bluuebunny/crossref_metadata_2025 huggingface dataset:
Supplementary Table S1 from Genetic Susceptibility to Nonalcoholic Fatty Liver Disease and Risk for Pancreatic Cancer: Mendelian Randomization
Authors: King Sontoria D. , Veliginti Swathi , Brouwers Martijn C.G.J. , Ren Zhewen , Zheng Wei , Setiawan Veronica W. , Wilkens Lynne R. , Shu Xiao-Ou , Arslan Alan A. , Beane Freeman Laura E. , Bracci Paige M. , Canzian Federico , Du Mengmeng , Gallinger Steven J. , Giles Graham G. , Goodman Phyllis J. , Haiman Christopher A. , Kogevinas Manolis , Kooperberg Charles , LeMarchand Loic , Neale Rachel E. , Visvanathan Kala , White Emily , Albanes Demetrius , Andreotti Gabriella , Babic Ana , Berndt Sonja I. , Brais Lauren K. , Brennan Paul , Buring Julie E. , Rabe Kari G. , Bamlet William R. , Chanock Stephen J. , Fuchs Charles S. , Gaziano J. Michael , Giovannucci Edward L. , Hackert Thilo , Hassan Manal M. , Katzke Verena , Kurtz Robert C. , Lee I.-Min , Malats Núria , Murphy Neil , Oberg Ann L. , Orlow Irene , Porta Miquel , Real Francisco X. , Rothman Nathaniel , Sesso Howard D. , Silverman Debra T. , Thompson Ian M. , Wactawski-Wende Jean , Wang Xiaoliang , Wentzensen Nicolas , Yu Herbert , Zeleniuch-Jacquotte Anne , Yu Kai , Wolpin Brian M. , Duell Eric J. , Li Donghui , Hung Rayjean J. , Perdomo Sandra , McCullough Marjorie L. , Freedman Neal D. , Patel Alpa V. , Peters Ulrike , Riboli Elio , Sund Malin , Tjønneland Anne , Zhong Jun , Van Den Eeden Stephen K. , Kraft Peter , Risch Harvey A. , Amundadottir Laufey T. , Klein Alison P. , Stolzenberg-Solomon Rachael Z. , Antwi Samuel O.
Published: July 2023

Supplementary Table S1 shows results of univariate analysis for 77 chronically elevated serum alanine aminotransferase (cALT)-defined nonalcoholic fatty liver disease SNPs in the Pancreatic Cancer Cohort Consortium (PanScan) data
Supplementary Figure S2 from Development of a Breast Cancer Risk Prediction Model Incorporating Polygenic Risk Scores and Nongenetic Risk Factors for Korean Women
Authors: Choi Jihye , Ha Tae-Woong , Choi Hye-Mi , Lee Han-Byoel , Shin Hee-Chul , Chung Woosung , Han Wonshik
Published: July 2023

The absolute risk of developing breast cancer was estimated using data from 20,434 Korean women. The absolute risk of breast cancer was estimated by PRS38_ASN+PRS190_EB for women in different percentiles and age categories. The dotted lines represent the average risks. (A) Lifetime absolute risk (B) 5-year absolute risk
Supplementary Table 4 from Intake of Proton-Pump Inhibitors and Gastric Cancer within the Stomach Cancer Pooling (StoP) Project
Authors: Sassano Michele , Mariani Marco , Pelucchi Claudio , Lunet Nuno , Morais Samantha , Martín Vicente , Moreno Victor , Curado Maria Paula , Dias-Neto Emmanuel , Leja Marcis , Gašenko Evita , La Vecchia Carlo , Boccia Stefania , Pastorino Roberta
Published: July 2023

Supplementary Table 4: Pooled adjusted odds ratios (ORs) and corresponding 95% confidence intervals (CIs) for the association between intake of proton-pump inhibitors and gastric cancer from the leave-one-out meta-analysis.
Supplementary Table 2 from Intake of Proton-Pump Inhibitors and Gastric Cancer within the Stomach Cancer Pooling (StoP) Project
Authors: Sassano Michele , Mariani Marco , Pelucchi Claudio , Lunet Nuno , Morais Samantha , Martín Vicente , Moreno Victor , Curado Maria Paula , Dias-Neto Emmanuel , Leja Marcis , Gašenko Evita , La Vecchia Carlo , Boccia Stefania , Pastorino Roberta
Published: July 2023

Supplementary Table 2: Questionnaire items used to assess exposure for each study included in the analysis.
Supplementary Table 1 from Intake of Proton-Pump Inhibitors and Gastric Cancer within the Stomach Cancer Pooling (StoP) Project
Authors: Sassano Michele , Mariani Marco , Pelucchi Claudio , Lunet Nuno , Morais Samantha , Martín Vicente , Moreno Victor , Curado Maria Paula , Dias-Neto Emmanuel , Leja Marcis , Gašenko Evita , La Vecchia Carlo , Boccia Stefania , Pastorino Roberta
Published: July 2023

Supplementary Table 1: Main characteristics of the studies included in the analysis.
Supplementary Figure 1 from Intake of Proton-Pump Inhibitors and Gastric Cancer within the Stomach Cancer Pooling (StoP) Project
Authors: Sassano Michele , Mariani Marco , Pelucchi Claudio , Lunet Nuno , Morais Samantha , Martín Vicente , Moreno Victor , Curado Maria Paula , Dias-Neto Emmanuel , Leja Marcis , Gašenko Evita , La Vecchia Carlo , Boccia Stefania , Pastorino Roberta
Published: July 2023

Supplementary Figure 1: Pooled adjusted odds ratios (ORs) and corresponding 95% confidence intervals (CIs) for the association between intake of proton-pump inhibitors and gastric cancer, stratified by H. pylori infection and socioeconomic status (SES).
Data from Relationship between ABO Blood Group Alleles and Pancreatic Cancer Is Modulated by Secretor (FUT2) Genotype, but Not Lewis Antigen (FUT3) Genotype
Authors: Kim Jihye , Yuan Chen , Amundadottir Laufey T. , Wolpin Brian M. , Klein Alison P. , Risch Harvey A. , Kraft Peter
Published: July 2023

