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279 results on '"Sjöström, Martin"'

1. Genomic and transcriptomic features of androgen receptor signaling inhibitor resistance in metastatic castration-resistant prostate cancer.

Author

Zhu, Xiaolin, Farsh, Tatyanah, Vis, Daniël, Yu, Ivan, Li, Haolong, Liu, Tianyi, Sjöström, Martin, Shrestha, Raunak, Kneppers, Jeroen, Severson, Tesa, Zhang, Meng, Lundberg, Arian, Moreno Rodriguez, Thaidy, Weinstein, Alana, Foye, Adam, Mehra, Niven, Aggarwal, Rahul, Bergman, Andries, Small, Eric, Lack, Nathan, Zwart, Wilbert, Quigley, David, van der Heijden, Michiel, and Feng, Felix

Subjects
Oncology, Prostate cancer, Male, Humans, Prostatic Neoplasms, Castration-Resistant, Receptors, Androgen, Drug Resistance, Neoplasm, Cell Line, Tumor, Signal Transduction, Transcriptome, Neoplasm Metastasis, Receptors, Somatostatin, Gene Expression Regulation, Neoplastic, Androgen Receptor Antagonists, Neoplasm Proteins
Abstract

BACKGROUNDAndrogen receptor signaling inhibitors (ARSIs) have improved outcomes for patients with metastatic castration-resistant prostate cancer (mCRPC), but their clinical benefit is limited by treatment resistance.METHODSTo investigate the mechanisms of ARSI resistance, we analyzed the whole-genome (n = 45) and transcriptome (n = 31) sequencing data generated from paired metastatic biopsies obtained before initiation of first-line ARSI therapy for mCRPC and after radiographic disease progression. We investigated the effects of genetic and pharmacologic modulation of SSTR1 in 22Rv1 cells, a representative mCRPC cell line.RESULTSWe confirmed the predominant role of tumor genetic alterations converging on augmenting androgen receptor (AR) signaling and the increased transcriptional heterogeneity and lineage plasticity during the emergence of ARSI resistance. We further identified amplifications involving a putative enhancer downstream of the AR and transcriptional downregulation of SSTR1, encoding somatostatin receptor 1, in ARSI-resistant tumors. We found that patients with SSTR1-low mCRPC tumors derived less benefit from subsequent ARSI therapy in a retrospective cohort. We showed that SSTR1 was antiproliferative in 22Rv1 cells and that the FDA-approved drug pasireotide suppressed 22Rv1 cell proliferation.CONCLUSIONOur findings expand the knowledge of ARSI resistance and point out actionable next steps, exemplified by potentially targeting SSTR1, to improve patient outcomes.FUNDINGNational Cancer Institute (NCI), NIH; Prostate Cancer Foundation; Conquer Cancer, American Society of Clinical Oncology Foundation; UCSF Benioff Initiative for Prostate Cancer Research; Netherlands Cancer Institute.

Published
2024

2. Integrated analyses highlight interactions between the three-dimensional genome and DNA, RNA and epigenomic alterations in metastatic prostate cancer.

Author

Zhao, Shuang, Bootsma, Matthew, Zhou, Stanley, Shrestha, Raunak, Moreno-Rodriguez, Thaidy, Lundberg, Arian, Pan, Chu, Arlidge, Christopher, Hawley, James, Foye, Adam, Weinstein, Alana, Sjöström, Martin, Zhang, Meng, Li, Haolong, Chesner, Lisa, Rydzewski, Nicholas, Helzer, Kyle, Shi, Yue, Lynch, Molly, Dehm, Scott, Lang, Joshua, Alumkal, Joshi, He, Hansen, Wyatt, Alexander, Aggarwal, Rahul, Zwart, Wilbert, Small, Eric, Quigley, David, Lupien, Mathieu, and Feng, Felix

Subjects
Humans, Male, DNA Methylation, 5-Methylcytosine, Gene Expression Regulation, Neoplastic, Epigenomics, Neoplasm Metastasis, Genome, Human, Prostatic Neoplasms, Epigenesis, Genetic, Receptors, Androgen, Chromatin, Prostatic Neoplasms, Castration-Resistant, Oncogene Proteins, Fusion, DNA, Whole Genome Sequencing, RNA, Prognosis
Abstract

The impact of variations in the three-dimensional structure of the genome has been recognized, but solid cancer tissue studies are limited. Here, we performed integrated deep Hi-C sequencing with matched whole-genome sequencing, whole-genome bisulfite sequencing, 5-hydroxymethylcytosine (5hmC) sequencing and RNA sequencing across a cohort of 80 biopsy samples from patients with metastatic castration-resistant prostate cancer. Dramatic differences were present in gene expression, 5-methylcytosine/5hmC methylation and in structural variation versus mutation rate between A and B (open and closed) chromatin compartments. A subset of tumors exhibited depleted regional chromatin contacts at the AR locus, linked to extrachromosomal circular DNA (ecDNA) and worse response to AR signaling inhibitors. We also identified topological subtypes associated with stark differences in methylation structure, gene expression and prognosis. Our data suggested that DNA interactions may predispose to structural variant formation, exemplified by the recurrent TMPRSS2-ERG fusion. This comprehensive integrated sequencing effort represents a unique clinical tumor resource.

Published
2024

4. The genomic and epigenomic landscape of double-negative metastatic prostate cancer

Author

Lundberg, Arian, Zhang, Meng, Aggarwal, Rahul, Li, Haolong, Zhang, Li, Foye, Adam, Sjöström, Martin, Chou, Jonathan, Chang, Kevin, Moreno-Rodriguez, Thaidy, Shrestha, Raunak, Baskin, Avi, Zhu, Xiaolin, Weinstein, Alana S, Younger, Noah, Alumkal, Joshi J, Beer, Tomasz M, N., Kim, Evans, Christopher P, Gleave, Martin, Lara, Primo N, Reiter, Rob E, Rettig, Matthew B, Witte, Owen N, Wyatt, Alexander W, Feng, Felix Y, Small, Eric J, and Quigley, David A

