation of the classical cell state is synergistic with KRAS inhibition, providing a preclinical proof of concept for this therapeutic strategy. Our findings motivate combining classical state–directed therapies with KRAS inhibitors to deepen responses and counteract resistance in pancreatic cancer.

Significance: KRAS inhibitors hold promise in pancreatic cancer, but responses are limited by acquired resistance. We find that a classical epithelial cancer cell state is acutely resistant to KRAS inhibition and serves as a reservoir for disease relapse. Targeting the classical state alongside KRAS inhibition deepens responses, revealing a potent therapeutic strategy.

See related commentary by Marasco and Misale, p. 2018
Advancing Cancer Prevention through an AI-Based Integration of Traditional and Western Medicine
Authors: Zhang Peng , Zhang Qian , Li Shao
Published: November 2024

Traditional Chinese medicine has accumulated a wealth of experiences in individualized cancer prevention and serves as a complement to Western medicine. We propose an artificial intelligence–based integration of traditional and Western medicine as a new paradigm for cancer prevention, encompassing cancer risk screening and preventive intervention, which will provide new solutions for cancer prevention and offer fresh perspectives for traditional medicine research worldwide.
Building an Organ-Wide Macroscopic View of Cancer Hallmarks
Authors: Liu Suling , Wang Yuan , Feng Jiawen , Liu Zhihua , Zhou Shengtao
Published: November 2024

Despite an increasingly detailed understanding of cancer hallmarks at molecular or atomic resolution, most studies, however, fall short of investigating the systemic interactions of cancer with the human body. We propose to investigate the hallmarks of cancer from an organ-wide macroscopic view, discuss the challenges in preclinical and clinical research to study the cross-organ regulation of cancer together with potential directions to overcome these challenges, and foresee how this holistic view may be translated into more effective therapies.
Supplementary Table 7 from Therapy-Related Myeloid Neoplasms: Complex Interactions among Cytotoxic Therapies, Genetic Factors, and Aberrant Microenvironment
Authors: Singhal Deepak , Kutyna Monika M. , Hahn Christopher N. , Shah Mithun Vinod , Hiwase Devendra K.
Published: November 2024

Supplementary Table 7 shows allogeneic stem cell transplant outcome across different studies in t-MN
Supplementary Table 1 from Therapy-Related Myeloid Neoplasms: Complex Interactions among Cytotoxic Therapies, Genetic Factors, and Aberrant Microenvironment
Authors: Singhal Deepak , Kutyna Monika M. , Hahn Christopher N. , Shah Mithun Vinod , Hiwase Devendra K.
Published: November 2024

Supplementary Table 1 shows distribution of t-MN cases according to type of primary cancer/diseases
Suppl. Table 4 from Tracking Rare Single Donor and Recipient Immune and Leukemia Cells after Allogeneic Hematopoietic Cell Transplantation Using Mitochondrial DNA Mutations
Authors: Penter Livius , Cieri Nicoletta , Maurer Katie , Kwok Marwan , Lyu Haoxiang , Lu Wesley S. , Oliveira Giacomo , Gohil Satyen H. , Leshchiner Ignaty , Lareau Caleb A. , Ludwig Leif S. , Neuberg Donna S. , Kim Haesook T. , Li Shuqiang , Bullinger Lars , Ritz Jerome , Getz Gad , Garcia Jacqueline S. , Soiffer Robert J. , Livak Kenneth J. , Wu Catherine J.
Published: November 2024

Total-seq B oligotags.
Suppl. Fig. 7 from Tracking Rare Single Donor and Recipient Immune and Leukemia Cells after Allogeneic Hematopoietic Cell Transplantation Using Mitochondrial DNA Mutations
Authors: Penter Livius , Cieri Nicoletta , Maurer Katie , Kwok Marwan , Lyu Haoxiang , Lu Wesley S. , Oliveira Giacomo , Gohil Satyen H. , Leshchiner Ignaty , Lareau Caleb A. , Ludwig Leif S. , Neuberg Donna S. , Kim Haesook T. , Li Shuqiang , Bullinger Lars , Ritz Jerome , Getz Gad , Garcia Jacqueline S. , Soiffer Robert J. , Livak Kenneth J. , Wu Catherine J.
Published: November 2024

Tracking co-evolution of somatic nuclear and mitochondrial DNA mutations in CLL and AML using single cell DNA and protein sequencing (Tapestri).
Suppl. Fig. 3 from Tracking Rare Single Donor and Recipient Immune and Leukemia Cells after Allogeneic Hematopoietic Cell Transplantation Using Mitochondrial DNA Mutations
Authors: Penter Livius , Cieri Nicoletta , Maurer Katie , Kwok Marwan , Lyu Haoxiang , Lu Wesley S. , Oliveira Giacomo , Gohil Satyen H. , Leshchiner Ignaty , Lareau Caleb A. , Ludwig Leif S. , Neuberg Donna S. , Kim Haesook T. , Li Shuqiang , Bullinger Lars , Ritz Jerome , Getz Gad , Garcia Jacqueline S. , Soiffer Robert J. , Livak Kenneth J. , Wu Catherine J.
Published: November 2024

Longitudinal changes of somatic nuclear and mitochondrial DNA mutations in genetically stable CLL.
Suppl. Fig. 20 from Tracking Rare Single Donor and Recipient Immune and Leukemia Cells after Allogeneic Hematopoietic Cell Transplantation Using Mitochondrial DNA Mutations
Authors: Penter Livius , Cieri Nicoletta , Maurer Katie , Kwok Marwan , Lyu Haoxiang , Lu Wesley S. , Oliveira Giacomo , Gohil Satyen H. , Leshchiner Ignaty , Lareau Caleb A. , Ludwig Leif S. , Neuberg Donna S. , Kim Haesook T. , Li Shuqiang , Bullinger Lars , Ritz Jerome , Getz Gad , Garcia Jacqueline S. , Soiffer Robert J. , Livak Kenneth J. , Wu Catherine J.
Published: November 2024

Co-evolution of somatic nuclear and mitochondrial DNA mutations in AML.
Suppl. Fig. 2 from Tracking Rare Single Donor and Recipient Immune and Leukemia Cells after Allogeneic Hematopoietic Cell Transplantation Using Mitochondrial DNA Mutations
Authors: Penter Livius , Cieri Nicoletta , Maurer Katie , Kwok Marwan , Lyu Haoxiang , Lu Wesley S. , Oliveira Giacomo , Gohil Satyen H. , Leshchiner Ignaty , Lareau Caleb A. , Ludwig Leif S. , Neuberg Donna S. , Kim Haesook T. , Li Shuqiang , Bullinger Lars , Ritz Jerome , Getz Gad , Garcia Jacqueline S. , Soiffer Robert J. , Livak Kenneth J. , Wu Catherine J.
Published: November 2024

Longitudinal changes of somatic nuclear and mitochondrial DNA mutations in naturally progressing CLL.