bluuebunny/crossref_metadata_2025 huggingface dataset:
Supplemental Figure 2 from Targeting YES1 Disrupts Mitotic Fidelity and Potentiates the Response to Taxanes in Triple-Negative Breast Cancer
Authors: Piemonte Katrina M. , Ingles Natasha N. , Weber-Bonk Kristen L. , Valentine Mitchell J. , Majmudar Parth R. , Singh Salendra , Keri Ruth A.
Published: November 2024

Loss of YES1 causes chromosomal instability dsDNA breaks, and decreased growth in TNBC cells.
Table S1 from Molecular Characterization and Classification of HER2-Positive Breast Cancer Inform Tailored Therapeutic Strategies
Authors: Li Yu-Wei , Dai Lei-Jie , Wu Xiang-Rong , Zhao Shen , Xu Yu-Zheng , Jin Xi , Xiao Yi , Wang Ying , Lin Cai-Jin , Zhou Yi-Fan , Fu Tong , Yang Wen-Tao , Li Ming , Lv Hong , Chen Siyuan , Grigoriadis Anita , Jiang Yi-Zhou , Ma Ding , Shao Zhi-Ming
Published: November 2024

Table S1
Figure S7 from Targeting BCL2 with Venetoclax Enhances the Efficacy of the KRASG12D Inhibitor MRTX1133 in Pancreatic Cancer
Authors: Becker Jeffrey H. , Metropulos Anastasia E. , Spaulding Christina , Marinelarena Alejandra M. , Shields Mario A. , Principe Daniel R. , Pham Thao D. , Munshi Hidayatullah G.
Published: November 2024

Effect of MRTX1133 on ‘small’ KPC tumors.
Supplementary Data 1 from NQO1 Triggers Neutrophil Recruitment and NET Formation to Drive Lung Metastasis of Invasive Breast Cancer
Authors: Wang Xinzhi , Qu Yi , Xu Qianqian , Jiang Zeyu , Wang Hang , Lin Binyan , Cao Zehong , Pan Yuqi , Li Sheng , Hu Yili , Yang Hui , He Li , Chang Hang , Hang Bo , Wen Hongmei , Wu Hao , Mao Jian-Hua
Published: November 2024

This file includes: Materials and Methods; Figures. S1 to S22; Tables. S1, S2, S3, S4, S5 and S7; Original Western-blot images
Supplementary Table 3 from CRISPR Screening of Transcribed Super-Enhancers Identifies Drivers of Triple-Negative Breast Cancer Progression
Authors: Lewis Michael W. , King Caitlin M. , Wisniewska Kamila , Regner Matthew J. , Coffey Alisha , Kelly Michael R. , Mendez-Giraldez Raul , Davis Eric S. , Phanstiel Douglas H. , Franco Hector L.
Published: November 2024

Guide RNA sequences for CRISPRi screen
Figure S6 from FOXP4 Is a Direct YAP1 Target That Promotes Gastric Cancer Stemness and Drives Metastasis
Authors: Liu Xiaoli , Chen Bonan , Xie Fuda , Wong Kit Yee , Cheung Alvin H.K. , Zhang Jinglin , Wu Qian , Fang Canbin , Hu Jintao , Wang Shouyu , Xu Dazhi , Chen Jianwu , Wang Yuzhi , Wong Chi Chun , Chen Huarong , Wu William K.K. , Yu Jun , Chan Michael W.Y. , Tsang Chi Man , Lo Kwok Wai , Tse Gary M.K. , To Ka-Fai , Kang Wei
Published: November 2024

Supplementary Figure S6
Data from Molecular Characterization and Classification of HER2-Positive Breast Cancer Inform Tailored Therapeutic Strategies
Authors: Li Yu-Wei , Dai Lei-Jie , Wu Xiang-Rong , Zhao Shen , Xu Yu-Zheng , Jin Xi , Xiao Yi , Wang Ying , Lin Cai-Jin , Zhou Yi-Fan , Fu Tong , Yang Wen-Tao , Li Ming , Lv Hong , Chen Siyuan , Grigoriadis Anita , Jiang Yi-Zhou , Ma Ding , Shao Zhi-Ming
Published: November 2024

Abstract
HER2-positive breast cancer is an aggressive subtype that accounts for 15% to 20% of all breast cancers. Recent studies have suggested that HER2-positive breast cancer is a group of heterogeneous diseases with different sensitivities to standard treatment regimens. Revealing the molecular heterogeneity of HER2-positive breast cancer could potentially enable more precise treatment strategies. In this study, we performed multiomics profiling on a HER2-positive breast cancer cohort and identified four transcriptome-based subtypes. The classical HER2 (HER2-CLA) subtype comprised 28.3% of the samples and displayed high ERBB2 activation and significant benefit from anti-HER2 therapy. The immunomodulatory (HER2-IM) subtype (20%) featured an immune-activated microenvironment, potentially suitable for de-escalated treatment and immunotherapy. The luminal-like (HER2-LUM) subtype (30.6%) possessed similar molecular features of hormone receptor–positive HER2-negative breast cancer, suggesting endocrine therapy and CDK4/6 inhibitors as a potential therapeutic strategy. Lastly, the basal/mesenchymal-like (HER2-BM) subtype (21.1%) had a poor response to current dual HER2-targeted therapy and could potentially benefit from tyrosine kinase inhibitors. The molecular characteristics and clinical features of the subtypes were further explored across multiple cohorts, and the feasibility of the proposed treatment strategies was validated in patient-derived organoid and patient-derived tumor fragment models. This study elucidates the molecular heterogeneity of HER2-positive breast cancer and paves the way for a more tailored treatment.

Significance: Illumination of the inherent heterogeneity within HER2-positive breast cancers through the delineation of distinct molecular subtypes lays the groundwork for developing more personalized treatment strategies based on specific patient characteristics.
PRDM16 Induces Methylation of FLT3 to Promote FLT3-ITD Signaling and Leukemia Progression
Authors: Zhai Fengxian , Pan Guozheng , Xue Lei , Cheng Can , Wang Jiabei , Liu Yao , Liu Lianxin
Published: November 2024

Internal tandem duplication (ITD) in the FMS-like receptor tyrosine kinase-3 (FLT3) is one of the most frequent mutations in acute myeloid leukemia (AML) and is associated with poor prognosis. FLT3-ITD mutations result in endoplasmic reticulum (ER) retention and constitutive autophosphorylation of FLT3. The PR/SET domain 16 (PRDM16) is highly expressed in patients with FLT3-ITD+ AML, suggesting it might play a role in leukemogenesis. Here, we revealed that genetic and pharmacologic suppression of PRDM16 greatly slowed the progression of FLT3-ITD–driven leukemia, sensitized leukemic cells to tyrosine kinase inhibitors, and extended the survival of leukemic mice. PRDM16 enhanced activation of oncogenic FLT3-ITD and ligand-dependent activation of wild-type FLT3 in leukemic cells. Mechanistically, PRDM16 mediated monomethylation of FLT3-ITD at lysine-614 and promoted its ER localization, resulting in enhanced FLT3 signaling in leukemia cells. Moreover, pharmacologic suppression of FLT3-ITD methylation in combination with tyrosine kinase inhibitors increased the elimination of FLT3-ITD+ AML cells. Altogether, these results suggest that PRDM16 boosts oncogenic FLT3 signaling in leukemic cells by prompting FLT3-ITD methylation. Therefore, PRDM16 may serve as a therapeutic target for AML.

