bluuebunny/crossref_metadata_2025 huggingface dataset:
Supplementary Figure 3 from Sources of Disparities in Surveillance Mammography Performance and Risk-Guided Recommendations for Supplemental Breast Imaging: A Simulation Study
Authors: Hubbard Rebecca A. , Pujol Toyya A. , Alhajjar Elie , Edoh Kossi , Martin Melissa L.
Published: July 2023

Supplementary Figure 3. Simulation results for surveillance mammography positive predictive value overall and stratified by race and ethnicity in simulated populations of women with a personal history of breast cancer
Supplementary Table S5 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 S5 shows results of univariate analysis for 77 chronically elevated serum alanine aminotransferase (cALT)-defined nonalcoholic fatty liver disease in the Pancreatic Cancer Case-Control Consortium (PanC4) data
Supplementary Table S4 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 S4 shows results of univariate analysis for 17 imaging and biopsy validated SNPs in the PanScan sample
Supplementary Table S6 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

Mean, SD of the multiple PRS (PRS38_ASN+PRS190_EB) and the integrated model (PRS38_ASN+PRS190_EB+NGRF) at age 80, stratified by percentiles
Supplementary Table 3 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 3: History of exposure to proton-pump inhibitors (PPIs) among cases and controls, according to different exposure definitions.
Data from Association between Sleep Duration and Colorectal Adenomas: Findings from a Case–Control Study in Vietnam
Authors: Tran Chi Thi-Du , Paragomi Pedram , Tran Mo Thi , Nguyen Mai Vu-Tuyet , Tuong Thuy Thi-Van , Tran Quang Hong , Le Linh Cu , Pham Huong Thi-Thu , Ha Hien Thi-Thu , Bui Nam Chi , Vu Hien Huy , Ta Phuong Que , Shrubsole Martha J. , Cai Qiuyin , Ye Fei , Le Song Huu , Vu Khien Van , Tran Huong Thi-Thanh , Tran Thuan Van , Boffetta Paolo , Shu Xiao-Ou , Luu Hung N.
Published: July 2023

AbstractBackground:
Colorectal cancer is one of the leading cancers worldwide and in Vietnam. Adenomas are important precursors of colorectal cancer. Study on the association between sleep duration and development of colorectal adenoma (CRA) is limited, particularly among Vietnamese population.
Methods:
We conducted an individually matched case–control study of 870 CRA cases and 870 controls in a large-scale colorectal screening program involving 103,542 individuals ages ≥40 years old in Hanoi, Vietnam. Sleep duration was categorized in three groups: short: ≤6 hours/day, normal: 7 to 8 hours/day, and long: >8 hours/day. Conditional logistic regression was used to evaluate the association between sleep duration and adenomas risk after controlling for potential confounders.
Results:
Overall, short-sleep duration was associated with increased risk of having CRA compared with normal duration [OR, 1.48; 95% confidence interval (CI), 1.12–1.97]. This pattern was present in both females (OR, 1.58; 95% CI, 1.14–2.18) and males (OR, 1.45; 95% CI, 1.08–1.93), with advanced adenomas (OR, 1.61; 95% CI, 1.09–2.38) and non-advanced adenomas (OR, 1.66; 95% CI, 1.19–2.32). Furthermore, the association between CRA development and short-sleep duration was more apparent among females who were nondrinker, nonobese, physically active, with proximal or both sided adenomas and with cardiometabolic disorder. Among males, the short-sleep duration was associated with CRA risk among never-smoking, cardiometabolic disorders, and obese.
Conclusions:
Short-sleep duration was associated with increased prevalence of both advanced and non-advanced CRAs among Vietnamese population.
Impact:
Findings from this study showed that maintaining an adequate sleep duration may have an important implication for colorectal adenoma prevention and control.
Data from Associations of Dietary Patterns with Colorectal Adenomas in the Prostate, Lung, Colorectal and Ovarian Cancer (PLCO) Cohort
Authors: Nepal Sushma , Aslani Zahra , Shi Ni , Tabung Fred K.
Published: July 2023

