bluuebunny/crossref_metadata_2025 huggingface dataset:
Supplementary figure legends from Glucocorticoid Receptor (GR) Activation Is Associated with Increased cAMP/PKA Signaling in Castration-Resistant Prostate Cancer
Authors: Bennett Lynda , Jaiswal Praveen Kumar , Harkless Ryan V. , Long Tiha M. , Gao Ning , Vandenburg Brianna , Selman Phillip , Durdana Ishrat , Lastra Ricardo R. , Vander Griend Donald , Adelaiye-Ogala Remi , Szmulewitz Russell Z. , Conzen Suzanne D.
Published: April 2024

Supplementary figure legends
Supplementary Figure 13 from Oncogenic Cells of Renal Embryonic Lineage Sensitive to the Small-Molecule Inhibitor QC6352 Display Depletion of KDM4 Levels and Disruption of Ribosome Biogenesis
Authors: Pichavaram Prahalathan , Jablonowski Carolyn M. , Fang Jie , Fleming Andrew M. , Gil Hyea Jin , Boghossian Andrew S. , Rees Matthew G. , Ronan Melissa M. , Roth Jennifer A. , Morton Christopher L. , Zambetti Gerard P. , Davidoff Andrew M. , Yang Jun , Murphy Andrew J.
Published: April 2024

Knockdown of KDM4A alters QC6352 sensitivity. (A) The PrestoBlue assay demonstrated that siRNA-mediated knockdown of KDM4A and C was associated with resistance to QC6352 when compared to parental cells and empty vector control in WiT49. (B) The PrestoBlue assay demonstrated that siRNA-mediated knockdown of KDM4A was associated with resistance to QC6352 when compared to parental cells and empty vector control in HEK293. (C)IC50 values for WiT49 and HEK293 with siKDM4A-C and NTC siRNA.
Supplementary Figure 11 from Oncogenic Cells of Renal Embryonic Lineage Sensitive to the Small-Molecule Inhibitor QC6352 Display Depletion of KDM4 Levels and Disruption of Ribosome Biogenesis
Authors: Pichavaram Prahalathan , Jablonowski Carolyn M. , Fang Jie , Fleming Andrew M. , Gil Hyea Jin , Boghossian Andrew S. , Rees Matthew G. , Ronan Melissa M. , Roth Jennifer A. , Morton Christopher L. , Zambetti Gerard P. , Davidoff Andrew M. , Yang Jun , Murphy Andrew J.
Published: April 2024

Gene set enrichment analysis demonstrated significant alteration of the GO_CHROMATIN_SILENCING_AT_RDNA pathways in WiT49 and HEK293 cells treated with QC6352.
Supplementary Figure 1 from Oncogenic Cells of Renal Embryonic Lineage Sensitive to the Small-Molecule Inhibitor QC6352 Display Depletion of KDM4 Levels and Disruption of Ribosome Biogenesis
Authors: Pichavaram Prahalathan , Jablonowski Carolyn M. , Fang Jie , Fleming Andrew M. , Gil Hyea Jin , Boghossian Andrew S. , Rees Matthew G. , Ronan Melissa M. , Roth Jennifer A. , Morton Christopher L. , Zambetti Gerard P. , Davidoff Andrew M. , Yang Jun , Murphy Andrew J.
Published: April 2024

KDM4A expression is upregulated in Wilms tumor and potentially associated with prognosis. (A) RNA-seq log2(FPKM) data demonstrated increased expression of KDM4A in Wilms tumor compared to fetal kidney (p=0.0015) and normal kidney (p=0.0434) samples. (B) Kaplan-Meier analysis (minimum group size 8, “high” expression determined by R2: Genomics Analysis and Visualization KaplanScanner tool) of gene expression microarray data from the NCI-TARGET discovery dataset (n=124 samples, exclusively anaplastic or relapsed favorable histology Wilms tumor) demonstrated a nonsignificant association between high expression of KDM4A and inferior overall survival probability (p=0.343). (C) However, in the NCI-TARGET validation dataset (n=148 samples, primarily favorable histology Wilms tumor), a significant association was found between high expression of KDM4A and inferior overall survival probability (p<0.0001). These relationships were not found in association with KDM4B (D-F) or KDM4C (G-I) expression.
Supplementary Data File 2 from Oncogenic Cells of Renal Embryonic Lineage Sensitive to the Small-Molecule Inhibitor QC6352 Display Depletion of KDM4 Levels and Disruption of Ribosome Biogenesis
Authors: Pichavaram Prahalathan , Jablonowski Carolyn M. , Fang Jie , Fleming Andrew M. , Gil Hyea Jin , Boghossian Andrew S. , Rees Matthew G. , Ronan Melissa M. , Roth Jennifer A. , Morton Christopher L. , Zambetti Gerard P. , Davidoff Andrew M. , Yang Jun , Murphy Andrew J.
Published: April 2024

RNA-seq gene set enrichment analysis for siRNA KDM4 A, B, C, A-C, and non-targeting control in WiT49 cells
Supplementary Figure S2 from Cereblon-based Bifunctional Degrader of SOS1, BTX-6654, Targets Multiple KRAS Mutations and Inhibits Tumor Growth
Authors: Begovich Kyle , Schoolmeesters Angela , Rajapakse Navin , Martinez-Terroba Elena , Kumar Maneesh , Shakya Arvind , Lai Chon , Greene Steven , Whitefield Brandon , Okano Akinori , Mali Venkat , Huang Shenlin , Chourasia Aparajita H. , Fung Leah
Published: April 2024

Supplementary Figure S2 shows the degradation-driven antiproliferative activity of BTX-6654 and BTX-7312 in K562 cells
Supplementary Figure S1 from Cereblon-based Bifunctional Degrader of SOS1, BTX-6654, Targets Multiple KRAS Mutations and Inhibits Tumor Growth
Authors: Begovich Kyle , Schoolmeesters Angela , Rajapakse Navin , Martinez-Terroba Elena , Kumar Maneesh , Shakya Arvind , Lai Chon , Greene Steven , Whitefield Brandon , Okano Akinori , Mali Venkat , Huang Shenlin , Chourasia Aparajita H. , Fung Leah
Published: April 2024

Supplementary Figure S1 displays the effects of SOS1 degraders on SOS1-complex interactors and neosusbstrates
Supplementary Table S3 from Neutrophil Elastase Remodels Mammary Tumors to Facilitate Lung Metastasis
Authors: Lulla Amriti R. , Akli Said , Karakas Cansu , Caruso Joseph A. , Warma Lucas D. , Fowlkes Natalie W. , Rao Xiayu , Wang Jing , Hunt Kelly K. , Watowich Stephanie S. , Keyomarsi Khandan
Published: April 2024