Significance: Monomethylation of FLT3-ITD at lysine-614 by PRDM16 induces FLT3 ER localization and enhanced signaling, which can be inhibited by targeting PRDM16 to suppress survival of FLT3-ITD+ AML cells and increase chemosensitivity.
ACE2 Enhances Sensitivity to PD-L1 Blockade by Inhibiting Macrophage-Induced Immunosuppression and Angiogenesis
Authors: Xie Peiyi , Guo Lei , Yu Qiang , Zhao Yufei , Yu Mincheng , Wang Hui , Wu Mengyuan , Xu Wenxin , Xu Min , Zhu Xiao-Dong , Xu Yongfeng , Xiao Yong-Sheng , Huang Cheng , Zhou Jian , Fan Jia , Hung Mien-Chie , Sun Huichuan , Ye Qing-Hai , Zhang Bo , Li Hui
Published: November 2024

Anti–PD-L1–based combination immunotherapy has become the first-line treatment for unresectable hepatocellular carcinoma (HCC). However, the objective response rate is lower than 40%, highlighting the need to identify mechanisms of tolerance to immune checkpoint inhibitors and accurate biomarkers of response. In this study, we used next-generation sequencing to analyze HCC samples from 10 patients receiving anti–PD-L1 therapy. Activation of the renin–angiotensin system was elevated in nonresponders compared with responders, and angiotensin-converting enzyme 2 (ACE2) expression was significantly downregulated in nonresponders. ACE2 deficiency promoted HCC development and anti–PD-L1 resistance, whereas ACE2 overexpression inhibited HCC progression in immune-competent mice. Mass cytometry by time of flight revealed that ACE2-deficient murine orthotopic tumor tissues featured elevated M2-like tumor-associated macrophages, displayed a CCR5+PD-L1+ immunosuppressive phenotype, and exhibited high VEGFα expression. ACE2 downregulated tumor-intrinsic chemokine (C–C motif) ligand 5 expression by suppressing NF-κB signaling through the ACE2/angiotensin-(1–7)/Mas receptor axis. The lower chemokine (C–C motif) ligand 5 levels led to reduced activation of the JAK–STAT3 pathway and suppressed PD-L1 and VEGFα expression in macrophages, blocking macrophage infiltration and M2-like polarization. Pharmacologic targeting of CCR5 using maraviroc enhanced the tumor-suppressive effect of anti–PD-L1 therapy. Together, these findings suggest that activation of the ACE2 axis overcomes the immunosuppressive microenvironment of HCC and may serve as an immunotherapeutic target and predictive biomarker of response to PD-L1 blockade.

Significance: ACE2 regulates the immune landscape of hepatocellular carcinoma by abrogating M2-like macrophage polarization and sensitizes tumors to anti–PD-L1, suggesting that harnessing the ACE2 axis could be a promising strategy to improve immunotherapy efficacy.
ASCL1 Drives the Development of Neuroendocrine Prostate Cancer
Authors: McQuillen Caden N. , Brady Nicholas J.
Published: November 2024

Therapeutic resistance to androgen receptor (AR)–targeting agents remains a significant clinical problem during the treatment of prostate cancer, with the incidence rate of resistant disease increasing as more men are treated with next-generation AR-targeted therapies. Lineage plasticity and progression to neuroendocrine prostate cancer (NEPC) are mechanisms by which prostate tumors lose dependence on androgen signaling and escape treatment. Although many known genetic alterations can predispose tumors to acquiring the NEPC phenotype, it remains unclear what, if any, drivers are essential to this progression. In this issue of Cancer Research, Rodarte and colleagues identified ASCL1 as one such essential regulator. Through the use of genetically engineered mouse models, the authors demonstrated that whereas ASCL1 was dispensable for tumor formation and growth, ASCL1 loss nearly completely abrogated the development of NEPC and instead redirected lineage trajectories toward a basal-like phenotype. This study provides an important new model for the study of NEPC, reveals the ability of ASCL1+ NEPC cells to also assume a NEUROD1+ state, and demonstrates the changes to tumor cell phenotypes following ASCL1 loss.

See related article by Rodarte et al., p. 3522
The Influence of DNA Repair Genes and Prenatal Tobacco Exposure on Risk of Childhood Acute Lymphoblastic Leukemia: A Gene–Environment Interaction Study
Authors: Wang Xinran , Zhong Charlie , Ma Xiaomei , Metayer Catherine , Mancuso Nicolas , Gauderman W. James , Wiemels Joseph L.
Published: November 2024

Background:

Acute lymphoblastic leukemia (ALL) is the most common type of cancer among children. Tobacco exposure during gestation has been investigated as a potential risk factor, but its role remains undefined. Given tobacco’s toxicologic profile as a DNA-damaging agent, we examined the impact of DNA repair gene variability as a source of vulnerability to tobacco exposure risk for ALL.

Methods:

Leveraging demographic and genotype data from two large California-based ALL epidemiology studies, we used logistic regression, MinimumP (minP) statistical method, and permutation tests to examine interactions between DNA repair genes and prenatal tobacco exposure.

Results:

We found statistically significant interactions between prenatal tobacco exposure and DNA repair genes RECQL (minP = 1.00 × 10−4, FDR-P value = 1.86 × 10−2) and TDG (minP = 1.00 × 10−4, FDR-P value = 1.86 × 10−2) with regard to childhood ALL risk. Notable interactions in the homologous recombination pathway were observed among Latino children, whereas non-Latino White children displayed significant interactions in the base excision repair and nucleotide excision repair pathways.

Conclusions:

Our study highlights the significance of DNA repair genes and pathways when evaluating environmental exposure to tobacco smoke, suggesting that genetic variability within these pathways could impact vulnerability in the development of childhood ALL.