Abstract
Background: Most Colorectal cancers arise from adenomas, and though insulinemic and inflammatory dietary patterns have been associated with colorectal cancer risk, these dietary patterns have not been studied in relation to adenoma risk.
Methods: Using data from 21,192 participants in the Prostate, Lung, Colorectal, and Ovarian (PLCO) Cancer screening cohort, we calculated the Empirical Dietary Index for Hyperinsulinemia (EDIH), Empirical Dietary Inflammatory Pattern (EDIP) and overall dietary quality measured via the Healthy Eating Index (HEI-2015), from food frequency questionnaires (FFQ). In multivariable-adjusted logistic regression, we investigated associations of these dietary indices with adenoma (any adenoma, advanced adenoma, n=19,493), and recurrent adenoma (n=1,699).
Results: EDIH was not associated with adenoma or advanced adenoma but was marginally associated with recurrent adenoma. The OR (95%CI) comparing highest (lowest insulinemic) versus lowest (most hyperinsulinemic) quintiles was 0.76 (0.55, 1.05) after multivariable adjustment including BMI. EDIP and HEI-2015 were not associated with any of the three outcomes.
Conclusions: In the PLCO cohort, we did not observe substantial associations between dietary patterns and risk of colorectal adenomas.
Impact: Pending confirmation in larger prospective studies, our findings suggest that these dietary patterns may not substantially affect colorectal cancer risk via the adenoma-carcinoma sequence.
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

Abstract
Background: 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 utilizing 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 odds ratios (ORs) and 95% confidence intervals (CIs) of the risk of PDAC adjusted for age and sex. We examined multiplicative interactions of ABO with secretor status and Lewis group by considering each product term between ABO and secretor and between ABO and Lewis group individually.

Results: We found that the increased risk associated with non-O blood groups was somewhat stronger among secretors than non-secretors (ORs 1.28 [95% CI: 1.15-1.42] and 1.17 [95% CI: 1.03-1.32] respectively; interaction p-value = 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.
Socioeconomic Status at Birth and Breast Tissue Composition in Adolescence and Adulthood
Authors: Kehm Rebecca D. , Lilge Lothar , Walter E. Jane , White Melissa , Herbstman Julie B. , Perera Frederica P. , Miller Rachel L. , Terry Mary Beth , Tehranifar Parisa
Published: July 2023

Background:

Socioeconomic status (SES) at birth is associated with breast cancer risk. Whether this association is driven by changes in breast tissue composition (BTC) prior to adulthood remains unclear.

Methods:

We used multivariable linear regression models to examine whether SES at birth is associated with BTC in adolescence and adulthood using data from a New York City cohort of daughters (n = 165, 11–20 years) and mothers (n = 160, 29–55 years). We used maternal-reported data on daughters’ household income and maternal education at birth, analyzed individually and in combination (SES index). Women also reported their own mothers’ education at birth. We used optical spectroscopy to evaluate BTC measures that positively (water content, collagen content, optical index) and negatively (lipid content) correlate with mammographic breast density, a recognized breast cancer risk factor.

Results:

Being in the highest versus lowest category of the SES index was associated with lower lipid content [βadjusted (βadj) = −0.80; 95% confidence interval (CI), −1.30 to –0.31] and higher collagen content (βadj = 0.54; 95% CI, 0.09–0.99) in adolescence. In women with a body mass index (BMI) <30 kg/m2, higher maternal education at birth (≥ vs. < high school degree) was associated with lower lipid content (βadj = −0.57; 95% CI, −0.97 to −0.17), higher water content (βadj = 0.70; 95% CI, 0.26–1.14), and higher optical index (βadj = 0.53; 95% CI, 0.10–0.95).

Conclusions:

This study supports that SES at birth is associated with BTC in adolescence and adulthood, although the latter association may depend on adult BMI.