Immune subsets and their associated cell surface markers used for gating in flow cytometric analysis
Supplementary Materials and Methods 1 from Neutrophil Elastase Remodels Mammary Tumors to Facilitate Lung Metastasis
Authors: Lulla Amriti R. , Akli Said , Karakas Cansu , Caruso Joseph A. , Warma Lucas D. , Fowlkes Natalie W. , Rao Xiayu , Wang Jing , Hunt Kelly K. , Watowich Stephanie S. , Keyomarsi Khandan
Published: April 2024

Supplementary Materials and Methods, clean copy version
Figure S8 from Neutrophil Elastase Remodels Mammary Tumors to Facilitate Lung Metastasis
Authors: Lulla Amriti R. , Akli Said , Karakas Cansu , Caruso Joseph A. , Warma Lucas D. , Fowlkes Natalie W. , Rao Xiayu , Wang Jing , Hunt Kelly K. , Watowich Stephanie S. , Keyomarsi Khandan
Published: April 2024

Supplementary Figure S8: (A) PK data for AZD9668, when administered by intraperitoneal (I.P.) injection at a concentration of 100mg/kg. N=3 mice were used per timepoint, and the t1/2 of the drug was calculated to 2.16 hours. (B) Specificity of AZD9668 to inhibit NE activity was confirmed in vitro using a NE-specific substrate, under indicated doses of AZD9668. AZD5069 (CXCR2 antagonist) was used as a negative control. (C) Whole body weights of PyMT NE+/+ mice treated with either Vehicle (black) or 100mg/kg AZD9668 (pink) every day, BID for 60 consecutive days. (D, E) Western blot analysis done on endpoint tumors, to confirm NE activity in (D) PyMT NE+/+ and PyMT NE-/- mice and (E) PyMT NE+/+ mice treated with either Vehicle or 100mg/kg AZD9668, as described in Figure 5 of main text.
Figure S7 from Neutrophil Elastase Remodels Mammary Tumors to Facilitate Lung Metastasis
Authors: Lulla Amriti R. , Akli Said , Karakas Cansu , Caruso Joseph A. , Warma Lucas D. , Fowlkes Natalie W. , Rao Xiayu , Wang Jing , Hunt Kelly K. , Watowich Stephanie S. , Keyomarsi Khandan
Published: April 2024

Supplementary Figure S7: Recurrence-free survival (A) and overall survival (C) for each individual gene used in the METABRIC patient cohort signature and progression-free survival (B) and overall survival (D) used in the and TCGA patient cohort signature.
Figure S4 from Neutrophil Elastase Remodels Mammary Tumors to Facilitate Lung Metastasis
Authors: Lulla Amriti R. , Akli Said , Karakas Cansu , Caruso Joseph A. , Warma Lucas D. , Fowlkes Natalie W. , Rao Xiayu , Wang Jing , Hunt Kelly K. , Watowich Stephanie S. , Keyomarsi Khandan
Published: April 2024

Supplementary Figure S4: A focused T-cell subset of immune cells composed of naïve, memory and regulatory T-cell markers was interrogated in 12-week old PyMT NE+/+ (N=4) and PyMT NE-
/- (N=3) mice. The percentage of each cell type (normalized to % CD45 cells) is shown. �45 cells were normalized to the live cell population in each tissue.
Figure S3 from Neutrophil Elastase Remodels Mammary Tumors to Facilitate Lung Metastasis
Authors: Lulla Amriti R. , Akli Said , Karakas Cansu , Caruso Joseph A. , Warma Lucas D. , Fowlkes Natalie W. , Rao Xiayu , Wang Jing , Hunt Kelly K. , Watowich Stephanie S. , Keyomarsi Khandan
Published: April 2024

Supplementary Figure S3: The immune milieu is unchanged between PyMT tumor bearing NE+/+ and NE-/- mice. A basic panel of immune cells composed of myeloid cells (neutrophils, monocytes, and macrophages), T-cells and B-cells was interrogated in 12-week old PyMT NE+/+ (N=5) and PyMT NE-/- (N=5) mice. (A) The total cell counts of each cell type is shown. Counts were obtained by normalizing to the CD45 counts, per mg of tissue. (B) The percentage of each cell type (interrogated in panel A and normalized to % CD45+ cells) is shown. �45 cells were normalized to the live cell population in each tissue.
Figure S2 from Neutrophil Elastase Remodels Mammary Tumors to Facilitate Lung Metastasis
Authors: Lulla Amriti R. , Akli Said , Karakas Cansu , Caruso Joseph A. , Warma Lucas D. , Fowlkes Natalie W. , Rao Xiayu , Wang Jing , Hunt Kelly K. , Watowich Stephanie S. , Keyomarsi Khandan
Published: April 2024

Supplementary Figure S2: (A) Percentage of tumor-free mice in PyMT NE+/+ (N=30) and PyMT NE-/- (N=21) mice, between 12-14 weeks of age. (B) Total tumor mass, (C) number of glands with tumors per mouse and (D) doubling time of tumors at end point (12-14 weeks age) in PyMT NE+/+ & PyMT NE-/- mice. (E) Frequency of the major histologies (solid, alveolar/tubular, papillary, and adenosquamous) detected in both PyMT NE+/+ and PyMT NE-/- primary tumors.
(F) Spontaneous tumors isolated from PyMT NE+/+ and PyMT NE-/- mice were implanted in FVB NE+/+ and FVB NE-/- respectively. Tumor growth curves, as a function of days post implantation are shown.
Table S7 from Development of a Novel DNA Mono-alkylator Platform for Antibody–Drug Conjugates
Authors: Thomas Joshua D. , Yurkovetskiy Aleksandr V. , Yin Mao , Bodyak Natalya D. , Tang Shuyi , Protopopova Marina , Kelleher Eugene , Jones Brian , Yang Liping , Custar Daniel , Catcott Kalli C. , Demady Damon R. , Collins Scott D. , Xu Ling , Bu Charlie , Qin LiuLiang , Ter-Ovanesyan Elena , Damelin Marc , Toader Dorin , Lowinger Timothy B.
Published: April 2024

Table shows Cytotoxicity comparisons between Biaryl PBD ADCs vs DGN549 ADCs
Supplemental Table S6 from The Methyltransferases METTL7A and METTL7B Confer Resistance to Thiol-Based Histone Deacetylase Inhibitors
Authors: Robey Robert W. , Fitzsimmons Christina M. , Guiblet Wilfried M. , Frye William J.E. , González Dalmasy José M. , Wang Li , Russell Drake A. , Huff Lyn M. , Perciaccante Andrew J. , Ali-Rahmani Fatima , Lipsey Crystal C. , Wade Heidi M. , Mitchell Allison V. , Maligireddy Siddhardha S. , Terrero David , Butcher Donna , Edmondson Elijah F. , Jenkins Lisa M. , Nikitina Tatiana , Zhurkin Victor B. , Tiwari Amit K. , Piscopio Anthony D. , Totah Rheem A. , Bates Susan E. , Arda H. Efsun , Gottesman Michael M. , Batista Pedro J.
Published: April 2024

