bluuebunny/crossref_metadata_2025 huggingface dataset:
Supplementary Table S3 from Proportional Hazards Violations in Phase III Cancer Clinical Trials: A Potential Source of Trial Misinterpretation
Authors: Lin Timothy A. , McCaw Zachary R. , Koong Alex , Lin Christine , Abi Jaoude Joseph , Patel Roshal , Kouzy Ramez , El Alam Molly B. , Sherry Alexander D. , Noticewala Sonal S. , Fuller Clifton D. , Thomas Charles R. , Sun Ryan , Lee J. Jack , Lin Ruitao , Yuan Ying , Shyr Yu , Meirson Tomer , Ludmir Ethan B.
Published: October 2024

Table S3: List of 341 trials included in the overall analysis. ADT, androgen deprivation therapy; mFOLFOX, folinic acid, fluorouracil, and oxaliplatin; FOLFIRI, folinic acid, fluorouracil, irinotecan; GM-CSF, granulocyte-macrophage colony-stimulating factor; R-DHAP; rituximab, dexamethasone, cytarabine, cisplatin; O-DHAP; ofatumumab, dexamethasone, cytarabine, cisplatin; EDP, etoposide doxorubicin cisplatin; G-CHOP, obintuzumab, cyclophosphamide, doxorubicin hydrochloride, vincristine, prednisone; RCHOP, rituximab, cyclophosphamide, doxorubicin hydrochloride, vincristine, prednisone; VR-CAP, rituximab, cyclophosphamide, doxorubicin, and prednisone with bortezomib; AC, Adriamycin with cyclophosphamide; T, paclitaxel; XT, capecitabine plus paclitaxel; GIST, gastrointestinal stromal tumor; IFN, interferon; 5FU, 5-fluorouracil; FA, folinic acid; recMAGE-A3, recombinant MAGE A-3; NGR-Htnf, NGR–human tumor necrosis factor; TACE, trans-arterial chemoembolization; T-DM1, Trastuzumab emtansine; Mf, mitomycin-C and fluoropyrimidine; iceMFP, intraperitoneal cisplatin (100 mg), intravenous mitomycin-C (15 mg/m(2)) on postoperative day 1, followed by oral doxifluridine for 12 months, and six monthly intravenous cisplatin (60 mg/m(2); RFA, radiofrequency ablation.
Supplementary Figure S3 from Proportional Hazards Violations in Phase III Cancer Clinical Trials: A Potential Source of Trial Misinterpretation
Authors: Lin Timothy A. , McCaw Zachary R. , Koong Alex , Lin Christine , Abi Jaoude Joseph , Patel Roshal , Kouzy Ramez , El Alam Molly B. , Sherry Alexander D. , Noticewala Sonal S. , Fuller Clifton D. , Thomas Charles R. , Sun Ryan , Lee J. Jack , Lin Ruitao , Yuan Ying , Shyr Yu , Meirson Tomer , Ludmir Ethan B.
Published: October 2024

Figure S3. Scatter Plot of the restricted mean survival time difference to trial hazard ratio for all Kaplan-Meier comparisons included in the study (N = 357). RMST, restricted mean survival time.
Supplementary Table S5 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 S5. Response and disease control according to local assessment (intention-to-treat population).
Supplementary Figure S2 from Proportional Hazards Violations in Phase III Cancer Clinical Trials: A Potential Source of Trial Misinterpretation
Authors: Lin Timothy A. , McCaw Zachary R. , Koong Alex , Lin Christine , Abi Jaoude Joseph , Patel Roshal , Kouzy Ramez , El Alam Molly B. , Sherry Alexander D. , Noticewala Sonal S. , Fuller Clifton D. , Thomas Charles R. , Sun Ryan , Lee J. Jack , Lin Ruitao , Yuan Ying , Shyr Yu , Meirson Tomer , Ludmir Ethan B.
Published: October 2024

Figure S2. Scatterplot of the reported hazard ratio based upon reconstructed data compared to the trial’s reported hazard ratio for accurate and inaccurate reconstructions (N = 384). Trials were considered accurate if the absolute value of the ratio of the natural logarithm of the reported reconstructed hazard ratios was less than 0.1, while those with values equal to or greater than 0.1 were considered inaccurate and excluded prior to analysis.
Supplementary Figure S1 from Proportional Hazards Violations in Phase III Cancer Clinical Trials: A Potential Source of Trial Misinterpretation
Authors: Lin Timothy A. , McCaw Zachary R. , Koong Alex , Lin Christine , Abi Jaoude Joseph , Patel Roshal , Kouzy Ramez , El Alam Molly B. , Sherry Alexander D. , Noticewala Sonal S. , Fuller Clifton D. , Thomas Charles R. , Sun Ryan , Lee J. Jack , Lin Ruitao , Yuan Ying , Shyr Yu , Meirson Tomer , Ludmir Ethan B.
Published: October 2024

Figure S1: Demonstration of the method of reconstruction of patient-level data from published Kaplan-Meier plots. Kaplan-Meier plots from published manuscripts were imported into WebPlot Digitizer, where event times for each Kaplan-Meier curve were manually selected. This data, along with the numbers ta risk corresponding to each time interval in the original Kaplan-Meier graph, was then converted into a CSV file. Data from this file was used to calculate the RMST difference using the survRM2 function in R (version 1.0-4). K-M, Kaplan-Meier.
Supplementary Data S1 from Proportional Hazards Violations in Phase III Cancer Clinical Trials: A Potential Source of Trial Misinterpretation
Authors: Lin Timothy A. , McCaw Zachary R. , Koong Alex , Lin Christine , Abi Jaoude Joseph , Patel Roshal , Kouzy Ramez , El Alam Molly B. , Sherry Alexander D. , Noticewala Sonal S. , Fuller Clifton D. , Thomas Charles R. , Sun Ryan , Lee J. Jack , Lin Ruitao , Yuan Ying , Shyr Yu , Meirson Tomer , Ludmir Ethan B.
Published: October 2024

