bluuebunny/crossref_metadata_2025 huggingface dataset:
Data from Rapalogs Efficacy Relies on the Modulation of Antitumor T-cell Immunity
Authors: Beziaud Laurent , Mansi Laura , Ravel Patrice , Marie-Joseph Elodie Lauret , Laheurte Caroline , Rangan Laurie , Bonnefoy Francis , Pallandre Jean-René , Boullerot Laura , Gamonet Clémentine , Vrecko Sindy , Queiroz Lise , Maurina Tristan , Mouillet Guillaume , Hon Thierry Nguyen Tan , Curtit Elsa , Royer Bernard , Gaugler Béatrice , Bayry Jagadeesh , Tartour Eric , Thiery-Vuillemin Antoine , Pivot Xavier , Borg Christophe , Godet Yann , Adotévi Olivier
Published: April 2023

Abstract
The rapalogs everolimus and temsirolimus that inhibit mTOR signaling are used as antiproliferative drugs in several cancers. Here we investigated the influence of rapalogs-mediated immune modulation on their antitumor efficacy. Studies in metastatic renal cell carcinoma patients showed that everolimus promoted high expansion of FoxP3+Helios+Ki67+ regulatory CD4 T cells (Tregs). In these patients, rapalogs strongly enhanced the suppressive functions of Tregs, mainly in a contact-dependent manner. Paradoxically, a concurrent activation of spontaneous tumor-specific Th1 immunity also occurred. Furthermore, a high rate of Eomes+CD8+ T cells was detected in patients after a long-term mTOR inhibition. We found that early changes in the Tregs/antitumor Th1 balance can differentially shape the treatment efficacy. Patients presenting a shift toward decreased Tregs levels and high expansion of antitumor Th1 cells showed better clinical responses. Studies conducted in tumor-bearing mice confirmed the deleterious effect of rapalogs-induced Tregs via a mechanism involving the inhibition of antitumor T-cell immunity. Consequently, the combination of temsirolimus plus CCR4 antagonist, a receptor highly expressed on rapalogs-exposed Tregs, was more effective than monotherapy. Altogether, our results describe for the first time a dual impact of host adaptive antitumor T-cell immunity on the clinical effectiveness of rapalogs and prompt their association with immunotherapies. Cancer Res; 76(14); 4100–12. ©2016 AACR.
Data from IL6 Trans-signaling Promotes KRAS-Driven Lung Carcinogenesis
Authors: Brooks Gavin D. , McLeod Louise , Alhayyani Sultan , Miller Alistair , Russell Prudence A. , Ferlin Walter , Rose-John Stefan , Ruwanpura Saleela , Jenkins Brendan J.
Published: April 2023

Abstract
Oncogenic KRAS mutations occur frequently in lung adenocarcinoma. The signaling pathways activated by IL6 promote Kras-driven lung tumorigenesis, but the basis for this cooperation is uncertain. In this study, we used the gp130F/F (Il6st) knock-in mouse model to examine the pathogenic contribution of hyperactivation of the STAT3 arm of IL6 signaling on KRAS-driven lung tumorigenesis. Malignant growths in the gp130F/F:KrasG12D model displayed features of atypical adenomatous hyperplasia, adenocarcinoma in situ, and invasive adenocarcinoma throughout the lung, as compared with parental KrasG12D mice, where STAT3 was not hyperactivated. Among IL6 family cytokines, only IL6 was upregulated in the lung. Accordingly, normalization of pulmonary STAT3 activity, by genetic ablation of either Il6 or Stat3, suppressed the extent of lung cancer in the model. Mechanistic investigations revealed elevation in the lung of soluble IL6 receptor (sIL6R), the key driver of IL6 trans-signaling, and blocking this mechanism via interventions with an anti-IL6R antibody or the inhibitor sgp130Fc ameliorated lung cancer pathogenesis. Clinically, expression of IL6 and sIL6R was increased significantly in human specimens of lung adenocarcinoma or patient serum. Our results offer a preclinical rationale to clinically evaluate IL6 trans-signaling as a therapeutic target for the treatment of KRAS-driven lung adenocarcinoma. Cancer Res; 76(4); 866–76. ©2016 AACR.
Data from Eritoran Suppresses Colon Cancer by Altering a Functional Balance in Toll-like Receptors That Bind Lipopolysaccharide
Authors: Kuo Wei-Ting , Lee Tsung-Chun , Yu Linda Chia-Hui
Published: April 2023

Abstract
Colorectal carcinogenesis is affected by overexpression of the lipopolysaccharide (LPS) receptors CD14 and TLR4, which antagonize each other by affecting epithelial cell proliferation and apoptosis. Eritoran is an investigational drug for sepsis treatment that resembles the lipid A moiety of LPS and therefore acts as a TLR4 inhibitor. In the present study, we explored the potential therapeutic uses and mechanisms of action of eritoran in reducing colon cancer progression. Eritoran administration via intracolonic, intragastric, or intravenous routes significantly reduced tumor burden in a chemically induced mouse model of colorectal carcinoma. Decreased proliferation and increased apoptosis were observed in mouse tumor cells after eritoran treatment. In vitro cultures of mouse primary tumor spheroids and human cancer cell lines displayed increased cell proliferation and cell-cycle progression following LPS challenge. This effect was inhibited by eritoran and by silencing CD14 or TLR4. In contrast, apoptosis induced by eritoran was eliminated by silencing CD14 or protein kinase Cζ (PKCζ) but not TLR4. Lastly, LPS and eritoran caused hyperphosphorylation of PKCζ in a CD14-dependent and TLR4-independent manner. Blocking PKCζ activation by a Src kinase inhibitor and a PKCζ-pseudosubstrate prevented eritoran-induced apoptosis. In summary, our work offers a preclinical proof of concept for the exploration of eritoran as a clinical treatment, with a mechanistic rationale to reposition this drug to improve the management of colorectal cancer. Cancer Res; 76(16); 4684–95. ©2016 AACR.
Data from Osteogenic Potential of Mesenchymal Stromal Cells Contributes to Primary Myelofibrosis
Authors: Martinaud Christophe , Desterke Christophe , Konopacki Johanna , Pieri Lisa , Torossian Frédéric , Golub Rachel , Schmutz Sandrine , Anginot Adrienne , Guerton Bernadette , Rochet Nathalie , Albanese Patricia , Henault Emilie , Pierre-Louis Olivier , Souraud Jean-Baptiste , de Revel Thierry , Dupriez Brigitte , Ianotto Jean-Christophe , Bourgeade Marie-Françoise , Vannucchi Alessandro M. , Lataillade Jean-Jacques , Le Bousse-Kerdilès Marie-Caroline
Published: April 2023