Supplemental Table S6 contains information about the cross-resistance profile of the Vector, 7A 1-2, 7A 1-4, 7B 1-3 and 7B 2-2 cells
Table S6 from Development of a Novel DNA Mono-alkylator Platform for Antibody–Drug Conjugates
Authors: Thomas Joshua D. , Yurkovetskiy Aleksandr V. , Yin Mao , Bodyak Natalya D. , Tang Shuyi , Protopopova Marina , Kelleher Eugene , Jones Brian , Yang Liping , Custar Daniel , Catcott Kalli C. , Demady Damon R. , Collins Scott D. , Xu Ling , Bu Charlie , Qin LiuLiang , Ter-Ovanesyan Elena , Damelin Marc , Toader Dorin , Lowinger Timothy B.
Published: April 2024

Table shows Cytotoxicity comparisons between Biaryl PBD payloads 4 and 20 vs IGN 2
Table S5 from Development of a Novel DNA Mono-alkylator Platform for Antibody–Drug Conjugates
Authors: Thomas Joshua D. , Yurkovetskiy Aleksandr V. , Yin Mao , Bodyak Natalya D. , Tang Shuyi , Protopopova Marina , Kelleher Eugene , Jones Brian , Yang Liping , Custar Daniel , Catcott Kalli C. , Demady Damon R. , Collins Scott D. , Xu Ling , Bu Charlie , Qin LiuLiang , Ter-Ovanesyan Elena , Damelin Marc , Toader Dorin , Lowinger Timothy B.
Published: April 2024

Table shows TROP2 receptor quantification on DLD1 and HT29 cells
Table S4 from Development of a Novel DNA Mono-alkylator Platform for Antibody–Drug Conjugates
Authors: Thomas Joshua D. , Yurkovetskiy Aleksandr V. , Yin Mao , Bodyak Natalya D. , Tang Shuyi , Protopopova Marina , Kelleher Eugene , Jones Brian , Yang Liping , Custar Daniel , Catcott Kalli C. , Demady Damon R. , Collins Scott D. , Xu Ling , Bu Charlie , Qin LiuLiang , Ter-Ovanesyan Elena , Damelin Marc , Toader Dorin , Lowinger Timothy B.
Published: April 2024

Table shows Impact of Tether length and Hydrophilic Modifier on ADC Aggregation and Hydrophobicity
Supplemental Table S4 from The Methyltransferases METTL7A and METTL7B Confer Resistance to Thiol-Based Histone Deacetylase Inhibitors
Authors: Robey Robert W. , Fitzsimmons Christina M. , Guiblet Wilfried M. , Frye William J.E. , González Dalmasy José M. , Wang Li , Russell Drake A. , Huff Lyn M. , Perciaccante Andrew J. , Ali-Rahmani Fatima , Lipsey Crystal C. , Wade Heidi M. , Mitchell Allison V. , Maligireddy Siddhardha S. , Terrero David , Butcher Donna , Edmondson Elijah F. , Jenkins Lisa M. , Nikitina Tatiana , Zhurkin Victor B. , Tiwari Amit K. , Piscopio Anthony D. , Totah Rheem A. , Bates Susan E. , Arda H. Efsun , Gottesman Michael M. , Batista Pedro J.
Published: April 2024

Supplemental Table S4 contains information about the cross-resistance profile of MCF7 DpVp300 cells with thiol-based HDACis
Table S3 from Development of a Novel DNA Mono-alkylator Platform for Antibody–Drug Conjugates
Authors: Thomas Joshua D. , Yurkovetskiy Aleksandr V. , Yin Mao , Bodyak Natalya D. , Tang Shuyi , Protopopova Marina , Kelleher Eugene , Jones Brian , Yang Liping , Custar Daniel , Catcott Kalli C. , Demady Damon R. , Collins Scott D. , Xu Ling , Bu Charlie , Qin LiuLiang , Ter-Ovanesyan Elena , Damelin Marc , Toader Dorin , Lowinger Timothy B.
Published: April 2024

Table shows Payload in vitro potency in various cell lines.
Figure S8 from Development of a Novel DNA Mono-alkylator Platform for Antibody–Drug Conjugates
Authors: Thomas Joshua D. , Yurkovetskiy Aleksandr V. , Yin Mao , Bodyak Natalya D. , Tang Shuyi , Protopopova Marina , Kelleher Eugene , Jones Brian , Yang Liping , Custar Daniel , Catcott Kalli C. , Demady Damon R. , Collins Scott D. , Xu Ling , Bu Charlie , Qin LiuLiang , Ter-Ovanesyan Elena , Damelin Marc , Toader Dorin , Lowinger Timothy B.
Published: April 2024

Figure shows Cytotoxicity of Mesothelin ADCs M-16, M-17, and M-19 in NCI-N87 cell line
Figure S7 from Development of a Novel DNA Mono-alkylator Platform for Antibody–Drug Conjugates
Authors: Thomas Joshua D. , Yurkovetskiy Aleksandr V. , Yin Mao , Bodyak Natalya D. , Tang Shuyi , Protopopova Marina , Kelleher Eugene , Jones Brian , Yang Liping , Custar Daniel , Catcott Kalli C. , Demady Damon R. , Collins Scott D. , Xu Ling , Bu Charlie , Qin LiuLiang , Ter-Ovanesyan Elena , Damelin Marc , Toader Dorin , Lowinger Timothy B.
Published: April 2024

Figure shows Efficacy in OVCAR-3 xenograft for A) targeted ADCs X-17 and X-19 and B) their corresponding non-binding control ADCs NB-17 and NB-19
Figure S6 from Development of a Novel DNA Mono-alkylator Platform for Antibody–Drug Conjugates
Authors: Thomas Joshua D. , Yurkovetskiy Aleksandr V. , Yin Mao , Bodyak Natalya D. , Tang Shuyi , Protopopova Marina , Kelleher Eugene , Jones Brian , Yang Liping , Custar Daniel , Catcott Kalli C. , Demady Damon R. , Collins Scott D. , Xu Ling , Bu Charlie , Qin LiuLiang , Ter-Ovanesyan Elena , Damelin Marc , Toader Dorin , Lowinger Timothy B.
Published: April 2024

Figure shows comet assay results
Figure S4 from Development of a Novel DNA Mono-alkylator Platform for Antibody–Drug Conjugates
Authors: Thomas Joshua D. , Yurkovetskiy Aleksandr V. , Yin Mao , Bodyak Natalya D. , Tang Shuyi , Protopopova Marina , Kelleher Eugene , Jones Brian , Yang Liping , Custar Daniel , Catcott Kalli C. , Demady Damon R. , Collins Scott D. , Xu Ling , Bu Charlie , Qin LiuLiang , Ter-Ovanesyan Elena , Damelin Marc , Toader Dorin , Lowinger Timothy B.
Published: April 2024

