bluuebunny/crossref_metadata_2025 huggingface dataset:
Supplementary Table 1 from p53 Negatively Regulates the Hepatoma Growth Factor HDGF
Authors: Sasaki Yasushi , Negishi Hideaki , Idogawa Masashi , Yokota Ikuko , Koyama Ryota , Kusano Masanobu , Suzuki Hiromu , Fujita Masahiro , Maruyama Reo , Toyota Minoru , Saito Tsuyoshi , Tokino Takashi
Published: April 2023

PDF file - 46K
Supplementary Methods from p53 Negatively Regulates the Hepatoma Growth Factor HDGF
Authors: Sasaki Yasushi , Negishi Hideaki , Idogawa Masashi , Yokota Ikuko , Koyama Ryota , Kusano Masanobu , Suzuki Hiromu , Fujita Masahiro , Maruyama Reo , Toyota Minoru , Saito Tsuyoshi , Tokino Takashi
Published: April 2023

PDF file - 103K
Supplementary Figure 1 from Lactate Influx through the Endothelial Cell Monocarboxylate Transporter MCT1 Supports an NF-κB/IL-8 Pathway that Drives Tumor Angiogenesis
Authors: Végran Frédérique , Boidot Romain , Michiels Carine , Sonveaux Pierre , Feron Olivier
Published: April 2023

Supplementary Figure 1 from Lactate Influx through the Endothelial Cell Monocarboxylate Transporter MCT1 Supports an NF-κB/IL-8 Pathway that Drives Tumor Angiogenesis
Supplementary Table 1 from MTGR1 Is Required for Tumorigenesis in the Murine AOM/DSS Colitis-Associated Carcinoma Model
Authors: Barrett Caitlyn W. , Fingleton Barbara , Williams Amanda , Ning Wei , Fischer Melissa A. , Washington Mary K. , Chaturvedi Rupesh , Wilson Keith T. , Hiebert Scott W. , Williams Christopher S.
Published: April 2023

Supplementary Table 1 from MTGR1 Is Required for Tumorigenesis in the Murine AOM/DSS Colitis-Associated Carcinoma Model
Supplementary Figure 4 from ZNF668 Functions as a Tumor Suppressor by Regulating p53 Stability and Function in Breast Cancer
Authors: Hu Ruozhen , Peng Guang , Dai Hui , Breuer Eun-Kyoung , Stemke-Hale Katherine , Li Kaiyi , Gonzalez-Angulo Ana M. , Mills Gordon B. , Lin Shiaw-Yih
Published: April 2023

PDF file - 1261KB
Supplementary References from Considerations for the Clinical Application of Chimeric Antigen Receptor T Cells: Observations from a Recombinant DNA Advisory Committee Symposium Held June 15, 2010
Authors: Ertl Hildegund C.J. , Zaia John , Rosenberg Steven A. , June Carl H. , Dotti Gianpietro , Kahn Jeffrey , Cooper Laurence J.N. , Corrigan-Curay Jacqueline , Strome Scott E.
Published: April 2023

Supplementary References from Considerations for the Clinical Application of Chimeric Antigen Receptor T Cells: Observations from a Recombinant DNA Advisory Committee Symposium Held June 15, 2010
Supplementary Legends for Figures 1-6 and Table 1 from Cell-Permeable NM23 Blocks the Maintenance and Progression of Established Pulmonary Metastasis
Authors: Lim Junghee , Jang Giyong , Kang Seeun , Lee Guewha , Nga Do Thi Thuy , Phuong Do Thi Lan , Kim Hyuncheol , El-Rifai Wael , Ruley H. Earl , Jo Daewoong
Published: April 2023

PDF file - 93K
Supplementary Table 2 from Cancer-Induced Immunosuppression: IL-18–Elicited Immunoablative NK Cells
Authors: Terme Magali , Ullrich Evelyn , Aymeric Laetitia , Meinhardt Kathrin , Coudert Jérôme D. , Desbois Mélanie , Ghiringhelli François , Viaud Sophie , Ryffel Bernard , Yagita Hideo , Chen Lieping , Mécheri Salaheddine , Kaplanski Gilles , Prévost-Blondel Armelle , Kato Masashi , Schultze Joachim L. , Tartour Eric , Kroemer Guido , Degli-Esposti Mariapia , Chaput Nathalie , Zitvogel Laurence
Published: April 2023

PDF file - 307K, Differentially expressed genes between Kit+ and Kit- samples, coding for annotated genes, FC >2, p-value <0.05, difference of mean > 100
Supplementary Figure 2 from Cancer-Induced Immunosuppression: IL-18–Elicited Immunoablative NK Cells
Authors: Terme Magali , Ullrich Evelyn , Aymeric Laetitia , Meinhardt Kathrin , Coudert Jérôme D. , Desbois Mélanie , Ghiringhelli François , Viaud Sophie , Ryffel Bernard , Yagita Hideo , Chen Lieping , Mécheri Salaheddine , Kaplanski Gilles , Prévost-Blondel Armelle , Kato Masashi , Schultze Joachim L. , Tartour Eric , Kroemer Guido , Degli-Esposti Mariapia , Chaput Nathalie , Zitvogel Laurence
Published: April 2023

PDF file - 105K, IL-18 does not promote the proliferation of Kit+ NK cells in vivo
Supplementary Methods, Figures 1-6, Table 1 from Overcoming Temozolomide Resistance in Glioblastoma via Dual Inhibition of NAD+ Biosynthesis and Base Excision Repair
Authors: Goellner Eva M. , Grimme Bradford , Brown Ashley R. , Lin Ying-Chih , Wang Xiao-Hong , Sugrue Kelsey F. , Mitchell Leah , Trivedi Ram N. , Tang Jiang-bo , Sobol Robert W.
Published: April 2023

Supplementary Methods, Figures 1-6, Table 1 from Overcoming Temozolomide Resistance in Glioblastoma via Dual Inhibition of NAD+ Biosynthesis and Base Excision Repair
Supplementary Figure 3 from A Role for Bone Morphogenetic Protein-4 in Lymph Node Vascular Remodeling and Primary Tumor Growth
Authors: Farnsworth Rae H. , Karnezis Tara , Shayan Ramin , Matsumoto Masataka , Nowell Cameron J. , Achen Marc G. , Stacker Steven A.
Published: April 2023

PDF file - 86K
Supplementary Tables 1-7 from Pivotal Role of Reduced let-7g Expression in Breast Cancer Invasion and Metastasis
Authors: Qian Pengxu , Zuo Zehua , Wu Zhengsheng , Meng Xianyi , Li Gaopeng , Wu Zhengzhou , Zhang Weijie , Tan Sheng , Pandey Vijay , Yao Yandan , Wang Puyue , Zhao Liqing , Wang Jun , Wu Qiang , Song Erwei , Lobie Peter E. , Yin Zhinan , Zhu Tao
Published: April 2023

