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View article: Supplementary Figures and Table from Inhibitor of Apoptosis Proteins Antagonist Induces T-cell Proliferation after Cross-Presentation by Dendritic Cells
Supplementary Figures and Table from Inhibitor of Apoptosis Proteins Antagonist Induces T-cell Proliferation after Cross-Presentation by Dendritic Cells Open
Supplementary Data file, Figure S1-S9, Table S1
View article: Cholesterol biosynthesis as a drug-induced vulnerability in diffuse large B cell lymphoma insensitive to EZH2 inhibition
Cholesterol biosynthesis as a drug-induced vulnerability in diffuse large B cell lymphoma insensitive to EZH2 inhibition Open
View article: Epigenetic profiling identifies markers of endocrine resistance and therapeutic options for metastatic castration-resistant prostate cancer
Epigenetic profiling identifies markers of endocrine resistance and therapeutic options for metastatic castration-resistant prostate cancer Open
View article: A functionally validated TCR-pMHC database for TCR specificity model development
A functionally validated TCR-pMHC database for TCR specificity model development Open
Summary Accurate prediction of TCR specificity forms a holy grail in immunology and large language models and computational structure predictions provide a path to achieve this. Importantly, current TCR-pMHC prediction models have been tra…
View article: Molecular dependencies and genomic consequences of a global DNA damage tolerance defect
Molecular dependencies and genomic consequences of a global DNA damage tolerance defect Open
Our data highlight the essential contribution of the DDT system to genome maintenance and type 3 deletions as mutational signature of replication stress. The unique characteristics of type 3 deletions implicate the existence of a novel del…
View article: Mixing time of the torus shuffle
Mixing time of the torus shuffle Open
We prove a theorem that reduces bounding the mixing time of a card shuffle to verifying a condition that involves only triplets of cards. Then we use it to analyze a classic model of card shuffling. In 1988, Diaconis introduced the followi…
View article: Figure S5 from Paradoxical Activation of Oncogenic Signaling as a Cancer Treatment Strategy
Figure S5 from Paradoxical Activation of Oncogenic Signaling as a Cancer Treatment Strategy Open
Figure S5: Combined toxicity of LB-100 and Adavosertib in PDAC and CCA models (A) and (B) Dose-response assays show the effect of LB-100 or Adavosertib in 4 PDAC and 4 CCA models, respectively. Cell viability was estimated by resazurin flu…
View article: Table S5 from Paradoxical Activation of Oncogenic Signaling as a Cancer Treatment Strategy
Table S5 from Paradoxical Activation of Oncogenic Signaling as a Cancer Treatment Strategy Open
Supplementary table 5: Stress-focused drug screens AUC differences in HT-29 cells Area Under the Curve (AUC) from each compound of the stress-focused drug screen in the presence or absence of LB-100. Compounds are ranked by the difference …
View article: Data from Paradoxical Activation of Oncogenic Signaling as a Cancer Treatment Strategy
Data from Paradoxical Activation of Oncogenic Signaling as a Cancer Treatment Strategy Open
Cancer homeostasis depends on a balance between activated oncogenic pathways driving tumorigenesis and engagement of stress response programs that counteract the inherent toxicity of such aberrant signaling. Although inhibition of oncogeni…
View article: Figure S1 from Paradoxical Activation of Oncogenic Signaling as a Cancer Treatment Strategy
Figure S1 from Paradoxical Activation of Oncogenic Signaling as a Cancer Treatment Strategy Open
Figure S1: LB-100 engages stress-related, inflammatory response, and mitogenic signaling transcriptional programs in CRC cells (A) Dose-response assays show the effect of LB-100 in 7 CRC models. Cell viability was estimated by resazurin fl…
View article: Data from Paradoxical Activation of Oncogenic Signaling as a Cancer Treatment Strategy
Data from Paradoxical Activation of Oncogenic Signaling as a Cancer Treatment Strategy Open