Figure shows In vitro activity of NaPi2b ADCs X-BG and X-19 and payload 4 in the OVCAR3 cell line
Figure S3 from Development of a Novel DNA Mono-alkylator Platform for Antibody–Drug Conjugates
Authors: Thomas Joshua D. , Yurkovetskiy Aleksandr V. , Yin Mao , Bodyak Natalya D. , Tang Shuyi , Protopopova Marina , Kelleher Eugene , Jones Brian , Yang Liping , Custar Daniel , Catcott Kalli C. , Demady Damon R. , Collins Scott D. , Xu Ling , Bu Charlie , Qin LiuLiang , Ter-Ovanesyan Elena , Damelin Marc , Toader Dorin , Lowinger Timothy B.
Published: April 2024

Figure shows DLD1 xenograft study comparing Biaryl PBD ADCs hR-13 vs hR-DGN549
Figure S2 from Development of a Novel DNA Mono-alkylator Platform for Antibody–Drug Conjugates
Authors: Thomas Joshua D. , Yurkovetskiy Aleksandr V. , Yin Mao , Bodyak Natalya D. , Tang Shuyi , Protopopova Marina , Kelleher Eugene , Jones Brian , Yang Liping , Custar Daniel , Catcott Kalli C. , Demady Damon R. , Collins Scott D. , Xu Ling , Bu Charlie , Qin LiuLiang , Ter-Ovanesyan Elena , Damelin Marc , Toader Dorin , Lowinger Timothy B.
Published: April 2024

Figure shows Structures of Platforms 6, and 8-16
Data from Multiomic-Based Molecular Landscape of FaDu Xenograft Tumors in Mice after a Combinatorial Treatment with Radiation and an HSP90 Inhibitor Identifies Adaptation-Induced Targets of Resistance and Therapeutic Intervention
Authors: Bylicky Michelle A. , Shankavaram Uma , Aryankalayil Molykutty J. , Chopra Sunita , Naz Sarwat , Sowers Anastasia L. , Choudhuri Rajani , Calvert Valerie , Petricoin Emanuel F. , Eke Iris , Mitchell James B. , Coleman C. Norman
Published: April 2024

Abstract
Treatments involving radiation and chemotherapy alone or in combination have improved patient survival and quality of life. However, cancers frequently evade these therapies due to adaptation and tumor evolution. Given the complexity of predicting response based solely on the initial genetic profile of a patient, a predetermined treatment course may miss critical adaptation that can cause resistance or induce new targets for drug and immunotherapy. To address the timescale for these evasive mechanisms, using a mouse xenograft tumor model, we investigated the rapidity of gene expression (mRNA), molecular pathway, and phosphoproteome changes after radiation, an HSP90 inhibitor, or combination. Animals received radiation, drug, or combination treatment for 1 or 2 weeks and were then euthanized along with a time-matched untreated group for comparison. Changes in gene expression occur as early as 1 week after treatment initiation. Apoptosis and cell death pathways were activated in irradiated tumor samples. For the HSP90 inhibitor and combination treatment at weeks 1 and 2 compared with Control Day 1, gene-expression changes induced inhibition of pathways including invasion of cells, vasculogenesis, and viral infection among others. The combination group included both drug-alone and radiation-alone changes. Our data demonstrate the rapidity of gene expression and functional pathway changes in the evolving tumor as it responds to treatment. Discovering these phenotypic adaptations may help elucidate the challenges in using sustained treatment regimens and could also define evolving targets for therapeutic efficacy.
Data from Oncogenic Cells of Renal Embryonic Lineage Sensitive to the Small-Molecule Inhibitor QC6352 Display Depletion of KDM4 Levels and Disruption of Ribosome Biogenesis
Authors: Pichavaram Prahalathan , Jablonowski Carolyn M. , Fang Jie , Fleming Andrew M. , Gil Hyea Jin , Boghossian Andrew S. , Rees Matthew G. , Ronan Melissa M. , Roth Jennifer A. , Morton Christopher L. , Zambetti Gerard P. , Davidoff Andrew M. , Yang Jun , Murphy Andrew J.
Published: April 2024

Abstract
The histone lysine demethylases KDM4A-C are involved in physiologic processes including stem cell identity and self-renewal during development, DNA damage repair, and cell-cycle progression. KDM4A-C are overexpressed and associated with malignant cell behavior in multiple human cancers and are therefore potential therapeutic targets. Given the role of KDM4A-C in development and cancer, we aimed to test the potent, selective KDM4A-C inhibitor QC6352 on oncogenic cells of renal embryonic lineage. The anaplastic Wilms tumor cell line WiT49 and the tumor-forming human embryonic kidney cell line HEK293 demonstrated low nanomolar QC6352 sensitivity. The cytostatic response to QC6352 in WiT49 and HEK293 cells was marked by induction of DNA damage, a DNA repair–associated protein checkpoint response, S-phase cell-cycle arrest, profound reduction of ribosomal protein gene and rRNA transcription, and blockade of newly synthesized proteins. QC6352 caused reduction of KDM4A-C levels by a proteasome-associated mechanism. The cellular phenotype caused by QC6352 treatment of reduced migration, proliferation, tumor spheroid growth, DNA damage, and S-phase cell-cycle arrest was most closely mirrored by knockdown of KDM4A as determined by siRNA knockdown of KDM4A-C. QC6352 sensitivity correlated with high basal levels of ribosomal gene transcription in more than 900 human cancer cell lines. Targeting KDM4A may be of future therapeutic interest in oncogenic cells of embryonic renal lineage or cells with high basal expression of ribosomal protein genes.
Data from Glucocorticoid Receptor (GR) Activation Is Associated with Increased cAMP/PKA Signaling in Castration-Resistant Prostate Cancer
Authors: Bennett Lynda , Jaiswal Praveen Kumar , Harkless Ryan V. , Long Tiha M. , Gao Ning , Vandenburg Brianna , Selman Phillip , Durdana Ishrat , Lastra Ricardo R. , Vander Griend Donald , Adelaiye-Ogala Remi , Szmulewitz Russell Z. , Conzen Suzanne D.
Published: April 2024