AbstractBackground:
In Western populations, pancreatic ductal adenocarcinoma (PDAC) risk has been found to be greater among individuals with non-O blood types than those with O blood type. However, the association has not been fully evaluated with respect to FUT2 (determining secretor status) and FUT3 (determining Lewis antigens) status, two biologically important genes in the expression of ABO blood groups with PDAC.
Methods:
We examined interactions in data from 8,027 cases and 11,362 controls in large pancreatic cancer consortia (PanScan I-III and PanC4) by using genetic variants to predict ABO blood groups (rs505922 and rs8176746), secretor status (rs601338), and Lewis antigens (rs812936, rs28362459, and rs3894326). Multivariable logistic regression was used to estimate ORs and 95% confidence intervals (CI) of the risk of PDAC adjusted for age and sex. We examined multiplicative interactions of ABO with secretor status and Lewis antigens by considering each product term between ABO and secretor and between ABO and Lewis antigens individually.
Results:
We found that the increased risk associated with non-O blood groups was somewhat stronger among secretors than nonsecretors [ORs, 1.28 (95% CI, 1.15–1.42) and 1.17 (95% CI, 1.03–1.32) respectively; Pinteraction = 0.002]. We did not find any interactions between ABO and Lewis antigens.
Conclusions:
Our large consortia data provide evidence of effect modification in the association between non-O blood type and pancreatic cancer risk by secretor status.
Impact:
Our results indicate that the association between ABO blood type and PDAC risk may vary by secretor status, but not by Lewis antigens.
Patterns of Evidence-Based Care for the Diagnosis, Staging, and First-line Treatment of Breast Cancer by Race–Ethnicity: A SEER-Medicare Study
Authors: Herbach Emma L. , Nash Sarah H. , Lizarraga Ingrid M. , Carnahan Ryan M. , Wang Kai , Ogilvie Amy C. , Curran Michaela , Charlton Mary E.
Published: July 2023

Background:

Racial and ethnic disparities in guideline-recommended breast cancer treatment are well documented, however studies including diagnostic and staging procedures necessary to determine treatment indications are lacking. The purpose of this study was to characterize patterns in delivery of evidence-based services for the diagnosis, clinical workup, and first-line treatment of breast cancer by race–ethnicity.

Methods:

SEER-Medicare data were used to identify women diagnosed with invasive breast cancer between 2000 and 2017 at age 66 or older (n = 2,15,605). Evidence-based services included diagnostic procedures (diagnostic mammography and breast biopsy), clinical workup (stage and grade determination, lymph node biopsy, and HR and HER2 status determination), and treatment initiation (surgery, radiation, chemotherapy, hormone therapy, and HER2-targeted therapy). Poisson regression was used to estimate rate ratios (RR) and 95% confidence intervals (CI) for each service.

Results:

Black and American Indian/Alaska Native (AIAN) women had significantly lower rates of evidence-based care across the continuum from diagnostics through first-line treatment compared to non-Hispanic White (NHW) women. AIAN women had the lowest rates of HER2-targeted therapy and hormone therapy initiation. While Black women also had lower initiation of HER2-targeted therapy than NHW, differences in hormone therapy were not observed.

Conclusions:

Our findings suggest patterns along the continuum of care from diagnostic procedures to treatment initiation may differ across race–ethnicity groups.

Impact:

Efforts to improve delivery of guideline-concordant treatment and mitigate racial–ethnic disparities in healthcare and survival should include procedures performed as part of the diagnosis, clinical workup, and staging processes.
Supplementary Fig. 4 from An Open-label Phase I Study of GDC-0927 in Postmenopausal Women with Locally Advanced or Metastatic Estrogen Receptor–Positive Breast Cancer
Authors: Chandarlapaty Sarat , Dickler Maura N. , Perez Fidalgo Jose Alejandro , Villanueva-Vázquez Rafael , Giltnane Jennifer , Gates Mary , Chang Ching-Wei , Cheeti Sravanthi , Fredrickson Jill , Wang Xiaojing , Collier Ann , Moore Heather M. , Metcalfe Ciara , Lauchle Jennifer , Humke Eric W. , Bardia Aditya
Published: July 2023

Supplementary Fig. S4. ESR1 mutation analysis in ctDNA.
Supplementary Fig. 1 from An Open-label Phase I Study of GDC-0927 in Postmenopausal Women with Locally Advanced or Metastatic Estrogen Receptor–Positive Breast Cancer
Authors: Chandarlapaty Sarat , Dickler Maura N. , Perez Fidalgo Jose Alejandro , Villanueva-Vázquez Rafael , Giltnane Jennifer , Gates Mary , Chang Ching-Wei , Cheeti Sravanthi , Fredrickson Jill , Wang Xiaojing , Collier Ann , Moore Heather M. , Metcalfe Ciara , Lauchle Jennifer , Humke Eric W. , Bardia Aditya
Published: July 2023

Supplementary Fig. S1. Study scheme.
Supplementary Data 1 from An Open-label Phase I Study of GDC-0927 in Postmenopausal Women with Locally Advanced or Metastatic Estrogen Receptor–Positive Breast Cancer
Authors: Chandarlapaty Sarat , Dickler Maura N. , Perez Fidalgo Jose Alejandro , Villanueva-Vázquez Rafael , Giltnane Jennifer , Gates Mary , Chang Ching-Wei , Cheeti Sravanthi , Fredrickson Jill , Wang Xiaojing , Collier Ann , Moore Heather M. , Metcalfe Ciara , Lauchle Jennifer , Humke Eric W. , Bardia Aditya
Published: July 2023

Supplementary Tables S1, S2, and S3.
Supplementary Data 1 from Comparative Genomic Analysis of Pancreatic Acinar Cell Carcinoma (PACC) and Pancreatic Ductal Adenocarcinoma (PDAC) Unveils New Actionable Genomic Aberrations in PACC
Authors: Florou Vaia , Elliott Andrew , Bailey Matthew H. , Stone David , Affolter Kajsa , Soares Heloisa P. , Nevala-Plagemann Chris , Scaife Courtney , Walker Phillip , Korn W. Michael , Lou Emil , Shroff Rachna T. , Hosein Peter J. , Garrido-Laguna Ignacio
Published: July 2023

Supplementary table
Supplementary Data 1 from Spatial Immunoprofiling of Adenoid Cystic Carcinoma Reveals B7-H4 Is a Therapeutic Target for Aggressive Tumors
Authors: Sousa Luana Guimaraes , McGrail Daniel J. , Lazar Neto Felippe , Li Kaiyi , Marques-Piubelli Mario L. , Ferri-Borgogno Sammy , Dai Hui , Mitani Yoshitsugu , Spardy Burr Nicole , Cooper Zachary A. , Kinneer Krista , Cortez Maria Angelica , Lin Shiaw-Yih , Bell Diana , El Naggar Adel , Burks Jared , Ferrarotto Renata
Published: July 2023

Supplementary material including methods, supplementary table 1, supplementary table 2, and supplementary table 3
Circulating Tumor DNA to Drive Treatment in Metastatic Colorectal Cancer
Authors: Patelli Giorgio , Mauri Gianluca , Tosi Federica , Amatu Alessio , Bencardino Katia , Bonazzina Erica , Pizzutilo Elio Gregory , Villa Federica , Calvanese Gabriele , Agostara Alberto Giuseppe , Stabile Stefano , Ghezzi Silvia , Crisafulli Giovanni , Di Nicolantonio Federica , Marsoni Silvia , Bardelli Alberto , Siena Salvatore , Sartore-Bianchi Andrea
Published: July 2023