Data Supplement S1: Clinical context of trials from Table 3 with proportional hazards violations and discordant alternative survival assessments that were cited in NCCN guidelines or led to FDA drug approval.
Supplementary Table S5 from Clinical and Molecular Risk Factors in Extracranial Malignant Rhabdoid Tumors: Toward an Integrated Model of High-Risk Tumors
Authors: Fincke Victoria E. , Steinbügl Mona , Chun Hye-Jung E. , Nemes Karolina , Mucha Marlena , Loßner Maurice , Dorn Felix , Gastberger Katharina , Bühner Sebastian , Sill Martin , Kröncke Thomas , Siebert Reiner , Melchior Patrick , Furtwängler Rhoikos , Schlesner Matthias , Vokuhl Christian , Röcken Christoph , Johann Pascal D. , Frühwald Michael C.
Published: October 2024

CpG Sites used for model generation
Supplementary Table S1 from Clinical and Molecular Risk Factors in Extracranial Malignant Rhabdoid Tumors: Toward an Integrated Model of High-Risk Tumors
Authors: Fincke Victoria E. , Steinbügl Mona , Chun Hye-Jung E. , Nemes Karolina , Mucha Marlena , Loßner Maurice , Dorn Felix , Gastberger Katharina , Bühner Sebastian , Sill Martin , Kröncke Thomas , Siebert Reiner , Melchior Patrick , Furtwängler Rhoikos , Schlesner Matthias , Vokuhl Christian , Röcken Christoph , Johann Pascal D. , Frühwald Michael C.
Published: October 2024

Cohort overview
Supplementary Figure S3 from Clinical and Molecular Risk Factors in Extracranial Malignant Rhabdoid Tumors: Toward an Integrated Model of High-Risk Tumors
Authors: Fincke Victoria E. , Steinbügl Mona , Chun Hye-Jung E. , Nemes Karolina , Mucha Marlena , Loßner Maurice , Dorn Felix , Gastberger Katharina , Bühner Sebastian , Sill Martin , Kröncke Thomas , Siebert Reiner , Melchior Patrick , Furtwängler Rhoikos , Schlesner Matthias , Vokuhl Christian , Röcken Christoph , Johann Pascal D. , Frühwald Michael C.
Published: October 2024

Copy number alterations for extracranial malignant rhabdoid tumors
Supplementary Figure S2 from Clinical and Molecular Risk Factors in Extracranial Malignant Rhabdoid Tumors: Toward an Integrated Model of High-Risk Tumors
Authors: Fincke Victoria E. , Steinbügl Mona , Chun Hye-Jung E. , Nemes Karolina , Mucha Marlena , Loßner Maurice , Dorn Felix , Gastberger Katharina , Bühner Sebastian , Sill Martin , Kröncke Thomas , Siebert Reiner , Melchior Patrick , Furtwängler Rhoikos , Schlesner Matthias , Vokuhl Christian , Röcken Christoph , Johann Pascal D. , Frühwald Michael C.
Published: October 2024

t-stochastic neighbor embedding (tSNE) plot displaying the DNA methylation of the three atypical teratoid rhabdoid tumor (ATRT) subgroups and the three extracranial malignant rhabdoid tumors (eMRT) subgroups. Triangles indicate which samples were unpublished before. (ATRT-MYC n=33, ATRT-SHH n=64, ATRT-TYR n=53, eMRT high risk I n=65, eMRT standard risk n=46, eMRT high risk II n=61)
Supplementary Figure S1 from Clinical and Molecular Risk Factors in Extracranial Malignant Rhabdoid Tumors: Toward an Integrated Model of High-Risk Tumors
Authors: Fincke Victoria E. , Steinbügl Mona , Chun Hye-Jung E. , Nemes Karolina , Mucha Marlena , Loßner Maurice , Dorn Felix , Gastberger Katharina , Bühner Sebastian , Sill Martin , Kröncke Thomas , Siebert Reiner , Melchior Patrick , Furtwängler Rhoikos , Schlesner Matthias , Vokuhl Christian , Röcken Christoph , Johann Pascal D. , Frühwald Michael C.
Published: October 2024

