bluuebunny/crossref_metadata_2025 huggingface dataset:
Data from Determinants of survival in HER2+ metastatic esophagogastric cancer
Authors: Maron Steven B. , Chatila Walid , Walch Henry , Chou Joanne F. , Ceglia Nicholas , Ptashkin Ryan , Do Richard Kinh Gian. , Paroder Viktoriya , Pandit-Taskar Neeta , Lewis Jason S. , Biachi De Castria TIago , Sabwa Shalom , Socolow Fiona , Feder Lara , Thomas Jasmine , Schulze Isabell , Kim Kwanghee , Elzein Arijh , Bojilova Viktoria , Zatzman Matthew , Bhanot Umesh , Nagy Rebecca J. , Lee Jeeyun , Simmons Marc , Segal Michal , Ku Geoffrey Y. , Ilson David H. , Capanu Marinela , Hechtman Jaclyn F. , Merghoub Taha , Shah Sohrab , Schultz Nikolaus , Solit David B. , Janjigian Yelena Y.
Published: September 2024

Abstract
Purpose: We report updated clinical outcomes from a phase II study of pembrolizumab, trastuzumab, and chemotherapy (PTC) in metastatic esophagogastric (EG) cancer in conjunction with outcomes from an independent MSK cohort. Experimental Design: The significance of pre-treatment 89Zr-trastuzumab PET, plasma circulating tumor DNA (ctDNA) dynamics, and tumor HER2 expression and whole exome sequencing was evaluated to identify prognostic biomarkers and mechanisms of resistance in patients treated on-protocol with PTC. Additional prognostic features were evaluated using a multivariable Cox regression model of trastuzumab-treated MSK patients (n=226). Single cell RNA sequencing data from MSK and Samsung were evaluated for mechanisms of therapy resistance. Results: 89Zr-trastuzumab PET, single cell RNA-seq (scRNAseq), and serial ctDNA with CT imaging identified how pre-treatment intrapatient genomic heterogeneity contributes to inferior progression-free survival (PFS). We demonstrated that presence of intensely-avid lesions by 89Zr-trastuzumab PET, decline in tumor-matched ctDNA by 3 weeks, and clearance of tumor-matched ctDNA by 9 weeks were minimally invasive biomarkers of durable PFS. Paired pre- and on-treatment scRNAseq identified rapid clearance of HER2-expressing tumor clones with expansion of clones expressing a transcriptional resistance program, which was associated with MT1H, MT1E, MT2A, and MSMB expression. Amongst trastuzumab-treated patients at MSK, ERBB2 amplification was associated with improved PFS, while alterations in MYC and CDKN2A/B were associated with inferior PFS. Conclusions: These findings highlight the clinical relevance of identifying baseline intrapatient heterogeneity and serial ctDNA monitoring of HER2-positive EG cancer patients to identify early evidence of treatment resistance, which could guide proactive therapy escalation or de-escalation.
Data from Transcriptomic Signatures of MSI-high Metastatic Colorectal Cancer Predict Efficacy of Immune Checkpoint Inhibitors
Authors: Gallois Claire , Landi Matteo , Taieb Julien , Sroussi Marine , Saberzadeh-Ardestani Bahar , Cazelles Antoine , Lonardi Sara , Bergamo Francesca , Intini Rossana , Maddalena Giulia , Pietrantonio Filippo , Corti Francesca , Ambrosini Margherita , Martinetti Antonia , Germani Marco Maria. , Boccaccio Chiara , Vetere Guglielmo , Mouillet-Richard Sophie , de Reynies Aurelien , Sinicrope Frank A. , Cremolini Chiara , Laurent-Puig Pierre
Published: September 2024

Abstract
Purpose: Microsatellite instability (MSI) is currently the only predictive biomarker of efficacy of immune checkpoint inhibitors (ICI) in metastatic colorectal cancers (mCRC). However, 10-40% of patients with MSI mCRC will experience a primary resistance to ICI. Experimental design: In 2 cohorts of patients with MSI mCRC treated with ICI (exploratory: N=103, validation: N=35), 3’RNAseq was performed from primary tumors. Previously described single-cell transcriptomic signatures of tumor microenvironment (TME) were analysed. Results: In the exploratory cohort, the unsupervised clustering allowed the identification of three clusters of tumors with distinct transcriptional profiles: cluster A (“stromalHIGH-proliferationLOW”), cluster B (“stromalHIGH-proliferationMED”), and cluster C (“stromalLOW-proliferationHIGH”), with an enrichment of patients progressing at first disease assessment under ICI in the cluster A (30% vs 12% in cluster B and 8.1% in cluster C, p=0.074). Progression-free survival (PFS) was also significantly shorter in patients belonging to cluster A, compared to clusters B or C (p<0.001) with 2-year PFS rates of 33.5%, 80.5% and 78.3%, respectively. In multivariate analysis, PFS was still significantly longer in patients belonging to cluster B (HR: 0.19 95%CI 0.08-0.45, p<0.001) and cluster C (HR: 0.25 95%CI 0.10-0.59, p=0.02), compared to patients belonging to cluster A. The association of this clustering with PFS under ICI was confirmed in the validation cohort. PFS related to non-ICI-based regimens was not significantly different according to cluster. Conclusion: This unsupervised transcriptomic classification identified three groups of MSI mCRCs with different compositions of TME cells and proliferative capacities of TME/tumor cells. The “stromalHIGH-proliferationLOW” cluster is associated with a poorer prognosis with ICI treatment.
Data from Poor outcome in postpartum breast cancer patients is associated with distinct molecular and immunological features
Authors: Lefrère Hanne , Moore Kat , Floris Giuseppe , Sanders Joyce , Seignette Iris M. , Bismeijer Tycho , Peters Dennis , Broeks Annegien , Hooijberg Erik , Van Calsteren Kristel , Neven Patrick , Warner Ellen , Peccatori Fedro Alessandro. , Loibl Sibylle , Maggen Charlotte , Han Sileny N. , Jerzak Katarzyna J. , Annibali Daniela , Lambrechts Diether , de Visser Karin E. , Wessels Lodewyk , Lenaerts Liesbeth , Amant Frédéric
Published: September 2024