Abstract
Primary myelofibrosis is a myeloproliferative neoplasm that is a precursor to myeloid leukemia. Dysmegakaryopoiesis and extramedullary hematopoiesis characterize primary myelofibrosis, which is also associated with bone marrow stromal alterations marked by fibrosis, neoangiogenesis, and osteomyelosclerosis. In particular, contributions to primary myelofibrosis from mesenchymal stromal cells (MSC) have been suggested by mouse studies, but evidence in humans remains lacking. In this study, we show that bone marrow MSCs from primary myelofibrosis patients exhibit unique molecular and functional abnormalities distinct from other myeloproliferative neoplasms and these abnormalities are maintained stably ex vivo in the absence of leukemic cells. Primary myelofibrosis-MSC overexpressed heparin-binding cytokines, including proinflammatory TGFβ1 and osteogenic BMP-2, as well as glycosaminoglycans such as heparan sulfate and chondroitin sulfate. Transcriptome and functional analyses revealed alterations in MSC differentiation characterized by an increased osteogenic potential and a TGFβ1 signaling signature. Accordingly, phospho-Smad2 levels were intrinsically increased in primary myelofibrosis-MSC along with enhanced expression of the master bone regulator RUNX2, while inhibition of the endogenous TGFβ1 receptor TGFβR1 impaired osteogenic differentiation in these MSCs. Taken together, our results define the source of a critical osteogenic function in primary myelofibrosis that supports its pathophysiology, suggesting that combined targeting of both the hematopoietic and stromal cell compartments in primary myelofibrosis patients may heighten therapeutic efficacy. Cancer Res; 75(22); 4753–65. ©2015 AACR.
Data from Multiplex H. pylori Serology and Risk of Gastric Cardia and Noncardia Adenocarcinomas
Authors: Shakeri Ramin , Malekzadeh Reza , Nasrollahzadeh Dariush , Pawilta Michael , Murphy Gwen , Islami Farhad , Sotoudeh Masoud , Michel Angelika , Etemadi Arash , Waterboer Tim , Poustchi Hossein , Brennan Paul , Boffetta Paolo , Dawsey Sanford M. , Kamangar Farin , Abnet Christian C.
Published: April 2023

Abstract
The reported associations with gastric adenocarcinoma and seropositivity to different Helicobacter pylori antigens using multiplex serology have not been consistent across studies. We aimed to investigate the association between 15 different multiplex serology antigens and the risk of gastric cardia (GCA) and gastric noncardia (GNCA) adenocarcinomas in northeastern Iran, a population with high rates of gastric adenocarcinoma. We included 272 cases of gastric adenocarcinoma (142 GCA, 103 GNCA, and 27 unspecified) and 524 controls who were individually matched to cases for age, sex, and place of residence in a population-based case–control study. Seropositivity to H. pylori was assessed using both multiplex serology and H. pylori IgG ELISA. Ninety-five percent of controls were seropositive to H. pylori. Of the 15 antibodies in the multiplex assay, 11 showed no significant association with gastric adenocarcinomas. CagA and VacA were associated with a significantly increased risk of all gastric adenocarcinoma and GNCA in multivariate models. Surprisingly, GroEL and NapA were significantly associated with a reduced risk of these tumors. Only CagA antigen was associated with significantly elevated risk of GCA. We found no associations between H. pylori seropositivity overall either by whole-cell ELISA test or multiplex serology, likely due to the high prevalence of seropositivity. Individual antigen testing showed that CagA positivity was associated with increased risk of both noncardia and cardia adenocarcinoma, which is similar to some other Asian populations, whereas two antigens were associated with lower risk of gastric cancer. This latter result was unexpected and should be retested in other populations. Cancer Res; 75(22); 4876–83. ©2015 AACR.
Data from JPO2/CDCA7L and LEDGF/p75 Are Novel Mediators of PI3K/AKT Signaling and Aggressive Phenotypes in Medulloblastoma
Authors: Chan Tiffany Sin Yu , Hawkins Cynthia , Krieger Jonathan R. , McGlade C. Jane , Huang Annie
Published: April 2023

Abstract
Substantial evidence links Myc–PI3K/AKT signaling to the most aggressive subtype of medulloblastoma and this axis in medulloblastoma therapy. In this study, we advance understanding of how Myc–PI3K/AKT signaling contributes to this malignancy, specifically, in identifying the Myc-interacting protein JPO2 and its partner binding protein LEDGF/p75 as critical modulators of PI3K/AKT signaling and metastasis in medulloblastoma. JPO2 overexpression induced metastatic medulloblastoma in vivo through two synergistic feed-forward regulatory circuits involving LEDGF/p75 and AKT that promote metastatic phenotypes in this setting. Overall, our findings highlight two novel prometastatic loci in medulloblastoma and point to the JPO2:LEDGF/p75 protein complex as a potentially new targetable component of PI3K/AKT signaling in medulloblastoma. Cancer Res; 76(9); 2802–12. ©2016 AACR.
Data from An Imbalance in TAZ and YAP Expression in Hepatocellular Carcinoma Confers Cancer Stem Cell–like Behaviors Contributing to Disease Progression
Authors: Hayashi Hiromitsu , Higashi Takaaki , Yokoyama Naomi , Kaida Takayoshi , Sakamoto Keita , Fukushima Yukiko , Ishimoto Takatsugu , Kuroki Hideyuki , Nitta Hidetoshi , Hashimoto Daisuke , Chikamoto Akira , Oki Eiji , Beppu Toru , Baba Hideo
Published: April 2023

