bluuebunny/crossref_metadata_2025 huggingface dataset:
Figure S5 from Comprehensive Metabolic Tracing Reveals the Origin and Catabolism of Cysteine in Mammalian Tissues and Tumors
Authors: Yoon Sang Jun , Combs Joseph A. , Falzone Aimee , Prieto-Farigua Nicolas , Caldwell Samantha , Ackerman Hayley D. , Flores Elsa R. , DeNicola Gina M.
Published: September 2024

Figure S5 contains the total metabolite levels in liver and pancreas cancer models related to Figure 4
Supplementary Information from Ablation of p57+ Quiescent Cancer Stem Cells Suppresses Recurrence After Chemotherapy of Intestinal Tumors
Authors: Oka Takeru , Higa Tsunaki , Sugahara Osamu , Koga Daisuke , Nakayama Shogo , Nakayama Keiichi I.
Published: September 2024

Supplementary Table Information
Supplementary Figures S1–S5
Supplementary Figure Legends
Source Data from Ablation of p57+ Quiescent Cancer Stem Cells Suppresses Recurrence After Chemotherapy of Intestinal Tumors
Authors: Oka Takeru , Higa Tsunaki , Sugahara Osamu , Koga Daisuke , Nakayama Shogo , Nakayama Keiichi I.
Published: September 2024

Source Data
Supplementary Methods from ANO1 reprograms cholesterol metabolism and the tumor microenvironment to promote cancer metastasis
Authors: Deng Chun-Miao , Zhang Guo-Geng , Liu Qin-Wen , Xu Jiao-Jiao , Liu Zhi-Chao , Yang Jing , Xu Tao-Yang , Li Zhi-Gang , Zhang Fan , Li Bin
Published: September 2024

Supplementary Methods shows supplementary Materials and Methods
Supplementary Figure 2 from Hypoxia potentiates the inflammatory fibroblast phenotype promoted by pancreatic cancer cell-derived cytokines
Authors: Schwoerer Simon , Cimino Francesco V. , Ros Manon , Tsanov Kaloyan M. , Ng Charles , Lowe Scott W. , Carmona-Fontaine Carlos , Thompson Craig B.
Published: September 2024

Supplementary Figure 2, related to Figure 2
Table S1, S2 from DAB2IP is a bifunctional tumor suppressor that regulates wildtype RAS and inflammatory cascades in KRAS mutant colon cancer
Authors: Miller Abigail L. , Perurena Naiara , Gardner Alycia , Hinoue Toshinori , Loi Patrick , Laird Peter W. , Cichowski Karen
Published: September 2024

Table S1: Genes enriched in tumor macrophages, Table S2: The methylation of RASGAPs in human colorectal cancer (TCGA)
Supplementary Materials and Methods from NAT10 drives cisplatin chemoresistance by enhancing ac4C-associated DNA repair in bladder cancer
Authors: Xie Ruihui , Cheng Liang , Huang Ming , Huang Lin , Chen Ziyue , Zhang Qiang , Li Hong , Lu Junlin , Wang Hongjin , Zhou Qianghua , Huang Jian , Chen Xu , Lin Tianxin
Published: September 2024

Supplementary Materials and Methods
Figure S1 from MEN1 degradation induced by neddylation and the CUL4B-DCAF7 axis promotes pancreatic neuroendocrine tumor progression
Authors: Xu Junfeng , Ye Zeng , Zhuo Qifeng , Gao Heli , Qin Yi , Llou Xin , Zhang Wuhu , Wang Fei , Wang Yan , Jing Desheng , Fan Guixiong , Zhang Yue , Chen Xuemin , Chen Jie , Xu Xiaowu , Yu Xianjun , Ji Shunrong
Published: September 2024

Representative tandem MS spectrum of the LPENYTDETWQK peptide from CUL4B as determined by IP-Mass Spec
Table S5 from Caffeine supplementation and FOXM1 inhibition enhance the antitumor effect of statins in neuroblastoma
Authors: Tran Gia-Buu , Ding Jane , Ye Bingwei , Liu Mengling , Yu Yajie , Zha Yunhong , Dong Zheng , Liu Kebin , Sudarshan Sunil , Ding Han-Fei
Published: September 2024

Go analysis of genes up-regulated by simvastatin
Supplementary Table from Ubiquitin ligases Siah1a/2 control alveolar macrophage functions to limit carcinogen-induced lung adenocarcinoma
Authors: Scortegagna Marzia , Du Yuanning , Bradley Linda M. , Wang Kun , Molinolo Alfredo , Ruppin Eytan , Murad Rabi , Ronai Ze'ev A.
Published: September 2024

Sup Table 2
Supplementary Data from Tumor-derived Small Extracellular Vesicles Inhibit the Efficacy of CAR T Cells against Solid Tumors
Authors: Guo Wei , Zhong Wenqun , Xiao Zebin , Qin Zhiyuan , Yang Jingbo , Wen Yi , Yu Ziyan , Li Yumei , Sheppard Neil C. , Fuchs Serge Y. , Xu Xiaowei , Herlyn Meenhard , June Carl H. , Pure Ellen
Published: September 2024

Supplementary Figures and Figure Legends
Supplementary Table 5 from CellMinerCDB: NCATS is a Web-Based Portal Integrating Public Cancer Cell Line Databases for Pharmacogenomic Explorations
Authors: Reinhold William C. , Wilson Kelli , Elloumi Fathi , Bradwell Katie R. , Ceribelli Michele , Varma Sudhir , Wang Yanghsin , Duveau Damien , Menon Nikhil , Trepel Jane , Zhang Xiaohu , Klumpp-Thomas Carleen , Michael Samuel , Shinn Paul , Luna Augustin , Thomas Craig , Pommier Yves
Published: September 2024

Multivariate prediction
Supplementary Table 1 from CellMinerCDB: NCATS is a Web-Based Portal Integrating Public Cancer Cell Line Databases for Pharmacogenomic Explorations
Authors: Reinhold William C. , Wilson Kelli , Elloumi Fathi , Bradwell Katie R. , Ceribelli Michele , Varma Sudhir , Wang Yanghsin , Duveau Damien , Menon Nikhil , Trepel Jane , Zhang Xiaohu , Klumpp-Thomas Carleen , Michael Samuel , Shinn Paul , Luna Augustin , Thomas Craig , Pommier Yves
Published: September 2024

Unique non-cancer drugs
Figure S3 from Ccr2+ monocyte-derived macrophages influence trajectories of acquired therapy resistance in Braf-mutant melanoma
Authors: Kim Dahihm , An Luye , Moon Jiwon , Maymi Viviana I. , McGurk Alexander I. , Rudd Brian D. , Fowell Deborah , White Andrew C.
Published: September 2024