Impact:

Further research is needed to identify the socially patterned early life factors influencing BTC.
Supplementary Figures 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 Figures
Data 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

AbstractPurpose:
Adenoid cystic carcinoma (ACC) is a heterogeneous malignancy, and no effective systemic therapy exists for metastatic disease. We previously described two prognostic ACC molecular subtypes with distinct therapeutic vulnerabilities, ACC-I and ACC-II. In this study, we explored the ACC tumor microenvironment (TME) using RNA-sequencing and spatial biology to identify potential therapeutic targets.
Experimental Design:
Tumor samples from 62 ACC patients with available RNA-sequencing data that had been collected as part of previous studies were stained with a panel of 28 validated metal-tagged antibodies. Imaging mass cytometry (IMC) was performed using the Fluidigm Helios CyTOF instrument and analyzed with Visiopharm software. The B7-H4 antibody–drug conjugate AZD8205 was tested in ACC patient-derived xenografts (PDX).
Results:
RNA deconvolution revealed that most ACCs are immunologically “cold,” with approximately 30% being “hot.” ACC-I tumors with a poor prognosis harbored a higher density of immune cells; however, spatial analysis by IMC revealed that ACC-I immune cells were significantly restricted to the stroma, characterizing an immune-excluded TME. ACC-I tumors overexpressed the immune checkpoint B7-H4, and the degree of immune exclusion was directly correlated with B7-H4 expression levels, an independent predictor of poor survival. Two ACC-I/B7-H4-high PDXs obtained 90% complete responses to a single dose of AZD8205, but none were observed with isotype-conjugated payload or in an ACC-II/B7-H4 low PDX.
Conclusions:
Spatial analysis revealed that ACC subtypes have distinct TMEs, with enrichment of ACC-I immune cells that are restricted to the stroma. B7-H4 is highly expressed in poor-prognosis ACC-I subtype and is a potential therapeutic target.
Data 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

AbstractBackground:
Pure pancreatic acinar cell carcinomas (PACC) are rare malignancies with no established treatment. PACC demonstrates significant genetic intertumoral heterogeneity with multiple pathways involved, suggesting using targeted cancer therapeutics to treat this disease. We aggregated one of the largest datasets of pure PACC to examine the genomic variability and explore patient-specific therapeutic targets.
Methods:
PACC specimens (n = 51) underwent next-generation sequencing of DNA (n = 29) or whole exome (n = 22) and RNA (whole transcriptome, n = 29) at a commercial laboratory. We performed comparative analyses of a genomic cohort of pancreatic ductal adenocarcinomas (PDAC; n = 4,205). In parallel, we conducted a retrospective review of patients with PACC treated at Huntsman Cancer Institute (HCI).
Results:
The real-world dataset included samples from 51 patients with PACC. We found key molecular differences between pure PACC and PDAC, highlighting the unique characteristics of pure PACC. Major differences in PACC include lower MAPK signaling and less stromal cell abundance compared with PDAC. Pure PACC showed genomic loss-of-heterozygosity to largely coincide with mutations in BRCA1, BRCA2, and PALB2. Of the 7 patients treated at HCI, one had a tumor that harbored a BRAF-V600E mutation. Leveraging precision oncology, this patient is being treated with encorafenib plus binimetinib, achieving an exceptionally durable and ongoing complete response of more than 3 years.
Conclusions:
There are major differences between PACC and PDAC, including downregulation of the MAPK signaling pathway, and less stromal cell abundance. In addition, genomic characterization of pure PACC revealed frequent targetable alterations, which can guide patient treatment.
Table S1 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 the IHC staining of HCK in ovarian cancer tissue microarrays.
Fig S4 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

The effect of GSIs on NOTCH3 ICD expression in HGSOC cells following HCK overexpression.
Fig 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

Cell line selection and engineering
Fig 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

The source of elevated HCK signature is not due to a bias in tumor purity or immune infiltration.
Supplementary Table 4 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

Supplementary Table 4. The Chi-squared and Fisher's Exact tests of metastases in the group of mice with orthotopic tumor.
Supplementary Table 3 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

Supplementary Table 3. The detailed information about orthotopic surgery, tumor sizes, and metastases.
Supplementary Table 1 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

Supplementary Table 1. Combinations of Abs used for IHC experiments.
Supplementary Methods and Materials 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