Abstract
Purpose: Postpartum breast cancer patients diagnosed after cessation of breastfeeding (post-weaning, PP-BCPW), have a particularly poor prognosis compared to patients diagnosed during lactation (PP-BCDL), or to pregnant (Pr-BC) and nulliparous (NP-BC) patients, irrespective of standard prognostic characteristics. Animal studies point to a role of the involution process in stimulation of tumor growth in the mammary gland. However, in women, the molecular mechanisms that underlie this poor prognosis of PP-BCPW patients remain vastly underexplored, due to of lack of adequate patient numbers and outcome data. Experimental Design: We explored whether distinct prognostic features, common to all breast cancer molecular subtypes, exist in postpartum tumor tissue. Using detailed breastfeeding data, we delineated the post-weaning period in PP-BC as a surrogate for mammary gland involution and performed whole transcriptome sequencing, immunohistochemical and (multiplex) immunofluorescent analyses on tumor tissue of PP-BCPW, PP-BCDL, Pr-BC and NP-BC patients. Results: We found that PP-BCPW patients having a low expression level of an immunoglobulin gene signature, but high infiltration of plasma B-cells, have an increased risk for metastasis and death. Although PP-BCPW tumor tissue was also characterized by an increase in CD8+ cytotoxic T-cells and reduced distance among these cell types, these parameters were not associated with differential clinical outcomes among groups. Conclusion: These data point to the importance of plasma B-cells in the post-weaning mammary tumor microenvironment regarding the poor prognosis of PP-BCPW patients. Future prospective and in-depth research needs to further explore the role of B-cell immunobiology in this specific group of young breast cancer patients.
Data from A phase 1/2a trial of yttrium-90 radioembolization in combination with durvalumab for locally advanced unresectable hepatocellular carcinoma
Authors: Lee Yun Bin , Nam Joon Yeul , Cho Eun Ju , Lee Jeong-Hoon , Yu Su Jong , Kim Hyo-Cheol , Paeng Jin Chul , Yoon Jung-Hwan , Kim Yoon Jun
Published: September 2024

Abstract
Purpose: Synergistic effect of radiotherapy and immunotherapy for the treatment of hepatocellular carcinoma (HCC) has been reported. This phase 1/2a pilot trial evaluated preliminary efficacy and safety of combination of radioembolization with yttrium-90 microspheres (Y90-radioembolization) and durvalumab in patients with locally advanced unresectable HCC. Patients and Methods: Patients with Child-Pugh score ≤7 and locally advanced HCC, defined as Barcelona Clinic Liver Cancer (BCLC) stage B HCC or BCLC-C disease without extrahepatic metastases, received Y90-radioembolization followed by intravenous durvalumab 1500 mg 7–14 days after Y90-radioembolization and every 4 weeks thereafter. Primary endpoint was time to progression (TTP) assessed by modified RECIST (mRECIST). Secondary endpoints included overall survival (OS), progression-free survival (PFS), objective response rate (ORR) determined by mRECIST, and safety. Results: All 24 patients enrolled received Y90-radioembolization and 23 received at least one dose of durvalumab. Median follow-up duration was 19.0 months (range, 2.2–24.2). Median TTP was 15.2 months (95% confidence interval [CI], 6.1–not estimated). Median OS was not reached and 18-month OS rate was 58.3% (95% CI, 36.4–75.0). Median PFS was 6.9 months (95% CI, 5.4–15.2). Seven (29.2%) patients had a complete response and 13 (54.2%) had a partial response; ORR was 83.3% (95% CI, 62.6–95.3). Eleven (47.8%) patients experienced any-grade treatment-related adverse events. Two (8.7%) patients had grade 3 treatment-related adverse events (neutropenia and fever). None experienced any treatment-related serious adverse events. Conclusions: In patients with locally advanced unresectable HCC, the combination of Y90-radioembolization and durvalumab demonstrated promising efficacy and safety, warranting further evaluation in large-scale controlled trials.
Data from Endoglin, a novel biomarker and therapeutical target to prevent malignant peripheral nerve sheath tumor growth and metastasis
Authors: González-Muñoz Teresa , Di Giannatale Angela , Garcia-Silva Susana , Santos Vanesa , Sanchez-Redondo Sara , Savini Claudia , Graña-Castro Osvaldo , Blanco-Aparicio Carmen , Fischer Suzanne , De Wever Olivier , Creus-Bachiller Edgar , Ortega-Bertran Sara , Pisapia David J. , Rodríguez-Peralto José L. , Fernández-Rodríguez Juana , Romagosa Cleofe , Alaggio Rita , Benassi Maria Serena , Pazzaglia Laura , Scotlandi Katia , Ratner Nancy , Yohay Kaleb , Theuer Charles P. , Peinado Héctor
Published: September 2024

Abstract
Purpose: Malignant peripheral nerve sheath tumors (MPNSTs) are highly aggressive soft-tissue sarcomas that lack effective treatments, underscoring the urgent need to uncover novel mediators of MPNST pathogenesis that may serve as potential therapeutic targets. Tumor angiogenesis is considered a critical event in MPNST transformation and progression. Here, we have investigated whether endoglin (ENG), a TGF-β coreceptor with a crucial role in angiogenesis, could be a novel therapeutic target in MPNSTs. Experimental Design: ENG expression was evaluated in human peripheral nerve sheath tumor tissues and plasma samples. Effects of tumor cell-specific ENG expression on gene expression, signaling pathway activation and in vivo MPNST growth and metastasis were investigated. The efficacy of ENG targeting in monotherapy or in combination with MEK inhibition was analyzed in xenograft models. Results: ENG expression was found to be upregulated in both human MPNST tumor tissues and plasma circulating small extracellular vesicles. We demonstrated that ENG modulates Smad1/5 and MAPK/ERK pathway activation and pro-angiogenic and pro-metastatic gene expression in MPNST cells and plays an active role in tumor growth and metastasis in vivo. Targeting with ENG-neutralizing antibodies (TRC105/M1043) decreased MPNST growth and metastasis in xenograft models by reducing tumor cell proliferation and angiogenesis. Moreover, combination of anti-ENG therapy with MEK inhibition effectively reduced tumor cell growth and angiogenesis. Conclusions: Our data unveil a tumor-promoting function of ENG in MPNSTs and support the use of this protein as a novel biomarker and a promising therapeutic target for this disease.
Data from Evaluation of somatic mutations in urine samples as a non-invasive method for the detection and molecular classification of endometrial cancer
Authors: Costas Laura , Onieva Irene , Pelegrina Beatriz , Marin Fátima , Carmona Alvaro , López-Querol Marta , Frias-Gomez Jon , Peremiquel-Trillas Paula , Martínez José Manuel , Dorca Eduard , Brunet Joan , Pineda Marta , Ponce Jordi , Matías-Guiu Xavier , de Sanjosé Silvia , Bosch Francesc Xavier , Alemany Laia , Paytubi Sonia
Published: September 2024