Ccr2 infiltration does not impact the growth of TBP tumors in an untreated setting.
Supplementary File 5 from Proteasome Inhibition Sensitizes Liposarcoma to MDM2 Inhibition with Nutlin-3 by Activating the ATF4/CHOP Stress Response Pathway
Authors: Ludwig Michael P. , Galbraith Matthew D. , Eduthan Neetha Paul. , Hill Amanda A. , Clay Michael R. , Moreno Tellez Cristiam , Wilky Breelyn A. , Elias Anthony , Espinosa Joaquín Maximiliano. , Sullivan Kelly D.
Published: September 2024

Nutlin-3-proteasome inhibitor drug interaction SRB data.
Supplementary Figures from Targeting CD44 variant 5 with an antibody-drug conjugate is an effective therapeutic strategy for intrahepatic cholangiocarcinoma
Authors: Bei Yuncheng , He Jian , Dong Xuhui , Wang Yuxin , Wang Sijie , Guo Wan , Cai Chengjie , Xu Zhiye , Wei Jia , Liu Baorui , Zhang Nan , Shen Pingping
Published: September 2024

Supplementary Figures and legends
Supplemental Information from Inter- and intra-metastatic heterogeneity shapes adaptive therapy cycling dynamics
Authors: Gallaher Jill , Strobl Maximilian , West Jeffrey , Gatenby Robert , Zhang Jingsong , Robertson-Tessi Mark , Anderson Alexander R.A.
Published: September 2024

Supplemental methods, tables, and figures
Figure S7 from BRCA1 Insufficiency Induces a Hypersialylated Acidic Tumor Microenvironment that Promotes Metastasis and Immunotherapy Resistance
Authors: Shu Xiaodong , Li Jianjie , Chan Un In , Su Sek Man , Shi Changxiang , Zhang Xin , An Tingting , Xu Jun , Mo Lihua , Liu Jianlin , Wang Yuqing , Li Xiaoling , Deng Min , Lei Josh Haipeng , Wang Chunfei , Tian Hao , Sun Heng , Shim Joong Sup , Zhang Xuanjun , Dai Yunlu , Yao Zhicheng , Kuang Xiaying , Lin Ying , Deng Chu-Xia , Xu Xiaoling
Published: September 2024

Original picture
Table S5 from Elevated Mast Cell Abundance is Associated with Enrichment of CCR2+ Cytotoxic T cells and Favorable Prognosis in Lung Adenocarcinoma
Authors: Fan Fanfan , Gao Jian , Zhao Yue , Wang Jun , Meng Lu , Ma Jiaqiang , Li Teng , Han Han , Lai Jinglei , Gao Zhendong , Li Xiongfei , Guo Ran , Cao Zhiwei , Zhang Yang , Zhang Xiaoming , Chen Haiquan
Published: September 2024

Table S5
Figure S6 from Oncogenic Transformation Drives DNA Methylation Loss and Transcriptional Activation of Transposable Element Loci
Authors: Kanholm Tomas , Rentia Uzma , Hadley Melissa , Karlow Jennifer A. , Cox Olivia L. , Diab Noor , Bendall Matthew L. , Dawson Tyson , McDonald James I. , Xie Wenbing , Crandall Keith A. , Burns Kathleen H. , Baylin Stephen B. , Easwaran Hariharan , Chiappinelli Katherine B.
Published: September 2024

Supplemental Figure 6
Figure S2 from Oncogenic Transformation Drives DNA Methylation Loss and Transcriptional Activation of Transposable Element Loci
Authors: Kanholm Tomas , Rentia Uzma , Hadley Melissa , Karlow Jennifer A. , Cox Olivia L. , Diab Noor , Bendall Matthew L. , Dawson Tyson , McDonald James I. , Xie Wenbing , Crandall Keith A. , Burns Kathleen H. , Baylin Stephen B. , Easwaran Hariharan , Chiappinelli Katherine B.
Published: September 2024

Supplemental Figure 2
Figure S1 from Oncogenic Transformation Drives DNA Methylation Loss and Transcriptional Activation of Transposable Element Loci
Authors: Kanholm Tomas , Rentia Uzma , Hadley Melissa , Karlow Jennifer A. , Cox Olivia L. , Diab Noor , Bendall Matthew L. , Dawson Tyson , McDonald James I. , Xie Wenbing , Crandall Keith A. , Burns Kathleen H. , Baylin Stephen B. , Easwaran Hariharan , Chiappinelli Katherine B.
Published: September 2024

Supplemental Figure 1
Table S6 from Breast cancer mutations HER2 V777L and PIK3CA H1047R activate the p21-CDK4/6 –Cyclin D1 axis driving tumorigenesis and drug resistance.
Authors: Cheng Xiaoqing , Sun Yirui , Highkin Maureen , Vemalapally Nagalaxmi , Jin Xiaohua , Zhou Brandon , Prior Julie L. , Tipton Ashley R. , Li Shunqiang , Iliuk Anton , Achilefu Samuel , Hagemann Ian S. , Edwards John R. , Bose Ron
Published: September 2024

Phosphopeptides in Heatmap
Figures S1-S8 from Breast cancer mutations HER2 V777L and PIK3CA H1047R activate the p21-CDK4/6 –Cyclin D1 axis driving tumorigenesis and drug resistance.
Authors: Cheng Xiaoqing , Sun Yirui , Highkin Maureen , Vemalapally Nagalaxmi , Jin Xiaohua , Zhou Brandon , Prior Julie L. , Tipton Ashley R. , Li Shunqiang , Iliuk Anton , Achilefu Samuel , Hagemann Ian S. , Edwards John R. , Bose Ron
Published: September 2024

Figures S1-S8
Supplementary Table S6 from Deficiency of the Polycomb protein RYBP and TET methylcytosine oxidases promotes extensive CpG island hypermethylation and malignant transformation
Authors: Cui Wei , Huang Zhijun , Jin Seung-Gi , Johnson Jennifer , Lau Kin H. , Hostetter Galen , Pfeifer Gerd P.
Published: September 2024

Hypermethylated DMR regions of R/TET123 QKO that intersect with CGIs and associated genes
Supplementary Table S4 from The EstroGene database reveals diverse temporal, context-dependent, and bidirectional estrogen receptor regulomes in breast cancer
Authors: Li Zheqi , Li Tianqin , Yates Megan E. , Wu Yang , Ferber Amanda , Chen Lyuqin , Brown Daniel D. , Carroll Jason S. , Sikora Matthew J. , Tseng George C. , Oesterreich Steffi , Lee Adrian V.
Published: September 2024

