bluuebunny/crossref_metadata_2025 huggingface dataset:
Supplementary Figure S1 from Single-Stranded DNA Gap Accumulation Is a Functional Biomarker for USP1 Inhibitor Sensitivity
Authors: da Costa Alexandre A. , Somuncu Ozge , Ravindranathan Ramya , Mukkavalli Sirisha , Martignetti David B. , Nguyen Huy , Jiao Yuqing , Lamarre Benjamin P. , Sadatrezaei Golbahar , Moreau Lisa , Liu Joyce , Iyer Divya R. , Lazaro Jean-Bernard , Shapiro Geoffrey I. , Parmar Kalindi , D’Andrea Alan D.
Published: October 2024

Supplementary Figure S1. USP1 inhibition causes accumulation of RAD18 at the replication fork in BRCA1-deficient cancer cells
Table S6 from Chromosome 7 Gain Compensates for Chromosome 10 Loss in Glioma
Authors: Nair Nishanth Ulhas , Schäffer Alejandro A. , Gertz E. Michael , Cheng Kuoyuan , Zerbib Johanna , Sahu Avinash Das , Leor Gil , Shulman Eldad D. , Aldape Kenneth D. , Ben-David Uri , Ruppin Eytan
Published: October 2024

Table S6
Supplementary Data from Targeting YAP Activity and Glutamine Metabolism Cooperatively Suppresses Tumor Progression by Preventing Extracellular Matrix Accumulation
Authors: Park Mihyang , Jin Jonghwa , An Da Young , Kim Dong-Ho , Lee Jaebon , Yun Jae Won , Hwang Ilseon , Park Jae Seok , Kim Mi Kyung , Lee You Mie , Byun Jun-Kyu , Choi Yeon-Kyung , Park Keun-Gyu
Published: October 2024

Supplementary Data
Figure S9 from Cancer-Associated Fibroblasts Expressing Sulfatase 1 Facilitate VEGFA-Dependent Microenvironmental Remodeling to Support Colorectal Cancer
Authors: Wang Huijuan , Chen Jiaxin , Chen Xiaoyu , Liu Yingqiang , Wang Jiawei , Meng Qing , Wang Huogang , He Ying , Song Yujia , Li Jingyun , Ju Zhenyu , Xiao Peng , Qian Junbin , Song Zhangfa
Published: October 2024

Figure S9.
Figure S8 from The USP1 Inhibitor KSQ-4279 Overcomes PARP Inhibitor Resistance in Homologous Recombination–Deficient Tumors
Authors: Cadzow Louise , Brenneman Jehrod , Tobin Erica , Sullivan Pamela , Nayak Sumeet , Ali Janid A. , Shenker Sol , Griffith Jim , McGuire Michael , Grasberger Paula , Mishina Yuji , Murray Morgan , Dodson Anne E. , Gannon Hugh , Krall Elsa , Hixon Jeff , Chipumuro Edmond , Sinkevicius Kerstin , Gokhale Prafulla C. , Ganapathy Suthakar , Matulonis Ursula A. , Liu Joyce F. , Olaharski Andrew , Sangurdekar Dipen , Liu Hanlan , Wilt Jeremy , Schlabach Michael , Stegmeier Frank , Wylie Andrew A.
Published: October 2024

Combination studies using KSQ-4279 and PARP inhibitors
Figure S5 from The USP1 Inhibitor KSQ-4279 Overcomes PARP Inhibitor Resistance in Homologous Recombination–Deficient Tumors
Authors: Cadzow Louise , Brenneman Jehrod , Tobin Erica , Sullivan Pamela , Nayak Sumeet , Ali Janid A. , Shenker Sol , Griffith Jim , McGuire Michael , Grasberger Paula , Mishina Yuji , Murray Morgan , Dodson Anne E. , Gannon Hugh , Krall Elsa , Hixon Jeff , Chipumuro Edmond , Sinkevicius Kerstin , Gokhale Prafulla C. , Ganapathy Suthakar , Matulonis Ursula A. , Liu Joyce F. , Olaharski Andrew , Sangurdekar Dipen , Liu Hanlan , Wilt Jeremy , Schlabach Michael , Stegmeier Frank , Wylie Andrew A.
Published: October 2024

IHC staining of KSQ-4279 treated tumors
Figure S4 from The USP1 Inhibitor KSQ-4279 Overcomes PARP Inhibitor Resistance in Homologous Recombination–Deficient Tumors
Authors: Cadzow Louise , Brenneman Jehrod , Tobin Erica , Sullivan Pamela , Nayak Sumeet , Ali Janid A. , Shenker Sol , Griffith Jim , McGuire Michael , Grasberger Paula , Mishina Yuji , Murray Morgan , Dodson Anne E. , Gannon Hugh , Krall Elsa , Hixon Jeff , Chipumuro Edmond , Sinkevicius Kerstin , Gokhale Prafulla C. , Ganapathy Suthakar , Matulonis Ursula A. , Liu Joyce F. , Olaharski Andrew , Sangurdekar Dipen , Liu Hanlan , Wilt Jeremy , Schlabach Michael , Stegmeier Frank , Wylie Andrew A.
Published: October 2024

KSQ-4279 CryoEM workflow and resolution distribution
Supplementary Table 1 from CD47-SIRPα Blockade Sensitizes Head and Neck Squamous Cell Carcinoma to Cetuximab by Enhancing Macrophage Adhesion to Cancer Cells
Authors: Li Bolei , Hao Yu , He Hongzhi , Fan Yu , Ren Biao , Peng Xian , Zhou Xuedong , Cheng Lei
Published: October 2024

sgRNA sequences of the CRISPR pooled library
Data from Single-Stranded DNA Gap Accumulation Is a Functional Biomarker for USP1 Inhibitor Sensitivity
Authors: da Costa Alexandre A. , Somuncu Ozge , Ravindranathan Ramya , Mukkavalli Sirisha , Martignetti David B. , Nguyen Huy , Jiao Yuqing , Lamarre Benjamin P. , Sadatrezaei Golbahar , Moreau Lisa , Liu Joyce , Iyer Divya R. , Lazaro Jean-Bernard , Shapiro Geoffrey I. , Parmar Kalindi , D’Andrea Alan D.
Published: October 2024

Abstract
Recent studies suggest that PARP and POLQ inhibitors confer synthetic lethality in BRCA1-deficient tumors by accumulation of single-stranded DNA (ssDNA) gaps at replication forks. Loss of USP1, a deubiquitinating enzyme, is also synthetically lethal with BRCA1 deficiency, and USP1 inhibitors are now undergoing clinical development for these cancers. Herein, we show that USP1 inhibitors also promote the accumulation of ssDNA gaps during replication in BRCA1-deficient cells, and this phenotype correlates with drug sensitivity. USP1 inhibition increased monoubiquitinated proliferating cell nuclear antigen at replication forks, mediated by the ubiquitin ligase RAD18, and knockdown of RAD18 caused USP1 inhibitor resistance and suppression of ssDNA gaps. USP1 inhibition overcame PARP inhibitor resistance in a BRCA1-mutated xenograft model and induced ssDNA gaps. Furthermore, USP1 inhibition was synergistic with PARP and POLQ inhibition in BRCA1-mutant cells, with enhanced ssDNA gap accumulation. Finally, in patient-derived ovarian tumor organoids, sensitivity to USP1 inhibition alone or in combination correlated with the accumulation of ssDNA gaps. Assessment of ssDNA gaps in ovarian tumor organoids represents a rapid approach for predicting response to USP1 inhibition in ongoing clinical trials.