Supplementary Figure 1: (A) Venn diagram displaying which patients clinical data were previously published in Nemes et al. 2022. (B) Cumulative distribution functions (CDF) of the consensus matrix for each k. (C-E) Histograms for k=2, k=3, k=4 after consensus clustering dispalying the frequency of samples being assigned to the same subgroup. (F,G) Heatmaps of the consensus matrices for k=2 and k=4 with samples as both rows and columns. Consensus values range from 0 to 1 marked by white to dark blue color. (H) Heatmap that displays the stability for k=5 NMF subgroups. (I) Plot displaying the cophenetic correlation coefficient which indicates the dispersion of the consensus matrix and measures the stability of clusters obtained from NMF. (J) Sankey plot displaying the overlap between the three eMRT subgroups obtained from NMF and consensus clustering. (K) Kaplan Meier plot dispalying the survival for the n=39 patients published in Chun et al. by their original subgroups. (L) Kaplan Meier plot displaying the survival of eMRT patients of each NMF subgroup, which were calculated in the same way as in Chun et al.
Supplementary Figure 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 Figure S6. Effects of HDAC inhibitors on t-SCLC cell lines.
Supplementary Table S1 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 S1. List of LMS patients with germline variants in this study.
Supplementary Figure 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 Figure S4. Characterization of two t-SCLC cell lines.
Supplementary Figure S1 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 S1. Tumor variant allelic frequency (VAF) vs matched normal VAF in germline pathogenic variants (PGV).
Supplementary Table S1 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 S1
Supplementary Figure S8 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 8. a-c) RNA class distribution of osteosarcoma (n=10) (a) and multiple myeloma (n=5) (b) patient plasma EVs, and normalized counts (rpm) of known (TLR-3 and RIG-I activating) inflammatory RNAs in osteosarcoma plasma EVs, MM plasma EVs and 143B EVs (c). d) Expression levels of (endosomal and cytosolic) pattern recognition receptors in MSCs based on normalized RNA-seq counts. e-h) Knockdown confirmation of TLR3 (e), RIG-I (f), MDA5 (g) and LGP2 (h) in primary MSCs as compared to control (shGFP-transduced) cells. i) IL8 protein production in MSCs transduced with indicated shRNAs upon exposure to 143B EVs. Graph shows data from a replicate experiment performed using MSCs from donor #2.
Data from Effectiveness of PARP Inhibitor Maintenance Therapy in Ovarian Cancer by BRCA1/2 and a Scar-Based HRD Signature in Real-World Practice
Authors: Richardson Debra L. , Quintanilha Julia C. F. , Danziger Natalie , Li Gerald , Sokol Ethan , Schrock Alexa B. , Ebot Ericka , Bhardwaj Neeru , Norris Tanesha , Afghahi Anosheh , Frachioni Anthony , Washington Christina , Dockery Lauren , Elvin Julia , Graf Ryon P. , Moore Kathleen N.
Published: October 2024

AbstractPurpose:
The purpose of the study was to compare the effectiveness of PARP inhibitor maintenance therapy (mPARPi) in real-world practice by biomarker status [BRCA1/2 alterations (BRCAalt) and a homologous recombination deficiency signature (HRDsig)] in advanced ovarian cancer.
Experimental Design:
Patients with ovarian cancer receiving first-line platinum-based chemotherapy and either mPARPi or no maintenance were included. Patient data were obtained by a US-based de-identified ovarian cancer Clinico-Genomic Database, from ∼280 US cancer clinics (01/2015–03/2023). Real-world progression-free survival (rwPFS) and overall survival (rwOS) were compared by biomarker status using Cox models, weighted by propensity scores.
Results:
Of 673 patients, 160 received mPARPi [31.2% BRCAalt and 51.9% HRDsig(+)] and 513 no maintenance [15.6% BRCAalt and 34.1% HRDsig(+)]. BRCAalt patients receiving mPARPi versus no maintenance had favorable rwPFS [HR, 0.48; 95% confidence interval (CI), 0.26–0.87; P = 0.0154], as did BRCA wild-type (WT; HR, 0.76; 95% CI, 0.57–1.01; P = 0.0595). Favorable rwOS was not observed with mPARPi for BRCAalt or BRCA-WT. HRDsig(+) patients receiving mPARPi versus no maintenance had favorable rwPFS (HR, 0.36; 95% CI, 0.24–0.55; P < 0.001) and numerically favorable rwOS (HR, 0.46; 95% CI, 0.21–1.02; P = 0.0561). No differences were observed for HRDsig(−). mPARPi treatment interaction was observed for HRDsig(+) versus HRDsig(−) (rwPFS P < 0.001/rwOS P = 0.016) but not for BRCAalt versus BRCA-WT. Patients with BRCA-WT/HRDsig(+) receiving mPARPi had favorable rwPFS (HR, 0.40; 95% CI, 0.22–0.72; P = 0.003), whereas no difference was observed for BRCA-WT/HRDsig(−).
Conclusions:
HRDsig predicted benefit of mPARPi better than BRCAalt. Patients with HRDsig(+) status experienced favorable outcomes, even if they had BRCA-WT status. In contrast, patients with HRDsig(−) status did not show significant benefit from mPARPi treatment. HRDsig might predict benefit from mPARPi regardless of BRCAalt status.
Data from KIR2DL2/DL3+NKs and Helios+Tregs in Peripheral Blood Predict Nivolumab Response in Patients with Metastatic Renal Cell Cancer
Authors: Santagata Sara , Trotta Anna Maria , D’Alterio Crescenzo , Napolitano Maria , Rea Giuseppina , Di Napoli Marilena , Portella Luigi , Ieranò Caterina , Guardascione Giuseppe , Coppola Elisabetta , Caux Christophe , Dubois Bertrand , Boyle Helen J. , Carles Joan , Rossetti Sabrina , Azzaro Rosa , Feroce Florinda , Perdonà Sisto , Fordellone Mario , Bello Anna Maria , Califano Daniela , Chiodini Paolo , Pignata Sandro , Scala Stefania
Published: October 2024