Subjects
Biological Sciences, Biomedical and Clinical Sciences, Clinical Sciences, Oncology and Carcinogenesis, Genetics, Cancer Genomics, Cancer, Urologic Diseases, Human Genome, Precision Medicine, Biotechnology, Prostate Cancer, Good Health and Well Being, Humans, Male, Prostatic Neoplasms, Castration-Resistant, Receptors, Androgen, Epigenomics, Androgen Antagonists, Androgens, Genomics, Neuroendocrine Tumors, Oncology & Carcinogenesis, Biochemistry and cell biology, Oncology and carcinogenesis
Abstract

Systemic targeted therapy in prostate cancer is primarily focused on ablating androgen signaling. Androgen deprivation therapy and second-generation androgen receptor (AR)-targeted therapy selectively favor the development of treatment-resistant subtypes of metastatic castration-resistant prostate cancer (mCRPC), defined by AR and neuroendocrine (NE) markers. Molecular drivers of double-negative (AR-/NE-) mCRPC are poorly defined. In this study, we comprehensively characterized treatment-emergent mCRPC by integrating matched RNA sequencing, whole-genome sequencing, and whole-genome bisulfite sequencing from 210 tumors. AR-/NE- tumors were clinically and molecularly distinct from other mCRPC subtypes, with the shortest survival, amplification of the chromatin remodeler CHD7, and PTEN loss. Methylation changes in CHD7 candidate enhancers were linked to elevated CHD7 expression in AR-/NE+ tumors. Genome-wide methylation analysis nominated Krüppel-like factor 5 (KLF5) as a driver of the AR-/NE- phenotype, and KLF5 activity was linked to RB1 loss. These observations reveal the aggressiveness of AR-/NE- mCRPC and could facilitate the identification of therapeutic targets in this highly aggressive disease.SignificanceComprehensive characterization of the five subtypes of metastatic castration-resistant prostate cancer identified transcription factors that drive each subtype and showed that the double-negative subtype has the worst prognosis.

Published
2023

5. Intrinsic Molecular Subtypes of Metastatic Castration-Resistant Prostate Cancer.

Author

Feng, Eric, Rydzewski, Nicholas R, Zhang, Meng, Lundberg, Arian, Bootsma, Matthew, Helzer, Kyle T, Lang, Joshua M, Aggarwal, Rahul, Small, Eric J, Quigley, David A, Sjöström, Martin, and Zhao, Shuang G

Subjects
Biomedical and Clinical Sciences, Oncology and Carcinogenesis, Prostate Cancer, Digestive Diseases, Genetics, Cancer, Urologic Diseases, Humans, Male, Prostatic Neoplasms, Castration-Resistant, Gene Expression Profiling, Adenocarcinoma, Nuclear Proteins, Repressor Proteins, Oncology & Carcinogenesis, Clinical sciences, Oncology and carcinogenesis
Abstract

PurposeAlthough numerous biology-driven subtypes have been described previously in metastatic castration-resistant prostate cancer (mCRPC), unsupervised molecular subtyping based on gene expression has been less studied, especially using large cohorts. Thus, we sought to identify the intrinsic molecular subtypes of mCRPC and assess molecular and clinical correlates in the largest combined cohort of mCRPC samples with gene expression data available to date.Experimental designWe combined and batch-effect corrected gene expression data from four mCRPC cohorts from the Fred Hutchinson Cancer Research Center (N = 157), a small-cell neuroendocrine (NE) prostate cancer (SCNC)-enriched cohort from Weill Cornell Medicine (N = 49), and cohorts from the Stand Up 2 Cancer/Prostate Cancer Foundation East Coast Dream Team (N = 266) and the West Coast Dream Team (N = 162).ResultsHierarchical clustering of RNA-sequencing data from these 634 mCRPC samples identified two distinct adenocarcinoma subtypes, one of which (adeno-immune) was characterized by higher gene expression of immune pathways, higher CIBERSORTx immune scores, diminished ASI benefit, and non-lymph node metastasis tropism compared with an adeno-classic subtype. We also identified two distinct subtypes with enrichment for an NE phenotype, including an NE-liver subgroup characterized by liver metastasis tropism, PTEN loss, and APC and SPOP mutations compared with an NE-classic subgroup.ConclusionsOur results emphasize the heterogeneity of mCRPC beyond currently accepted molecular phenotypes, and suggest that future studies should consider incorporating transcriptome-wide profiling to better understand how these differences impact treatment responses and outcomes.

Published
2022

6. TROP2 Expression Across Molecular Subtypes of Urothelial Carcinoma and Enfortumab Vedotin-resistant Cells.

Author

Chou, Jonathan, Trepka, Kai, Sjöström, Martin, Egusa, Emily, Chu, Carissa, Zhu, Jun, Chan, Emily, Gibb, Ewan, Badura, Michelle, Contreras-Sanz, Alberto, Stohr, Bradley, Meng, Maxwell, Pruthi, Raj, Lotan, Yair, Black, Peter, Porten, Sima, Koshkin, Vadim, Friedlander, Terence, and Feng, Felix

Subjects
Antibody-drug conjugate, Bladder cancer, Enfortumab vedotin, Molecular subtypes, Sacituzumab govitecan, Urothelial cancer, Humans, Carcinoma, Transitional Cell, Urinary Bladder Neoplasms, Immunoconjugates, Cell Adhesion Molecules, RNA, Messenger
Abstract

Sacituzumab govitecan (SG) is an antibody-drug conjugate (ADC) targeting TROP2, which has recently been approved for treatment-refractory metastatic urothelial cancer (UC). However, the variability of TROP2 expression across different bladder cancer (BC) subtypes, as well as after enfortumab vedotin (EV) exposure, remains unknown. Using gene expression data from four clinical cohorts with >1400 patient samples of muscle-invasive BC and a BC tissue microarray, we found that TROP2 mRNA and protein are highly expressed across basal, luminal, and stroma-rich subtypes, but depleted in the neuroendocrine subtype. In addition, TROP2 mRNA levels are correlated with NECTIN4 mRNA but are more highly expressed than NECTIN4 mRNA in patient cohorts and BC cell lines. Moreover, CRISPR/Cas9-mediated knockdown of TROP2 demonstrates that its expression is one factor governing SG sensitivity. After prolonged EV exposure, cells can downregulate NECTIN4, leading to EV resistance, but retain TROP2 expression and remain sensitive to SG, suggesting nonoverlapping resistance mechanisms to these ADCs. While our findings warrant further validation, they have significant implications for biomarker development, patient selection, and treatment sequencing in the clinic as well as clinical trial design and stratification for metastatic BC patients. PATIENT SUMMARY: In this report, we investigated the expression levels of the drug target TROP2 across different molecular subtypes of bladder cancer in multiple patient cohorts and cell lines. We found high levels of TROP2 in most subtypes except in the neuroendocrine subtype. Overall, TROP2 gene expression is higher than NECTIN4 gene expression, and cells resistant to enfortumab vedotin (EV), a NECTIN4-targeting antibody-drug conjugate, remain sensitive to sacituzumab govitecan (SG). Our findings suggest that SG may be effective across most bladder cancer subtypes, including the bladder cancers previously treated with EV.