Significance: USP1 inhibitors kill BRCA1-deficient cells and cause ssDNA gap accumulation, supporting the potential of using ssDNA gap detection as a functional biomarker for clinical trials on USP1 inhibitors.
Data from FANCI Inhibition Induces PARP1 Redistribution to Enhance the Efficacy of PARP Inhibitors in Breast Cancer
Authors: Huang Yu-Zhou , Sang Ming-Yi , Xi Pei-Wen , Xu Ruo-Xi , Cai Meng-Yuan , Wang Zi-Wen , Zhao Jian-Yi , Li Yi-Han , Wei Ji-Fu , Ding Qiang
Published: October 2024

Abstract
Breast cancer is a global public health concern with high mortality rates, necessitating the development of innovative treatment strategies. PARP inhibitors have shown efficacy in certain patient populations, but their application is largely limited to cancers with homologous recombination deficiency. Here, we identified the suppression of FANCI as a therapeutic strategy to enhance the efficacy of PARP inhibitors in breast cancer. Elevated FANCI expression in breast cancer was associated with poor prognosis and increased cell proliferation and migration. FANCI interacted with PARP1, and suppressing FANCI limited the nuclear localization and functionality of PARP1. Importantly, FANCI inhibition sensitized breast cancer cells to the PARP inhibitor talazoparib in the absence of BRCA mutations. Additionally, the CDK4/6 inhibitor palbociclib enhanced the sensitivity of breast cancer cells to talazoparib through FANCI inhibition. These findings highlight the potential of targeting FANCI to enhance the efficacy of PARP inhibitors in treating breast cancer.

Significance: Targeting FANCI is a promising therapeutic strategy for enhancing PARP inhibitor sensitivity in breast cancer that holds potential for broader therapeutic applications beyond cancers harboring BRCA mutations.
Supplementary Figure S7 from YAP1 Status Defines Two Intrinsic Subtypes of LCNEC with Distinct Molecular Features and Therapeutic Vulnerabilities
Authors: Stewart C. Allison , Diao Lixia , Xi Yuanxin , Wang Runsheng , Ramkumar Kavya , Serrano Alejandra G. , Tanimoto Azusa , Rodriguez B. Leticia , Morris Benjamin B. , Shen Li , Zhang Bingnan , Yang Yan , Hamad Samera H. , Cardnell Robert J. , Duarte Alberto , Sahu Moushumi , Novegil Veronica Y. , Weissman Bernard E. , Frumovitz Michael , Kalhor Neda , Solis Soto Luisa , da Rocha Pedro , Vokes Natalie , Gibbons Don L. , Wang Jing , Heymach John V. , Glisson Bonnie , Byers Lauren Averett , Gay Carl M.
Published: October 2024

Supplementary Figure S7. Surfaceome targets in LCNEC.
Supplementary Figure S4 from YAP1 Status Defines Two Intrinsic Subtypes of LCNEC with Distinct Molecular Features and Therapeutic Vulnerabilities
Authors: Stewart C. Allison , Diao Lixia , Xi Yuanxin , Wang Runsheng , Ramkumar Kavya , Serrano Alejandra G. , Tanimoto Azusa , Rodriguez B. Leticia , Morris Benjamin B. , Shen Li , Zhang Bingnan , Yang Yan , Hamad Samera H. , Cardnell Robert J. , Duarte Alberto , Sahu Moushumi , Novegil Veronica Y. , Weissman Bernard E. , Frumovitz Michael , Kalhor Neda , Solis Soto Luisa , da Rocha Pedro , Vokes Natalie , Gibbons Don L. , Wang Jing , Heymach John V. , Glisson Bonnie , Byers Lauren Averett , Gay Carl M.
Published: October 2024

Supplementary Figure S4. Single-cell transcriptional analyses of subtype-defining genes in LCNEC biopsies.
Table 2 from A Phase Ib/II Randomized Clinical Trial of Oleclumab with or without Durvalumab plus Chemotherapy in Patients with Metastatic Pancreatic Ductal Adenocarcinoma
Authors: Coveler Andrew L. , Reilley Matthew J. , Zalupski Mark , Macarulla Teresa , Fountzilas Christos , Ponz-Sarvisé Mariano , Nagrial Adnan , Uboha Nataliya V. , Frentzas Sophia , Overman Michael , Noonan Anne , Messersmith Wells A. , Pavlakis Nick , Mettu Niharika B. , Bisha Ina , Wang Ying , Smith Paul , Murtomaki Elina , Bielska Agata A. , Bragulat Veronique , Cooper Zachary A. , Kumar Rakesh , Spigel David R.
Published: October 2024

TEAEs occurring at any severity in ≥20% of patients in any arm in the dose-expansion phase (as-treated population; N = 170).
Supplementary Table S5 from Integrative Multiomic Profiling of Triple-Negative Breast Cancer for Identifying Suitable Therapies
Authors: Jovanović Bojana , Church Sarah E. , Gorman Kara M. , North Khrystyna , Richardson Edward T. , DiLullo Molly , Attaya Victoria , Kasparian Julie , Mohammed-Abreu Ayesha , Kirkner Gregory , Hughes Melissa E. , Lin Nancy U. , Mittendorf Elizabeth A. , Schnitt Stuart J. , Tolaney Sara M. , Goel Shom
Published: October 2024

Supplementary Table S5. Differential genes and signature for luminal AR clusters.
Supplementary Figure S6 from Integrative Multiomic Profiling of Triple-Negative Breast Cancer for Identifying Suitable Therapies
Authors: Jovanović Bojana , Church Sarah E. , Gorman Kara M. , North Khrystyna , Richardson Edward T. , DiLullo Molly , Attaya Victoria , Kasparian Julie , Mohammed-Abreu Ayesha , Kirkner Gregory , Hughes Melissa E. , Lin Nancy U. , Mittendorf Elizabeth A. , Schnitt Stuart J. , Tolaney Sara M. , Goel Shom
Published: October 2024