Abstract
Transcriptional coactivator with PDZ-binding motif (TAZ) and yes-associated protein (YAP) are equivalently placed downstream effectors of the Hippo pathway with oncogenic roles in human cancers. However, the expression profiles of TAZ/YAP differ depending on the cancer cell type, suggesting that these proteins have different roles during cancer progression, yet no studies have examined the biologic significance of the balance between TAZ and YAP expression levels. Here we examined the functional roles of TAZ/YAP in hepatocellular carcinoma progression. We found that TAZ, but not YAP, was predominantly expressed in HCC. TAZ knockdown under normal conditions attenuated cell growth in HCC cells; however, TAZ knockdown combined with 5-fluorouracil treatment significantly increased chemoresistance compared with control cells. Notably, TAZ knockdown induced compensatory YAP expression and was accompanied by upregulation of CD90, a HCC–specific cancer stem cell marker. Continuous treatment with 5-fluorouracil also induced YAP expression and promoted tumor formation in vivo. Conversely, double knockdown of TAZ/YAP reduced chemoresistance and tumorigenicity. Moreover, YAP knockdown aggravated HCC cell growth to a greater degree than TAZ knockdown, and YAP overexpression was strongly associated with poor prognoses in patients with HCC. Collectively, these studies demonstrate that TAZ and YAP exhibit different functional roles in cancer progression, and a shift to predominant YAP expression upon TAZ depletion conferred cancer stem cell–like properties including chemoresistance and tumorigenicity in HCC. Therefore, targeting of both TAZ/YAP will be required for a complete antitumor response in HCC. Cancer Res; 75(22); 4985–97. ©2015 AACR.
Data from Low-Dose Paclitaxel Reduces S100A4 Nuclear Import to Inhibit Invasion and Hematogenous Metastasis of Cholangiocarcinoma
Authors: Cadamuro Massimiliano , Spagnuolo Gaia , Sambado Luisa , Indraccolo Stefano , Nardo Giorgia , Rosato Antonio , Brivio Simone , Caslini Chiara , Stecca Tommaso , Massani Marco , Bassi Nicolò , Novelli Eugenio , Spirli Carlo , Fabris Luca , Strazzabosco Mario
Published: April 2023

Abstract
Nuclear expression of the calcium-binding protein S100A4 is a biomarker of increased invasiveness in cholangiocarcinoma, a primary liver cancer with scarce treatment opportunities and dismal prognosis. In this study, we provide evidence that targeting S100A4 nuclear import by low-dose paclitaxel, a microtubule-stabilizing agent, inhibits cholangiocarcinoma invasiveness and metastatic spread. Administration of low-dose paclitaxel to established (EGI-1) and primary (CCA-TV3) cholangiocarcinoma cell lines expressing nuclear S100A4 triggered a marked reduction in nuclear expression of S100A4 without modifying its cytoplasmic levels, an effect associated with a significant decrease in cell migration and invasiveness. While low-dose paclitaxel did not affect cellular proliferation, apoptosis, or cytoskeletal integrity, it significantly reduced SUMOylation of S100A4, a critical posttranslational modification that directs its trafficking to the nucleus. This effect of low-dose paclitaxel was reproduced by ginkolic acid, a specific SUMOylation inhibitor. Downregulation of nuclear S100A4 by low-dose paclitaxel was associated with a strong reduction in RhoA and Cdc42 GTPase activity, MT1-MMP expression, and MMP-9 secretion. In an SCID mouse xenograft model, low-dose metronomic paclitaxel treatment decreased lung dissemination of EGI-1 cells without significantly affecting their local tumor growth. In the tumor mass, nuclear S100A4 expression by cholangiocarcinoma cells was significantly reduced, whereas rates of proliferation and apoptosis were unchanged. Overall, our findings highlight nuclear S100A4 as a candidate therapeutic target in cholangiocarcinoma and establish a mechanistic rationale for the use of low-dose paclitaxel in blocking metastatic progression of cholangiocarcinoma. Cancer Res; 76(16); 4775–84. ©2016 AACR.
Data from IL17 Functions through the Novel REG3β–JAK2–STAT3 Inflammatory Pathway to Promote the Transition from Chronic Pancreatitis to Pancreatic Cancer
Authors: Loncle Celine , Bonjoch Laia , Folch-Puy Emma , Lopez-Millan Maria Belen , Lac Sophie , Molejon Maria Inés , Chuluyan Eduardo , Cordelier Pierre , Dubus Pierre , Lomberk Gwen , Urrutia Raul , Closa Daniel , Iovanna Juan L.
Published: April 2023

Abstract
Pancreatic ductal adenocarcinoma (PDAC) offers an optimal model for discovering “druggable” molecular pathways that participate in inflammation-associated cancer development. Chronic pancreatitis, a common prolonged inflammatory disease, behaves as a well-known premalignant condition that contributes to PDAC development. Although the mechanisms underlying the pancreatitis-to-cancer transition remain to be fully elucidated, emerging evidence supports the hypothesis that the actions of proinflammatory mediators on cells harboring Kras mutations promote neoplastic transformation. Recent elegant studies demonstrated that the IL17 pathway mediates this phenomenon and can be targeted with antibodies, but the downstream mechanisms by which IL17 functions during this transition are currently unclear. In this study, we demonstrate that IL17 induces the expression of REG3β, a well-known mediator of pancreatitis, during acinar-to-ductal metaplasia and in early pancreatic intraepithelial neoplasia (PanIN) lesions. Furthermore, we found that REG3β promotes cell growth and decreases sensitivity to cell death through activation of the gp130-JAK2-STAT3-dependent pathway. Genetic inactivation of REG3β in the context of oncogenic Kras-driven PDAC resulted in reduced PanIN formation, an effect that could be rescued by administration of exogenous REG3β. Taken together, our findings provide mechanistic insight into the pathways underlying inflammation-associated pancreatic cancer, revealing a dual and contextual pathophysiologic role for REG3β during pancreatitis and PDAC initiation. Cancer Res; 75(22); 4852–62. ©2015 AACR.
Data from Ras Signaling Is a Key Determinant for Metastatic Dissemination and Poor Survival of Luminal Breast Cancer Patients
Authors: Wright Katherine L. , Adams Jessica R. , Liu Jeff C. , Loch Amanda J. , Wong Ruth G. , Jo Christine E.B. , Beck Lauren A. , Santhanam Divya R. , Weiss Laura , Mei Xue , Lane Timothy F. , Koralov Sergei B. , Done Susan J. , Woodgett James R. , Zacksenhaus Eldad , Hu Pingzhao , Egan Sean E.
Published: April 2023

Abstract
Breast cancer is associated with alterations in a number of growth factor and hormone-regulated signaling pathways. Mouse models of metastatic breast cancer typically feature mutated oncoproteins that activate PI3K, Stat3, and Ras signaling, but the individual and combined roles of these pathways in breast cancer progression are poorly understood. In this study, we examined the relationship between oncogenic pathway activation and breast cancer subtype by analyzing mouse mammary tumor formation in which each pathway was activated singly or pairwise. All three oncogenes showed cooperation during primary tumor formation, but efficient dissemination was only dependent on Ras. In addition, transcriptional profiling demonstrated that Ras induced adenocarcinomas with molecular characteristics related to human basal-like and HER2+ tumors. In contrast, Ras combined with PIK3CAH1047R, an oncogenic mutant linked to ERα+/luminal breast cancer in humans, induced metastatic luminal B-like tumors. Consistent with these data, elevated Ras signaling was associated with basal-like and HER2+ subtype tumors in humans and showed a statistically significant negative association with estrogen receptor (ER) signaling across all breast cancer. Despite this, there are luminal tumors with elevated Ras signaling. Importantly, when considered as a continuous variable, Ras pathway activation was strongly linked to reduced survival of patients with ERα+ disease independent of PI3K or Stat3 activation. Therefore, our studies suggest that Ras activation is a key determinant for dissemination and poor prognosis of ERα+/luminal breast cancer in humans, and hormone therapy supplemented with Ras-targeting agents may be beneficial for treating this aggressive subtype. Cancer Res; 75(22); 4960–72. ©2015 AACR.
Data from Molecular Insights of Pathways Resulting from Two Common PIK3CA Mutations in Breast Cancer
Authors: Bhat-Nakshatri Poornima , Goswami Chirayu P. , Badve Sunil , Magnani Luca , Lupien Mathieu , Nakshatri Harikrishna
Published: April 2023