Published
2022

7. The 5-Hydroxymethylcytosine Landscape of Prostate Cancer

Author

Sjöström, Martin, Zhao, Shuang G, Levy, Samuel, Zhang, Meng, Ning, Yuhong, Shrestha, Raunak, Lundberg, Arian, Herberts, Cameron, Foye, Adam, Aggarwal, Rahul, Hua, Junjie T, Li, Haolong, Bergamaschi, Anna, Maurice-Dror, Corinne, Maheshwari, Ashutosh, Chen, Sujun, Ng, Sarah WS, Ye, Wenbin, Petricca, Jessica, Fraser, Michael, Chesner, Lisa, Perry, Marc D, Moreno-Rodriguez, Thaidy, Chen, William S, Alumkal, Joshi J, Chou, Jonathan, Morgans, Alicia K, Beer, Tomasz M, Thomas, George V, Gleave, Martin, Lloyd, Paul, Phillips, Tierney, McCarthy, Erin, Haffner, Michael C, Zoubeidi, Amina, Annala, Matti, Reiter, Robert E, Rettig, Matthew B, Witte, Owen N, Fong, Lawrence, Bose, Rohit, Huang, Franklin W, Luo, Jianhua, Bjartell, Anders, Lang, Joshua M, Mahajan, Nupam P, Lara, Primo N, Evans, Christopher P, Tran, Phuoc T, Posadas, Edwin M, He, Chuan, Cui, Xiao-Long, Huang, Jiaoti, Zwart, Wilbert, Gilbert, Luke A, Maher, Christopher A, Boutros, Paul C, N., Kim, Ashworth, Alan, Small, Eric J, He, Housheng H, Wyatt, Alexander W, Quigley, David A, and Feng, Felix Y

Subjects
Biological Sciences, Biomedical and Clinical Sciences, Genetics, Clinical Sciences, Oncology and Carcinogenesis, Urologic Diseases, Cancer, Prostate Cancer, Human Genome, Aging, Cancer Genomics, 4.1 Discovery and preclinical testing of markers and technologies, 2.1 Biological and endogenous factors, 4.2 Evaluation of markers and technologies, Good Health and Well Being, Male, Humans, 5-Methylcytosine, Prostatic Neoplasms, Prostate, Biopsy, Oncology & Carcinogenesis, Biochemistry and cell biology, Oncology and carcinogenesis
Abstract

Analysis of DNA methylation is a valuable tool to understand disease progression and is increasingly being used to create diagnostic and prognostic clinical biomarkers. While conversion of cytosine to 5-methylcytosine (5mC) commonly results in transcriptional repression, further conversion to 5-hydroxymethylcytosine (5hmC) is associated with transcriptional activation. Here we perform the first study integrating whole-genome 5hmC with DNA, 5mC, and transcriptome sequencing in clinical samples of benign, localized, and advanced prostate cancer. 5hmC is shown to mark activation of cancer drivers and downstream targets. Furthermore, 5hmC sequencing revealed profoundly altered cell states throughout the disease course, characterized by increased proliferation, oncogenic signaling, dedifferentiation, and lineage plasticity to neuroendocrine and gastrointestinal lineages. Finally, 5hmC sequencing of cell-free DNA from patients with metastatic disease proved useful as a prognostic biomarker able to identify an aggressive subtype of prostate cancer using the genes TOP2A and EZH2, previously only detectable by transcriptomic analysis of solid tumor biopsies. Overall, these findings reveal that 5hmC marks epigenomic activation in prostate cancer and identify hallmarks of prostate cancer progression with potential as biomarkers of aggressive disease.SignificanceIn prostate cancer, 5-hydroxymethylcytosine delineates oncogene activation and stage-specific cell states and can be analyzed in liquid biopsies to detect cancer phenotypes. See related article by Wu and Attard, p. 3880.

Published
2022

8. Drug-Induced Epigenomic Plasticity Reprograms Circadian Rhythm Regulation to Drive Prostate Cancer toward Androgen Independence.

Author

Linder, Simon, Hoogstraat, Marlous, Stelloo, Suzan, Eickhoff, Nils, Schuurman, Karianne, de Barros, Hilda, Alkemade, Maartje, Bekers, Elise M, Severson, Tesa M, Sanders, Joyce, Huang, Chia-Chi Flora, Morova, Tunc, Altintas, Umut Berkay, Hoekman, Liesbeth, Kim, Yongsoo, Baca, Sylvan C, Sjöström, Martin, Zaalberg, Anniek, Hintzen, Dorine C, de Jong, Jeroen, Kluin, Roelof JC, de Rink, Iris, Giambartolomei, Claudia, Seo, Ji-Heui, Pasaniuc, Bogdan, Altelaar, Maarten, Medema, René H, Feng, Felix Y, Zoubeidi, Amina, Freedman, Matthew L, Wessels, Lodewyk FA, Butler, Lisa M, Lack, Nathan A, van der Poel, Henk, Bergman, Andries M, and Zwart, Wilbert

Subjects
Biomedical and Clinical Sciences, Clinical Sciences, Oncology and Carcinogenesis, Prostate Cancer, Aging, Urologic Diseases, Biotechnology, Cancer, 5.1 Pharmaceuticals, Development of treatments and therapeutic interventions, 2.1 Biological and endogenous factors, Aetiology, ARNTL Transcription Factors, Androgens, Cell Line, Tumor, Circadian Rhythm, Drug Resistance, Neoplasm, Epigenomics, Humans, Male, Nitriles, Prostatic Neoplasms, Castration-Resistant, Receptors, Androgen, Biochemistry and cell biology, Oncology and carcinogenesis
Abstract