PDF file - 249K
Supplementary Table 3 from Sonic Hedgehog Pathway Promotes Metastasis and Lymphangiogenesis via Activation of Akt, EMT, and MMP-9 Pathway in Gastric Cancer
Authors: Yoo Young A. , Kang Myoung Hee , Lee Hyun Joo , Kim Baek-hui , Park Jong Kuk , Kim Hyun Koo , Kim Jun Suk , Oh Sang Cheul
Published: April 2023

PDF file - 17K
Supplementary Table 2 from Sonic Hedgehog Pathway Promotes Metastasis and Lymphangiogenesis via Activation of Akt, EMT, and MMP-9 Pathway in Gastric Cancer
Authors: Yoo Young A. , Kang Myoung Hee , Lee Hyun Joo , Kim Baek-hui , Park Jong Kuk , Kim Hyun Koo , Kim Jun Suk , Oh Sang Cheul
Published: April 2023

PDF file - 15K
Supplementary Movie 2 from Spatial Regulation of RhoA Activity during Pancreatic Cancer Cell Invasion Driven by Mutant p53
Authors: Timpson Paul , McGhee Ewan J. , Morton Jennifer P. , von Kriegsheim Alex , Schwarz Juliane P. , Karim Saadia A. , Doyle Brendan , Quinn Jean A. , Carragher Neil O. , Edward Mike , Olson Michael F. , Frame Margaret C. , Brunton Valerie G. , Sansom Owen J. , Anderson Kurt I.
Published: April 2023

Supplementary Movie 2 from Spatial Regulation of RhoA Activity during Pancreatic Cancer Cell Invasion Driven by Mutant p53
Supplemental Methods from Evolutionary Action Score of TP53 Identifies High-Risk Mutations Associated with Decreased Survival and Increased Distant Metastases in Head and Neck Cancer
Authors: Neskey David M. , Osman Abdullah A. , Ow Thomas J. , Katsonis Panagiotis , McDonald Thomas , Hicks Stephanie C. , Hsu Teng-Kuei , Pickering Curtis R. , Ward Alexandra , Patel Ameeta , Yordy John S. , Skinner Heath D. , Giri Uma , Sano Daisuke , Story Michael D. , Beadle Beth M. , El-Naggar Adel K. , Kies Merrill S. , William William N. , Caulin Carlos , Frederick Mitchell , Kimmel Marek , Myers Jeffrey N. , Lichtarge Olivier
Published: April 2023

Supplemental Methods. Description of additional methods and procedures used in the study.
Supplemental Figure Legends from Carbonic Anhydrase IX Promotes Myeloid-Derived Suppressor Cell Mobilization and Establishment of a Metastatic Niche by Stimulating G-CSF Production
Authors: Chafe Shawn C. , Lou Yuanmei , Sceneay Jaclyn , Vallejo Marylou , Hamilton Melisa J. , McDonald Paul C. , Bennewith Kevin L. , Möller Andreas , Dedhar Shoukat
Published: April 2023

Figure legends for supplemental figures 1-3
Supplemental Figure Legends from Evolutionary Action Score of TP53 Identifies High-Risk Mutations Associated with Decreased Survival and Increased Distant Metastases in Head and Neck Cancer
Authors: Neskey David M. , Osman Abdullah A. , Ow Thomas J. , Katsonis Panagiotis , McDonald Thomas , Hicks Stephanie C. , Hsu Teng-Kuei , Pickering Curtis R. , Ward Alexandra , Patel Ameeta , Yordy John S. , Skinner Heath D. , Giri Uma , Sano Daisuke , Story Michael D. , Beadle Beth M. , El-Naggar Adel K. , Kies Merrill S. , William William N. , Caulin Carlos , Frederick Mitchell , Kimmel Marek , Myers Jeffrey N. , Lichtarge Olivier
Published: April 2023

Legends for Supplemental Figures S1-S4.
Supplemental Figure 1 from Jak1–STAT3 Signals Are Essential Effectors of the USP6/TRE17 Oncogene in Tumorigenesis
Authors: Quick Laura , Young Robert , Henrich Ian C. , Wang Xiaoke , Asmann Yan W. , Oliveira Andre M. , Chou Margaret M.
Published: April 2023

P-STAT3 IHC
Figure S6 from S-nitrosylation of the Mitochondrial Chaperone TRAP1 Sensitizes Hepatocellular Carcinoma Cells to Inhibitors of Succinate Dehydrogenase
Authors: Rizza Salvatore , Montagna Costanza , Cardaci Simone , Maiani Emiliano , Di Giacomo Giuseppina , Sanchez-Quiles Virginia , Blagoev Blagoy , Rasola Andrea , De Zio Daniela , Stamler Jonathan S. , Cecconi Francesco , Filomeni Giuseppe
Published: April 2023

Meta-analysis of the association between GSNOR expression and HCC.
Supplemental figure legends from p120 Catenin Suppresses Basal Epithelial Cell Extrusion in Invasive Pancreatic Neoplasia
Authors: Hendley Audrey M. , Wang Yue J. , Polireddy Kishore , Alsina Janivette , Ahmed Ishrat , Lafaro Kelly J. , Zhang Hao , Roy Nilotpal , Savidge Samuel G. , Cao Yanna , Hebrok Matthias , Maitra Anirban , Reynolds Albert B. , Goggins Michael , Younes Mamoun , Iacobuzio-Donahue Christine A. , Leach Steven D. , Bailey Jennifer M.
Published: April 2023

This document provides detailed captions for figures S1-S8.
Supplementary Figure S12 from Mutational Landscape and Antiproliferative Functions of ELF Transcription Factors in Human Cancer
Authors: Ando Mizuo , Kawazu Masahito , Ueno Toshihide , Koinuma Daizo , Ando Koji , Koya Junji , Kataoka Keisuke , Yasuda Takahiko , Yamaguchi Hiroyuki , Fukumura Kazutaka , Yamato Azusa , Soda Manabu , Sai Eirin , Yamashita Yoshihiro , Asakage Takahiro , Miyazaki Yasushi , Kurokawa Mineo , Miyazono Kohei , Nimer Stephen D. , Yamasoba Tatsuya , Mano Hiroyuki
Published: April 2023