Abstract
The PI3K pathway is activated in approximately 70% of breast cancers. PIK3CA gene mutations or amplifications that affect the PI3K p110α subunit account for activation of this pathway in 20% to 40% of cases, particularly in estrogen receptor alpha (ERα)-positive breast cancers. AKT family of kinases, AKT1–3, are the downstream targets of PI3K and these kinases activate ERα. Although several inhibitors of PI3K have been developed, none has proven effective in the clinic, partly due to an incomplete understanding of the selective routing of PI3K signaling to specific AKT isoforms. Accordingly, we investigated in this study the contribution of specific AKT isoforms in connecting PI3K activation to ERα signaling, and we also assessed the utility of using the components of PI3K–AKT isoform–ERα signaling axis as predictive biomarkers of response to PI3K inhibitors. Using a variety of physiologically relevant model systems with defined natural or knock-in PIK3CA mutations and/or PI3K hyperactivation, we show that PIK3CA-E545K mutations (found in ∼20% of PIK3CA-mutant breast cancers), but not PIK3CA-H1047R mutations (found in 55% of PIK3CA-mutant breast cancers), preferentially activate AKT1. Our findings argue that AKT1 signaling is needed to respond to estrogen and PI3K inhibitors in breast cancer cells with PIK3CA-E545K mutation, but not in breast cancer cells with other PIK3CA mutations. This study offers evidence that personalizing treatment of ER-positive breast cancers to PI3K inhibitor therapy may benefit from an analysis of PIK3CA–E545K–AKT1–estrogen signaling pathways. Cancer Res; 76(13); 3989–4001. ©2016 AACR.
Supplementary Methods from Modeling of the Growth Kinetics of Occult Breast Tumors: Role in Interpretation of Studies of Prevention and Menopausal Hormone Therapy
Authors: Santen Richard J. , Yue Wei , Heitjan Daniel F.
Published: April 2023

PDF file, 126KB.
Supplementary Figure 1 from Modeling of the Growth Kinetics of Occult Breast Tumors: Role in Interpretation of Studies of Prevention and Menopausal Hormone Therapy
Authors: Santen Richard J. , Yue Wei , Heitjan Daniel F.
Published: April 2023

PDF file, 33KB, Data from the computer simulated model.
Supplementary Figure 1 from Collaborative Cancer Epidemiology in the 21st Century: The Model of Cancer Consortia
Authors: Burgio Michael R. , Ioannidis John P.A. , Kaminski Brett M. , DeRycke Eric , Rogers Scott , Khoury Muin J. , Seminara Daniela
Published: April 2023

PDF - 418KB, Global distribution of EGRP-supported cancer epidemiology consortia (CEC)-affiliated teams.
Supplemental Figure 3 from Medical Care Cost of Oropharyngeal Cancer among Texas Patients
Authors: Lairson David R. , Wu Chi-Fang , Chan Wenyaw , Dahlstrom Kristina R. , Tam Samantha , Sturgis Erich M.
Published: April 2023

The unadjusted cost of pre- and post-period between cases and controls
Supplementary Figure S1 from Heme Iron Intake, Dietary Antioxidant Capacity, and Risk of Colorectal Adenomas in a Large Cohort Study of French Women
Authors: Bastide Nadia , Morois Sophie , Cadeau Claire , Kangas Suvi , Serafini Mauro , Gusto Gaëlle , Dossus Laure , Pierre Fabrice H. , Clavel-Chapelon Françoise , Boutron-Ruault Marie-Christine
Published: April 2023

Supplemental Figure S1: Risk of colorectal adenomas according to the total heme iron /TRAP ratio
Supplementary Table 2 from Using Genetic Proxies for Lifecourse Sun Exposure to Assess the Causal Relationship of Sun Exposure with Circulating Vitamin D and Prostate Cancer Risk
Authors: Bonilla Carolina , Gilbert Rebecca , Kemp John P. , Timpson Nicholas J. , Evans David M. , Donovan Jenny L. , Hamdy Freddie C. , Neal David E. , Fraser William D. , Davey Smith George , Lewis Sarah J. , Lathrop Mark , Martin Richard M.
Published: April 2023

PDF file - 37K, Distribution of pigmentation genetic scores across the nine centers contributing participants to ProtecT.
Supplemental Table 3 from Prevalence of Major Risk Factors and Use of Screening Tests for Cancer in the United States
Authors: Fedewa Stacey A. , Sauer Ann Goding , Siegel Rebecca L. , Jemal Ahmedin
Published: April 2023

Supplemental Table 3. Prevalence of physical activity measures, high school students, by state, Youth Risk Behavior Survey, 2013.
Supplementary Table 3 from Metabolomics in Epidemiology: Sources of Variability in Metabolite Measurements and Implications
Authors: Sampson Joshua N. , Boca Simina M. , Shu Xiao Ou , Stolzenberg-Solomon Rachael Z. , Matthews Charles E. , Hsing Ann W. , Tan Yu Ting , Ji Bu-Tian , Chow Wong-Ho , Cai Qiuyin , Liu Da Ke , Yang Gong , Xiang Yong Bing , Zheng Wei , Sinha Rashmi , Cross Amanda J. , Moore Steven C.
Published: April 2023

PDF file - 94K, Metabolite Classification
Supplementary Methods and Figure Legend from Metabolomics in Epidemiology: Sources of Variability in Metabolite Measurements and Implications
Authors: Sampson Joshua N. , Boca Simina M. , Shu Xiao Ou , Stolzenberg-Solomon Rachael Z. , Matthews Charles E. , Hsing Ann W. , Tan Yu Ting , Ji Bu-Tian , Chow Wong-Ho , Cai Qiuyin , Liu Da Ke , Yang Gong , Xiang Yong Bing , Zheng Wei , Sinha Rashmi , Cross Amanda J. , Moore Steven C.
Published: April 2023