Abstract
Purpose: Current diagnostic methods for endometrial cancer lack specificity, leading to many women undergoing invasive procedures. The aim of this study was to evaluate somatic mutations in urine to accurately discriminate endometrial cancer patients from controls. Experimental Design: Overall, 72 samples were analyzed using next-generation sequencing with molecular identifiers targeting 47 genes. We evaluated urine supernatant samples from women with endometrial cancer (n=19) and age-matched controls (n=20). Cell pellets from urine and plasma samples from seven cases were sequenced; further, we also evaluated paired tumor samples from all cases. Finally, immunohistochemical markers for molecular profiling were evaluated in all tumor samples. Results: Overall, we were able to identify mutations in DNA from urine supernatant samples in 100% of endometrial cancers. In contrast, only one control (5%) showed variants at a variant allele frequency (VAF)≥2% in the urine supernatant samples. The molecular classification obtained by using tumor samples and urine samples showed good agreement. Analyses in paired samples revealed a higher number of mutations and VAFs in urine supernatants than in urine cell pellets and blood samples. Conclusions: Evaluation of somatic mutations using urine samples may offer a user-friendly and reliable tool for endometrial cancer detection and molecular classification. The diagnostic performance for endometrial cancer detection was very high, and cases could be molecularly classified using these noninvasive and self-collected samples. Additional multi-center evaluations using larger sample sizes are needed to validate the results and understand the potential of urine samples for the early detection and prognosis of endometrial cancer.
Data from Novel Genomic Risk Stratification Model for Primary Gastrointestinal Stromal Tumors (GIST) in the Imatinib and Adjuvant Therapy Era
Authors: Dermawan Josephine K. , Kelly Ciara , Gao Zhidong , Smith Shaleigh , Jadeja Bhumika , Singer Samuel , Tap William D. , Chi Ping , Antonescu Cristina R.
Published: September 2024

Abstract
Purpose: Traditional risk stratification schemes in gastrointestinal stromal tumors (GIST) had been defined in the pre-imatinib era and rely solely on clinicopathologic metrics. We hypothesize that genomic-based risk stratification is prognostically relevant in the current era of tyrosine kinase inhibitor (TKI) therapeutics. Experimental Design: Comprehensive mutational and copy number profiling using MSK-IMPACT was performed. We integrated clinicopathologic and genomic parameters and utilized an elastic-net penalized Cox proportional hazards machine learning model for outcome risk stratification. Results: A 3-tier genomic risk stratification model for recurrence-free survival (RFS) in 152 primary localized gastric and 80 small bowel GISTs was proposed. Gastric GISTs were classified as high risk if chr1p deletion or SDHB loss was present, and intermediate risk if chr14q deletion was present or KIT exon 11 mutation was absent. Small bowel GISTs were classified as high risk if MAX/MGA/MYC, CDKN2A or RB1 alterations was present, and intermediate risk if chr1p deletion or chr5q amplification was present. Compared to conventional risk stratification, genomic risk stratification both upgrades and downgrades, suggesting that conventional risk stratification may underestimate or overtreat some high-risk and low-risk patients, respectively. Longitudinal sequencing detected most KIT-independent genomic alterations at baseline. Subanalysis in 26 SDH-deficient GISTs revealed that presence of TP53 mutations or chr1q amplifications portends worse RFS and disease-free survival. Conclusions: We developed a novel, next-generation genomic risk stratification model for primary gastric and small bowel GISTs, complementing traditional clinicopathologic models. Future independent validation of our model in external cohorts is essential.
Data from Memory-like differentiation, tumor targeting monoclonal antibodies, and chimeric antigen receptors enhance natural killer cell responses to head and neck cancer
Authors: Jacobs Miriam T. , Wong Pamela , Zhou Alice Y. , Becker-Hapak Michelle , Marin Nancy D. , Marsala Lynne , Foster Mark , Foltz Jennifer A. , Cubitt Celia C. , Tran Jennifer , Russler-Germain David A. , Neal Carly , Kersting-Schadek Samantha , Chang Lily , Schappe Timothy , Pence Patrick , McClain Ethan , Zevallos Jose P. , Rich Jason T. , Paniello Randal C. , Jackson Ryan S. , Pipkorn Patrik , Adkins Douglas R. , DeSelm Carl J. , Berrien-Elliott Melissa M. , Puram Sidharth V. , Fehniger Todd A.
Published: September 2024

Abstract
Purpose: Head and neck squamous cell carcinoma (HNSCC) is an aggressive tumor with low response rates to frontline PD-1 blockade. Natural killer (NK) cells are a promising cellular therapy for T cell therapy–refractory cancers, but are frequently dysfunctional in patients with HNSCC. Strategies are needed to enhance NK cell responses against HNSCC. We hypothesized that ML NK cell differentiation, tumor-targeting with cetuximab, and engineering with an anti-EphA2 chimeric antigen receptor (CAR) enhance NK cell responses against HNSCC. Experimental Design: We generated ML NK and conventional (c)NK cells from healthy donors then evaluated their ability to produce IFN-γ, TNF, degranulate, and kill HNSCC cell lines and primary HNSCC cells, alone or in combination with cetuximab, in vitro and in vivo using xenograft models. ML and cNK cells were engineered to express anti-EphA2 CAR-CD8A-41BB-CD3z, and functional responses were assessed in vitro against HNSCC cell lines and primary HNSCC tumor cells. Results: Human ML NK cells displayed enhanced IFN-γ and TNF production and both short- and long-term killing of HNSCC cell lines and primary targets, compared to cNK cells. These enhanced responses were further improved by cetuximab. Compared to controls, ML NK cells expressing anti-EphA2 CAR had increased IFN-γ and cytotoxicity in response to EphA2+ cell lines and primary HNSCC targets. Conclusions: These pre-clinical findings demonstrate that ML differentiation alone or coupled with either cetuximab-directed targeting or EphA2 CAR engineering were effective against HNSCCs and provide the rationale for investigating these combination approaches in early phase clinical trials for HNSCC patients.
Data from Efficacy and safety of stereotactic body radiotherapy combined with Camrelizumab and Apatinib in hepatocellular carcinoma patients with portal vein tumor thrombus
Authors: Hu Yue , Zhou Min , Tang Jing , Li Shuang , Liu Hongli , Hu Jianli , Ma Hong , Liu Junli , Qin Tingting , Yu Xiongjie , Chen Yongshun , Peng Jin , Zou Yanmei , Zhang Tao , Xue Jun
Published: September 2024