ChIP-seq analysis on DLX3 and HRK loci
Data from Macrophage Infiltration and Alternative Activation during Wound Healing Promote MEK1-Induced Skin Carcinogenesis
Authors: Weber Christine , Telerman Stephanie B. , Reimer Andreas S. , Sequeira Ines , Liakath-Ali Kifayathullah , Arwert Esther N. , Watt Fiona M.
Published: April 2023

Abstract
Macrophages are essential for the progression and maintenance of many cancers, but their role during the earliest stages of tumor formation is unclear. To test this, we used a previously described transgenic mouse model of wound-induced skin tumorigenesis, in which expression of constitutively active MEK1 in differentiating epidermal cells results in chronic inflammation (InvEE mice). Upon wounding, the number of epidermal and dermal monocytes and macrophages increased in wild-type and InvEE skin, but the increase was greater, more rapid, and more sustained in InvEE skin. Macrophage ablation reduced tumor incidence. Furthermore, bioluminescent imaging in live mice to monitor macrophage flux at wound sites revealed that macrophage accumulation was predictive of tumor formation; wounds with the greatest number of macrophages at day 5 went on to develop tumors. Gene expression profiling of flow-sorted monocytes, macrophages, and T cells from InvEE and wild-type skin showed that as wound healing progressed, InvEE macrophages altered their phenotype. Throughout wound healing and after wound closure, InvEE macrophages demonstrated sustained upregulation of several markers implicated in alternative macrophage activation including arginase-1 (ARG1) and mannose receptor (CD206). Notably, inhibition of ARG1 activity significantly reduced tumor formation and epidermal proliferation in vivo, whereas addition of L-arginase to cultured keratinocytes stimulated proliferation. We conclude that macrophages play a key role in early, inflammation-mediated skin tumorigenesis, with mechanistic evidence suggesting that ARG1 secretion drives tumor development by stimulating epidermal cell proliferation. These findings highlight the importance of cancer immunotherapies aiming to polarize tumor-associated macrophages toward an antitumor phenotype. Cancer Res; 76(4); 805–17. ©2016 AACR.
Data from Neuropilin-2 Regulates Endosome Maturation and EGFR Trafficking to Support Cancer Cell Pathobiology
Authors: Dutta Samikshan , Roy Sohini , Polavaram Navatha S. , Stanton Marissa J. , Zhang Heyu , Bhola Tanvi , Hönscheid Pia , Donohue Terrence M. , Band Hamid , Batra Surinder K. , Muders Michael H. , Datta Kaustubh
Published: April 2023

Abstract
Neuropilin-2 (NRP2) is a non-tyrosine kinase receptor frequently overexpressed in various malignancies, where it has been implicated in promoting many protumorigenic behaviors, such as imparting therapeutic resistance to metastatic cancer cells. Here, we report a novel function of NRP2 as a regulator of endocytosis, which is enhanced in cancer cells and is often associated with increased metastatic potential and drug resistance. We found that NRP2 depletion in human prostate and pancreatic cancer cells resulted in the accumulation of EEA1/Rab5-positive early endosomes concomitant with a decrease in Rab7-positive late endosomes, suggesting a delay in early-to-late endosome maturation. NRP2 depletion also impaired the endocytic transport of cell surface EGFR, arresting functionally active EGFR in endocytic vesicles that consequently led to aberrant ERK activation and cell death. Mechanistic investigations revealed that WD-repeat– and FYVE-domain–containing protein 1 (WDFY1) functioned downstream of NRP2 to promote endosome maturation, thereby influencing the endosomal trafficking of EGFR and the formation of autolysosomes responsible for the degradation of internalized cargo. Overall, our results indicate that the NRP2/WDFY1 axis is required for maintaining endocytic activity in cancer cells, which supports their oncogenic activities and confers drug resistance. Therefore, therapeutically targeting endocytosis may represent an attractive strategy to selectively target cancer cells in multiple malignancies. Cancer Res; 76(2); 418–28. ©2015 AACR.
Data from RASSF1A Suppresses the Invasion and Metastatic Potential of Human Non–Small Cell Lung Cancer Cells by Inhibiting YAP Activation through the GEF-H1/RhoB Pathway
Authors: Dubois Fatéméh , Keller Maureen , Calvayrac Olivier , Soncin Fabrice , Hoa Lily , Hergovich Alexander , Parrini Maria-Carla , Mazières Julien , Vaisse-Lesteven Mélissa , Camonis Jacques , Levallet Guénaëlle , Zalcman Gérard
Published: April 2023

Abstract
Inactivation of the tumor suppressor gene RASSF1A by promoter hypermethylation represents a key event underlying the initiation and progression of lung cancer. RASSF1A inactivation is also associated with poor prognosis and may promote metastatic spread. In this study, we investigated how RASSF1A inactivation conferred invasive phenotypes to human bronchial cells. RNAi-mediated silencing of RASSF1A induced epithelial-to-mesenchymal transition (EMT), fomenting a motile and invasive cellular phenotype in vitro and increased metastatic prowess in vivo. Mechanistic investigations revealed that RASSF1A blocked tumor growth by stimulating cofilin/PP2A–mediated dephosphorylation of the guanine nucleotide exchange factor GEF-H1, thereby stimulating its ability to activate the antimetastatic small GTPase RhoB. Furthermore, RASSF1A reduced nuclear accumulation of the Hippo pathway transcriptional cofactor Yes-associated protein (YAP), which was reinforced by RhoB activation. Collectively, our results indicated that RASSF1 acts to restrict EMT and invasion by indirectly controlling YAP nuclear shuttling and activation through a RhoB-regulated cytoskeletal remodeling process, with potential implications to delay the progression of RASSF1-hypermethylated lung tumors. Cancer Res; 76(6); 1627–40. ©2016 AACR.
Data from Quantitative Phosphotyrosine Profiling of Patient-Derived Xenografts Identifies Therapeutic Targets in Pediatric Leukemia
Authors: Dolai Sibasish , Sia Keith C.S. , Robbins Alissa K. , Zhong Ling , Heatley Sue L. , Vincent Tiffaney L. , Hochgräfe Falko , Sutton Rosemary , Kurmasheva Raushan T. , Revesz Tamas , White Deborah L. , Houghton Peter J. , Smith Malcolm A. , Teachey David T. , Daly Roger J. , Raftery Mark J. , Lock Richard B.
Published: April 2023

