bluuebunny/crossref_metadata_2025 huggingface dataset:
Data from And-1 Coordinates with the FANCM Complex to Regulate Fanconi Anemia Signaling and Cisplatin Resistance
Authors: Zhang Yi , Li Jing , Zhou Yuan , Li Zhuqing , Peng Changmin , Pei Huadong , Zhu Wenge
Published: March 2023

Abstract
The Fanconi anemia (FA) pathway is essential for repairing DNA interstrand crosslinks (ICL). ICLs induce stalled DNA replication forks and trigger activation of the FA pathway by promoting recruitment of the FANCM/FAAP24/MHF complex to ICL sites. Given that stalled replication forks are proximal to ICL sites, fork-associated proteins may coordinate with FA factors to rapidly sense ICLs for activation of FA signaling. Here we report that And-1, a replisome protein, is critical for activation of the FA pathway by sensing ICL-stalled forks and recruiting the FANCM/FAAP24 complex to ICLs. In response to ICLs, And-1 rapidly accumulated at ICL-stalled forks in a manner dependent on ataxia telangiectasia and Rad3-related protein–induced phosphorylation at T826. And-1 phosphorylation triggered an intramolecular change that promoted the interaction of And-1 with FANCM/FAAP24, resulting in recruitment of the FANCM/FAAP24 complex to ICLs. Furthermore, p-T826 And-1 was elevated in cisplatin-resistant ovarian cancer cells, and activated And-1 contributed to cisplatin resistance. Collectively, these studies elucidate a mechanism by which And-1 regulates FA signaling and identify And-1 as a potential target for developing therapeutic approaches to treat platinum-resistant ovarian cancer.
Significance:
This work shows that phosphorylation of And-1 by ATR activates Fanconi anemia signaling at interstrand crosslink–stalled replication forks by recruiting the FANCM/FAAP24 complex, revealing And-1 as a potential therapeutic target in cancer.
Data from Intratumoral Heterogeneity and Immune Modulation in Lung Adenocarcinoma in Female Smokers and Never Smokers
Authors: Trefzer Timo B. , Schneider Marc A. , Jechow Katharina , Chua Robert Lorenz , Muley Thomas , Winter Hauke , Kriegsmann Mark , Meister Michael , Eils Roland , Conrad Christian
Published: March 2023

Abstract
Lung cancer remains the leading cause of cancer-related death worldwide, despite declining smoking prevalence in industrialized countries. Although lung cancer is highly associated with smoking status, a significant proportion of lung cancer cases develop in patients who have never smoked, with an observable bias toward female never smokers. A better understanding of lung cancer heterogeneity and immune system involvement during tumor evolution and progression in never smokers is therefore highly needed. Here, we used single-nucleus transcriptomics of surgical lung adenocarcinoma (LUAD) and normal lung tissue samples from patients with or without a history of smoking. Immune cells as well as fibroblasts and endothelial cells responded to tobacco smoke exposure by inducing a highly inflammatory state in normal lung tissue. In LUAD, characterization of differentially expressed transcriptional programs in macrophages and cancer-associated fibroblasts provided insight into how the niche favors tumor progression. Within tumors, eight subpopulations of neoplastic cells were identified in female smokers and never smokers. Pseudotemporal ordering inferred a trajectory toward two differentiated tumor cell states implicated in cancer progression and invasiveness. A proliferating cell population sustaining tumor growth exhibited differential immune modulating signatures in both patient groups. Collectively, these results resolve cellular heterogeneity and immune interactions in LUAD, with a special emphasis on female never smokers.
Significance:
Single-cell analysis of healthy lung tissue and lung cancer reveals distinct tumor cell populations, including cells with differential immune modulating capacity between smokers and never smokers, which could guide future therapeutic strategies.
Data from Bimodal Gene Expression in Patients with Cancer Provides Interpretable Biomarkers for Drug Sensitivity
Authors: Ba-Alawi Wail , Nair Sisira Kadambat , Li Bo , Mammoliti Anthony , Smirnov Petr , Mer Arvind Singh , Penn Linda Z. , Haibe-Kains Benjamin
Published: March 2023

Abstract
Identifying biomarkers predictive of cancer cell response to drug treatment constitutes one of the main challenges in precision oncology. Recent large-scale cancer pharmacogenomic studies have opened new avenues of research to develop predictive biomarkers by profiling thousands of human cancer cell lines at the molecular level and screening them with hundreds of approved drugs and experimental chemical compounds. Many studies have leveraged these data to build predictive models of response using various statistical and machine learning methods. However, a common pitfall to these methods is the lack of interpretability as to how they make predictions, hindering the clinical translation of these models. To alleviate this issue, we used the recent logic modeling approach to develop a new machine learning pipeline that explores the space of bimodally expressed genes in multiple large in vitro pharmacogenomic studies and builds multivariate, nonlinear, yet interpretable logic-based models predictive of drug response. The performance of this approach was showcased in a compendium of the three largest in vitro pharmacogenomic datasets to build robust and interpretable models for 101 drugs that span 17 drug classes with high validation rates in independent datasets. These results along with in vivo and clinical validation support a better translation of gene expression biomarkers between model systems using bimodal gene expression.
Significance:
A new machine learning pipeline exploits the bimodality of gene expression to provide a reliable set of candidate predictive biomarkers with a high potential for clinical translatability.
Data from Inhibition of Melanoma Cell–Intrinsic Tim-3 Stimulates MAPK-Dependent Tumorigenesis
Authors: Schatton Tobias , Itoh Yuta , Martins Christina , Rasbach Erik , Singh Praveen , Silva Mariana , Mucciarone Kyla , Heppt Markus V. , Geddes-Sweeney Jenna , Stewart Kate , Brandenburg Anne , Liang Jennifer , Dimitroff Charles J. , Mihm Martin C. , Landsberg Jennifer , Schlapbach Christoph , Lian Christine G. , Murphy George F. , Kupper Thomas S. , Ramsey Matthew R. , Barthel Steven R.
Published: March 2023