Cancer homeostasis depends on a balance between activated oncogenic pathways driving tumorigenesis and engagement of stress response programs that counteract the inherent toxicity of such aberrant signaling. Although inhibition of oncogeni…
View article: Figure S2 from Paradoxical Activation of Oncogenic Signaling as a Cancer Treatment Strategy
Figure S2 from Paradoxical Activation of Oncogenic Signaling as a Cancer Treatment Strategy Open
Figure S1: LB-100 engages stress-related, inflammatory response, and mitogenic signaling transcriptional programs in CRC cells (A) Dose-response assays show the effect of LB-100 in 7 CRC models. Cell viability was estimated by resazurin fl…
View article: Figure S1 from Paradoxical Activation of Oncogenic Signaling as a Cancer Treatment Strategy
Figure S1 from Paradoxical Activation of Oncogenic Signaling as a Cancer Treatment Strategy Open
Figure S1: LB-100 engages stress-related, inflammatory response, and mitogenic signaling transcriptional programs in CRC cells (A) Dose-response assays show the effect of LB-100 in 7 CRC models. Cell viability was estimated by resazurin fl…
View article: Figure S2 from Paradoxical Activation of Oncogenic Signaling as a Cancer Treatment Strategy
Figure S2 from Paradoxical Activation of Oncogenic Signaling as a Cancer Treatment Strategy Open
Figure S1: LB-100 engages stress-related, inflammatory response, and mitogenic signaling transcriptional programs in CRC cells (A) Dose-response assays show the effect of LB-100 in 7 CRC models. Cell viability was estimated by resazurin fl…
View article: Table S7 from Paradoxical Activation of Oncogenic Signaling as a Cancer Treatment Strategy
Table S7 from Paradoxical Activation of Oncogenic Signaling as a Cancer Treatment Strategy Open
Supplementary table 7: Full list of genes whose knockout was selectively toxic in the presence of LB-100 in SW-480 cells in the CRISPR-KO screen FDR smaller or equal to 0.25 and log2 fold change smaller or equal to -1 in treated/untreated …
View article: Table S3 from Paradoxical Activation of Oncogenic Signaling as a Cancer Treatment Strategy
Table S3 from Paradoxical Activation of Oncogenic Signaling as a Cancer Treatment Strategy Open
Supplementary table 3: Full list of genes whose knockout attenuated LB-100 toxicity in SW-480 cells in the CRISPR-KO screen FDR smaller or equal to 0.25 and log2 fold change greater or equal to 1 in treated/untreated comparison were criter…
View article: Figure S10 from Paradoxical Activation of Oncogenic Signaling as a Cancer Treatment Strategy
Figure S10 from Paradoxical Activation of Oncogenic Signaling as a Cancer Treatment Strategy Open
Figure S10: Acquired resistance to the combination of LB-100 and Adavosertib suppress anchorage-independent and tumor growth in CRC models (A) Endpoint proliferation of HT-29 and SW-480 parental and resistant cells growing attached or in a…
View article: Figure S4 from Paradoxical Activation of Oncogenic Signaling as a Cancer Treatment Strategy
Figure S4 from Paradoxical Activation of Oncogenic Signaling as a Cancer Treatment Strategy Open
Figure S4: Combined toxicity of LB-100 and Adavosertib in CRC models (A) Dose-response assays show the effect of Adavosertib in 7 CRC models. Cell viability was estimated by resazurin fluorescence after 5 days in the presence of the drug o…
View article: Table S7 from Paradoxical Activation of Oncogenic Signaling as a Cancer Treatment Strategy
Table S7 from Paradoxical Activation of Oncogenic Signaling as a Cancer Treatment Strategy Open
Supplementary table 7: Full list of genes whose knockout was selectively toxic in the presence of LB-100 in SW-480 cells in the CRISPR-KO screen FDR smaller or equal to 0.25 and log2 fold change smaller or equal to -1 in treated/untreated …
View article: Table S4 from Paradoxical Activation of Oncogenic Signaling as a Cancer Treatment Strategy
Table S4 from Paradoxical Activation of Oncogenic Signaling as a Cancer Treatment Strategy Open
Supplementary table 4: The composition of the stress-focused drug library Compounds comprising the stress-focused drug library with their respective targets.