Metadata of four ER ChIP-seq data sets for inter-data set concordance analysis
Supplementary Table S2 from The EstroGene database reveals diverse temporal, context-dependent, and bidirectional estrogen receptor regulomes in breast cancer
Authors: Li Zheqi , Li Tianqin , Yates Megan E. , Wu Yang , Ferber Amanda , Chen Lyuqin , Brown Daniel D. , Carroll Jason S. , Sikora Matthew J. , Tseng George C. , Oesterreich Steffi , Lee Adrian V.
Published: September 2024

Log2 (CPM+1) expression level of all genes and indication of low expression genes
Supplementary Table 3. from The genomic and epigenomic landscape of double-negative metastatic prostate cancer
Authors: Lundberg Arian , Zhang Meng , Aggarwal Rahul , Li Haolong , Zhang Li , Foye Adam , Sjöström Martin , Chou Jonathan , Chang Kevin , Moreno-Rodriguez Thaidy , Shrestha Raunak , Baskin Avi , Zhu Xiaolin , Weinstein Alana S. , Younger Noah , Alumkal Joshi J. , Beer Tomasz M. , Chi Kim N. , Evans Christopher P. , Gleave Martin , Lara Primo N. , Reiter Rob E. , Rettig Matthew B. , Witte Owen N. , Wyatt Alexander W. , Feng Felix Y. , Small Eric J. , Quigley David A.
Published: September 2024

ETS family fusions detected in the WCDT samples
Table S2 from Mesenchymal-like tumor cells and myofibroblastic cancer-associated fibroblasts are associated with progression and immunotherapy response of clear-cell renal cell carcinoma
Authors: Davidson Guillaume , Helleux Alexandra , Vano Yann A. , Lindner Véronique , Fattori Antonin , Cerciat Marie , Elaidi Reza Thierry. , Verkarre Virginie , Sun Cheng-Ming , Chevreau Christine , Bennamoun Mostefa , Lang Hervé , Tricard Thibault , Fridman Wolf Herman. , Sautes-Fridman Catherine , Su Xiaoping , Plassard Damien , Keime Celine , Thibault-Carpentier Christelle , Barthélémy Philippe , Oudard Stéphane Marie. , Davidson Irwin , Malouf Gabriel G.
Published: September 2024

Single-cell RNA sequencing markers for each global cluster and each re-clustering
Supplementary Figure Annotations from Mesenchymal-like tumor cells and myofibroblastic cancer-associated fibroblasts are associated with progression and immunotherapy response of clear-cell renal cell carcinoma
Authors: Davidson Guillaume , Helleux Alexandra , Vano Yann A. , Lindner Véronique , Fattori Antonin , Cerciat Marie , Elaidi Reza Thierry. , Verkarre Virginie , Sun Cheng-Ming , Chevreau Christine , Bennamoun Mostefa , Lang Hervé , Tricard Thibault , Fridman Wolf Herman. , Sautes-Fridman Catherine , Su Xiaoping , Plassard Damien , Keime Celine , Thibault-Carpentier Christelle , Barthélémy Philippe , Oudard Stéphane Marie. , Davidson Irwin , Malouf Gabriel G.
Published: September 2024

Annotation of supplementary figures
Supplementary Data from SENP1 decreases RNF168 phase separation to promote DNA damage repair and drug resistance in colon cancer
Authors: Wei Min , Huang Xinping , Liao Liming , Tian Yonglu , Zheng Xiaofeng
Published: September 2024

Supplementary video 1
Supplemental Figures and Figure Legends from Abemaciclib is effective in palbociclib-resistant hormone receptor-positive metastatic breast cancers
Authors: Navarro-Yepes Juliana , Kettner Nicole M. , Rao Xiayu , Bishop Cassandra Santaella. , Bui Tuyen N. , Wingate Hannah F. , Singareeka Raghavendra Akshara , Wang Yan , Wang Jing , Sahin Aysegul A. , Meric-Bernstam Funda , Hunt Kelly K. , Damodaran Senthil , Tripathy Debu , Keyomarsi Khandan
Published: September 2024

The attached file contains 12 Supplemental Figures and Figure Legnds
Supplementary Figure 6 from Galectin-1 mediates chronic STING activation in tumors to promote metastasis through MDSC recruitment
Authors: Nambiar Dhanya K. , Viswanathan Vignesh , Cao Hongbin , Zhang Weiruo , Guan Li , Chamoli Manish , Holmes Brittany , Kong Christina , Hildebrand Rachel , Koong Amanda Jeanette. , von Eyben Rie , Plevritis Sylvia , Li Lingyin , Giaccia Amato , Engleman Edgar , Le Quynh-Thu
Published: September 2024

Immunoblot showing knockdown of STING in MOC2 WT/KO cells.
Supplementary Figure 1 from Galectin-1 mediates chronic STING activation in tumors to promote metastasis through MDSC recruitment
Authors: Nambiar Dhanya K. , Viswanathan Vignesh , Cao Hongbin , Zhang Weiruo , Guan Li , Chamoli Manish , Holmes Brittany , Kong Christina , Hildebrand Rachel , Koong Amanda Jeanette. , von Eyben Rie , Plevritis Sylvia , Li Lingyin , Giaccia Amato , Engleman Edgar , Le Quynh-Thu
Published: September 2024

A. Terminal Tumor volume of MOC2 WT/KO-Gal1 tumors in Rag2-/- IL2rg-/- mice. B. Gating strategy used for analyses of PMN-MDSCs and M-MDSCs in tumor and lung tissues. C. Unsupervised tSNE clustering of live cells in MOC2 WT/KO-Gal1 tumor showing the proportion of M-MDSC, PMN-MDSC, and CD8+ T cells. D. Visual representation of the spleens isolated from either naïve mice or mice bearing WT- or KO-Gal1 tumors. E. Comparison of MDSC enrichment scores between smaller T1-2 and larger T3-4 tumors in the HNSCC TCGA cohort. The student’s t-test was used to assess the significance of the difference between the two groups. F. Heat map showing gene expression clustering based on the MDSC enrichment score in the HNSCC TCGA cohort. Differentially expressed genes (DEGs) were defined by a false discovery rate smaller than 0.05 and fold change higher than 1.5. G. Representative images showing low and high staining Gal1 or LOX1 (OLR1, established marker of PMN-MDSCs) using immunohistochemistry (IHC). H. Table showing the distribution of tumors expressing high or low Gal1 and high or low LOX1 (PMN-MDSCs) in 81 patients with oral cavity tumors. Gal1 and LOX1 staining distribution was analyzed using a chi-square test and was not statistically significant.
Table S5 from Intratumoral Microbiota Composition Regulates Chemoimmunotherapy Response in Esophageal Squamous Cell Carcinoma
Authors: Wu Hong , Leng Xuefeng , Liu Qianshi , Mao Tianqin , Jiang Tao , Liu Yiqiang , Li Feifei , Cao Chenhui , Fan Jun , Chen Liang , Chen Yaqi , Yao Quan , Lu Shun , Liang Renchuan , Hu Lanlin , Liu Mingxin , Wan Yejian , Li Zhaoshen , Peng Jun , Luo Qiyu , Zhou Hang , Yin Jun , Xu Ke , Lan Mei , Peng Xinhao , Lan Haitao , Li Gang , Han Yongtao , Zhang Xia , Xiao Zhi-Xiong Jim. , Lang Jinyi , Wang Guihua , Xu Chuan
Published: September 2024