In the evolving molecular treatment landscape of metastatic colorectal cancer (mCRC), the identification of druggable alterations is pivotal to achieve the best therapeutic opportunity for each patient. Because the number of actionable targets is expanding, there is the need to timely detect their presence or emergence to guide the choice of different available treatment options. Liquid biopsy, through the analysis of circulating tumor DNA (ctDNA), has proven safe and effective as a complementary method to address cancer evolution while overcoming the limitations of tissue biopsy. Even though data are accumulating regarding the potential for ctDNA-guided treatments applied to targeted agents, still major gaps in knowledge exist as for their application to different areas of the continuum of care. In this review, we recapitulate how ctDNA information could be exploited to drive different targeted treatment strategies in mCRC patients, by refining molecular selection before treatment by addressing tumor heterogeneity beyond tumor tissue biopsy; longitudinally monitoring early-tumor response and resistance mechanisms to targeted agents, potentially leading to tailored, molecular-driven, therapeutic options; guiding the molecular triage towards rechallenge strategies with anti-EGFR agents, suggesting the best time for retreatment; and providing opportunities for an “enhanced rechallenge” through additional treatments or combos aimed at overcoming acquired resistance. Besides, we discuss future perspectives concerning the potential role of ctDNA to fine-tune investigational strategies such as immuno-oncology.
A Phase Ib Trial of AVID200, a TGFβ 1/3 Trap, in Patients with Myelofibrosis
Authors: Mascarenhas John , Migliaccio Anna Rita , Kosiorek Heidi , Bhave Rupali , Palmer Jeanne , Kuykendall Andrew , Mesa Ruben , Rampal Raajit K. , Gerds Aaron T. , Yacoub Abdulraheem , Pettit Kristen , Talpaz Moshe , Komrokji Rami , Kremyanskaya Marina , Gonzalez Agapito , Fabris Frank , Johnson Kathryn , Dougherty Mikaela , McGovern Erin , Arango Ossa Juan , Domenico Dylan , Farnoud Noushin , Weinberg Rona Singer , Kong Amy , Najfeld Vesna , Vannucchi Alessandro Maria , Arciprete Francesca , Zingariello Maria , Falchi Mario , Salama Mohamed E. , Mead-Harvey Carolyn , Dueck Amylou , Varricchio Lilian , Hoffman Ronald
Published: July 2023

Purpose:

Myelofibrosis (MF) is a clonal myeloproliferative neoplasm characterized by systemic symptoms, cytopenias, organomegaly, and bone marrow fibrosis. JAK2 inhibitors afford symptom and spleen burden reduction but do not alter the disease course and frequently lead to thrombocytopenia. TGFβ, a pleiotropic cytokine elaborated by the MF clone, negatively regulates normal hematopoiesis, downregulates antitumor immunity, and promotes bone marrow fibrosis. Our group previously showed that AVID200, a potent and selective TGFβ 1/3 trap, reduced TGFβ1-induced proliferation of human mesenchymal stromal cells, phosphorylation of SMAD2, and collagen expression. Moreover, treatment of MF mononuclear cells with AVID200 led to increased numbers of progenitor cells (PC) with wild-type JAK2 rather than JAK2V617F.

Patients and Methods:

We conducted an investigator-initiated, multicenter, phase Ib trial of AVID200 monotherapy in 21 patients with advanced MF.

Results:

No dose-limiting toxicity was identified at the three dose levels tested, and grade 3/4 anemia and thrombocytopenia occurred in 28.6% and 19.0% of treated patients, respectively. After six cycles of therapy, two patients attained a clinical benefit by IWG-MRT criteria. Spleen and symptom benefits were observed across treatment cycles. Unlike other MF-directed therapies, increases in platelet counts were noted in 81% of treated patients with three patients achieving normalization. Treatment with AVID200 resulted in potent suppression of plasma TGFβ1 levels and pSMAD2 in MF cells.

Conclusions:

AVID200 is a well-tolerated, rational, therapeutic agent for the treatment of patients with MF and should be evaluated further in patients with thrombocytopenic MF in combination with agents that target aberrant MF intracellular signaling pathways.
Table S3 from HCK Promotes High-grade Serous Ovarian Cancer Tumorigenesis through CD44 and NOTCH3 Signaling
Authors: Khella Christen A. , Franciosa Lucyann , Rodirguez-Rodriguez Lorna , Rajkarnikar Resha , Mythreye Karthikeyan , Gatza Michael L.
Published: July 2023

Summary of differentially expressed proteins (RPPA analysis) following HCK silencing in CAOV3 cells
Table S2 from HCK Promotes High-grade Serous Ovarian Cancer Tumorigenesis through CD44 and NOTCH3 Signaling
Authors: Khella Christen A. , Franciosa Lucyann , Rodirguez-Rodriguez Lorna , Rajkarnikar Resha , Mythreye Karthikeyan , Gatza Michael L.
Published: July 2023

CAOV3 RPPA data summary
Supplementary Figure 9 from Targeting the ATF6-Mediated ER Stress Response and Autophagy Blocks Integrin-Driven Prostate Cancer Progression
Authors: Macke Amanda J. , Pachikov Artem N. , Divita Taylor E. , Morris Mary E. , LaGrange Chad A. , Holzapfel Melissa S. , Kubyshkin Anatoly V. , Zyablitskaya Evgeniya Y. , Makalish Tatiana P. , Eremenko Sergey N. , Qiu Haowen , Riethoven Jean-Jack M. , Hemstreet George P. , Petrosyan Armen
Published: July 2023

Figure S9. (A) Left Panels: representative images of triple IHC staining of Na+/K+-ATPase (green), Integrin αv (red), and Gal-3 (brown) in the orthotopic tumor samples from the indicated group of mice; bars, 100 µm. Middle panel: IF of Golgi stained by GM130 in the prostate tumor foci; bars, 10 µm. White boxes indicate areas enlarged at the right. (B) Quantification of Golgi fragments per cell in tumor foci from samples in A; median ± SD. (C) ATF6 IF in the orthotopic tumor samples from the indicated group of mice; bars, 20 µm. Areas of mice prostate epithelium is highlighted by dotted lines. (D) Quantification of ATF6 IF intensity from samples in C; median ± SD. For all graphs: pairwise comparisons using Wilcoxon rank sum exact test, p-adjusted using Benjamini-Hochberg; ****p<0.0001, **p<0.01, and *p<0.05; n indicates the number of foci counted. (E) IF staining of the prostate tumor foci from the indicated group of mice to visualize Na+/K+-ATPase (magenta), Integrin αv (red), and Gal-3 (green); bars, 10 µm. (F, G) Quantification of IF intensity of Integrin αv (F) and Gal-3 (G) at the PM in samples from C; median ± SD.
Supplementary Figure 6 from Targeting the ATF6-Mediated ER Stress Response and Autophagy Blocks Integrin-Driven Prostate Cancer Progression
Authors: Macke Amanda J. , Pachikov Artem N. , Divita Taylor E. , Morris Mary E. , LaGrange Chad A. , Holzapfel Melissa S. , Kubyshkin Anatoly V. , Zyablitskaya Evgeniya Y. , Makalish Tatiana P. , Eremenko Sergey N. , Qiu Haowen , Riethoven Jean-Jack M. , Hemstreet George P. , Petrosyan Armen
Published: July 2023