Abstract
In castration-resistant prostate cancer (CRPC), increased glucocorticoid receptor (GR) expression and ensuing transcriptional activity have been proposed as an oncogenic “bypass” mechanism in response to androgen receptor (AR) signaling inhibition (ARSi). Here, we report that GR transcriptional activity acquired following ARSi is associated with the upregulation of cyclic adenosine monophosphate (cAMP)-associated gene expression pathways in both model systems and metastatic prostate cancer patient samples. In the context of ARSi, the expression of GR-mediated genes encoding cAMP signaling pathway-associated proteins can be inhibited by treatment with selective GR modulators (SGRMs). For example, in the context of ARSi, we found that GR activation resulted in upregulation of protein kinase inhibitor beta (PKIB) mRNA and protein levels, leading to nuclear accumulation of the cAMP-dependent protein kinase A catalytic subunit (PKA-c). Increased PKA-c, in turn, is associated with increased cAMP response element-binding protein phosphorylation and activity. Furthermore, enzalutamide and SGRM combination therapy in mice bearing CRPC xenografts delayed CRPC progression compared with enzalutamide therapy alone, and reduced tumor PKIB mRNA expression. Supporting the clinical importance of GR/PKA signaling activation in CRPC, we found a significant enrichment of both cAMP pathway signaling-associated gene expression and high NR3C1 (GR) activity in patient-derived xenograft models and metastatic human CRPC samples. These findings suggest a novel mechanism linking CRPC-induced GR transcriptional activity with increased cAMP signaling in AR-antagonized CRPC. Furthermore, our findings suggest that GR-specific modulation in addition to AR antagonism may delay GR+ CRPC time to recurrence, at least in part, by inhibiting tumor cAMP/PKA pathways.
Data from Cereblon-based Bifunctional Degrader of SOS1, BTX-6654, Targets Multiple KRAS Mutations and Inhibits Tumor Growth
Authors: Begovich Kyle , Schoolmeesters Angela , Rajapakse Navin , Martinez-Terroba Elena , Kumar Maneesh , Shakya Arvind , Lai Chon , Greene Steven , Whitefield Brandon , Okano Akinori , Mali Venkat , Huang Shenlin , Chourasia Aparajita H. , Fung Leah
Published: April 2024

Abstract
Mutations within the oncogene KRAS drive an estimated 25% of all cancers. Only allele-specific KRAS G12C inhibitors are currently available and are associated with the emergence of acquired resistance, partly due to upstream pathway reactivation. Given its upstream role in the activation of KRAS, son of sevenless homolog 1 (SOS1), has emerged as an attractive therapeutic target. Agents that target SOS1 for degradation could represent a potential pan-KRAS modality that may be capable of circumventing certain acquired resistance mechanisms. Here, we report the development of two SOS1 cereblon-based bifunctional degraders, BTX-6654 and BTX-7312, cereblon-based bifunctional SOS1 degraders. Both compounds exhibited potent target-dependent and -specific SOS1 degradation. BTX-6654 and BTX-7312 reduced downstream signaling markers, pERK and pS6, and displayed antiproliferative activity in cells harboring various KRAS mutations. In two KRAS G12C xenograft models, BTX-6654 degraded SOS1 in a dose-dependent manner correlating with tumor growth inhibition, additionally exhibiting synergy with KRAS and MEK inhibitors. Altogether, BTX-6654 provided preclinical proof of concept for single-agent and combination use of bifunctional SOS1 degraders in KRAS-driven cancers.
Data from Neutrophil Elastase Remodels Mammary Tumors to Facilitate Lung Metastasis
Authors: Lulla Amriti R. , Akli Said , Karakas Cansu , Caruso Joseph A. , Warma Lucas D. , Fowlkes Natalie W. , Rao Xiayu , Wang Jing , Hunt Kelly K. , Watowich Stephanie S. , Keyomarsi Khandan
Published: April 2024

Abstract
Metastatic disease remains the leading cause of death due to cancer, yet the mechanism(s) of metastasis and its timely detection remain to be elucidated. Neutrophil elastase (NE), a serine protease secreted by neutrophils, is a crucial mediator of chronic inflammation and tumor progression. In this study, we used the PyMT model (NE+/+ and NE−/−) of breast cancer to interrogate the tumor-intrinsic and -extrinsic mechanisms by which NE can promote metastasis. Our results showed that genetic ablation of NE significantly reduced lung metastasis and improved metastasis-free survival. RNA-sequencing analysis of primary tumors indicated differential regulation of tumor-intrinsic actin cytoskeleton signaling pathways by NE. These NE-regulated pathways are critical for cell-to-cell contact and motility and consistent with the delay in metastasis in NE−/− mice. To evaluate whether pharmacologic inhibition of NE inhibited pulmonary metastasis and phenotypically mimicked PyMT NE−/− mice, we utilized AZD9668, a clinically available and specific NE inhibitor. We found AZD9668 treated PyMT-NE+/+ mice showed significantly reduced lung metastases, improved recurrence-free, metastasis-free and overall survival, and their tumors showed similar molecular alterations as those observed in PyMT-NE−/− tumors. Finally, we identified a NE-specific signature that predicts recurrence and metastasis in patients with breast cancer. Collectively, our studies suggest that genetic ablation and pharmacologic inhibition of NE reduces metastasis and extends survival of mouse models of breast cancer, providing rationale to examine NE inhibitors as a treatment strategy for the clinical management of patients with metastatic breast cancer.
Data from The Methyltransferases METTL7A and METTL7B Confer Resistance to Thiol-Based Histone Deacetylase Inhibitors
Authors: Robey Robert W. , Fitzsimmons Christina M. , Guiblet Wilfried M. , Frye William J.E. , González Dalmasy José M. , Wang Li , Russell Drake A. , Huff Lyn M. , Perciaccante Andrew J. , Ali-Rahmani Fatima , Lipsey Crystal C. , Wade Heidi M. , Mitchell Allison V. , Maligireddy Siddhardha S. , Terrero David , Butcher Donna , Edmondson Elijah F. , Jenkins Lisa M. , Nikitina Tatiana , Zhurkin Victor B. , Tiwari Amit K. , Piscopio Anthony D. , Totah Rheem A. , Bates Susan E. , Arda H. Efsun , Gottesman Michael M. , Batista Pedro J.
Published: April 2024

Abstract
Histone deacetylase inhibitors (HDACi) are part of a growing class of epigenetic therapies used for the treatment of cancer. Although HDACis are effective in the treatment of T-cell lymphomas, treatment of solid tumors with this class of drugs has not been successful. Overexpression of the multidrug resistance protein P-glycoprotein (P-gp), encoded by ABCB1, is known to confer resistance to the HDACi romidepsin in vitro, yet increased ABCB1 expression has not been associated with resistance in patients, suggesting that other mechanisms of resistance arise in the clinic. To identify alternative mechanisms of resistance to romidepsin, we selected MCF-7 breast cancer cells with romidepsin in the presence of the P-gp inhibitor verapamil to reduce the likelihood of P-gp-mediated resistance. The resulting cell line, MCF-7 DpVp300, does not express P-gp and was found to be selectively resistant to romidepsin but not to other HDACis such as belinostat, panobinostat, or vorinostat. RNA-sequencing analysis revealed upregulation of the mRNA coding for the putative methyltransferase, METTL7A, whose paralog, METTL7B, was previously shown to methylate thiol groups on hydrogen sulfide and captopril. As romidepsin has a thiol as the zinc-binding moiety, we hypothesized that METTL7A could inactivate romidepsin and other thiol-based HDACis via methylation of the thiol group. We demonstrate that expression of METTL7A or METTL7B confers resistance to thiol-based HDACis and that both enzymes are capable of methylating thiol-containing HDACis. We thus propose that METTL7A and METTL7B confer resistance to thiol-based HDACis by methylating and inactivating the zinc-binding thiol.
Supplementary Figure 3 from RETRACTED: Minocycline Targets the NF-κB Nexus through Suppression of TGF-β1-TAK1-IκB Signaling in Ovarian Cancer
Authors: Ataie-Kachoie Parvin , Badar Samina , Morris David L. , Pourgholami Mohammad H.
Published: April 2024