PDF file - 65K
Supplementary figure legends from Night Shift Work Increases the Risks of Multiple Primary Cancers in Women: A Systematic Review and Meta-analysis of 61 Articles
Authors: Yuan Xia , Zhu Chenjing , Wang Manni , Mo Fei , Du Wei , Ma Xuelei
Published: April 2023

Supplementary figure legends
Figure S2 from Night Shift Work Increases the Risks of Multiple Primary Cancers in Women: A Systematic Review and Meta-analysis of 61 Articles
Authors: Yuan Xia , Zhu Chenjing , Wang Manni , Mo Fei , Du Wei , Ma Xuelei
Published: April 2023

Supplementary Figure 2. Begg's funnel plot was used to assess potential publication bias
Supplementary Table 5 from N-acetyltransferase 2 Phenotype, Occupation, and Bladder Cancer Risk: Results from the EPIC Cohort
Authors: Pesch Beate , Gawrych Katarzyna , Rabstein Sylvia , Weiss Tobias , Casjens Swaantje , Rihs Hans-Peter , Ding Hui , Angerer Jürgen , Illig Thomas , Klopp Norman , Bueno-de-Mesquita Bas , Ros Martine M. , Kaaks Rudolf , Chang-Claude Jenny , Roswall Nina , Tjønneland Anne , Overvad Kim , Clavel-Chapelon Françoise , Boutron-Ruault Marie-Christine , Dossus Laure , Boeing Heiner , Weikert Steffen , Trichopoulos Dimitrios , Palli Domenico , Sieri Sabina , Tumino Rosario , Panico Salvatore , Quirós José Ramón , González Carlos , Sánchez Mariá José , Dorronsoro Miren , Navarro Carmen , Barricarte Aurelio , Ljungberg Börje , Johansson Mattias , Ulmert David , Ehrnström Roy , Khaw Kay-Tee , Wareham Nick , Key Timothy J. , Ferrari Pietro , Romieu Isabelle , Riboli Elio , Brüning Thomas , Vineis Paolo
Published: April 2023

PDF - 80KB, Association of smoking and occupational exposure with bladder cancer by NAT2 acetylation in cases and controls from EPIC.
Supplementary Table 4 from N-acetyltransferase 2 Phenotype, Occupation, and Bladder Cancer Risk: Results from the EPIC Cohort
Authors: Pesch Beate , Gawrych Katarzyna , Rabstein Sylvia , Weiss Tobias , Casjens Swaantje , Rihs Hans-Peter , Ding Hui , Angerer Jürgen , Illig Thomas , Klopp Norman , Bueno-de-Mesquita Bas , Ros Martine M. , Kaaks Rudolf , Chang-Claude Jenny , Roswall Nina , Tjønneland Anne , Overvad Kim , Clavel-Chapelon Françoise , Boutron-Ruault Marie-Christine , Dossus Laure , Boeing Heiner , Weikert Steffen , Trichopoulos Dimitrios , Palli Domenico , Sieri Sabina , Tumino Rosario , Panico Salvatore , Quirós José Ramón , González Carlos , Sánchez Mariá José , Dorronsoro Miren , Navarro Carmen , Barricarte Aurelio , Ljungberg Börje , Johansson Mattias , Ulmert David , Ehrnström Roy , Khaw Kay-Tee , Wareham Nick , Key Timothy J. , Ferrari Pietro , Romieu Isabelle , Riboli Elio , Brüning Thomas , Vineis Paolo
Published: April 2023

PDF - 73KB, Joint effects of NAT2 acetylation status and occupational exposure to aromatic amines on the risk of bladder cancer (492 cases and 569 controls).
Table S1 from The Premenopausal Breast Cancer Collaboration: A Pooling Project of Studies Participating in the National Cancer Institute Cohort Consortium
Authors: Nichols Hazel B. , Schoemaker Minouk J. , Wright Lauren B. , McGowan Craig , Brook Mark N. , McClain Kathleen M. , Jones Michael E. , Adami Hans-Olov , Agnoli Claudia , Baglietto Laura , Bernstein Leslie , Bertrand Kimberly A. , Blot William J. , Boutron-Ruault Marie-Christine , Butler Lesley , Chen Yu , Doody Michele M. , Dossus Laure , Eliassen A. Heather , Giles Graham G. , Gram Inger T. , Hankinson Susan E. , Hoffman-Bolton Judy , Kaaks Rudolf , Key Timothy J. , Kirsh Victoria A. , Kitahara Cari M. , Koh Woon-Puay , Larsson Susanna C. , Lund Eiliv , Ma Huiyan , Merritt Melissa A. , Milne Roger L. , Navarro Carmen , Overvad Kim , Ozasa Kotaro , Palmer Julie R. , Peeters Petra H. , Riboli Elio , Rohan Thomas E. , Sadakane Atsuko , Sund Malin , Tamimi Rulla M. , Trichopoulou Antonia , Vatten Lars , Visvanathan Kala , Weiderpass Elisabete , Willett Walter C. , Wolk Alicja , Zeleniuch-Jacquotte Anne , Zheng Wei , Sandler Dale P. , Swerdlow Anthony J.
Published: April 2023

Supplementary table 1: Overview of the number of cohort studies providing information on each type of risk factor in the pooled data set
Supplementary Table 2 from N-acetyltransferase 2 Phenotype, Occupation, and Bladder Cancer Risk: Results from the EPIC Cohort
Authors: Pesch Beate , Gawrych Katarzyna , Rabstein Sylvia , Weiss Tobias , Casjens Swaantje , Rihs Hans-Peter , Ding Hui , Angerer Jürgen , Illig Thomas , Klopp Norman , Bueno-de-Mesquita Bas , Ros Martine M. , Kaaks Rudolf , Chang-Claude Jenny , Roswall Nina , Tjønneland Anne , Overvad Kim , Clavel-Chapelon Françoise , Boutron-Ruault Marie-Christine , Dossus Laure , Boeing Heiner , Weikert Steffen , Trichopoulos Dimitrios , Palli Domenico , Sieri Sabina , Tumino Rosario , Panico Salvatore , Quirós José Ramón , González Carlos , Sánchez Mariá José , Dorronsoro Miren , Navarro Carmen , Barricarte Aurelio , Ljungberg Börje , Johansson Mattias , Ulmert David , Ehrnström Roy , Khaw Kay-Tee , Wareham Nick , Key Timothy J. , Ferrari Pietro , Romieu Isabelle , Riboli Elio , Brüning Thomas , Vineis Paolo
Published: April 2023

