bluuebunny/crossref_metadata_2025 huggingface dataset:
Supplementary Table S1 from Serum Lipidome Profiling Reveals a Distinct Signature of Ovarian Cancer in Korean Women
Authors: Sah Samyukta , Bifarin Olatomiwa O. , Moore Samuel G. , Gaul David A. , Chung Hyewon , Kwon Sun Young , Cho Hanbyoul , Cho Chi-Heum , Kim Jae-Hoon , Kim Jaeyeon , Fernández Facundo M.
Published: May 2024

Supplementary Table S1 shows Matched Cohort Characteristics.
Supplementary Figure 7 from Diffsig: Associating Risk Factors with Mutational Signatures
Authors: Park Ji-Eun , Smith Markia A. , Van Alsten Sarah C. , Walens Andrea , Wu Di , Hoadley Katherine A. , Troester Melissa A. , Love Michael I.
Published: May 2024

This figure shows TCGA results with a different set of breast cancer signatures
Supplementary Figure 6 from Diffsig: Associating Risk Factors with Mutational Signatures
Authors: Park Ji-Eun , Smith Markia A. , Van Alsten Sarah C. , Walens Andrea , Wu Di , Hoadley Katherine A. , Troester Melissa A. , Love Michael I.
Published: May 2024

This figure shows the evaluation results of false positives with simulation data on Diffsig
Supplementary Data from Diffsig: Associating Risk Factors with Mutational Signatures
Authors: Park Ji-Eun , Smith Markia A. , Van Alsten Sarah C. , Walens Andrea , Wu Di , Hoadley Katherine A. , Troester Melissa A. , Love Michael I.
Published: May 2024

This data includes the variables used in the analysis including HRD scores (HRD_Score) and breast cancer subtypes (Call)
Data from Risk of Clinically Significant Prostate Cancer after a Nonsuspicious Prostate MRI—A Comparison with the General Population
Authors: Pylväläinen Juho , Hoffström Jaakko , Kenttämies Anu , Auvinen Anssi , Mirtti Tuomas , Rannikko Antti
Published: May 2024

AbstractBackground:
We compare the risk of clinically significant (csPCa; ISUP Grade Group ≥ 2) and insignificant prostate cancer (isPCa; ISUP Grade Group 1) in men with a nonsuspicious prostate MRI (nMRI; PI-RADS ≤ 2) with the general population, and assess the value of PSA density (PSAD) in stratification.
Methods:
In this retrospective population-based cohort study we identified 1,682 50–79-year-old men, who underwent nMRI at HUS (2016–2019). We compared their age-standardized incidence rates (IR) of csPCa and the odds of isPCa to a local age- and sex-matched general population (n = 230,458) during a six-year follow-up. Comparisons were performed by calculating incidence rate ratios (IRR) and ORs with 95% confidence intervals (CI). We repeated the comparison for the 920 men with nMRI and PSAD < 0.15 ng/mL/cm3.
Results:
Compared with the general population, the IR of csPCa was significantly higher after nMRI [1,852 vs. 552 per 100,000 person-years; IRR 3.4 (95% CI, 2.8–4.1)]. However, the IR was substantially lower if PSAD was low [778 per 100,000 person-years; IRR 1.4 (95% CI, 0.9–2.0)]. ORs for isPCa were 2.4 (95% CI, 1.7–3.5) for all men with nMRI and 5.0 (95% CI, 2.8–9.1) if PSAD was low.
Conclusions:
Compared with the general population, the risk of csPCa is not negligible after nMRI. However, men with nMRI and PSAD <0.15 ng/mL/cm3 have worse harm-benefit balance than men in the general population.
Impact:
Prostate biopsies for men with nMRI should be reserved for cases indicated by additional risk stratification.

See related In the Spotlight, p. 641
Supplementary Figure S2 from Breast Cancer Index and Prediction of Extended Aromatase Inhibitor Therapy Benefit in Hormone Receptor-Positive Breast Cancer from the NRG Oncology/NSABP B-42 Trial
Authors: Mamounas Eleftherios P. , Bandos Hanna , Rastogi Priya , Zhang Yi , Treuner Kai , Lucas Peter C. , Geyer Charles E. , Fehrenbacher Louis , Chia Stephen K. , Brufsky Adam M. , Walshe Janice M. , Soori Gamini S. , Dakhil Shaker , Paik Soonmyung , Swain Sandra M. , Sgroi Dennis C. , Schnabel Catherine A. , Wolmark Norman
Published: May 2024

Supplemental Figure SF2. Exploratory Kaplan-Meier analysis based on A, any new primary cancer and B, new breast primary
cancer comparing extended letrozole vs placebo in the overall Breast Cancer Index (BCI) NSABP B-42 translational cohort.
Supplementary Table S9 from Molecular and Pathologic Characterization of YAP1-Expressing Small Cell Lung Cancer Cell Lines Leads to Reclassification as SMARCA4-Deficient Malignancies
Authors: Ng Jin , Cai Ling , Girard Luc , Prall Owen W.J. , Rajan Neeha , Khoo Christine , Batrouney Ahida , Byrne David J. , Boyd Danielle K. , Kersbergen Ariena J. , Christie Michael , Minna John D. , Burr Marian L. , Sutherland Kate D.
Published: May 2024

SMARCA4-UT cell lines and patient samples based on unsupervised hierarchical clustering using YAP1 signature genes.
Supplementary Table S1 from Molecular and Pathologic Characterization of YAP1-Expressing Small Cell Lung Cancer Cell Lines Leads to Reclassification as SMARCA4-Deficient Malignancies
Authors: Ng Jin , Cai Ling , Girard Luc , Prall Owen W.J. , Rajan Neeha , Khoo Christine , Batrouney Ahida , Byrne David J. , Boyd Danielle K. , Kersbergen Ariena J. , Christie Michael , Minna John D. , Burr Marian L. , Sutherland Kate D.
Published: May 2024

Immunohistochemistry antibodies, protocols and evaluation criteria.
Supplementary Figure S2 from Selective CDK7 Inhibition Suppresses Cell Cycle Progression and MYC Signaling While Enhancing Apoptosis in Therapy-resistant Estrogen Receptor–positive Breast Cancer
Authors: Guarducci Cristina , Nardone Agostina , Russo Douglas , Nagy Zsuzsanna , Heraud Capucine , Grinshpun Albert , Zhang Qi , Freelander Allegra , Leventhal Mathew Joseph , Feit Avery , Cohen Feit Gabriella , Feiglin Ariel , Liu Weihan , Hermida-Prado Francisco , Kesten Nikolas , Ma Wen , De Angelis Carmine , Morlando Antonio , O'Donnell Madison , Naumenko Sergey , Huang Shixia , Nguyen Quang-Dé , Huang Ying , Malorni Luca , Bergholz Johann S. , Zhao Jean J. , Fraenkel Ernest , Lim Elgene , Schiff Rachel , Shapiro Geoffrey I. , Jeselsohn Rinath
Published: May 2024