Table S5 shows sequences of the primers used for qRT-PCR.
Table S4 from Intratumoral Microbiota Composition Regulates Chemoimmunotherapy Response in Esophageal Squamous Cell Carcinoma
Authors: Wu Hong , Leng Xuefeng , Liu Qianshi , Mao Tianqin , Jiang Tao , Liu Yiqiang , Li Feifei , Cao Chenhui , Fan Jun , Chen Liang , Chen Yaqi , Yao Quan , Lu Shun , Liang Renchuan , Hu Lanlin , Liu Mingxin , Wan Yejian , Li Zhaoshen , Peng Jun , Luo Qiyu , Zhou Hang , Yin Jun , Xu Ke , Lan Mei , Peng Xinhao , Lan Haitao , Li Gang , Han Yongtao , Zhang Xia , Xiao Zhi-Xiong Jim. , Lang Jinyi , Wang Guihua , Xu Chuan
Published: September 2024

Table S4 shows reagents and antibodies.
Figure S8 from Intratumoral Microbiota Composition Regulates Chemoimmunotherapy Response in Esophageal Squamous Cell Carcinoma
Authors: Wu Hong , Leng Xuefeng , Liu Qianshi , Mao Tianqin , Jiang Tao , Liu Yiqiang , Li Feifei , Cao Chenhui , Fan Jun , Chen Liang , Chen Yaqi , Yao Quan , Lu Shun , Liang Renchuan , Hu Lanlin , Liu Mingxin , Wan Yejian , Li Zhaoshen , Peng Jun , Luo Qiyu , Zhou Hang , Yin Jun , Xu Ke , Lan Mei , Peng Xinhao , Lan Haitao , Li Gang , Han Yongtao , Zhang Xia , Xiao Zhi-Xiong Jim. , Lang Jinyi , Wang Guihua , Xu Chuan
Published: September 2024

Figure S8 shows intra-tumoral bacterial contents were stable during tumor growth.
Figure S5 from Integrative genomic analyses identify lncRNA regulatory networks across pediatric leukemias and solid tumors
Authors: Modi Apexa , Lopez Gonzalo , Conkrite Karina L. , Su Chun , Leung Tsz Ching , Ramanan Sathvik , Manduchi Elisabetta , Johnson Matthew E. , Cheung Daphne , Gadd Samantha , Zhang Jinghui , Smith Malcolm A. , Guidry Auvil Jaime M. , Meshinchi Soheil , Perlman Elizabeth J. , Hunger Stephen P. , Maris John M. , Wells Andrew D. , Grant Struan F.A. , Diskin Sharon J.
Published: September 2024

Figure S5: Characteristics of lncMod analysis and results
Supplementary Data from Temozolomide Sensitizes ARID1A-Mutated Cancers to PARP Inhibitors
Authors: Yu Zheng-Cheng , Li Tianhe , Tully Ellen , Huang Peng , Chen Chih-Ning , Oberdoerffer Philipp , Gaillard Stephanie , Shih Ie-Ming , Wang Tian-Li
Published: September 2024

Supplementary Figures
Data from Mutated HRAS activates YAP1-AXL signaling to drive metastasis of head and neck cancer
Authors: Jagadeeshan Sankar , Prasad Manu , Badarni Mai , Ben Lulu Talal , Liju Vijayasteltar Belsamma. , Mathukkada Sooraj , Saunders Claire , Shnerb Avital Beeri. , Zorea Jonathan , Yegodayev Ksenia M. , Wainer Monica , Vtorov Liza , Allon Irit , Cohen Ofir , Gausdal Gro , Friedmann-Morvinski Dinorah , Cheong Sok Ching , Ho Alan L. , Rosenberg Ari J. , Kessler Linda , Burrows Francis , Kong Dexin , Grandis Jennifer R. , Gutkind J Silvio , Elkabets Moshe
Published: September 2024

Abstract
The survival rate for head and neck cancer (HNC) patients diagnosed with cervical lymph node (cLN) or distant metastasis is low. Genomic alterations in the HRAS oncogene are associated with advanced tumor stage and metastasis in HNC. Elucidation of the molecular mechanisms by which mutated HRAS (HRASmut) facilitates HNC metastasis could lead to improved treatment options for patients. Here, we examined metastasis driven by mutant HRAS in vitro and in vivo using HRASmut human HNC cell lines, patient-derived xenografts (PDXs), and a novel HRASmut syngeneic model. Genetic and pharmacological manipulations indicated that HRASmut was sufficient to drive invasion in vitro and metastasis in vivo. Targeted proteomic analysis showed that HRASmut promoted AXL expression via suppressing the Hippo pathway and stabilizing YAP1 activity. Pharmacological blockade of HRAS signaling with the farnesyltransferase inhibitor tipifarnib activated the Hippo pathway and reduced the nuclear export of YAP1, thus suppressing YAP1-mediated AXL expression and metastasis. AXL was required for HRASmut cells to migrate and invade in vitro and to form regional cLN and lung metastases in vivo. In addition, AXL-depleted HRASmut tumors displayed reduced lymphatic and vascular angiogenesis in the primary tumor. Tipifarnib treatment also reduced AXL expression and attenuated VEGFA and VEGFC expression, thus regulating tumor-induced vascular formation and metastasis. Our results indicate that YAP1 and AXL are crucial factors for HRASmut-induced metastasis and that tipifarnib treatment can limit the metastasis of HNC tumors with HRAS mutations by enhancing YAP1 cytoplasmic sequestration and downregulating AXL expression.
Data from Spatial transcriptomics depict ligand-receptor crosstalk heterogeneity at the tumor-stroma interface in long-term ovarian cancer survivors
Authors: Ferri-Borgogno Sammy , Zhu Ying , Sheng Jianting , Burks Jared K. , Gomez Javier A. , Wong Kwong Kwok , Wong Stephen T. C. , Mok Samuel C.
Published: September 2024