In prostate cancer, androgen receptor (AR)-targeting agents are very effective in various disease stages. However, therapy resistance inevitably occurs, and little is known about how tumor cells adapt to bypass AR suppression. Here, we performed integrative multiomics analyses on tissues isolated before and after 3 months of AR-targeting enzalutamide monotherapy from patients with high-risk prostate cancer enrolled in a neoadjuvant clinical trial. Transcriptomic analyses demonstrated that AR inhibition drove tumors toward a neuroendocrine-like disease state. Additionally, epigenomic profiling revealed massive enzalutamide-induced reprogramming of pioneer factor FOXA1 from inactive chromatin sites toward active cis-regulatory elements that dictate prosurvival signals. Notably, treatment-induced FOXA1 sites were enriched for the circadian clock component ARNTL. Posttreatment ARNTL levels were associated with patients' clinical outcomes, and ARNTL knockout strongly decreased prostate cancer cell growth. Our data highlight a remarkable cistromic plasticity of FOXA1 following AR-targeted therapy and revealed an acquired dependency on the circadian regulator ARNTL, a novel candidate therapeutic target.SignificanceUnderstanding how prostate cancers adapt to AR-targeted interventions is critical for identifying novel drug targets to improve the clinical management of treatment-resistant disease. Our study revealed an enzalutamide-induced epigenomic plasticity toward prosurvival signaling and uncovered the circadian regulator ARNTL as an acquired vulnerability after AR inhibition, presenting a novel lead for therapeutic development. See related commentary by Zhang et al., p. 2017. This article is highlighted in the In This Issue feature, p. 2007.

Published
2022

15. A phenocopy signature of TP53 loss predicts response to chemotherapy.

Author

Bakhtiar, Hamza, Sharifi, Marina N., Helzer, Kyle T., Shi, Yue, Bootsma, Matthew L., Shang, Tianfu A., Chrostek, Matthew R., Berg, Tracy J., Carson Callahan, S., Carreno, Viridiana, Blitzer, Grace C., West, Malinda T., O'Regan, Ruth M., Wisinski, Kari B., Sjöström, Martin, and Zhao, Shuang G.

Subjects
PATHOLOGIC complete response, NEOADJUVANT chemotherapy, BREAST cancer, GENE expression, PROOF of concept
Abstract

In preclinical studies, p53 loss of function impacts chemotherapy response, but this has not been consistently validated clinically. We trained a TP53-loss phenocopy gene expression signature from pan-cancer clinical samples in the TCGA. In vitro, the TP53-loss phenocopy signature predicted chemotherapy response across cancer types. In a clinical dataset of 3003 breast cancer samples treated with neoadjuvant chemotherapy, the TP53-loss phenocopy samples were 56% more likely to have a pathologic complete response (pCR), with a significant association between TP53-loss phenocopy and pCR in both ER positive and ER negative tumors. In an independent clinical validation in the I-SPY2 trial (N = 987), we confirmed the association with neoadjuvant chemotherapy pCR and found higher rates of chemoimmunotherapy response in TP53-loss phenocopy tumors compared to non-TP53-loss phenocopy tumors (64% vs. 28%). The TP53-loss phenocopy signature predicts chemotherapy response across cancer types in vitro, and in a proof-of-concept clinical validation is associated with neoadjuvant chemotherapy response across multiple clinical breast cancer cohorts. [ABSTRACT FROM AUTHOR]

Published
2024
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16. Supplementary Figure S4 from Integrating Tumor-Intrinsic and Immunologic Factors to Identify Immunogenic Breast Cancers from a Low-Risk Cohort: Results from the Randomized SweBCG91RT Trial

Author

Stenmark Tullberg, Axel, primary, Sjöström, Martin, primary, Niméus, Emma, primary, Killander, Fredrika, primary, Chang, S. Laura, primary, Feng, Felix Y., primary, Speers, Corey W., primary, Pierce, Lori J., primary, Kovács, Anikó, primary, Lundstedt, Dan, primary, Holmberg, Erik, primary, and Karlsson, Per, primary

Published
2024
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17. Supplementary Tables S5-S11 from Integrating Tumor-Intrinsic and Immunologic Factors to Identify Immunogenic Breast Cancers from a Low-Risk Cohort: Results from the Randomized SweBCG91RT Trial

Author

Stenmark Tullberg, Axel, primary, Sjöström, Martin, primary, Niméus, Emma, primary, Killander, Fredrika, primary, Chang, S. Laura, primary, Feng, Felix Y., primary, Speers, Corey W., primary, Pierce, Lori J., primary, Kovács, Anikó, primary, Lundstedt, Dan, primary, Holmberg, Erik, primary, and Karlsson, Per, primary

Published
2024
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18. Study protocol S1 from Integrating Tumor-Intrinsic and Immunologic Factors to Identify Immunogenic Breast Cancers from a Low-Risk Cohort: Results from the Randomized SweBCG91RT Trial

Author

Stenmark Tullberg, Axel, primary, Sjöström, Martin, primary, Niméus, Emma, primary, Killander, Fredrika, primary, Chang, S. Laura, primary, Feng, Felix Y., primary, Speers, Corey W., primary, Pierce, Lori J., primary, Kovács, Anikó, primary, Lundstedt, Dan, primary, Holmberg, Erik, primary, and Karlsson, Per, primary

Published
2024
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21. Data from The Genomic and Epigenomic Landscape of Double-Negative Metastatic Prostate Cancer

Author

Lundberg, Arian, primary, Zhang, Meng, primary, Aggarwal, Rahul, primary, Li, Haolong, primary, Zhang, Li, primary, Foye, Adam, primary, Sjöström, Martin, primary, Chou, Jonathan, primary, Chang, Kevin, primary, Moreno-Rodriguez, Thaidy, primary, Shrestha, Raunak, primary, Baskin, Avi, primary, Zhu, Xiaolin, primary, Weinstein, Alana S., primary, Younger, Noah, primary, Alumkal, Joshi J., primary, Beer, Tomasz M., primary, Chi, Kim N., primary, Evans, Christopher P., primary, Gleave, Martin, primary, Lara, Primo N., primary, Reiter, Rob E., primary, Rettig, Matthew B., primary, Witte, Owen N., primary, Wyatt, Alexander W., primary, Feng, Felix Y., primary, Small, Eric J., primary, and Quigley, David A., primary