Effect of SY-1365 on WT and KI-Y537S mutant MCF7 cells after SY-1365 treatment over time
Figure 2 from Molecular and Pathologic Characterization of YAP1-Expressing Small Cell Lung Cancer Cell Lines Leads to Reclassification as SMARCA4-Deficient Malignancies
Authors: Ng Jin , Cai Ling , Girard Luc , Prall Owen W.J. , Rajan Neeha , Khoo Christine , Batrouney Ahida , Byrne David J. , Boyd Danielle K. , Kersbergen Ariena J. , Christie Michael , Minna John D. , Burr Marian L. , Sutherland Kate D.
Published: May 2024

SMARCA4-deficient SCLC cell lines are morphologically and immunophenotypically similar to SMARCA4-UT. A, Outline of the methodology employed for assessing SMARCA4-deficient SCLC cell lines by a panel of five anatomical pathologists. B, Representative H&E images of cell line xenografts diagnosed as high-grade NE carcinoma (SCLC) and other malignant neoplasms (non-SCLC). Scale bar = 100 μm. C, Heatmap of re-evaluated diagnosis of SCLC cell line xenografts (row) and each pathologists’ classification (column). Abbreviations: LCNEC, large cell neuroendocrine cancer; SMARCA4-UT, SMARCA4-deficient undifferentiated tumor; SCLC/LCNEC, combined SCLC and LCNEC components; Other, undifferentiated tumor or small blue round cell tumor.
Supplementary Figure S1 from Platinum-Based Chemotherapy Attenuates the Effector Response of CD8 T Cells to Concomitant PD-1 Blockade
Authors: Mariniello Annapaola , Nasti Tahseen H. , Chang Daniel Y. , Hashimoto Masao , Malik Sakshi , McManus Daniel T. , Lee Judong , McGuire Donald J. , Cardenas Maria A. , Umana Pablo , Nicolini Valeria , Antia Rustom , Saha Ananya , Buchwald Zachary , Kissick Hayden , Ghorani Ehsan , Novello Silvia , Sangiolo Dario , Scagliotti Giorgio V. , Ramalingam Suresh S. , Ahmed Rafi
Published: May 2024

(A) Number of total lymphocytes, CD8 and CD4 T cells in the spleen across the treatment groups. (B-C) Frequency of PD-1+ and LCMV-specific CD8 T cells in the spleen and in the lung. Data are pooled from 2-3 experiments of 4-5 mice per group. For statistical analysis, the one-way ANOVA test was used; total numbers were Log10 transformed. Bars represent mean and SEM. *p<0.05; ** p<0.01; *** p<0.001; **** p<0.0001.
Supplementary Table S1 from Improved Risk-Stratification Scheme for Mismatch-Repair Proficient Stage II Colorectal Cancers Using the Digital Pathology Biomarker QuantCRC
Authors: Wu Christina , Pai Reetesh K. , Kosiorek Heidi , Banerjee Imon , Pfeiffer Ashlyn , Hagen Catherine E. , Hartley Christopher P. , Graham Rondell P. , Sonbol Mohamad B. , Bekaii-Saab Tanios , Xie Hao , Sinicrope Frank A. , Patel Bhavik , Westerling-Bui Thomas , Shivji Sameer , Conner James , Swallow Carol , Savage Paul , Cyr David P. , Kirsch Richard , Pai Rish K.
Published: May 2024

Supplementary Table S1. Univariate and multivariate analysis of QuantCRC risk classification, pT stage, and any high-risk pathologic feature.
Supplementary Figure S2 from Improved Risk-Stratification Scheme for Mismatch-Repair Proficient Stage II Colorectal Cancers Using the Digital Pathology Biomarker QuantCRC
Authors: Wu Christina , Pai Reetesh K. , Kosiorek Heidi , Banerjee Imon , Pfeiffer Ashlyn , Hagen Catherine E. , Hartley Christopher P. , Graham Rondell P. , Sonbol Mohamad B. , Bekaii-Saab Tanios , Xie Hao , Sinicrope Frank A. , Patel Bhavik , Westerling-Bui Thomas , Shivji Sameer , Conner James , Swallow Carol , Savage Paul , Cyr David P. , Kirsch Richard , Pai Rish K.
Published: May 2024

Supplementary Figure S2. Scatter plots of QuantCRC features stratified by QuantCRC-integrated and ASCO risk schemes.
Supplementary Figure S1 from Improved Risk-Stratification Scheme for Mismatch-Repair Proficient Stage II Colorectal Cancers Using the Digital Pathology Biomarker QuantCRC
Authors: Wu Christina , Pai Reetesh K. , Kosiorek Heidi , Banerjee Imon , Pfeiffer Ashlyn , Hagen Catherine E. , Hartley Christopher P. , Graham Rondell P. , Sonbol Mohamad B. , Bekaii-Saab Tanios , Xie Hao , Sinicrope Frank A. , Patel Bhavik , Westerling-Bui Thomas , Shivji Sameer , Conner James , Swallow Carol , Savage Paul , Cyr David P. , Kirsch Richard , Pai Rish K.
Published: May 2024

Supplementary Figure S1. Flow diagram outlining the steps undertaken in this study.
Supplementary Table S1 from Improved Innate Immune Function in Patients with Chronic Lymphocytic Leukemia Treated with Targeted Therapy in Clinical Trials
Authors: Svanberg Teglgaard Rebecca , Marquart Hanne Vibeke , Hartling Hans Jakob , Bay Jakob Thaning , da Cunha-Bang Caspar , Brieghel Christian , Faitová Tereza , Enggaard Lisbeth , Kater Arnon P. , Levin Mark-David , Kersting Sabina , Ostrowski Sisse Rye , Niemann Carsten U.
Published: May 2024

Supplementary Table S1. Overview over the applied 10-color flow cytometry panel for the two tubes included in this study.
Supplementary Video S5 from Mesothelin CAR T Cells Secreting Anti-FAP/Anti-CD3 Molecules Efficiently Target Pancreatic Adenocarcinoma and its Stroma
Authors: Wehrli Marc , Guinn Samantha , Birocchi Filippo , Kuo Adam , Sun Yi , Larson Rebecca C. , Almazan Antonio J. , Scarfò Irene , Bouffard Amanda A. , Bailey Stefanie R. , Anekal Praju Vikas , Montero Llopis Paula , Nieman Linda T. , Song Yuhui , Xu Katherine H. , Berger Trisha R. , Kann Michael C. , Leick Mark B. , Silva Harrison , Salas-Benito Diego , Kienka Tamina , Grauwet Korneel , Armstrong Todd D. , Zhang Rui , Zhu Qingfeng , Fu Juan , Schmidts Andrea , Korell Felix , Jan Max , Choi Bryan D. , Liss Andrew S. , Boland Genevieve M. , Ting David T. , Burkhart Richard A. , Jenkins Russell W. , Zheng Lei , Jaffee Elizabeth M. , Zimmerman Jacquelyn W. , Maus Marcela V.
Published: May 2024