AbstractPurpose:
To identify predictive factors of nivolumab sensitivity, peripheral blood NKs and regulatory T-cell (Treg) were evaluated in patients with metastatic renal cell carcinoma (mRCC) enrolled in the REVOLUTION trial.
Experimental Design:
Fifty-seven mRCCs being treated with nivolumab, as at least second-line of therapy, and 62 healthy donors were longitudinally evaluated (0–1–3–6–12 months) for peripheral NKs and Tregs, phenotype, and function. Multivariable logistic regression was conducted to identify the independent predictors. The 0.632+ internal cross-validation was used to avoid overfitting. The best cutoff value based on a 3-month clinical response was applied to progression-free survival (PFS) and overall survival (OS). Kaplan–Meier curves for PFS and OS were produced.
Results:
At pretreatment, mRCCs displayed high frequency of NKp46+NKs, NKp30+NKs, KIR2DL1+NKs, KIR2DL2/DL3+NKs, and PD1+NKs with reduced NK degranulation as well as high frequency of Tregs, PD1+Tregs, Helios+Tregs, and ENTPD1+Tregs. Responder patients, identified as a clinical response after 3 months of treatment, presented at pretreatment significantly low CD3+, high KIR2DL2/DL3+NKs, high PD1+Tregs, and high Helios+Tregs. Upon multivariate analysis, only KIR2DL2/DL3NKs and Helios+Tregs held as independent predictors of nivolumab responsiveness. The KIR2DL2/DL3+NKs >35.3% identified patients with longer OS, whereas the Helios+Tregs >34.3% displayed significantly longer PFS. After 1-month of nivolumab, responder patients showed low CD3+, high NKs, KIR2DL2/DL3+NKs, and ICOS+Tregs. Among these subpopulations, CD3+ and KIR2DL2/DL3+NKs held as independent predictors of nivolumab efficacy. Low CD3+ (≤71%) was significantly associated with longer PFS, whereas high KIR2DL2/DL3+NKs (>23.3%) were associated with both PFS and OS.
Conclusions:
Pretreatment evaluation of Helios+Tregs/KIR2DL2/DL3+NKs and 1-month posttreatment CD3+/ KIR2DL2/DL3+NKs will predict nivolumab response in mRCCs.
Data from Pembrolizumab and Cabozantinib in Recurrent and/or Metastatic Head and Neck Squamous Cell Carcinoma: Long-term Survival Update with a Biomarker Analysis
Authors: Saba Nabil F. , Chaudhary Ritu , Kirtane Kedar , Marra Angelo , Ekpenyong Asari , McCook-Veal Ashley , Schmitt Nicole C. , Gross Jennifer H. , Patel Mihir R. , Remick Jill , Bates James E. , McDonald Mark W. , Rudra Soumon F. , Stokes William A. , Biernacki Maria , Song Xiaofei , Slebos Robbert J.C. , Liu Yuan , Steuer Conor E. , Shin Dong M. , Teng Yong , Chung Christine H.
Published: October 2024

AbstractPurpose:
Anti-programmed cell death protein 1 (PD-1) therapy is a standard of care in recurrent and/or metastatic head and neck squamous cell carcinoma (RMHNSCC). Vascular endothelial growth factor receptor tyrosine kinase inhibitors (VEGFR-TKI) have immunomodulatory properties and improve clinical outcomes in combination with anti-PD-1 therapy in different malignancies. We report the long-term efficacy and safety of pembrolizumab and cabozantinib in patients with RMHNSCC and include a correlative biomarker analysis.
Patients and Methods:
This open-label, single-arm, multicenter, phase 2 study screened 50 patients with RMHNSCC, of whom 36 received pembrolizumab and cabozantinib. The primary endpoint was overall response rate (ORR), safety, and tolerability. Secondary endpoints included progression-free survival (PFS), overall survival (OS), and correlative studies of tissue and blood. We report the long-term PFS, OS, and safety of treated patients and describe correlative biomarkers evaluating p-MET expression and tumor immune microenvironment (TIME) using multiplex immunohistochemistry.
Results:
With median follow-up of 22.4 months, the median PFS was 12.8 months with a 2-year PFS of 32.6% (95% CI, 18.8%–56.3%) and the median OS was 27.7 months with a 2-year OS of 54.7% [95% confidence interval (CI), 38.9%–76.8%]. The median duration of response was 12.6 months with a 2-year rate of 38.5% (95% CI, 30.8%–81.8%). Long-term treatment-related adverse events included manageable hypothyroidism (5.5%) and grade 1 elevated aspartate aminotransferase and alanine aminotransferase (2.8%). Baseline tumor p-MET expression correlated with ORR (P = 0.0055). Higher density of CD8+, CD103+, and CSF1-R+ cells at baseline correlated with improved OS [hazard ratio (HR) = 5.27, P = 0.030; HR = 8.79, P = 0.017; HR = 6.87, P = 0.040, respectively].
Conclusions:
Pembrolizumab and cabozantinib provided prolonged encouraging long-term disease control and survival with a maintained favorable safety profile. The prognostic significance of higher density of CD8+, CD103+, and CSF1-R+ cells in TIME deserve further evaluation in similar clinical settings.
Data 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