PDF file - 1507K, Effect of minocycline on constitutive and TNF-α-induce NF-кB activation in HUVEC and HOSE cells.
Supplementary Figure Legends from Identification of Colorectal Cancer Cell Stemness from Single-Cell RNA Sequencing
Authors: Lin Kangyu , Chowdhury Saikat , Zeineddine Mohammad A. , Zeineddine Fadl A. , Hornstein Nicholas J. , Villarreal Oscar E. , Maru Dipen M. , Haymaker Cara L. , Vauthey Jean-Nicolas , Chang George J. , Bogatenkova Elena , Menter David , Kopetz Scott , Shen John Paul
Published: April 2024

Supplementary Figure Legends 1-3
Supplementary Materials from Peritoneal Microenvironment Promotes Appendiceal Adenocarcinoma Growth: A Multi-omics Approach Using Patient-Derived Xenografts
Authors: Pattalachinti Vinay K. , Ito Ichiaki , Chowdhury Saikat , Yousef Abdelrahman , Gu Yue , Gunes Betul Beyza , Salle Emma R. , Taggart Melissa W. , Fournier Keith , Fowlkes Natalie W. , Shen John Paul
Published: April 2024

Supplementary Materials and methods
Supplementary Figure 1 from Identification of Colorectal Cancer Cell Stemness from Single-Cell RNA Sequencing
Authors: Lin Kangyu , Chowdhury Saikat , Zeineddine Mohammad A. , Zeineddine Fadl A. , Hornstein Nicholas J. , Villarreal Oscar E. , Maru Dipen M. , Haymaker Cara L. , Vauthey Jean-Nicolas , Chang George J. , Bogatenkova Elena , Menter David , Kopetz Scott , Shen John Paul
Published: April 2024

A single-cell transcriptome map of CRC
Figure S7 from Mass Spectrometry–Based Proteomics Identifies Serpin B9 as a Key Protein in Promoting Bone Metastases in Lung Cancer
Authors: Huang Yufeng , Gong Ming , Chen Hongmin , Deng Chuangzhong , Zhu Xiaojun , Lin Jiaming , Huang Anfei , Xu Yanyang , Tai Yi , Song Guohui , Xu Huaiyuan , Hu Jinxin , Feng Huixiong , Tang Qinglian , Lu Jinchang , Wang Jin
Published: April 2024

Bone metastases of lung cancer patients’ demographic and clinical data
Figure S1 from Mass Spectrometry–Based Proteomics Identifies Serpin B9 as a Key Protein in Promoting Bone Metastases in Lung Cancer
Authors: Huang Yufeng , Gong Ming , Chen Hongmin , Deng Chuangzhong , Zhu Xiaojun , Lin Jiaming , Huang Anfei , Xu Yanyang , Tai Yi , Song Guohui , Xu Huaiyuan , Hu Jinxin , Feng Huixiong , Tang Qinglian , Lu Jinchang , Wang Jin
Published: April 2024

Highly bone-metastatic LLC1-BM3 cells were established using a bone metastatic mouse model by CA injection.
A-D: Representative BLI images of differnt organic metastases.(n=10); A: lung metastases; B: bone metastases of lower limb; C: bone metastases of spine; D: brain metastases.
Figure S5 from miR-217 Regulates Normal and Tumor Cell Fate Following Induction of Endoplasmic Reticulum Stress
Authors: Dey Neekkan , Koumenis Costas , Ruggero Davide , Fuchs Serge Y. , Diehl J. Alan
Published: April 2024

S5. Relative band intensities compared to actin controls (a) for Fig 2a, (b) for Fig 2b, (c) for Fig 2c, (d) for Fig 5b.
Figure S3 from miR-217 Regulates Normal and Tumor Cell Fate Following Induction of Endoplasmic Reticulum Stress
Authors: Dey Neekkan , Koumenis Costas , Ruggero Davide , Fuchs Serge Y. , Diehl J. Alan
Published: April 2024

S3. (a) The 3’UTR of EZH2 mRNA contains the binding sequence of miR-217 as predicted by TargetScan. (b) Map of luciferase reporter vector Wt-EZH2-3’UTR (MmiT073625-MT06, GeneCopoeia).
Figure S2 from miR-217 Regulates Normal and Tumor Cell Fate Following Induction of Endoplasmic Reticulum Stress
Authors: Dey Neekkan , Koumenis Costas , Ruggero Davide , Fuchs Serge Y. , Diehl J. Alan
Published: April 2024

S2. AGS cells infected with either control or miR-217 were exposed to Tg (300nM) for 0, 2, 5 and 8 hours. Cells were exposed to actinomycin D (2 ᵰ7g/ml) where indicated after 5 hours of Tg treatment (and kept throughout the indicated timepoint). MiR-211 and miR-217 expression levels were quantified by qPCR. Error bars represent standard deviation for three independent experiments.
Figure S6 from NRAS Mutant Dictates AHCYL1-Governed ER Calcium Homeostasis for Melanoma Tumor Growth
Authors: Cai Chufan , Tu Jiayi , Najarro Jeronimo , Zhang Rukang , Fan Hao , Zhang Freya Q. , Li Jiacheng , Xie Zhicheng , Su Rui , Dong Lei , Arellano Nicole , Ciboddo Michele , Elf Shannon E. , Gao Xue , Chen Jing , Wu Rong
Published: April 2024

Supplementary Figure 6. AHCYL1 deficiency triggers apoptosis resulted from the UPR activation.
Data from miR-217 Regulates Normal and Tumor Cell Fate Following Induction of Endoplasmic Reticulum Stress
Authors: Dey Neekkan , Koumenis Costas , Ruggero Davide , Fuchs Serge Y. , Diehl J. Alan
Published: April 2024