Figure S6. (A) Immunostaining of Gal-3 (green) and Na+/K+-ATPase (red) in control and HCQ-treated PC-3 cells; bars, 20 µm. (B) Quantification of Gal-3 integrated intensity at PM in cells from A. Mann Whitney test; *p<0.05, mean ± SD; n indicates number of cells.
Supplementary Figure 5 from Targeting the ATF6-Mediated ER Stress Response and Autophagy Blocks Integrin-Driven Prostate Cancer Progression
Authors: Macke Amanda J. , Pachikov Artem N. , Divita Taylor E. , Morris Mary E. , LaGrange Chad A. , Holzapfel Melissa S. , Kubyshkin Anatoly V. , Zyablitskaya Evgeniya Y. , Makalish Tatiana P. , Eremenko Sergey N. , Qiu Haowen , Riethoven Jean-Jack M. , Hemstreet George P. , Petrosyan Armen
Published: July 2023

Figure S5. (A, B) Representative EM images of PC-3 (A) and DU145 (B) cells. Note phagophore nucleation from Golgi (arrowheads) and autophagosomes localizing close to the Golgi (arrow). Orange boxes indicate the areas magnified at the right. (C) WIPI2 W-B of the Golgi fractions isolated from LNCaP, PC-3, and DU145 cells. Samples were normalized by GM130.
Supplementary Figure 8 from Continuous Administration of Anti-VEGFA Antibody Upregulates PAI-1 Secretion from Ovarian Cancer Cells via miR-143-3p Downregulation
Authors: Yagi Taro , Sawada Kenjiro , Miyamoto Mayuko , Shimizu Aasa , Oi Yukako , Toda Aska , Nakamura Koji , Kinose Yasuto , Kodama Michiko , Hashimoto Kae , Kimura Tadashi
Published: July 2023

Supplementary Figure 8 shows the representative images of immunohistochemical staining of a human normal kidney for PAI-1 and CD31.
Supplementary Figure 6 from Continuous Administration of Anti-VEGFA Antibody Upregulates PAI-1 Secretion from Ovarian Cancer Cells via miR-143-3p Downregulation
Authors: Yagi Taro , Sawada Kenjiro , Miyamoto Mayuko , Shimizu Aasa , Oi Yukako , Toda Aska , Nakamura Koji , Kinose Yasuto , Kodama Michiko , Hashimoto Kae , Kimura Tadashi
Published: July 2023

Supplementary Figure 6 shows that the transduction of miR-143-3p does not attenuate in vitro tube formation in HUVECs incubated with the culture media of SKOV3ip1 cells.
Supplementary Figure 2 from Targeting the ATF6-Mediated ER Stress Response and Autophagy Blocks Integrin-Driven Prostate Cancer Progression
Authors: Macke Amanda J. , Pachikov Artem N. , Divita Taylor E. , Morris Mary E. , LaGrange Chad A. , Holzapfel Melissa S. , Kubyshkin Anatoly V. , Zyablitskaya Evgeniya Y. , Makalish Tatiana P. , Eremenko Sergey N. , Qiu Haowen , Riethoven Jean-Jack M. , Hemstreet George P. , Petrosyan Armen
Published: July 2023

Figure S2. (A) Representative images of triple IHC staining of Integrin αvβ5 (green), Gal-3 (red), and E-cadherin (brown) in the normal prostate and tumor tissues from PCa patients with different grades. Deconvoluted images of Integrin αvβ5 are shown on the right; bars, 100 µm. (B) Quantification of Integrin αvβ5 H-score at PM from samples in A. Dunn Test (1964) Kruskal-Wallis multiple comparisons, p-adjusted using Benjamini-Hochberg; ****p<0.0001 and ***p<0.001, median ± SD. (C) Quantification of Integrin αvβ5 and Gal-3 colocalization at PM in normal prostate and PCa, grades 2-5. Kruskal-Wallis test; ***p<0.001, mean ± SD.
Supplementary Figure 4 from Continuous Administration of Anti-VEGFA Antibody Upregulates PAI-1 Secretion from Ovarian Cancer Cells via miR-143-3p Downregulation
Authors: Yagi Taro , Sawada Kenjiro , Miyamoto Mayuko , Shimizu Aasa , Oi Yukako , Toda Aska , Nakamura Koji , Kinose Yasuto , Kodama Michiko , Hashimoto Kae , Kimura Tadashi
Published: July 2023

Supplementary Figure 4 shows that the knockdown of VEGFA significantly inhibited the expression level of miR-143-3p, followed by the upregulation of PAI secretion from OC cells.
Movie S4 from Targeting the ATF6-Mediated ER Stress Response and Autophagy Blocks Integrin-Driven Prostate Cancer Progression
Authors: Macke Amanda J. , Pachikov Artem N. , Divita Taylor E. , Morris Mary E. , LaGrange Chad A. , Holzapfel Melissa S. , Kubyshkin Anatoly V. , Zyablitskaya Evgeniya Y. , Makalish Tatiana P. , Eremenko Sergey N. , Qiu Haowen , Riethoven Jean-Jack M. , Hemstreet George P. , Petrosyan Armen
Published: July 2023

PC-3 cell treated with HCQ, stained for Integrin αv (red), Gal-3 (green), EEA1 (magenta). Areas of 3-color colocalization are highlighted with white. Surfaces were reconstructed by Imaris.
Supplementary Figure 2 from Continuous Administration of Anti-VEGFA Antibody Upregulates PAI-1 Secretion from Ovarian Cancer Cells via miR-143-3p Downregulation
Authors: Yagi Taro , Sawada Kenjiro , Miyamoto Mayuko , Shimizu Aasa , Oi Yukako , Toda Aska , Nakamura Koji , Kinose Yasuto , Kodama Michiko , Hashimoto Kae , Kimura Tadashi
Published: July 2023

Supplementary Figure 2 shows that PAI-1 enhanced in vitro tube formation not only in the absence of anti-VEGFA antibody but also in the presence of anti-VEGFA antibody.
Supplementary Figure 1 from Continuous Administration of Anti-VEGFA Antibody Upregulates PAI-1 Secretion from Ovarian Cancer Cells via miR-143-3p Downregulation
Authors: Yagi Taro , Sawada Kenjiro , Miyamoto Mayuko , Shimizu Aasa , Oi Yukako , Toda Aska , Nakamura Koji , Kinose Yasuto , Kodama Michiko , Hashimoto Kae , Kimura Tadashi
Published: July 2023