AbstractPurpose:
Triple-negative breast cancer (TNBC) is a heterogeneous disease that carries the poorest prognosis of all breast cancers. Although novel TNBC therapies in development are frequently targeted toward tumors carrying a specific genomic, transcriptomic, or protein biomarker, it is poorly understood how these biomarkers are correlated.
Experimental Design:
To better understand the molecular features of TNBC and their correlation with one another, we performed multimodal profiling on a cohort of 95 TNBC. Our approach involved quantifying tumor-infiltrating lymphocytes through hematoxylin and eosin staining, assessing the abundance of retinoblastoma, androgen receptor, and PDL1 proteins through IHC, and carrying out transcriptomic profiling using the NanoString BC360 platform, targeted DNA sequencing on a subset of cases, as well as evaluating associations with overall survival.
Results:
Levels of RB1 mRNA and RB proteins are better correlated with markers of retinoblastoma functionality than RB1 mutational status. Luminal androgen receptor tumors clustered into two groups with transcriptomes that cluster with either basal or mesenchymal tumors. Tumors classified as PDL1-positive by the presence of immune or tumor cells showed similar biological characteristics. HER2-low TNBC showed no distinct biological phenotype when compared with HER2-zero. The majority of TNBC were classified as basal or HER2-enriched by PAM50, the latter showing significantly improved overall survival.
Conclusions:
Our study contributes new insights into biomarker utility for identifying suitable TNBC therapies and the intercorrelations between genomic, transcriptomic, protein, and cellular biomarkers. Additionally, our rich data resource can be used by other researchers to explore the interplay between DNA, RNA, and protein biomarkers in TNBC.
Data from Integrated Clinical Genotype–Phenotype Characteristics of STAT3-Mutated Myeloid Neoplasms
Authors: Ye Matthew T. , Zuo Zhuang , Calin Steliana , Ye Fengxi , He Hua , Kamata Wataru , Yang Yaling , You M. James
Published: October 2024

AbstractPurpose:
STAT3 is a key transcription factor that mediates cancer progression through phosphorylation or gain-of-function mutations. STAT3 activation in myeloid neoplasms (MN) is primarily mediated through phosphorylation. STAT3 mutation has only rarely been reported in MNs.
Experimental Design:
We assessed the clinicopathologic and molecular genetic features of 32 STAT3-mutated MNs.
Results:
The frequency of STAT3 mutation in MNs was <0.5%. Twenty (62.5%) cases were classified as acute myeloid leukemia, 7 (21.9%) as myelodysplastic syndrome, and 5 (15.6%) as chronic myelomonocytic leukemia, but none as myeloproliferative neoplasms. STAT3 mutations occurred at initial diagnosis in 22 (88%) cases or at relapse or upon leukemic transformation. Clonal hierarchy analysis revealed that STAT3 mutations represented the dominant clone in 30% of acute myeloid leukemia cases but were subclonal in myelodysplastic syndrome and chronic myelomonocytic leukemia. Most were missense mutations located at the SH2 domain, Y640F being the most common. STAT3 mutation was accompanied by coexisting mutations in all cases, most frequently SRSF2, TET2, ASXL1, and SETBP1. STAT3 mutations were usually associated with morphologic dysplasia, increased blasts, and monosomy 7/del7q. With a median follow-up of 24.5 months, 21 patients died, 6 had persistent disease, and 5 achieved complete remission after stem cell transplantation.
Conclusions:
STAT3 mutation is present in various MNs but not in myeloproliferative neoplasms. It is often an early event or occurs upon leukemic transformation, which suggests an important role in the pathogenesis and progression of MNs by activating the JAK-STAT pathway. It may help determine a subset of patients with MNs who may benefit from targeted therapy.

See related commentary by Hochman and Frank, p. 4554
Data 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

AbstractPurpose:
Chimeric antigen receptor (CAR) T-cell therapy is a potent immunotherapy for hematologic malignancies, but patients can develop long-term adverse events, including second primary malignancies (SPM) that impact morbidity and mortality. To delineate the frequency and subtypes of SPMs following CAR-T in lymphoma and myeloma, we performed a systematic review and meta-analysis.
Experimental Design:
A literature search was conducted in the MEDLINE, Embase, and Cochrane CENTRAL databases. Following the extraction of SPM cases and assignment of malignant origin, we analyzed SPM point estimates using random effects models.
Results:
We identified 326 SPMs across 5,517 patients from 18 clinical trials and 7 real-world studies. With a median follow-up of 21.7 months, the overall SPM point estimate was 6.0% (95% confidence interval, 4.8%–7.4%). SPM estimates were associated with treatment setting (clinical trials > real-world studies), duration of follow-up, and number of prior treatment lines, which were each confirmed as independent study-level risk factors of SPM in a meta-regression model. A subgroup meta-analysis of the four trials that randomized CAR-T versus standard-of-care revealed a similar risk of SPM with either treatment strategy (P = 0.92). In a distribution analysis of SPM subtypes, hematologic malignancies were the most common entity (37%), followed by solid tumors (27%) and non-melanoma skin cancers (16%). T-cell malignancies represented a small minority of events (1.5%). We noted disease- and product-specific variations in SPM distribution.
Conclusions:
These data raise awareness of SPM as a clinically relevant long-term adverse event in patients receiving CAR T-cell therapy. However, our findings do not indicate that SPM frequency is higher with CAR-T versus previous standard-of-care strategies.
Data from A Phase Ib Study of Linperlisib in the Treatment of Patients with Relapsed and/or Refractory Peripheral T-cell Lymphoma
Authors: Jin Jie , Cen Hong , Zhou Keshu , Xu Xiaohong , Li Fei , Wu Tao , Yang Haiyan , Wang Zhen , Li Zhiming , Huang Wenyang , Bao Hanying , Xu Zusheng , Qiu Lugui
Published: October 2024