Abstract
T-cell immunoglobulin mucin family member 3 (Tim-3) is an immune checkpoint receptor that dampens effector functions and causes terminal exhaustion of cytotoxic T cells. Tim-3 inhibitors are under investigation in immuno-oncology (IO) trials, because blockade of T-cell-Tim-3 enhances antitumor immunity. Here, we identify an additional role for Tim-3 as a growth-suppressive receptor intrinsic to melanoma cells. Inhibition of melanoma cell-Tim-3 promoted tumor growth in both immunocompetent and immunocompromised mice, while melanoma-specific Tim-3 overexpression attenuated tumorigenesis. Ab-mediated Tim-3 blockade inhibited growth of immunogenic murine melanomas in T-cell–competent hosts, consistent with established antitumor effects of T-cell-Tim-3 inhibition. In contrast, Tim-3 Ab administration stimulated tumorigenesis of both highly and lesser immunogenic murine and human melanomas in T-cell–deficient mice, confirming growth-promoting effects of melanoma-Tim-3 antagonism. Melanoma-Tim-3 activation suppressed, while its blockade enhanced, phosphorylation of pro-proliferative downstream MAPK signaling mediators. Finally, pharmacologic MAPK inhibition reversed unwanted Tim-3 Ab-mediated tumorigenesis in T-cell–deficient mice and enhanced desired antitumor activity of Tim-3 interference in T-cell–competent hosts. These results identify melanoma-Tim-3 blockade as a mechanism that antagonizes T-cell-Tim-3–directed IO therapeutic efficacy. They further reveal MAPK targeting as a combination strategy for circumventing adverse consequences of unintended melanoma-Tim-3 inhibition.
Significance:
Tim-3 is a growth-suppressive receptor intrinsic to melanoma cells, the blockade of which promotes MAPK-dependent tumorigenesis and thus counteracts antitumor activity of T-cell–directed Tim-3 inhibition.
Data from Epithelial-to-Mesenchymal Transition Supports Ovarian Carcinosarcoma Tumorigenesis and Confers Sensitivity to Microtubule Targeting with Eribulin
Authors: Ho Gwo Yaw , Kyran Elizabeth L. , Bedo Justin , Wakefield Matthew J. , Ennis Darren P. , Mirza Hasan B. , Vandenberg Cassandra J. , Lieschke Elizabeth , Farrell Andrew , Hadla Anthony , Lim Ratana , Dall Genevieve , Vince James E. , Chua Ngee Kiat , Kondrashova Olga , Upstill-Goddard Rosanna , Bailey Ulla-Maja , Dowson Suzanne , Roxburgh Patricia , Glasspool Rosalind M. , Bryson Gareth , Biankin Andrew V. , Cooke Susanna L. , Ratnayake Gayanie , McNally Orla , Traficante Nadia , DeFazio Anna , Weroha S. John , Bowtell David D. , McNeish Iain A. , Papenfuss Anthony T. , Scott Clare L. , Barker Holly E.
Published: March 2023

Abstract
Ovarian carcinosarcoma (OCS) is an aggressive and rare tumor type with limited treatment options. OCS is hypothesized to develop via the combination theory, with a single progenitor resulting in carcinomatous and sarcomatous components, or alternatively via the conversion theory, with the sarcomatous component developing from the carcinomatous component through epithelial-to-mesenchymal transition (EMT). In this study, we analyzed DNA variants from isolated carcinoma and sarcoma components to show that OCS from 18 women is monoclonal. RNA sequencing indicated that the carcinoma components were more mesenchymal when compared with pure epithelial ovarian carcinomas, supporting the conversion theory and suggesting that EMT is important in the formation of these tumors. Preclinical OCS models were used to test the efficacy of microtubule-targeting drugs, including eribulin, which has previously been shown to reverse EMT characteristics in breast cancers and induce differentiation in sarcomas. Vinorelbine and eribulin more effectively inhibited OCS growth than standard-of-care platinum-based chemotherapy, and treatment with eribulin reduced mesenchymal characteristics and N-MYC expression in OCS patient-derived xenografts. Eribulin treatment resulted in an accumulation of intracellular cholesterol in OCS cells, which triggered a downregulation of the mevalonate pathway and prevented further cholesterol biosynthesis. Finally, eribulin increased expression of genes related to immune activation and increased the intratumoral accumulation of CD8+ T cells, supporting exploration of immunotherapy combinations in the clinic. Together, these data indicate that EMT plays a key role in OCS tumorigenesis and support the conversion theory for OCS histogenesis. Targeting EMT using eribulin could help improve OCS patient outcomes.
Significance:
Genomic analyses and preclinical models of ovarian carcinosarcoma support the conversion theory for disease development and indicate that microtubule inhibitors could be used to suppress EMT and stimulate antitumor immunity.
Data from SMG8/SMG9 Heterodimer Loss Modulates SMG1 Kinase to Drive ATR Inhibitor Resistance
Authors: Llorca-Cardenosa Marta J. , Aronson Lauren I. , Krastev Dragomir B. , Nieminuszczy Jadwiga , Alexander John , Song Feifei , Dylewska Malgorzata , Broderick Ronan , Brough Rachel , Zimmermann Astrid , Zenke Frank T. , Gurel Bora , Riisnaes Ruth , Ferreira Ana , Roumeliotis Theodoros , Choudhary Jyoti , Pettitt Stephen J. , de Bono Johann , Cervantes Andres , Haider Syed , Niedzwiedz Wojciech , Lord Christopher J. , Chong Irene Y.
Published: March 2023

Abstract
Gastric cancer represents the third leading cause of global cancer mortality and an area of unmet clinical need. Drugs that target the DNA damage response, including ATR inhibitors (ATRi), have been proposed as novel targeted agents in gastric cancer. Here, we sought to evaluate the efficacy of ATRi in preclinical models of gastric cancer and to understand how ATRi resistance might emerge as a means to identify predictors of ATRi response. A positive selection genome-wide CRISPR-Cas9 screen identified candidate regulators of ATRi resistance in gastric cancer. Loss-of-function mutations in either SMG8 or SMG9 caused ATRi resistance by an SMG1-mediated mechanism. Although ATRi still impaired ATR/CHK1 signaling in SMG8/9-defective cells, other characteristic responses to ATRi exposure were not seen, such as changes in ATM/CHK2, γH2AX, phospho-RPA, or 53BP1 status or changes in the proportions of cells in S- or G2–M-phases of the cell cycle. Transcription/replication conflicts (TRC) elicited by ATRi exposure are a likely cause of ATRi sensitivity, and SMG8/9-defective cells exhibited a reduced level of ATRi-induced TRCs, which could contribute to ATRi resistance. These observations suggest ATRi elicits antitumor efficacy in gastric cancer but that drug resistance could emerge via alterations in the SMG8/9/1 pathway.
Significance:
These findings reveal how cancer cells acquire resistance to ATRi and identify pathways that could be targeted to enhance the overall effectiveness of these inhibitors.
Data from Genomic Landscapes and Hallmarks of Mutant RAS in Human Cancers
Authors: Scharpf Robert B. , Balan Archana , Ricciuti Biagio , Fiksel Jacob , Cherry Christopher , Wang Chenguang , Lenoue-Newton Michele L. , Rizvi Hira A. , White James R. , Baras Alexander S. , Anaya Jordan , Landon Blair V. , Majcherska-Agrawal Marta , Ghanem Paola , Lee Jocelyn , Raskin Leon , Park Andrew S. , Tu Huakang , Hsu Hil , Arbour Kathryn C. , Awad Mark M. , Riely Gregory J. , Lovly Christine M. , Anagnostou Valsamo
Published: March 2023