Abstract
Purpose: This study aimed to evaluate the efficacy and safety of camrelizumab plus apatinib with or without stereotactic body radiotherapy (SBRT) as first-line therapy for hepatocellular carcinoma (HCC) patients with portal vein tumor thrombus (PVTT). Patients and Methods: This is a multicenter, open-label, non-comparative, randomized trial that recruited HCC patients with type II/III/IV PVTT, who had not previously received systemic therapy. Patients were randomly assigned (2:1) to receive camrelizumab (200 mg, Q3W) and apatinib (250 mg, QD) with or without SBRT (95% PTV, 36 - 40 Gy/6 - 8 Gy). The primary endpoint was overall survival (OS), and the secondary endpoints were progression-free survival (PFS), objective response rate (ORR), disease control rate (DCR), duration of response (DOR), time to progression (TTP) and safety. Results: Sixty patients were enrolled and randomly assigned to two prospective cohorts. Median OS were 12.7 months (95% CI, 10.2-NA) and 8.6 months (95% CI, 5.6-NA), and median PFS were 4.6 months (95% CI, 3.3-7.0) and 2.5 months (95% CI, 2.0-7.6) for the SBRT and non-SBRT cohorts, respectively. The ORR and DCR were 47.5% and 72.5% in the SBRT cohort, and 20.0% and 40.0% in the non-SBRT cohort. The most common treatment-related adverse events of any grade were hypertension (55.0%), hand-foot syndrome (51.7%), and leukopenia (50.0%). Grade ≥ 3 was reported in 13 (21.7%) patients. Conclusion: First-line treatment with camrelizumab-apatinib combined with or without SBRT showed clinical benefits in HCC patients with PVTT, with an acceptable safety profile. Thus, these combination regimens may be potential options for such patients.
Supplementary Figure 23 from Arginase 1/2 inhibitor OATD-02: from discovery to first-in-man setup in cancer immunotherapy
Authors: Borek Bartlomiej , Nowicka Julita , Gzik Anna , Dziegielewski Marek , Jedrzejczak Karol , Brzezinska Joanna , Grzybowski Marcin , Stanczak Paulina , Pomper Paulina , Zagozdzon Agnieszka , Rejczak Tomasz , Matyszewski Krzysztof , Golebiowski Adam , Olczak Jacek , Lisiecki Kamil , Tyszkiewicz Magdalena , Kania Magdalena , Piasecka Sylwia , Cabaj Anna , Dera Paulina , Mulewski Krzysztof , Chrzanowski Jacek , Kusmirek Damian , Sobolewska Elzbieta , Magdycz Marta , Mucha Lukasz , Masnyk Marek , Golab Jakub , Nowotny Marcin , Nowak Elzbieta , Napiorkowska-Gromadzka Agnieszka , Pikul Stanislaw , Jazwiec Radoslaw , Dzwonek Karolina , Dobrzanski Pawel , Meyring Michael , Skowronek Krzysztof , Iwanowski Piotr , Zaslona Zbigniew , Blaszczyk Roman
Published: September 2024

Simulated human plasma concentration time profiles of OATD-02
Supplementary Figure S4 from Tyrosine Kinase Inhibitors Diminish Renal Neoplasms in a Tuberous Sclerosis Model via induction of Apoptosis
Authors: Unachukwu Uchenna , Sonett Jarrod , Woode Denzel , Shiomi Takayuki , Chada Kiran , D'Armiento Jeanine M.
Published: September 2024

Ingenuity Pathway Analysis of Drug-Induced Pulmonary LAM Tumor Cells
Supplementary Fig.S3 from Preclinical Evaluation of 9MW2821, a Site-Specific Monomethyl Auristatin E-based Antibody-Drug Conjugate for treatment of Nectin-4-expressing Cancers
Authors: Zhou Wei , Fang Peng , Yu Dongan , Ren Hongyuan , You Meng , Yin Long , Mei Fei , Zhu Huikai , Wang Zhenzhen , Xu Hui , Cao Yuxia , Sun Xiaowei , Xu Xiaohong , Bi Jianjun , Wang Jin , Ma Lanping , Wang Xin , Chen Lin , Zhang Yongliang , Cen Xiaowei , Zhu Xi , Lou Liguang , Liu Datao , Tan Xiaoding , Yang Jinliang , Meng Tao , Shen Jingkang
Published: September 2024

Comparison of the structure of 9MW2821 and enfortumab vedotin.
Supplementary Fig.S12 from Preclinical Evaluation of 9MW2821, a Site-Specific Monomethyl Auristatin E-based Antibody-Drug Conjugate for treatment of Nectin-4-expressing Cancers
Authors: Zhou Wei , Fang Peng , Yu Dongan , Ren Hongyuan , You Meng , Yin Long , Mei Fei , Zhu Huikai , Wang Zhenzhen , Xu Hui , Cao Yuxia , Sun Xiaowei , Xu Xiaohong , Bi Jianjun , Wang Jin , Ma Lanping , Wang Xin , Chen Lin , Zhang Yongliang , Cen Xiaowei , Zhu Xi , Lou Liguang , Liu Datao , Tan Xiaoding , Yang Jinliang , Meng Tao , Shen Jingkang
Published: September 2024

Mouse body weight from BL3578, CV13641, LU3073, BR9457, BR9479, BR1282 and BR1458 patient-derived xenograft studies.
Figure S8 from APR-246 enhances colorectal cancer sensitivity to radiotherapy
Authors: Xie Xuqin , Fan Chuanwen , Luo Bin , Zhang Jing , Jensen Lasse D. , Burman Jonas , Jonsson Carolin , Ljusberg Anna , Larsson Peter , Zhao Zengren , Sun Xiao-Feng
Published: September 2024

Supplementary figure 8
Supplementary Figure S4 from Schlafen 11 (SLFN11) kills cancer cells undergoing unscheduled re-replication
Authors: Murai Junko , Ceribelli Michele , Fu Haiqing , Redon Christophe E. , Jo Ukhyun , Murai Yasuhisa , Aladjem Mirit I. , Thomas Craig J. , Pommier Yves
Published: September 2024

Figure S4
Supplementary Figure 4 from Vincristine Enhances the Efficacy of MEK Inhibitors in Preclinical Models of KRAS-mutant Colorectal Cancer
Authors: Ghosh Susmita , Fan Fan , Powell Reid T. , Roszik Jason , Park Yongsung , Stephan Clifford , Sebastian Manu , Tan Lin , Sorokin Alexey V. , Lorenzi Philip L. , Kopetz Scott , Ellis Lee M. , Bhattacharya Rajat
Published: September 2024

Supplementary Figure 4 shows that the combination of trametinib and vincristine is well tolerated in mice.
Table S1 from T cell-intrinsic immunomodulatory effects of TAK-981 (subasumstat), a SUMO-activating enzyme inhibitor, in chronic lymphocytic leukemia
Authors: Lam Vi , Roleder Carly , Liu Tingting , Bruss Nur , Best Scott , Wang Xiaoguang , Phillips Tycel , Shouse Geoffrey , Berger Allison J. , Alinari Lapo , Wang Lili , Siddiqi Tanya , Pennock Nathan D. , Danilov Alexey V.
Published: September 2024

