bluuebunny/crossref_metadata_2025 huggingface dataset:
Supplementary Figure 1 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

The immunosuppressive character of ARG1 and ARG2 in the tumor microenvironment (TME)
Figure S3 from Antitumor Immune Mechanisms of the Anti-Complement Factor H Antibody GT103
Authors: Bushey Ryan T. , Saxena Ruchi , Campa Michael J. , Gottlin Elizabeth B. , He You-Wen , Patz Edward F.
Published: September 2024

Flow cytometry histograms of C3b/iC3b or C1q binding to NSCLC cells incubated with normal human serum (NHS) or depleted (Dpl) NHS + antibodies.
Figure S2 from Antitumor Immune Mechanisms of the Anti-Complement Factor H Antibody GT103
Authors: Bushey Ryan T. , Saxena Ruchi , Campa Michael J. , Gottlin Elizabeth B. , He You-Wen , Patz Edward F.
Published: September 2024

Deposition of intratumoral C3dg and C3d.
Supplementary Figure 8 from BET inhibition sensitizes immunologically-cold Rb-deficient prostate cancer to immune checkpoint blockade
Authors: Olson Brian M. , Chaudagar Kiranj , Bao Riyue , Saha Sweta Sharma. , Hong Christina , Li Marguerite , Rameshbabu Srikrishnan , Chen Raymond , Thomas Alison , Patnaik Akash
Published: September 2024

Generation of STING-deficient Myc-CaP cell lines.
Supplementary Figure 5 from BET inhibition sensitizes immunologically-cold Rb-deficient prostate cancer to immune checkpoint blockade
Authors: Olson Brian M. , Chaudagar Kiranj , Bao Riyue , Saha Sweta Sharma. , Hong Christina , Li Marguerite , Rameshbabu Srikrishnan , Chen Raymond , Thomas Alison , Patnaik Akash
Published: September 2024

Pharmacological inhibition of BET family members by JQ-1.
Supplementary Figure 10 from BET inhibition sensitizes immunologically-cold Rb-deficient prostate cancer to immune checkpoint blockade
Authors: Olson Brian M. , Chaudagar Kiranj , Bao Riyue , Saha Sweta Sharma. , Hong Christina , Li Marguerite , Rameshbabu Srikrishnan , Chen Raymond , Thomas Alison , Patnaik Akash
Published: September 2024

JQ-1 treatment in vivo increases PD-L1 expression on myeloid suppressive cells.
Figure S1-S5 from Activating an Adaptive Immune Response with a Telomerase-mediated Telomere Targeting Therapeutic in Hepatocellular Carcinoma
Authors: Mender Ilgen , Siteni Silvia , Barron Summer , Flusche Ann Marie , Kubota Naoto , Yu Chunhua , Cornelius Crystal , Tedone Enzo , Maziveyi Mazvita , Grichuk Anthony , Venkateswaran Niranjan , Conacci Sorrell Maralice , Hoshida Yujin , Kang Rui , Tang Daolin , Gryaznov Sergei , Shay Jerry W.
Published: September 2024

Supplementary Data
Supplementary Figure S7 from Efficacy and Imaging Enabled Pharmacodynamic Profiling of KRAS G12C Inhibitors in Xenograft and Genetically Engineered Mouse Models of Cancer
Authors: Lee Catherine , Jiang Ziyue Karen , Planken Simon , Manzuk Lisa K. , Ortiz Roberto , Hall Michael , Noorbehesht Kavon , Ram Sripad , Affolter Timothy , Troche Gabriel E. , Ihle Nathan T. , Johnson Theodore , Ahn Youngwook , Kraus Manfred , Giddabasappa Anand
Published: September 2024

G12C KP model survival data from long-term treatment with Compound A
Supplementary Figure S3 from Efficacy and Imaging Enabled Pharmacodynamic Profiling of KRAS G12C Inhibitors in Xenograft and Genetically Engineered Mouse Models of Cancer
Authors: Lee Catherine , Jiang Ziyue Karen , Planken Simon , Manzuk Lisa K. , Ortiz Roberto , Hall Michael , Noorbehesht Kavon , Ram Sripad , Affolter Timothy , Troche Gabriel E. , Ihle Nathan T. , Johnson Theodore , Ahn Youngwook , Kraus Manfred , Giddabasappa Anand
Published: September 2024

Tolerability and individual MiaPaCa2 tumor growth data from animals treated with two weeks of Compound A
Supplementary Table S4 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

Patient information for breast cancer formalin-fixed paraffin-embedded samples
Supplementary Fig.S11 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

The nectin-4 expression for BR1282
Materials and Methods 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

Supplementary Materials and Methods
Supplementary Data 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

p53Wt_log2FC of genes
Figure S7 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 7
Figure S6 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 6
Supplementary Table S3 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

Data for Figure 4B
Supplementary Table S1 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