Impact:

This study highlights the significant impact of genetic variation interacting with prenatal tobacco exposure on ALL risk. Further research is needed to understand these interactions and their implications for ALL etiology. Expanding studies to other gene–environment interactions will aid in developing targeted prevention, diagnosis, and treatment strategies for pediatric oncology.
Supplementary Table 3 from Circulating Tumor DNA Analysis Detects FGFR2 Amplification and Concurrent Genomic Alterations Associated with FGFR Inhibitor Efficacy in Advanced Gastric Cancer
Authors: Jogo Tomoko , Nakamura Yoshiaki , Shitara Kohei , Bando Hideaki , Yasui Hisateru , Esaki Taito , Terazawa Tetsuji , Satoh Taroh , Shinozaki Eiji , Nishina Tomohiro , Sunakawa Yu , Komatsu Yoshito , Hara Hiroki , Oki Eiji , Matsuhashi Nobuhisa , Ohta Takashi , Kato Takeshi , Ohtsubo Koushiro , Kawakami Takeshi , Okano Naohiro , Yamamoto Yoshiyuki , Yamada Takanobu , Tsuji Akihito , Odegaard Justin I. , Taniguchi Hiroya , Doi Toshihiko , Fujii Satoshi , Yoshino Takayuki
Published: November 2024

Alterations detected by ctDNA sequencing
Supplementary Table 2 from Circulating Tumor DNA Analysis Detects FGFR2 Amplification and Concurrent Genomic Alterations Associated with FGFR Inhibitor Efficacy in Advanced Gastric Cancer
Authors: Jogo Tomoko , Nakamura Yoshiaki , Shitara Kohei , Bando Hideaki , Yasui Hisateru , Esaki Taito , Terazawa Tetsuji , Satoh Taroh , Shinozaki Eiji , Nishina Tomohiro , Sunakawa Yu , Komatsu Yoshito , Hara Hiroki , Oki Eiji , Matsuhashi Nobuhisa , Ohta Takashi , Kato Takeshi , Ohtsubo Koushiro , Kawakami Takeshi , Okano Naohiro , Yamamoto Yoshiyuki , Yamada Takanobu , Tsuji Akihito , Odegaard Justin I. , Taniguchi Hiroya , Doi Toshihiko , Fujii Satoshi , Yoshino Takayuki
Published: November 2024

Association between the FGFR2 amplification status and clinicopathological features
Supplementary Data from Improving Risk Stratification for Pediatric Patients with Rhabdomyosarcoma by Molecular Detection of Disseminated Disease
Authors: Lak Nathalie S.M. , Voormanns Timon L. , Zappeij-Kannegieter Lily , van Zogchel Lieke M.J. , Fiocco Marta , van Noesel Max M. , Merks Johannes H.M. , van der Schoot C. Ellen , Tytgat Godelieve A.M. , Stutterheim Janine
Published: November 2024

Supplementary tables and figures
Figure 1 from Kinobead Profiling Reveals Reprogramming of BCR Signaling in Response to Therapy within Primary CLL Cells
Authors: Linley Adam J. , Karydis Laura I. , Mondru Anil K. , D'Avola Annalisa , Al Shmrany Humood , Cicconi Silvia , Griffin Rebecca , Forconi Francesco , Pettitt Andrew R. , Kalakonda Nagesh , Rawstron Andrew C. , Hillmen Peter , Steele Andrew J. , MacEwan David J. , Packham Graham , Prior Ian A. , Slupsky Joseph R.
Published: November 2024

Kinobead analysis of MEC-1 cells. A, Schematic of the kinobead-MS approach for MEC-1 cells. B, Pie graphs illustrating the numbers of kinase and non-kinase proteins isolated from MEC-1 cell lysates using six different kinobeads. C, Heatmaps constructed using average data from experiments involving MEC-1 cells (n = 3), which were treated with 500 nmol/L ibrutinib or dasatinib or left untreated as a control. After 60 minutes, cell lysates were prepared and kinase binding to Ki-NET beads was assessed using MS. Kinases are grouped by subfamilies. Heatmap shows mean change (log2) in kinase binding for ibrutinib- or dasatinib-treated cells relative to control cells for the core 107 kinases derived from three independent experiments. D, Graph showing results for ibrutinib for selected kinases, including direct targets (i.e., inhibited by ibrutinib in in vitro assays with IC50 < 500 nmol/L), kinases which are modulated by ibrutinib but are not direct targets, and kinases which are unaffected by ibrutinib. Graph shows mean (±error) binding normalized to control cells (set to 100%) with statistical significance of differences indicated (Student t test; *, P < 0.05; **, P < 0.01; ****, P < 0.0001).
Figure S4 from Prognostic Utility of Breast Cancer Index to Stratify Distant Recurrence Risk in Invasive Lobular Carcinoma
Authors: Nunes Raquel , Sella Tal , Treuner Kai , Atkinson Jennifer M. , Wong Jenna , Zhang Yi , Exman Pedro , Dabbs David , Richardson Andrea L. , Schnabel Catherine A. , Sgroi Dennis C. , Oesterreich Steffi , Cimino-Mathews Ashley , Metzger Otto
Published: November 2024

Prognostic performance of BCI for overall 10-year, early (0-5 years), and late (5-10 years) distant recurrence (DR) rate for patients that received adjuvant endocrine therapy in the lobular cohort.
Figure S2 from Prognostic Utility of Breast Cancer Index to Stratify Distant Recurrence Risk in Invasive Lobular Carcinoma
Authors: Nunes Raquel , Sella Tal , Treuner Kai , Atkinson Jennifer M. , Wong Jenna , Zhang Yi , Exman Pedro , Dabbs David , Richardson Andrea L. , Schnabel Catherine A. , Sgroi Dennis C. , Oesterreich Steffi , Cimino-Mathews Ashley , Metzger Otto
Published: November 2024

Concordance of BCI scores between manual microdissection versus laser capture microdissection (A) and the relationship of BCI score difference versus tumor content (B).
Supplementary Figure 3 from A Phase I Study of LSZ102, an Oral Selective Estrogen Receptor Degrader, with or without Ribociclib or Alpelisib, in Patients with Estrogen Receptor–Positive Breast Cancer
Authors: Jhaveri Komal , Juric Dejan , Yap Yoon-Sim , Cresta Sara , Layman Rachel M. , Duhoux Francois P. , Terret Catherine , Takahashi Shunji , Huober Jens , Kundamal Nicole , Sheng Qing , Balbin Alejandro , Ji Yan , He Wei , Crystal Adam , De Vita Serena , Curigliano Giuseppe
Published: November 2024

Supplementary figure 3 shows progression-free survival (Kaplan-Meier) in each treatment arm.
Supplementary Data from Single-Agent Ibrutinib for Rituximab-Refractory Waldenström Macroglobulinemia: Final Analysis of the Substudy of the Phase III InnovateTM Trial
Authors: Trotman Judith , Buske Christian , Tedeschi Alessandra , Matous Jeffrey V. , MacDonald David , Tam Constantine S. , Tournilhac Olivier , Ma Shuo , Treon Steven P. , Oriol Albert , Ping Jerry , Briso Eva M. , Arango-Hisijara Israel , Dimopoulos Meletios A.
Published: November 2024

Supplemental Figure S1
Unearthing a Prostate Cancer cfDNA Signature that “Stems” from AR Alterations
Authors: Nawfal Rashad , El Hajj Chehade Razane , Berchuck Jacob E.
Published: November 2024

Androgen receptor alterations portend a poor prognosis in patients with advanced prostate cancer. A recent study identified a stemness signature enriched in cell-free DNA from androgen receptor–altered patients, associated with worse outcomes. These findings highlight the potential of epigenomic liquid biopsy tools to discover novel clinically relevant tumor molecular subtypes.