Supplementary Video S5. Meso^CD19 CAR T cells on AsPC1 + CAF
Data from Randomized Phase II Trial of Imiquimod with or without 9-Valent HPV Vaccine versus Observation in Patients with High-grade Pre-neoplastic Cervical Lesions (NCT02864147)
Authors: Sheth Sangini S. , Oh Ji Eun , Bellone Stefania , Siegel Eric R. , Greenman Michelle , Mutlu Levent , McNamara Blair , Pathy Shefali , Clark Mitchell , Azodi Masoud , Altwerger Gary , Andikyan Vaagn , Huang Gloria , Ratner Elena , Kim Daniel J. , Iwasaki Akiko , Levi Angelique W. , Buza Natalia , Hui Pei , Flaherty Sean , Schwartz Peter E. , Santin Alessandro D.
Published: May 2024

AbstractPurpose:
We report the results of a randomized phase II trial of imiquimod, a topical immune-response modulator versus imiquimod plus a 9-valent human papillomavirus (HPV) vaccine (9vHPV) versus clinical surveillance in cervical intraepithelial neoplasia (CIN2/3) patients.
Patients and Methods:
We randomly allocated 133 patients with untreated CIN2/3 in equal proportions to a 4-month treatment with self-applied vaginal suppositories containing imiquimod (Arm B) or imiquimod plus a 9vHPV (Arm C) versus clinical surveillance (Arm A). The main outcome was efficacy, defined as histologic regression to CIN1 or less. Secondary outcomes were HPV clearance and tolerability. Exploratory objectives included the comparison of cervical CD4/CD8 T-cell infiltration at baseline, mid-study, and posttreatment by flow cytometry among study arms.
Results:
Of the 114 evaluable patients 77% and 23% harbored CIN2 and CIN3, respectively. Regression to CIN1 or less was observed in 95% of patients in the imiquimod group (Arm B) compared with 79% in the control/surveillance (Arm A); P = 0.043 and 84% in the imiquimod+9vHPV group (Arm C; P = 0.384 vs. Arm A). Neither of the treatment-arm differences from Arm A reached the prespecified α = 0.025 significance level. No significant differences were noted in the secondary outcome of rate of HPV clearance. The number of tissue-resident memory CD4/CD8 T cells in cytobrush samples demonstrated a >5-fold increase in Arm B/imiquimod when compared with Arm A/surveillance (P < 0.01). In contrast, there was no significant difference in T-cell responses among participants in Arm C when compared with Arm A. Imiquimod treatment was well tolerated.
Conclusions:
Although imiquimod induced a higher regression to CIN1 or less and significant increases in CD4/CD8 T cells infiltrating the cervix, it did not meet its prespecified statistical outcome for efficacy. A higher regression rate than expected was observed in the surveillance arm of this prospective trial. Future clinical trials with imiquimod targeting CIN3 patients are warranted.
Data from Phase I/II Study of Combined BCL-xL and MEK Inhibition with Navitoclax and Trametinib in KRAS or NRAS Mutant Advanced Solid Tumors
Authors: Corcoran Ryan B. , Do Khanh T. , Kim Jeong E. , Cleary James M. , Parikh Aparna R. , Yeku Oladapo O. , Xiong Niya , Weekes Colin D. , Veneris Jennifer , Ahronian Leanne G. , Mauri Gianluca , Tian Jun , Norden Bryanna L. , Michel Alexa G. , Van Seventer Emily E. , Siravegna Giulia , Camphausen Kyle , Chi Gary , Fetter Isobel J. , Brugge Joan S. , Chen Helen , Takebe Naoko , Penson Richard T. , Juric Dejan , Flaherty Keith T. , Sullivan Ryan J. , Clark Jeffrey W. , Heist Rebecca S. , Matulonis Ursula A. , Liu Joyce F. , Shapiro Geoffrey I.
Published: May 2024

AbstractPurpose:
MEK inhibitors (MEKi) lack monotherapy efficacy in most RAS-mutant cancers. BCL-xL is an anti-apoptotic protein identified by a synthetic lethal shRNA screen as a key suppressor of apoptotic response to MEKi.
Patients and Methods:
We conducted a dose escalation study (NCT02079740) of the BCL-xL inhibitor navitoclax and MEKi trametinib in patients with RAS-mutant tumors with expansion cohorts for: pancreatic, gynecologic (GYN), non–small cell lung cancer (NSCLC), and other cancers harboring KRAS/NRAS mutations. Paired pretreatment and day 15 tumor biopsies and serial cell-free (cf)DNA were analyzed.
Results:
A total of 91 patients initiated treatment, with 38 in dose escalation. Fifty-eight percent had ≥3 prior therapies. A total of 15 patients (17%) had colorectal cancer, 19 (11%) pancreatic, 15 (17%) NSCLC, and 32 (35%) GYN cancers. The recommended phase II dose (RP2D) was established as trametinib 2 mg daily days 1 to 14 and navitoclax 250 mg daily days 1 to 28 of each cycle. Most common adverse events included diarrhea, thrombocytopenia, increased AST/ALT, and acneiform rash. At RP2D, 8 of 49 (16%) evaluable patients achieved partial response (PR). Disease-specific differences in efficacy were noted. In patients with GYN at the RP2D, 7 of 21 (33%) achieved a PR and median duration of response 8.2 months. No PRs occurred in patients with colorectal cancer, NSCLC, or pancreatic cancer. MAPK pathway inhibition was observed in on-treatment tumor biopsies. Reductions in KRAS/NRAS mutation levels in cfDNA correlated with clinical benefit.
Conclusions:
Navitoclax in combination with trametinib was tolerable. Durable clinical responses were observed in patients with RAS-mutant GYN cancers, warranting further evaluation in this population.
Data from Improved Innate Immune Function in Patients with Chronic Lymphocytic Leukemia Treated with Targeted Therapy in Clinical Trials
Authors: Svanberg Teglgaard Rebecca , Marquart Hanne Vibeke , Hartling Hans Jakob , Bay Jakob Thaning , da Cunha-Bang Caspar , Brieghel Christian , Faitová Tereza , Enggaard Lisbeth , Kater Arnon P. , Levin Mark-David , Kersting Sabina , Ostrowski Sisse Rye , Niemann Carsten U.
Published: May 2024