Results of HTS in CCRF-CEM parent and SLFN11-KO cells
Supplementary Figure S1 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 S1
Figure S3 from Bromo- and Extra-Terminal Domain Inhibitors Induce Mitochondrial Stress in Pancreatic Ductal Adenocarcinoma
Authors: Rana Manjul , Kansal Rita G. , Bisunke Bijay , Fang Jie , Shibata David , Bajwa Amandeep , Yang Jun , Glazer Evan S.
Published: September 2024

Figure S3
Supplementary Figure 8 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

In vitro efficacy and bystander effect of AMT-562.
Supplementary Figure 7 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

Orthogonal combination experiments of HER3 targeting ADCs and trafficking parameters of AMT-562.
Supplementary Figure 2 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

HER3 expression level and hydrophilicity of Ab562 ADCs.
Supplementary Figure 11 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

In vivo antitumor efficacy of AMT-562 in pancreatic and gastric cancer.
Supplementary Figure 9 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

Organoids homogeneity and pharmacodynamics of AMT-562 in organoids.
Supplementary Figure 13 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

HER3 expression in NSCLC and clinical trial status of U3-1402.
Supplementary File 2 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

HTS data using 3D CRC spheroids showing growth curves and heat maps to demonstrate efficacy of different compounds when combined with trametinib.
Supplementary Fig.S5 from MTX-13, a novel PTK7-directed antibody-drug conjugate with widened therapeutic index shows sustained tumor regressions for a broader spectrum of PTK7-positive tumors
Authors: Kong Chao , Pu Junyi , Zhao Qianqian , Weng Weining , Ma Linjie , Qian Yu , Hu Wenhao , Meng Xun , Meng Tao
Published: September 2024

Supplementary Fig.S5 shows in vitro and in vivo efficacy of MTX-13
Supplementary Fig.S1 from MTX-13, a novel PTK7-directed antibody-drug conjugate with widened therapeutic index shows sustained tumor regressions for a broader spectrum of PTK7-positive tumors
Authors: Kong Chao , Pu Junyi , Zhao Qianqian , Weng Weining , Ma Linjie , Qian Yu , Hu Wenhao , Meng Xun , Meng Tao
Published: September 2024

Supplementary Fig.S1 shows the development and characterization of Ab13, a PTK7-targeting antibody
Figure S5 from S-531011, a novel anti-human CCR8 antibody, induces potent anti-tumor responses through depletion of tumor-infiltrating CCR8-expressing regulatory T cells
Authors: Nagira Yoji , Nagira Morio , Nagai Ryohei , Nogami Wataru , Hirata Michinari , Ueyama Azumi , Yoshida Tetsuya , Yoshikawa Mai , Shinonome Satomi , Yoshida Hiroshi , Haruna Miya , Miwa Hiroto , Chatani Natsumi , Ohkura Naganari , Wada Hisashi , Tanaka Hidekazu
Published: September 2024

In vivo anti-tumor activity of S-531011 in CT26.WT or EMT6 tumor-bearing mice model.
Figure S3 from S-531011, a novel anti-human CCR8 antibody, induces potent anti-tumor responses through depletion of tumor-infiltrating CCR8-expressing regulatory T cells
Authors: Nagira Yoji , Nagira Morio , Nagai Ryohei , Nogami Wataru , Hirata Michinari , Ueyama Azumi , Yoshida Tetsuya , Yoshikawa Mai , Shinonome Satomi , Yoshida Hiroshi , Haruna Miya , Miwa Hiroto , Chatani Natsumi , Ohkura Naganari , Wada Hisashi , Tanaka Hidekazu
Published: September 2024

Concentration of S-531011 in serum and tumor after a single intravenous administration of S-531011 in CT26.WT tumor-bearing hCCR8 KI mice.
Figure S1 from S-531011, a novel anti-human CCR8 antibody, induces potent anti-tumor responses through depletion of tumor-infiltrating CCR8-expressing regulatory T cells
Authors: Nagira Yoji , Nagira Morio , Nagai Ryohei , Nogami Wataru , Hirata Michinari , Ueyama Azumi , Yoshida Tetsuya , Yoshikawa Mai , Shinonome Satomi , Yoshida Hiroshi , Haruna Miya , Miwa Hiroto , Chatani Natsumi , Ohkura Naganari , Wada Hisashi , Tanaka Hidekazu
Published: September 2024

The binding activity of S-531011 against various chemokine receptors, PD-1, PD-L1, CTLA4, or mouse CCR8
Supplementary Table S2 from Safety and Tolerability of a Novel Anti-HER2 Antibody-Drug Conjugate (PF-06804103) in Patients With HER2-Expressing Solid Tumors: A Phase 1 Dose Escalation Study
Authors: Meric-Bernstam Funda , Calvo Emiliano , Lee Keun Seok , Moreno Victor , Park Yeon Hee , Rha Sun Young , Chalasani Pavani , Zhong Wei , Zhou Li , Pirie-Shepherd Steven , Leung Abraham CF. , Curigliano Giuseppe
Published: September 2024