Supplementary Figure S6. Biological profiles and clinical outcomes for TNBC based on HER2-low versus HER2-zero status.
Supplementary Figure S3 from A Phase Ib/II Randomized Clinical Trial of Oleclumab with or without Durvalumab plus Chemotherapy in Patients with Metastatic Pancreatic Ductal Adenocarcinoma
Authors: Coveler Andrew L. , Reilley Matthew J. , Zalupski Mark , Macarulla Teresa , Fountzilas Christos , Ponz-Sarvisé Mariano , Nagrial Adnan , Uboha Nataliya V. , Frentzas Sophia , Overman Michael , Noonan Anne , Messersmith Wells A. , Pavlakis Nick , Mettu Niharika B. , Bisha Ina , Wang Ying , Smith Paul , Murtomaki Elina , Bielska Agata A. , Bragulat Veronique , Cooper Zachary A. , Kumar Rakesh , Spigel David R.
Published: October 2024

ctDNA-derived genomic analysis of tumors from patients with plasma at baseline and IHC biomarkers from the dose-expansion phase of Cohort A
Supplementary Table S3 from Second Primary Malignancies after CAR T-Cell Therapy: A Systematic Review and Meta-analysis of 5,517 Lymphoma and Myeloma Patients
Authors: Tix Tobias , Alhomoud Mohammad , Shouval Roni , Cliff Edward R. Scheffer , Perales Miguel-Angel , Cordas dos Santos David M. , Rejeski Kai
Published: October 2024

Detailled breakdown of SPM entities: Solid tumors.
Supplementary Table S2 from Second Primary Malignancies after CAR T-Cell Therapy: A Systematic Review and Meta-analysis of 5,517 Lymphoma and Myeloma Patients
Authors: Tix Tobias , Alhomoud Mohammad , Shouval Roni , Cliff Edward R. Scheffer , Perales Miguel-Angel , Cordas dos Santos David M. , Rejeski Kai
Published: October 2024

Detailled breakdown of SPM entities: Hematological Malignancies.
Supplementary Data 1 from Remote Neuroinflammation in Newly Diagnosed Glioblastoma Correlates with Unfavorable Clinical Outcome
Authors: Bartos Laura M. , Quach Stefanie , Zenatti Valerio , Kirchleitner Sabrina V. , Blobner Jens , Wind-Mark Karin , Kolabas Zeynep Ilgin , Ulukaya Selin , Holzgreve Adrien , Ruf Viktoria C. , Kunze Lea H. , Kunte Sebastian T. , Hoermann Leonie , Härtel Marlies , Park Ha Eun , Groß Mattes , Franzmeier Nicolai , Zatcepin Artem , Zounek Adrian , Kaiser Lena , Riemenschneider Markus J. , Perneczky Robert , Rauchmann Boris-Stephan , Stöcklein Sophia , Ziegler Sibylle , Herms Jochen , Ertürk Ali , Tonn Joerg C. , Thon Niklas , von Baumgarten Louisa , Prestel Matthias , Tahirovic Sabina , Albert Nathalie L. , Brendel Matthias
Published: October 2024

Supplementary Figures 1, 2 Supplementary Tables 1 - 3 inlucing Representativeness of Study Participants" supplementary table (Supplementary Table 1)
Figure 3 from Remote Neuroinflammation in Newly Diagnosed Glioblastoma Correlates with Unfavorable Clinical Outcome
Authors: Bartos Laura M. , Quach Stefanie , Zenatti Valerio , Kirchleitner Sabrina V. , Blobner Jens , Wind-Mark Karin , Kolabas Zeynep Ilgin , Ulukaya Selin , Holzgreve Adrien , Ruf Viktoria C. , Kunze Lea H. , Kunte Sebastian T. , Hoermann Leonie , Härtel Marlies , Park Ha Eun , Groß Mattes , Franzmeier Nicolai , Zatcepin Artem , Zounek Adrian , Kaiser Lena , Riemenschneider Markus J. , Perneczky Robert , Rauchmann Boris-Stephan , Stöcklein Sophia , Ziegler Sibylle , Herms Jochen , Ertürk Ali , Tonn Joerg C. , Thon Niklas , von Baumgarten Louisa , Prestel Matthias , Tahirovic Sabina , Albert Nathalie L. , Brendel Matthias
Published: October 2024

Contralateral TSPO-PET signal elevation is associated with persisting epileptic seizures and worse overall survival. A, Contralateral TSPO-PET shows no quantitative difference between patients presenting with (n = 20) and without (n = 20) epileptic seizures at inital diagnosis (top). Significant increase of contralateral TSPO expression in patients experiencing persisting epileptic seizures after treatment of the primary tumor site (n = 8) compared to patients with discontinued seizures (n = 12; bottom). B, Heatmap of contralateral TSPO-PET signal in anatomically and functionally predefined brain regions (n = 15) of all patients experiencing epileptic seizures at initial diagnosis highlights two patients (age: in their 70s) with strongest contralateral TSPO expression. Coronal slices of TSPO-PET of these two patients are illustrated in comparison to group average images of patients with discontinued and persisting epileptic seizures after tumor therapy. White arrows point toward the tumor. C, Patients with persisting epileptic seizures indicate significant signal elevation in several contralateral brain regions with predominance in motor cortex, mesial temporal lobe, and occipital lobe compared to patients with discontinued epileptic seizures. *, P < 0.01. D, Matrix of regional TSPO-PET inter-correlation coefficients in comparison of patients with discontinued and persisting seizures as well as controls. Single boxes indicate interregional Pearson’s R. E, Significant increase of the contralateral TSPO-PET signal in patients with short overall survival (≤10.7 months; median split). F, High contralateral TSPO-PET signal (>0.88 SUVr; median split) at initial diagnosis is associated with worse overall survival in patients with glioblastoma. Multivariate Cox regression was adjusted for age, glucocorticoid medication, subsequent radiotherapy, and TSPO-PET signal of the tumor. **, P < 0.01. G and H, Distinct predictive value of contralateral TSPO-PET signal in different sub-regions on overall survival. *, P < 0.05.
Supplementary Figure S10 from Second Primary Malignancies after CAR T-Cell Therapy: A Systematic Review and Meta-analysis of 5,517 Lymphoma and Myeloma Patients
Authors: Tix Tobias , Alhomoud Mohammad , Shouval Roni , Cliff Edward R. Scheffer , Perales Miguel-Angel , Cordas dos Santos David M. , Rejeski Kai
Published: October 2024

Follow-up of studies reporting below median age show an increased follow-up.
Supplementary Table S4 from Evaluating Debio 1347 in Patients with FGFR Fusion-Positive Advanced Solid Tumors from the FUZE Multicenter, Open-Label, Phase II Basket Trial
Authors: Grivas Petros , Garralda Elena , Meric-Bernstam Funda , Mellinghoff Ingo K. , Goyal Lipika , Harding James J. , Dees E. Claire , Bahleda Rastislav , Azad Nilofer S. , Karippot Asha , Kurzrock Razelle , Tabernero Josep , Kononen Juha , Ng Matthew C.H. , Mehta Rutika , Uboha Nataliya V. , Bigot Frédéric , Boni Valentina , Bowyer Samantha E. , Breder Valeriy , Cervantes Andrés , Chan Nancy , Cleary James M. , Dhawan Mallika , Eefsen Rikke L. , Ewing James , Graham Donna M. , Guren Tormod K. , Won Kim Jin , Koynov Krassimir , Oh Do-Youn , Redman Rebecca , Yen Chia-Jui , Spetzler David , Roubaudi-Fraschini Marie-Claude , Nicolas-Metral Valerie , Ait-Sarkouh Rafik , Zanna Claudio , Ennaji Abdallah , Pokorska-Bocci Anna , Flaherty Keith T.
Published: October 2024