See related article by Chauhan et al., p. 151
Supplemental Figure 9 from SC134-TCB Targeting Fucosyl-GM1, a T Cell–Engaging Antibody with Potent Antitumor Activity in Preclinical Small Cell Lung Cancer Models
Authors: Dave Foram , Vaghela Poonam , Heath Bryony , Dunster Zuzana , Dubinina Elena , Thakker Dhruma , Mann Katie , Chadwick Joe , Cane Gaëlle , Kaira Bubacarr G. , Mohammed Omar J. , Choudhury Ruhul , Paston Samantha , Parsons Tina , Vankemmelbeke Mireille , Durrant Lindy
Published: November 2024

Further in vivo validation: growth curves, IHC
Supplemental Figure 10 from SC134-TCB Targeting Fucosyl-GM1, a T Cell–Engaging Antibody with Potent Antitumor Activity in Preclinical Small Cell Lung Cancer Models
Authors: Dave Foram , Vaghela Poonam , Heath Bryony , Dunster Zuzana , Dubinina Elena , Thakker Dhruma , Mann Katie , Chadwick Joe , Cane Gaëlle , Kaira Bubacarr G. , Mohammed Omar J. , Choudhury Ruhul , Paston Samantha , Parsons Tina , Vankemmelbeke Mireille , Durrant Lindy
Published: November 2024

Individual tumour growth curves Atezolizumab study
Figure 5 from SC134-TCB Targeting Fucosyl-GM1, a T Cell–Engaging Antibody with Potent Antitumor Activity in Preclinical Small Cell Lung Cancer Models
Authors: Dave Foram , Vaghela Poonam , Heath Bryony , Dunster Zuzana , Dubinina Elena , Thakker Dhruma , Mann Katie , Chadwick Joe , Cane Gaëlle , Kaira Bubacarr G. , Mohammed Omar J. , Choudhury Ruhul , Paston Samantha , Parsons Tina , Vankemmelbeke Mireille , Durrant Lindy
Published: November 2024

PDL1 inhibition and dose modulation further improve SC134-TCB antitumor impact. SC134-TCB treatment induces PDL1 expression. A, Dose-dependent PDL1 expression in ex vivo 48-hour cocultures (DMS79: huPBMCs at 5:1). B,In vivo SC134-TCB–induced PDL1 expression on DMS79 cells (at termination) from NSG antitumor study, Mann–Whitney test, P = 0.0220. Antitumor study investigating the efficacy of SC134-TCB on implanted DMS79 tumor in NSG mice. DMS79 cells were implanted on day 1 and PBMCs dosed on days 8 and 22 at an E:T of 5:1. Gray arrows show biweekly administration of SC134-TCB (100 μg); upward ticks show atezolizumab dosing (200 μg). C, Tumor volume analysis, mixed-effects model P < 0.0001. Individual growth curves shown in Supplementary Fig. S10; D, OS analysis, log-rank Mantel–Cox P < 0.01. E, Phenotyping data assessing the percentage of live T cells (Tils) and (F) the percentage PD1/TIM3 double-positive Tils in terminal tumor samples, Mann–Whitney test, P = 0.0142. Antitumor study investigating the efficacy of reduced dose or reduced dose frequency of SC134-TCB on implanted DMS79 tumor in NSG mice. DMS79 cells were implanted on day 1 and PBMCs dosed on days 7 and 21 at an E:T of 5:1. SC134-TCB dosing either biweekly (six doses of 10 or 100 μg) or weekly (three doses of 100 μg). G, Tumor volume analysis, two-way ANOVA, P = 0.0004. Individual growth curves shown in Supplementary Fig. S11. H, OS, log-rank Mantel–Cox, P < 0.0001. Atez, atezolizumab.
Supplementary Table 1 from Novel Inhibition of Central Carbon Metabolism Pathways by Rac and CDC42 inhibitor MBQ167 and Paclitaxel
Authors: Cruz-Collazo Ailed M. , Katsara Olga , Grafals-Ruiz Nilmary , Colon Gonzalez Jessica , Dorta-Estremera Stephanie , Carlo Victor P. , Chorna Nataliya , Schneider Robert J. , Dharmawardhane Suranganie
Published: November 2024

Supplementary Table 1
Figure 1 from SC134-TCB Targeting Fucosyl-GM1, a T Cell–Engaging Antibody with Potent Antitumor Activity in Preclinical Small Cell Lung Cancer Models
Authors: Dave Foram , Vaghela Poonam , Heath Bryony , Dunster Zuzana , Dubinina Elena , Thakker Dhruma , Mann Katie , Chadwick Joe , Cane Gaëlle , Kaira Bubacarr G. , Mohammed Omar J. , Choudhury Ruhul , Paston Samantha , Parsons Tina , Vankemmelbeke Mireille , Durrant Lindy
Published: November 2024

SC134 specifically binds FucGM1, a SCLC selective target. Glycolipid binding specificity by hybridoma-derived SC134. A, ELISA analysis of FucGM1-binding specificity of SC134. FucGM1 binding is observed, in contrast to lack of binding to closely related gangliosides. Positive control antibody reactivity for the respective gangliosides is shown in Supplementary Fig. S1A. B, Immuno-TLC analysis of SC134 showing reactivity toward DMS79 lipid extract as well as purified FucGM1, combined with lack of GM1 reactivity. C, SC134-binding efficiency for FucGM1 on ELISA. D, SC134 cell surface–binding efficiency on a range of SCLC cell lines. h134 characterization: (E) FucGM1 lipid binding compared with GM1 by ch134 and h134 on ELISA. F, SCLC cell line binding by h134. MFI assessed by flow cytometry. FucGM1 distribution in SCLC tumor tissues: (G) IHC FucGM1 expression analysis using h134 (huIgG1) of frozen patient-derived xenograft SCLC tissues. H, FucGM1 expression by DMS79 in culture. I, FucGM1 expression by DMS79 after growing in NSG mice. J, Restricted FucGM1 expression in frozen normal healthy human tissues, immunostained with h134 (J). The pituitary (a), skin (b), and thymus (c) were the only positive tissues from the 30 normal healthy tissues analyzed. The full arrays are shown in Supplementary Fig. S1D. ch134, chimeric (human IgG1) SC134; MFI, median fluorescence intensity; TLC, thin-layer chromatography.
Figure S2 from YAP1 Suppression by ZDHHC7 Is Associated with Ferroptosis Resistance and Poor Prognosis in Ovarian Clear Cell Carcinoma
Authors: Furutake Yoko , Yamaguchi Ken , Yamanoi Koji , Kitamura Sachiko , Takamatsu Shiro , Taki Mana , Ukita Masayo , Hosoe Yuko , Murakami Ryusuke , Abiko Kaoru , Horie Akihito , Hamanishi Junzo , Baba Tsukasa , Matsumura Noriomi , Mandai Masaki
Published: November 2024