Supplementary Table S2 shows the PK results
Supplementary Figure S2 from Safety and Tolerability of a Novel Anti-HER2 Antibody-Drug Conjugate (PF-06804103) in Patients With HER2-Expressing Solid Tumors: A Phase 1 Dose Escalation Study
Authors: Meric-Bernstam Funda , Calvo Emiliano , Lee Keun Seok , Moreno Victor , Park Yeon Hee , Rha Sun Young , Chalasani Pavani , Zhong Wei , Zhou Li , Pirie-Shepherd Steven , Leung Abraham CF. , Curigliano Giuseppe
Published: September 2024

Supplementary Figure S2 shows the duration of treatment including response and tumor type (the safety analysis set)
Table S6 from Pan-cancer pharmacogenomic analysis of patient-derived tumor cells utilizing clinically relevant drug exposures
Authors: Chang Stephen H. , Ice Ryan J. , Chen Michelle , Sidorov Maxim , Woo Rinette W.L. , Rodriguez-Brotons Aida , Jian Damon , Kim Han Kyul , Kim Angela , Stone David E. , Nazarian Ari , Oh Alyssia , Tranah Gregory J. , Nosrati Mehdi , de Semir David , Dar Altaf A. , Desprez Pierre-Yves , Kashani-Sabet Mohammed , Soroceanu Liliana , McAllister Sean D.
Published: September 2024

Supplementary Table 6 ROC formulae training and test
Table S3 from Pan-cancer pharmacogenomic analysis of patient-derived tumor cells utilizing clinically relevant drug exposures
Authors: Chang Stephen H. , Ice Ryan J. , Chen Michelle , Sidorov Maxim , Woo Rinette W.L. , Rodriguez-Brotons Aida , Jian Damon , Kim Han Kyul , Kim Angela , Stone David E. , Nazarian Ari , Oh Alyssia , Tranah Gregory J. , Nosrati Mehdi , de Semir David , Dar Altaf A. , Desprez Pierre-Yves , Kashani-Sabet Mohammed , Soroceanu Liliana , McAllister Sean D.
Published: September 2024

Supplementary Table 3 binarization sensitivity 19 drugs
Supplementary Data Figure S1 from Pan-cancer pharmacogenomic analysis of patient-derived tumor cells utilizing clinically relevant drug exposures
Authors: Chang Stephen H. , Ice Ryan J. , Chen Michelle , Sidorov Maxim , Woo Rinette W.L. , Rodriguez-Brotons Aida , Jian Damon , Kim Han Kyul , Kim Angela , Stone David E. , Nazarian Ari , Oh Alyssia , Tranah Gregory J. , Nosrati Mehdi , de Semir David , Dar Altaf A. , Desprez Pierre-Yves , Kashani-Sabet Mohammed , Soroceanu Liliana , McAllister Sean D.
Published: September 2024

Figure S1
Table S1 from Intratumoral interleukin-15 improves efficacy of near-infrared photoimmunotherapy
Authors: Fukushima Hiroshi , Furusawa Aki , Kato Takuya , Wakiyama Hiroaki , Takao Seiichiro , Okuyama Shuhei , Choyke Peter L. , Kobayashi Hisataka
Published: September 2024

Supplementary Table S1. List of key resource identifiers in this study.
Figure S9 from Intratumoral interleukin-15 improves efficacy of near-infrared photoimmunotherapy
Authors: Fukushima Hiroshi , Furusawa Aki , Kato Takuya , Wakiyama Hiroaki , Takao Seiichiro , Okuyama Shuhei , Choyke Peter L. , Kobayashi Hisataka
Published: September 2024

Supplementary Fig. S9. In vivo therapeutic efficacy of intratumoral IL-15 injection combined with CD44-targeted NIR-PIT against MC38 tumors using T cell-deficient athymic nude mice.
Figure S6 from Intratumoral interleukin-15 improves efficacy of near-infrared photoimmunotherapy
Authors: Fukushima Hiroshi , Furusawa Aki , Kato Takuya , Wakiyama Hiroaki , Takao Seiichiro , Okuyama Shuhei , Choyke Peter L. , Kobayashi Hisataka
Published: September 2024

Supplementary Fig. S6. Expression of immunogenic signals after in vitro CD44-targeted NIR-PIT in hIL-15-MC38 or parental MC38 cells.
Figure S4 from Intratumoral interleukin-15 improves efficacy of near-infrared photoimmunotherapy
Authors: Fukushima Hiroshi , Furusawa Aki , Kato Takuya , Wakiyama Hiroaki , Takao Seiichiro , Okuyama Shuhei , Choyke Peter L. , Kobayashi Hisataka
Published: September 2024

Supplementary Fig. S4. Comparison of immune cell expressions between hIL-15-MC38 and MC38 tumors.
Figure S12 from Intratumoral interleukin-15 improves efficacy of near-infrared photoimmunotherapy
Authors: Fukushima Hiroshi , Furusawa Aki , Kato Takuya , Wakiyama Hiroaki , Takao Seiichiro , Okuyama Shuhei , Choyke Peter L. , Kobayashi Hisataka
Published: September 2024