Supplementary Table S4. Baseline characteristics and outcomes of patients in the intention-to-treat population with response according to central review.
Supplementary Table S10 from Evaluating Debio 1347 in Patients with FGFR Fusion-Positive Advanced Solid Tumors from the FUZE Multicenter, Open-Label, Phase II Basket Trial
Authors: Grivas Petros , Garralda Elena , Meric-Bernstam Funda , Mellinghoff Ingo K. , Goyal Lipika , Harding James J. , Dees E. Claire , Bahleda Rastislav , Azad Nilofer S. , Karippot Asha , Kurzrock Razelle , Tabernero Josep , Kononen Juha , Ng Matthew C.H. , Mehta Rutika , Uboha Nataliya V. , Bigot Frédéric , Boni Valentina , Bowyer Samantha E. , Breder Valeriy , Cervantes Andrés , Chan Nancy , Cleary James M. , Dhawan Mallika , Eefsen Rikke L. , Ewing James , Graham Donna M. , Guren Tormod K. , Won Kim Jin , Koynov Krassimir , Oh Do-Youn , Redman Rebecca , Yen Chia-Jui , Spetzler David , Roubaudi-Fraschini Marie-Claude , Nicolas-Metral Valerie , Ait-Sarkouh Rafik , Zanna Claudio , Ennaji Abdallah , Pokorska-Bocci Anna , Flaherty Keith T.
Published: October 2024

Supplementary Table S10. Treatment-emergent adverse events considered by the investigator to be related to the study drug occurring at any grade in ≥10% of patients (safety population).
Supplementary Table S1 from Evaluating Debio 1347 in Patients with FGFR Fusion-Positive Advanced Solid Tumors from the FUZE Multicenter, Open-Label, Phase II Basket Trial
Authors: Grivas Petros , Garralda Elena , Meric-Bernstam Funda , Mellinghoff Ingo K. , Goyal Lipika , Harding James J. , Dees E. Claire , Bahleda Rastislav , Azad Nilofer S. , Karippot Asha , Kurzrock Razelle , Tabernero Josep , Kononen Juha , Ng Matthew C.H. , Mehta Rutika , Uboha Nataliya V. , Bigot Frédéric , Boni Valentina , Bowyer Samantha E. , Breder Valeriy , Cervantes Andrés , Chan Nancy , Cleary James M. , Dhawan Mallika , Eefsen Rikke L. , Ewing James , Graham Donna M. , Guren Tormod K. , Won Kim Jin , Koynov Krassimir , Oh Do-Youn , Redman Rebecca , Yen Chia-Jui , Spetzler David , Roubaudi-Fraschini Marie-Claude , Nicolas-Metral Valerie , Ait-Sarkouh Rafik , Zanna Claudio , Ennaji Abdallah , Pokorska-Bocci Anna , Flaherty Keith T.
Published: October 2024

Supplementary Table S1. Representativeness of study participants.
Supplementary Table S6 from Transcriptomic Heterogeneity of EGFR-Mutant Non–Small Cell Lung Cancer Evolution Toward Small-Cell Lung Cancer
Authors: Oh Songji , Koh Jaemoon , Kim Tae Min , Kim Soyeon , Youk Jeonghwan , Kim Miso , Keam Bhumsuk , Jeon Yoon Kyung , Ku Ja-Lok , Kim Dong-Wan , Chung Doo Hyun , Heo Dae Seog
Published: October 2024

Supplementary Table S6. The RNA-seq results of two t-SCLC cell lines (log2(FPKM+1)).
Supplementary Table S4 from Transcriptomic Heterogeneity of EGFR-Mutant Non–Small Cell Lung Cancer Evolution Toward Small-Cell Lung Cancer
Authors: Oh Songji , Koh Jaemoon , Kim Tae Min , Kim Soyeon , Youk Jeonghwan , Kim Miso , Keam Bhumsuk , Jeon Yoon Kyung , Ku Ja-Lok , Kim Dong-Wan , Chung Doo Hyun , Heo Dae Seog
Published: October 2024

Supplementary Table S4. The analysis results of DEGs for EGFR-mutant LADC versus SCLC.
Supplementary Table S2 from The Impact of Li‐Fraumeni and Germline Retinoblastoma Mutations on Leiomyosarcoma Initiation, Outcomes, and Genetic Testing Recommendations
Authors: Dermawan Josephine K. , Abramson David H. , Chiang Sarah , Hensley Martee L. , Tap William D. , Movva Sujana , Maki Robert G. , Mandelker Diana , Antonescu Cristina R.
Published: October 2024

Supplementary Table S2. Representativeness of Study Participants.
Supplementary Figure S3 from The Impact of Li‐Fraumeni and Germline Retinoblastoma Mutations on Leiomyosarcoma Initiation, Outcomes, and Genetic Testing Recommendations
Authors: Dermawan Josephine K. , Abramson David H. , Chiang Sarah , Hensley Martee L. , Tap William D. , Movva Sujana , Maki Robert G. , Mandelker Diana , Antonescu Cristina R.
Published: October 2024

Supplementary Figure S3. Outcome of germline vs sporadic uterine leiomyosarcoma (ULMS) patients.
Supplementary Figure S1 from Transcriptomic Heterogeneity of EGFR-Mutant Non–Small Cell Lung Cancer Evolution Toward Small-Cell Lung Cancer
Authors: Oh Songji , Koh Jaemoon , Kim Tae Min , Kim Soyeon , Youk Jeonghwan , Kim Miso , Keam Bhumsuk , Jeon Yoon Kyung , Ku Ja-Lok , Kim Dong-Wan , Chung Doo Hyun , Heo Dae Seog
Published: October 2024

Supplementary Figure S1. Whole transcriptome data production using GeoMx® digital spatial profiler (DSP) system.
Supplementary Table S2 from HER2 Antibody–Drug Conjugates Are Active against Desmoplastic Small Round Cell Tumor
Authors: Zhang Tom , Febres-Aldana Christopher A. , Liu Zebing , Dix Jenna-Marie , Cheng Ryan , Dematteo Raymond G. , Lui Allan J.W. , Khodos Inna , Gili Leo , Mattar Marissa S. , Lisanti Jeanine , Kwong Charlene , Linkov Irina , Tipping Murray J. , de Stanchina Elisa , Odintsov Igor , Ladanyi Marc , Somwar Romel
Published: October 2024

Supplementary Table S2
Supplementary Figure S7 from Tumor-Secreted Extracellular Vesicles Counteract Therapy Response by Triggering Inflammatory Mesenchymal Stem Cell Development
Authors: Massaro Crescenzo , Sensoy Hilal N. , Mulders Manon , De Schrijver Celine , Gómez-Martín Cristina , Simon Nieto Juan , Lagerweij Tonny , Atmopawiro Alisha , Pérez-Boza Jennifer , Bebelman Maarten , Bosch Leontien , Foderaro Simone , Neves Ferreira Mafalda , van Eijndhoven Monique A.J. , van Weering Jan R.T. , Dell’Aversana Carmela , Altucci Lucia , Savci-Heijink Cemile Dilara , van de Donk Niels W.C.J. , Giorgio Cristina , Brandolini Laura , Allegretti Marcello , Pegtel Dirk Michiel , Baglio Serena Rubina
Published: October 2024