Supplementary Figure 2
Figure S4 from A DXd/TLR7-Agonist Dual-Conjugate Anti-HER2 ADC Exerts Robust Antitumor Activity Through Tumor Cell Killing and Immune Activation
Authors: Yue Hangtian , Xu Hui , Ma Lanping , Li Xiyuan , Yang Biyu , Wang Xiyuan , Zeng Qingzhong , Li Han , Zhang Deqiang , Geng Meiyu , Meng Tao , Xie Zuoquan
Published: November 2024

Figure S4 ESI-MS analysis (deconvoluted mass spectra) and DAR calculation. (A) Tras-MTL1. (B) Tras-DXd. (C) Tras-DXd-MTL1.
Figure S1 from A DXd/TLR7-Agonist Dual-Conjugate Anti-HER2 ADC Exerts Robust Antitumor Activity Through Tumor Cell Killing and Immune Activation
Authors: Yue Hangtian , Xu Hui , Ma Lanping , Li Xiyuan , Yang Biyu , Wang Xiyuan , Zeng Qingzhong , Li Han , Zhang Deqiang , Geng Meiyu , Meng Tao , Xie Zuoquan
Published: November 2024

Figure S1. Synthetic procedure of drug-linker MTL1 (A) and 1H-NMR spectrum of MTL1 (B).
Supplementary Table 4 from Trastuzumab-MMAU Antibody-Auristatin Conjugates: Valine-Glucoserine Linker with Stabilized Maleimide Conjugation Improves In Vivo Efficacy and Tolerability
Authors: Goldberg Shalom D. , Satomaa Tero , Aina Olulanu , Aitio Olli , Burke Krista , Dudkin Vadim , Geist Brian , Irrechukwu Onyi , Hänninen Anna-Liisa , Heiskanen Annamari , Helin Jari , Hiltunen Jukka O. , Kinyamu-Akunda Jacqueline , Klein Donna M. , Kohli Neeraj , Kotiranta Titta , Lähteenmäki Tuula , Niemelä Ritva , Pitkänen Virve , Pynnönen Henna , Rittase William , Wiley Kristen , Zhou Junguo , Saarinen Juhani
Published: November 2024

Individual and mean serum MMAU toxicokinetic parameters following three i.v. bolus doses of T-mavg-MMAU DAR4 in male cynomolgus monkeys.
Supplementary Figure 8 from Trastuzumab-MMAU Antibody-Auristatin Conjugates: Valine-Glucoserine Linker with Stabilized Maleimide Conjugation Improves In Vivo Efficacy and Tolerability
Authors: Goldberg Shalom D. , Satomaa Tero , Aina Olulanu , Aitio Olli , Burke Krista , Dudkin Vadim , Geist Brian , Irrechukwu Onyi , Hänninen Anna-Liisa , Heiskanen Annamari , Helin Jari , Hiltunen Jukka O. , Kinyamu-Akunda Jacqueline , Klein Donna M. , Kohli Neeraj , Kotiranta Titta , Lähteenmäki Tuula , Niemelä Ritva , Pitkänen Virve , Pynnönen Henna , Rittase William , Wiley Kristen , Zhou Junguo , Saarinen Juhani
Published: November 2024

Digestion of T-mavg-MMAU DAR8 with recombinant cathepsin B.
Supplementary Figure 6 from Trastuzumab-MMAU Antibody-Auristatin Conjugates: Valine-Glucoserine Linker with Stabilized Maleimide Conjugation Improves In Vivo Efficacy and Tolerability
Authors: Goldberg Shalom D. , Satomaa Tero , Aina Olulanu , Aitio Olli , Burke Krista , Dudkin Vadim , Geist Brian , Irrechukwu Onyi , Hänninen Anna-Liisa , Heiskanen Annamari , Helin Jari , Hiltunen Jukka O. , Kinyamu-Akunda Jacqueline , Klein Donna M. , Kohli Neeraj , Kotiranta Titta , Lähteenmäki Tuula , Niemelä Ritva , Pitkänen Virve , Pynnönen Henna , Rittase William , Wiley Kristen , Zhou Junguo , Saarinen Juhani
Published: November 2024

Digestion of T-mavg-MMAU DAR8 with bovine liver β-glucuronidase.
Supplementary Figure 14 from Trastuzumab-MMAU Antibody-Auristatin Conjugates: Valine-Glucoserine Linker with Stabilized Maleimide Conjugation Improves In Vivo Efficacy and Tolerability
Authors: Goldberg Shalom D. , Satomaa Tero , Aina Olulanu , Aitio Olli , Burke Krista , Dudkin Vadim , Geist Brian , Irrechukwu Onyi , Hänninen Anna-Liisa , Heiskanen Annamari , Helin Jari , Hiltunen Jukka O. , Kinyamu-Akunda Jacqueline , Klein Donna M. , Kohli Neeraj , Kotiranta Titta , Lähteenmäki Tuula , Niemelä Ritva , Pitkänen Virve , Pynnönen Henna , Rittase William , Wiley Kristen , Zhou Junguo , Saarinen Juhani
Published: November 2024

Digestion of lintuzumab-mavg-MMAU DAR8 by cynomolgus monkey liver microsomes at pH 4.5.
Fig. S2 from Inhibition of SUMOylation Induces Adaptive Antitumor Immunity against Pancreatic Cancer through Multiple Effects on the Tumor Microenvironment
Authors: Erdem Suna , Lee Hyojae James , Shankara Narayanan Jayanth Surya Narayanan , Tharuka Mohottige Don Neranjan , De la Torre Jorge , Ren Tianchen , Kuang Yixuan , Abeywardana Tharindumala , Li Kevin , Berger Allison J. , Lowy Andrew M. , White Rebekah R. , Chen Yuan
Published: November 2024

Fig. S2
Data from SC134-TCB Targeting Fucosyl-GM1, a T Cell–Engaging Antibody with Potent Antitumor Activity in Preclinical Small Cell Lung Cancer Models
Authors: Dave Foram , Vaghela Poonam , Heath Bryony , Dunster Zuzana , Dubinina Elena , Thakker Dhruma , Mann Katie , Chadwick Joe , Cane Gaëlle , Kaira Bubacarr G. , Mohammed Omar J. , Choudhury Ruhul , Paston Samantha , Parsons Tina , Vankemmelbeke Mireille , Durrant Lindy
Published: November 2024