Abstract
Rapidly proliferating cancer cells require a microenvironment where essential metabolic nutrients like glucose, oxygen, and growth factors become scarce as the tumor volume surpasses the established vascular capacity of the tissue. Limits in nutrient availability typically trigger growth arrest and/or apoptosis to prevent cellular expansion. However, tumor cells frequently co-opt cellular survival pathways thereby favoring cell survival under this environmental stress. The unfolded protein response (UPR) pathway is typically engaged by tumor cells to favor adaptation to stress. PERK, an endoplasmic reticulum (ER) protein kinase and UPR effector is activated in tumor cells and contributes tumor cell adaptation by limiting protein translation and balancing redox stress. PERK also induces miRNAs that contribute to tumor adaptation. miR-211 and miR-216b were previously identified as PERK-ATF4–regulated miRNAs that regulate cell survival. We have identified another PERK-responsive miRNA, miR-217, with increased expression under prolonged ER stress. Key targets of miR-217 are identified as TRPM1, the host gene for miR-211 and EZH2. Evidence is provided that miR-217 expression is essential for the rapid loss of miR-211 in prolonged ER stress and provides a functional link for determining whether cells adapt to stress or commit to apoptosis.
Implications:
PERK-dependent induction of miR-217 limits accumulation and function of the prosurvival miRNA, miR-211, to establish cell fate and promote cell commitment to apoptosis.
Data from Semi-Supervised, Attention-Based Deep Learning for Predicting TMPRSS2:ERG Fusion Status in Prostate Cancer Using Whole Slide Images
Authors: Omar Mohamed , Xu Zhuoran , Rand Sophie B. , Alexanderani Mohammad K. , Salles Daniela C. , Valencia Itzel , Schaeffer Edward M. , Robinson Brian D. , Lotan Tamara L. , Loda Massimo , Marchionni Luigi
Published: April 2024

Abstract
Prostate cancer harbors several genetic alterations, the most prevalent of which is TMPRSS2:ERG gene fusion, affecting nearly half of all cases. Capitalizing on the increasing availability of whole-slide images (WSI), this study introduces a deep learning (DL) model designed to detect TMPRSS2:ERG fusion from H&E-stained WSIs of radical prostatectomy specimens. Leveraging the TCGA prostate adenocarcinoma cohort, which comprises 436 WSIs from 393 patients, we developed a robust DL model, trained across 10 different splits, each consisting of distinct training, validation, and testing sets. The model's best performance achieved an AUC of 0.84 during training, and 0.72 on the TCGA test set. This model was subsequently validated on an independent cohort comprising 314 WSIs from a different institution, in which it has a robust performance at predicting TMPRSS2:ERG fusion with an AUC of 0.73. Importantly, the model identifies highly-attended tissue regions associated with TMPRSS2:ERG fusion, characterized by higher neoplastic cell content and altered immune and stromal profiles compared with fusion-negative cases. Multivariate survival analysis revealed that these morphologic features correlate with poorer survival outcomes, independent of Gleason grade and tumor stage. This study underscores the potential of DL in deducing genetic alterations from routine slides and identifying their underlying morphologic features, which might harbor prognostic information.
Implications:
Our study illuminates the potential of deep learning in effectively inferring key prostate cancer genetic alterations from the tissue morphology depicted in routinely available histology slides, offering a cost-effective method that could revolutionize diagnostic strategies in oncology.
Supplementary Table S3 from The Effects of Black Raspberry as a Whole Food–Based Approach on Biomarkers of Oxidative Stress in Buccal Cells and Urine of Smokers
Authors: Chen Kun-Ming , Sun Yuan-Wan , Krebs Nicolle M. , Reinhart Lisa , Sun Dongxiao , Liao Jiangang , Cook Rachel , Bond Paige Elizabeth , Mallery Susan R. , El-Bayoumy Karam
Published: April 2024

Supplementary Table S3: The effects of BRB on levels of oxidative stress biomarkers in urine and buccal cells of smokers as well as on levels of cotinine at baseline (a), mid-BRB (b), end-BRB (c), and the washout period (d) are shown. This table also provides the levels of urinary creatinine.
Supplemental Table 1 from Differences in Serum miRNA Profiles by Race, Ethnicity, and Socioeconomic Status: Implications for Developing an Equitable Ovarian Cancer Screening Test
Authors: Alimena Stephanie , Stephenson Briana Joy K. , Webber James W. , Wollborn Laura , Sussman Chad B. , Packard Daniel George , Williams Marta , Comrie Cameron Elizabeth , Wang Joyce Y. , Markert Tahireh , Spiegel Julia , Rodriguez Carmen B. , Lightfoot Maya , Graye Amia , O'Connor Sean , Elias Kevin M.
Published: April 2024

Supplemental Table 1: Differences in 179 individual miRNA studied by white vs non-white race/ethnicity. Here we show p-values for both univariate analysis and multiple linear regression analysis controlling for confounding factors. The association with human cancers in the literature is listed for those miRNA that remained significant on multiple linear regression analysis in a separate column.
Supplemental Figure 1 from Differences in Serum miRNA Profiles by Race, Ethnicity, and Socioeconomic Status: Implications for Developing an Equitable Ovarian Cancer Screening Test
Authors: Alimena Stephanie , Stephenson Briana Joy K. , Webber James W. , Wollborn Laura , Sussman Chad B. , Packard Daniel George , Williams Marta , Comrie Cameron Elizabeth , Wang Joyce Y. , Markert Tahireh , Spiegel Julia , Rodriguez Carmen B. , Lightfoot Maya , Graye Amia , O'Connor Sean , Elias Kevin M.
Published: April 2024

Supplemental Figure 1: Differences by individual racial subtypes for each of the eight miRNA related to ovarian cancer risk. Values for individual miRNAs were compared across different racial subtypes using pairwise t-tests. The images in this figure are binary, where a 0 (or blue box) indicates a significant p value (p < 0.05) for the pair-wise race-miRNA relation, and a 1 (or yellow box) indicates an insignificant relationship (p ≥ 0.05) between the two racial subtypes compared.
Data from The Effects of Black Raspberry as a Whole Food–Based Approach on Biomarkers of Oxidative Stress in Buccal Cells and Urine of Smokers
Authors: Chen Kun-Ming , Sun Yuan-Wan , Krebs Nicolle M. , Reinhart Lisa , Sun Dongxiao , Liao Jiangang , Cook Rachel , Bond Paige Elizabeth , Mallery Susan R. , El-Bayoumy Karam
Published: April 2024