Table S1 shows fluorochrome-conjugated anti-human antibodies used for flow cytometry or FACS experiments
Supplementary Fig. S3 from Preclinical development of brain permeable ERβ agonist for the treatment of glioblastoma
Authors: Pratap Uday P. , Tidwell Michael , Balinda Henriette U. , Clanton Nicholas A. , Yang Xue , Viswanadhapalli Suryavathi , Sareddy Gangadhara R. , Liang Dong , Xie Huan , Chen Yidong , Lai Zhao , Tekmal Rajeshwar R. , McHardy Stanton F. , Brenner Andrew J. , Vadlamudi Ratna K.
Published: September 2024

Supplementary Fig.S3 shows efficacy of CIDD-0149897 combination therapy.
Table S2 from Co-targeting Phosphoinositide 3-Kinase and Focal Adhesion Kinase Pathways Inhibits Proliferation of NF2 Schwannoma Cells
Authors: Hardin Haley M. , Dinh Christine T. , Huegel Julianne , Petrilli Alejandra M. , Bracho Olena , Allaf Abdulrahman , Karajannis Matthias A. , Griswold Anthony J. , Ivan Michael E. , Morcos Jacques , Gultekin Sakir H. , Telischi Fred F. , Liu Xue Zhong , Fernandez-Valle Cristina
Published: September 2024

Supplemental Table 2. Selectivity Score of Top Three Drug Combinations for Merlin-deficient Over Isogenic Normal Human Schwann Cells.
Supplementary Table 2 from Conditional dependency of LP-184 on prostaglandin reductase 1 is synthetic lethal in pancreatic cancers with DNA damage repair deficiencies
Authors: Restifo Diana , McDermott Joseph R. , Cvetkovic Dusica , Dos Santos Troy , Ogier Charline , Surumbayeva Aizhan , Handorf Elizabeth A. , Schimke Caleb , Ma Charlie , Cai Kathy Q. , Olszanski Anthony J. , Kathad Umesh , Bhatia Kishor , Sharma Panna , Kulkarni Aditya , Astsaturov Igor
Published: September 2024

Characteristics of PDX models
Supplementary Figure S1 from Interferon Gamma Induces Higher Neutrophil Extracellular Traps Leading to Tumor-Killing Activity in Microsatellite Stable Colorectal Cancer
Authors: Teng Hao-Wei , Wang Tean-Ya , Lin Chun-Chi , Tong Zhen-Jie , Cheng Hsiao-Wei , Wang Hsiang-Tsui
Published: September 2024

Supplementary Figure 1 shows the surface marker CD66b expression and neutrophil function in isolated neutrophils Surface marker CD66b expression and neutrophil function in isolated neutrophils of CRC patients and healthy donors.
Data from Tumor and stromal cell targeting with Nintedanib and Alpelisib overcomes intrinsic bladder cancer resistance
Authors: Marqués Miriam , Corral Sonia , Sánchez-Díaz María , del Pozo Natalia , Martínez de Villarreal Jaime , Schweifer Norbert , Zagorac Ivana , Hilberg Frank , Real Francisco X.
Published: September 2024

Abstract
Bladder cancer is a highly prevalent tumor, requiring the urgent development of novel therapies, especially for locally advanced and metastatic disease. Nintedanib is a potent anti-fibrotic angio-kinase inhibitor, which has shown clinical efficacy in combination with chemotherapy in locally advanced muscle invasive BC patients. Nintedanib inhibits Fibroblast Growth Factor receptors (FGFRs), validated targets in patients with BC harboring FGFR3/2 genetic alterations. Here, we aimed at studying its mechanisms of action to understand therapy resistance, identify markers predictive of response, and improve the design of future clinical trials. We have used a panel of genetically well-characterized human BC cells in order to identify the molecular and transcriptomic changes induced upon treatment with Nintedanib, in vitro and in vivo, at the tumor and stroma cell levels. We showed that BC cells display an intrinsic resistance to Nintedanib treatment in vitro, independently of their FGFR3 status. However, Nintedanib has higher antitumor activity on mouse xenografts. We have identified PI3K activation as a resistance mechanism against Nintedanib in BC and evidenced that the combination of Nintedanib with the PI3K inhibitor Alpelisib has synergistic antitumor activity. Treatment with this combination is associated with cell cycle inhibition at the tumoral and stromal levels and potent non-tumor cell autonomous effects on -smooth muscle (SMA)-positive tumor infiltrating cells and tumor vasculature. The combination of Nintedanib with PI3K inhibitors not only reversed BC resistance to Nintedanib but also enhanced its anti-angiogenic effects.
Data from Novel arginase inhibitor, AZD0011, demonstrates immune cell stimulation and anti-tumor efficacy with diverse combination partners
Authors: Doshi Aatman S. , Cantin Susan , Hernandez Marylens , Srinivasan Srimathi , Tentarelli Sharon , Griffin Matthew , Wang Yanjun , Pop-Damkov Petar , Prickett Laura B. , Kankkonen Cecilia , Shen Minhui , San Martin Maryann , Wu Song , Castaldi M Paola , Ghadially Hormas , Varnes Jeffrey , Gales Sonya , Henry David , Hoover Clare , Mele Deanna A. , Simpson Iain , Gangl Eric T. , Mlynarski Scott N. , Finlay M. Raymond V. , Drew Lisa , Fawell Stephen E. , Shao Wenlin , Schuller Alwin G.
Published: September 2024

Abstract
Anti-tumor immunity can be hampered by immunosuppressive mechanisms in the tumor microenvironment including recruitment of arginase (ARG) expressing myeloid cells which deplete L-arginine essential for optimal T cell and natural killer cell function. Hence, ARG inhibition can reverse immunosuppression enhancing anti-tumor immunity. We describe AZD0011, a novel peptidic boronic acid prodrug to deliver an orally available, highly potent, ARG inhibitor payload (AZD0011-PL). We demonstrate that AZD0011-PL is unable to permeate cells, suggesting this compound will only inhibit extracellular ARG. In vivo, AZD0011 monotherapy leads to arginine increases, immune cell activation, and tumor growth inhibition (TGI) in various syngeneic models. Anti-tumor responses increase when AZD0011 is combined with anti-PD-L1 treatment, correlating with increases in multiple tumor immune cell populations. We demonstrate a novel triple combination of AZD0011, anti-PD-L1 and anti-NKG2A, and combination benefits with type I interferon (IFN) inducers including polyI:C and radiation. Our pre-clinical data demonstrates AZD0011’s ability to reverse tumor immunosuppression and enhance immune stimulation and anti-tumor responses with diverse combination partners providing potential strategies to increase immuno-oncology therapies clinically.
Data from Pharmacokinetic/Pharmacodynamic Analysis of Savolitinib Plus Osimertinib in an EGFR-Mutation Positive, MET-Amplified Non-Small Cell Lung Cancer Model
Authors: Jones Rhys D.O. , Petersson Klas , Tabatabai Areya , Bao Larry , Tomkinson Helen , Schuller Alwin G.
Published: September 2024