Suppl. Figure 7. a) Dynasore-mediated inhibition of PKH67-labeled EV uptake by MSCs as assessed by FACS. b-e) Relative expression levels of CXCL2, CXCL5, CXCL3, CXCL6 in MSCs treated with 143B EVs in the presence or absence of dynasore. Transcript levels are normalized to GAPDH and expressed as fold increase relative to the experimental controls (untreated or dynasore-treated MSCs). Graphs show the average of 3 (CXCL2 and CXCL6) or 2 (CXCL3 and CXCL5) experiments. Statistics was calculated on normalized expression data, *p < 0.05, two-tailed t test. f) Volcano plots depicting differentially expressed interferon stimulated genes (ISGs) in MSCs exposed to 143B EVs, and relative log2FC and FDR values. Human fibroblast (hF) EVs were used as control vesicles. g-j) Expression of the ISGs IFIT1, IFITM1, MX1 and OAS2 in BM-MSCs upon transfection with (143B) EV RNA pre-treated or not with RNase III or RNase A. k-n) Syntenin, IL8, CXCL2 and CXCL3 mRNA expression levels in 143B stably transduced with dox-inducible shRNAs against syntenin or GFP as non-targeting control, in the presence or absence of doxycycline. o-r) RAB35, IL8, CXCL2 and CXCL3 mRNA expression levels in 143B stably transduced with dox-inducible shRab35 or shGFP in the presence or absence of doxycycline.
Supplementary Figure S6 from Tumor-Secreted Extracellular Vesicles Counteract Therapy Response by Triggering Inflammatory Mesenchymal Stem Cell Development
Authors: Massaro Crescenzo , Sensoy Hilal N. , Mulders Manon , De Schrijver Celine , Gómez-Martín Cristina , Simon Nieto Juan , Lagerweij Tonny , Atmopawiro Alisha , Pérez-Boza Jennifer , Bebelman Maarten , Bosch Leontien , Foderaro Simone , Neves Ferreira Mafalda , van Eijndhoven Monique A.J. , van Weering Jan R.T. , Dell’Aversana Carmela , Altucci Lucia , Savci-Heijink Cemile Dilara , van de Donk Niels W.C.J. , Giorgio Cristina , Brandolini Laura , Allegretti Marcello , Pegtel Dirk Michiel , Baglio Serena Rubina
Published: October 2024

Suppl. Figure 6. a-b) Expression of the most upregulated TGFβ-dependent (a) and independent/partially dependent (b) genes in bone marrow MSCs based on RNA-seq normalized counts. c-f) Relative expression levels of CXCL1, CXCL2, CXCL5, CXCL6 mRNAs in bone marrow MSCs (donor #1) exposed to 143B EVs in the presence or absence of the TGFBR1 inhibitor SB-431542 as assessed by RT-qPCR. g-m) Relative expression levels of IL6, IL8, CXCL1, CXCL2, CXCL3, CXCL5, CXCL6 mRNAs in bone marrow MSCs (donor #2) exposed to 143B EVs in the presence or absence of the TGFBR1 inhibitor EW-7197. n-o) Relative expression of IL6 and IL8 mRNAs in adipose-derived MSCs (donor #3) exposed to 143B EVs in the presence or absence of EW-7197.
Supplementary Figure S5 from Tumor-Secreted Extracellular Vesicles Counteract Therapy Response by Triggering Inflammatory Mesenchymal Stem Cell Development
Authors: Massaro Crescenzo , Sensoy Hilal N. , Mulders Manon , De Schrijver Celine , Gómez-Martín Cristina , Simon Nieto Juan , Lagerweij Tonny , Atmopawiro Alisha , Pérez-Boza Jennifer , Bebelman Maarten , Bosch Leontien , Foderaro Simone , Neves Ferreira Mafalda , van Eijndhoven Monique A.J. , van Weering Jan R.T. , Dell’Aversana Carmela , Altucci Lucia , Savci-Heijink Cemile Dilara , van de Donk Niels W.C.J. , Giorgio Cristina , Brandolini Laura , Allegretti Marcello , Pegtel Dirk Michiel , Baglio Serena Rubina
Published: October 2024

Suppl. Figure 5. a-b) CD63 (a) and CD81 (b) protein quantification (western blot pixel density) in EVs released by engineered (shGFP, shSyntenin, shRab11b, shRab35) 143B cells. c) Growth curve of wt and engineered (shGFP, shRab11b, shRab35, shSyntenin) 143B showing no differences in cell growth over 72 hours). d-e) Relative mRNA expression levels of IL6 (d) and IL8 (e) in MSCs exposed to indicated volumes of wild type 143B EVs.
Supplementary Figure S3 from Tumor-Secreted Extracellular Vesicles Counteract Therapy Response by Triggering Inflammatory Mesenchymal Stem Cell Development
Authors: Massaro Crescenzo , Sensoy Hilal N. , Mulders Manon , De Schrijver Celine , Gómez-Martín Cristina , Simon Nieto Juan , Lagerweij Tonny , Atmopawiro Alisha , Pérez-Boza Jennifer , Bebelman Maarten , Bosch Leontien , Foderaro Simone , Neves Ferreira Mafalda , van Eijndhoven Monique A.J. , van Weering Jan R.T. , Dell’Aversana Carmela , Altucci Lucia , Savci-Heijink Cemile Dilara , van de Donk Niels W.C.J. , Giorgio Cristina , Brandolini Laura , Allegretti Marcello , Pegtel Dirk Michiel , Baglio Serena Rubina
Published: October 2024

Suppl. Figure 3. a-e) Relative expression levels of IL6, IL8, CXCL2, CXCL3 and CXCL6 in MSCs from an independent donor (MSC#2) exposed to plasma-derived EVs from healthy donor #1 (H#1) and MM patient #1 (MM#1).
Data from Artificial Intelligence-Powered Spatial Analysis of Tumor-Infiltrating Lymphocytes as a Potential Biomarker for Immune Checkpoint Inhibitors in Patients with Biliary Tract Cancer
Authors: Bang Yeong Hak , Lee Choong-kun , Bang Kyunghye , Kim Hyung-Don , Kim Kyu-pyo , Jeong Jae Ho , Park Inkeun , Ryoo Baek-Yeol , Lee Dong Ki , Choi Hye Jin , Chung Taek , Jeon Seung Hyuck , Shin Eui-Cheol , Oum Chiyoon , Kim Seulki , Lim Yoojoo , Park Gahee , Ahn Chang Ho , Lee Taebum , Finn Richard S. , Ock Chan-Young , Shin Jinho , Yoo Changhoon
Published: October 2024