Supplementary Figure 1 shows Kaplan–Meier plotter analysis of genes that were upregulated during anti-VEGFA treatment.
Movie S2 from Targeting the ATF6-Mediated ER Stress Response and Autophagy Blocks Integrin-Driven Prostate Cancer Progression
Authors: Macke Amanda J. , Pachikov Artem N. , Divita Taylor E. , Morris Mary E. , LaGrange Chad A. , Holzapfel Melissa S. , Kubyshkin Anatoly V. , Zyablitskaya Evgeniya Y. , Makalish Tatiana P. , Eremenko Sergey N. , Qiu Haowen , Riethoven Jean-Jack M. , Hemstreet George P. , Petrosyan Armen
Published: July 2023

PC-3 cell treated with HCQ, stained for Golgi (GRASP65, green) and MGAT3 (red). Surfaces were reconstructed by Imaris.
Supplementary Figure 6 from Oncostatin-M and OSM-Receptor Feed-Forward Activation of MAPK Induces Separable Stem-like and Mesenchymal Programs
Authors: Polak Kelsey L. , Tamagno Ilaria , Parameswaran Neetha , Smigiel Jacob , Chan E. Ricky , Yuan Xueer , Rios Brenda , Jackson Mark W.
Published: July 2023

S6. Generation and analysis of SMAD3 knock-out cells.
Supplementary Figure 5 from Oncostatin-M and OSM-Receptor Feed-Forward Activation of MAPK Induces Separable Stem-like and Mesenchymal Programs
Authors: Polak Kelsey L. , Tamagno Ilaria , Parameswaran Neetha , Smigiel Jacob , Chan E. Ricky , Yuan Xueer , Rios Brenda , Jackson Mark W.
Published: July 2023

S5. MEK inhibitors block OSM-driven conversion to a CD44HI/mesenchymal state.
Supplementary Figure 7 from Targeting c-Jun Is a Potential Therapy for Luminal Breast Cancer Bone Metastasis
Authors: Han Yuxuan , Katayama Shota , Futakuchi Mitsuru , Nakamichi Kazuya , Wakabayashi Yutaro , Sakamoto Mai , Nakayama Jun , Semba Kentaro
Published: July 2023

Evaluation of JNK-IN-8 inhibition of MCF7-BM cells.
Supplementary Figure 8 from Nrf2 Drives Hepatocellular Carcinoma Progression through Acetyl-CoA–mediated Metabolic and Epigenetic Regulatory Networks
Authors: Xi Caixia , Pang Junfeng , Barrett Amanda , Horuzsko Anatolij , Ande Satyanarayana , Mivechi Nahid F. , Zhu Xingguo
Published: July 2023

S8. GCK and ALDOA gene expression in glucose-deprived shNRF2 HepG2 cells after energy-refeeding.
Supplementary Figure 6 from Nrf2 Drives Hepatocellular Carcinoma Progression through Acetyl-CoA–mediated Metabolic and Epigenetic Regulatory Networks
Authors: Xi Caixia , Pang Junfeng , Barrett Amanda , Horuzsko Anatolij , Ande Satyanarayana , Mivechi Nahid F. , Zhu Xingguo
Published: July 2023

S6. A glucose dependency of NRF2 regulation in HepG2 cells.
Supplementary Figure 4 from Simultaneous Targeting of DNA Polymerase Theta and PARP1 or RAD52 Triggers Dual Synthetic Lethality in Homologous Recombination–Deficient Leukemia Cells
Authors: Sullivan-Reed Katherine , Toma Monika M. , Drzewiecka Malgorzata , Nieborowska-Skorska Margaret , Nejati Reza , Karami Adam , Wasik Mariusz A. , Sliwinski Tomasz , Skorski Tomasz
Published: July 2023

S4. Targeting Polθ + PARP and Polθ + RAD52 induced dual synthetic lethality against HR -deficient MPN cells.
Supplementary Figure 1 from Simultaneous Targeting of DNA Polymerase Theta and PARP1 or RAD52 Triggers Dual Synthetic Lethality in Homologous Recombination–Deficient Leukemia Cells
Authors: Sullivan-Reed Katherine , Toma Monika M. , Drzewiecka Malgorzata , Nieborowska-Skorska Margaret , Nejati Reza , Karami Adam , Wasik Mariusz A. , Sliwinski Tomasz , Skorski Tomasz
Published: July 2023

S1. Genetic aberrations and mRNA expression variabilities of POLQ, PARP1 and RAD52 do not coexist in 519 AML samples from the BEAT-AML cohort.
Supplementary Figure 1 from Nrf2 Drives Hepatocellular Carcinoma Progression through Acetyl-CoA–mediated Metabolic and Epigenetic Regulatory Networks
Authors: Xi Caixia , Pang Junfeng , Barrett Amanda , Horuzsko Anatolij , Ande Satyanarayana , Mivechi Nahid F. , Zhu Xingguo
Published: July 2023

S1. RF2 promotes hepatocarcinogenesis.
Supplemental Table 1 from Nrf2 Drives Hepatocellular Carcinoma Progression through Acetyl-CoA–mediated Metabolic and Epigenetic Regulatory Networks
Authors: Xi Caixia , Pang Junfeng , Barrett Amanda , Horuzsko Anatolij , Ande Satyanarayana , Mivechi Nahid F. , Zhu Xingguo
Published: July 2023

Supplemental Table 1. DNA Oligos
Supplementary Fig S3 from Chromatin-Associated SIN3B Protects Cancer Cells from Genotoxic Stress-Induced Apoptosis and Dictates DNA Damage Repair Pathway Choice
Authors: Morales-Valencia Jorge , Petit Coralie , Calderon Alexander , Saini Siddharth , David Gregory
Published: July 2023

Cell cycle effect on DNA damage-induced apoptosis
Supplementary Fig S1 from Chromatin-Associated SIN3B Protects Cancer Cells from Genotoxic Stress-Induced Apoptosis and Dictates DNA Damage Repair Pathway Choice
Authors: Morales-Valencia Jorge , Petit Coralie , Calderon Alexander , Saini Siddharth , David Gregory
Published: July 2023

SIN3B protects against DNA damage-induced apoptosis.
Data from Simultaneous Targeting of DNA Polymerase Theta and PARP1 or RAD52 Triggers Dual Synthetic Lethality in Homologous Recombination–Deficient Leukemia Cells
Authors: Sullivan-Reed Katherine , Toma Monika M. , Drzewiecka Malgorzata , Nieborowska-Skorska Margaret , Nejati Reza , Karami Adam , Wasik Mariusz A. , Sliwinski Tomasz , Skorski Tomasz
Published: July 2023