Abstract
Activating mutations in tyrosine kinases (TK) drive pediatric high-risk acute lymphoblastic leukemia (ALL) and confer resistance to standard chemotherapy. Therefore, there is urgent need to characterize dysregulated TK signaling axes in patients with ALL and identify actionable kinase targets for the development of therapeutic strategies. Here, we present the first study to quantitatively profile TK activity in xenografted patient biopsies of high-risk pediatric ALL. We integrated a quantitative phosphotyrosine profiling method with “spike-in” stable isotope labeling with amino acids in cell culture (SILAC) and quantified 1394 class I phosphorylation sites in 16 ALL xenografts. Moreover, hierarchical clustering of phosphotyrosine sites could accurately classify these leukemias into either B- or T-cell lineages with the high-risk early T-cell precursor (ETP) and Ph-like ALL clustering as a distinct group. Furthermore, we validated this approach by using specific kinase pathway inhibitors to perturb ABL1, FLT3, and JAK TK signaling in four xenografted patient samples. By quantitatively assessing the tyrosine phosphorylation status of activated kinases in xenograft models of ALL, we were able to identify and validate clinically relevant targets. Therefore, this study highlights the application and potential of phosphotyrosine profiling for identifying clinically relevant kinase targets in leukemia. Cancer Res; 76(9); 2766–77. ©2016 AACR.
Supplemental Table 2 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 2. Age-Adjusted Prevalence of Physical Activity (%), Adults 18 Years and Older, US, National Health Interview Survey, 2013.
Supplementary Figure 1 from The TMPRSS2:ERG Rearrangement, ERG Expression, and Prostate Cancer Outcomes: A Cohort Study and Meta-analysis
Authors: Pettersson Andreas , Graff Rebecca E. , Bauer Scott R. , Pitt Michael J. , Lis Rosina T. , Stack Edward C. , Martin Neil E. , Kunz Lauren , Penney Kathryn L. , Ligon Azra H. , Suppan Catherine , Flavin Richard , Sesso Howard D. , Rider Jennifer R. , Sweeney Christopher , Stampfer Meir J. , Fiorentino Michelangelo , Kantoff Philip W. , Sanda Martin G. , Giovannucci Edward L. , Ding Eric L. , Loda Massimo , Mucci Lorelei A.
Published: April 2023

PDF file, 130K, Selection process for the study inclusion in the meta-analysis.
Supplementary Table 1 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 - 59K, A list of the identified metabolites with the lowest values of between-subject variability, (e.g. the highest within-subject variability), among all metabolites with an ICC > 0.8. Rows include metabolite name, , the equivalent value from the age and gender adjusted (A.G.A) model, the equivalent from a female-only model, p-value for the metabolite's association with age, and p-value for the metabolite's association with gender.
Figure S3 from Cellular Expression of PD-L1 in the Peripheral Blood of Lung Cancer Patients is Associated with Worse Survival
Authors: Boffa Daniel J. , Graf Ryon P. , Salazar Michelle C. , Hoag Jessica , Lu David , Krupa Rachel , Louw Jessica , Dugan Lyndsey , Wang Yipeng , Landers Mark , Suraneni Mahipal , Greene Stephanie B. , Magaña Marisa , Makani Samir , Bazhenova Lyudmila , Dittamore Ryan V. , Nieva Jorge
Published: April 2023

'CK(-)PD-L1(+) Circulating Cells Associated with Malignancy (CCAM) at Diagnosis is a Prognostic Factor for Overall Survival in Lung Cancer Patients.'
Supplementary Figure Legend from Adult Stature and Risk of Cancer at Different Anatomic Sites in a Cohort of Postmenopausal Women
Authors: Kabat Geoffrey C. , Anderson Matthew L. , Heo Moonseong , Hosgood H. Dean , Kamensky Victor , Bea Jennifer W. , Hou Lifang , Lane Dorothy S. , Wactawski-Wende Jean , Manson JoAnn E. , Rohan Thomas E.
Published: April 2023

PDF - 22KB, Legends for supplementary figures 1-5.
Supplementary Figure 19 from Sex Disparities in Cancer Mortality and Survival
Authors: Cook Michael B. , McGlynn Katherine A. , Devesa Susan S. , Freedman Neal D. , Anderson William F.
Published: April 2023

PDF file - 96K
Data from Mental and Physical Health–Related Quality of Life among U.S. Cancer Survivors: Population Estimates from the 2010 National Health Interview Survey
Authors: Weaver Kathryn E. , Forsythe Laura P. , Reeve Bryce B. , Alfano Catherine M. , Rodriguez Juan L. , Sabatino Susan A. , Hawkins Nikki A. , Rowland Julia H.
Published: April 2023

Abstract
Background: Despite extensive data on health-related quality of life (HRQOL) among cancer survivors, we do not yet have an estimate of the percentage of survivors with poor mental and physical HRQOL compared with population norms. HRQOL population means for adult-onset cancer survivors of all ages and across the survivorship trajectory also have not been published.

Methods: Survivors (N = 1,822) and adults with no cancer history (N = 24,804) were identified from the 2010 National Health Interview Survey. The PROMIS® Global Health Scale was used to assess HRQOL. Poor HRQOL was defined as 1 SD or more below the PROMIS® population norm.

Results: Poor physical and mental HRQOL were reported by 24.5% and 10.1% of survivors, respectively, compared with 10.2% and 5.9% of adults without cancer (both P < 0.0001). This represents a population of approximately 3.3 million and 1.4 million U.S. survivors with poor physical and mental HRQOL. Adjusted mean mental and physical HRQOL scores were similar for breast, prostate, and melanoma survivors compared with adults without cancer. Survivors of cervical, colorectal, hematologic, short-survival, and other cancers had worse physical HRQOL; cervical and short-survival cancer survivors reported worse mental HRQOL.

Conclusion: These data elucidate the burden of cancer diagnosis and treatment among U.S. survivors and can be used to monitor the impact of national efforts to improve survivorship care and outcomes.

Impact: We present novel data on the number of U.S. survivors with poor HRQOL. Interventions for high-risk groups that can be easily implemented are needed to improve survivor health at a population level. Cancer Epidemiol Biomarkers Prev; 21(11); 2108–17. ©2012 AACR.
Data from Work Loss Duration and Predictors Following Rectal Cancer Treatment among Patients with and without Prediagnostic Work Loss
Authors: Chen Lingjing , Glimelius Ingrid , Neovius Martin , Ekberg Sara , Martling Anna , Eloranta Sandra , Smedby Karin E.
Published: April 2023

Abstract
Background: The number of working-age rectal cancer survivors is increasing due to early detection and improved treatment. However, work loss duration and predictors among them have not been studied thoroughly.

Methods: We identified 3,438 patients with stage I–III rectal cancer, 18 to 61 years of age in the Swedish Colorectal Cancer Register 1996–2009. Information on work loss due to sick leave or disability pension was collected from 2 years before diagnosis to 5 years after (until December 31st, 2013). Incidence rate ratios (IRR) of work loss were estimated in a negative binominal model by clinical characteristics for the 1st and 2nd–5th years after diagnosis. Patients were stratified by prediagnostic work loss.