Abstract
The RAS family of small GTPases represents the most commonly activated oncogenes in human cancers. To better understand the prevalence of somatic RAS mutations and the compendium of genes that are coaltered in RAS-mutant tumors, we analyzed targeted next-generation sequencing data of 607,863 mutations from 66,372 tumors in 51 cancer types in the AACR Project GENIE Registry. Bayesian hierarchical models were implemented to estimate the cancer-specific prevalence of RAS and non-RAS somatic mutations, to evaluate co-occurrence and mutual exclusivity, and to model the effects of tumor mutation burden and mutational signatures on comutation patterns. These analyses revealed differential RAS prevalence and comutations with non-RAS genes in a cancer lineage-dependent and context-dependent manner, with differences across age, sex, and ethnic groups. Allele-specific RAS co-mutational patterns included an enrichment in NTRK3 and chromatin-regulating gene mutations in KRAS G12C-mutant non–small cell lung cancer. Integrated multiomic analyses of 10,217 tumors from The Cancer Genome Atlas (TCGA) revealed distinct genotype-driven gene expression programs pointing to differential recruitment of cancer hallmarks as well as phenotypic differences and immune surveillance states in the tumor microenvironment of RAS-mutant tumors. The distinct genomic tracks discovered in RAS-mutant tumors reflected differential clinical outcomes in TCGA cohort and in an independent cohort of patients with KRAS G12C-mutant non–small cell lung cancer that received immunotherapy-containing regimens. The RAS genetic architecture points to cancer lineage–specific therapeutic vulnerabilities that can be leveraged for rationally combining RAS-mutant allele-directed therapies with targeted therapies and immunotherapy.
Significance:
The complex genomic landscape of RAS-mutant tumors is reflective of selection processes in a cancer lineage–specific and context-dependent manner, highlighting differential therapeutic vulnerabilities that can be clinically translated.
Data from Elevated Methionine Flux Drives Pyroptosis Evasion in Persister Cancer Cells
Authors: El-Kenawi Asmaa , Berglund Anders , Estrella Veronica , Zhang Yonghong , Liu Min , Putney Ryan M. , Yoder Sean J. , Johnson Joseph , Brown Joel , Gatenby Robert
Published: March 2023

Abstract
Induction of cell death represents a primary goal of most anticancer treatments. Despite the efficacy of such approaches, a small population of “persisters” develop evasion strategies to therapy-induced cell death. While previous studies have identified mechanisms of resistance to apoptosis, the mechanisms by which persisters dampen other forms of cell death, such as pyroptosis, remain to be elucidated. Pyroptosis is a form of inflammatory cell death that involves formation of membrane pores, ion gradient imbalance, water inflow, and membrane rupture. Herein, we investigate mechanisms by which cancer persisters resist pyroptosis, survive, then proliferate in the presence of tyrosine kinase inhibitors (TKI). Lung, prostate, and esophageal cancer persister cells remaining after treatments exhibited several hallmarks indicative of pyroptosis resistance. The inflammatory attributes of persisters included chronic activation of inflammasome, STING, and type I interferons. Comprehensive metabolomic characterization uncovered that TKI-induced pyroptotic persisters display high methionine consumption and excessive taurine production. Elevated methionine flux or exogenous taurine preserved plasma membrane integrity via osmolyte-mediated effects. Increased dependency on methionine flux decreased the level of one carbon metabolism intermediate S-(5′-adenosyl)-L-homocysteine, a determinant of cell methylation capacity. The consequent increase in methylation potential induced DNA hypermethylation of genes regulating metal ion balance and intrinsic immune response. This enabled thwarting TKI resistance by using the hypomethylating agent decitabine. In summary, the evolution of resistance to pyroptosis can occur via a stepwise process of physical acclimation and epigenetic changes without existing or recurrent mutations.
Significance:
Methionine enables cancer cells to persist by evading pyroptotic osmotic lysis, which leads to genome-wide hypermethylation that allows persisters to gain proliferative advantages.
Data from Genome-Wide Analysis of Rare Haplotypes Associated with Breast Cancer Risk
Authors: Wang Fan , Moon Wonjong , Letsou William , Sapkota Yadav , Wang Zhaoming , Im Cindy , Baedke Jessica L. , Robison Leslie , Yasui Yutaka
Published: March 2023

Abstract
Numerous common genetic variants have been linked to breast cancer risk, but they only partially explain the total breast cancer heritability. Inference from Nordic population-based twin data indicates rare high-risk loci as the chief determinant of breast cancer risk. Here, we use haplotypes, rather than single variants, to identify rare high-risk loci for breast cancer. With computationally phased genotypes from 181,034 white British women in the UK Biobank, a genome-wide haplotype–breast cancer association analysis was conducted using sliding windows of 5 to 500 consecutive array-genotyped variants. In the discovery stage, haplotype–breast cancer associations were evaluated retrospectively in the prestudy-enrollment data including 5,487 breast cancer cases. Breast cancer hazard ratios (HR) for additive haplotypic effects were estimated using Cox regression. The replication analysis included a prospective cohort of women free of breast cancer at enrollment, of whom 3,524 later developed breast cancer. This two-stage analysis detected 13 rare loci (frequency <1%), each associated with an appreciable breast cancer-risk increase (discovery: HRs = 2.84–6.10, P < 5 × 10–8; replication: HRs = 2.08–5.61, P < 0.01). In contrast, the variants that formed these rare haplotypes individually exhibited much smaller effects. Functional annotation revealed extensive cis-regulatory DNA elements in breast cancer–related cells underlying the replicated rare haplotypes. Using phased, imputed genotypes from 30,064 cases and 25,282 controls in the DRIVE OncoArray case–control study, 6 of the 13 rare–loci associations were found generalizable (odds ratio estimates: 1.48–7.67, P < 0.05). This study demonstrates the complementary advantage of utilizing rare haplotypes to capture novel risk loci and suggests the potential for the discovery of more genetic elements contributing to cancer heritability as large data sets of germline whole-genome sequencing become available.
Significance:
A genome-wide two-stage haplotype analysis identifies rare haplotypes associated with breast cancer risk and suggests that the rare risk haplotypes represent long-range interactions with regulatory consequences influencing cancer risk.
Data from MEX3A Mediates p53 Degradation to Suppress Ferroptosis and Facilitate Ovarian Cancer Tumorigenesis
Authors: Wang Cheng-Kai , Chen Tzu-Jou , Tan Grace Y.T. , Chang Fang-Pei , Sridharan Samyuktha , Yu Chen-Hsin Albert , Chang Yen-Hou , Chen Yi-Jen , Cheng Li-Tzu , Hwang-Verslues Wendy W.
Published: March 2023