Abstract
DNA polymerase theta (Polθ, encoded by POLQ gene) plays an essential role in Polθ-mediated end-joining (TMEJ) of DNA double-strand breaks (DSB). Inhibition of Polθ is synthetic lethal in homologous recombination (HR)-deficient tumor cells. However, DSBs can be also repaired by PARP1 and RAD52-mediated mechanisms. Because leukemia cells accumulate spontaneous DSBs, we tested if simultaneous targeting of Polθ and PARP1 or RAD52 enhance the synthetic lethal effect in HR-deficient leukemia cells. Transformation potential of the oncogenes inducing BRCA1/2-deficiency (BCR-ABL1 and AML1-ETO) was severely limited in Polq−/−;Parp1−/− and Polq−/−;Rad52−/− cells when compared with single knockouts, which was associated with accumulation of DSBs. Small-molecule inhibitor of Polθ (Polθi) when combined with PARP or RAD52 inhibitors (PARPi, RAD52i) caused accumulation of DSBs and exerted increased effect against HR-deficient leukemia and myeloproliferative neoplasm cells.
Implications:
In conclusion, we show that PARPi or RAD52i might improve therapeutic effect of Polθi against HR-deficient leukemias.
Data from Chromatin-Associated SIN3B Protects Cancer Cells from Genotoxic Stress-Induced Apoptosis and Dictates DNA Damage Repair Pathway Choice
Authors: Morales-Valencia Jorge , Petit Coralie , Calderon Alexander , Saini Siddharth , David Gregory
Published: July 2023

Abstract
Transcription and DNA damage repair act in a coordinated manner. The scaffolding protein SIN3B serves as a transcriptional co-repressor of hundreds of cell cycle–related genes. However, the contribution of SIN3B during the DNA damage response remains unknown. Here, we show that SIN3B inactivation delays the resolution of DNA double-strand breaks and sensitizes cancer cells to DNA-damaging agents, including the chemotherapeutic drugs cisplatin and doxorubicin. Mechanistically, SIN3B is rapidly recruited to DNA damage sites where it directs the accumulation of Mediator of DNA Damage Checkpoint 1 (MDC1). In addition, we show that SIN3B inactivation favors the engagement of the alternative nonhomologous end joining (NHEJ) repair pathway over the canonical NHEJ. Altogether, our findings impute an unexpected function for the transcriptional co-repressor SIN3B as a gatekeeper of genomic integrity and a determining factor in the DNA repair choice pathway, and point to the inhibition of the SIN3B chromatin-modifying complex as a novel therapeutic vulnerability in cancer cells.
Implications:
Identifying SIN3B as a modulator of DNA damage repair choice provides novel potential therapeutic avenues to sensitize cancer cells to cytotoxic therapies.
Data from Clinical activity and exploratory resistance mechanism of milademetan, an MDM2 inhibitor, in intimal sarcoma with MDM2 amplification: an open-label phase 1b/2 study
Authors: Koyama Takafumi , Shimizu Toshio , Kojima Yuki , Sudo Kazuki , Okuma Hitomi Sumiyoshi. , Shimoi Tatsunori , Ichikawa Hitoshi , Kohsaka Shinji , Sadachi Ryo , Hirakawa Akihiro , Yoshida Akihiko , Ando Reiko Makihara. , Ueno Toshihide , Yanagaki Mitsuru , Matsui Naoko , Nakamura Kenichi , Yamamoto Noboru , Yonemori Kan
Published: July 2023

Abstract
Intimal sarcoma is an extremely rare life-threatening malignant neoplasm. Murine double minute 2 (MDM2) amplification is observed in > 70% of intimal sarcomas. Milademetan, an MDM2 inhibitor, may provide a clinical benefit in this patient population. We conducted a phase 1b/2 study in patients with MDM2-amplified wild-type TP53 intimal sarcoma as a sub-study of a large nationwide registry for rare cancers in Japan. Milademetan (260 mg) was administered orally once daily for three days every 14 days, twice in a 28-day cycle. Of 11 patients enrolled, 10 were included in the efficacy analysis. Two patients (20%) showed durable responses for >15 months. Anti-tumor activity correlated with TWIST1 amplification (P = 0.028) and negatively with CDKN2A loss (P = 0.071). Acquired TP53 mutations were detected in sequential liquid biopsies as a novel exploratory resistance mechanism to milademetan. These results suggest that milademetan could be a potential therapeutic strategy for intimal sarcoma.
Table S5 from Systemic Treatments and Molecular Biomarkers for Perivascular Epithelioid Cell Tumors: A Single-institution Retrospective Analysis
Authors: Testa Stefano , Bui Nam Q. , Ganjoo Kristen N.
Published: July 2023

Table S5 shows DCR and ORR based on biomarker status and primary tumor site, considering all treatment episodes, and mTOR inhibitors only.
Table S4 from Systemic Treatments and Molecular Biomarkers for Perivascular Epithelioid Cell Tumors: A Single-institution Retrospective Analysis
Authors: Testa Stefano , Bui Nam Q. , Ganjoo Kristen N.
Published: July 2023

Table S4 shows the best disease control rate (DCR) and overall response rate (ORR) for mTOR inhibitors compared to other treatments based on histotype.
Table S3 from Systemic Treatments and Molecular Biomarkers for Perivascular Epithelioid Cell Tumors: A Single-institution Retrospective Analysis
Authors: Testa Stefano , Bui Nam Q. , Ganjoo Kristen N.
Published: July 2023

Table S3 shows the best overall response rate (ORR) and disease control rate (DCR) for different treatment types based on histology, tumor location, TFE3 positivity, as well as TSC1, TSC2, and TP53 mutational status.
Table S2 from Systemic Treatments and Molecular Biomarkers for Perivascular Epithelioid Cell Tumors: A Single-institution Retrospective Analysis
Authors: Testa Stefano , Bui Nam Q. , Ganjoo Kristen N.
Published: July 2023

Table S2 shows the results of molecular testing available for each patient in the study.
Table S12 from Systemic Treatments and Molecular Biomarkers for Perivascular Epithelioid Cell Tumors: A Single-institution Retrospective Analysis
Authors: Testa Stefano , Bui Nam Q. , Ganjoo Kristen N.
Published: July 2023

Table S12 shows results of Cox proportional hazard analysis for progression-free survival for all treatment episodes combined, regardless of line of therapy in patients with malignant PEComa only.
Table S10 from Systemic Treatments and Molecular Biomarkers for Perivascular Epithelioid Cell Tumors: A Single-institution Retrospective Analysis
Authors: Testa Stefano , Bui Nam Q. , Ganjoo Kristen N.
Published: July 2023

Table S10 shows median clinical PFS from first-line therapy in months, as well as 5-year clinical PFS rate from first-line therapy in patients with malignant PEComa.
Figure S9 from Systemic Treatments and Molecular Biomarkers for Perivascular Epithelioid Cell Tumors: A Single-institution Retrospective Analysis
Authors: Testa Stefano , Bui Nam Q. , Ganjoo Kristen N.
Published: July 2023

Figure S9 shows Kaplan-Meier curves for combined clinical PFS in patients with malignant PEComas. Specifically, figure shows effects on combined clinical PFS of TFE3 positivity, treatment type, and TP53 and TSC1/TSC2 mutational status.
Figure S8 from Systemic Treatments and Molecular Biomarkers for Perivascular Epithelioid Cell Tumors: A Single-institution Retrospective Analysis
Authors: Testa Stefano , Bui Nam Q. , Ganjoo Kristen N.
Published: July 2023