Abstract
Advanced high-grade serous ovarian cancer (HGSC) is an aggressive disease that accounts for 70% of all ovarian cancer deaths. Nevertheless, 15% of patients diagnosed with advanced HGSC survive more than 10 years. The elucidation of predictive markers of these long-term survivors (LTS) could help identify therapeutic targets for the disease, and thus improve patient survival rates. To investigate the stromal heterogeneity of the tumor microenvironment (TME) in ovarian cancer, we used spatial transcriptomics to generate spatially resolved transcript profiles in treatment naïve advanced HGSC from LTS and short-term survivors (STS) and determined the association between cancer-associated fibroblasts (CAF) heterogeneity and survival in patients with advanced HGSC. Spatial transcriptomics and single-cell RNA sequencing data were integrated to distinguish tumor and stroma regions, and a computational method was developed to investigate spatially resolved ligand-receptor interactions between various tumor and CAF subtypes in the TME. A specific subtype of CAFs and its spatial location relative to a particular ovarian cancer cell subtype in the TME correlated with long-term survival in advanced HGSC patients. Also, increased APOE-LRP5 crosstalk occurred at the stroma-tumor interface in tumor tissues from STS compared to LTS. These findings were validated using multiplex immunohistochemistry. Overall, this spatial transcriptomics analysis revealed spatially resolved CAF-tumor crosstalk signaling networks in the ovarian TME that are associated with long-term survival of HGSC patients. Further studies to confirm whether such crosstalk plays a role in modulating the malignant phenotype of HGSC and could serve as a predictive biomarker of patient survival are warranted.
Data from Comprehensive Metabolic Tracing Reveals the Origin and Catabolism of Cysteine in Mammalian Tissues and Tumors
Authors: Yoon Sang Jun , Combs Joseph A. , Falzone Aimee , Prieto-Farigua Nicolas , Caldwell Samantha , Ackerman Hayley D. , Flores Elsa R. , DeNicola Gina M.
Published: September 2024

Abstract
Cysteine plays critical roles in cellular biosynthesis, enzyme catalysis, and redox metabolism. The intracellular cysteine pool can be sustained by cystine uptake or de novo synthesis from serine and homocysteine. Demand for cysteine is increased during tumorigenesis for generating glutathione to deal with oxidative stress. While cultured cells have been shown to be highly dependent on exogenous cystine for proliferation and survival, how diverse tissues obtain and use cysteine in vivo has not been characterized. We comprehensively interrogated cysteine metabolism in normal murine tissues and cancers that arise from them using stable isotope 13C1-serine and 13C6-cystine tracing. De novo cysteine synthesis was highest in normal liver and pancreas and absent in lung tissue, while cysteine synthesis was either inactive or downregulated during tumorigenesis. By contrast, cystine uptake and metabolism to downstream metabolites was a universal feature of normal tissues and tumors. However, differences in glutathione labeling from cysteine were evident across tumor types. Thus, cystine is a major contributor to the cysteine pool in tumors, and glutathione metabolism is differentially active across tumor types.
Data from ASS1-mediated reductive carboxylation of cytosolic glutamine confers ferroptosis resistance in cancer cells
Authors: Hu Qiangsheng , Dai Jie , Zhang Zheng , yu Huansha , Zhang Jing , Zhu Xinsheng , Qin Yi , Zhang Lele , Zhang Peng
Published: September 2024

Abstract
Induction of ferroptosis, a recently defined form of nonapoptotic cell death caused by iron-dependent lipid peroxidation, has emerged as an anti-cancer strategy. Erastin is a ferroptosis activator that promotes cell death that not only depends on the depletion of cellular cysteine but also relies on mitochondrial oxidative metabolism of glutamine. Here, we demonstrate that ASS1, a key enzyme involved in the urea cycle, plays a crucial role in ferroptosis resistance. Loss of ASS1 increased the sensitivity of non-small cell lung cancer (NSCLC) cells to erastin in vitro and decreased tumor growth in vivo. Metabolomics analysis with stable isotope-labeled glutamine showed that ASS1 promotes reductive carboxylation of cytosolic glutamine and compromises the oxidative TCA cycle from glutamine anaplerosis, reducing mitochondrial-derived lipid reactive oxygen species. Moreover, transcriptome sequencing showed that ASS1 activates the mTORC1-SREBP1-SCD5 axis to promote de novo monounsaturated fatty acid synthesis by utilizing acetyl-CoA derived from the glutamine reductive pathway. Treating ASS1-deficient NSCLC cells with erastin combined with arginine deprivation significantly enhanced cell death compared to either treatment alone. Collectively, these results reveal a previously unknown regulatory role of ASS1 in ferroptosis resistance and provide a potential therapeutic target for ASS1-deficient NSCLC.
Data from Hypoxia potentiates the inflammatory fibroblast phenotype promoted by pancreatic cancer cell-derived cytokines
Authors: Schwoerer Simon , Cimino Francesco V. , Ros Manon , Tsanov Kaloyan M. , Ng Charles , Lowe Scott W. , Carmona-Fontaine Carlos , Thompson Craig B.
Published: September 2024

Abstract
Cancer-associated fibroblasts (CAFs) are a major cell type in the stroma of solid tumors and can exert both tumor-promoting and tumor-restraining functions. CAF heterogeneity is frequently observed in pancreatic ductal adenocarcinoma (PDAC), a tumor characterized by a dense and hypoxic stroma that features myofibroblastic CAFs (myCAFs) and inflammatory CAFs (iCAFs) that are thought to have opposing roles in tumor progression. While CAF heterogeneity can be driven in part by tumor cell-produced cytokines, other determinants shaping CAF identity and function are largely unknown. In vivo, we found that iCAFs displayed a hypoxic gene expression and biochemical profile and were enriched in hypoxic regions of PDAC tumors, while myCAFs were excluded from these regions. Hypoxia led fibroblasts to acquire an inflammatory gene expression signature and synergized with cancer cell-derived cytokines to promote an iCAF phenotype in a HIF-1α dependent fashion. Furthermore, HIF-1α stabilization was sufficient to induce an iCAF phenotype in stromal cells introduced into PDAC organoid co-cultures and to promote PDAC tumor growth. These findings indicate hypoxia-induced HIF-1α as a regulator of CAF heterogeneity and promoter of tumor progression in PDAC.
Data from Genome-wide splicing QTL analysis identifies causal risk variants for non-small cell lung cancer
Authors: Jin Meng , Liu Bo , Chen Can , Huang Yongbiao , Zhang Huixian , Chen Bingliang , Song Guoda , Zhao Dong , Duan Limin , Liu Wei , Yang Haizhen , Yue Fang , Liu Peijun , Yuan Xianglin , Chu Qian , Tian Jianbo , Hu Ke
Published: September 2024