AbstractPurpose:
Recently, anti-programmed cell death-1/anti-programmed cell death ligand-1 (anti-PD1/L1) immunotherapy has been demonstrated for its efficacy when combined with cytotoxic chemotherapy in randomized phase 3 trials for advanced biliary tract cancer (BTC). However, no biomarker predictive of benefit has been established for anti-PD1/L1 in BTC. Here, we evaluated tumor-infiltrating lymphocytes (TIL) using artificial intelligence-powered immune phenotype (AI-IP) analysis in advanced BTC treated with anti-PD1.
Experimental Design:
Pretreatment hematoxylin and eosin (H&E)–stained whole-slide images from 339 patients with advanced BTC who received anti-PD1 as second-line treatment or beyond, were employed for AI-IP analysis and correlative analysis between AI-IP and efficacy outcomes with anti-PD1. Next, data and images of the BTC cohort from The Cancer Genome Atlas (TCGA) were additionally analyzed to evaluate the transcriptomic and mutational characteristics of various AI-IP in BTC.
Results:
Overall, AI-IP were classified as inflamed [high intratumoral TIL (iTIL)] in 40 patients (11.8%), immune-excluded (low iTIL and high stromal TIL) in 167 patients (49.3%), and immune-desert (low TIL overall) in 132 patients (38.9%). The inflamed IP group showed a substantially higher overall response rate compared with the noninflamed IP groups (27.5% vs. 7.7%, P < 0.001). Median overall survival and progression-free survival were significantly longer in the inflamed IP group than in the noninflamed IP group (OS, 12.6 vs. 5.1 months; P = 0.002; PFS, 4.5 vs. 1.9 months; P < 0.001). In the TCGA cohort analysis, the inflamed IP showed increased cytolytic activity scores and IFNγ signature compared with the noninflamed IP.
Conclusions:
AI-IP based on spatial TIL analysis was effective in predicting the efficacy outcomes in patients with BTC treated with anti-PD1 therapy. Further validation is necessary in the context of anti-PD1/L1 plus gemcitabine–cisplatin.
Data from Transcriptomic Heterogeneity of EGFR-Mutant Non–Small Cell Lung Cancer Evolution Toward Small-Cell Lung Cancer
Authors: Oh Songji , Koh Jaemoon , Kim Tae Min , Kim Soyeon , Youk Jeonghwan , Kim Miso , Keam Bhumsuk , Jeon Yoon Kyung , Ku Ja-Lok , Kim Dong-Wan , Chung Doo Hyun , Heo Dae Seog
Published: October 2024

AbstractPurpose:
Histologic transformation from EGFR-mutant non–small cell lung cancer (NSCLC) to small-cell lung cancer (SCLC) is a key mechanism of resistance to EGFR tyrosine kinase inhibitors (TKI). However, transcriptomic changes between NSCLC and transformed SCLC (t-SCLC) remain unexplored.
Experimental Design:
We conducted whole-transcriptome analysis of 59 regions of interest through the spatial profiling of formalin-fixed, paraffin-embedded tissues obtained from 10 patients (lung adenocarcinoma, 22; combined SCLC/NSCLC, 7; and t-SCLC, 30 regions of interests). Transcriptomic profiles and differentially expressed genes were compared between pre- and post-transformed tumors.
Results:
Following EGFR-TKI treatment, 93.7% (15/16) of t-SCLC components evolved into neuroendocrine-high subtypes (SCLC-A or SCLC-N). The transition to t-SCLC occurred regardless of EGFR-TKI treatment and EGFR mutational status, with a notable decrease in EGFR expression (P < 0.001) at both mRNA and protein levels. Pathway analysis revealed that gene overexpression was related to epigenetic alterations in t-SCLC. Interestingly, histone deacetylase inhibitors restored EGFR expression in SNU-2962A cells and their organoid model. The synergistic effects of third-generation EGFR-TKI osimertinib and the histone deacetylase inhibitor fimepinostat were validated in both in vitro and in vivo models.
Conclusions:
Our study demonstrated that most t-SCLC cases showed neuronal subtypes with low EGFR expression. Differentially expressed gene analysis and t-SCLC preclinical models identified an epigenetic modifier as a promising treatment strategy for t-SCLC.
Data from The Impact of Li‐Fraumeni and Germline Retinoblastoma Mutations on Leiomyosarcoma Initiation, Outcomes, and Genetic Testing Recommendations
Authors: Dermawan Josephine K. , Abramson David H. , Chiang Sarah , Hensley Martee L. , Tap William D. , Movva Sujana , Maki Robert G. , Mandelker Diana , Antonescu Cristina R.
Published: October 2024

AbstractPurpose:
Leiomyosarcomas (LMS) are clinically and molecularly heterogeneous, occurring mostly in sporadic but also syndromic settings. The role of pathogenic germline variants (PGV) as LMS drivers and their impact on outcomes remains uncertain.
Experimental Design:
We performed a comprehensive clinicopathologic and molecular analysis using a tumor-normal DNA next-generation sequencing assay (Memorial Sloan Kettering–Integrated Mutational Profiling of Actionable Cancer Targets) of germline-associated LMS compared with sporadic LMS.
Results:
Among 285 LMS [120 soft-tissue LMS (STLMS) and 165 uterine LMS (ULMS)] with germline testing, 78 (27%, 43 STLMS and 35 ULMS) cases harbored PGV, with 35/78 (45%) of PGV carriers showing biallelic inactivation of the corresponding gene in the tumor (26 STLMS and nine ULMS). The most frequent germline predispositions were TP53 (Li‐Fraumeni syndrome; 17 patients, 16 in STLMS) and RB1 (retinoblastoma; 13 patients, 11 in STLMS). Germline TP53 and somatic RB1 alterations often co-occurred in the tumor andvice versa. Other biallelically inactivated PGV were enriched in DNA damage repair–related genes: CHEK2, MSH2, MSH6, RAD51D, BRCA2, and FANCA. Monoallelic PGV were mostly in ULMS and associated with co-occurring TP53 and RB1 somatic alterations. Patients with STLMS with biallelic but not monoallelic PGV were significantly younger than patients with sporadic STLMS (median ages 38 vs. 52 vs. 58 years). No differences in disease-specific or progression-free survival were observed in germline-associated versus sporadic LMS regardless of biallelic status.
Conclusions:
Although patients with ULMS had a relatively low proportion of PGV, a high percentage of patients with STLMS with PGV had tumor biallelic status, indicating that PGV drive tumorigenesis in these individuals. These findings have significant implications for genetic testing recommendations.
Table S1 from Oncogenic Mutant p53 Sensitizes Non–Small Cell Lung Cancer Cells to Proteasome Inhibition via Oxidative Stress–Dependent Induction of Mitochondrial Apoptosis
Authors: Chougoni Kranthi Kumar , Neely Victoria , Ding Boxiao , Oduah Eziafa , Lam Vianna T. , Hu Bin , Koblinski Jennifer E. , Windle Bradford E. , Palit Deb Swati , Deb Sumitra , Nieva Jorge J. , Radhakrishnan Senthil K. , Harada Hisashi , Grossman Steven R.
Published: October 2024