Figure S8 shows combined clinical progression-free survival (cPFS) in the whole cohort comparing each mTOR inhibitors to other treatments.
Figure S5 from Systemic Treatments and Molecular Biomarkers for Perivascular Epithelioid Cell Tumors: A Single-institution Retrospective Analysis
Authors: Testa Stefano , Bui Nam Q. , Ganjoo Kristen N.
Published: July 2023

Figure S5 shows Kaplan-Meier Curves of Overall Survival for patients with Malignant PEComas treated with chemotherapy or mTOR inhibitors, and for patients with and without TP53 mutations, with and without TSC1/TSC2 mutations, and for those that are TFE3 positive versus TFE3 negative.
Figure S3 from Systemic Treatments and Molecular Biomarkers for Perivascular Epithelioid Cell Tumors: A Single-institution Retrospective Analysis
Authors: Testa Stefano , Bui Nam Q. , Ganjoo Kristen N.
Published: July 2023

Figure S3 shows a bar graph with the number of treatment episodes in each disease group classified based on type and line of treatment.
FIGURE 2 from Systemic Treatments and Molecular Biomarkers for Perivascular Epithelioid Cell Tumors: A Single-institution Retrospective Analysis
Authors: Testa Stefano , Bui Nam Q. , Ganjoo Kristen N.
Published: July 2023

OS and cPFS. A, Kaplan–Meier curve shows OS in patients treated with first-line chemotherapy versus mTOR inhibitors. B, Kaplan–Meier curve shows OS of patients with TFE3 positivity as detected through either IHC or FISH compared with those that were TFE3 negative. C, Kaplan–Meier curve shows cPFS from first-line treatment in patients that received chemotherapy compared with those treated with mTOR inhibitors. D, Kaplan–Meier curve shows cPFS from first-line treatment in patients with (TP53_MUT) and without (TP53_WT) a TP53 mutation. E, Kaplan–Meier curve showing cPFS for all treatment episodes regardless of line of therapy, and comparing chemotherapy, ICI, mTOR inhibitors, and other treatments. F, Kaplan–Meier curve shows cPFS for all treatment episodes regardless of line of therapy in patients that are TFE3 positive versus those that are TFE3 negative. log-rank P values are shown. Othera included: olaparib (n = 1), pazopanib (n = 1), pazopanib-everolimus (n = 1), anastrozole (n = 1), and levantinib-everolimus (n = 1). NR, not reachable.
Figure S6 from Remodeling of Stromal Immune Microenvironment by Urolithin A Improves Survival with Immune Checkpoint Blockade in Pancreatic Cancer
Authors: Mehra Siddharth , Garrido Vanessa T. , Dosch Austin R. , Lamichhane Purushottam , Srinivasan Supriya , Singh Samara P. , Zhou Zhiqun , De Castro Silva Iago , Joshi Chandrashekar , Ban Yuguang , Datta Jashodeep , Gilboa Eli , Merchant Nipun B. , Nagathihalli Nagaraj S.
Published: July 2023

PD-L1 expression in Uro A or PI3Ki treated KPC cells.
Figure S5 from Remodeling of Stromal Immune Microenvironment by Urolithin A Improves Survival with Immune Checkpoint Blockade in Pancreatic Cancer
Authors: Mehra Siddharth , Garrido Vanessa T. , Dosch Austin R. , Lamichhane Purushottam , Srinivasan Supriya , Singh Samara P. , Zhou Zhiqun , De Castro Silva Iago , Joshi Chandrashekar , Ban Yuguang , Datta Jashodeep , Gilboa Eli , Merchant Nipun B. , Nagathihalli Nagaraj S.
Published: July 2023

Cytokine profiling of PKT tumors and KPC cells treated with PI3Ki or Uro A.
Figure S1 from Remodeling of Stromal Immune Microenvironment by Urolithin A Improves Survival with Immune Checkpoint Blockade in Pancreatic Cancer
Authors: Mehra Siddharth , Garrido Vanessa T. , Dosch Austin R. , Lamichhane Purushottam , Srinivasan Supriya , Singh Samara P. , Zhou Zhiqun , De Castro Silva Iago , Joshi Chandrashekar , Ban Yuguang , Datta Jashodeep , Gilboa Eli , Merchant Nipun B. , Nagathihalli Nagaraj S.
Published: July 2023

Raw uncropped images of Western blot membranes for Figs.1e and 3d.
FIGURE 4 from Remodeling of Stromal Immune Microenvironment by Urolithin A Improves Survival with Immune Checkpoint Blockade in Pancreatic Cancer
Authors: Mehra Siddharth , Garrido Vanessa T. , Dosch Austin R. , Lamichhane Purushottam , Srinivasan Supriya , Singh Samara P. , Zhou Zhiqun , De Castro Silva Iago , Joshi Chandrashekar , Ban Yuguang , Datta Jashodeep , Gilboa Eli , Merchant Nipun B. , Nagathihalli Nagaraj S.
Published: July 2023

PD-1/PD-L1 expression in the PDAC TME with Uro A treatment. A, Immunofluorescence-based histologic analysis depicting PD-L1–positive cells within pancreatic tumor sections harvested from vehicle or Uro A-treated PKT mice. Mean of positive cells per field of view within the tumor area for each mouse is shown in adjacent plot, n = 4 mice per group. B, Western blot analysis demonstrating PD-L1 protein expression in whole pancreatic tumor lysates from vehicle- or Uro A-treated PKT mice. C, Flow cytometric analysis of PD-L1 expression in the macrophage population with representative PD-L1 histogram overlay of vehicle- and Uro A-treated PKT mice (right). Flow cytometric analysis of PD-1 expression on CD4+ T cells (D) and CD8+ T cells (E) with representative PD-1 histogram overlay of vehicle- and Uro A-treated groups (right) of pancreatic tumors from PKT mice. Individual datapoints with mean ± SEM are shown and compared by two-tailed unpaired t test. *, P < 0.05; ***, P < 0.001; ns, P > 0.05; MFI, mean fluorescence intensity.
FIGURE 3 from Remodeling of Stromal Immune Microenvironment by Urolithin A Improves Survival with Immune Checkpoint Blockade in Pancreatic Cancer
Authors: Mehra Siddharth , Garrido Vanessa T. , Dosch Austin R. , Lamichhane Purushottam , Srinivasan Supriya , Singh Samara P. , Zhou Zhiqun , De Castro Silva Iago , Joshi Chandrashekar , Ban Yuguang , Datta Jashodeep , Gilboa Eli , Merchant Nipun B. , Nagathihalli Nagaraj S.
Published: July 2023