Supplementary Fig. S12. Therapeutic efficacy of in vivo CD44-targeted NIR-PIT in a bilateral tumor mouse model (R: MC38 tumor, L: MC38 tumor).
Figure S1 from Intratumoral interleukin-15 improves efficacy of near-infrared photoimmunotherapy
Authors: Fukushima Hiroshi , Furusawa Aki , Kato Takuya , Wakiyama Hiroaki , Takao Seiichiro , Okuyama Shuhei , Choyke Peter L. , Kobayashi Hisataka
Published: September 2024

Supplementary Fig. S1. Host immune responses after intraperitoneal or intratumoral injection of IL-15.
Supplementary table S1 from Efficacy and safety of glycosphingolipid SSEA-4 targeting CAR-T cells
in an ovarian carcinoma model
Authors: Monzo Hector J. , Kalander Kerttu , Hyytiäinen Marko M. , Elbasani Endrit , Wall Johanna , Moyano-Galceran Lidia , Tanjore Ramanathan Jayendrakishore , Jukonen Joonas J.J. , Laakkonen Pirjo , Ristimäki Ari , Carlson Joseph W. , Lehti Kaisa , Salehi Sahar , Puolakkainen Pauli , Haglund Caj , Seppänen Hanna , Leppä Sirpa , Ojala Päivi M.
Published: September 2024

SSEA-4 expression in an ovarian cancer cohort.
Supplementary Figure S2 from Efficacy and safety of glycosphingolipid SSEA-4 targeting CAR-T cells
in an ovarian carcinoma model
Authors: Monzo Hector J. , Kalander Kerttu , Hyytiäinen Marko M. , Elbasani Endrit , Wall Johanna , Moyano-Galceran Lidia , Tanjore Ramanathan Jayendrakishore , Jukonen Joonas J.J. , Laakkonen Pirjo , Ristimäki Ari , Carlson Joseph W. , Lehti Kaisa , Salehi Sahar , Puolakkainen Pauli , Haglund Caj , Seppänen Hanna , Leppä Sirpa , Ojala Päivi M.
Published: September 2024

Supplementary Figure S2. Short-term in vivo study, dose-response, and weight monitoring. A. Treatment groups and used T cell doses. B. Weight monitoring in the indicated mice groups. CAR-T 3M treated mice showed a trend of mild weight loss. (M=1x106).
Supplementary Data from Use of Payload Binding Selectivity Enhancers to Improve Therapeutic Index of Maytansinoid-Antibody-Drug Conjugates
Authors: Nguyen Toan Duc. , Bordeau Brandon M. , Balthasar Joseph P.
Published: September 2024

Supplementary methods and results
Supplementary Fig. S1 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.S1 shows scheme for synthesis of ER beta agonist CIDD-0149897
Analytical Data from Targeted Investigational Oncology Agents (IOA) in the NCI60: A Phenotypic Systems-Based Resource
Authors: Morris Joel , Kunkel Mark W. , White Stephen L. , Wishka Donn G. , Lopez Omar D. , Bowles Lori , Sellers Brady Penny , Ramsey Patricia , Grams Julie , Rohrer Tiffany , Martin Karen , Dexheimer Thomas S. , Coussens Nathan P. , Evans David , Risbood Prabhakar , Sonkin Dmitriy , Williams John D. , Polley Eric C. , Collins Jerry M. , Doroshow James H. , Teicher Beverly A.
Published: September 2024

Analytical Data
Supplementary Figure 1 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

Supplementary Figure 1
Supplementary Figure S6 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 6 shows the effect of IFNgamma combined PD-1 antibody in orthotropic CT-26 colon cancer.
Supplementary table 1 from Activation of Hepatocyte Growth Factor/MET Signaling as a Mechanism of Acquired Resistance to a Novel YAP1/TEAD Small Molecule Inhibitor
Authors: Moure Casey J. , Vara Brandon , Cheng Mangeng M. , Sondey Christopher , Muise Eric , Park Eunsil , Vela Ramirez Julia Eulalia , Su Dan , D’Souza Shanti , Yan Qingyun , Yeung Charles S. , Zhang Minjia , Mansueto My Sam , Linn Doug , Buchanan Mark , Foti Robert , DiMauro Erin , Long Brian , Simov Vladimir , Barry Evan R.
Published: September 2024

Supplementary table 1
Data from Identification of a First-in-Class Small Molecule Inhibitor of the eIF4E-RBM38 Complex that Enhances wild-type p53 Protein Translation for Tumor Growth Suppression
Authors: Lucchesi Christopher A. , Zhang Jin , Gao Mingchun , Shaw Jared , Chen Xinbin
Published: September 2024