PDF - 84KB, Joint effects of smoking and occupational exposure to aromatic amines and polycyclic aromatic hydrocarbons on the risk of bladder cancer (754 cases and 833 controls).
Supplementary Figure 1 from Germline Missense Variants in the BTNL2 Gene Are Associated with Prostate Cancer Susceptibility
Authors: FitzGerald Liesel M. , Kumar Akash , Boyle Evan A. , Zhang Yuzheng , McIntosh Laura M. , Kolb Suzanne , Stott-Miller Marni , Smith Tiffany , Karyadi Danielle M. , Ostrander Elaine A. , Hsu Li , Shendure Jay , Stanford Janet L.
Published: April 2023

PDF - 53K, Flow diagram of results from family- and bioinformatics-based filtering of whole-exome sequencing data and confirmation steps.
Supplementary Table S1 from Pleiotropic Analysis of Cancer Risk Loci on Esophageal Adenocarcinoma Risk
Authors: Lee Eunjung , Stram Daniel O. , Ek Weronica E. , Onstad Lynn E. , MacGregor Stuart , Gharahkhani Puya , Ye Weimin , Lagergren Jesper , Shaheen Nicholas J. , Murray Liam J. , Hardie Laura J. , Gammon Marilie D. , Chow Wong-Ho , Risch Harvey A. , Corley Douglas A. , Levine David M. , Whiteman David C. , Bernstein Leslie , Bird Nigel C. , Vaughan Thomas L. , Wu Anna H.
Published: April 2023

Association between 387 SNPs and risk of EA, BE, or EA/BE combined
Supplementary Figure legends from A Newly Identified Susceptibility Locus near FOXP1 Modifies the Association of Gastroesophageal Reflux with Barrett's Esophagus
Authors: Dai James Y. , de Dieu Tapsoba Jean , Buas Matthew F. , Onstad Lynn E. , Levine David M. , Risch Harvey A. , Chow Wong-Ho , Bernstein Leslie , Ye Weimin , Lagergren Jesper , Bird Nigel C. , Corley Douglas A. , Shaheen Nicholas J. , Wu Anna H. , Reid Brian J. , Hardie Laura J. , Whiteman David C. , Vaughan Thomas L.
Published: April 2023

Figure legends
Editorial for This Article from Contribution of Screening and Survival Differences to Racial Disparities in Colorectal Cancer Rates
Authors: Lansdorp-Vogelaar Iris , Kuntz Karen M. , Knudsen Amy B. , van Ballegooijen Marjolein , Zauber Ann G. , Jemal Ahmedin
Published: April 2023

Editorial for This Article from Contribution of Screening and Survival Differences to Racial Disparities in Colorectal Cancer Rates
Supplementary Table 1 from A Pooled Analysis of Alcohol Consumption and Risk of Multiple Myeloma in the International Multiple Myeloma Consortium
Authors: Andreotti Gabriella , Birmann Brenda , De Roos Anneclaire J. , Spinelli John , Cozen Wendy , Camp Nicola J. , Moysich Kirsten , Chiu Brian , Steplowski Emily , Krzystan Joseph , Boffetta Paolo , Benhaim-Luzon Véronique , Brennan Paul , de Sanjosé Silvia , Costas Laura , Costantini Adele Seniori , Miligi Lucia , Cocco Pierluigi , Becker Nikolaus , Foretová Lenka , Maynadié Marc , Nieters Alexandra , Staines Anthony , Tricot Guido , Milliken Kevin , Weisenburger Dennis , Zheng Tongzhang , Baris Dalsu , Purdue Mark P.
Published: April 2023

PDF - 41KB, Characteristics of Study Population.
Supplemental Table S1 from Insurance-Based Differences in Time to Diagnostic Follow-up after Positive Screening Mammography
Authors: Durham Danielle D. , Robinson Whitney R. , Lee Sheila S. , Wheeler Stephanie B. , Reeder-Hayes Katherine E. , Bowling J. Michael , Olshan Andrew F. , Henderson Louise M.
Published: April 2023

Supplemental Table
Supplementary tables 1-3 from Circulating Beta-2 Microglobulin and Risk of Cancer: The Atherosclerosis Risk in Communities Study (ARIC)
Authors: Prizment Anna E. , Linabery Amy M. , Lutsey Pamela L. , Selvin Elizabeth , Nelson Heather H. , Folsom Aaron R. , Church Timothy R. , Drake Charles G. , Platz Elizabeth A. , Joshu Corinne
Published: April 2023

Supplementary table 1. Hazard ratios (95% CI) for the incidence of total cancer and cancer types by quartile of serum β-2-microglobulin (B2M), ARIC, 1990-2006. Supplementary table 2a. Hazard ratios (95% CI) a for colorectal cancer incidence in strata of select characteristics. ARIC, 1990-2006. Supplementary table 2b. Hazard ratiosa (95% CI) for lung cancer incidence in strata of selected participants' characteristics; ARIC, 1990-2006. Supplementary table 3. Hazard ratios (95% CIs)a for colorectal cancer by quartiles of combined scores based on B2M and CRP; ARIC, 1990-2006.
Table 2 from Prior Autoimmune Disease and Risk of Monoclonal Gammopathy of Undetermined Significance and Multiple Myeloma: A Systematic Review
Authors: McShane Charlene M. , Murray Liam J. , Landgren Ola , O'Rorke Michael A. , Korde Neha , Kunzmann Andrew T. , Ismail Mohammad Roshidi , Anderson Lesley A.
Published: April 2023

Table 2. Summary characteristics of studies included within meta-analysis of autoimmune disease and subsequent risk of MGUS
Characteristics of studies included in meta-analysis of prior autoimmune disease and subsequent risk of MGUS from Prior Autoimmune Disease and Risk of Monoclonal Gammopathy of Undetermined Significance and Multiple Myeloma: A Systematic Review
Authors: McShane Charlene M. , Murray Liam J. , Landgren Ola , O'Rorke Michael A. , Korde Neha , Kunzmann Andrew T. , Ismail Mohammad Roshidi , Anderson Lesley A.
Published: April 2023

Summary characteristics of studies included within meta-analysis of autoimmune disease and subsequent risk of MGUS
Supplementary Table 1 from RAZOR: A Phase II Open Randomized Trial of Screening Plus Goserelin and Raloxifene Versus Screening Alone in Premenopausal Women at Increased Risk of Breast Cancer
Authors: Howell Anthony , Ashcroft Linda , Fallowfield Lesley , Eccles Diana M. , Eeles Rosalind A. , Ward Ann , Brentnall Adam R. , Dowsett Mitchell , Cuzick Jack M. , Greenhalgh Rosemary , Boggis Caroline , Motion Jamie , Sergeant Jamie C. , Adams Judith , Evans D. Gareth
Published: April 2023