Abstract
Epithelial ovarian cancer is a highly heterogeneous and malignant female cancer with an overall low survival rate. Mutations in p53 are prevalent in the major ovarian cancer histotype, high-grade serous ovarian carcinoma (HGSOC), while p53 mutations are much less frequent in other ovarian cancer subtypes, particularly in ovarian clear cell carcinoma (OCCC). Advanced stage OCCC with wild-type (WT) p53 has a worse prognosis and increased drug resistance, metastasis, and recurrence than HGSOC. The mechanisms responsible for driving the aggressiveness of WT p53-expressing ovarian cancer remain poorly understood. Here, we found that upregulation of MEX3A, a dual-function protein containing a RING finger domain and an RNA-binding domain, was critical for tumorigenesis in WT p53-expressing ovarian cancer. MEX3A overexpression enhanced the growth and clonogenicity of OCCC cell lines. In contrast, depletion of MEX3A in OCCC cells, as well as ovarian teratocarcinoma cells, reduced cell survival and proliferative ability. MEX3A depletion also inhibited tumor growth and prolonged survival in orthotopic xenograft models. MEX3A depletion did not alter p53 mRNA level but did increase p53 protein stability. MEX3A-mediated p53 protein degradation was crucial to suppress ferroptosis and enhance tumorigenesis. Consistently, p53 knockdown reversed the effects of MEX3A depletion. Together, our observations identified MEX3A as an important oncogenic factor promoting tumorigenesis in ovarian cancer cells expressing WT p53.
Significance:
Degradation of p53 mediated by MEX3A drives ovarian cancer growth by circumventing p53 tumor suppressive functions, suggesting targeting MEX3A as a potential strategy for treating of ovarian cancer expressing WT p53.
Supplementary Tables 1-2 from Associations of Plasma C-Peptide and IGFBP-1 Levels with Risk of Colorectal Adenoma in a Multiethnic Population
Authors: Le Marchand Loïc , Wang Hansong , Rinaldi Sabina , Kaaks Rudolf , Vogt Thomas M. , Yokochi Lance , Decker Robert
Published: March 2023

Supplementary Tables 1-2 from Associations of Plasma C-Peptide and IGFBP-1 Levels with Risk of Colorectal Adenoma in a Multiethnic Population
Supplementary Figure 1 Legend from The Paracrine Hormone for the GUCY2C Tumor Suppressor, Guanylin, Is Universally Lost in Colorectal Cancer
Authors: Wilson Chantell , Lin Jieru E. , Li Peng , Snook Adam E. , Gong Jianping , Sato Takahiro , Liu Chengbao , Girondo Melanie A. , Rui Hallgeir , Hyslop Terry , Waldman Scott A.
Published: March 2023

Supplementary Figure 1 Legend
Supplementary Table Legend from The 6q22.33 Locus and Breast Cancer Susceptibility
Authors: Kirchhoff Tomas , Chen Zhang-qun , Gold Bert , Pal Prodipto , Gaudet Mia M. , Kosarin Kristi , Levine Douglas A. , Gregersen Peter , Spencer Sara , Harlan Megan , Robson Mark , Klein Robert J. , Hudis Clifford A. , Norton Larry , Dean Michael , Offit Kenneth
Published: March 2023

Supplementary Table Legend from The 6q22.33 Locus and Breast Cancer Susceptibility
Supplementary Figures 1 through 4 from Salivary Auto-Antibodies as Noninvasive Diagnostic Markers of Oral Cavity Squamous Cell Carcinoma
Authors: Wu Chih-Ching , Chang Ya-Ting , Chang Kai-Ping , Liu Yu-Ling , Liu Hao-Ping , Lee I-Ling , Yu Jau-Song , Chiang Wei-Fan
Published: March 2023

PDf - 299K, Supplementary Fig. S1, establishment of a multiplexed bead-based system for auto-Ab detection. Supplementary Fig. S2, measurement of salivary levels of auto-Abs in OSCC patients. Supplementary Fig. S3, efficacy of auto-Abs as early-detection markers of OSCC. Supplementary Fig. S4. efficacy of auto-Abs as early-detection markers of OSCC.
Supplementary Information from Identification of Potential Serum Biomarkers of Glioblastoma: Serum Osteopontin Levels Correlate with Poor Prognosis
Authors: Sreekanthreddy Peddagangannagari , Srinivasan Harish , Kumar Durairaj Mohan , Nijaguna Mamatha Bangalore , Sridevi Sambandam , Vrinda Marigowda , Arivazhagan Arimappamagan , Balasubramaniam Anandh , Hegde Alangar Sathyaranjandas , Chandramouli Bangalore A. , Santosh Vani , Rao Manchanahalli R.S. , Kondaiah Paturu , Somasundaram Kumaravel
Published: March 2023

Supplementary Information from Identification of Potential Serum Biomarkers of Glioblastoma: Serum Osteopontin Levels Correlate with Poor Prognosis
Supplementary Figure 1 from Identification of Potential Serum Biomarkers of Glioblastoma: Serum Osteopontin Levels Correlate with Poor Prognosis
Authors: Sreekanthreddy Peddagangannagari , Srinivasan Harish , Kumar Durairaj Mohan , Nijaguna Mamatha Bangalore , Sridevi Sambandam , Vrinda Marigowda , Arivazhagan Arimappamagan , Balasubramaniam Anandh , Hegde Alangar Sathyaranjandas , Chandramouli Bangalore A. , Santosh Vani , Rao Manchanahalli R.S. , Kondaiah Paturu , Somasundaram Kumaravel
Published: March 2023

Supplementary Figure 1 from Identification of Potential Serum Biomarkers of Glioblastoma: Serum Osteopontin Levels Correlate with Poor Prognosis
Supplementary Figure S4 from Circulating Mitochondrial DNA Level, a Noninvasive Biomarker for the Early Detection of Gastric Cancer
Authors: Fernandes Julien , Michel Valérie , Camorlinga-Ponce Margarita , Gomez Alejandro , Maldonado Carmen , De Reuse Hilde , Torres Javier , Touati Eliette
Published: March 2023

Supplementary Figure S4 : Comparison of circulating leukocytes mtDNA levels at various steps of the gastric carcinogenesis process in patients in Cohort 2. MtDNA was measured in NAG, IM and GC patients, by quantitative PCR as described in material and methods. Each symbol corresponds to a single patient. Bars represent mean{plus minus}SEM. Samples were tested in triplicate in three independent experiments.
Supplementary Tables 1-9, Supplementary Figure 1 from Genetic Variation in Prostaglandin E2 Synthesis and Signaling, Prostaglandin Dehydrogenase, and the Risk of Colorectal Adenoma
Authors: Poole Elizabeth M. , Hsu Li , Xiao Liren , Kulmacz Richard J. , Carlson Christopher S. , Rabinovitch Peter S. , Makar Karen W. , Potter John D. , Ulrich Cornelia M.
Published: March 2023