Abstract
Osimertinib is a third-generation, irreversible, oral epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI), recommended as first-line treatment for patients with locally advanced/metastatic EGFR-mutation positive (EGFRm) non-small cell lung cancer (NSCLC). However, MET-amplification/overexpression is a common acquired osimertinib resistance mechanism. Savolitinib is an oral, potent, and highly selective MET-TKI; preliminary data suggest that combining osimertinib with savolitinib may overcome MET-driven resistance.
A patient-derived xenograft (PDX) mouse model with EGFRm, MET-amplified NSCLC was tested with a fixed osimertinib dose (10 mg/kg, for exposures equivalent to [≈] 80 mg), combined with doses of savolitinib (0–15 mg/kg, ≈0–600 mg once-daily), both with 1-aminobenzotriazole (to better match clinical half-life). After 20 days of oral dosing, samples were taken at various timepoints to follow the time-course of drug exposure in addition to phosphorylated MET and EGFR (pMET; pEGFR) change. Population pharmacokinetics, savolitinib concentration versus percentage inhibition from baseline in pMET, and the relationship between pMET and tumor growth inhibition (TGI) were also modeled.
As single agents, savolitinib (15 mg/kg) showed significant anti-tumor activity, reaching ~84% TGI and osimertinib (10 mg/kg) showed no significant anti-tumor activity (34% TGI, P>0.05 vs. vehicle). Upon combination, at a fixed dose of osimertinib, significant savolitinib dose-related anti-tumor activity was shown, ranging from 81% TGI (0.3 mg/kg) to 84% tumor regression (15 mg/kg). Pharmacokinetic-pharmacodynamic modeling showed that the maximum inhibition of both pEGFR and pMET increased with increasing savolitinib doses.
Savolitinib demonstrated exposure-related combination anti-tumor activity when combined with osimertinib in the EGFRm MET-amplified NSCLC PDX model.
Data from AMT-562, a novel HER3-targeting antibody drug conjugate, demonstrates a potential to broaden therapeutic opportunities for HER3-expressing tumors
Authors: Weng Weining , Meng Tao , Pu Junyi , Ma Linjie , Shen Yi , Wang Zhaohui , Pan Rong , Wang Mingqiao , Chen Caiwei , Wang Lijun , Zhang Jianjian , Zhou Biao , Shao Siyuan , Qian Yu , Liu Shu-Hui , Hu Wenhao , Meng Xun
Published: September 2024

Abstract
HER3 is a unique member of the epidermal growth factor receptor family of tyrosine kinases, which is broadly expressed in several cancers, including breast, lung, pancreatic, colorectal, gastric, prostate, and bladder cancers and is often associated with poor patient outcomes and therapeutic resistance. U3-1402/Patritumab-GGFG-DXd is the first successful HER3-targeting ADC molecule with clinical efficacy in non-small cell lung cancer (NSCLC). However, over 60% of patients are non-responsive to U3-1402 due to low target expression levels and responses tend to be in patients with higher target expression levels. U3-1402 is also ineffective in more challenging tumor types such as colorectal cancer. AMT-562 was generated by a novel anti-HER3 antibody Ab562 and a modified self-immolative PABC spacer (T800) to conjugate exatecan. Exatecan showed higher cytotoxic potency than its derivative DXd. Ab562 was selected due to its moderate affinity for minimizing potential toxicity and improving tumor penetration purposes. Both alone or in combination therapies, AMT-562 showed potent and durable antitumor response in low HER3 expression xenograft and heterogeneous patient-derived xenograft/organoid (PDX/PDO) models, including digestive system and lung tumors representing of unmet needs. Combination therapies pairing AMT-562 with therapeutic antibodies, inhibitors of CHEK1, KRAS and TKI showed higher synergistic efficacy than Patritumab-GGFG-DXd. Pharmacokinetics and safety profiles of AMT-562 were favorable and the highest dose lacking severe toxicity was 30 mg/kg in cynomolgus monkeys. AMT-562 has potential to be a superior HER3-targeting ADC with a higher therapeutic window that can overcome resistance to generate higher percentage and more durable responses in U3-1402-insensitive tumors.
Figure S2 from UBE2C-mediated autophagy inhibition via ubiquitination of SIRT1 contributes to endometrial cancer progression
Authors: Zhao Rong , Liu Yan , Wang Ziwei , Zhang Jun , Zhang Wei , Zhou Xing , Tsedendorj Sevjid , Enkhtur Amarsanaa , Feng Dilu , Wang Hongbo
Published: September 2024

Figure S2
Supplementary Fig. 3 from Disruption of the MYC Super-Enhancer Complex by Dual Targeting of FLT3 and LSD1 in Acute Myeloid Leukemia
Authors: Yashar William M. , Curtiss Brittany M. , Coleman Daniel J. , VanCampen Jake , Kong Garth , Macaraeg Jommel , Estabrook Joseph , Demir Emek , Long Nicola , Bottomly Daniel , McWeeney Shannon K. , Tyner Jeffrey W. , Druker Brian J. , Maxson Julia E. , Braun Theodore P.
Published: September 2024

Epigenetic impact of dual FLT3/LSD1 inhibition.
Supplementary Tables and Figures from Triple-negative breast cancer-derived extracellular vesicles promote a hepatic pre-metastatic niche via a cascade of microenvironment remodeling
Authors: Heo Woohang , Lee Woochan , Cheun Jong Ho , Lee Eun-Shin , Li Songbin , Kim Hoe suk , Son Hye-Youn , Kim Ju Hee , Woo Yeon Duk , Chung Doo Hyun , Yun Jihui , Jung Ji Gwang , Lee Han-Byoel , Han Wonshik , Kim Hong-Kyu , Kim Jong-Il , Moon Hyeong-Gon
Published: September 2024

Supplementary Table 1. Information about patients derived xenograft models and derived patient.
Supplementary Table 2. Ontology of differentially expressed genes in metastasis-harboring liver of PDX models.
Supplementary Table 3. Differentially expressed genes in liver and lung of metastasis-harboring PDX models.
Supplementary Table 4. Human ratio in lung and liver of additional PDX models identified by RNA sequencing.
Supplementary Table 5. Gene ontology of co-expressed genes with Cx3cr1 in liver of PDX models identified by RNA sequencing.
Supplementary Table 6. Top ranked genes having significant correlation with Cx3cr1 in liver of PDX models identified by RNA sequencing.
Supplementary Table 7. Demographic and clinical characteristics of all patients.
Supplementary Table 8. Information about used primer sequences for quantitative real-time PCR