Supplementary Table 1. DXA scan measurements (Baseline, 1-yr and 2-yr.)
Supplementary Figure 1, Tables 1-2 from Fine-Mapping CASP8 Risk Variants in Breast Cancer
Authors: Camp Nicola J. , Parry Marina , Knight Stacey , Abo Ryan , Elliott Graeme , Rigas Sushilaben H. , Balasubramanian Sabapathy P. , Reed Malcolm W. R. , McBurney Helen , Latif Ayse , Newman William G. , Cannon-Albright Lisa A. , Evans D. Gareth , Cox Angela
Published: April 2023

PDF file - 410K
Table S2. Sixty-three types of HPV used for Agilent baits from Targeted, Deep Sequencing Reveals Full Methylation Profiles of Multiple HPV Types and Potential Biomarkers for Cervical Cancer Progression
Authors: Liu Pengyuan , Iden Marissa , Fye Samantha , Huang Yi-Wen , Hopp Elizabeth , Chu Chen , Lu Yan , Rader Janet S.
Published: April 2023

List of base pair coverage and sequence references used by Agilent for designing custom HPV baits.
Supplementary Methods, Tables 1 - 6, Figures 1 - 3, PRISMA Checklist from Diagnostic and Prognostic Value of microRNA-21 in Colorectal Cancer: An Original Study and Individual Participant Data Meta-analysis
Authors: Zhang Honghe , Li Peiwei , Ju Haixing , Pesta Martin , Kulda Vlastimil , Jin Wenjun , Cai Mao , Liu Changbao , Wu Han , Xu Jinming , Ye Yao , Zhang Guanglin , Xu Enping , Cai Jianting , Lai Maode , Xia Dajing , Yang Jun , Wu Yihua
Published: April 2023

Supplementary Table 1 Instrument used for the evaluation of the risk of bias and applicability concerns of the included prognostic studies (adapted from QUADAS-2). Supplementary Table 2 Characteristics of studies included in the diagnostic meta-analysis. Supplementary Table 3 Characteristics of studies included in the prognostic meta-analysis. Supplementary Table 4 Quality assessment of the included diagnostic studies according to QUADAS-2. Supplementary Table 5 Risk of bias and applicability concerns of included prognostic studies. Supplementary Table 6 Methodological quality of included prognostic studies according to STROBE criteria. Supplementary Figure 1 Receiver operating characteristic curves of plasma miR-21 for discrimination CRC patients from controls. Supplementary Figure 2 Kaplanâ€“Meier curve of tissue miR-21 expression in relation to the survival of CRC patients in the original study. Supplementary Figure 3 Funnel plots of the meta-analyses (A) Funnel plot of tissue miR-21 and CRC OS (B) Funnel plot of tissue miR-21 and CRC DFS (3) Funnel plot of circulating miR-21 and CRC diagnosis. PRISMA Checklist.
Supplementary Figure S6. Sensitivity and specificity of methylation as a quantitative classifier of cervical precancer and cancer samples from Targeted, Deep Sequencing Reveals Full Methylation Profiles of Multiple HPV Types and Potential Biomarkers for Cervical Cancer Progression
Authors: Liu Pengyuan , Iden Marissa , Fye Samantha , Huang Yi-Wen , Hopp Elizabeth , Chu Chen , Lu Yan , Rader Janet S.
Published: April 2023

AUC values of different HPV genes for distinguishing (A) ICC from CIN or (B) SCC from CIN3. AUC values of across all CpGs for distinguishing HPV 16-positive (C) ICC from CIN or (D) SCC from CIN3. G, Global.
Supplementary Methods, Figure Legends, Tables 1 - 6 from Biomarker Discovery for Heterogeneous Diseases
Authors: Wallstrom Garrick , Anderson Karen S. , LaBaer Joshua
Published: April 2023

PDF file - 145K, Table S1: Normal Samples Homogeneous Disease Summary Statistics Table S2: Normal Samples Heterogeneous Disease Summary Statistics Table S3: T3 Homogeneous Disease Summary Statistics Table S4: T3 Heterogeneous Disease Summary Statistics Table S5: Summary Statistics for Significant Hits in Breast Cancer Screening Study Table S6: Highly Significant Hits in Breast Cancer Screening Study
Supplementary Figure S3. Distribution of HPV types among CIN and ICC samples from Targeted, Deep Sequencing Reveals Full Methylation Profiles of Multiple HPV Types and Potential Biomarkers for Cervical Cancer Progression
Authors: Liu Pengyuan , Iden Marissa , Fye Samantha , Huang Yi-Wen , Hopp Elizabeth , Chu Chen , Lu Yan , Rader Janet S.
Published: April 2023

HPV types in CIN and ICC samples were determined by their read counts. For a sample to be considered positive for a specific HPV type, the proportion of mapped reads for that type had to be {greater than or equal to}15% of the total HPV read count. Two samples were the exception, as they were called positive for an HPV type with only 10% of the total HPV reads (due to identification of an integration event in that HPV type).
Supplementary Figure 5 from Biomarker Discovery for Heterogeneous Diseases
Authors: Wallstrom Garrick , Anderson Karen S. , LaBaer Joshua
Published: April 2023

PDF file - 5101K, Figure S5. Estimated power with FDR controlled at 50% for a two-stage design using 100 total patients and 100 total controls with normal samples for a (a) homogeneous disease and a (b) heterogeneous disease.
Supplementary Figure S1. HPV capture methodology from Targeted, Deep Sequencing Reveals Full Methylation Profiles of Multiple HPV Types and Potential Biomarkers for Cervical Cancer Progression
Authors: Liu Pengyuan , Iden Marissa , Fye Samantha , Huang Yi-Wen , Hopp Elizabeth , Chu Chen , Lu Yan , Rader Janet S.
Published: April 2023