AbstractPurpose:
Relapsed and/or refractory peripheral T-cell lymphoma (r/r PTCL) is an aggressive and heterogeneous hematologic malignancy with high unmet need. Previously, PI3K inhibitors were shown to be efficacious in B- and T-cell lymphomas, but as a drug class, these agents have frequently been observed to have tolerability limitations. Next-generation agents that improve the tolerability while maintaining efficacy are desirable.
Patients and Methods:
A phase Ib clinical study was conducted with the oral PI3K-delta isoform-selective small-molecule inhibitor, linperlisib, in patients with r/r PTCL, and the clinical benefit was explored by the evaluation of safety and efficacy.
Results:
In this clinical study, 43 patients with r/r PTCL in China were treated with continuous dosing of 80-mg linperlisib once a day. Treatment-related adverse events (AE) were manageable. The most frequently reported grade 3 AE were neutropenia (21%), pneumonia (11.6%), and hypertriglyceridemia (7%). All other AE were either absent or reported in <5% of the patients. Linperlisib treatment for these patients with r/r PTCL, consisting of the major PTCL subtypes, was observed to have a 60.5% overall response rate with 35% complete responses and led to a median duration of response of 11.1 months, median progression-free survival of 11.8 months, and a median overall survival of >38 months (not reached).
Conclusions:
With the very promising clinical activity against r/r PTCL, the results of this study support the further investigation of linperlisib for the treatment of r/r PTCL.
Data 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

AbstractPurpose:
Current therapy strategies still provide only limited success in the treatment of glioblastoma, the most frequent primary brain tumor in adults. In addition to the characterization of the tumor microenvironment, global changes in the brain of patients with glioblastoma have been described. However, the impact and molecular signature of neuroinflammation distant of the primary tumor site have not yet been thoroughly elucidated.
Experimental Design:
We performed translocator protein (TSPO)-PET in patients with newly diagnosed glioblastoma (n = 41), astrocytoma WHO grade 2 (n = 7), and healthy controls (n = 20) and compared TSPO-PET signals of the non-lesion (i.e., contralateral) hemisphere. Back-translation into syngeneic SB28 glioblastoma mice was used to characterize Pet alterations on a cellular level. Ultimately, multiplex gene expression analyses served to profile immune cells in remote brain.
Results:
Our study revealed elevated TSPO-PET signals in contralateral hemispheres of patients with newly diagnosed glioblastoma compared to healthy controls. Contralateral TSPO was associated with persisting epileptic seizures and shorter overall survival independent of the tumor phenotype. Back-translation into syngeneic glioblastoma mice pinpointed myeloid cells as the predominant source of contralateral TSPO-PET signal increases and identified a complex immune signature characterized by myeloid cell activation and immunosuppression in distant brain regions.
Conclusions:
Neuroinflammation within the contralateral hemisphere can be detected with TSPO-PET imaging and associates with poor outcome in patients with newly diagnosed glioblastoma. The molecular signature of remote neuroinflammation promotes the evaluation of immunomodulatory strategies in patients with detrimental whole brain inflammation as reflected by high TSPO expression.
Data from Proportional Hazards Violations in Phase III Cancer Clinical Trials: A Potential Source of Trial Misinterpretation
Authors: Lin Timothy A. , McCaw Zachary R. , Koong Alex , Lin Christine , Abi Jaoude Joseph , Patel Roshal , Kouzy Ramez , El Alam Molly B. , Sherry Alexander D. , Noticewala Sonal S. , Fuller Clifton D. , Thomas Charles R. , Sun Ryan , Lee J. Jack , Lin Ruitao , Yuan Ying , Shyr Yu , Meirson Tomer , Ludmir Ethan B.
Published: October 2024

AbstractPurpose:
Survival analyses of novel agents with long-term responders often exhibit differential hazard rates over time. Such proportional hazards violations (PHV) may reduce the power of the log-rank test and lead to misinterpretation of trial results. We aimed to characterize the incidence and study attributes associated with PHVs in phase III oncology trials and assess the utility of restricted mean survival time and maximum combination test as additional analyses.
Experimental Design:
Clinicaltrials.gov and PubMed were searched to identify two-arm, randomized, phase III superiority-design cancer trials with time-to-event primary endpoints and published results through 2020. Patient-level data were reconstructed from published Kaplan–Meier curves. PHVs were assessed using Schoenfeld residuals.
Results:
Three hundred fifty-seven Kaplan–Meier comparisons across 341 trials were analyzed, encompassing 292,831 enrolled patients. PHVs were identified in 85/357 [23.8%; 95% confidence interval (CI), 19.7%, 28.5%] comparisons. In multivariable analysis, non–overall survival endpoints [OR, 2.16 (95% CI, 1.21, 3.87); P = 0.009] were associated with higher odds of PHVs, and immunotherapy comparisons [OR 1.94 (95% CI, 0.98, 3.86); P = 0.058] were weakly suggestive of higher odds of PHVs. Few trials with PHVs (25/85, 29.4%) prespecified a statistical plan to account for PHVs. Fourteen trials with PHVs exhibited discordant statistical signals with restricted mean survival time or maximum combination test, of which 10 (71%) reported negative results.
Conclusions:
PHVs are common across therapy types, and attempts to account for PHVs in statistical design are lacking despite the potential for results exhibiting nonproportional hazards to be misinterpreted.
Figure S4 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