Published
2023
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22. Supplementary Figure 8. from The Genomic and Epigenomic Landscape of Double-Negative Metastatic Prostate Cancer

Author

Lundberg, Arian, primary, Zhang, Meng, primary, Aggarwal, Rahul, primary, Li, Haolong, primary, Zhang, Li, primary, Foye, Adam, primary, Sjöström, Martin, primary, Chou, Jonathan, primary, Chang, Kevin, primary, Moreno-Rodriguez, Thaidy, primary, Shrestha, Raunak, primary, Baskin, Avi, primary, Zhu, Xiaolin, primary, Weinstein, Alana S., primary, Younger, Noah, primary, Alumkal, Joshi J., primary, Beer, Tomasz M., primary, Chi, Kim N., primary, Evans, Christopher P., primary, Gleave, Martin, primary, Lara, Primo N., primary, Reiter, Rob E., primary, Rettig, Matthew B., primary, Witte, Owen N., primary, Wyatt, Alexander W., primary, Feng, Felix Y., primary, Small, Eric J., primary, and Quigley, David A., primary

Published
2023
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23. Supplementary Figure 4. from The Genomic and Epigenomic Landscape of Double-Negative Metastatic Prostate Cancer

Author

Lundberg, Arian, primary, Zhang, Meng, primary, Aggarwal, Rahul, primary, Li, Haolong, primary, Zhang, Li, primary, Foye, Adam, primary, Sjöström, Martin, primary, Chou, Jonathan, primary, Chang, Kevin, primary, Moreno-Rodriguez, Thaidy, primary, Shrestha, Raunak, primary, Baskin, Avi, primary, Zhu, Xiaolin, primary, Weinstein, Alana S., primary, Younger, Noah, primary, Alumkal, Joshi J., primary, Beer, Tomasz M., primary, Chi, Kim N., primary, Evans, Christopher P., primary, Gleave, Martin, primary, Lara, Primo N., primary, Reiter, Rob E., primary, Rettig, Matthew B., primary, Witte, Owen N., primary, Wyatt, Alexander W., primary, Feng, Felix Y., primary, Small, Eric J., primary, and Quigley, David A., primary

Published
2023
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24. Supplementary Figure 6. from The Genomic and Epigenomic Landscape of Double-Negative Metastatic Prostate Cancer

Author

Lundberg, Arian, primary, Zhang, Meng, primary, Aggarwal, Rahul, primary, Li, Haolong, primary, Zhang, Li, primary, Foye, Adam, primary, Sjöström, Martin, primary, Chou, Jonathan, primary, Chang, Kevin, primary, Moreno-Rodriguez, Thaidy, primary, Shrestha, Raunak, primary, Baskin, Avi, primary, Zhu, Xiaolin, primary, Weinstein, Alana S., primary, Younger, Noah, primary, Alumkal, Joshi J., primary, Beer, Tomasz M., primary, Chi, Kim N., primary, Evans, Christopher P., primary, Gleave, Martin, primary, Lara, Primo N., primary, Reiter, Rob E., primary, Rettig, Matthew B., primary, Witte, Owen N., primary, Wyatt, Alexander W., primary, Feng, Felix Y., primary, Small, Eric J., primary, and Quigley, David A., primary

Published
2023
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25. Supplementary Figure 1. from The Genomic and Epigenomic Landscape of Double-Negative Metastatic Prostate Cancer

Author

Lundberg, Arian, primary, Zhang, Meng, primary, Aggarwal, Rahul, primary, Li, Haolong, primary, Zhang, Li, primary, Foye, Adam, primary, Sjöström, Martin, primary, Chou, Jonathan, primary, Chang, Kevin, primary, Moreno-Rodriguez, Thaidy, primary, Shrestha, Raunak, primary, Baskin, Avi, primary, Zhu, Xiaolin, primary, Weinstein, Alana S., primary, Younger, Noah, primary, Alumkal, Joshi J., primary, Beer, Tomasz M., primary, Chi, Kim N., primary, Evans, Christopher P., primary, Gleave, Martin, primary, Lara, Primo N., primary, Reiter, Rob E., primary, Rettig, Matthew B., primary, Witte, Owen N., primary, Wyatt, Alexander W., primary, Feng, Felix Y., primary, Small, Eric J., primary, and Quigley, David A., primary

Published
2023
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26. Supplementary Figure 5. from The Genomic and Epigenomic Landscape of Double-Negative Metastatic Prostate Cancer

Author

Lundberg, Arian, primary, Zhang, Meng, primary, Aggarwal, Rahul, primary, Li, Haolong, primary, Zhang, Li, primary, Foye, Adam, primary, Sjöström, Martin, primary, Chou, Jonathan, primary, Chang, Kevin, primary, Moreno-Rodriguez, Thaidy, primary, Shrestha, Raunak, primary, Baskin, Avi, primary, Zhu, Xiaolin, primary, Weinstein, Alana S., primary, Younger, Noah, primary, Alumkal, Joshi J., primary, Beer, Tomasz M., primary, Chi, Kim N., primary, Evans, Christopher P., primary, Gleave, Martin, primary, Lara, Primo N., primary, Reiter, Rob E., primary, Rettig, Matthew B., primary, Witte, Owen N., primary, Wyatt, Alexander W., primary, Feng, Felix Y., primary, Small, Eric J., primary, and Quigley, David A., primary

Published
2023
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27. Supplementary Table 3. from The Genomic and Epigenomic Landscape of Double-Negative Metastatic Prostate Cancer