Abstract
eIF4E, an mRNA cap-binding protein, is necessary for cap-dependent translation. Overexpression of eIF4E is known to promote cancer development by preferentially translating a group of oncogenic mRNAs. Thus, 4EGI-1, a disruptor of eIF4E-eIF4G interaction, was developed to inhibit oncoprotein expression for cancer therapy. Interestingly, RBM38, an RNA-binding protein, interacts with eIF4E on p53 mRNA, prevents eIF4E from binding to p53 mRNA cap, and inhibits p53 expression. Thus, Pep8, an eight amino acid peptide derived from RBM38, was developed to disrupt the eIF4E-RBM38 complex, leading to increased p53 expression and decreased tumor cell growth. Herein, we have developed a first-in-class small molecule compound 094, which interacts with eIF4E via the same pocket as does Pep8, dissociates RBM38 from eIF4E, and enhances p53 translation in RBM38- and eIF4E-dependent manners. Structure-activity relationship (SAR) studies identified that both the fluorobenzene and ethyl benzamide are necessary for compound 094 to interact with eIF4E. Further, we showed that compound 094 is capable of suppressing 3D tumor spheroid growth in RBM38- and p53-dependent manners. Additionally, we found that compound 094 cooperates with chemotherapeutic agent doxorubicin and eIF4E inhibitor 4EGI-1 to suppress tumor cell growth. Collectively, we showed that two distinct approaches can be used together to target eIF4E for cancer therapy by enhancing wild-type p53 expression (094), and by suppressing oncoprotein expression (4EGI-1).
Data from Antitumor Immune Mechanisms of the Anti-Complement Factor H Antibody GT103
Authors: Bushey Ryan T. , Saxena Ruchi , Campa Michael J. , Gottlin Elizabeth B. , He You-Wen , Patz Edward F.
Published: September 2024

Abstract
Development of novel therapeutic antibodies that not only kill tumor cells but modulate the adaptive immune response has the potential to produce long term anti-cancer immunity and a durable clinical response. We previously reported the discovery of anti-complement factor H (CFH) autoantibodies in lung cancer patients that were associated with early stage disease and exceptional outcomes. The human monoclonal antibody GT103, produced from a single CFH autoantibody-expressing B cell of a lung cancer patient, recognizes a conformationally distinct epitope on tumor cells, kills tumor cells, and inhibits tumor growth in animal studies. Recent experiments have shown that GT103 restructures the tumor microenvironment and initiates a robust antitumoral adaptive immune response. The current study further elucidates several mechanisms by which GT103 kills tumor cells and drives the immune program. Here we show GT103 has specificity for tumor cells without binding to native soluble CFH or normal tissues. GT103 causes complement C3 split product deposition on tumor cells in vitro and in vivo, triggers antibody-dependent cellular phagocytosis, and increases translocation of the danger associated molecular pattern molecule calreticulin to the plasma membrane. We also demonstrate that GT103 causes B cell activation in vitro and in vivo, and that GT103 antitumor activity in vivo is B cell dependent. The complex mechanism of GT103, a tumor specific antibody that kills tumor cells and stimulates an immune response, supports further development of this human-derived antibody as a novel therapeutic option for patients with lung cancer.
Data from Targeting Glutamine Metabolism with a Novel Na+/K+-ATPase Inhibitor RX108 in Hepatocellular Carcinoma
Authors: Wei Daoyan , Chen Dongmei , Mou Hongyuan , Chakraborty Sharmistha , Wei Bo , Tan Lin , Lorenzi Philip L. , Qian Xiangping , Yang Peiying
Published: September 2024

Abstract
The poor prognosis and limited therapeutic options for human hepatocellular carcinoma (HCC), the most common form of liver cancer, highlight the urgent need to identify novel therapeutic modalities. Here we describe the antitumor activity and underlying molecular mechanisms of a novel Na+/K+-ATPase inhibitor RX108 in human HCC cells and its xenograft model. RX108 dose-dependently inhibited HCC cell proliferation in vitro and tumor growth in a xenograft mouse model, and that the inhibition was associated with induction of apoptosis. Mechanistically, RX108 significantly downregulated alanine serine cysteine transporter 2 (ASCT2) protein expression and reduced glutamine and glutamate concentration in HCC cells and tumors. Additionally, RX108 exposure led to a significant decrease in cell energy metabolism in Huh7 and Hep3B cells, including decreased levels of glutathione, NADH, NADPH, and mitochondrial respiration oxygen consumption rate (OCR). Furthermore, HCC cells exhibited evidence of glutamine addiction; the antiproliferative effect of RX108 was dependent on glutamine transport. Clinically, elevated ASCT2 mRNA expression in HCCs was associated with unfavorable survival. Taken together, these findings reveal a novel approach to target glutamine metabolism through inhibiting Na+/K+-ATPase and provide a rationale for using RX108 to treat HCC in patients whose tumors express ASCT2 at high levels. RX108 is currently under clinical development.
Data from Identification of 2',4',6'-trihydroxyacetophenone as promising cysteine conjugate beta-lyase inhibitor for preventing cisplatin-induced nephrotoxicity
Authors: Sukeda Nao , Fujigaki Hidetsugu , Ando Tatsuya , Ando Honomi , Yamamoto Yasuko , Saito Kuniaki
Published: September 2024