Results: Patients without prediagnostic work loss (74%) experienced median 147 days (25th and 75th percentile: 55 and 281) of work loss during the 1st year after diagnosis. Work loss rates (2nd–5th years) were significantly increased among relapse-free patients diagnosed in stage III [IRR = 1.92; 95% confidence interval (CI), 1.52–2.43], operated with abdominoperineal resection (IRR = 1.26; 95% CI, 1.03–1.56), and treated with neoadjuvant (chemo)radiotherapy (IRR = 1.46; 95% CI, 1.06–2.02). Patients with prediagnostic work loss (26%) experienced median 336 days (25th and 75th percentile: 183 and 365) of work loss during the 1st year, and rates did not vary clinically till 5 years.

Conclusion: Without prediagnostic work loss, disease- and treatment-related factors could help identify rectal cancer patients in need of early interventions to facilitate return to work.

Impact: Clinical awareness around prediagnostic and postdiagnostic work loss and individualized cancer rehabilitation programs should be emphasized among cancer survivors. Cancer Epidemiol Biomarkers Prev; 25(6); 987–94. ©2016 AACR.
Data from Plasma Alkylresorcinol Metabolites as Biomarkers for Whole-Grain Intake and Their Association with Prostate Cancer: A Swedish Nested Case–Control Study
Authors: Drake Isabel , Sonestedt Emily , Gullberg Bo , Bjartell Anders , Olsson Håkan , Adlercreutz Herman , Tikkanen Matti J. , Wirfält Elisabet , Wallström Peter
Published: April 2023

Abstract
Background: Observational studies have mostly found no association between self-reported whole-grain intake and prostate cancer. Plasma alkylresorcinol metabolites have been suggested as biomarkers for whole-grain intake in free-living populations.

Methods: We investigated the major dietary and lifestyle determinants of plasma alkylresorcinol metabolites in a nested case–control study (1,016 cases and 1,817 controls) in the Malmö Diet and Cancer Study. Multivariate adjusted ORs and 95% confidence intervals (95% CI) were estimated to assess the association between plasma alkylresorcinol metabolites and prostate cancer using logistic regression.

Results: Whole-grain intake, waist circumference, educational level, and smoking status were the main determinants of alkylresorcinol metabolites. We observed significant correlations between alkylresorcinol metabolites and whole-grain (r = 0.31) and fiber (r = 0.27) intake. Metabolite concentration was positively associated with prostate cancer risk (Poverall effect = 0.0004) but the association was not linear (P = 0.04). The lowest risk was seen among men with moderate plasma concentrations. The OR for high compared with moderate plasma alkylresorcinol metabolites was 1.41 (95% CI, 1.10–1.80) for prostate cancer.

Conclusions: Results suggest that plasma alkylresorcinol metabolites are mainly determined by whole-grain intake in this nested case–control study of Swedish men. The increased risk of prostate cancer seen among men with high plasma alkylresorcinol metabolites requires further study, but residual confounding, detection bias, or competing risks of nonprostate cancer–related deaths are plausible explanations that could not be ruled out.

Impact: We found no evidence of a protective effect of whole grains on incident prostate cancer. Further validation of alkylresorcinol metabolites as a biomarker for whole-grain intake is needed. Cancer Epidemiol Biomarkers Prev; 23(1); 73–83. ©2013 AACR.
Data from Total Nut, Tree Nut, Peanut, and Peanut Butter Consumption and the Risk of Pancreatic Cancer in the Netherlands Cohort Study
Authors: Nieuwenhuis Lisette , van den Brandt Piet A.
Published: April 2023

Abstract
Background: Nut intake has been associated with decreased cancer-related mortality, but few studies have examined the potential of nuts in the chemoprevention of pancreatic cancer. We prospectively investigated the association of total nut, tree nut, peanut, and peanut butter consumption with pancreatic cancer risk.

Methods: In the Netherlands Cohort Study, 120,852 men and women completed a baseline questionnaire, including a food frequency questionnaire, in 1986. After 20.3 years of follow-up, 583 incident pancreatic cancer cases, including 349 microscopically confirmed pancreatic cancer (MCPC) cases, were included in multivariable case–cohort analyses.

Results: Increased total nut consumption was associated with a nonsignificantly decreased MCPC risk in men [HR (95% confidence interval) for 10+ g/d vs. nonconsumers = 0.72 (0.47–1.11), Ptrend = 0.163]. No clear association was found in women. For tree nut and peanut consumption, nonsignificant inverse associations were observed in men. In women, no or unclear associations were found for tree nut and peanut consumption. Peanut butter intake was related to a significantly reduced risk of MCPC in men [HR (95% confidence interval) for 5+ g/d vs. nonconsumers = 0.53 (0.28–1.00), Ptrend = 0.047], but this relation was not clear in women. Evidence for a nonlinear dose–response relation with MCPC was found for tree nut intake only. The associations were weaker when looking at total pancreatic cancer.

Conclusions: Our results suggest that nuts and peanut butter might reduce pancreatic cancer risk in men. In women, no or unclear associations were found.

Impact: Nut consumption might reduce the risk of pancreatic cancer in men. Cancer Epidemiol Biomarkers Prev; 27(3); 274–84. ©2018 AACR.
Data from Secondhand Smoke Exposure Among Community-Dwelling Adult Cancer Survivors in the United States: 1999–2012
Authors: Akinboro Oladimeji , Olorunfemi Odunayo , Basak Prasanta , Phillips Elizabeth , Pomerantz Daniel , Bernhardt Bernard , Gucalp Rasim , Jesmajian Stephen , Ostroff Jamie S.
Published: April 2023

Abstract
Background: Little is known about the prevalence of secondhand smoke exposure (SHSe) among cancer survivors. We sought to determine the prevalence, trends, and correlates of SHSe among nonsmoking adult cancer survivors in the United States.

Methods: Interview and serum cotinine data for nonsmoking adults, age 20 years and older, with a history of cancer (N = 686) were obtained from consecutive two-year cross-sectional cycles of the National Health and Nutrition Examination Survey from 1999 to 2012. SHSe was defined as serum cotinine 0.05–10 ng/mL among nonsmokers. We calculated and trended the prevalence of SHSe among nonsmoking cancer survivors. Multivariable logistic regression was used to examine the associations of SHSe with sociodemographic, smoking, and clinical characteristics. Survey weights were applied in estimating prevalence rates, adjusted ORs, and confidence intervals (CI).