Author

Lundberg, Arian, primary, Zhang, Meng, primary, Aggarwal, Rahul, primary, Li, Haolong, primary, Zhang, Li, primary, Foye, Adam, primary, Sjöström, Martin, primary, Chou, Jonathan, primary, Chang, Kevin, primary, Moreno-Rodriguez, Thaidy, primary, Shrestha, Raunak, primary, Baskin, Avi, primary, Zhu, Xiaolin, primary, Weinstein, Alana S., primary, Younger, Noah, primary, Alumkal, Joshi J., primary, Beer, Tomasz M., primary, Chi, Kim N., primary, Evans, Christopher P., primary, Gleave, Martin, primary, Lara, Primo N., primary, Reiter, Rob E., primary, Rettig, Matthew B., primary, Witte, Owen N., primary, Wyatt, Alexander W., primary, Feng, Felix Y., primary, Small, Eric J., primary, and Quigley, David A., primary

Published
2023
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28. Supplementary Data 1. from The Genomic and Epigenomic Landscape of Double-Negative Metastatic Prostate Cancer

Author

Lundberg, Arian, primary, Zhang, Meng, primary, Aggarwal, Rahul, primary, Li, Haolong, primary, Zhang, Li, primary, Foye, Adam, primary, Sjöström, Martin, primary, Chou, Jonathan, primary, Chang, Kevin, primary, Moreno-Rodriguez, Thaidy, primary, Shrestha, Raunak, primary, Baskin, Avi, primary, Zhu, Xiaolin, primary, Weinstein, Alana S., primary, Younger, Noah, primary, Alumkal, Joshi J., primary, Beer, Tomasz M., primary, Chi, Kim N., primary, Evans, Christopher P., primary, Gleave, Martin, primary, Lara, Primo N., primary, Reiter, Rob E., primary, Rettig, Matthew B., primary, Witte, Owen N., primary, Wyatt, Alexander W., primary, Feng, Felix Y., primary, Small, Eric J., primary, and Quigley, David A., primary

Published
2023
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29. Supplementary Figure 3. from The Genomic and Epigenomic Landscape of Double-Negative Metastatic Prostate Cancer

Author

Lundberg, Arian, primary, Zhang, Meng, primary, Aggarwal, Rahul, primary, Li, Haolong, primary, Zhang, Li, primary, Foye, Adam, primary, Sjöström, Martin, primary, Chou, Jonathan, primary, Chang, Kevin, primary, Moreno-Rodriguez, Thaidy, primary, Shrestha, Raunak, primary, Baskin, Avi, primary, Zhu, Xiaolin, primary, Weinstein, Alana S., primary, Younger, Noah, primary, Alumkal, Joshi J., primary, Beer, Tomasz M., primary, Chi, Kim N., primary, Evans, Christopher P., primary, Gleave, Martin, primary, Lara, Primo N., primary, Reiter, Rob E., primary, Rettig, Matthew B., primary, Witte, Owen N., primary, Wyatt, Alexander W., primary, Feng, Felix Y., primary, Small, Eric J., primary, and Quigley, David A., primary

Published
2023
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30. Supplementary Figure 7. from The Genomic and Epigenomic Landscape of Double-Negative Metastatic Prostate Cancer

Author

Lundberg, Arian, primary, Zhang, Meng, primary, Aggarwal, Rahul, primary, Li, Haolong, primary, Zhang, Li, primary, Foye, Adam, primary, Sjöström, Martin, primary, Chou, Jonathan, primary, Chang, Kevin, primary, Moreno-Rodriguez, Thaidy, primary, Shrestha, Raunak, primary, Baskin, Avi, primary, Zhu, Xiaolin, primary, Weinstein, Alana S., primary, Younger, Noah, primary, Alumkal, Joshi J., primary, Beer, Tomasz M., primary, Chi, Kim N., primary, Evans, Christopher P., primary, Gleave, Martin, primary, Lara, Primo N., primary, Reiter, Rob E., primary, Rettig, Matthew B., primary, Witte, Owen N., primary, Wyatt, Alexander W., primary, Feng, Felix Y., primary, Small, Eric J., primary, and Quigley, David A., primary

Published
2023
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31. Supplementary Data 2. from The Genomic and Epigenomic Landscape of Double-Negative Metastatic Prostate Cancer

Author

Lundberg, Arian, primary, Zhang, Meng, primary, Aggarwal, Rahul, primary, Li, Haolong, primary, Zhang, Li, primary, Foye, Adam, primary, Sjöström, Martin, primary, Chou, Jonathan, primary, Chang, Kevin, primary, Moreno-Rodriguez, Thaidy, primary, Shrestha, Raunak, primary, Baskin, Avi, primary, Zhu, Xiaolin, primary, Weinstein, Alana S., primary, Younger, Noah, primary, Alumkal, Joshi J., primary, Beer, Tomasz M., primary, Chi, Kim N., primary, Evans, Christopher P., primary, Gleave, Martin, primary, Lara, Primo N., primary, Reiter, Rob E., primary, Rettig, Matthew B., primary, Witte, Owen N., primary, Wyatt, Alexander W., primary, Feng, Felix Y., primary, Small, Eric J., primary, and Quigley, David A., primary

Published
2023
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32. Supplementary Figure 2. from The Genomic and Epigenomic Landscape of Double-Negative Metastatic Prostate Cancer

Author

Lundberg, Arian, primary, Zhang, Meng, primary, Aggarwal, Rahul, primary, Li, Haolong, primary, Zhang, Li, primary, Foye, Adam, primary, Sjöström, Martin, primary, Chou, Jonathan, primary, Chang, Kevin, primary, Moreno-Rodriguez, Thaidy, primary, Shrestha, Raunak, primary, Baskin, Avi, primary, Zhu, Xiaolin, primary, Weinstein, Alana S., primary, Younger, Noah, primary, Alumkal, Joshi J., primary, Beer, Tomasz M., primary, Chi, Kim N., primary, Evans, Christopher P., primary, Gleave, Martin, primary, Lara, Primo N., primary, Reiter, Rob E., primary, Rettig, Matthew B., primary, Witte, Owen N., primary, Wyatt, Alexander W., primary, Feng, Felix Y., primary, Small, Eric J., primary, and Quigley, David A., primary

Published
2023
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33. Supplementary Table 1. from The Genomic and Epigenomic Landscape of Double-Negative Metastatic Prostate Cancer