AbstractPurpose:
Patients with chronic lymphocytic leukemia (CLL) have increased risk of severe infections. Although adaptive immune dysfunction is well described, clinical tools for identifying patients at risk are lacking, warranting investigation of additional immune components. In contrast to chemotherapy, targeted agents could spare or even improve innate immune function. Therefore, we investigated innate immune phenotypes and function in patients with CLL before and during targeted treatment.
Experimental Design:
Baseline and consecutive blood samples were collected from patients with CLL treated with acalabrutinib (n = 17) or ibrutinib+venetoclax (n = 18) in clinical trials. Innate immune function was assessed by TruCulture, a whole-blood ligand-stimulation assay quantifying cytokine release in response to standardized stimuli. Innate immune phenotypes were characterized by flow cytometry. As a proxy for infections, we mapped antimicrobial use before and during treatment.
Results:
At baseline, patients with CLL displayed impaired stimulated cytokine responses to the endotoxin lipopolysaccharide (LPS) along with deactivated monocytes, enrichment of myeloid-derived suppressor cells and metamyelocytes, and elevated (unstimulated) proinflammatory cytokines. Two/three cycles of acalabrutinib or ibrutinib normalized LPS-stimulated responses, in parallel with decreased duration of infections. Innate immune profiles and elevated proinflammatory cytokines further normalized during longer-term acalabrutinib or ibrutinib+venetoclax, paralleled by decreased infection frequency.
Conclusions:
Innate immune impairment and infection susceptibility in patients with CLL were restored in parallel during targeted therapy. Thus, targeted treatment may reduce the risk of infections in CLL, as currently under investigation in the PreVent-ACaLL phase 2 trial of acalabrutinib+venetoclax for high-risk CLL (NCT03868722).
Data from Impact of Circulating Tumor Cell–Expressed Prostate-Specific Membrane Antigen and Prostate-Specific Antigen Transcripts in Different Stages of Prostate Cancer
Authors: Cho Hyungseok , Byun Seok-Soo , Son Nak-Hoon , Chung Jae Il , Seo Won Ik , Lee Chan Ho , Morgan Todd M. , Han Ki-Ho , Chung Jae-Seung
Published: May 2024

AbstractPurpose:
Prostate-specific membrane antigen (PSMA)–based images, which visually quantify PSMA expression, are used to determine prostate cancer micrometastases. This study evaluated whether a circulating tumor cell (CTC)–based transcript platform, including PSMA mRNA, could help identify potential prognostic markers in prostate cancer.
Experimental Design:
We prospectively enrolled 21 healthy individuals and 247 patients with prostate cancer [localized prostate cancer (LPCa), n = 94; metastatic hormone–sensitive prostate cancer (mHSPC), n = 44; and metastatic castration-resistant prostate cancer (mCRPC), n = 109]. The mRNA expression of six transcripts [PSMA, prostate-specific antigen (PSA), AR, AR-V7, EpCAM, and KRT 19] from CTCs was measured, and their relationship with biochemical recurrence (BCR) in LPCa and mCRPC progression-free survival (PFS) rate in mHSPC was assessed. PSA-PFS and radiological-PFS were also calculated to identify potential biomarkers for predicting androgen receptor signaling inhibitor (ARSI) and taxane-based chemotherapy resistance in mCRPC.
Results:
CTC detection rates were 75.5%, 95.3%, and 98.0% for LPCa, mHSPC, and mCRPC, respectively. In LPCa, PSMA [hazard ratio (HR), 3.35; P = 0.028) and PSA mRNA (HR, 1.42; P = 0.047] expressions were associated with BCR. Patients with mHSPC with high PSMA (HR, 4.26; P = 0.020) and PSA mRNA (HR, 3.52; P = 0.042) expressions showed significantly worse mCRPC-PFS rates than those with low expression. Increased PSA and PSMA mRNA expressions were significantly associated with shorter PSA-PFS and radiological PFS in mCPRC, indicating an association with drug resistance.
Conclusions:
PSMA and PSA mRNA expressions are associated with BCR in LPCa. In advanced prostate cancer, PSMA and PSA mRNA can also predict rapid progression from mHSPC to mCRPC and ARSI or taxane-based chemotherapy resistance.
Figure S7 from Early Immune Remodeling Steers Clinical Response to First-Line Chemoimmunotherapy in Advanced Gastric Cancer
Authors: An Minae , Mehta Arnav , Min Byung Hoon , Heo You Jeong , Wright Samuel J. , Parikh Milan , Bi Lynn , Lee Hyuk , Kim Tae Jun , Lee Song-Yi , Moon Jeonghyeon , Park Ryan J. , Strickland Matthew R. , Park Woong-Yang , Kang Won Ki , Kim Kyoung-Mee , Kim Seung Tae , Klempner Samuel J. , Lee Jeeyun
Published: May 2024

Figure S7. (A) UMAP embedding of single cell transcriptomes from epithelial cells
obtained from all samples in this trial. Shown are UMAP embeddings with
expression of key epithelial genes. (B) UMAP embeddings color coded by
predicted annotation of tumor cell v.s. normal cell using Numbat.
Figure S27 from Early Immune Remodeling Steers Clinical Response to First-Line Chemoimmunotherapy in Advanced Gastric Cancer
Authors: An Minae , Mehta Arnav , Min Byung Hoon , Heo You Jeong , Wright Samuel J. , Parikh Milan , Bi Lynn , Lee Hyuk , Kim Tae Jun , Lee Song-Yi , Moon Jeonghyeon , Park Ryan J. , Strickland Matthew R. , Park Woong-Yang , Kang Won Ki , Kim Kyoung-Mee , Kim Seung Tae , Klempner Samuel J. , Lee Jeeyun
Published: May 2024

Figure S27. Boxplots showing usage of T cell cNMF programs in T cells of fast and slow progressors (A) post-chemotherapy (FU1) and (B) post-immunotherapy (FU2). (C) Expression of CD39, CD103, CXCL13, 4-1BB and GITR in single CD8 T cells segregated by timepoint (BL, FU1, FU2) and by fast versus slow progressing patients. Statistical comparison performed using a Wilcoxon signedrank test.
Figure S2 from Early Immune Remodeling Steers Clinical Response to First-Line Chemoimmunotherapy in Advanced Gastric Cancer
Authors: An Minae , Mehta Arnav , Min Byung Hoon , Heo You Jeong , Wright Samuel J. , Parikh Milan , Bi Lynn , Lee Hyuk , Kim Tae Jun , Lee Song-Yi , Moon Jeonghyeon , Park Ryan J. , Strickland Matthew R. , Park Woong-Yang , Kang Won Ki , Kim Kyoung-Mee , Kim Seung Tae , Klempner Samuel J. , Lee Jeeyun
Published: May 2024