Abstract
Alternative RNA splicing is an essential mechanism linking genetic variation to human diseases. While the signals from genome-wide association studies(GWAS) have been linked to expression quantitative trait loci(eQTLs) in previous studies,further work is needed to better elucidate the relationship to other genetic regulatory mechanisms,such as splicing QTLs(sQTLs). Here,we performed a genome-wide sQTL analysis to identify variants that might affect RNA splicing in 1,010 non-small cell lung cancer(NSCLC) samples from The Cancer Genome Atlas(TCGA).The identified sQTLs were largely independent of eQTLs and were predominantly enriched in exonic regions,genetic regulatory elements,RNA binding protein(RBP) binding sites, and known NSCLC risk loci. Additionally, target genes affected by sQTLs(sGenes) were involved in multiple processes in cancer,including cell growth,apoptosis,metabolism,immune infiltration,and drug responses,and sGenes were frequently altered genetically in NSCLC. Systematic screening of sQTLs associated with NSCLC risk using GWAS data from 15,474 cases and 12,375 controls identified an sQTL variant rs156697-G allele that was significantly associated with an increased risk of NSCLC. The association between the rs156697-G variant and NSCLC risk was further validated in two additional large population cohorts. The risk variant promoted inclusion of GSTO2 alternative exon 5 and led to higher expression of the GSTO2 full-length isoform(GSTO2-V1) and lower expression of the truncated GSTO2 isoform(GSTO2-V2),which was induced by RBP quaking(QKI). Mechanistically,compared with GSTO2-V1,GSTO2-V2 inhibited NSCLC cells proliferation by increasing S-glutathionylation of AKT1 and thereby functionally blocking AKT1 phosphorylation and activation. Overall,this study provides a comprehensive view of splicing variants linked to NSCLC risk and provides a set of genetic targets with therapeutic potential.
Data from DAB2IP is a bifunctional tumor suppressor that regulates wildtype RAS and inflammatory cascades in KRAS mutant colon cancer
Authors: Miller Abigail L. , Perurena Naiara , Gardner Alycia , Hinoue Toshinori , Loi Patrick , Laird Peter W. , Cichowski Karen
Published: September 2024

Abstract
The DAB2IP tumor suppressor encodes a RAS GTPase-activating protein (RASGAP). Accordingly, DAB2IP has been shown to be mutated or suppressed in tumor types that typically lack RAS mutations. However, here we report that DAB2IP is mutated or selectively silenced in the vast majority of KRAS and BRAF mutant CRCs. In this setting, DAB2IP loss promoted tumor development by activating wild-type H- and NRAS proteins, which was surprisingly required to achieve robust activation of RAS effector pathways in KRAS-mutant tumors. DAB2IP loss also triggered production of inflammatory mediators and the recruitment of pro-tumorigenic macrophages in vivo. Importantly, tumor growth was suppressed by depleting macrophages or inhibiting cytokine/inflammatory mediator expression with a JAK/TBK1 inhibitor. In human tumors DAB2IP was lost at early stages of tumor development, and its depletion was associated with an enrichment of macrophage and inflammatory signatures. Together, these findings demonstrate that DAB2IP restrains the activation of the RAS pathway and inflammatory cascades in the colon and that its loss represents a common and unappreciated mechanism for amplifying these two critical oncogenic signals in colorectal cancer.
Data from CellMinerCDB: NCATS is a Web-Based Portal Integrating Public Cancer Cell Line Databases for Pharmacogenomic Explorations
Authors: Reinhold William C. , Wilson Kelli , Elloumi Fathi , Bradwell Katie R. , Ceribelli Michele , Varma Sudhir , Wang Yanghsin , Duveau Damien , Menon Nikhil , Trepel Jane , Zhang Xiaohu , Klumpp-Thomas Carleen , Michael Samuel , Shinn Paul , Luna Augustin , Thomas Craig , Pommier Yves
Published: September 2024

Abstract
Major advances have been made in the field of precision medicine for treating cancer. However, many open questions remain that need to be answered to realize the goal of matching every cancer patient to the most efficacious therapy. To facilitate these efforts, we have developed CellMinerCDB:NCATS (https://discover.nci.nih.gov/rsconnect/cellminercdb_ncats/), which makes available activity information for 2,675 drugs and compounds, including multiple non-oncology drugs and 1,866 drugs and compounds unique to the National Center for Advancing Translational Sciences (NCATS). CellMinerCDB:NCATS comprises 183 cancer cell lines with 72 unique to NCATS including some from previously understudied tissues of origin. Multiple forms of data from different institutes are integrated, including single and combination drug activity, DNA copy number, methylation and mutation, transcriptome, protein levels, histone acetylation and methylation, metabolites, CRISPR and miscellaneous signatures. Curation of cell lines and drug names enables cross-database (CDB) analyses. Comparison of the datasets is made possible by the overlap between cell lines and drugs across databases. Multiple univariate and multivariate analysis tools are built-in, including linear regression and LASSO. Examples have been presented here for the clinical topoisomerase I (TOP1) inhibitors topotecan and irinotecan/SN-38. This web-application provides both substantial new data and significant pharmacogenomic integration allowing exploration of interrelationships.
Data from A germline variant in the BET1L 3’-UTR confers colorectal cancer susceptibility by reducing miRNA binding and m6A modification
Authors: Li Shuwei , Du Mulong , Xu Kaili , Ben Shuai , Zhu Tianru , Guo Mengfan , Xin Junyi , Zhu Lingjun , Gu Dongying , Zhang Zhengdong , Wang Meilin
Published: September 2024

Abstract
Genetic variants in regions encoding 3’-untranslated regions (UTR) of mRNA potentially alter miRNA binding affinity and N6-methyladenosine (m6A) levels to affect gene expression. A better understanding of the association of these variants with colorectal cancer susceptibility could facilitate development of cancer prevention and treatment approaches. Here, we analyzed miRNA expression profiles and integrated genetic analyses from 8,533 individuals to evaluate the effects of altered miRNA-binding sites on colorectal cancer risk. The single nucleotide polymorphism rs11245997 in the BET1L 3’-UTR was significantly associated with colorectal cancer risk. The rs11245997 A allele facilitated BET1L expression by disrupting miR-140-3p binding. It also reduced BET1L m6A modification, which upregulated BET1L mRNA and protein expression levels through a mechanism mediated by the m6A methyltransferases (METTL14 and WTAP) and the m6A demethylase ALKBH5. Moreover, higher expression of BET1L was associated with advanced tumor stages and poor patient prognosis. Increased BET1L expression promoted growth of colorectal cancer cells in vitro and in vivo, which could be partially rescued with miR-140-3p overexpression. RNA-Seq and pathway analyses indicated that BET1L is associated with the steroid biosynthesis pathway through regulation of HSD17B7, CYP27B1 and COMT. These findings provide insights into the involvement of genetic variants of BET1L in the development and progression of colorectal cancer.
Data from Tumor-derived Small Extracellular Vesicles Inhibit the Efficacy of CAR T Cells against Solid Tumors
Authors: Guo Wei , Zhong Wenqun , Xiao Zebin , Qin Zhiyuan , Yang Jingbo , Wen Yi , Yu Ziyan , Li Yumei , Sheppard Neil C. , Fuchs Serge Y. , Xu Xiaowei , Herlyn Meenhard , June Carl H. , Pure Ellen
Published: September 2024