Supplementary Methods and Materials
Supplementary Figure 8 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 S8. AST (A) and ALT (B) serum activity from the indicated mice. ALT and AST activity were examined using the ALT Assay Kit (Abcam, ab241035) and the AST Assay Kit (Abcam, ab105135), respectively, per the manufacturer's protocol. Kruskal-Wallis test, all p>0.05, mean ± SD; n represents number of mice tested.
Supplementary Figure 7 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 7 shows that the transduction of miR-143-3p did not affect tumor growth in a murine model of ovarian cancer.
Supplementary Figure 10 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 S10. (A) Evaluation of MGAT5-mediated Integrin αv glycosylation in the orthotopic tumor samples. Tissue samples were co-stained with Integrin αv (green) and Cy3 labeled PHA-L lectin (red). Representative Z-stack images were collected by SIM and reconstructed using Imaris for clarity. (B) Mander's colocalization between red and green in the samples from A. Kruskal-Wallis test; n indicates the number of foci counted. For all statistics: median ± SD, ****p<0.0001, ***p<0.001, **p<0.005, *p<0.05. (C) Evaluation of MGAT3-mediated Integrin αv glycosylation in the orthotopic tumor samples. Tissue samples were co-stained with Integrin αv (green) and Cy3 labeled PHA-E lectin (red). Representative Z-stack images were collected by SIM and reconstructed using Imaris for clarity; bars, 3 µm. (D) Mander's colocalization between red and green in the samples from C. Kruskal-Wallis test; n indicates the number of foci counted; mean ± SD, ****p<0.0001, **p<0.01, and *p<0.05.
Supplementary Figure 3 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 3 shows the correlation analysis between miR-10a-5p expression and PAI-1 concentration.
Supplementary Figure Legends 1-6 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

Supplementary Figure Legends 1-6
Supplementary Figure 4 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

S4. OSM-expressing cells are distinct from CD44HI/mesenchymal cells created by EMT transcription factors.
Supplementary Figure 6 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

Mineralization assay co-cultured with MCF7 cells.
Supplementary Figure 2 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

S2. Kaplan Meier comparison of IL-6 family member receptors.
Supplementary Figure 1 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

S1. OSM induces tumor initiation.
Supplementary Figure 4 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

Extraction of c-Jun-regulated bone metastasis gene signatures from the MCF7 cell lines.
Supplementary Figure 3 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

c-Jun expression is heterogeneous in BM section.
Supplementary Figure 2 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

TAM67 suppressed osteolytic bone metastasis of MCF7-BM02 cells.
Supplementary Figure 1 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

Characterization of c-Jun overexpression in MCF7-BM cells.
Supplementary Figure 5 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

S5. Targeting Polθ + PARP1 and Polθ + RAD52 induced dual synthetic lethality against HR-deficient leukemia cells.
Supplementary Figure 5 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

S5. Hypoxia shows no contribution to the NRF2 regulated histone acetylation.
Supplementary Figure 3 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

S3. Nrf2 ablation shows no effect on the levels of acetyl-CoA or CoASH in tumor adjacent liver tissues.
Supplementary Figure 2 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

S2. Nrf2 ablation affects gene expression in mouse liver tumors.
Supplemental material and methods 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 material and methods
Supplementary Fig S4 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 deletion results in unchanged H4K16 Acetylation levels upon DSB induction.
Supplementary Fig S2 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 from drug-induced cytotoxicity, independently of its ability to interact with its cognate partners.
Data 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

Abstract
Although bevacizumab (BEV) plays a key role in ovarian cancer treatment, BEV resistance is often observed in clinical settings. This study aimed to identify the genes responsible for BEV resistance. C57BL/6 mice inoculated with ID-8 murine ovarian cancer cells were treated with anti-VEGFA antibody or IgG (control) twice weekly for 4 weeks. The mice were sacrificed, then, RNA was extracted from the disseminated tumors. qRT-PCR assays were performed to identify angiogenesis-related genes and miRNAs that were altered by anti-VEGFA treatment. SERPINE1/PAI-1 was found to be upregulated during BEV treatment. Therefore, we focused on miRNAs to elucidate the mechanism underlying the upregulation of PAI-1 during BEV treatment. Kaplan–Meier plotter analysis revealed that higher expression levels of SERPINE1/PAI-1 were associated with poor prognoses among BEV-treated patients, suggesting that SERPINE1/PAI may be involved in the acquisition of BEV resistance. miRNA microarray analysis followed by in silico and functional assays revealed that miR-143-3p targeted SERPINE1 and negatively regulated PAI-1 expression. The transfection of miR-143-3p suppressed PAI-1 secretion from ovarian cancer cells and inhibited in vitro angiogenesis in HUVECs. Next, miR-143-3p-overexpressing ES2 cells were intraperitoneally injected into BALB/c nude mice. ES2-miR-143-3p cells downregulated PAI-1 production, attenuated angiogenesis, and significantly inhibited intraperitoneal tumor growth following treatment with anti-VEGFA antibody. Continuous anti-VEGFA treatment downregulated miR-143-3p expression, which upregulated PAI-1 and activated an alternative angiogenic pathway in ovarian cancer. In conclusion, the substitution of this miRNA during BEV treatment may help overcome BEV resistance, and this may be used as a novel treatment strategy in clinical settings.
Implications:
Continuous administration of VEGFA antibody upregulates SERPINE1/PAI-1 expression via the downregulation of miR-143-3p, which contributes to acquiring bevacizumab resistance in ovarian cancer.
Data 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