Supplementary Tables 1-9, Supplementary Figure 1 from Genetic Variation in Prostaglandin E2 Synthesis and Signaling, Prostaglandin Dehydrogenase, and the Risk of Colorectal Adenoma
Supplementary Figure S3 from Circulating Mitochondrial DNA Level, a Noninvasive Biomarker for the Early Detection of Gastric Cancer
Authors: Fernandes Julien , Michel Valérie , Camorlinga-Ponce Margarita , Gomez Alejandro , Maldonado Carmen , De Reuse Hilde , Torres Javier , Touati Eliette
Published: March 2023

Supplementary Figure S3 : Effect of smoking on the levels of mtDNA in peripheral leukocytes and serological IL-8 levels in NAG and GC patients, compared to healthy blood donors in cohort 1. A) Quantification of MtDNA levels by quantitative PCR as described in material and methods and B) Measure of IL-8 levels by ELISA. Cohort 1 included 47%, 48% and 56% of smokers in controls, NAG and GC groups respectively. Smokers are in black symbols and non-smokers in white symbols, circled symbols among GC cases in B) correspond to samples related to mtDNA inteval II. Each symbol represents a single patient, bars correspond to mean{plus minus}SEM. Each sample was tested in triplicate in three independent experiments. *p-value>0.05 ; **p-value<0.01.
Supplementary Figure Legend from Subtype-Specific Risk of Testicular Tumors among Immigrants and Their Descendants in Sweden, 1960 to 2007
Authors: Beiki Omid , Granath Fredrik , Allebeck Peter , Akre Olof , Moradi Tahereh
Published: March 2023

Supplementary Figure Legend from Subtype-Specific Risk of Testicular Tumors among Immigrants and Their Descendants in Sweden, 1960 to 2007
Supplementary Tables 3-4 from Exposure to Smoking Imagery in the Movies and Experimenting with Cigarettes among Mexican Heritage Youth
Authors: Wilkinson Anna V. , Spitz Margaret R. , Prokhorov Alexander V. , Bondy Melissa L. , Shete Sanjay , Sargent James D.
Published: March 2023

Supplementary Tables 3-4 from Exposure to Smoking Imagery in the Movies and Experimenting with Cigarettes among Mexican Heritage Youth
Supplementary Table 2 from Global Levels of Specific Histone Modifications and an Epigenetic Gene Signature Predict Prostate Cancer Progression and Development
Authors: Bianco-Miotto Tina , Chiam Karen , Buchanan Grant , Jindal Shalini , Day Tanya K. , Thomas Mervyn , Pickering Marie A. , O'Loughlin Melissa A. , Ryan Natalie K. , Raymond Wendy A. , Horvath Lisa G. , Kench James G. , Stricker Phillip D. , Marshall Villis R. , Sutherland Robert L. , Henshall Susan M. , Gerald William L. , Scher Howard I. , Risbridger Gail P. , Clements Judith A. , Butler Lisa M. , Tilley Wayne D. , Horsfall David J. , Ricciardelli Carmela
Published: March 2023

Supplementary Table 2 from Global Levels of Specific Histone Modifications and an Epigenetic Gene Signature Predict Prostate Cancer Progression and Development
Supplementary Table 1 from Global Levels of Specific Histone Modifications and an Epigenetic Gene Signature Predict Prostate Cancer Progression and Development
Authors: Bianco-Miotto Tina , Chiam Karen , Buchanan Grant , Jindal Shalini , Day Tanya K. , Thomas Mervyn , Pickering Marie A. , O'Loughlin Melissa A. , Ryan Natalie K. , Raymond Wendy A. , Horvath Lisa G. , Kench James G. , Stricker Phillip D. , Marshall Villis R. , Sutherland Robert L. , Henshall Susan M. , Gerald William L. , Scher Howard I. , Risbridger Gail P. , Clements Judith A. , Butler Lisa M. , Tilley Wayne D. , Horsfall David J. , Ricciardelli Carmela
Published: March 2023

Supplementary Table 1 from Global Levels of Specific Histone Modifications and an Epigenetic Gene Signature Predict Prostate Cancer Progression and Development
Supplementary Appendix A from Association of Insurance and Race/Ethnicity with Disease Severity among Men Diagnosed with Prostate Cancer, National Cancer Database 2004-2006
Authors: Fedewa Stacey A. , Etzioni Ruth , Flanders W. Dana , Jemal Ahmedin , Ward Elizabeth M.
Published: March 2023

Supplementary Appendix A from Association of Insurance and Race/Ethnicity with Disease Severity among Men Diagnosed with Prostate Cancer, National Cancer Database 2004-2006
Supplementary Table 2 from Associations of Lifestyle Factors and Anthropometric Measures with Repeat PSA Levels During Active Surveillance/Monitoring
Authors: Burton Anya J. , Martin Richard M. , Donovan Jenny L. , Lane J. Athene , Davis Michael , Hamdy Freddie C. , Neal David E. , Tilling Kate
Published: March 2023

PDF file, 74K, Age, recruitment PSA and repeat PSAs by anthropometric measures.
Supplementary Table 1, Supplementary Figure 1 from Systematic Error in Gas Chromatography-Mass Spectrometry–Based Quantification of Hydrolyzed Urinary Steroids
Authors: Moon Ju-Yeon , Ha Young Wan , Moon Myeong Hee , Chung Bong Chul , Choi Man Ho
Published: March 2023

Supplementary Table 1, Supplementary Figure 1 from Systematic Error in Gas Chromatography-Mass Spectrometry–Based Quantification of Hydrolyzed Urinary Steroids
Supplementary Figure 1 from Global Levels of Specific Histone Modifications and an Epigenetic Gene Signature Predict Prostate Cancer Progression and Development
Authors: Bianco-Miotto Tina , Chiam Karen , Buchanan Grant , Jindal Shalini , Day Tanya K. , Thomas Mervyn , Pickering Marie A. , O'Loughlin Melissa A. , Ryan Natalie K. , Raymond Wendy A. , Horvath Lisa G. , Kench James G. , Stricker Phillip D. , Marshall Villis R. , Sutherland Robert L. , Henshall Susan M. , Gerald William L. , Scher Howard I. , Risbridger Gail P. , Clements Judith A. , Butler Lisa M. , Tilley Wayne D. , Horsfall David J. , Ricciardelli Carmela
Published: March 2023