Figure S2. (A) CoMut plot demonstrating TCGA subtype, tumor mutational
burden, mutational signature enrichment and mutational profiles of key driver
genes for all patient samples at baseline in the reported clinical trial. (B) PD-L1
expression for each patient sample at baseline in the reported clinical trial.
Figure S19 from Early Immune Remodeling Steers Clinical Response to First-Line Chemoimmunotherapy in Advanced Gastric Cancer
Authors: An Minae , Mehta Arnav , Min Byung Hoon , Heo You Jeong , Wright Samuel J. , Parikh Milan , Bi Lynn , Lee Hyuk , Kim Tae Jun , Lee Song-Yi , Moon Jeonghyeon , Park Ryan J. , Strickland Matthew R. , Park Woong-Yang , Kang Won Ki , Kim Kyoung-Mee , Kim Seung Tae , Klempner Samuel J. , Lee Jeeyun
Published: May 2024

Figure S19. (A) UMAP embedding of single cell transcriptomes of all
macrophages obtained from all samples in this trial. Labeled are granular
macrophage subsets separated by tumor v.s. normal tissue, and by timepoint. (B)
UMAP embeddings showing marker gene expression for macrophage subsets in
(A). (C) Relative M1 macrophage proportion in fast and slow progressing patients
separated by timepoint. (D) Macrophage subtype proportions at baseline and FU1
in fast versus slow progressing patients, and in non-responder and responder
patients. (E) Relative M1 macrophage proportion in non-responder and responder
patients separated by timepoint. (F) Proportion of SPP1+ macrophages in nonresponder
and responder patients split by timepoint. Statistical comparisons
performed using a Wilcoxon signed-rank test. (G) Change in relative M1
proportion from BL to FU1 plotted against change in tumor volume after 1 cycle of
chemotherapy, segregated by non-responder and responder patients. (H) GSVA
performed for M2 signatures on bulk RNA-seq samples split by timepoints and
progression status.
Figure S11 from Early Immune Remodeling Steers Clinical Response to First-Line Chemoimmunotherapy in Advanced Gastric Cancer
Authors: An Minae , Mehta Arnav , Min Byung Hoon , Heo You Jeong , Wright Samuel J. , Parikh Milan , Bi Lynn , Lee Hyuk , Kim Tae Jun , Lee Song-Yi , Moon Jeonghyeon , Park Ryan J. , Strickland Matthew R. , Park Woong-Yang , Kang Won Ki , Kim Kyoung-Mee , Kim Seung Tae , Klempner Samuel J. , Lee Jeeyun
Published: May 2024

Figure S11. Mean usage of myeloid cNMF programs per myeloid cell subset at (A)
baseline, (B) post-chemotherapy (FU1) and (C) post-immunotherapy (FU2). Mean
usage of T cell cNMF programs per T cell cell subset at (D) baseline, (E) postchemotherapy
(FU1) and (F) post-immunotherapy (FU2).
Supplementary Table S4 from Pan-Cancer Comparative and Integrative Analyses of Driver Alterations Using Japanese and International Genomic Databases
Authors: Horie Sara , Saito Yuki , Kogure Yasunori , Mizuno Kota , Ito Yuta , Tabata Mariko , Kanai Takanori , Murakami Koichi , Koya Junji , Kataoka Keisuke
Published: May 2024

Details of gene rearrangements forming putative driver fusions in C-CAT
Supplementary Figures S1-S7 from Sotorasib Is a Pan-RASG12C Inhibitor Capable of Driving Clinical Response in NRASG12C Cancers
Authors: Rubinson Douglas A. , Tanaka Noritaka , Fece de la Cruz Ferran , Kapner Kevin S. , Rosenthal Michael H. , Norden Bryanna L. , Barnes Haley , Ehnstrom Sara , Morales-Giron Alvin A. , Brais Lauren K. , Lemke Christopher T. , Aguirre Andrew J. , Corcoran Ryan B.
Published: May 2024

Supplementary Figure S1 shows IC50 values of KRASG12C inhibitors for KRASG12C, NRASG12C, HRASG12C.

Supplementary Figure S2 shows inhibition of NRASG12C by sotorasib in 293T and MOLT-4 cells.

Supplementary Figure S3 shows effect of amino acid substitutions in NRASG12C or KRASG12C on signaling in response to sotorasib and adagrasib.

Supplementary Figure S4 who's location of isoform-variable residues relative to Switch-II binders.

Supplementary Figure S5 shows crystal structures of KRASG12C inhibitors and interactions with His95.

Supplementary Figure S6 shows chemical structures of switch-II pocket-binding KRASG12C inhibitors.

Supplementary Figure S7 shows structural model of sotorasib interaction with Leu95.
Supplementary Tables from Acquired Cross-Resistance in Small Cell Lung Cancer due to Extrachromosomal DNA Amplification of MYC Paralogs
Authors: Pal Choudhuri Shreoshi , Girard Luc , Lim Jun Yi Stanley , Wise Jillian F. , Freitas Braeden , Yang Di , Wong Edmond , Hamilton Seth , Chien Victor D. , Kim Yoon Jung , Gilbreath Collin , Zhong Jun , Phat Sarah , Myers David T. , Christensen Camilla L. , Mazloom-Farsibaf Hanieh , Stanzione Marcello , Wong Kwok-Kin , Hung Yin P. , Farago Anna F. , Meador Catherine B. , Dyson Nicholas J. , Lawrence Michael S. , Wu Sihan , Drapkin Benjamin J.
Published: May 2024

Supplementary Table S1. Clinical Histories of PDX Models.

Supplementary Table S2. Differential Gene Expression for MGH1518 Serial Models.

Supplementary Table S3. Mutations in the ecMYC region in MGH1518-3A.

Supplementary Table S4. Mutations in the chromosome 17 ecDNA region in MGH1531-5BX.

Supplementary Table S5. Mutations at ecMYC junctions.

Supplementary Table S6. Focused PDX model clinical, molecular, and functional profiles.