View article: Figure S7 from Paradoxical Activation of Oncogenic Signaling as a Cancer Treatment Strategy
Figure S7 from Paradoxical Activation of Oncogenic Signaling as a Cancer Treatment Strategy Open
Figure S7: Normal tissues from the orthotopic CRC PDXs are not affected by LB-100, adavosertib, or the combination. Representative Hematoxylin & Eosin (H&E) stainings of the heart, liver, lung, and spleen from the PDOX1 PDXs treated as ind…
View article: Table S1 from Paradoxical Activation of Oncogenic Signaling as a Cancer Treatment Strategy
Table S1 from Paradoxical Activation of Oncogenic Signaling as a Cancer Treatment Strategy Open
Supplementary table 1: Cancer cell lines with oncogenic drivers The mutational status of the cell lines was compiled from the ATCC, Catalogue of Somatic Mutations in Cancer (COSMIC) and Cell Model Passport, Wellcome Trust Sanger Institute,…
View article: Figure S8 from Paradoxical Activation of Oncogenic Signaling as a Cancer Treatment Strategy
Figure S8 from Paradoxical Activation of Oncogenic Signaling as a Cancer Treatment Strategy Open
Figure S8: Acquired resistance to the combination of LB-100 and adavosertib suppressed malignant traits in CRC models (A) IncuCyte-based proliferation assays from HT-29 and SW-480 parental and resistant cells in the absence or presence of …
View article: Figure S6 from Paradoxical Activation of Oncogenic Signaling as a Cancer Treatment Strategy
Figure S6 from Paradoxical Activation of Oncogenic Signaling as a Cancer Treatment Strategy Open
Figure S6: LB-100 and adavosertib induce histological response in orthotopic CRC PDXs (A) Representative Hematoxylin & Eosin (H&E) stainings at endpoint from PDOX2 and PDOX3 treated as indicated. Original magnification middle images: 15x, …
View article: Figure S3 from Paradoxical Activation of Oncogenic Signaling as a Cancer Treatment Strategy
Figure S3 from Paradoxical Activation of Oncogenic Signaling as a Cancer Treatment Strategy Open
Figure S3: High N-Myc levels sensitize neuroblastoma cells to LB-100, and PP2A knockdown sensitizes CRC cells to WEE1 inhibition (A) Western blots comparing N-Myc levels in isogenic neuroblastoma models. GAPDH was used as a loading control…
View article: Table S6 from Paradoxical Activation of Oncogenic Signaling as a Cancer Treatment Strategy
Table S6 from Paradoxical Activation of Oncogenic Signaling as a Cancer Treatment Strategy Open
Supplementary table 6: Stress-focused drug screens AUC differences in SW-480 cells Area Under the Curve (AUC) from each compound of the stress-focused drug screen in the presence or absence of LB-100. Compounds are ranked by the difference…
View article: Table S5 from Paradoxical Activation of Oncogenic Signaling as a Cancer Treatment Strategy
Table S5 from Paradoxical Activation of Oncogenic Signaling as a Cancer Treatment Strategy Open
Supplementary table 5: Stress-focused drug screens AUC differences in HT-29 cells Area Under the Curve (AUC) from each compound of the stress-focused drug screen in the presence or absence of LB-100. Compounds are ranked by the difference …
View article: Figure S4 from Paradoxical Activation of Oncogenic Signaling as a Cancer Treatment Strategy
Figure S4 from Paradoxical Activation of Oncogenic Signaling as a Cancer Treatment Strategy Open
Figure S4: Combined toxicity of LB-100 and Adavosertib in CRC models (A) Dose-response assays show the effect of Adavosertib in 7 CRC models. Cell viability was estimated by resazurin fluorescence after 5 days in the presence of the drug o…
View article: Figure S8 from Paradoxical Activation of Oncogenic Signaling as a Cancer Treatment Strategy
Figure S8 from Paradoxical Activation of Oncogenic Signaling as a Cancer Treatment Strategy Open
Figure S8: Acquired resistance to the combination of LB-100 and adavosertib suppressed malignant traits in CRC models (A) IncuCyte-based proliferation assays from HT-29 and SW-480 parental and resistant cells in the absence or presence of …
View article: Figure S10 from Paradoxical Activation of Oncogenic Signaling as a Cancer Treatment Strategy
Figure S10 from Paradoxical Activation of Oncogenic Signaling as a Cancer Treatment Strategy Open
Figure S10: Acquired resistance to the combination of LB-100 and Adavosertib suppress anchorage-independent and tumor growth in CRC models (A) Endpoint proliferation of HT-29 and SW-480 parental and resistant cells growing attached or in a…