Supplementary Figure 1 from Global Levels of Specific Histone Modifications and an Epigenetic Gene Signature Predict Prostate Cancer Progression and Development
Supplementary Table 1 from Glutathione Pathway Genetic Polymorphisms and Lung Cancer Survival After Platinum-Based Chemotherapy
Authors: Moyer Ann M. , Sun Zhifu , Batzler Anthony J. , Li Liang , Schaid Daniel J. , Yang Ping , Weinshilboum Richard M.
Published: March 2023

Supplementary Table 1 from Glutathione Pathway Genetic Polymorphisms and Lung Cancer Survival After Platinum-Based Chemotherapy
Supplementary Table 3 from Genetic Polymorphisms in Adaptive Immunity Genes and Childhood Acute Lymphoblastic Leukemia
Authors: Chang Jeffrey S. , Wiemels Joseph L. , Chokkalingam Anand P. , Metayer Catherine , Barcellos Lisa F. , Hansen Helen M. , Aldrich Melinda C. , Guha Neela , Urayama Kevin Y. , Scélo Ghislaine , Green Janet , May Suzanne L. , Kiley Vincent A. , Wiencke John K. , Buffler Patricia A.
Published: March 2023

Supplementary Table 3 from Genetic Polymorphisms in Adaptive Immunity Genes and Childhood Acute Lymphoblastic Leukemia
Supplementary Table 1 from Genetic Polymorphisms in Adaptive Immunity Genes and Childhood Acute Lymphoblastic Leukemia
Authors: Chang Jeffrey S. , Wiemels Joseph L. , Chokkalingam Anand P. , Metayer Catherine , Barcellos Lisa F. , Hansen Helen M. , Aldrich Melinda C. , Guha Neela , Urayama Kevin Y. , Scélo Ghislaine , Green Janet , May Suzanne L. , Kiley Vincent A. , Wiencke John K. , Buffler Patricia A.
Published: March 2023

Supplementary Table 1 from Genetic Polymorphisms in Adaptive Immunity Genes and Childhood Acute Lymphoblastic Leukemia
Supplementary Figure 2 from Genetic Polymorphisms in Adaptive Immunity Genes and Childhood Acute Lymphoblastic Leukemia
Authors: Chang Jeffrey S. , Wiemels Joseph L. , Chokkalingam Anand P. , Metayer Catherine , Barcellos Lisa F. , Hansen Helen M. , Aldrich Melinda C. , Guha Neela , Urayama Kevin Y. , Scélo Ghislaine , Green Janet , May Suzanne L. , Kiley Vincent A. , Wiencke John K. , Buffler Patricia A.
Published: March 2023

Supplementary Figure 2 from Genetic Polymorphisms in Adaptive Immunity Genes and Childhood Acute Lymphoblastic Leukemia
Legend for Supplementary Figures 1-5 from Relationship between Epidermal Growth Factor Receptor Status, p16INK4A, and Outcome in Head and Neck Squamous Cell Carcinoma
Authors: Young Richard J. , Rischin Danny , Fisher Richard , McArthur Grant A. , Fox Stephen B. , Peters Lester J. , Corry June , Lim Annette , Waldeck Kelly , Solomon Benjamin
Published: March 2023

Legend for Supplementary Figures 1-5 from Relationship between Epidermal Growth Factor Receptor Status, p16INK4A, and Outcome in Head and Neck Squamous Cell Carcinoma
Supplementary Table 7 from Distribution and Hepatocellular Carcinoma–Related Viral Properties of Hepatitis B Virus Genotypes in Mainland China: A Community-Based Study
Authors: Yin Jianhua , Zhang Hongwei , He Yongchao , Xie Jiaxin , Liu Shijian , Chang Wenjun , Tan Xiaojie , Gu Chunying , Lu Wei , Wang Hongyang , Bi Shengli , Cui Fuqiang , Liang Xiaofeng , Schaefer Stephan , Cao Guangwen
Published: March 2023

Supplementary Table 7 from Distribution and Hepatocellular Carcinoma–Related Viral Properties of Hepatitis B Virus Genotypes in Mainland China: A Community-Based Study
Supplementary Table 5 from Distribution and Hepatocellular Carcinoma–Related Viral Properties of Hepatitis B Virus Genotypes in Mainland China: A Community-Based Study
Authors: Yin Jianhua , Zhang Hongwei , He Yongchao , Xie Jiaxin , Liu Shijian , Chang Wenjun , Tan Xiaojie , Gu Chunying , Lu Wei , Wang Hongyang , Bi Shengli , Cui Fuqiang , Liang Xiaofeng , Schaefer Stephan , Cao Guangwen
Published: March 2023

Supplementary Table 5 from Distribution and Hepatocellular Carcinoma–Related Viral Properties of Hepatitis B Virus Genotypes in Mainland China: A Community-Based Study
Supplementary Table 3 from Distribution and Hepatocellular Carcinoma–Related Viral Properties of Hepatitis B Virus Genotypes in Mainland China: A Community-Based Study
Authors: Yin Jianhua , Zhang Hongwei , He Yongchao , Xie Jiaxin , Liu Shijian , Chang Wenjun , Tan Xiaojie , Gu Chunying , Lu Wei , Wang Hongyang , Bi Shengli , Cui Fuqiang , Liang Xiaofeng , Schaefer Stephan , Cao Guangwen
Published: March 2023

Supplementary Table 3 from Distribution and Hepatocellular Carcinoma–Related Viral Properties of Hepatitis B Virus Genotypes in Mainland China: A Community-Based Study
Supplementary Table 1 from Genetic Variants of Methyl Metabolizing Enzymes and Epigenetic Regulators: Associations with Promoter CpG Island Hypermethylation in Colorectal Cancer
Authors: de Vogel Stefan , Wouters Kim A.D. , Gottschalk Ralph W.H. , van Schooten Frederik J. , de Goeij Anton F.P.M. , de Bruïne Adriaan P. , Goldbohm Royle A. , van den Brandt Piet A. , Weijenberg Matty P. , van Engeland Manon
Published: March 2023

Supplementary Table 1 from Genetic Variants of Methyl Metabolizing Enzymes and Epigenetic Regulators: Associations with Promoter CpG Island Hypermethylation in Colorectal Cancer
Supplementary Table 1 from TP53 Arg72Pro Polymorphism and Colorectal Cancer Risk: A Systematic Review and Meta-Analysis
Authors: Dahabreh Issa J. , Linardou Helena , Bouzika Peggy , Varvarigou Vasileia , Murray Samuel
Published: March 2023

Supplementary Table 1 from TP53 Arg72Pro Polymorphism and Colorectal Cancer Risk: A Systematic Review and Meta-Analysis
Supplementary Figure 2 from TP53 Arg72Pro Polymorphism and Colorectal Cancer Risk: A Systematic Review and Meta-Analysis
Authors: Dahabreh Issa J. , Linardou Helena , Bouzika Peggy , Varvarigou Vasileia , Murray Samuel
Published: March 2023