Abstract
Patients diagnosed with Pancreatic Ductal Adenocarcinoma (PDAC) frequently present with advanced metastatic disease and exhibit a poor response to therapy, resulting in poor outcomes. The tumor microenvironment cytokine Oncostatin-M (OSM) initiates PDAC plasticity, inducing the reprogramming to a stem-like/mesenchymal state, which enhances metastasis and therapy resistance. Using a panel of PDAC cells driven through epithelial-mesenchymal transition (EMT) by OSM or the transcription factors ZEB1 or SNAI1, we find that OSM uniquely induces tumor-initiation and gemcitabine resistance independently of its ability to induce a CD44HI/mesenchymal phenotype. In contrast, while ZEB1 and SNAI1 induce a CD44HI/mesenchymal phenotype and migration comparable to OSM, they are unable to promote tumor-initiation or robust gemcitabine resistance. Transcriptomic analysis identified that OSM-mediated stemness requires MAPK activation and sustained, feed-forward transcription of OSMR. MEK and ERK inhibitors prevented OSM-driven transcription of select target genes and stem-like/mesenchymal reprogramming, resulting in reduced tumor growth and re-sensitization to gemcitabine. We propose that the unique properties of OSMR, which hyperactivates MAPK signaling when compared to other IL-6 family receptors, make it an attractive therapeutic target, and that disrupting the OSM-OSMR-MAPK feed-forward loop may be a novel way to therapeutically target the stem-like behaviors common to aggressive PDAC.

Implications: Small molecule MAPK inhibitors may effectively target the OSM/OSMR-axis that leads to EMT and tumor initiating properties that promote aggressive PDAC.
Table 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

Table S9 shows Cox proportional hazard analysis results for clinical progression-free survival from first-line therapy in patients with malignant PEComa.
TABLE 3 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

Cox PH analysis for PFS from first-line treatment
TABLE 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

Cox PH analysis for OS
TABLE 1 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

Baseline patient characteristics
Figure S6 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 S6 shows Kaplan-Meier curves for clinical PFS from first-line therapy in patients with PEComas, and specifically effect of TFE3 positivity, TSC1/TSC2 mutational status, and uterine versus extra-uterine location on clinical PFS.
Figure 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

Figure S10 shows a Kaplan-Meier curve that represents effects of different treatments on combined clinical PFS only in patients with malignant PEComa.
FIGURE 1 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

Best change in maximum tumor dimension for treatment episodes regardless of line of therapy. Waterfall plot shows the percent change in the sum of maximum tumor diameters pretreatment and posttreatment for the 40 treatment episodes for which radiographic imaging was directly available for assessment of response based on RECIST 1.1. The bars are color coded on the basis of the type of treatment. Information about TSC1/TSC2 and TP53 mutational status is shown for each patient, where available, and as described in the legend. Patients with epithelioid AML are indicated with an asterisk while those with a diagnosis of tuberous sclerosis complex are indicated with a hexagon. TFE3 + indicates both patients with TFE3 gene rearrangement or amplification on FISH as well as those with TFE3 protein overexpression on IHC. AML: angiomyolipoma; ICI: immune checkpoint inhibitors; LAM: lymphangioleiomyomatosis; PEComa: perivascular epithelioid cell tumors; XRT: radiotherapy.
Supplementary Tables S1-S2 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