Abstract
Small cell lung cancer (SCLC) is an aggressive disease with limited treatment options. Fucosyl-GM1 (FucGM1) is a glycolipid overexpressed in the majority of SCLC tumors but virtually absent from normal healthy tissues. In this study, we validate a FucGM1-targeting T cell–redirecting bispecific (TCB) antibody for the treatment of SCLC. More than 80% of patient-derived xenograft tissues of SCLC expressed FucGM1, whereas only three normal human tissues: pituitary, thymus, and skin expressed low and focal FucGM1. A FucGM1-targeting TCB (SC134-TCB), based on the Fc-silenced humanized SC134 antibody, exhibited nanomolar efficiency in FucGM1 glycolipid and SCLC cell surface binding. SC134-TCB showed potent ex vivo killing of SCLC cell lines with donor-dependent EC50 ranging from 7.2 pmol/L up to 211.0 pmol/L, effectively activating T cells, with picomolar efficiency, coinciding with target-dependent cytokine production such as IFNγ, IL2, and TNFα and robust proliferation of both CD4 and CD8 T cells. The ex vivo SC134-TCB tumor controlling activity translated into an effective in vivo anti-DMS79 tumor therapy, resulting in 100% tumor-free survival in a human peripheral blood mononuclear cell admixed setting and 40% overall survival (55% tumor growth inhibition) with systemically administered human peripheral blood mononuclear cells. Combination treatment with atezolizumab further enhanced survival and tumor growth inhibition (up to 73%). A 10-fold SC134-TCB dose reduction maintained the strong in vivo antitumor impact, translating into 70% overall survival (P < 0.0001). Whole-blood incubation with SC134-TCB, as well as healthy human primary cells analysis, revealed no target-independent cytokine production. SC134-TCB presents an attractive candidate to deliver an effective immunotherapy treatment option for patients with SCLC.
Data from Novel Inhibition of Central Carbon Metabolism Pathways by Rac and CDC42 inhibitor MBQ167 and Paclitaxel
Authors: Cruz-Collazo Ailed M. , Katsara Olga , Grafals-Ruiz Nilmary , Colon Gonzalez Jessica , Dorta-Estremera Stephanie , Carlo Victor P. , Chorna Nataliya , Schneider Robert J. , Dharmawardhane Suranganie
Published: November 2024

Abstract
Triple negative breast cancer (TNBC) represents a therapeutic challenge in which standard chemotherapy is limited to paclitaxel. MBQ167, a clinical stage small molecule inhibitor that targets Rac and Cdc42, inhibits tumor growth and metastasis in mouse models of TNBC. Herein, we investigated the efficacy of MBQ167 in combination with paclitaxel in TNBC preclinical models, as a prelude to safety trials of this combination in patients with advanced breast cancer. Individual MBQ167 or combination therapy with paclitaxel was more effective at reducing TNBC cell viability and increasing apoptosis compared with paclitaxel alone. In orthotopic mouse models of human TNBC (MDA-MB231 and MDA-MB468), individual MBQ167, paclitaxel, or the combination reduced mammary tumor growth with similar efficacy, with no apparent liver toxicity. However, paclitaxel single agent treatment significantly increased lung metastasis, whereas MBQ167, single or combined, reduced lung metastasis. In the syngeneic 4T1/BALB/c model, combined MBQ167 and paclitaxel decreased established lung metastases by ∼80%. To determine the molecular basis for the improved efficacy of the combined treatment on metastasis, 4T1 tumor extracts from BALB/c mice treated with MBQ167, paclitaxel, or the combination were subjected to transcriptomic analysis. Gene set enrichment identified specific downregulation of central carbon metabolic pathways by the combination of MBQ167 and paclitaxel but not individual compounds. Biochemical validation, by immunoblotting and metabolic Seahorse analysis, shows that combined MBQ167 and paclitaxel reduces glycolysis. This study provides a strong rationale for the clinical testing of MBQ167 in combination with paclitaxel as a potential therapeutic for TNBC and identifies a unique mechanism of action.
Data from Trastuzumab-MMAU Antibody-Auristatin Conjugates: Valine-Glucoserine Linker with Stabilized Maleimide Conjugation Improves In Vivo Efficacy and Tolerability
Authors: Goldberg Shalom D. , Satomaa Tero , Aina Olulanu , Aitio Olli , Burke Krista , Dudkin Vadim , Geist Brian , Irrechukwu Onyi , Hänninen Anna-Liisa , Heiskanen Annamari , Helin Jari , Hiltunen Jukka O. , Kinyamu-Akunda Jacqueline , Klein Donna M. , Kohli Neeraj , Kotiranta Titta , Lähteenmäki Tuula , Niemelä Ritva , Pitkänen Virve , Pynnönen Henna , Rittase William , Wiley Kristen , Zhou Junguo , Saarinen Juhani
Published: November 2024

Abstract
Antibody–drug conjugates (ADC) have shown impressive clinical activity with approval of many agents in hematologic and solid tumors. However, challenges remain with both efficacy and safety of ADCs. This study describes novel trastuzumab–auristatin conjugates with the hydrophilic monomethylauristatin E (MMAE) prodrug MMAU, and optimization of a glycopeptide linker leading to a wider therapeutic window. Trastuzumab was conjugated with auristatin payloads via a series of linkers using a stabilized maleimide handle. The ADCs were characterized in vitro and their relative in vivo antitumor efficacies were assessed in HER2+ xenograft models. Relative linker stabilities and the mechanism of linker cleavage were studied using in vitro assays. Toxicity and toxicokinetics of the best performing ADC were evaluated in cynomolgus monkey (cyno). The trastuzumab–MMAU ADC with stabilized glycopeptide linker showed maleimide stabilization and higher resistance to cleavage by serum and lysosomal enzymes compared with a valine–citrulline conjugated trastuzumab ADC (trastuzumab–vc-MMAE). A single dose of 1 or 2 mg/kg of trastuzumab–MMAU at drug-to-antibody ratios (DAR) of eight and four respectively resulted in xenograft tumor growth inhibition, with superior efficacy to trastuzumab–vc-MMAE. Trastuzumab–MMAUDAR4 was tolerated at doses up to 12 mg/kg in cyno, which represents 2- to 4-fold higher dose than that observed with vedotin ADCs, and had increased terminal half-life and exposure. The optimized trastuzumab–MMAU ADC showed potent antitumor activity and was well tolerated with excellent pharmacokinetics in nonhuman primates, leading to a superior preclinical therapeutic window. The data support potential utility of trastuzumab–MMAU for treatment of HER2+ tumors.
Data from Inhibition of SUMOylation Induces Adaptive Antitumor Immunity against Pancreatic Cancer through Multiple Effects on the Tumor Microenvironment
Authors: Erdem Suna , Lee Hyojae James , Shankara Narayanan Jayanth Surya Narayanan , Tharuka Mohottige Don Neranjan , De la Torre Jorge , Ren Tianchen , Kuang Yixuan , Abeywardana Tharindumala , Li Kevin , Berger Allison J. , Lowy Andrew M. , White Rebekah R. , Chen Yuan
Published: November 2024