Figure S4
Figure S3 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

Figure S3
Figure 1 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 regulates basal levels of 20S proteasome activity and is required for BTZ-induced cytotoxicity in NSCLC cells. A, 20S proteasome activity was determined in the indicated cell lines using a fluorometric proteosome activity assay and plotted as mean fluorescence units (MFU). All pairwise comparisons were made using the Student t test. B, (Left) Relative 20S proteasome activity in lysates of H1975-Control vs. H1975-p53KO cells. (Right) Cell lysates of H1975-Control and H1975-p53KO (p53KO) cell lines generated using CRISPR/Cas9 were immunoblotted with p53 and GAPDH antibodies. C, The indicated cells were treated with vehicle or increasing concentrations of BTZ (left) or CFZ (right) for 72 hours, and cell viability was determined by the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. A paired t test was performed to analyze differences in viability among the cell lines. D, (Left) H1975-Control or H1975-p53KO cells expressing GFP or p53R273H were treated with BTZ (5 nmol/L) for 48 hours, and cell viability was determined by trypan blue exclusion assay. (Right) Lysates of the indicated cell lines were immunoblotted with p53 and GAPDH antibodies. E, (Left) H460 or H460-p53KO (18) cells were treated with vehicle (−) or BTZ (5 nmol/L) for 72 hours, and cell viability was determined by WST-1 assay. (Right) Cell lysates of H460 and H460-p53KO cells were immunoblotted with p53 and GAPDH antibodies. F, (Left) H460-p53KO cells stably expressing GFP or p53R273H were treated with increasing concentrations of BTZ for 72 hours, and cell viability was determined by WST-1 assay. (Right) Cell lysates of H460-p53KO cells stably expressing GFP or p53R273H were immunoblotted with p53 and GAPDH antibodies. *, P < 0.05; **, P < 0.01; ***, P < 0.005; ns, P > 0.05. Error bars indicate ± 1.0 SD.
Data 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

Abstract
Non–small cell lung cancer (NSCLC) cells with oncogenic mutant p53 (Onc-p53) alleles exhibit significantly higher levels of proteasome activity, indicating that Onc-p53 induces proteotoxic stress which may be leveraged as a therapeutic vulnerability. Proteasome inhibitors (PI) are most active in cells under proteotoxic stress, so we investigated whether PIs exhibit preferential cytotoxicity in Onc-p53 NSCLC cells. Indeed, bortezomib (BTZ) and other PIs exhibited IC50 values 6- to 15-fold lower in Onc-p53 cells versus wild-type (WT) p53 cells. BTZ cytotoxic effects in Onc-p53 cells were abrogated by antioxidants such as N-acetyl-L-cysteine, indicating that oxidative stress is the critical driver of BTZ-dependent cytotoxic effects in Onc-p53 cells. Importantly, we observed oxidative stress–dependent transcriptional induction of the proapoptotic BH3-only protein NOXA, leading to cleavage of caspase-3, consistent with an apoptotic mechanism of cell death in Onc-p53 but not in WT p53 cells treated with BTZ. BTZ-generated oxidative stress was linked to nuclear translocation of NRF2 and transcriptional activation of ATF3, which in turn was required for NOXA induction. Validating the translational potential of BTZ in Onc-p53 NSCLC cells, BTZ and the BH3-mimetic navitoclax were synergistically cytotoxic in Onc-p53 but not in WTp53 cells in vitro, and BTZ effectively limited the growth of Onc-p53 NSCLC xenografts when combined with navitoclax and carboplatin (a standard-of-care chemotherapeutic in NSCLC) in vivo. Our data therefore support further investigation of the therapeutic utility of PIs combined with BH3-mimetics and chemotherapy in Onc-p53 human NSCLC as a novel therapeutic strategy.
Significance:
NSCLC is the leading cause of cancer death due, in part, to a lack of active therapies in advanced disease. We demonstrate that combination therapy with a proteasome inhibitor, BH3-mimetic, and chemotherapy is an active precision therapy in NSCLC cells and tumors expressing Onc-p53 alleles.
Association Between Neurological Status and Outcomes in Cardiac Arrest Patients Undergoing PCI in Contemporary Practice: Insights From BMC2
Authors: Hamilton David E. , Kobe Daniel S. , Seth Milan , Sharma Manoj , LaLonde Thomas , Shah Ibrahim , Gurm Hitinder S. , Sukul Devraj
Published: October 2024

BACKGROUND:

Coronary artery disease remains the largest contributor to cardiac arrests worldwide; yet, long-term outcomes are often driven by neurological status after resuscitation. We examined the association between pre–percutaneous coronary intervention (PCI) level of consciousness (LOC) and outcomes among patients with cardiac arrest who underwent PCI.

METHODS:

The study cohort included patients undergoing PCI after cardiac arrest between April 2018 and March 2022 at 48 hospitals in the state of Michigan. Pre-PCI LOC was categorized as mentally alert, partially responsive, unresponsive, and unable to assess. In-hospital outcomes included mortality, bleeding, and acute kidney injury.

RESULTS:

Among 3021 patients who underwent PCI after cardiac arrest, 1394 (49%) were mentally alert, 132 (5%) were partially responsive, 698 (24%) were unresponsive, and 631 (22%) were unable to assess. The mentally alert cohort had lower mortality (4.59%) compared with the partially responsive (17.42%), unresponsive (50.14%), and unable to assess cohorts (38.03%;
P
<0.001). After adjusting for baseline differences, compared with mentally alert patients, the odds of mortality were markedly elevated in patients who were partially responsive (adjusted odds ratio, 4.63 [95% CI, 2.67–8.04];
P
<0.001), unable to assess (adjusted odds ratio, 13.95 [95% CI, 9.97–19.51];
P
<0.001), and unresponsive (adjusted odds ratio, 24.36 [17.34–34.23];
P
<0.001). After adjustment, patients with impaired LOC also had higher risks of acute kidney injury and bleeding compared with mentally alert patients.