Primary antibodies for flow cytometry, immunohistochemistry and Western blot analysis.
Figure S2 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. 2e, 2f, S3a and S3b.
FIGURE 5 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

Addition of αPD-1 blockade to Uro A treatment further decreases PDAC tumor burden and improves overall survival in PKT mice. A, Schematic representation of PKT mice treated with vehicle, Uro A, or Uro A in combination with aPD-1. B, Kaplan–Meier plot and log-rank test analysis showing superior survival of PKT mice treated with Uro A in combination with aPD-1 when compared with all other groups. C, Representative H&E-stained tumor sections after 3 weeks of drug treatment depicting significant presence of normal pancreatic architecture (highlighted in green) in PKT mice treated with combination therapy of Uro A and αPD-1 as compared with other treatment cohorts (scale bar = 50 μm). D, Percentage of tumor area (brown bar) relative to the normal pancreas (green bar) quantified within the whole pancreas, by capturing multiple fields of view in lower magnification. E–J, Flow cytometric assessment of the tumor-infiltrating adaptive immune compartment in mice treated with vehicle, Uro A (same mice cohort used in previous figures) or Uro A+aPD-1 depicting frequency of CD4+ (E) and CD8+ (F) T cells naïve, central memory, and effector memory populations. PD-1 MFI expression in CD8+ T cells (G) and PD-1 MFI expression in CD4+ T cells (H). Flow cytometric analysis of tumor-infiltrating effector memory CD4+ T cells showing frequency of Tregs (I), and Th1 (J) cells in mice treated with vehicle, Uro A or Uro A+aPD-1. Individual datapoints with mean ± SEM are shown and compared by one-way ANOVA test. *, P < 0.05; **, P < 0.01; ***, P < 0.001; ****, P < 0.0001; ns, P > 0.05.
FIGURE 2 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

Treatment with PI3Ki (Omipalisib) recapitulates antitumor and immunomodulatory benefits of Uro A in PDAC. A, Schematic of PI3Ki (Omipalisib) treatment in PKT mice. B, Pancreas weight analysis of PI3Ki- or vehicle-treated PKT mice, n = 3–4 mice/group. C, Representative H&E-stained tumor sections in PI3Ki-treated mice and vehicle-treated mice. D, Cytokine array profiling of pancreatic tumor tissues harvested from PKT mice treated with PI3Ki or vehicle. Western blot analysis demonstrating decreased phosphorylation of AKT (band marked by red arrow) in murine KPC PDAC tumor cell line upon PI3Ki (0–10 μmol/L; E) and Uro A (0–75 μmol/L; F) treatment for 3 hours. G, Representative heat map showing fold change of immunomodulatory gene transcripts (qPCR analysis) associated with PI3Ki (1 μmol/L) or Uro A (25 μmol/L) treatment in KPC PDAC tumor cells for 3 hours. Individual datapoints with mean ± SEM are shown and compared by two-tailed unpaired t test; *, P < 0.05.
Data 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