Abstract
Improvement of outcome in patients with pancreatic ductal adenocarcinoma (PDAC) requires exploration of novel therapeutic targets. Thus far, most studies of PDAC therapies, including those inhibiting small ubiquitin-like modifications (SUMOylation), have focused on PDAC epithelial cell biology, yet SUMOylation occurs in a variety of cell types. The mechanisms by which SUMOylation impacts PDAC in the context of its tumor microenvironment are poorly understood. We used clinically relevant orthotopic PDAC mouse models to investigate the effect of SUMOylation inhibition using a specific, clinical-stage compound, TAK-981. In contrast to its inhibition of PDAC cell proliferation in vitro, the survival benefit conferred by TAK-981 in vivo is dependent on the presence of T cells, suggesting that induction of adaptive antitumor immunity is an important antitumor effect of SUMOylation inhibition in vivo. To understand how this adaptive antitumor immunity is promoted, we investigated how SUMOylation inhibition in vivo alters major cell types/subtypes and their communications in the PDAC tumor microenvironment by performing transcriptomic analyses at single-cell resolution, which allowed mapping of cells in our orthotopic mouse model to cells in human PDAC tumors based on gene expression profiles. Findings are further validated by flow cytometry, immunofluorescence, IHC, western blots, and qPCR. The single-cell transcriptome dataset provided here suggests several combination strategies to augment adaptive immune responses that are necessary for durable disease control in patients with PDAC.
ASAP1 and ARF1 Regulate Myogenic Differentiation in Rhabdomyosarcoma by Modulating TAZ Activity
Authors: Hebron Katie E. , Perkins Olivia L. , Kim Angela , Jian Xiaoying , Girald-Berlingeri Sofia A. , Lei Haiyan , Shern Jack F. , Conner Elizabeth A. , Randazzo Paul A. , Yohe Marielle E.
Published: November 2024

Despite aggressive, multimodal therapies, the prognosis of patients with refractory or recurrent rhabdomyosarcoma (RMS) has not improved in four decades. Because RMS resembles skeletal muscle precursor cells, differentiation-inducing therapy has been proposed for patients with advanced disease. In RAS-mutant PAX fusion–negative RMS (FN-RMS) preclinical models, MEK1/2 inhibition (MEKi) induces differentiation, slows tumor growth, and extends survival. However, the response is short-lived. A better understanding of the molecular mechanisms regulating FN-RMS differentiation could improve differentiation therapy. In this study, we identified a role in FN-RMS differentiation for ASAP1, an ADP ribosylation factor (ARF) GTPase–activating protein (GAP) with both proinvasive and tumor-suppressor functions. We found that ASAP1 knockdown inhibited differentiation in FN-RMS cells. Interestingly, knockdown of the GTPases ARF1 or ARF5, targets of ASAP1 GAP activity, also blocked differentiation of FN-RMS. We discovered that loss of ARF pathway components blocked myogenic transcription factor expression. Therefore, we examined the effects on transcriptional regulators. MEKi led to the phosphorylation and inactivation of WW domain–containing transcriptional regulator 1 (WWTR1; TAZ), a homolog of the pro-proliferative transcriptional co-activator YAP1, regulated by the Hippo pathway. However, loss of ASAP1 or ARF1 blocked this inactivation, which inhibits MEKi-induced differentiation. Finally, MEKi-induced differentiation was rescued by dual knockdown of ASAP1 and WWTR1. This study shows that ASAP1 and ARF1 are necessary for myogenic differentiation, providing a deeper understanding of differentiation in FN-RMS and illuminating an opportunity to advance differentiation therapy.

Implications: ASAP1 and ARF1 regulate MEKi-induced differentiation of FN-RMS cells by modulating WWTR1 (TAZ) activity, supporting YAP1/TAZ inhibition as a FN-RMS differentiation therapy strategy.
Supplementary Figure S3 from Viewing Native American Cervical Cancer Disparities through the Lens of the Vaginal Microbiome: A Pilot Study
Authors: Łaniewski Paweł , Joe Tawnjerae R. , Jimenez Nicole R. , Eddie Tristen L. , Bordeaux Skyler J. , Quiroz Verity , Peace Donna J. , Cui Haiyan , Roe Denise J. , Caporaso J. Gregory , Lee Naomi R. , Herbst-Kralovetz Melissa M.
Published: November 2024

Supplementary Figure S3: Associations of Lactobacillus abundance with race, vaginal pH, and HPV status.
Supplementary Figure 16 from Organ-Specific Immune Setpoints Underlie Divergent Immune Profiles across Metastatic Sites in Breast Cancer
Authors: Egelston Colt A. , Guo Weihua , Simons Diana L. , Ye Jian , Avalos Christian , Solomon Shawn T. , Nwangwu Mary , Nelson Michael S. , Tan Jiayi , Bacon Eliza R. , Ihle Kena , Schmolze Daniel , Tumyan Lusine , Waisman James R. , Lee Peter P.
Published: November 2024

PD-L1 expression assessment in metastatic tumor tissues. A, PD-L1 expression in tumor-involved tissues as assessed by a pathologist. B, Representative images of chromogenic PD-L1 staining in tumor-involved tissues. PD-L1 assessment percentages are shown. C, Densities of immune cell subsets were compared across PD-L1+ (>1%) and PD-L1- tumor-involved tissues. Capacity for production IFN-γ, IL-2, and TNF-α by D, CD8+ T cells and E, CD4+ T cells were compared between PD-L1+ and PD-L1- tissues. Frequencies of individual immune cell subsets that compose all PD-L1+ immune cells for F, tumor-free and G, tumor-involved tissues. Statistics generated by Kruskal–Wallis test by ranks (a,f,g) and Wilcoxon rank sum tests (c,d). Calculated p values are displayed as *, p < 0.05; **, p < 0.01; ***, p < 0.001; ****, p < 0.0001.
Supplementary Figure 1 from Organ-Specific Immune Setpoints Underlie Divergent Immune Profiles across Metastatic Sites in Breast Cancer
Authors: Egelston Colt A. , Guo Weihua , Simons Diana L. , Ye Jian , Avalos Christian , Solomon Shawn T. , Nwangwu Mary , Nelson Michael S. , Tan Jiayi , Bacon Eliza R. , Ihle Kena , Schmolze Daniel , Tumyan Lusine , Waisman James R. , Lee Peter P.
Published: November 2024

Flow cytometry gating strategy. Shown for CD8+ T cell panel (A) and CD4+ T cell panel (B).
Supplementary Table S6 from CD36+ Proinflammatory Macrophages Interact with ZCCHC12+ Tumor Cells in Papillary Thyroid Cancer Promoting Tumor Progression and Recurrence
Authors: Zhang Xin , Guo Limei , Tian Wenyu , Yang Ying , Yin Yue , Qiu Yaruo , Wang Weixuan , Li Yang , Zhang Guangze , Zhao Xuyang , Wang Guangxi , Lin Zhiqiang , Yang Meng , Zhao Wei , Lu Dan
Published: November 2024

Supplementary Table S6 PTC-specific markers based on spatial transcriptome screening.
Supplementary Fig S9 from CD36+ Proinflammatory Macrophages Interact with ZCCHC12+ Tumor Cells in Papillary Thyroid Cancer Promoting Tumor Progression and Recurrence
Authors: Zhang Xin , Guo Limei , Tian Wenyu , Yang Ying , Yin Yue , Qiu Yaruo , Wang Weixuan , Li Yang , Zhang Guangze , Zhao Xuyang , Wang Guangxi , Lin Zhiqiang , Yang Meng , Zhao Wei , Lu Dan
Published: November 2024