Supplementary Figure 2 from TP53 Arg72Pro Polymorphism and Colorectal Cancer Risk: A Systematic Review and Meta-Analysis
Supplementary Figure Legends from Collagen XXIII: A Potential Biomarker for the Detection of Primary and Recurrent Non–Small Cell Lung Cancer
Authors: Spivey Kristin A. , Banyard Jacqueline , Solis Luisa M. , Wistuba Ignacio I. , Barletta Justine A. , Gandhi Leena , Feldman Henry A. , Rodig Scott J. , Chirieac Lucian R. , Zetter Bruce R.
Published: March 2023

Supplementary Figure Legends from Collagen XXIII: A Potential Biomarker for the Detection of Primary and Recurrent Non–Small Cell Lung Cancer
Supplementary Figure 5 from Collagen XXIII: A Potential Biomarker for the Detection of Primary and Recurrent Non–Small Cell Lung Cancer
Authors: Spivey Kristin A. , Banyard Jacqueline , Solis Luisa M. , Wistuba Ignacio I. , Barletta Justine A. , Gandhi Leena , Feldman Henry A. , Rodig Scott J. , Chirieac Lucian R. , Zetter Bruce R.
Published: March 2023

Supplementary Figure 5 from Collagen XXIII: A Potential Biomarker for the Detection of Primary and Recurrent Non–Small Cell Lung Cancer
Supplementary Table 1 from Cigarette Smoking and Pulmonary Function in Adult Survivors of Childhood Cancer Exposed to Pulmonary-Toxic Therapy: Results from the St. Jude Lifetime Cohort Study
Authors: Oancea S. Cristina , Gurney James G. , Ness Kirsten K. , Ojha Rohit P. , Tyc Vida L. , Klosky James L. , Srivastava DeoKumar , Stokes Dennis C. , Robison Leslie L. , Hudson Melissa M. , Green Daniel M.
Published: March 2023

PDF file - 57K, Frequency of demographic and treatment characteristics among SJLIFE participants who did or did not undergo PFT and non-participants exposed to pulmonary toxic therapy.
Supplemental Tables 1 - 2 from 1,3-Butadiene Exposure and Metabolism among Japanese American, Native Hawaiian, and White Smokers
Authors: Park Sungshim Lani , Kotapati Srikanth , Wilkens Lynne R. , Tiirikainen Maarit , Murphy Sharon E. , Tretyakova Natalia , Le Marchand Loïc
Published: March 2023

Supplemental Table 1. Spearman's partial correlations (r)a between 1,3 butadiene urinary metabolites and nicotine equivalents.Supplemental Table 2. Geometric means (95% Confidence Limits) for the 1,3 butadiene metabolite, MHBMA (ng/mg Cr),stratified by cigarettes per day (CPD), nicotine equivalents, and CYP2A6 activityb
Supplementary Appendix from The Potential of Genes and Other Markers to Inform about Risk
Authors: Pepe Margaret S. , Gu Jessie W. , Morris Daryl E.
Published: March 2023

Supplementary Appendix from The Potential of Genes and Other Markers to Inform about Risk
Supplementary Table 1 from Analgesic Use and Sex Steroid Hormone Concentrations in Postmenopausal Women
Authors: Gates Margaret A. , Tworoger Shelley S. , Eliassen A. Heather , Missmer Stacey A. , Hankinson Susan E.
Published: March 2023

Supplementary Table 1 from Analgesic Use and Sex Steroid Hormone Concentrations in Postmenopausal Women
Supplementary Figures 1-5, Supplementary Tables 1-3, Full List of Authors and Affiliations from Saliva-Derived DNA Performs Well in Large-Scale, High-Density Single-Nucleotide Polymorphism Microarray Studies
Authors: Bahlo Melanie , Stankovich Jim , Danoy Patrick , Hickey Peter F. , Taylor Bruce V. , Browning Sharon R. , Brown Matthew A. , Rubio Justin P.
Published: March 2023

Supplementary Figures 1-5, Supplementary Tables 1-3, Full List of Authors and Affiliations from Saliva-Derived DNA Performs Well in Large-Scale, High-Density Single-Nucleotide Polymorphism Microarray Studies
Supplementary Figure 8 from Global Patterns of Cancer Incidence and Mortality Rates and Trends
Authors: Jemal Ahmedin , Center Melissa M. , DeSantis Carol , Ward Elizabeth M.
Published: March 2023

Supplementary Figure 8 from Global Patterns of Cancer Incidence and Mortality Rates and Trends
Supplementary Table 4 from Confirmation of 5p12 As a Susceptibility Locus for Progesterone-Receptor–Positive, Lower Grade Breast Cancer
Authors: Milne Roger L. , Goode Ellen L. , García-Closas Montserrat , Couch Fergus J. , Severi Gianluca , Hein Rebecca , Fredericksen Zachary , Malats Núria , Zamora M. Pilar , Pérez Jose Ignacio Arias , Benítez Javier , Dörk Thilo , Schürmann Peter , Karstens Johann H. , Hillemanns Peter , Cox Angela , Brock Ian W. , Elliot Graeme , Cross Simon S. , Seal Sheila , Turnbull Clare , Renwick Anthony , Rahman Nazneen , Shen Chen-Yang , Yu Jyh-Cherng , Huang Chiun-Sheng , Hou Ming-Feng , Nordestgaard Børge G. , Bojesen Stig E. , Lanng Charlotte , Alnæs Grethe Grenaker , Kristensen Vessela , Børrensen-Dale Anne-Lise , Hopper John L. , Dite Gillian S. , Apicella Carmel , Southey Melissa C. , Lambrechts Diether , Yesilyurt Betül T. , Floris Giuseppe , Leunen Karin , Sangrajrang Suleeporn , Gaborieau Valerie , Brennan Paul , McKay James , Chang-Claude Jenny , Wang-Gohrke Shan , Radice Paolo , Peterlongo Paolo , Manoukian Siranoush , Barile Monica , Giles Graham G. , Baglietto Laura , John Esther M. , Miron Alexander , Chanock Stephen J. , Lissowska Jolanta , Sherman Mark E. , Figueroa Jonine D. , Bogdanova Natalia V. , Antonenkova Natalia N. , Zalutsky Iosif V. , Rogov Yuri I. , Fasching Peter A. , Bayer Christian M. , Ekici Arif B. , Beckmann Matthias W. , Brenner Hermann , Müller Heiko , Arndt Volker , Stegmaier Christa , Andrulis Irene L. , Knight Julia A. , Glendon Gord , Mulligan Anna Marie , Mannermaa Arto , Kataja Vesa , Kosma Veli-Matti , Hartikainen Jaana M. , Meindl Alfons , Heil Joerg , Bartram Claus R. , Schmutzler Rita K. , Thomas Gilles D. , Hoover Robert N. , Fletcher Olivia , Gibson Lorna J. , dos Santos Silva Isabel , Peto Julian , Nickels Stefan , Flesch-Janys Dieter , Anton-Culver Hoda , Ziogas Argyrios , Sawyer Elinor , Tomlinson Ian , Kerin Michael , Miller Nicola , Schmidt Marjanka K. , Broeks Annegien , Van ‘t Veer Laura J. , Tollenaar Rob A.E.M. , Pharoah Paul D.P. , Dunning Alison M. , Pooley Karen A. , Marme Frederik , Schneeweiss Andreas , Sohn Christof , Burwinkel Barbara , Jakubowska Anna , Lubinski Jan , Jaworska Katarzyna , Durda Katarzyna , Kang Daehee , Yoo Keun-Young , Noh Dong-Young , Ahn Sei-Hyun , Hunter David J. , Hankinson Susan E. , Kraft Peter , Lindstrom Sara , Chen Xiaoqing , Beesley Jonathan , Hamann Ute , Harth Volker , Justenhoven Christina , Winqvist Robert , Pylkäs Katri , Jukkola-Vuorinen Arja , Grip Mervi , Hooning Maartje , Hollestelle Antoinette , Oldenburg Rogier A. , Tilanus-Linthorst Madeleine , Khusnutdinova Elza , Bermisheva Marina , Prokofieva Darya , Farahtdinova Albina , Olson Janet E. , Wang Xianshu , Humphreys Manjeet K. , Wang Qin , Chenevix-Trench Georgia , Easton Douglas F.
Published: March 2023