Pancreatic ductal adenocarcinoma (PDAC) is a significant contributor to cancer-related morbidity and mortality, and it is known for its resistance to conventional treatment regimens, including chemotherapy and immune checkpoint blockade (ICB)-based therapies. We have previously shown that Urolithin A (Uro A), a gut microbial metabolite derived from pomegranates, can target and inhibit KRAS-dependent PI3K/AKT/mTOR signaling pathways to overcome therapeutic resistance and improve survival in PDAC. However, the effect of Uro A on the tumor immune microenvironment and its ability to enhance ICB efficacy has not been explored. This study demonstrates that Uro A treatment reduces stromal fibrosis and reinvigorates the adaptive T-cell immune response to overcome resistance to PD-1 blockade in a genetically engineered mouse model (GEMM) of PDAC. Flow cytometric–based analysis of Uro A-treated mouse tumors revealed a significant attenuation of immunosuppressive tumor-associated M2-like macrophages with a concurrent increase in the infiltration of CD4+ and CD8+ T cells with memory-like phenotype along with reduced expression of the exhaustion-associated protein, PD-1. Importantly, the combination of Uro A treatment with anti-PD-1 immunotherapy promoted enhancement of the antitumor response with increased infiltration of CD4+ Th1 cells, ultimately resulting in a remarkable improvement in overall survival in GEMM of PDAC. Overall, our findings provide preclinical evidence for the potential of Uro A as a novel therapeutic agent to increase sensitivity to immunotherapy in PDAC and warrant further mechanistic exploration in preclinical and clinical studies.
Significance:
Immunotherapeutic agents are ineffective against pancreatic cancer, mainly due to the immunosuppressive tumor microenvironment and stromal desmoplasia. Our current study demonstrates the therapeutic utility of a novel gut microbial metabolite, Uro A, to remodel the stromal-immune microenvironment and improve overall survival with anti-PD-1 therapy in pancreatic cancer.
СУЧАСНИЙ ПОГЛЯД НА ВИДОВИЙ СПЕКТР ЗБУДНИКІВ «КЛАСИЧНИХ» ІНФЕКЦІЙНИХ БАКТЕРІЙНИХ ХВОРОБ
Authors: Корнійчук О. П. , Надрага О. Б. , Мотика О. І.
Published: July 2023

Представлено сучасні погляди на «класичні» інфекційні хвороби на прикладі дифтерії, кашлюка, бешихи та псевдомембранозного коліту, спричиненого Clostridium difficile. Розглядаються таксономічні аспекти та роль молекулярно-генетичних методів у дослідженні факторів патогенності бактерій.
Проаналізовано дані останніх років, на підставі яких до збудників інфекційних хвороб людини включають нові види бактерій. Так, розглядається розширення кола збудників кашлюкоподібних захворювань, зокрема значення Bordetella holmensii в розвитку хвороби. Останніми роками переглядається структура виду Corynebacterium diphtheriae, сформувалась думка про «комплекс видів збудників дифтерії». Проілюстровано приклади протилежної ситуації, коли застосування молекулярних методів дало змогу звузити коло імовірних збудників для інфекцій із схожими клінічними картинами. Відповідно до результатів досліджень останніх років, роль інших видів, крім Streptococcus pyogenes, у виникненні бешихи видається дискусійною. Для псевдомембранозного коліту основним етіологічним агентом визначено Clostridium difficile.
АНАЛІЗ ОСОБЛИВОСТЕЙ ПЕРЕБІГУ COVID-19 У ПАЦІЄНТІВ ІЗ МЕТАБОЛІЧНИМИ ПОРУШЕННЯМИ
Authors: Антонюк О. Я.
Published: July 2023

Мета: виділення прогностичних критеріїв тяжкого перебігу COVID-19 у пацієнтів із метаболічними порушеннями залежно від індексу маси тіла, віку і наявної коморбідної патології, клініко-лабораторних даних.
Матеріали і методи. Методи дослідження: системного підходу, медико-статистичний, структурно-логічного аналізу, клінічні методи, лабораторні, інструментальні.
Результати. Виявлено високу частоту метаболічної патології, зокрема частоти цукрового діабету та гіперглікемії у пацієнтів із тяжким перебігом коронавірусного захворювання, що потребує корекції ризику як на індивідуальному, так і на популяційному рівнях. Надмір жирової тканини в організмі людини є модифікованим фактором, на відміну від віку і статі.
Висновки.
1. Надання медичної допомоги в умовах масових санітарних втрат під час пандемії потребувало ранжування пацієнтів за індивідуальним ризиком. Триває пошук засобів оцінки предикторів тяжкого перебігу коронавірусної хвороби.
2. При коронавірусній хворобі механізм впливу визначається як прямою дією вірусу на органи-мішені, так і опосередковано через імунне запалення. Рівень фонового хронічного запалення до початку коронавірусного захворювання у пацієнтів із метаболічними порушеннями із надміром жирової тканини є незалежним фактором ризику і потребує вчасного призначення терапії, а також оцінки груп ризику, що потребують госпіталізації.
3. Тактика лікування пацієнтів залежить від вихідної оцінки антропометричних даних, вихідних клініко-лабораторних даних та наявної супутньої патології.