Abstract
Cisplatin is a chemotherapeutic agent used to treat many types of malignant tumors. However, irrespective of its potent anticancer properties and efficacy, nephrotoxicity is the dose-limiting factor of cisplatin treatment. Cisplatin infiltrates renal tubular cells in the kidneys and is metabolized by cysteine conjugate-beta lyase 1 (CCBL1) to form highly reactive thiol-cisplatin; this may mediate cisplatin's nephrotoxicity. Therefore, CCBL1 inhibition may prevent cisplatin-induced nephrotoxicity. Using a high-throughput screening assay, we identified 2',4',6'-trihydroxyacetophenone (THA) as an inhibitor of CCBL1. THA inhibited human CCBL1 beta-elimination activity in a concentration-dependent manner. We further investigated the preventive effect of THA on cisplatin-induced nephrotoxicity. THA attenuated the effect of cisplatin on the viability of confluent renal tubular cells (LLC-PK1 cells) but had no effect on cisplatin-induced reduction of proliferation in the tumor cell lines (LLC and MDA-MB-231). THA pre-treatment significantly attenuated cisplatin-induced increases in blood urea nitrogen, creatinine, cell damage score, and apoptosis of renal tubular cells in mice in a dose-dependent manner. Furthermore, THA pre-treatment attenuated cisplatin-induced nephrotoxicity without compromising its anti-tumor activities in mice bearing subcutaneous syngeneic LLC tumors. THA could help prevent cisplatin-induced nephrotoxicity and may provide a new strategy for cisplatin-inclusive cancer treatments.
Data 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

Abstract
Tuberous Sclerosis Complex (TSC) tumors are presently incurable despite a cytostatic response to mTOR pathway inhibition since recurrence of disease occurs after discontinuation of treatment. Here, we explored the hypothesis that inhibiting tyrosine kinase activity in mesenchymal lineage specific platelet derived growth factor receptor beta (PDGFRβ) signaling in TSC tumors is cytocidal and attenuates tumorigenesis at significantly higher levels than treatment with an mTOR inhibitor. Rapamycin- versus tyrosine kinase inhibitor (TKI)-induced renal angiomyolipoma (AML) and pulmonary lymphangioleiomyomatosis (LAM) tumor cells were comparatively analyzed using cell survival assays, and RNA sequencing and bioinformatics to distinguish tumoricidal mechanisms adopted by each drug type. The efficacy of imatinib therapy was validated against spontaneously developing renal cystadenomas in Tuberous Sclerosis Tsc2+/- mouse models (C57BL/6J mice; N=6; 400mg/kg/day; oral gavage) compared to Tsc2+/- mice treated with phosphate buffered saline (PBS) (C57BL/6J mice; N=6). Our study revealed that TKIs imatinib and nilotinib were cytocidal to both pulmonary LAM and renal AML cell cultures through the downregulation of the glycoprotein GPVI pathway and resultant disruption in mitochondrial permeability, increased cytosolic cytochrome C, and caspase 3 activation. Importantly, renal tumor growth was significantly attenuated in imatinib-treated Tsc2+/- mice compared to PBS treatment. The preclinical studies reported here provide evidence documenting the effectiveness of TKIs in limiting LAM and AML cell growth and viability with important clinical potential. Furthermore, these drugs elicit their effects by targeting a PDGF pathway-dependent apoptotic mechanism supporting the investigation of these drugs as a novel class of TSC therapeutics.
Data from The role of protein arginine methyltransferases in pathogenesis and treatment of digestive system carcinoma
Authors: Wang Bin , Ding Dong , Zhang Xiaoan , Zhang Junxi , Zhang Huanhuan , Liu Xinxin , Chang Hui , Gao Zhan , Yu Zengli
Published: September 2024

Abstract
Post-translational modification of proteins increases their diversity and maintains the stability of the intracellular environment. Protein arginine methyltransferases (PRMTs) are an important family of epigenetic modification enzymes, which play a critical role in post-translational modification. In recent years, with the in-depth study of the role of epigenetics, the structure and function of PRMTs have been gradually understood. PRMT enzymatic activity is related to a variety of cellular processes in digestive system malignancies, such as inflammation and immune response, activation of cell cycle and proliferation, inhibition of apoptosis, DNA damage repair, epithelial-mesenchymal transition (EMT). A variety of chemical tools are developed to inhibit PRMT activity, which have been verified by tumor models and clinical trials. This review summarizes the structure and functions of PRMTs as a prelude to our further studies on their role in tumors. The involvement of different PRMTs in the pathogenesis of gastrointestinal tumors is then reviewed. In addition, the application of PRMT inhibitors as therapeutic agents for digestive system cancers is highlighted. In conclusion, PRMTs play an important role in the pathogenesis of gastrointestinal tumors, and their prognostic and therapeutic potential warrants further investigation.
Data from Pan-cancer pharmacogenomic analysis of patient-derived tumor cells utilizing clinically relevant drug exposures
Authors: Chang Stephen H. , Ice Ryan J. , Chen Michelle , Sidorov Maxim , Woo Rinette W.L. , Rodriguez-Brotons Aida , Jian Damon , Kim Han Kyul , Kim Angela , Stone David E. , Nazarian Ari , Oh Alyssia , Tranah Gregory J. , Nosrati Mehdi , de Semir David , Dar Altaf A. , Desprez Pierre-Yves , Kashani-Sabet Mohammed , Soroceanu Liliana , McAllister Sean D.
Published: September 2024