Results: The weighted aggregate SHSe and self-reported indoor SHSe prevalence rates over the study period were 28.26% (95% CI: 24.97%–31.55%) and 4.53% (95% CI: 3.48%–5.57%), respectively. SHS exposure declined from 39.61% (95% CI: 27.88%–51.34%) in 1999/2000 to 15.68% (95% CI: 9.38%–21.98%) in 2011/2012 (Ptrend < 0.001). Age ≥ 60 years was protective against SHSe, while being black, having less than high school education, poverty, and a smoking-related cancer history were associated with higher odds of SHSe.

Conclusions: Fortunately, SHSe among nonsmoking cancer survivors in the United States is on the decline, although certain subgroups remain disproportionately burdened.

Impact: These findings highlight clinical and public health imperatives to target socioeconomically disadvantaged nonsmoking cancer survivors to reduce their SHSe. Cancer Epidemiol Biomarkers Prev; 26(8); 1296–305. ©2017 AACR.
Data from Cervical Infection with Cutaneous Beta and Mucosal Alpha Papillomaviruses
Authors: Sichero Laura , El-Zein Mariam , Nunes Emily M. , Ferreira Silvaneide , Franco Eduardo L. , Villa Luisa L.
Published: April 2023

Abstract
Background: Alpha-human papillomavirus (α-HPV) plays a causal role in cervical cancer, but little is known about the epidemiology of genital Beta-human papillomavirus (β-HPV) infection.

Methods: We used Luminex and PCR hybridization to detect β- and α-HPVs prevalence at enrollment and 12-month follow-up in cervical samples from 505 women enrolled in the Ludwig-McGill cohort study. We compared epidemiologic correlates of both β- and α-HPVs and compared genotypes between these genera with respect to co-occurrence and association with cervical cytologic abnormalities.

Results: Infection with β-HPV types was more prevalent than that with α-HPV types at both visits (cumulative prevalences: 27.3% vs. 21.6%, respectively, P = 0.034). β-HPVs were mostly transient; however, only 1.98% women retained their original positivity at 12 months, whereas persistence was higher for α-HPVs (5.15%; P = 0.007). Age, parity, and sexual activity variables were predictors of α-HPV but not of β-HPV. α- and β-HPV types occurred independently. Increased risk of cervical abnormalities was restricted to women infected with α-9 or α-6 HPV types. We found no epidemiologic correlates for β-HPV infections.

Conclusions: Detection of β-HPV types in the cervix tends to occur as random and transient episodes not explained via the sexual-transmission correlates that characterize infections by α-HPVs.

Impact: Although it is plausible that β-HPVs may play a direct or indirect carcinogenic role, the lack of epidemiologic correlates for detection episodes of these viruses and lack of association with cervical lesions speak against their ancillary role as sexually transmitted agents in cervical carcinogenesis. Cancer Epidemiol Biomarkers Prev; 26(8); 1312–20. ©2017 AACR.
Data from Aristolochic Acid in the Etiology of Renal Cell Carcinoma
Authors: Hoang Margaret L. , Chen Chung-Hsin , Chen Pau-Chung , Roberts Nicholas J. , Dickman Kathleen G. , Yun Byeong Hwa , Turesky Robert J. , Pu Yeong-Shiau , Vogelstein Bert , Papadopoulos Nickolas , Grollman Arthur P. , Kinzler Kenneth W. , Rosenquist Thomas A.
Published: April 2023

Abstract
Background:Aristolochia species used in the practice of traditional herbal medicine contains aristolochic acid (AA), an established human carcinogen contributing to urothelial carcinomas of the upper urinary tract. AA binds covalently to genomic DNA, forming aristolactam (AL)–DNA adducts. Here we investigated whether AA is also an etiologic factor in clear cell renal cell carcinoma (ccRCC).

Methods: We conducted a population-based case–control study to investigate the linkage between Aristolochia prescription history, cumulative AA consumption, and ccRCC incidence in Taiwan (5,709 cases and 22,836 matched controls). The presence and level of mutagenic dA-AL-I adducts were determined in the kidney DNA of 51 Taiwanese ccRCC patients. The whole-exome sequences of ccRCC tumors from 10 Taiwanese ccRCC patients with prior exposure to AA were determined.

Results: Cumulative ingestion of more than 250 mg of AA increased risk of ccRCC (OR, 1.25), and we detected dA-AL-I adducts in 76% of Taiwanese ccRCC patients. Furthermore, the distinctive AA mutational signature was evident in six of 10 sequenced ccRCC exomes from Taiwanese patients.

Conclusions: This study strongly suggests that AA contributes to the etiology of certain RCCs.

Impact: The current study offers compelling evidence implicating AA in a significant fraction of the RCC arising in Taiwan and illustrates the power of integrating epidemiologic, molecular, and genetic data in the investigation of cancer etiology. Cancer Epidemiol Biomarkers Prev; 25(12); 1600–8. ©2016 AACR.
Supplementary Table 1 from Ursolic Acid Inhibits Growth and Metastasis of Human Colorectal Cancer in an Orthotopic Nude Mouse Model by Targeting Multiple Cell Signaling Pathways: Chemosensitization with Capecitabine
Authors: Prasad Sahdeo , Yadav Vivek R. , Sung Bokyung , Reuter Simone , Kannappan Ramaswamy , Deorukhkar Amit , Diagaradjane Parmeswaran , Wei Caimiao , Baladandayuthapani Veerabhadran , Krishnan Sunil , Guha Sushovan , Aggarwal Bharat B.
Published: April 2023

PDF file, 52K, Assessment of synergistic drug combination treatments between ursolic acid and capecitabine.
Supplementary Figure 3 from Omental Adipose Tissue–Derived Stromal Cells Promote Vascularization and Growth of Endometrial Tumors
Authors: Klopp Ann H. , Zhang Yan , Solley Travis , Amaya-Manzanares Felipe , Marini Frank , Andreeff Michael , Debeb Bisrat , Woodward Wendy , Schmandt Rosemarie , Broaddus Russell , Lu Karen , Kolonin Mikhail G.
Published: April 2023

PDF file - 202K, Quantification of histological and immunofluorescence tissue analysis.
Supplementary Table 3 from High ALK Receptor Tyrosine Kinase Expression Supersedes ALK Mutation as a Determining Factor of an Unfavorable Phenotype in Primary Neuroblastoma
Authors: Schulte Johannes H. , Bachmann Hagen S. , Brockmeyer Bent , DePreter Katleen , Oberthür André , Ackermann Sandra , Kahlert Yvonne , Pajtler Kristian , Theissen Jessica , Westermann Frank , Vandesompele Jo , Speleman Frank , Berthold Frank , Eggert Angelika , Brors Benedikt , Hero Barbara , Schramm Alexander , Fischer Matthias
Published: April 2023