Supplementary Table S7. MYC paralog amplifications in cell lines, PDX models and patient tumor samples.
Supplementary Figure S16 from Long-term Multimodal Recording Reveals Epigenetic Adaptation Routes in Dormant Breast Cancer Cells
Authors: Rosano Dalia , Sofyali Emre , Dhiman Heena , Ghirardi Chiara , Ivanoiu Diana , Heide Timon , Vingiani Andrea , Bertolotti Alessia , Pruneri Giancarlo , Canale Eleonora , Dewhurst Hannah F. , Saha Debjani , Slaven Neil , Barozzi Iros , Li Tong , Zemlyanskiy Grigory , Phillips Henry , James Chela , Győrffy Balázs , Lynn Claire , Cresswell George D. , Rehman Farah , Noberini Roberta , Bonaldi Tiziana , Sottoriva Andrea , Magnani Luca
Published: May 2024

Morphological inspection of cells along adaptation
Table S7 from Large-scale Pan-cancer Cell Line Screening Identifies Actionable and Effective Drug Combinations
Authors: Bashi Azadeh C. , Coker Elizabeth A. , Bulusu Krishna C. , Jaaks Patricia , Crafter Claire , Lightfoot Howard , Milo Marta , McCarten Katrina , Jenkins David F. , van der Meer Dieudonne , Lynch James T. , Barthorpe Syd , Andersen Courtney L. , Barry Simon T. , Beck Alexandra , Cidado Justin , Gordon Jacob A. , Hall Caitlin , Hall James , Mali Iman , Mironenko Tatiana , Mongeon Kevin , Morris James , Richardson Laura , Smith Paul D. , Tavana Omid , Tolley Charlotte , Thomas Frances , Willis Brandon S. , Yang Wanjuan , O'Connor Mark J. , McDermott Ultan , Critchlow Susan E. , Drew Lisa , Fawell Stephen E. , Mettetal Jerome T. , Garnett Mathew J.
Published: May 2024

Supplementary Table 7 shows the top combination-cancer type pairs in hematological cancers showing activity in at least 10% of tested cell lines in that specific cancer type ranked based on their activity (% responders) and disease selectivity
Supplementary Figure S10 from Long-term Multimodal Recording Reveals Epigenetic Adaptation Routes in Dormant Breast Cancer Cells
Authors: Rosano Dalia , Sofyali Emre , Dhiman Heena , Ghirardi Chiara , Ivanoiu Diana , Heide Timon , Vingiani Andrea , Bertolotti Alessia , Pruneri Giancarlo , Canale Eleonora , Dewhurst Hannah F. , Saha Debjani , Slaven Neil , Barozzi Iros , Li Tong , Zemlyanskiy Grigory , Phillips Henry , James Chela , Győrffy Balázs , Lynn Claire , Cresswell George D. , Rehman Farah , Noberini Roberta , Bonaldi Tiziana , Sottoriva Andrea , Magnani Luca
Published: May 2024

Drug holiday regimen
Table S16 from Large-scale Pan-cancer Cell Line Screening Identifies Actionable and Effective Drug Combinations
Authors: Bashi Azadeh C. , Coker Elizabeth A. , Bulusu Krishna C. , Jaaks Patricia , Crafter Claire , Lightfoot Howard , Milo Marta , McCarten Katrina , Jenkins David F. , van der Meer Dieudonne , Lynch James T. , Barthorpe Syd , Andersen Courtney L. , Barry Simon T. , Beck Alexandra , Cidado Justin , Gordon Jacob A. , Hall Caitlin , Hall James , Mali Iman , Mironenko Tatiana , Mongeon Kevin , Morris James , Richardson Laura , Smith Paul D. , Tavana Omid , Tolley Charlotte , Thomas Frances , Willis Brandon S. , Yang Wanjuan , O'Connor Mark J. , McDermott Ultan , Critchlow Susan E. , Drew Lisa , Fawell Stephen E. , Mettetal Jerome T. , Garnett Mathew J.
Published: May 2024

Supplementary Table 16 shows emergent biomarkers associated with top 5 enriched pathways for each drug combination category used in this study (CD = cell death, CS = cell signaling
Figure 1 from Long-term Multimodal Recording Reveals Epigenetic Adaptation Routes in Dormant Breast Cancer Cells
Authors: Rosano Dalia , Sofyali Emre , Dhiman Heena , Ghirardi Chiara , Ivanoiu Diana , Heide Timon , Vingiani Andrea , Bertolotti Alessia , Pruneri Giancarlo , Canale Eleonora , Dewhurst Hannah F. , Saha Debjani , Slaven Neil , Barozzi Iros , Li Tong , Zemlyanskiy Grigory , Phillips Henry , James Chela , Győrffy Balázs , Lynn Claire , Cresswell George D. , Rehman Farah , Noberini Roberta , Bonaldi Tiziana , Sottoriva Andrea , Magnani Luca
Published: May 2024

Genetic profile of tumor awakening in the clinical setting. A, High-depth profiling (median 105.47×) of ER+ breast cancer (BC; estrogen receptor–positive breast cancer) late relapses using a custom targeted panel. The simplified treatment scheme of patients is shown on the left. The heat map shows the mutations in ET resistance drivers in ER+ breast cancer passing the filters for allele depth ≥20, Alternate F1R2 + F2R1 ≥4, allele frequency ≥0.1, and consequence level of moderate or high. Time to relapse (years), recurrence in the data set, allele frequency, and relapse site are indicated. Significant genes are indicated based on dN/dS analysis from the q-value of neutrality test at the gene level (*qglobal_cv ≤0.1). B, Clinical histories of patients 2–5. The table shows age and response time to ET for each patient (letrozole). C, Scatter plots of VAF from whole-genome sequencing (WGS) data. Pairwise comparisons were done for pretreatment (diagnostic biopsies) versus progression (surgical biopsies). All patients were managed with primary endocrine therapy until progression. Labeled genes passed two filters: bona fide breast cancer drivers and ET resistance drivers in ER+ breast cancer and FATHMM significant score >0.6 (predicted damaging). Detected variants are labeled and color-coded according to detection at diagnosis (teal), progression (magenta), or both (gray). The highlighted gene (TP53) is annotated as a variant detected in ET resistance drivers in ER+ breast cancer according to the comprehensive ET-resistance driver gene list compiled based on Bertucci et al. (14). Marginal histograms of VAFs are shown on the sides of each plot. D, Spatial transcriptomics analysis of patients 1–3. On the left, representative images of regions of interest (ROI) from patient 3, pre- and post-treatment, are shown with the relevant staining. Green, pan cytokeratin (CK+); yellow, immune cells (CD45+); purple, stroma. On the right side, GeoMx UMAPs of previously identified pre-adapted SWNE up and down signatures from (2), and G2–M checkpoint signatures are shown for patients 1–3 (CK+ segment). D1 L biopsy was not suitable for spatial transcriptomics analysis due to poor specimen quality and was excluded from further examinations. S1L: surgical biopsy in the left breast; S1R: surgical biopsy in the right breast; R1R: loco-regional relapse after surgery in the right breast.
Figure S8 from EGFR-Driven Lung Adenocarcinomas Co-opt Alveolar Macrophage Metabolism and Function to Support EGFR Signaling and Growth
Authors: Kuhlmann-Hogan Alexandra , Cordes Thekla , Xu Ziyan , Kuna Ramya S. , Traina Kacie A. , Robles-Oteíza Camila , Ayeni Deborah , Kwong Elizabeth M. , Levy Stellar , Globig Anna-Maria , Nobari Matthew M. , Cheng George Z. , Leibel Sandra L. , Homer Robert J. , Shaw Reuben J. , Metallo Christian M. , Politi Katerina , Kaech Susan M.
Published: May 2024