Supplementary Figure 1. Liver and lung H&E staining pictures of eight nonmetastatic PDX models a. Microscopic images of non-metastasis harboring PDX mouse model’s liver (left) and lung (right) taken at 400x magnification.
Supplementary Figure 2. Immunohistochemistry about CX3CR1 in liver and lung of breast cancer metastasis patients.
Supplementary Figure 3. Hepatic metastasis after four weeks after orthotopic injection of 4T1 breast cancer cells identified by H&E staining.
Supplementary Figure 4. Identification of pre-metastatic niche in liver tissues of 4T1 bearing mice a. mRNA expression of inflammation associated genes identified by real-time PCR in liver tissues of 4T1 bearing mice.
Supplementary Figure 5. Identification of CX3CR1 positive cell population.
Supplementary Figure 6. FACS analysis with anti-CX3CR1 of Raw264.7 macrophage cell lines.
Supplementary Figure 7. Trans-well migration assay of BMDM with or without CX3CL1.
Supplementary Figure 8. Mmp9 mRNA expression having significant correlation with Cx3cr1 mRNA expression in liver of PDX models.
Supplementary Figure 9. MMP9 expression of macrophages with CX3CL1 treatment.
Supplementary Figure 10. Signaling pathway of CX3CL1 treated macrophages.
Supplementary Figure 11. Splenic injection of 4T1 cells inducing hepatic metastasis within two weeks in most cases.
Supplementary Figure 12. mRNA expression about Cx3cr1 and Mmp9 in liver of vehicle or AZD8797 treated BALB/C mice identified by real-time PCR.
Supplementary Figure 13. Correlation plot of Tnfa and Cx3cr1 mRNA expression in liver and lung of PDX models.
Supplementary Figure 14. EVs isolation of CD63-mRuby-4T1.
Figure S3 from Dynamic intestinal stem cell plasticity and lineage remodeling by a nutritional environment relevant to human risk for tumorigenesis
Authors: Choi Jiahn , Zhang Xusheng , Li Wenge , Houston Michele , Peregrina Karina , Dubin Robert , Ye Kenny , Augenlicht Leonard
Published: September 2024

The western diet suppresses expression of a large number of genes encoding subunits of each of the 5 complexes of mitochondrial electron transport.
Supplementary Figure S6 from Overlaid transcriptome and proteome analyses identify mitotic kinesins as important targets of arylsulfonamide-mediated RBM39 degradation
Authors: Coomar Seemon , Mota Pedro , Penson Alexander , Schwaller Juerg , Abdel-Wahab Omar , Gillingham Dennis
Published: September 2024

Supplementary Figure S6
Figure S6 from A comparative study of neuroendocrine heterogeneity in small cell lung cancer and neuroblastoma
Authors: Cai Ling , DeBerardinis Ralph J. , Xie Yang , Minna John D. , Xiao Guanghua
Published: September 2024

Examples of different and similar compound sensitivity dynamic ranges in SCLC and NBL.
Supplementary Table S6 from Identification of a ΔNp63-Dependent Basal-Like A Subtype-Specific Transcribed Enhancer Program (B-STEP) in Aggressive Pancreatic Ductal Adenocarcinoma
Authors: Wang Xin , Kutschat Ana P. , Aggrey-Fynn Joana , Hamdan Feda H. , Graham Rondell P. , Wixom Alexander Q. , Souto Yara , Ladigan-Badura Swetlana , Yonkus Jennifer A. , Abdelrahman Amro M. , Alva-Ruiz Roberto , Gaedcke Jochen , Strobel Philipp , Kosinsky Robyn Laura , Wegwitz Florian , Hermann Patrick , Truty Mark J. , Siveke Jens T. , Hahn Stephan A. , Hessmann Elisabeth , Johnsen Steven A. , Najafova Zeynab
Published: September 2024

Supplementary Table S6 contains list of qPCR primers used in the study.
Supplementary Table S4 from Identification of a ΔNp63-Dependent Basal-Like A Subtype-Specific Transcribed Enhancer Program (B-STEP) in Aggressive Pancreatic Ductal Adenocarcinoma
Authors: Wang Xin , Kutschat Ana P. , Aggrey-Fynn Joana , Hamdan Feda H. , Graham Rondell P. , Wixom Alexander Q. , Souto Yara , Ladigan-Badura Swetlana , Yonkus Jennifer A. , Abdelrahman Amro M. , Alva-Ruiz Roberto , Gaedcke Jochen , Strobel Philipp , Kosinsky Robyn Laura , Wegwitz Florian , Hermann Patrick , Truty Mark J. , Siveke Jens T. , Hahn Stephan A. , Hessmann Elisabeth , Johnsen Steven A. , Najafova Zeynab
Published: September 2024

Supplementary Table S4 contains L3.6pl TP63-dependent enhancer regions.
Supplementary Table S2 from Identification of a ΔNp63-Dependent Basal-Like A Subtype-Specific Transcribed Enhancer Program (B-STEP) in Aggressive Pancreatic Ductal Adenocarcinoma
Authors: Wang Xin , Kutschat Ana P. , Aggrey-Fynn Joana , Hamdan Feda H. , Graham Rondell P. , Wixom Alexander Q. , Souto Yara , Ladigan-Badura Swetlana , Yonkus Jennifer A. , Abdelrahman Amro M. , Alva-Ruiz Roberto , Gaedcke Jochen , Strobel Philipp , Kosinsky Robyn Laura , Wegwitz Florian , Hermann Patrick , Truty Mark J. , Siveke Jens T. , Hahn Stephan A. , Hessmann Elisabeth , Johnsen Steven A. , Najafova Zeynab
Published: September 2024

Supplementary Table S2 contains GöPdx4 super enhancers regions overlapping TP63
Supplementary Figure S2 from Identification of a ΔNp63-Dependent Basal-Like A Subtype-Specific Transcribed Enhancer Program (B-STEP) in Aggressive Pancreatic Ductal Adenocarcinoma
Authors: Wang Xin , Kutschat Ana P. , Aggrey-Fynn Joana , Hamdan Feda H. , Graham Rondell P. , Wixom Alexander Q. , Souto Yara , Ladigan-Badura Swetlana , Yonkus Jennifer A. , Abdelrahman Amro M. , Alva-Ruiz Roberto , Gaedcke Jochen , Strobel Philipp , Kosinsky Robyn Laura , Wegwitz Florian , Hermann Patrick , Truty Mark J. , Siveke Jens T. , Hahn Stephan A. , Hessmann Elisabeth , Johnsen Steven A. , Najafova Zeynab
Published: September 2024