Abstract
Chimeric antigen receptor (CAR) T cell therapy has shown remarkable success in the treatment of hematologic malignancies. Unfortunately, it has limited efficacy against solid tumors, even when the targeted antigens are well expressed. A better understanding of the underlying mechanisms of CAR T cell therapy resistance in solid tumors is necessary to develop strategies to improve efficacy. Here we report that solid tumors release small extracellular vesicles (sEVs) that carry both targeted tumor antigens and the immune checkpoint protein PD-L1. These sEVs acted as cell-free functional units to preferentially interact with cognate CAR T cells and efficiently inhibited their proliferation, migration, and function. In syngeneic mouse tumor models, blocking tumor sEV secretion not only boosted the infiltration and anti-tumor activity of CAR T cells but also improved endogenous anti-tumor immunity. These results suggest that solid tumors use sEVs as an active defense mechanism to resist CAR T cells and implicate tumor sEVs as a potential therapeutic target to optimize CAR T cell therapy against solid tumors.
Data from Tumor-derived Small Extracellular Vesicles Inhibit the Efficacy of CAR T Cells against Solid Tumors
Authors: Zhong Wenqun , Xiao Zebin , Qin Zhiyuan , Yang Jingbo , Wen Yi , Yu Ziyan , Li Yumei , Sheppard Neil C. , Fuchs Serge Y. , Xu Xiaowei , Herlyn Meenhard , June Carl H. , Pure Ellen , Guo Wei
Published: September 2024

Abstract
Chimeric antigen receptor (CAR) T cell therapy has shown remarkable success in the treatment of hematologic malignancies. Unfortunately, it has limited efficacy against solid tumors, even when the targeted antigens are well expressed. A better understanding of the underlying mechanisms of CAR T cell therapy resistance in solid tumors is necessary to develop strategies to improve efficacy. Here we report that solid tumors release small extracellular vesicles (sEVs) that carry both targeted tumor antigens and the immune checkpoint protein PD-L1. These sEVs acted as cell-free functional units to preferentially interact with cognate CAR T cells and efficiently inhibited their proliferation, migration, and function. In syngeneic mouse tumor models, blocking tumor sEV secretion not only boosted the infiltration and anti-tumor activity of CAR T cells but also improved endogenous anti-tumor immunity. These results suggest that solid tumors use sEVs as an active defense mechanism to resist CAR T cells and implicate tumor sEVs as a potential therapeutic target to optimize CAR T cell therapy against solid tumors.
Data from Breast cancer mutations HER2 V777L and PIK3CA H1047R activate the p21-CDK4/6 –Cyclin D1 axis driving tumorigenesis and drug resistance.
Authors: Cheng Xiaoqing , Sun Yirui , Highkin Maureen , Vemalapally Nagalaxmi , Jin Xiaohua , Zhou Brandon , Prior Julie L. , Tipton Ashley R. , Li Shunqiang , Iliuk Anton , Achilefu Samuel , Hagemann Ian S. , Edwards John R. , Bose Ron
Published: September 2024

Abstract
In metastatic breast cancer, HER2 activating mutations frequently co-occur with mutations in the PIK3CA, TP53, or E-cadherin genes. Of these co-occurring mutations, HER2 and PIK3CA mutations are the most prevalent gene pair, with approximately 40% of HER2 mutated breast cancers also having activating mutations in PIK3CA. To study the effects of co-occurring HER2 and PIK3CA mutations, we bred genetically engineered mice with the HER2V777L; PIK3CAH1047R transgenes (HP mice) and studied the resulting breast cancers both in vivo as well as ex vivo using cancer organoids. HP breast cancers show accelerated tumor formation in vivo and increased invasion and migration in in vitro assays. HP breast cancers have resistance to the pan-HER tyrosine kinase inhibitor, neratinib, but are effectively treated by neratinib plus trastuzumab deruxtecan. Proteomic and RNA-Seq analysis of HP breast cancers showed increased gene expression of Cyclin D1 and p21WAF1/Cip1 and changes in cell cycle markers. Combining neratinib with CDK4/6 inhibitors was another effective strategy for HP breast cancers with neratinib plus palbociclib showing a statistically significant reduction in mouse HP tumors as compared to either drug alone. We validated both the neratinib plus trastuzumab deruxtecan and neratinib plus palbociclib combinations using a human breast cancer patient-derived xenograft with very similar HER2 and PIK3CA mutations. Further, these two drug combinations effectively treated spontaneous lung metastasis in syngeneic mice transplanted with HP breast cancer organoids. Both of these drug combinations are being tested in phase 1 clinical trials and this study provides valuable preclinical evidence for them.
Data from Scribble Deficiency Promotes Pancreatic Ductal Adenocarcinoma Development and Metastasis
Authors: Bermejo-Rodriguez Camino , Araos Henríquez Joaquín , Caligiuri Giuseppina , Pinto Teles Sara , Park Youngkyu , Evans Anthony , Barrera Lawrence N. , Neesse Albrecht , Grützmann Robert , Aust Daniela , Rümmele Petra , Knösel Thomas , Narita Masako , Narita Masashi , Campbell Fiona , Öhlund Daniel , Pilarsky Christian , Dow Lukas E. , Humbert Patrick O. , Biffi Giulia , Tuveson David A. , Perez-Mancera Pedro A.
Published: September 2024

Abstract
Perturbation of cell polarity is a hallmark of pancreatic ductal adenocarcinoma (PDAC) progression. Scribble (SCRIB) is a well-characterized polarity regulator that has diverse roles in the pathogenesis of human neoplasms. To investigate the impact of SCRIB deficiency in PDAC development and progression, Scrib expression was genetically ablated in well-established mouse models of PDAC. Scrib loss in combination with KrasG12D did not influence development of pancreatic intraepithelial neoplasms in mice. However, Scrib deletion cooperated with KrasG12D and concomitant Trp53 heterozygous deletion to promote invasive PDAC and metastatic dissemination, leading to reduced overall survival. Immunohistochemical and transcriptome analyses revealed that Scrib-null tumors display a pronounced reduction of collagen content and an abundance of cancer-associated fibroblasts (CAF). Mechanistically, IL1α levels were reduced in Scrib-deficient tumors, and Scrib knockdown downregulated IL1α in mouse PDAC organoids (mPDO), which impaired CAF activation. Furthermore, Scrib loss increased YAP activation in mPDOs and established PDAC cell lines, enhancing cell survival. Clinically, SCRIB expression was decreased in human PDAC, and SCRIB mislocalization was associated with poorer patient outcome. These results indicate that SCRIB deficiency enhances cancer cell survival and remodels the tumor microenvironment to accelerate PDAC development and progression, establishing the tumor suppressor function of SCRIB in advanced pancreatic cancer.