Table S1
Figure 5 from Oncogenic Mutant p53 Sensitizes Non–Small Cell Lung Cancer Cells to Proteasome Inhibition via Oxidative Stress–Dependent Induction of Mitochondrial Apoptosis
Authors: Chougoni Kranthi Kumar , Neely Victoria , Ding Boxiao , Oduah Eziafa , Lam Vianna T. , Hu Bin , Koblinski Jennifer E. , Windle Bradford E. , Palit Deb Swati , Deb Sumitra , Nieva Jorge J. , Radhakrishnan Senthil K. , Harada Hisashi , Grossman Steven R.
Published: October 2024

Navitoclax enhances BTZ-induced cytotoxicity. A and B, H1975 and H460 cells were treated with vehicle or the indicated concentrations of navitoclax with/without BTZ (2 nmol/L) for 96 hours. Cell viability was determined by WST-1 assay. C, H1975-Control or H1975-p53KO cells were treated with vehicle or the indicated concentrations of navitoclax with/without BTZ (5 nmol/L) for 96 hours. Cell viability was determined by WST-1 assay. D and E, NOD-SCID-II.2 receptor gamma null (NSG) mice were injected with 3.0 × 106 H1975 (D) or 1.0 × 106 H460 cells (E), and once tumors became palpable, mice were treated for 3 weeks with vehicle (control) or the combination of BTZ (1.0 mg/kg) 2×/week via intraperitoneal injection + navitoclax (NAV; 80 mg/kg) 3×/week via oral gavage + carboplatin (CBP; 25 mg/kg) once weekly via intraperitoneal injection. The period of treatment is indicated by the horizontal bar, and tumor volumes were measured twice weekly (N = 6 mice/group). *, P < 0.05; **, P < 0.01; ***, P < 0.005; ns indicates P > 0.05. Error bars indicate ± 1.0 SD., except in D and E in which error bars indicate SEM.
Figure 3 from Oncogenic Mutant p53 Sensitizes Non–Small Cell Lung Cancer Cells to Proteasome Inhibition via Oxidative Stress–Dependent Induction of Mitochondrial Apoptosis
Authors: Chougoni Kranthi Kumar , Neely Victoria , Ding Boxiao , Oduah Eziafa , Lam Vianna T. , Hu Bin , Koblinski Jennifer E. , Windle Bradford E. , Palit Deb Swati , Deb Sumitra , Nieva Jorge J. , Radhakrishnan Senthil K. , Harada Hisashi , Grossman Steven R.
Published: October 2024

BTZ induces ATF3/NOXA and caspase-dependent apoptosis. A, H1975 cells were pretreated (30 minutes) with vehicle or the pan-caspase inhibitor QVD-OPh (QVD; 1 µmol/L) and then treated with vehicle or BTZ (5 nmol/L) for 48 hours. Cell viability was determined by trypan blue exclusion assay. B, H1975 cells were treated as in A, and the percentage of apoptotic cells was determined by annexin V–propidium iodide staining followed by FACS analysis. C, Cell lysates from A were immunoblotted with the indicated antibodies. D, H1975 or H460 cells were treated with vehicle or 2 or 5 nmol/L of BTZ for 48 hours, and cell lysates were immunoblotted with the indicated antibodies. E, RNA from D was extracted and subjected to qRT-PCR with NOXA primers. F, H1975 cells stably expressing shC or shNOXA were treated with vehicle or BTZ (5 nmol/L) for 48 hours, and cell lysates were immunoblotted with the indicated antibodies. G, H1975 cells were treated with vehicle or 2 or 5 nmol/L of BTZ for 48 hours, and mRNA expression of ATF3 was analyzed by qRT-PCR. H, H1975 cells were treated with vehicle, NAC (1 mmol/L), BTZ (5 nmol/L), or BTZ + NAC for 48 hours, and cell lysates were immunoblotted with indicated antibodies. I, H1975 cells stably expressing control shRNA (shC) or ATF3 shRNA (shATF3) were treated with vehicle or BTZ (5 nmol/L) for 48 hours, and cell lysates were immunoblotted with the indicated antibodies. J, H1975 cells stably expressing shC or shATF3 were treated with vehicle or BTZ (5 nmol/L) for 48 hours, and the percentage of apoptotic cells was determined by annexin V–propidium iodide staining followed by FACS analysis. **, P < 0.01; ***, P < 0.005; ns indicates P > 0.05. Error bars indicate ± 1.0 SD. Cl. Casp 3, cleaved caspase-3.
Figure 2 from Oncogenic Mutant p53 Sensitizes Non–Small Cell Lung Cancer Cells to Proteasome Inhibition via Oxidative Stress–Dependent Induction of Mitochondrial Apoptosis
Authors: Chougoni Kranthi Kumar , Neely Victoria , Ding Boxiao , Oduah Eziafa , Lam Vianna T. , Hu Bin , Koblinski Jennifer E. , Windle Bradford E. , Palit Deb Swati , Deb Sumitra , Nieva Jorge J. , Radhakrishnan Senthil K. , Harada Hisashi , Grossman Steven R.
Published: October 2024

Onc-p53 NSCLC cells exhibit basal and PI-induced oxidative stress. A, Average oxidized (GSSG) vs. reduced (GSH) levels of GSH obtained from metabolomic profiles (DepMap) of NSCLC cell lines that either express Onc-p53 protein (Onc-p53) or lack p53 protein expression due to homozygous deletion/frameshift/premature termination mutations (loss of function; LOF). Data were analyzed using the unpaired t test. B, GSH concentration was determined in lysates of the indicated cell lines. C, Relative GSH concentrations were determined in lysates of H1975-Control vs. H1975-p53KO cells. D, Levels of ROS were determined in the indicated cell lines using a fluorescent ROS detection assay and plotted as mean fluorescence units (MFU). E, H460 or H1975 cells were treated with vehicle, BTZ (5 nmol/L), NAC (1 mmol/L), or BTZ + NAC for 24 hours. Relative ROS levels normalized to vehicle treatment for each cell line were determined by staining with DCFH-DA followed by flow cytometry. F, H1975 cells were treated as per E for 48 hours, and cell viability was assessed by trypan blue exclusion. All pairwise comparisons were made using the Student t test. *, P < 0.05; **, P < 0.01; ***, P < 0.005. Error bars indicate ± 1.0 SD.
Study of Molecular Docking, Molecular Dynamics, Pharmacokinetics and Toxicity Prediction: Compounds from Nigella sativa Linn, Andrographis paniculata Nees, and Propolis as Inhibitors of Mycobacterium tuberculosis Growth
Authors: Asarini  , Abdillah Syamsudin , Sani Yulvian , Alam Gemini
Published: October 2024