PDF file - 70K
Supplementary Table 1 from Confirmation of 5p12 As a Susceptibility Locus for Progesterone-Receptor–Positive, Lower Grade Breast Cancer
Authors: Milne Roger L. , Goode Ellen L. , García-Closas Montserrat , Couch Fergus J. , Severi Gianluca , Hein Rebecca , Fredericksen Zachary , Malats Núria , Zamora M. Pilar , Pérez Jose Ignacio Arias , Benítez Javier , Dörk Thilo , Schürmann Peter , Karstens Johann H. , Hillemanns Peter , Cox Angela , Brock Ian W. , Elliot Graeme , Cross Simon S. , Seal Sheila , Turnbull Clare , Renwick Anthony , Rahman Nazneen , Shen Chen-Yang , Yu Jyh-Cherng , Huang Chiun-Sheng , Hou Ming-Feng , Nordestgaard Børge G. , Bojesen Stig E. , Lanng Charlotte , Alnæs Grethe Grenaker , Kristensen Vessela , Børrensen-Dale Anne-Lise , Hopper John L. , Dite Gillian S. , Apicella Carmel , Southey Melissa C. , Lambrechts Diether , Yesilyurt Betül T. , Floris Giuseppe , Leunen Karin , Sangrajrang Suleeporn , Gaborieau Valerie , Brennan Paul , McKay James , Chang-Claude Jenny , Wang-Gohrke Shan , Radice Paolo , Peterlongo Paolo , Manoukian Siranoush , Barile Monica , Giles Graham G. , Baglietto Laura , John Esther M. , Miron Alexander , Chanock Stephen J. , Lissowska Jolanta , Sherman Mark E. , Figueroa Jonine D. , Bogdanova Natalia V. , Antonenkova Natalia N. , Zalutsky Iosif V. , Rogov Yuri I. , Fasching Peter A. , Bayer Christian M. , Ekici Arif B. , Beckmann Matthias W. , Brenner Hermann , Müller Heiko , Arndt Volker , Stegmaier Christa , Andrulis Irene L. , Knight Julia A. , Glendon Gord , Mulligan Anna Marie , Mannermaa Arto , Kataja Vesa , Kosma Veli-Matti , Hartikainen Jaana M. , Meindl Alfons , Heil Joerg , Bartram Claus R. , Schmutzler Rita K. , Thomas Gilles D. , Hoover Robert N. , Fletcher Olivia , Gibson Lorna J. , dos Santos Silva Isabel , Peto Julian , Nickels Stefan , Flesch-Janys Dieter , Anton-Culver Hoda , Ziogas Argyrios , Sawyer Elinor , Tomlinson Ian , Kerin Michael , Miller Nicola , Schmidt Marjanka K. , Broeks Annegien , Van ‘t Veer Laura J. , Tollenaar Rob A.E.M. , Pharoah Paul D.P. , Dunning Alison M. , Pooley Karen A. , Marme Frederik , Schneeweiss Andreas , Sohn Christof , Burwinkel Barbara , Jakubowska Anna , Lubinski Jan , Jaworska Katarzyna , Durda Katarzyna , Kang Daehee , Yoo Keun-Young , Noh Dong-Young , Ahn Sei-Hyun , Hunter David J. , Hankinson Susan E. , Kraft Peter , Lindstrom Sara , Chen Xiaoqing , Beesley Jonathan , Hamann Ute , Harth Volker , Justenhoven Christina , Winqvist Robert , Pylkäs Katri , Jukkola-Vuorinen Arja , Grip Mervi , Hooning Maartje , Hollestelle Antoinette , Oldenburg Rogier A. , Tilanus-Linthorst Madeleine , Khusnutdinova Elza , Bermisheva Marina , Prokofieva Darya , Farahtdinova Albina , Olson Janet E. , Wang Xianshu , Humphreys Manjeet K. , Wang Qin , Chenevix-Trench Georgia , Easton Douglas F.
Published: March 2023

PDF file - 137K
Supplementary Figure 1, Table 1 from Identification of Adipophilin as a Potential Plasma Biomarker for Colorectal Cancer Using Label-Free Quantitative Mass Spectrometry and Protein Microarray
Authors: Matsubara Junichi , Honda Kazufumi , Ono Masaya , Sekine Shigeki , Tanaka Yoshinori , Kobayashi Michimoto , Jung Giman , Sakuma Tomohiro , Nakamori Shoji , Sata Naohiro , Nagai Hideo , Ioka Tatsuya , Okusaka Takuji , Kosuge Tomoo , Tsuchida Akihiko , Shimahara Masashi , Yasunami Yohichi , Chiba Tsutomu , Yamada Tesshi
Published: March 2023

PDF file - 52K
Supplementary Table 1 from Validation of a Light Questionnaire with Real-life Photopic Illuminance Measurements: the Harvard Light Exposure Assessment Questionnaire
Authors: Bajaj Archna , Rosner Bernard , Lockley Steven W. , Schernhammer Eva S.
Published: March 2023

Supplementary Table 1 from Validation of a Light Questionnaire with Real-life Photopic Illuminance Measurements: the Harvard Light Exposure Assessment Questionnaire