Defining the specificity and P63-dependence of B-STEP
Movie S4 from Targeting the ATF6-mediated ER stress response and autophagy blocks integrin-driven prostate cancer progression
Authors: Macke Amanda J. , Pachikov Artem N. , Divita Taylor E. , Morris Mary E. , LaGrange Chad A. , Holzapfel Melissa S. , Kubyshkin Anatoly V. , Zyablitskaya Evgeniya Y. , Makalish Tatiana P. , Eremenko Sergey N. , Qiu Haowen , Riethoven Jean-Jack M. , Hemstreet George P. , Petrosyan Armen
Published: September 2024

PC-3 cell treated with HCQ, stained for Integrin αv (red), Gal-3 (green), EEA1 (magenta). Areas of 3-color colocalization are highlighted with white. Surfaces were reconstructed by Imaris.
Supplemental Figure 5 from Allele-specific gene regulation, phenotypes, and therapeutic vulnerabilities in estrogen receptor alpha mutant endometrial cancer
Authors: Blanchard Zannel , Rush Craig M. , Arnesen Spencer , Vahrenkamp Jeffery M. , Rodriguez Adriana C. , Jarboe Elke A. , Brown Callie , Chang Matthew E.K. , Flory Mark R. , Mohammed Hisham , Modzelewska Katarzyna , Lum David H. , Gertz Jason
Published: September 2024

ER-Y537S and ER-D538G mutants drive proliferative gene expression signatures in vivo
Supplemental Figure 2 from Allele-specific gene regulation, phenotypes, and therapeutic vulnerabilities in estrogen receptor alpha mutant endometrial cancer
Authors: Blanchard Zannel , Rush Craig M. , Arnesen Spencer , Vahrenkamp Jeffery M. , Rodriguez Adriana C. , Jarboe Elke A. , Brown Callie , Chang Matthew E.K. , Flory Mark R. , Mohammed Hisham , Modzelewska Katarzyna , Lum David H. , Gertz Jason
Published: September 2024

Comparison of mutant ER regulated genes and genes regulated by sustained estrogen signaling
Supplemental Figure 1 from Allele-specific gene regulation, phenotypes, and therapeutic vulnerabilities in estrogen receptor alpha mutant endometrial cancer
Authors: Blanchard Zannel , Rush Craig M. , Arnesen Spencer , Vahrenkamp Jeffery M. , Rodriguez Adriana C. , Jarboe Elke A. , Brown Callie , Chang Matthew E.K. , Flory Mark R. , Mohammed Hisham , Modzelewska Katarzyna , Lum David H. , Gertz Jason
Published: September 2024

Validation and gene expression analysis of ER mutant models
Supplementary Table 6 from LncRNA-encoded Micropeptide ACLY‍-‍BP drives lipid deposition and cell proliferation in Clear Cell Renal Cell Carcinoma via maintenance of ACLY acetylation
Authors: Zhang Shenghua , Zhang Zheng , Liu Xiaolong , Deng Yibin , Zheng Jian , Deng Jieqiong , Wang Yirong , Guo Binbin , Li Fanrong , Chen Xiaoyue , Pan Yacheng , Wang Jieyu , Lu Jiachun , Wu Siqi , Guo Qiang , Zhou Yifeng
Published: September 2024

The genomic position of the predicted ORFs of the six lncRNAs
Supplementary Table 5 from LncRNA-encoded Micropeptide ACLY‍-‍BP drives lipid deposition and cell proliferation in Clear Cell Renal Cell Carcinoma via maintenance of ACLY acetylation
Authors: Zhang Shenghua , Zhang Zheng , Liu Xiaolong , Deng Yibin , Zheng Jian , Deng Jieqiong , Wang Yirong , Guo Binbin , Li Fanrong , Chen Xiaoyue , Pan Yacheng , Wang Jieyu , Lu Jiachun , Wu Siqi , Guo Qiang , Zhou Yifeng
Published: September 2024

Sequences of LINC00887 and ACLY-BP cDNA
Supplementary Table 4 from LncRNA-encoded Micropeptide ACLY‍-‍BP drives lipid deposition and cell proliferation in Clear Cell Renal Cell Carcinoma via maintenance of ACLY acetylation
Authors: Zhang Shenghua , Zhang Zheng , Liu Xiaolong , Deng Yibin , Zheng Jian , Deng Jieqiong , Wang Yirong , Guo Binbin , Li Fanrong , Chen Xiaoyue , Pan Yacheng , Wang Jieyu , Lu Jiachun , Wu Siqi , Guo Qiang , Zhou Yifeng
Published: September 2024

Sequences of shRNAs and siRNAs used in this study
Supplementary Figure 4 from LncRNA-encoded Micropeptide ACLY‍-‍BP drives lipid deposition and cell proliferation in Clear Cell Renal Cell Carcinoma via maintenance of ACLY acetylation
Authors: Zhang Shenghua , Zhang Zheng , Liu Xiaolong , Deng Yibin , Zheng Jian , Deng Jieqiong , Wang Yirong , Guo Binbin , Li Fanrong , Chen Xiaoyue , Pan Yacheng , Wang Jieyu , Lu Jiachun , Wu Siqi , Guo Qiang , Zhou Yifeng
Published: September 2024

Related information to figure 6
Supplementary Table 1 from TRIM50 inhibits gastric cancer progression by regulating the ubiquitination and nuclear translocation of JUP
Authors: Hu Jiajia , Huang Runjie , Liang Chengcai , Wang Yingnan , Wang Min , Chen Yanxing , Wu Chenyi , Zhang Jinling , Liu Zekun , Zhao Qi , Liu Zexian , Wang Feng , Yuan Shuqiang
Published: September 2024

The primer sequences used.
Figure S6 from TRIM50 inhibits gastric cancer progression by regulating the ubiquitination and nuclear translocation of JUP
Authors: Hu Jiajia , Huang Runjie , Liang Chengcai , Wang Yingnan , Wang Min , Chen Yanxing , Wu Chenyi , Zhang Jinling , Liu Zekun , Zhao Qi , Liu Zexian , Wang Feng , Yuan Shuqiang
Published: September 2024

Figure S6: Immunoblotting analysis of JUP in TRIM50 overexpressing versus control empty vector MKN45 cells.
Supplementary Figure 7 from Podoplanin drives amoeboid invasion in canine and human mucosal melanoma
Authors: Shinada Masahiro , Kato Daiki , Motegi Tomoki , Tsuboi Masaya , Ikeda Namiko , Aoki Susumu , Iguchi Takaaki , Li Toshio , Kodera Yuka , Ota Ryosuke , Hashimoto Yuko , Takahashi Yosuke , Chambers James , Uchida Kazuyuki , Kato Yukinari , Nishimura Ryohei , Nakagawa Takayuki
Published: September 2024

ROCK inhibition leads to cell cycle arrest and cellular senescence.