Abstract
As a result of tumor heterogeneity and solid cancers harboring multiple molecular defects, precision medicine platforms in oncology are most effective when both genetic and pharmacological determinants of a tumor are evaluated. Expandable patient-derived xenograft (PDX) mouse tumor and corresponding PDX culture (PDXC) models recapitulate many of the biological and genetic characteristics of the original patient tumor, allowing for a comprehensive pharmacogenomic analysis. Here, the somatic mutations of 23 matched patient tumor and PDX samples encompassing four cancers were first evaluated using next generation sequencing (NGS). 19 antitumor agents were evaluated across 78 patient-derived tumor cultures using clinically relevant drug exposures. A binarization threshold sensitivity classification determined in culture (PDXC) was used to identify tumors that best respond to drug in vivo (PDX). Utilizing this sensitivity classification, logic models of DNA mutations were developed for 19 antitumor agents to predict drug response. We determined that the concordance of somatic mutations across patient and corresponding PDX samples increased as variant allele frequency (VAF) increased. Notable individual PDXC responses to specific drugs, as well as lineage-specific drug responses where identified. Robust responses identified in PDXC were recapitulated in vivo in PDX-bearing mice and logic modeling determined somatic gene mutation(s) defining response to specific antitumor agents. In conclusion, combining NGS of primary patient tumors, high-throughput drug screen (HTDS) using clinically relevant doses, and logic modeling, can provide a platform for understanding response to therapeutic drugs targeting cancer.
Data from Discovery and Preclinical Characterization of XMT-1660, an Optimized B7-H4-Targeted Antibody-Drug Conjugate for the Treatment of Cancer
Authors: Toader Dorin , Fessler Shawn P. , Collins Scott D. , Conlon Patrick R. , Bollu Reddy , Catcott Kalli C. , Chin Chen-Ni , Dirksen Anouk , Du Bingfan , Duvall Jeremy R. , Higgins Stacy , Kozytska Mariya V. , Bellovoda Kamela , Faircloth Chelsey , Lee David , Li Fu , Qin Liuliang , Routhier Caitlin , Shaw Pamela , Stevenson Cheri A. , Wang Jason , Wongthida Phonphimon , Ter-Ovanesyan Elena , Ditty Elizabeth , Bradley Stephen P. , Xu Ling , Yin Mao , Yurkovetskiy Aleksandr V. , Mosher Rebecca , Damelin Marc , Lowinger Timothy B.
Published: September 2024

Abstract
Antibody-drug conjugates (ADCs) achieve targeted drug delivery to a tumor and have demonstrated clinical success in many tumor types. The activity and safety profile of an ADC depends on its construction: antibody, payload, linker, and conjugation method, as well as the number of payload drugs per antibody (drug-to-antibody ratio, DAR). To allow for ADC optimization for a given target antigen, we developed Dolasynthen, a novel ADC platform based on the payload auristatin hydroxypropylamide (AF-HPA), that enables precise DAR-ranging and site-specific conjugation. We used the new platform to optimize an ADC that targets B7-H4 (VTCN1), an immune-suppressive protein that is overexpressed in breast, ovarian, and endometrial cancers. XMT-1660 is a site-specific Dolasynthen DAR 6 ADC that induced complete tumor regressions in xenograft models of breast and ovarian cancer as well as in a syngeneic breast cancer model that is refractory to PD-1 immune checkpoint inhibition. In a panel of 28 breast cancer patient-derived xenografts (PDX), XMT-1660 demonstrated activity that correlated with B7-H4 expression. XMT-1660 has recently entered clinical development in a Phase 1 study (NCT05377996) in cancer patients.
Data from Targeted Investigational Oncology Agents (IOA) in the NCI60: A Phenotypic Systems-Based Resource
Authors: Morris Joel , Kunkel Mark W. , White Stephen L. , Wishka Donn G. , Lopez Omar D. , Bowles Lori , Sellers Brady Penny , Ramsey Patricia , Grams Julie , Rohrer Tiffany , Martin Karen , Dexheimer Thomas S. , Coussens Nathan P. , Evans David , Risbood Prabhakar , Sonkin Dmitriy , Williams John D. , Polley Eric C. , Collins Jerry M. , Doroshow James H. , Teicher Beverly A.
Published: September 2024

Abstract
The NCI-60 human tumor cell line panel has proved to be a useful tool for the global cancer research community in the search for novel chemotherapeutics. The publicly available cell-line characterization and compound screening data from the NCI-60 assay have significantly contributed to the understanding of cellular mechanisms targeted by new oncology agents. Signature sensitivi-ty/resistance patterns generated for a given chemotherapeutic agent against the NCI-60 panel have long served as fingerprint presentations that encompass target information and the mechanism of action associated with the tested agent. We report the establishment of a new public NCI-60 resource based on the cell-line screening of a large and growing set of 175 FDA-approved oncolo-gy drugs (AOD) plus >825 clinical and investigational oncology agents (IOA), representing a diverse set (>250) of therapeutic targets and mechanisms. This data resource is available to the public (https://ioa.cancer.gov) and includes the raw data from the screening of the IOA and AOD collection along with an ex-tensive set of visualization and analysis tools to allow for comparative study of individual test compounds and multiple compound sets.
Data 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