XLS file - 10K
Supplementary Figure 3 from PI3K/mTOR Inhibitor PF-04691502 Antitumor Activity Is Enhanced with Induction of Wild-Type TP53 in Human Xenograft and Murine Knockout Models of Head and Neck Cancer
Authors: Herzog Amanda , Bian Yansong , Vander Broek Robert , Hall Bradford , Coupar Jamie , Cheng Hui , Sowers Anastasia L. , Cook John D. , Mitchell James B. , Chen Zhong , Kulkarni Ashok B. , Van Waes Carter
Published: April 2023

PDF file - 107K, Photomicrographs of Effects of PF502 and pifithrin.
Supplementary Figure 2 from Gliomas Promote Immunosuppression through Induction of B7-H1 Expression in Tumor-Associated Macrophages
Authors: Bloch Orin , Crane Courtney A. , Kaur Rajwant , Safaee Michael , Rutkowski Martin J. , Parsa Andrew T.
Published: April 2023

PDF file - 42K, Figure S2. Glioma-derived soluble factors can further induce B7-H1 expression in non-autologous GBM patient peripheral monocytes, but not in autologous patient monocytes. Quantification of mean fluorescence intensity for B7-H1 staining measured by flow cytometry is shown for monocytes stimulated with IL-10 (10 ng/ml) or glioma-conditioned media (SF1U-CM). In monocytes from healthy control patients, B7-H1 intensity was significantly increased by IL-10, and further increased by conditioned media (* p<0.05). Similar results were observed with stimulation of non-autologous monocytes from a GBM patient (* p<0.05, **p<0.01). Monocytes from an autologous GBM patient, SF1U, had high initial B7-H1 expression and could not be further increased with stimulation. Columns represent mean fluorescence intensity plus-minus SEM for each sample repeated in triplicate.
Supplementary Figure Legends 1-4 from Molecular Determinants of Retinoic Acid Sensitivity in Pancreatic Cancer
Authors: Gupta Sonal , Pramanik Dipankar , Mukherjee Radha , Campbell Nathaniel R. , Elumalai Sathyanarayanan , de Wilde Roeland F. , Hong Seung-Mo , Goggins Michael G. , De Jesus-Acosta Ana , Laheru Daniel , Maitra Anirban
Published: April 2023

PDF file - 80K
Supplementary Figure A1 from Identification of Prognosis-Relevant Subgroups in Patients with Chemoresistant Triple-Negative Breast Cancer
Authors: Yu Ke-Da , Zhu Rui , Zhan Ming , Rodriguez Angel A. , Yang Wei , Wong Stephen , Makris Andreas , Lehmann Brian D. , Chen Xi , Mayer Ingrid , Pietenpol Jennifer A. , Shao Zhi-Ming , Symmans W. Fraser , Chang Jenny C.
Published: April 2023

Supplementary Figure A1 PDF file 73K, Subgroup analysis of the extended validation cohort
Supplementary Figure 3 from Use of [11C]Choline PET-CT as a Noninvasive Method for Detecting Pelvic Lymph Node Status from Prostate Cancer and Relationship with Choline Kinase Expression
Authors: Contractor Kaiyumars , Challapalli Amarnath , Barwick Tara , Winkler Mathias , Hellawell Giles , Hazell Steve , Tomasi Giampaolo , Al-Nahhas Adil , Mapelli Paola , Kenny Laura M. , Tadrous Paul , Coombes R. Charles , Aboagye Eric O. , Mangar Stephen
Published: April 2023

PDF file - 62K
Supplemental Figure 3 from Anticancer Effects of Niclosamide in Human Glioblastoma
Authors: Wieland Anja , Trageser Daniel , Gogolok Sabine , Reinartz Roman , Höfer Heike , Keller Mihaela , Leinhaas Anke , Schelle Ramona , Normann Sabine , Klaas Lil , Waha Andreas , Koch Philipp , Fimmers Rolf , Pietsch Torsten , Yachnis Anthony T. , Pincus David W. , Steindler Dennis A. , Brüstle Oliver , Simon Matthias , Glas Martin , Scheffler Björn
Published: April 2023

Cell cycle analysis of pGBM #046 after niclosamide exposure.
Supplementary Figure 3 from Proliferation in the Normal FTE Is a Hallmark of the Follicular Phase, Not BRCA Mutation Status
Authors: George Sophia H.L. , Milea Anca , Shaw Patricia A.
Published: April 2023

PDF file, 957K, Spectrum output algorithm showing annotations made to include the interleukocyte population in normal FTE and intratumor leukocyte population in both STICs and HGSC where yellow, orange and red represent positively stained cells and blue is negative.
Supplementary Figure 1 from Evaluation and Clinical Analyses of Downstream Targets of the Akt Inhibitor GDC-0068
Authors: Yan Yibing , Serra Violeta , Prudkin Ludmila , Scaltriti Maurizio , Murli Sumati , Rodríguez Olga , Guzman Marta , Sampath Deepak , Nannini Michelle , Xiao Yuanyuan , Wagle Marie-Claire , Wu Jenny Q. , Wongchenko Matthew , Hampton Garret , Ramakrishnan Vanitha , Lackner Mark R. , Saura Cristina , Roda Desamparados , Cervantes Andrés , Tabernero Josep , Patel Premal , Baselga José
Published: April 2023

PDF file 285K, Biomarker validation by Western blot
Supplementary Data from Detection of Mutant Free Circulating Tumor DNA in the Plasma of Patients with Gastrointestinal Stromal Tumor Harboring Activating Mutations of CKIT or PDGFRA
Authors: Maier Jacqueline , Lange Thoralf , Kerle Irina , Specht Katja , Bruegel Melanie , Wickenhauser Claudia , Jost Philipp , Niederwieser Dietger , Peschel Christian , Duyster Justus , von Bubnoff Nikolas
Published: April 2023

Supplementary Data - PDF file 158K, Supplementary Table S1. Target mutations and ligation probes for mutation specific and wild type CKIT or PDGFRA hybridisation. Patient numbers corresponding to Figure 2, their specific tumor/target mutations and the sequences of the hybridisation probes. Supplementary Table S2. Overview of test results in relation to clinical setting for patients with active disease. Allocation of test results corresponding to Table 2 and to patient numbers corresponding to Figure 2. Supplementary Figure S1. LINE1 levels of GIST patients in complete remission versus progression and relapse. Shown are the median LINE1 fragment numbers in 2 microl plasma DNA
Supplementary Methods from The Pivotal Role of Integrin β1 in Metastasis of Head and Neck Squamous Cell Carcinoma
Authors: Wang Dongsheng , Müller Susan , Amin A.R.M. Ruhul , Huang Donghai , Su Ling , Hu Zhongliang , Rahman Mohammad Aminur , Nannapaneni Sreenivas , Koenig Lydia , Chen Zhengjia , Tighiouart Mourad , Shin Dong M. , Chen Zhuo G.
Published: April 2023