Background: Tuberculosis (TB) is caused by *Mycobacterium tuberculosis*, and Multiple Drug-Resistant Tuberculosis (MDR-TB) arises from resistance to first-line treatments like Rifampicin and Isoniazid. Since current TB medications have been used for over four decades, discovering new drug candidates is critical. This research focuses on herbal compounds—Black cumin (*Nigella sativa*), Sambiloto (*Andrographis paniculata*), and propolis—as potential inhibitors of *M. tuberculosis* by targeting DHFR. The objective of the study is to predict the activity of these herbal compounds prior to in vitro and in vivo testing.
Methods: This study employed computational tools, including Molegro Virtual Docking (MVD) and Molecular Dynamics (MD), to assess the interactions of the herbal compounds with DHFR (PDB ID: 2CIG). Pharmacokinetic predictions were also conducted to evaluate the absorption and toxicity of the compounds.
Results: Molecular docking and MD simulations indicated that Andrographolide, Thymoquinone, and Caffeic Acid Phenethyl Ester effectively inhibited the growth of *M. tuberculosis*. The analysis revealed favorable binding interactions and conformational changes in DHFR, with significant activity observed for Thymoquinone.
Conclusion: This study suggests that Andrographolide, Thymoquinone, and Caffeic Acid Phenethyl Ester may serve as promising candidates for further development as anti-tuberculosis drugs. Subsequent in vitro and in vivo studies are warranted to validate their therapeutic potential.
Morpho-phylogenetic evidence reveals Pseudobionectria phoenicis gen. et sp. nov. (Bionectriaceae) from a mangrove habitat
Authors: ZHANG SHENG-NAN , HYDE KEVIN D. , LIU JIAN-KUI
Published: October 2024

A bionectriaceous ascomycete was collected from palm rachides in a mangrove habitat. Multi-gene phylogenetic analyses indicated this fungus belongs within the Bionectriaceae, forming a sister lineage to Septofusidium herbarum and distinct from other known genera. In this study, we proposed the new genus Pseudobionectria to accommodate the novel species P. phoenicis. Pseudobionectria is distinguished from other genera in Bionectriaceae by its superficial, globose, brownish-orange ascomata with a black crown that is flattened on the top and hyphal appendages that merge with the subiculum below. The asci are unitunicate, lacking a visible apical ring, and the ascospores are 1-septate, oblong-ellipsoidal to fusiform, hyaline, and exhibit spinose ornamentation. The establishment of this new genus is supported by morphological and phylogenetic evidence. Additionally, this paper provides a synopsis of the genera within Bionectriaceae, including information on the type species, morphological characteristics, lifestyles, molecular data and key publications.
Erratum: V. A. PAITHANE, A. S. BHUKTAR, A. R. CHORGHE, K. V. C. GOSAVI, R. P. KASHETTI & S. B. PATIL (2024) Dimeria anandibaiana (Poaceae: Panicoideae): a new species from Konkan region of Maharashtra, India. Phytotaxa 661 (2): 150–156.
Authors: PAITHANE V. A. , BHUKTAR A. S. , CHORGHE A. R. , GOSAVI K. V. C. , KASHETTI R. P. , PATIL S. B.
Published: October 2024

N/A
A new species of the Genus Margattea (Blattodea: Pseudophyllodromiidae) from Yonaguni-jima Island, the Ryukyus, Japan
Authors: HAYASHI KOKI
Published: October 2024

A new species of the cockroach genus Margattea Shellford, 1911 (Blattodea: Pseudophyllodromiidae) is described from Yonaguni-jima Island, the Ryukyus, Japan. The new species M. ventrinigra sp. nov. was compared with three species of the same genus on the basis of morphology and mitochondrial DNA sequences (COI and COII): M. satsumana, M. ogatai and M. nimbata.
The imagines of Platybaetis selvai Kubendran et al., 2021 (Ephemeroptera: Baetidae) from China
Authors: WANG NING-NING , SUN YU-XIAN , ZHOU CHANG-FA
Published: October 2024

Both the male and female imagines of Platybaetis selvai Kubendran, Vasanth & Subramanian, 2021 are described for the first time, some key characters of nymphs are also presented. Nymphs of this species have 10–11 segments of terminal filament, and its imagines have the palest bodies among the known five imagines, but their wings have pigmented basal half. Its relatively large body and colorful imaginal wings, and long terminal filament of nymphs can be seen its plesiomorphies.
Two new species of the genus Anabropsis Rehn, 1901 (Orthoptera: Anostostomatidae) from Yunnan, China
Authors: XU HAO , SHI FUMING
Published: October 2024

In this paper, two new species of the genus Anabropsis Rehn, 1901 from Yunnan, China, i.e. Anabropsis (Apteranabropsis) papiliomaculata sp. nov. and Anabropsis (Paterdecolyus) dulongjiangensis sp. nov. are described. In addition, the male of Anabropsis (Pseudapteranabropsis) nigrimaculatis Pang, Lu & Bian, 2023 is reported for the first time, and the species is transferred into Anabropsis (Apteranabropsis) Gorochov, 1988. All specimens are deposited in the Museum of Hebei University.
Myocardial Perfusion Scintigraphy in Diagnosic of Coronary Heart Disease
Authors: Lacko Anton , Straka Jan , Hrubon Anton , Babecka Jozef , Lacko Lukas
Published: October 2024

Introduction: Atherosclerosis plays a key role in the etiopathogenesis of cardiovascular diseases. Atherosclerosis is a generalized chronic inflammatory disease of the vascular wall, which results in anatomical and histological changes that, together with functional changes, lead to endothelial dysfunction, narrowing of the arterial lumen, and insufficient blood supply to the tissues. The shift in the incidence of cardiovascular diseases to younger age groups is alarming. The presence of microvascular changes in the myocardium is significant. The high incidence of cardiovascular diseases, especially ischemic heart disease, requires early diagnosis and modern treatment. Aim: The aim of the paper is to analyse and point out early diagnosis of coronary heart disease using nuclear medicine methods. Set of examined patients and methodology: Using nuclear medicine methods, we try to detect these changes in time and thus prevent the occurrence of acute coronary events. In nuclear cardiology, instead of a large-area scintillation detector, a new type of cardio-gamma camera "Discovery CZT 530c" based on the principle of semiconductor detectors began to be used. The abbreviation CZT stands for semiconductor composition (Cadmium-Zinc-Tellur). The set of respondents consisted of 4270 people examined in the years 2014-2016 by myocardial perfusion scintigraphy. There were 950 diabetic patients in the analysed group of the 4270 examined. Results: In the analysed group of 4270 respondents, 61% had negative findings and 39% had positive findings in terms of the presence of ischemic heart disease. In the group of diabetic patients, there was a negative finding in 28% of respondents and a positive finding in 72% of the respondents in the sense of positive ischemic heart disease. Using myocardial perfusion scintigraphy in the diagnosis of functional changes, we confirmed a great benefit in detecting early changes in coronary heart disease, including in the diagnosis of microvascular angina. Conclusion: Nuclear medicine methods are of great benefit for the diagnosis of small vessel disease, diabetic cardiomyopathy and cardiac autonomic neuropathy in patients with diabetes mellitus. The new type of cardio gamma camera "Discovery CZT 530c" allows more accurate assessment of myocardial perfusion abnormalities and at the same time the reduction of the radiopharmaceutical dose reduces the patient's radiation load by 50%.