Uro A treatment reduces immunosuppressive TAM populations, facilitates intratumoral T-cell infiltration and controls PDAC growth in a T cell–dependent manner. Single-cell suspensions of pancreatic tumors obtained from PKT mice treated with vehicle or Uro A were subjected to immunophenotyping analysis. Flow cytometric analysis demonstrating significant reduction in the percentage (%) of TAMs (CD11b+ F4/80+; A), and M2-like (F4/80+Arg1+CD206+; B) macrophages with Uro A as compared with vehicle mice. C, Comparison of mean fluorescence intensity (MFI) of MHCII expression on CD11b+ F4/80+ macrophages between vehicle- and Uro A-treated mice with representative MHCII histogram (right). Flow cytometric assessment of the tumor-infiltrating adaptive immune compartment depicting frequency of total T cells (CD45+ TCRβ+; D), CD4+ T cells (CD45+ TCRβ+ CD4+; E), CD8+ T cells (CD45+ TCRβ+ CD8+; F), CD8/Treg ratio (G), and frequency of naïve (CD62L+ CD44−), central memory (CD62L+ CD44+), and effector memory (CD62L− CD44+) in CD4+ (H) and CD8+ (I) T cells in mice treated with vehicle or Uro A. J, Schematic representation of PKT GEMM treated with vehicle, Uro A, or Uro A following T-cell depletion with anti-CD4 and anti-CD8 antibodies. K, Pancreas weight comparison among vehicle- and Uro A-treated mice with or without T-cell depletion. L, Kaplan–Meier plot and log-rank test analysis showing impaired antitumor efficacy of Uro A treatment in PKT mice subjected to T-cell depletion compared with non–T cell–depleted Uro A- and vehicle-treated mice. Individual datapoints with mean ± SEM are shown and compared by two-tailed unpaired t test. *, P < 0.05; **, P < 0.01; ****, P < 0.0001; ns, P > 0.05.
ЕКСТРЕНА ПРОФІЛАКТИКА СКАЗУ ТА ЇЇ УСКЛАДНЕННЯ
Authors: Копча В. С.
Published: July 2023

Наведено відомості про епідеміологію, патогенез, клініку сказу у тварин і людей, а також екстрену специфічну профілактику цієї хвороби. На прикладі клінічного випадку показана можливість розвитку сироваткової хвороби після використання гетерологічного антирабічного імуноглобуліну, а також виникнення цього ускладнення у разі використання зазначеного препарату без достатніх на це показань.
ЦИФРОВІ МЕДІА ТА ЇХ ВПЛИВ НА ДІТЕЙ ПІДЛІТКОВОГО ВІКУ
Authors: Бондарчук Н. Б. , Гордійчук С. В. , Шатило В. Й. , Горай О. В. , Поплавська С. Д.
Published: July 2023

Мета: проаналізувати цифрові та соціальні медіа і виявити ризики та вплив на життя та здоров’я дітей підліткового віку, розкрити значення інформаційно-комунікативних технологій у процесі деформації ціннісних орієнтирів.

Матеріали і методи. Використані матеріали досліджень вітчизняних та іноземних авторів, а також особисті дослідження серед дітей підліткового віку.

Результати. У сучасному інформаційному суспільстві, що базується на найновіших технологіях, засоби масової інформації мають як позитивний, так і негативний вплив на підлітків. Позитивні аспекти полягають у збагаченні знань та розширенні світогляду, але деякі підлітки використовують їх як засіб проведення вільного часу. Одним із можливих рішень для зменшення негативного впливу ЗМІ є розвиток критичного мислення, яке допоможе підліткам свідомо сприймати та аналізувати інформацію з урахуванням власних потреб, інтересів та цінностей. Таким чином, освіта повинна відігравати провідну роль у формуванні такої здатності у підлітків. Дослідження показали, що вплив соціальних медіа на здоров’я дітей і молодих людей був найбільшим на психічне здоров’я, зокрема у сферах самооцінки та благополуччя, з проблемами, пов’язаними з кіберзалякуванням і «депресією у Facebook», із зв’язком між використанням соціальних медіа й самооцінкою та образом тіла.

Висновки. Проведеним дослідженням виявлені позитивні результати для молоді, яка використовує різні види цифрових технологій, які проявляються в процесі соціалізації, отриманні знань про здоров’я, покращенні загального розвитку й успішності, опануванні додаткових навичок. Негативними результатами є гіподинамія, депресія, витіснення суспільно значущих цінностей, непоодинокі факти кіберзалякування, сексуальні домагання. Нові цифрові та соціальні медіа полегшують і сприяють соціальній взаємодії, участі та залученню, що включає як споживання, так і створення контенту. Однак наслідки використання медіа мають багатофакторний характер і залежать від типу медіа, обсягу використання та особливостей окремої дитини чи підлітка, які використовують медіа.
МОНІТОРИНГ СТАНУ ЗДОРОВ’Я ЯК ОСНОВНИЙ ЕЛЕМЕНТ ВИЗНАЧЕННЯ ПРОБЛЕМ ГРОМАДСЬКОГО ЗДОРОВ’Я В УКРАЇНІ
Authors: Романюк Н. Є. , Романюк Л. М. , Нагорна О. П.
Published: July 2023

Мета: розробити концептуальні підходи до організації та здійснення моніторингу стану здоров’я як основного механізму визначення проблем громадського здоров’я. Проаналізувати сучасні методики планування, розробки і впровадження системи моніторингу та оцінки покращення превентивних заходів у сфері громадського здоров’я на локальному рівні з урахуванням глобальних викликів і системних змін.

Матеріали і методи. В дослідженні використані такі методи: статистичні, викопіювання статистичних даних, метод експертних оцінок і динамічний аналіз.

Дослідження проведено на основі аналізу звітів комунального некомерційного підприємства «Тернопільський обласний центр громадського здоров’я» Тернопільської обласної ради, статистичних довідників центру медичної статистики МОЗ України, оперативної та довідкової інформації центру громадського здоров’я МОЗ України, стратегічних положень «Про систему громадського здоров’я».

Результати. Головними функціями системи та центрів громадського здоров’я є профілактика захворювань як на індивідуальному, так і на популяційному рівнях. Новостворені державні установи у сфері громадського здоров’я повинні зосереджувати свою діяльність на профілактику, безперервний моніторинг інфекційних та основних неіфекційних хвороб, які становлять значний тягар для суспільства і спричиняють значні соціально-економічні втрати. У сучасних умовах загрозливих викликів та наслідків, пов’язаних з існуючою пандемією Covid-19 та поглибленням негативних світових економічних проблем, особливо зростає роль функціонального забезпечення діяльності установ у сфері охорони громадського здоров’я.

Висновки. Проведений аналіз та моніторинг діяльності центру показали наявність загрозливих тенденцій у стані здоров’я населення області. З року в рік фіксується зменшення чисельності населення області, зростання показників смертності та захворюваності і зниження рівня народжуваності. Також у роботі шляхом моніторингу чітко визначені стратегічні завдання та перспективи розвитку центрів громадського здоров’я в Україні.