Supplementary Figure S9
Supplementary Fig S2 from CD36+ Proinflammatory Macrophages Interact with ZCCHC12+ Tumor Cells in Papillary Thyroid Cancer Promoting Tumor Progression and Recurrence
Authors: Zhang Xin , Guo Limei , Tian Wenyu , Yang Ying , Yin Yue , Qiu Yaruo , Wang Weixuan , Li Yang , Zhang Guangze , Zhao Xuyang , Wang Guangxi , Lin Zhiqiang , Yang Meng , Zhao Wei , Lu Dan
Published: November 2024

Supplementary Fig S2
Table S16 from The Spatial Structure of the Tumor Immune Microenvironment Can Explain and Predict Patient Response in High-Grade Serous Carcinoma
Authors: Van Kleunen Lucy B. , Ahmadian Mansooreh , Post Miriam D. , Wolsky Rebecca J. , Rickert Christian , Jordan Kimberly R. , Hu Junxiao , Richer Jennifer K. , Brubaker Lindsay W. , Marjon Nicole , Behbakht Kian , Sikora Matthew J. , Bitler Benjamin G. , Clauset Aaron
Published: November 2024

Table S16. Clustering analysis results.
Table S12 from The Spatial Structure of the Tumor Immune Microenvironment Can Explain and Predict Patient Response in High-Grade Serous Carcinoma
Authors: Van Kleunen Lucy B. , Ahmadian Mansooreh , Post Miriam D. , Wolsky Rebecca J. , Rickert Christian , Jordan Kimberly R. , Hu Junxiao , Richer Jennifer K. , Brubaker Lindsay W. , Marjon Nicole , Behbakht Kian , Sikora Matthew J. , Bitler Benjamin G. , Clauset Aaron
Published: November 2024

Table S12. Random forest predictive performance results. Full results for all random forest models using 15 different feature sets. Mean and standard deviation AUC results across 500 evaluations are reported for both OS and PFS.
Supplementary Fig S13 from CD36+ Proinflammatory Macrophages Interact with ZCCHC12+ Tumor Cells in Papillary Thyroid Cancer Promoting Tumor Progression and Recurrence
Authors: Zhang Xin , Guo Limei , Tian Wenyu , Yang Ying , Yin Yue , Qiu Yaruo , Wang Weixuan , Li Yang , Zhang Guangze , Zhao Xuyang , Wang Guangxi , Lin Zhiqiang , Yang Meng , Zhao Wei , Lu Dan
Published: November 2024

Supplementary Figure S13
Supplementary Fig S12 from CD36+ Proinflammatory Macrophages Interact with ZCCHC12+ Tumor Cells in Papillary Thyroid Cancer Promoting Tumor Progression and Recurrence
Authors: Zhang Xin , Guo Limei , Tian Wenyu , Yang Ying , Yin Yue , Qiu Yaruo , Wang Weixuan , Li Yang , Zhang Guangze , Zhao Xuyang , Wang Guangxi , Lin Zhiqiang , Yang Meng , Zhao Wei , Lu Dan
Published: November 2024

Supplementary Figure S12
Table S10 from The Spatial Structure of the Tumor Immune Microenvironment Can Explain and Predict Patient Response in High-Grade Serous Carcinoma
Authors: Van Kleunen Lucy B. , Ahmadian Mansooreh , Post Miriam D. , Wolsky Rebecca J. , Rickert Christian , Jordan Kimberly R. , Hu Junxiao , Richer Jennifer K. , Brubaker Lindsay W. , Marjon Nicole , Behbakht Kian , Sikora Matthew J. , Bitler Benjamin G. , Clauset Aaron
Published: November 2024

Table S10. Correlation coefficients between other cell type percentages and tumor cell percentages. Full list of Pearson correlation coefficients between tumor cell percentage and cell type percentage, two-sided p-values and false discovery rate adjusted p-values are reported, with significance determined by the latter.
Table S1 from The Spatial Structure of the Tumor Immune Microenvironment Can Explain and Predict Patient Response in High-Grade Serous Carcinoma
Authors: Van Kleunen Lucy B. , Ahmadian Mansooreh , Post Miriam D. , Wolsky Rebecca J. , Rickert Christian , Jordan Kimberly R. , Hu Junxiao , Richer Jennifer K. , Brubaker Lindsay W. , Marjon Nicole , Behbakht Kian , Sikora Matthew J. , Bitler Benjamin G. , Clauset Aaron
Published: November 2024

Table S1. Antibody panel design. List of proteins used in multiplexed imaging.
Figure S8 from The Spatial Structure of the Tumor Immune Microenvironment Can Explain and Predict Patient Response in High-Grade Serous Carcinoma
Authors: Van Kleunen Lucy B. , Ahmadian Mansooreh , Post Miriam D. , Wolsky Rebecca J. , Rickert Christian , Jordan Kimberly R. , Hu Junxiao , Richer Jennifer K. , Brubaker Lindsay W. , Marjon Nicole , Behbakht Kian , Sikora Matthew J. , Bitler Benjamin G. , Clauset Aaron
Published: November 2024

Fig S8. Random forest feature importance results with features derived from missing cell types all treated as NA. Main text Figure 7 repeated with missing cell types handled differently in data preprocessing.
Figure S6 from The Spatial Structure of the Tumor Immune Microenvironment Can Explain and Predict Patient Response in High-Grade Serous Carcinoma
Authors: Van Kleunen Lucy B. , Ahmadian Mansooreh , Post Miriam D. , Wolsky Rebecca J. , Rickert Christian , Jordan Kimberly R. , Hu Junxiao , Richer Jennifer K. , Brubaker Lindsay W. , Marjon Nicole , Behbakht Kian , Sikora Matthew J. , Bitler Benjamin G. , Clauset Aaron
Published: November 2024

Fig S6. Univariate Cox regression results with features derived from missing cell types all treated as NA. Covariates found to be significant in Univariate Cox regressions for (A) OS and (B) PFS outcomes. Results are shown for main text Figure 5 if missing cell types in samples are handled differently in the data pre-processing. Hazard ratio estimates are colored by feature category.
Supplementary Data 1 from CD36+ Proinflammatory Macrophages Interact with ZCCHC12+ Tumor Cells in Papillary Thyroid Cancer Promoting Tumor Progression and Recurrence
Authors: Zhang Xin , Guo Limei , Tian Wenyu , Yang Ying , Yin Yue , Qiu Yaruo , Wang Weixuan , Li Yang , Zhang Guangze , Zhao Xuyang , Wang Guangxi , Lin Zhiqiang , Yang Meng , Zhao Wei , Lu Dan
Published: November 2024

Cell line authentication of BCPAP