Figure S8: AMs transfer nutrients to tumor cells.
Figure S7 from EGFR-Driven Lung Adenocarcinomas Co-opt Alveolar Macrophage Metabolism and Function to Support EGFR Signaling and Growth
Authors: Kuhlmann-Hogan Alexandra , Cordes Thekla , Xu Ziyan , Kuna Ramya S. , Traina Kacie A. , Robles-Oteíza Camila , Ayeni Deborah , Kwong Elizabeth M. , Levy Stellar , Globig Anna-Maria , Nobari Matthew M. , Cheng George Z. , Leibel Sandra L. , Homer Robert J. , Shaw Reuben J. , Metallo Christian M. , Politi Katerina , Kaech Susan M.
Published: May 2024

Figure S7: PPARγ antagonist GW9662 rewires Alveolar macrophage metabolism within the TME.
Supplementary Figures S1-6 from Cancer Mutations Converge on a Collection of Protein Assemblies to Predict Resistance to Replication Stress
Authors: Zhao Xiaoyu , Singhal Akshat , Park Sungjoon , Kong JungHo , Bachelder Robin , Ideker Trey
Published: May 2024

Supplementary Figure S1. Aspects of replication stress addressed by cancer therapeutics.
Supplementary Figure S2. Nested systems in tumors (NeST).
Supplementary Figure S3. VNN schematic.
Supplementary Figure S4. Performance and interpretation of the multi-drug VNN.
Supplementary Figure S5. Evaluation of assemblies by systematic drug sensitivity screens.
Supplementary Figure S6. Survival analysis of cisplatin-treated TCGA cohorts.
Enhanced Molecular Response in Myeloproliferative Neoplasms with Complete JAK2V617F Inhibition
Authors: Celik Hamza , Challen Grant A.
Published: May 2024

Dunbar, Bowman, and colleagues present here a novel genetic mouse model with inducible and reversible expression of the JAK2V617F mutation in the endogenous locus. Results from this study clearly demonstrate an absolute requirement for myeloproliferative neoplasm–initiating cells for this mutation in their survival and imply that more efficacious inhibitors could be curative for these patients even in the setting of additional cooperating mutations.

See related article by Dunbar et al., p. 737 (8).
RAS G12C Inhibitors: Three Birds with One Stone
Authors: Seale Tessa , Misale Sandra
Published: May 2024

In this issue, Rubinson, Tanaka, and colleagues demonstrate that differences among G12C inhibitors rely on their ability to covalently bind not only G12C mutant KRAS but also NRAS and HRAS, proposing sotorasib as a potent NRAS G12C inhibitor.

See related article by Rubinson et al., p. 727 (6).
Supplementary Table 4 from Spatial Mapping of Hematopoietic Clones in Human Bone Marrow
Authors: Young Andrew L. , Davis Hannah C. , Cox Maggie J. , Parsons Tyler M. , Burkart Samantha C. , Bender Diane E. , Sun Lulu , Oh Stephen T. , Challen Grant A.
Published: May 2024

Supplementary Table 4. Hematopoietic subpopulations sorted from a bone marrow (BM) specimen (top) or a peripheral blood (PB) specimen (bottom) from UPN978825. Table includes the flow markers and total number of cells sorted from each subpopulation for ddPCR analysis. For each subpopulation, somatic mutations were identified by ddPCR.
Figure S8 from Acquired Multidrug Resistance in AML Is Caused by Low Apoptotic Priming in Relapsed Myeloblasts
Authors: Olesinski Elyse A. , Bhatia Karanpreet Singh , Wang Chuqi , Pioso Marissa S. , Lin Xiao Xian , Mamdouh Ahmed M. , Ng Shu Xuan , Sandhu Vedant , Jasdanwala Shaista Shabbir , Yilma Binyam , Bohl Stephan , Ryan Jeremy A. , Malani Disha , Luskin Marlise R. , Kallioniemi Olli , Porkka Kimmo , Adamia Sophia , Chng Wee Joo , Osato Motomi , Weinstock David M. , Garcia Jacqueline S. , Letai Anthony , Bhatt Shruti
Published: May 2024

Supplemental Figure 8 shows ex vivo DBP profiling in AML PDX models guides generation of drug-resistant PDXs.
Data from Acute Lymphoblastic Leukemia with Myeloid Mutations Is a High-Risk Disease Associated with Clonal Hematopoiesis
Authors: Saygin Caner , Zhang Pu , Stauber Jacob , Aldoss Ibrahim , Sperling Adam S. , Weeks Lachelle D. , Luskin Marlise R. , Knepper Todd C. , Wanjari Pankhuri , Wang Peng , Lager Angela M. , Fitzpatrick Carrie , Segal Jeremy P. , Gharghabi Mehdi , Gurbuxani Sandeep , Venkataraman Girish , Cheng Jason X. , Eisfelder Bart J. , Bohorquez Oliver , Patel Anand A. , Umesh Nagalakshmi Sheethal , Jayaram Savita , Odenike Olatoyosi M. , Larson Richard A. , Godley Lucy A. , Arber Daniel A. , Gibson Christopher J. , Munshi Nikhil C. , Marcucci Guido , Ebert Benjamin L. , Greally John M. , Steidl Ulrich , Lapalombella Rosa , Shah Bijal D. , Stock Wendy
Published: May 2024

Abstract
Myeloid neoplasms arise from preexisting clonal hematopoiesis (CH); however, the role of CH in the pathogenesis of acute lymphoblastic leukemia (ALL) is unknown. We found that 18% of adult ALL cases harbored TP53, and 16% had myeloid CH-associated gene mutations. ALL with myeloid mutations (MyM) had distinct genetic and clinical characteristics, associated with inferior survival. By using single-cell proteogenomic analysis, we demonstrated that myeloid mutations were present years before the diagnosis of ALL, and a subset of these clones expanded over time to manifest as dominant clones in ALL. Single-cell RNA sequencing revealed upregulation of genes associated with cell survival and resistance to apoptosis in B-ALL with MyM, which responds better to newer immunotherapeutic approaches. These findings define ALL with MyM as a high-risk disease that can arise from antecedent CH and offer new mechanistic insights to develop better therapeutic and preventative strategies.
Significance:
CH is a precursor lesion for lymphoblastic leukemogenesis. ALL with MyM has distinct genetic and clinical characteristics, associated with adverse survival outcomes after chemotherapy. CH can precede ALL years before diagnosis, and ALL with MyM is enriched with activated T cells that respond to immunotherapies such as blinatumomab.