Author

Lundberg, Arian, primary, Zhang, Meng, primary, Aggarwal, Rahul, primary, Li, Haolong, primary, Zhang, Li, primary, Foye, Adam, primary, Sjöström, Martin, primary, Chou, Jonathan, primary, Chang, Kevin, primary, Moreno-Rodriguez, Thaidy, primary, Shrestha, Raunak, primary, Baskin, Avi, primary, Zhu, Xiaolin, primary, Weinstein, Alana S., primary, Younger, Noah, primary, Alumkal, Joshi J., primary, Beer, Tomasz M., primary, Chi, Kim N., primary, Evans, Christopher P., primary, Gleave, Martin, primary, Lara, Primo N., primary, Reiter, Rob E., primary, Rettig, Matthew B., primary, Witte, Owen N., primary, Wyatt, Alexander W., primary, Feng, Felix Y., primary, Small, Eric J., primary, and Quigley, David A., primary

Published
2023
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34. Supplementary Table 2. from The Genomic and Epigenomic Landscape of Double-Negative Metastatic Prostate Cancer

Author

Lundberg, Arian, primary, Zhang, Meng, primary, Aggarwal, Rahul, primary, Li, Haolong, primary, Zhang, Li, primary, Foye, Adam, primary, Sjöström, Martin, primary, Chou, Jonathan, primary, Chang, Kevin, primary, Moreno-Rodriguez, Thaidy, primary, Shrestha, Raunak, primary, Baskin, Avi, primary, Zhu, Xiaolin, primary, Weinstein, Alana S., primary, Younger, Noah, primary, Alumkal, Joshi J., primary, Beer, Tomasz M., primary, Chi, Kim N., primary, Evans, Christopher P., primary, Gleave, Martin, primary, Lara, Primo N., primary, Reiter, Rob E., primary, Rettig, Matthew B., primary, Witte, Owen N., primary, Wyatt, Alexander W., primary, Feng, Felix Y., primary, Small, Eric J., primary, and Quigley, David A., primary

Published
2023
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35. Reply to V. Nardone et al

Author

Sjöström, Martin, primary, Fyles, Anthony, additional, Liu, Fei-Fei, additional, McCready, David, additional, Feng, Felix Y., additional, Speers, Corey W., additional, Pierce, Lori J., additional, Holmberg, Erik, additional, Fernö, Mårten, additional, Malmström, Per, additional, and Karlsson, Per, additional

Published
2023
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36. Transcriptomic Heterogeneity of Expansile Cribriform and Other Gleason Pattern 4 Prostate Cancer Subtypes

Author

Chappidi, Meera R., primary, Sjöström, Martin, additional, Greenland, Nancy Y., additional, Cowan, Janet E., additional, Baskin, Avi S., additional, Shee, Kevin, additional, Simko, Jeffry P., additional, Chan, Emily, additional, Stohr, Bradley A., additional, Washington, Samuel L., additional, Nguyen, Hao G., additional, Quigley, David A., additional, Davicioni, Elai, additional, Feng, Felix Y., additional, Carroll, Peter R., additional, and Cooperberg, Matthew R., additional

Published
2023
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38. Somatostatin receptor 1 (SSTR1) expression as a potential predictive biomarker for response to androgen receptor signaling inhibitor (ARSI) therapy in metastatic castration-resistant prostate cancer (mCRPC).

Author

Zhu, Xiaolin, Vis, Daniel J, Sjöström, Martin, Shrestha, Raunak, Kneppers, Jeroen, Severson, Tessa, Zhu, Yanyun, Li, Haolong, Farsh, Tatyanah, Zhang, Meng, Lundberg, Arian, Moreno Rodriguez, Thaidy, Foye, Adam, Bergman, Andre M., Zwart, Wilbert, Quigley, David Alan, Aggarwal, Rahul Raj, Small, Eric J., Van Der Heijden, Michiel Simon, and Feng, Felix Y

Published
2024
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39. Supplementary Figure S1 from Integrating Tumor-Intrinsic and Immunologic Factors to Identify Immunogenic Breast Cancers from a Low-Risk Cohort: Results from the Randomized SweBCG91RT Trial

Author

Stenmark Tullberg, Axel, primary, Sjöström, Martin, primary, Niméus, Emma, primary, Killander, Fredrika, primary, Chang, S. Laura, primary, Feng, Felix Y., primary, Speers, Corey W., primary, Pierce, Lori J., primary, Kovács, Anikó, primary, Lundstedt, Dan, primary, Holmberg, Erik, primary, and Karlsson, Per, primary

Published
2023
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40. Study protocol S1 from Integrating Tumor-Intrinsic and Immunologic Factors to Identify Immunogenic Breast Cancers from a Low-Risk Cohort: Results from the Randomized SweBCG91RT Trial

Author

Stenmark Tullberg, Axel, primary, Sjöström, Martin, primary, Niméus, Emma, primary, Killander, Fredrika, primary, Chang, S. Laura, primary, Feng, Felix Y., primary, Speers, Corey W., primary, Pierce, Lori J., primary, Kovács, Anikó, primary, Lundstedt, Dan, primary, Holmberg, Erik, primary, and Karlsson, Per, primary

Published
2023
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41. Supplementary Tables S1-S4 from Integrating Tumor-Intrinsic and Immunologic Factors to Identify Immunogenic Breast Cancers from a Low-Risk Cohort: Results from the Randomized SweBCG91RT Trial

Author

Stenmark Tullberg, Axel, primary, Sjöström, Martin, primary, Niméus, Emma, primary, Killander, Fredrika, primary, Chang, S. Laura, primary, Feng, Felix Y., primary, Speers, Corey W., primary, Pierce, Lori J., primary, Kovács, Anikó, primary, Lundstedt, Dan, primary, Holmberg, Erik, primary, and Karlsson, Per, primary

Published
2023
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42. Data from Integrating Tumor-Intrinsic and Immunologic Factors to Identify Immunogenic Breast Cancers from a Low-Risk Cohort: Results from the Randomized SweBCG91RT Trial

Author

Stenmark Tullberg, Axel, primary, Sjöström, Martin, primary, Niméus, Emma, primary, Killander, Fredrika, primary, Chang, S. Laura, primary, Feng, Felix Y., primary, Speers, Corey W., primary, Pierce, Lori J., primary, Kovács, Anikó, primary, Lundstedt, Dan, primary, Holmberg, Erik, primary, and Karlsson, Per, primary