Abstract
Many patients with colorectal cancer do not respond to immune checkpoint blockade (ICB) therapy, highlighting the urgent need to understand tumor resistance mechanisms. Recently, the link between the IFNγ signaling pathway integrity and ICB resistance in the colorectal cancer tumor microenvironment has been revealed. The immunosuppressive microenvironment poses a significant challenge to antitumor immunity in colorectal cancer development. Tumor-associated neutrophils found in tumor tissues exhibit an immunosuppressive phenotype and are associated with colorectal cancer patient prognosis. Neutrophil extracellular traps (NET), DNA meshes containing cytotoxic enzymes released into the extracellular space, may be promising therapeutic targets in cancer. This study showed increased NETs in tumor tissues and peripheral neutrophils of high levels of microsatellite instability (MSI-H) patients with colorectal cancer compared with microsatellite stable (MSS) patients with colorectal cancer. IFNγ response genes were enriched in MSI-H patients with colorectal cancer compared with patients with MSS colorectal cancer. Co-culturing neutrophils with MSI-H colorectal cancer cell lines induced more NET formation and higher cellular apoptosis than MSS colorectal cancer cell lines. IFNγ treatment induced more NET formation and apoptosis in MSS colorectal cancer cell lines. Using subcutaneous or orthotopic CT-26 (MSS) tumor-bearing mice models, IFNγ reduced tumor size and enhanced PD-1 antibody-induced tumor-killing activity, accompanied by upregulated NETs and cellular apoptosis. These findings suggest that IFNγ could be a therapeutic strategy for MSS colorectal cancer.
Supplementary Tables 1-5 from FOXA1 reprogramming dictates retinoid X receptor response in ESR1 mutant breast cancer
Authors: Wu Yang , Li Zheqi , Wedn Abdalla M. , Casey Allison N. , Brown Daniel , Rao Shalini V. , Omarjee Soleilmane , Hooda Jagmohan , Carroll Jason S. , Gertz Jason , Atkinson Jennifer M. , Lee Adrian V. , Oesterreich Steffi
Published: September 2024

Table S1. Data Sets Used
Table S2. FOXA1 and ER Chip-seq peaks
Table S3. DE genes
Table S4. Enriched FOXA1 peak motifs
Table S5. Enriched IPA pathways
Supplementary Figures 1-8 from FOXA1 reprogramming dictates retinoid X receptor response in ESR1 mutant breast cancer
Authors: Wu Yang , Li Zheqi , Wedn Abdalla M. , Casey Allison N. , Brown Daniel , Rao Shalini V. , Omarjee Soleilmane , Hooda Jagmohan , Carroll Jason S. , Gertz Jason , Atkinson Jennifer M. , Lee Adrian V. , Oesterreich Steffi
Published: September 2024

S1. FOXA1 redistribution in ESR1 mutant cells causes distinct ER-FOXA1 interaction.
S2. FOXA1 gained peaks annotated genes are significantly associated with novel target genes.
S3. FOXA1 redistribution in ESR1 mutant cells confers potential RXR binding sites.
S4. RXR agonist LG100268 can promote colonization and growth of ESR1 mutant cells.
S5. Clonogenic survival assay and 2D growth assay to test RXR
response in Park and Gertz MCF7 cell models.
S6. FOXA1 knockdown drastically attenuated the base line growth of both ESR1 WT and mutant cells.
S7. RXR antagonist HX531 can inhibit the response of ESR1 mutant
cells to RXR agonist.
S8. RXR antagonist HX531 can inhibit the basal and agonist
promoted growth of IPM-PDXO-073 organoid.
Figure S8 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 S8
Supplementary Table 8 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

RNA PolII Pause Index Analysis from MOLM13 RBP1 CUT&Tag (6 Hours After Drug Treatment)
Supplementary Table 4 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

Transcription Factor Enrichment Analysis of Differentially Downregulated Genes by The Drug Combination Previously Identified as Depleting Genes in a Genome-Wide CRISPR Dropout Screen
Supplementary Table 18 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

Single Cell ATAC Cell Type Populations
Supplementary Table 17 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

GSEA of Primary AML Bulk RNA-Seq (24 Hours After Drug Treatment)
Supplementary Table 15 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

Log2 Normalized Counts of Differentially Expressed Genes from Primary AML Blast Bulk RNA-seq (24 Hours After Drug Treatment)
Supplementary Table 1 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

Log2 Normalized Counts of Differentially Expressed Genes from MOLM13 Bulk RNA-seq (24 Hours After Drug Treatment)
Supplementary Materials and Methods 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

Supplementary Materials and Methods
Supplementary Fig. 10 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

Efficacy of dual FLT3/LSD1 inhibition in primary AML samples.