See related commentary by Iacobucci, p. 142.
Estado estético e vida ética absoluta: entre Schiller e Hegel
Authors: Nascimento Norton Gabriel
Published: May 2024

O artigo trata de demonstrar a validade da pressuposta relação entre o pensamento de Schiller e de Hegel, a partir de dois conceitos, à primeira vista, independentes ou mesmo divergentes entre si: estado estético [ästhetischer Staat] e vida ética absoluta [absolute Sittlichkeit]. A partir de um plano de fundo comum, isto é, o momento de passagem entre os séculos XVIII e XIX, o diagnóstico da modernidade como um estado de privação e a cisão entre os domínios sensível e racional, surge a exigência de uma solução para tal problema, que leve em conta a reciprocidade e a unidade dos âmbitos humanos, o particular e o universal, na construção de um estado pautado pela liberdade. Dessa tarefa, como o presente trabalho defende, resultam dois projetos únicos, que podem ser lidos em complementariedade, uma vez que ambos almejam um fim próximo e sua execução pode ocorrer de forma coordenada. Sustenta-se que, enquanto a proposta de Schiller por uma educação estética da humanidade incide na construção de um estado estético alinhado a uma concepção de ética e justiça que exige liberdade, autonomia e reconciliação, a proposta de Hegel igualmente pressupõe, no desenvolvimento da chamada vida ética absoluta, uma formação estética da sociedade moderna.
Coronary Sinus Metabolite 12,13-diHOME Is a Novel Biomarker for Left Atrial Remodeling in Patients With Atrial Fibrillation
Authors: Tang Xixiang , Wang Jiafu , Ouyang Xiaolan , Chen Qian , Dong Ruimin , Luo Yanting , Zhong Junlin , Huang Zhuoshan , Peng Long , Xie Xujing , Zhu Jieming , Zheng Zhenda , Li Suhua
Published: May 2024

BACKGROUND:

12,13-dihydroxy-9Z-octadecenoic acid (12,13-diHOME) has shown potential in protecting against heart disease, but its relationship with atrial fibrillation (AF) remains unknown.

METHODS:

Coronary sinus (CS) and femoral vein blood samplings were synchronously collected from AF and non-AF subjects (paroxysmal supraventricular tachycardia or idiopathic premature ventricular complexes) who underwent catheter ablation. First, untargeted metabolomic profiling was performed in a discovery cohort (including 12 AF and 12 non-AF subjects) to identify the most promising CS or femoral vein metabolite. Then, the selected metabolite was further measured in a validation cohort (including 119 AF and 103 non-AF subjects) to confirm its relationship with left atrium remodeling and 1-year postablation recurrence of AF. Finally, the biological function of the selected metabolite was validated in a rapid-paced cultured HL-1 atrial cardiomyocytes model.

RESULTS:

Metabolomic analysis identified CS 12,13-diHOME as the most pronounced change metabolite correlated with left atrium remodeling in the discovery cohort. In the validation cohort, CS 12,13-diHOME was significantly lower in patients with AF than non-AF controls (84.32±20.13 versus 96.24±23.56 pg/mL;
P
<0.01), and associated with worse structural, functional, and electrical remodeling of left atrium. Multivariable regression analyses further demonstrated that decreased CS 12,13-diHOME was an independent predictor of 1-year postablation recurrence of AF (odds ratio, 0.754 [95% CI, 0.648–0.920];
P
=0.005). Biological function validations showed that 12,13-diHOME treatment significantly protect the cell viability, improved the expression of MHC (myosin heavy chain) and Cav1.2 (L-type calcium channel α1c), and attenuated mitochondrial damage in the rapid-paced cultured HL-1 cardiomyocytes model.

CONCLUSIONS:

CS metabolite 12,13-diHOME is decreased in patients with AF and can serve as a novel biomarker for left atrium remodeling.
Beating Backsliding? Episodes and Outcomes of Democratic Backsliding in Indo-Pacific Asia in the Period 1950–2022
Authors: Croissant Aurel , Hengge Anna , Wintergerst Carmen
Published: May 2024

The paper presents the first comprehensive analysis of all episodes of backsliding in democratic regimes in Indo-Pacific Asia from 1950–2022. Based on the experience of this sample of cases, this paper aims to generate insights into why some Asian democracies are more resilient to this gradual decline in the quality of democratic institutions. Using Haggard and Kaufman’s framework of the “weak democracy syndrome” and the three different kinds of mechanisms of accountability that, in theory, can beat democratic backsliding, our analysis aims to show not only how but also when different accountability mechanisms succeed or fail in stopping autocratization.
‘Where there are many cattle’ in the Eocene of Ukraine: Review of Ambositra Masner (Hymenoptera, Diapriidae, Ambositrinae) from Rovno amber, with the description of three new species
Authors: CHEMYREVA VASILISA G. , VASILENKO DMITRY V. , PERKOVSKY EVGENY E.
Published: May 2024

Three species of the genus Ambositra: A. epicnemia sp. nov., A. bicarinata sp. nov. and A. masneri sp. nov. are described from Eocene Rovno amber. The new combination Ambositra villumi (Brazidec & Vilhelmsen) comb. nov. is suggested for the extinct diapriid wasp Basalys villumi described from Baltic amber. The female of A. villumi is described. A detailed illustration of the single extant species Ambositra famosa Masner and the original illustrated key for all known Ambositra species is given. The diagnosis of the genus Ambositra is clarified.
The genus Phanagenia Banks, 1933 (Hymenoptera: Pompilidae) from China with descriptions of two new species and a key to the world species
Authors: HE YI , LI QIANG , MA LI
Published: May 2024

The genus Phanagenia Banks, 1933 from China is reviewed. Two new species, Phanagenia bidenticulata He & Ma, sp. nov. from the Oriental region (Yunnan) and Ph. cornuta He & Ma, sp. nov. from the Palaearctic region (Hebei and Inner-Mongolia), are described and illustrated from China. The genus Phanagenia and the species Ph. takasago Tsuneki, 1989 is newly recorded from the Palaearctic region. A key to the world species of the genus Phanagenia is given.
The eye in forensic practice: In the dead
Authors: Atreya Alok , Ateriya Navneet , Menezes Ritesh G
Published: May 2024

Post-mortem examination of the eye provides valuable forensic information yet is often overlooked. This brief review focuses on determining the cause/manner of death and post-mortem interval. External eye findings like corneal haziness and tache noire, combined with post-mortem changes in the iris, lens, retina and vitreous humour, can help estimate time since death. Ocular biometrics (iris/retinal scans) may facilitate identification. Age-related ocular changes can provide insights. The eye offers clues into personality (corneal tattooing, trichotillomania) and cause of death (petechiae in strangulation, retinal haemorrhages in abusive head trauma). Ocular trauma and underlying eye disease may be evident. Toxicology of vitreous humour can detect drugs/poisons. As a window into systemic disease and age-related changes, the eye aids pathology interpretations and, accordingly, post-mortem examinations have value. Ocular findings should not be overlooked in forensic examinations as they provide distinct information in determining cause/manner of death and post-mortem interval.