Abstract
Cigarette smoke is a rich source of free radicals that can promote oxidative stress and carcinogenesis, including head and neck squamous cell carcinoma (HNSCC) development; importantly, 8-oxo-7,8-dihydro-2′-deoxyguanosine (8-oxodG) and 8-iso-prostaglandin F2α (8-isoprostane) are biomarkers of oxidative stress. Several mechanisms, including the antioxidant properties of black raspberry (BRB), account for their chemopreventive effects. In the present clinical trial, we tested the hypothesis that BRB administration reduces biomarkers levels of oxidative stress in buccal cells and urine of smokers. One week after enrolling 21 smokers, baseline buccal cells and urine samples were collected before the administration of BRB lozenges for 8 weeks (5/day, 1 gm BRB/lozenge). Buccal cells and urine samples were collected at the middle and the end of BRB administration. The last samples were collected after the BRB cessation (washout period). We analyzed levels of 8-oxodG and 8-isoprostane (LC/MS-MS), urinary cotinine (ELISA), and creatinine (spectrophotometry). BRB significantly reduced the levels of 8-oxodG by 17.08% (P = 0.00079) in buccal cells and 12.44% (P = 0.034) in urine at the middle of BRB administration as compared with baseline; the corresponding values at the end of BRB administration were 16.46% (P = 0.026) in buccal cells and 25.72% (P = 0.202) in urine. BRB had no significant effect on the levels of urinary 8-isoprostane. BRB's capacity to inhibit 8-oxodG formation of smokers’ buccal cells and urine is clearly evident and the reduction in 8-oxodG suggests that antioxidant abilities are central to BRB's HNSCC chemopreventive properties.
Prevention Relevance:
Cigarette smoke contains highly active components namely free radicals that can promote oxidative stress and oral cancer. We found that black raspberry (BRB) inhibited the formation of oxidative stress markers in the oral cavity and urine of smokers suggesting the antioxidant abilities of BRB in preventing oral cancer.
Supplementary Figure 8 from The Immune Suppressor IGSF1 as a Potential Target for Cancer Immunotherapy
Authors: Koh Dong-In , Lee Minki , Park Yoon Sun , Shin Jae-Sik , Kim Joseph , Ryu Yea Seong , Lee Jun Hyung , Bae Seunggeon , Lee Mi So , Hong Jun Ki , Jeong Hong-Rae , Choi Mingee , Hong Seung-Woo , Kim Dong Kwan , Lee Hyun-kyung , Kim Bomi , Yoon Yoo Sang , Jin Dong-Hoon
Published: April 2024

Anticancer activity of WM-A1 in a PBMC humanized mouse models of NSCLC cancer cell lines.
Supplementary Table 1 from Tumor Burden Dictates the Neoantigen Features Required to Generate an Effective Cancer Vaccine
Authors: Garzia Irene , Nocchi Linda , Avalle Lidia , Troise Fulvia , Leoni Guido , Seclì Laura , Antonucci Laura , Cotugno Gabriella , Allocca Simona , Romano Giuseppina , Conti Laura , Caiazza Carmen , Mallardo Massimo , Poli Valeria , Scarselli Elisa , D'Alise Anna Morena
Published: April 2024

List of the GAd encoded CT26 neoantigens selected according to: binding predictions for MHC-I (IC50 ≤ 500nM) and MHC-II (binding score ≤ 1); tumor allele frequency (MAF≥ 25%) and RNA expression (mutated RNA reads ≥ 1). The mutated amino acid is underlined. MAF = Minor Allele Frequency.
Supplementary Figure 2 from The Immune Suppressor IGSF1 as a Potential Target for Cancer Immunotherapy
Authors: Koh Dong-In , Lee Minki , Park Yoon Sun , Shin Jae-Sik , Kim Joseph , Ryu Yea Seong , Lee Jun Hyung , Bae Seunggeon , Lee Mi So , Hong Jun Ki , Jeong Hong-Rae , Choi Mingee , Hong Seung-Woo , Kim Dong Kwan , Lee Hyun-kyung , Kim Bomi , Yoon Yoo Sang , Jin Dong-Hoon
Published: April 2024

Analysis of IGSF1 expression and the physiological characteristics.
Supplementary Figure 5 from Gut Mycobiota Dysbiosis Is Associated with Melanoma and Response to Anti–PD-1 Therapy
Authors: Szóstak Natalia , Handschuh Luiza , Samelak-Czajka Anna , Tomela Katarzyna , Pietrzak Bernadeta , Schmidt Marcin , Galus Łukasz , Mackiewicz Jacek , Mackiewicz Andrzej , Kozlowski Piotr , Philips Anna
Published: April 2024

Supplementary Figure 5. The relative fungi abundance of melanoma and healthy samples at different taxonomical levels: (A) Phylum (B) Class (C) Order (D) Family.
Supplementary Figure 3 from Gut Mycobiota Dysbiosis Is Associated with Melanoma and Response to Anti–PD-1 Therapy
Authors: Szóstak Natalia , Handschuh Luiza , Samelak-Czajka Anna , Tomela Katarzyna , Pietrzak Bernadeta , Schmidt Marcin , Galus Łukasz , Mackiewicz Jacek , Mackiewicz Andrzej , Kozlowski Piotr , Philips Anna
Published: April 2024

Supplementary Figure 3. Relative abundance of Candida glabrata in normal (18.5
Figure S6. from High-Specificity CRISPR-Mediated Genome Engineering in Anti-BCMA Allogeneic CAR T Cells Suppresses Allograft Rejection in Preclinical Models
Authors: Degagné Émilie , Donohoue Paul D. , Roy Suparna , Scherer Jessica , Fowler Tristan W. , Davis Ryan T. , Reyes Gustavo A. , Kwong George , Stanaway Morena , Larroca Vicena Vanina , Mutha Devin , Guo Raymond , Edwards Leslie , Schilling Benjamin , Shaw McKay , Smith Stephen C. , Kohrs Bryan , Kufeldt Heinrich J. , Churchward Glen , Ruan Finey , Nyer David B. , McSweeney Kyle , Irby Matthew J. , Fuller Christopher K. , Banh Lynda , Toh Mckenzi S. , Thompson Matthew , Owen Arthur L.G. , An Zili , Gradia Scott , Skoble Justin , Bryan Mara , Garner Elizabeth , Kanner Steven B.
Published: April 2024

Antitumor activity of CB-011 CAR-T cells in a xenograft model of multiple myeloma.
Figure S4. from High-Specificity CRISPR-Mediated Genome Engineering in Anti-BCMA Allogeneic CAR T Cells Suppresses Allograft Rejection in Preclinical Models
Authors: Degagné Émilie , Donohoue Paul D. , Roy Suparna , Scherer Jessica , Fowler Tristan W. , Davis Ryan T. , Reyes Gustavo A. , Kwong George , Stanaway Morena , Larroca Vicena Vanina , Mutha Devin , Guo Raymond , Edwards Leslie , Schilling Benjamin , Shaw McKay , Smith Stephen C. , Kohrs Bryan , Kufeldt Heinrich J. , Churchward Glen , Ruan Finey , Nyer David B. , McSweeney Kyle , Irby Matthew J. , Fuller Christopher K. , Banh Lynda , Toh Mckenzi S. , Thompson Matthew , Owen Arthur L.G. , An Zili , Gradia Scott , Skoble Justin , Bryan Mara , Garner Elizabeth , Kanner Steven B.
Published: April 2024

Gamma-secretase inhibitor RO4929097 increases BCMA expression on-target cell lines but does not improve CB-011 antitumor efficacy.