 Significance: SCRIB loss promotes invasive pancreatic cancer development via both cell-autonomous and non–cell-autonomous processes and is associated with poorer outcomes, denoting SCRIB as a tumor suppressor and potential biomarker for the prediction of recurrence.
Supplementary Table 7 from Associations between MICA and MICB genetic variants, protein levels, and colorectal cancer: Atherosclerosis Risk in Communities (ARIC)
Authors: Wang Shuo , Onyeaghala Guillaume C. , Pankratz Nathan , Nelson Heather H. , Thyagarajan Bharat , Tang Weihong , Norby Faye L. , Ugoji Chinenye , Joshu Corinne E. , Gomez Christian R. , Couper David J. , Coresh Josef , Platz Elizabeth A. , Prizment Anna E.
Published: September 2024

Supplemental Table 7 shows the association of sMICA and sMICB levels (continuous variables) and pre-selected SNPsa with risk of CRC stratified by family history of CRC.
Supplementary Table 3 from Somatic mosaic chromosomal alterations and death of cardiovascular disease causes among cancer survivors
Authors: Sun Maxine , Cyr Marie-Christyne , Sandoval Johanna , Lemieux Perreault Louis-Philippe , Busque Lambert , Tardif Jean-Claude , Dubé Marie-Pierre
Published: September 2024

Supplementary Table 3: Sensitivity analyses by Cox regression considering additional covariates
Table S6 from Exploring the complex relationship between gut microbiota and risk of colorectal neoplasia using bidirectional Mendelian Randomization analysis
Authors: Li Wanxin , Zhou Xuan , Yuan Shuai , Wang Lijuan , Yu Lili , Sun Jing , Chen Jie , Xiao Qian , Wan Zhongxiao , Zheng Ju-Sheng , Zhang Cai-Xia , Larsson Susanna C. , Farrington Susan M. , Law Philip , Houlston Richard S. , Tomlinson Ian , Ding Ke-Feng , Dunlop Malcolm G. , Theodoratou Evropi , Li Xue
Published: September 2024

Table S6 shows the forward MR analyses of 24 gut microbiota with the risk of colorectal cancer.
Supplementary Table S1 from Genetic susceptibility to nonalcoholic fatty liver disease and risk for pancreatic cancer: Mendelian randomization
Authors: King Sontoria D. , Veliginti Swathi , Brouwers Martijn C G J. , Ren Zhewen , Zheng Wei , Setiawan Veronica Wendy. , Wilkens Lynne R. , Shu Xiao-Ou , Arslan Alan A. , Beane Freeman Laura E. , Bracci Paige M. , Canzian Federico , Du Mengmeng , Gallinger Steven J. , Giles Graham G. , Goodman Phyllis J. , Haiman Christopher A. , Kogevinas Manolis , Kooperberg Charles , Le Marchand Loic , Neale Rachel E. , Visvanathan Kala , White Emily , Albanes Demetrius , Andreotti Gabriella , Babic Ana , Berndt Sonja I. , Brais Lauren K. , Brennan Paul , Buring Julie E. , Rabe Kari G. , Bamlet William R. , Chanock Stephen J. , Fuchs Charles S. , Gaziano J. Michael , Giovannucci Edward L. , Hackert Thilo , Hassan Manal M. , Katzke Verena , Kurtz Robert C. , Lee I-Min , Malats Nuria , Murphy Neil , Oberg Ann L. , Orlow Irene , Porta Miquel , Real Francisco X. , Rothman Nathaniel , Sesso Howard D. , Silverman Debra T. , Thompson Ian M. , Wactawski-Wende Jean , Wang Xiaoliang , Wentzensen Nicolas , Yu Herbert , Zeleniuch-Jacquotte Anne , Yu Kai , Wolpin Brian M. , Duell Eric J. , Li Donghui , Hung Rayjean J. , Perdomo Sandra , McCullough Marjorie L. , Freedman Neal D. , Patel Alpa V. , Peters Ulrike , Riboli Elio , Sund Malin , Tjønneland Anne , Zhong Jun , Van Den Eeden Stephen K. , Kraft Peter , Risch Harvey A. , Amundadottir Laufey T. , Klein Alison P. , Stolzenberg-Solomon Rachael Z. , Antwi Samuel O.
Published: September 2024

Supplementary Table S1 shows results of univariate analysis for 77 chronically elevated serum alanine aminotransferase (cALT)-defined nonalcoholic fatty liver disease SNPs in the Pancreatic Cancer Cohort Consortium (PanScan) data
Supplementary Table S5 from Heritable Traits and Lung Cancer Risk: A Two-Sample Mendelian Randomization Study
Authors: Pettit Rowland W. , Byun Jinyoung , Han Younghun , Ostrom Quinn T. , Coarfa Cristian , Bondy Melissa L. , Amos Christopher I.
Published: September 2024

Supplementary Table S5. Multivariate MR estimates of direct causal effects of traits on lung cancer dually conditioned on genetically influenced smoking and educational attainment
Supplementary Figure S3 from Heritable Traits and Lung Cancer Risk: A Two-Sample Mendelian Randomization Study
Authors: Pettit Rowland W. , Byun Jinyoung , Han Younghun , Ostrom Quinn T. , Coarfa Cristian , Bondy Melissa L. , Amos Christopher I.
Published: September 2024

Supplementary Figure S3. IVW multivariate MR estimation of direct impact of traits on small cell lung cancer development, conditioned on smoking (pack years per lifespan), income, and education.
Data from Updated Review of Major Cancer Risk Factors and Screening Test Use in the United States, with a Focus on Changes During the COVID-19 Pandemic
Authors: Star Jessica , Bandi Priti , Nargis Nigar , Islami Farhad , Yabroff K Robin , Minihan Adair K. , Smith Robert A. , Jemal Ahmedin
Published: September 2024

Abstract
We present national and state representative prevalence estimates of modifiable cancer risk factors, preventive behaviors and services, and screening, with a focus on changes during the COVID-19 pandemic. Between 2019 and 2021, current smoking, physical inactivity, and heavy alcohol consumption declined, and human papillomavirus vaccination and stool testing for colorectal cancer screening uptake increased. In contrast, obesity prevalence increased, while fruit consumption and cervical cancer screening declined during the same timeframe. Favorable and unfavorable trends were evident during the 2nd year of the COVID-19 pandemic that must be monitored as more years of consistent data are collected. Yet disparities by racial/ethnic and socioeconomic status persisted, highlighting the continued need for interventions to address suboptimal levels among these population subgroups.