Published
2023
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43. Combining histological grade, TILs, and the PD-1/PD-L1 pathway to identify immunogenic tumors and de-escalate radiotherapy in early breast cancer: a secondary analysis of a randomized clinical trial

Author

Stenmark Tullberg, Axel, primary, Sjöström, Martin, additional, Tran, Lena, additional, Niméus, Emma, additional, Killander, Fredrika, additional, Kovács, Anikó, additional, Lundstedt, Dan, additional, Holmberg, Erik, additional, and Karlsson, Per, additional

Published
2023
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45. Integrating Tumor-Intrinsic and Immunologic Factors to Identify Immunogenic Breast Cancers from a Low-Risk Cohort: Results from the Randomized SweBCG91RT Trial

Author

Stenmark Tullberg, Axel, primary, Sjöström, Martin, additional, Niméus, Emma, additional, Killander, Fredrika, additional, Chang, S. Laura, additional, Feng, Felix Y., additional, Speers, Corey W., additional, Pierce, Lori J., additional, Kovács, Anikó, additional, Lundstedt, Dan, additional, Holmberg, Erik, additional, and Karlsson, Per, additional

Published
2023
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46. Supplementary Figure from Drug-Induced Epigenomic Plasticity Reprograms Circadian Rhythm Regulation to Drive Prostate Cancer toward Androgen Independence

Author

Linder, Simon, primary, Hoogstraat, Marlous, primary, Stelloo, Suzan, primary, Eickhoff, Nils, primary, Schuurman, Karianne, primary, de Barros, Hilda, primary, Alkemade, Maartje, primary, Bekers, Elise M., primary, Severson, Tesa M., primary, Sanders, Joyce, primary, Huang, Chia-Chi Flora, primary, Morova, Tunc, primary, Altintas, Umut Berkay, primary, Hoekman, Liesbeth, primary, Kim, Yongsoo, primary, Baca, Sylvan C., primary, Sjöström, Martin, primary, Zaalberg, Anniek, primary, Hintzen, Dorine C., primary, de Jong, Jeroen, primary, Kluin, Roelof J.C., primary, de Rink, Iris, primary, Giambartolomei, Claudia, primary, Seo, Ji-Heui, primary, Pasaniuc, Bogdan, primary, Altelaar, Maarten, primary, Medema, René H., primary, Feng, Felix Y., primary, Zoubeidi, Amina, primary, Freedman, Matthew L., primary, Wessels, Lodewyk F.A., primary, Butler, Lisa M., primary, Lack, Nathan A., primary, van der Poel, Henk, primary, Bergman, Andries M., primary, and Zwart, Wilbert, primary

Published
2023
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47. Supplementary Data from Drug-Induced Epigenomic Plasticity Reprograms Circadian Rhythm Regulation to Drive Prostate Cancer toward Androgen Independence

Author

Linder, Simon, primary, Hoogstraat, Marlous, primary, Stelloo, Suzan, primary, Eickhoff, Nils, primary, Schuurman, Karianne, primary, de Barros, Hilda, primary, Alkemade, Maartje, primary, Bekers, Elise M., primary, Severson, Tesa M., primary, Sanders, Joyce, primary, Huang, Chia-Chi Flora, primary, Morova, Tunc, primary, Altintas, Umut Berkay, primary, Hoekman, Liesbeth, primary, Kim, Yongsoo, primary, Baca, Sylvan C., primary, Sjöström, Martin, primary, Zaalberg, Anniek, primary, Hintzen, Dorine C., primary, de Jong, Jeroen, primary, Kluin, Roelof J.C., primary, de Rink, Iris, primary, Giambartolomei, Claudia, primary, Seo, Ji-Heui, primary, Pasaniuc, Bogdan, primary, Altelaar, Maarten, primary, Medema, René H., primary, Feng, Felix Y., primary, Zoubeidi, Amina, primary, Freedman, Matthew L., primary, Wessels, Lodewyk F.A., primary, Butler, Lisa M., primary, Lack, Nathan A., primary, van der Poel, Henk, primary, Bergman, Andries M., primary, and Zwart, Wilbert, primary

Published
2023
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48. Data from Drug-Induced Epigenomic Plasticity Reprograms Circadian Rhythm Regulation to Drive Prostate Cancer toward Androgen Independence

Author

Linder, Simon, primary, Hoogstraat, Marlous, primary, Stelloo, Suzan, primary, Eickhoff, Nils, primary, Schuurman, Karianne, primary, de Barros, Hilda, primary, Alkemade, Maartje, primary, Bekers, Elise M., primary, Severson, Tesa M., primary, Sanders, Joyce, primary, Huang, Chia-Chi Flora, primary, Morova, Tunc, primary, Altintas, Umut Berkay, primary, Hoekman, Liesbeth, primary, Kim, Yongsoo, primary, Baca, Sylvan C., primary, Sjöström, Martin, primary, Zaalberg, Anniek, primary, Hintzen, Dorine C., primary, de Jong, Jeroen, primary, Kluin, Roelof J.C., primary, de Rink, Iris, primary, Giambartolomei, Claudia, primary, Seo, Ji-Heui, primary, Pasaniuc, Bogdan, primary, Altelaar, Maarten, primary, Medema, René H., primary, Feng, Felix Y., primary, Zoubeidi, Amina, primary, Freedman, Matthew L., primary, Wessels, Lodewyk F.A., primary, Butler, Lisa M., primary, Lack, Nathan A., primary, van der Poel, Henk, primary, Bergman, Andries M., primary, and Zwart, Wilbert, primary

Published
2023
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50. Supplementary Figure S2 from G Protein–Coupled Estrogen Receptor Is Apoptotic and Correlates with Increased Distant Disease-Free Survival of Estrogen Receptor–Positive Breast Cancer Patients

Author

Broselid, Stefan, primary, Cheng, Benxu, primary, Sjöström, Martin, primary, Lövgren, Kristina, primary, Klug-De Santiago, Heather L.P., primary, Belting, Mattias, primary, Jirström, Karin, primary, Malmström, Per, primary, Olde, Björn, primary, Bendahl, Pär-Ola, primary, Hartman, Linda, primary, Fernö, Mårten, primary, and Leeb-Lundberg, L.M. Fredrik, primary

Published
2023
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