PDF file, 89K.
Supplementary Figure 4 from Novel Role of MDA-9/Syntenin in Regulating Urothelial Cell Proliferation by Modulating EGFR Signaling
Authors: Dasgupta Santanu , Menezes Mitchell E. , Das Swadesh K. , Emdad Luni , Janjic Aleksandar , Bhatia Shilpa , Mukhopadhyay Nitai D. , Shao Chunbo , Sarkar Devanand , Fisher Paul B.
Published: April 2023

PDF file - 120K, Supplementary Figure S4: Map of the wild type and mutant MDA-9/Syntenin construct lacking N and C terminal domains with a C terminal HA tag
Data Supplement from Functional p38 MAPK Identified by Biomarker Profiling of Pancreatic Cancer Restrains Growth through JNK Inhibition and Correlates with Improved Survival
Authors: Zhong Yi , Naito Yoshiki , Cope Leslie , Naranjo-Suarez Salvador , Saunders Tyler , Hong Seung-Mo , Goggins Michael G. , Herman Joseph M. , Wolfgang Christopher L. , Iacobuzio-Donahue Christine A.
Published: April 2023

Supplemental Figure 2. Kaplan Meier Plots.
Supplementary Table 3 from Sorafenib or Placebo with Either Gemcitabine or Capecitabine in Patients with HER-2–Negative Advanced Breast Cancer That Progressed during or after Bevacizumab
Authors: Schwartzberg Lee S. , Tauer Kurt W. , Hermann Robert C. , Makari-Judson Grace , Isaacs Claudine , Beck J. Thaddeus , Kaklamani Virginia , Stepanski Edward J. , Rugo Hope S. , Wang Wei , Bell-McGuinn Katherine , Kirshner Jeffrey J. , Eisenberg Peter , Emanuelson Richard , Keaton Mark , Levine Ellis , Medgyesy Diana C. , Qamar Rubina , Starr Alexander , Ro Sunhee Kwon , Lokker Nathalie A. , Hudis Clifford A.
Published: April 2023

PDF file - 55K, Study Drug Dosing (Safety Population)
Supplementary Figure 5 from Targeting Epithelial-to-Mesenchymal Transition with Met Inhibitors Reverts Chemoresistance in Small Cell Lung Cancer
Authors: Cañadas Israel , Rojo Federico , Taus Álvaro , Arpí Oriol , Arumí-Uría Montserrat , Pijuan Lara , Menéndez Silvia , Zazo Sandra , Dómine Manuel , Salido Marta , Mojal Sergi , García de Herreros Antonio , Rovira Ana , Albanell Joan , Arriola Edurne
Published: April 2023

PDF file - 150K, PF-2341066 sensitizes mesenchymal SCLC cells to chemotherapy.
Supplementary Figure 2 from Targeting Epithelial-to-Mesenchymal Transition with Met Inhibitors Reverts Chemoresistance in Small Cell Lung Cancer
Authors: Cañadas Israel , Rojo Federico , Taus Álvaro , Arpí Oriol , Arumí-Uría Montserrat , Pijuan Lara , Menéndez Silvia , Zazo Sandra , Dómine Manuel , Salido Marta , Mojal Sergi , García de Herreros Antonio , Rovira Ana , Albanell Joan , Arriola Edurne
Published: April 2023

PDF file - 110K, Karyotypic and gene expression differences between H69 and H69M.
Supplementary Appendix from Ultrasound Molecular Imaging in a Human CD276 Expression–Modulated Murine Ovarian Cancer Model
Authors: Lutz Amelie M. , Bachawal Sunitha V. , Drescher Charles W. , Pysz Marybeth A. , Willmann Jürgen K. , Gambhir Sanjiv Sam
Published: April 2023

PDF file - 86K
Supplementary Figures from Tumor Imaging and Interferon-γ–Inducible Protein-10 Gene Transfer Using a Highly Efficient Transferrin-Conjugated Liposome System in Mice
Authors: Zhuo Huiqin , Peng Yi , Yao Qin , Zhou Nuo , Zhou Sufang , He Jian , Fang Yuan , Li Xi , Jin Hongwei , Lu Xiaoling , Zhao Yongxiang
Published: April 2023

Supplementary Figures - PDF file 1800K, Figure S1: Transmission electron microscopy images of P-Ls (A), P-Ls entrapped; Figure S2: High-resolution X-ray photoelectron spectra on nitrogen of Lipid mixture (A), P-Ls (B), PTf-Ls (C) and sulfur atom of PTf-Ls (D); Figure S3: Confocal fluorescence images showing uptake of rhodamine-labeled PTf-Ls by MCF-7 cells. DAPI/nuclei (blue), rhodamine (red); Figure S4: Fluorescence micrographs and differential interference contrast (DIC) images of HeLa cells incubated with PTf-Ls entrapped pEGFP-N1 for 5 h (A), or pretreated for 1 h with 4 microg (B) or 40 microg (C) of transferrin in 1 mL of medium containing 10 % FBS for competition experiment. Images were taken 48 h after transfection; Figure S5: Fluorescence micrographs of HeLa cells transfected with PTf-Ls entrapped pEGFP-N1 (100�x magnification). (A and B) Images taken 48 h after transfection without (A) or with (B) FBS. (C) EGFP expression 24 h after transfection with PTf-Ls entrapped pEGFP-N1 with FBS. (D) EGFP expression 48 h after transfection with PTf-Ls entrapped pEGFP-N1 with FBS; Figure S6: Fluorescence micrographs of HeLa cells incubated with PTf-Ls entrapped pEGFP-N1 for 5 h (I), 24 h (II) or 48 h (III, the transfection medium was changed once at 24 h) (200�x, magnification); Figure S7: Dynamic light scattering particle size distributions for liposomes prepared on 4 June 2011 P-Ls (1) and PTf-Ls (2) or 11 August 2012 P-Ls (2) & PTf-Ls (4), respectively; Figure S8: Cytotoxicity of P-Ls and PTf-Ls measured at 4 h and 24 h after the addition of P-Ls or PTf-Ls to HeLa or MCF-7 cells; Figure S9: Cell cycle profiles of liposome-transfected HeLa cells. Numbers in figure indicate the percentage of cells in each cell cycle phase. Untreated group (A), HeLa cells transfected with P-Ls (B) or PTf-Ls (C)