CONCLUSIONS:

Pre-PCI LOC is a strong predictor of in-hospital outcomes after PCI among cardiac arrest patients. A patient’s pre-PCI LOC should be considered an important factor when weighing treatment options, designing clinical trials, and counseling patients and their families regarding prognosis after PCI.
Power, Politics, and Personification: Toward a Critique of Postone’s Theory of Antisemitism
Authors: Levi Neil
Published: October 2024

This essay offers an immanent critique of Moishe Postone’s theory of antisemitism. It argues that his account of modern antisemitism as a form of fetishistic anti-capitalism contains a decisive ambiguity. Postone oscillates between two distinct conceptions of anti-capitalism: explicit and implicit. These conceptions are conflated when Postone draws a line from his paradigm case of modern antisemitism to recent anti-imperialist criticism of particular nation-states. This conflation also allows him implicitly to suggest that anti-communism is a form of anti-capitalism. More attention to the differences between these senses of anti-capitalism could have led Postone to a richer theoretical account of the place of abstraction in the distinctively political dangers that obsessed modern antisemitism, which might, in turn, have drawn his attention in the present toward contemporary Islamophobia, rather than criticism of the US, as redolent of certain aspects of the modern antisemitic imaginary.
The Astronomical Observatory of the Abbot de Beauchamp in Baghdad
Authors: Deias Dalia , Bret Patrice
Published: October 2024

In 1786, the Abbé Joseph de Beauchamp, vicar general of the bishopric of Babylon, vice-consul in Baghdad and correspondent of the Royal Academy of Sciences in Paris, completed the description of the astronomical observatory he had installed on a terrace of the house of the Missionary Fathers of the Congregation of the Faith in Baghdad. A crossroads between Parisian and Middle Eastern astronomical practice, between scholarly, religious and diplomatic networks in France and abroad, Beauchamp’s observatory was destroyed by the wind in 1783, then carefully reconstructed and well equipped with observation and measurement instruments received from France. The notes, descriptions and detailed drawings carefully recorded by the astronomer explain the organization of this learned space, the function, construction and operation of each of the elements for the various types of observations (stars, the Sun and the planet Mercury, in particular) made within it.
New species diversity and host association of Lactarius sect. Deliciosi: describing L. gibbosus and L. parvihatsudake (Russulaceae, Russulales) in southern China
Authors: PU JIN-BAO , CAO SHU-QIN , WANG RAN , CHEN XIA , PANG CHUN-MEI , WANG XIANG-HUA
Published: October 2024

Lactarius gibbosus and L. parvihatsudake, two red-colored species of Lactarius sect. Deliciosi are described as new from southern China. Lactarius gibbosus is a rare species, growing in fagaceous forest in southwestern China, similar to L. subindigo. Its pileipellis with slightly thick-walled swollen cells is unique in the section. The macrocystidia filled with golden yellow contents are another good character. This is the first report of red-colored species of L. sect. Deliciosi growing in fagaceous forest. Lactarius parvihatsudake grows in forest of Pseudolarix amabilis, an ancient relict Chinese tree only in eastern China. It has smaller basidiocarps and bigger spores than L. hatsudake. The discovery of this species added Pseudolarix to the potential host list of L. sect. Deliciosi. Phylogenetic analyses of the ITS region and glyceraldehyde-3-phophate dehydrogenase gene showed that L. gibbosus was a sibling of L. subindigo. These two species formed an early diverging lineage of L. sect. Deliciosi. Lactarius parvihatsudake was nested deeply in L. sect. Deliciosi but its closest relatives cannot be determined. These data update our understanding of the diversity of L. sect. Deliciosi in Asia and will hopefully help to understand the role of host shift in speciation of ectomycorrhizal fungi.
Freshwater Sordariomycetes: a new species Nais submersa and a new record Natantispora unipolaris in Halosphaeriaceae from China
Authors: YANG RANG , GAO YI-BO , ZHANG DI , ZHANG HUANG , YU ZE-FEN
Published: October 2024

During our ongoing surveys of freshwater fungi in Yunnan Province, two halosphaeriaceous species were collected from submerged wood. Based on their morphological characters and phylogenetic analyses of combined LSU, SSU and ITS sequence data, a new species Nais submersa and a new habitat record Natantispora unipolaris are reported. Descriptions and illustration of two taxa are provided.
Type catalogue of Hymenoptera (Insecta) housed in the Museo Nacional de Historia Natural de Cuba
Authors: DUARTE SANDRA , BRETO DAYRON
Published: October 2024

A total of 26 holotypes and 125 paratypes of Hymenoptera housed in the Museo Nacional de Historia Natural de Cuba are catalogued. Original publications were reviewed to compile all accompanying information and verify the status of the material. Data on the specimens are provided, grouped by families, and holotypes were photographed, making them more accessible for study by the scientific community. In addition, as Camponotus taino Snelling & Torres, 1998 is an unresolved homonym of C. taino Fontenla, 1997, we propose Camponotus boriquen as a replacement name for the former.