(1) Genomic DNA (gDNA) was sheared into ~300 bp fragments that were end-repaired, adenylated, and ligated to Illumina TruSeq adapters. (2) The prepared library was hybridized with Agilent's Custom HPV Capture Library and IDT's xGen Lockdown Probes. (3) Streptavidin-coated beads were used to target and separate the 5'-biotinylated end of the bound hybrids. Unbound gDNA was washed away, and captured hybrids were eluted. (4) For methylation analysis, samples were treated with BS, which converts unmethylated cytosines to uracil. (5) Captured hybrids were PCR-amplified with primers specific to the Illumnia TruSeq Adapters. Finally, libraries were indexed to provide each with a unique 6 base pair code. Pooled libraries were sequenced using the Illumina HiSeq 2000 workflow.
Supplementary Data from Urinary Metabolite Risk Biomarkers of Lung Cancer: A Prospective Cohort Study
Authors: Haznadar Majda , Cai Qiuyin , Krausz Kristopher W. , Bowman Elise D. , Margono Ezra , Noro Rintaro , Thompson Matthew D. , Mathé Ewy A. , Munro Heather M. , Steinwandel Mark D. , Gonzalez Frank J. , Blot William J. , Harris Curtis C.
Published: April 2023

Ultra Performance Liquid Chromatography-Mass Spectrometry (UPLC-MS).
Supplementary Methods, Table 1 from Prognostic Value of Angiopoietin-2 for Death Risk Stratification in Patients with Metastatic Colorectal Carcinoma
Authors: Jary Marine , Vernerey Dewi , Lecomte Thierry , Dobi Erion , Ghiringhelli François , Monnien Franck , Godet Yann , Kim Stefano , Bouché Olivier , Fratte Serge , Gonçalves Anthony , Leger Julie , Queiroz Lise , Adotevi Olivier , Bonnetain Franck , Borg Christophe
Published: April 2023

Supplementary Methods, Table 1. Supplementary methods: - Ang-2 plasma sample measurement - Statistical analysis interpretation Supplementary table 1: - Cox Univariate analyses for OS prediction with and without the stratified approach (sensitivity analysis) Supplementary references
Supplemental Table 3 from Opportunities and Challenges for the Use of Large-Scale Surveys in Public Health Research: A Comparison of the Assessment of Cancer Screening Behaviors
Authors: Hamilton Jada G. , Breen Nancy , Klabunde Carrie N. , Moser Richard P. , Leyva Bryan , Breslau Erica S. , Kobrin Sarah C.
Published: April 2023

Supplemental Table 3. New cancer screening constructs from the National Health Interview Survey (NHIS), Health Information National Trends Survey (HINTS), Behavioral Risk Factor Surveillance Survey (BRFSS), and California Health Information Survey (CHIS)
Supplemental Table 1 from Family History of Breast Cancer, Breast Density, and Breast Cancer Risk in a U.S. Breast Cancer Screening Population
Authors: Ahern Thomas P. , Sprague Brian L. , Bissell Michael C.S. , Miglioretti Diana L. , Buist Diana S.M. , Braithwaite Dejana , Kerlikowske Karla
Published: April 2023

Supplemental Table 1. Characteristics of the study population (one random observation per woman, n=222,019) according to closest family history. Frequency and row percent.
Supplementary Table 1 from Alcohol Consumption in Relation to Plasma Sex Hormones, Prolactin, and Sex Hormone–Binding Globulin in Premenopausal Women
Authors: Hirko Kelly A. , Spiegelman Donna , Willett Walter C. , Hankinson Susan E. , Eliassen A. Heather
Published: April 2023

Spearman rank correlation coefficients for sex hormone concentrations among 2,000 premenopausal women in the Nursesâ€™ Health Study II.
Supplementary Table S4 from Expanding Epigenomics to Archived FFPE Tissues: An Evaluation of DNA Repair Methodologies
Authors: Siegel Erin M. , Berglund Anders E. , Riggs Bridget M. , Eschrich Steven A. , Putney Ryan M. , Ajidahun Abidemi O. , Coppola Domenico , Shibata David
Published: April 2023

Supplementary Table S4. Summary of Î²-value correlation (R2) and discordance (|Î”Î²|) between FF-FFPE pairs for Repli-g Ligation and the Restore methods by normalization: (A) DASEN, (B) minfi-Illumina, (C) SWAN and (D) raw Î²-values.
Supplementary Table S2 from Expanding Epigenomics to Archived FFPE Tissues: An Evaluation of DNA Repair Methodologies
Authors: Siegel Erin M. , Berglund Anders E. , Riggs Bridget M. , Eschrich Steven A. , Putney Ryan M. , Ajidahun Abidemi O. , Coppola Domenico , Shibata David
Published: April 2023

Supplementary Table S2. The number and overlap of discordant loci (|Î”Î²|>0.3) across internal replicates of the Restore and REPLI-g Ligase methods for each patient sample.
Supplementary Figure S3 from Expanding Epigenomics to Archived FFPE Tissues: An Evaluation of DNA Repair Methodologies
Authors: Siegel Erin M. , Berglund Anders E. , Riggs Bridget M. , Eschrich Steven A. , Putney Ryan M. , Ajidahun Abidemi O. , Coppola Domenico , Shibata David
Published: April 2023

Supplementary Figure S3: The distribution of Î²-values across all CpG loci measured on the Illumina 450K array for (a) the FFPE colon tumors and (b) the 121 FFPE samples from RTOG compared to FF tissues. All samples, regardless of storage type, had Î²-value peaks at 0.2 and 0.8 and variability between Î²-values of 0.3 and 0.6.
Supplementary Figure 6 from Fine-Mapping of IL16 Gene and Prostate Cancer Risk in African Americans
Authors: Batai Ken , Shah Ebony , Murphy Adam B. , Newsome Jennifer , Ruden Maria , Ahaghotu Chiledum , Kittles Rick A.
Published: April 2023

PDF file, 122K, -log10 P-value plot of association tests after imputation masking 24 genotyped SNPs. In this analysis, rs7175701 was masked and imputed yet remained the most significant SNP.
Supplementary Figure 5 from Fine-Mapping of IL16 Gene and Prostate Cancer Risk in African Americans
Authors: Batai Ken , Shah Ebony , Murphy Adam B. , Newsome Jennifer , Ruden Maria , Ahaghotu Chiledum , Kittles Rick A.
Published: April 2023

PDF file, 93K, Distribution of percent global West African Ancestry estimates in the discovery and replication cases (mean global WAA in discovery cases = 81.2%, mean global WAA in replication cases = 79.1 %; T-test P=0.342).
Supplementary Figure 4 from Fine-Mapping of IL16 Gene and Prostate Cancer Risk in African Americans
Authors: Batai Ken , Shah Ebony , Murphy Adam B. , Newsome Jennifer , Ruden Maria , Ahaghotu Chiledum , Kittles Rick A.
Published: April 2023

PDF file, 125K, -log10 P-value plot of association tests using genotyped and imputed SNPs from MACH and HapMap data analysis showing that the same three SNPs have the strongest association.