Article
|
Open Access
Featured
-
-
Article
| Open Access
African-specific molecular taxonomy of prostate cancer
A molecular taxonomy for prostate cancer reveals a subtype associated with copy-number loss found in African and European populations that predicts poor outcomes and two subtypes—one associated with high mutational noise and one with copy-number gain—specific to African populations.
- Weerachai Jaratlerdsiri
- , Jue Jiang
- & Vanessa M. Hayes
-
Article |
Deep whole-genome ctDNA chronology of treatment-resistant prostate cancer
Deep whole-genome sequencing of serial blood samples and matched metastatic tissue reveals that circulating tumour DNA profiling enables detailed study of treatment-driven subclone dynamics, epigenomics and genome-wide somatic evolution in metastatic human cancers.
- Cameron Herberts
- , Matti Annala
- & Alexander W. Wyatt
-
Article
| Open Access
Targeting SWI/SNF ATPases in enhancer-addicted prostate cancer
PROTAC degrader–induced SWI/SNF inactivation abolishes DNA accessibility at enhancer elements of oncogenes and also tempers supra-physiologic expression of driver transcription factors, resulting in potent inhibition of tumour growth in mouse models.
- Lanbo Xiao
- , Abhijit Parolia
- & Arul M. Chinnaiyan
-
Article |
A genomic and epigenomic atlas of prostate cancer in Asian populations
Genomic, transcriptomic and DNA methylation data from tissue samples from 208 Chinese patients with prostate cancer define the landscape of alterations in this population, and comparison with data from Western cohorts suggests that the disease may stratify into different molecular subtypes.
- Jing Li
- , Chuanliang Xu
- & Yinghao Sun
-
Letter |
FOXA1 mutations alter pioneering activity, differentiation and prostate cancer phenotypes
Mutations in the transcription factor FOXA1 that are common in prostate cancer result in gain-of-function effects that promote changes in the differentiation of tumour cells.
- Elizabeth J. Adams
- , Wouter R. Karthaus
- & Charles L. Sawyers
-
Article |
Progenitors from the central nervous system drive neurogenesis in cancer
In a mouse model of prostate cancer, neural progenitors from the central nervous system that express doublecortin infiltrate tumours and metastases, and can generate new adrenergic neurons in tumours.
- Philippe Mauffrey
- , Nicolas Tchitchek
- & Claire Magnon
-
Article |
IL-23 secreted by myeloid cells drives castration-resistant prostate cancer
IL-23 produced by myeloid-derived suppressor cells regulates castration resistance in prostate cancer by sustaining androgen receptor signalling.
- Arianna Calcinotto
- , Clarissa Spataro
- & Andrea Alimonti
-
Letter |
ERF mutations reveal a balance of ETS factors controlling prostate oncogenesis
In prostate cancer, the oncogenicity of transcription factor ERG is mediated, in part, by competition with another member of the ETS family, ERF.
- Rohit Bose
- , Wouter R. Karthaus
- & Charles L. Sawyers
-
Letter |
Synthetic essentiality of chromatin remodelling factor CHD1 in PTEN-deficient cancer
The gene CHD1 is synthetic essential in PTEN-deficient prostate and breast cancers.
- Di Zhao
- , Xin Lu
- & Ronald A. DePinho
-
Article |
Genomic hallmarks of localized, non-indolent prostate cancer
Genomic analyses of localized, non-indolent prostate cancer identify recurrent aberrations that can predict relapse, and also highlight differences between early prostate cancer and metastatic, castration-resistant disease.
- Michael Fraser
- , Veronica Y. Sabelnykova
- & Paul C. Boutros
-
Letter |
Redirecting abiraterone metabolism to fine-tune prostate cancer anti-androgen therapy
The prostate cancer drug abiraterone can be metabolized into several substances with different effects, and optimization of this process could be helpful for fine-tuning the treatment of prostate cancer.
- Zhenfei Li
- , Mohammad Alyamani
- & Nima Sharifi
-
Letter |
Conversion of abiraterone to D4A drives anti-tumour activity in prostate cancer
The drug abiraterone is converted to Δ4-abiraterone (D4A) in mice and patients with prostate cancer, which has more potent anti-tumour activity and may lead to more effective therapies.
- Zhenfei Li
- , Andrew C. Bishop
- & Nima Sharifi
-
Outlook |
Statistics: Attacking an epidemic
Despite a huge amount of funding and research, regional and individual differences in cancer trends make it a hard disease to wipe out. By Mike May.
- Mike May
-
Letter |
COUP-TFII inhibits TGF-β-induced growth barrier to promote prostate tumorigenesis
A cell-autonomous role for the COUP-TFII transcription factor in prostate cancer cells is identified, in which COUP-TFII inhibits TGF-β signalling by binding to SMAD4; COUP-TFII promotes prostate tumorigenesis and metastasis in a mouse model, and is associated with more aggressive disease in human prostate cancers.
- Jun Qin
- , San-Pin Wu
- & Sophia Y. Tsai
-
Letter |
The mutational landscape of lethal castration-resistant prostate cancer
Exome sequencing is used to investigate the role of mutations and copy number aberrations in metastatic castration-resistant prostate cancer, revealing recurrent mutations in multiple chromatin/histone modifying genes, as well as genes involved in androgen signalling.
- Catherine S. Grasso
- , Yi-Mi Wu
- & Scott A. Tomlins
-
Research Highlights |
Blocking tumour sugar metabolism
-
Letter |
Structures of cytochrome P450 17A1 with prostate cancer drugs abiraterone and TOK-001
The structures of CYP17A1 with steroid inhibitors abiraterone or TOK-001 provide a better understanding of the enzyme’s catalytic capabilities and inhibition, and hence assist in understanding steroidogenic diseases and designing drugs to improve the treatment of prostate and other steroid-responsive cancers.
- Natasha M. DeVore
- & Emily E. Scott
-
Editorial |
The PSA position
The US government must take a firm stance on whether prostate-cancer screening is justified.
-
News |
Urine predicts prostate cancer risk
Test could reduce unnecessary needle biopsies.
- Virginia Gewin
-
Letter |
COP1 is a tumour suppressor that causes degradation of ETS transcription factors
- Alberto C. Vitari
- , Kevin G. Leong
- & Vishva M. Dixit
-
Letter |
Reprogramming transcription by distinct classes of enhancers functionally defined by eRNA
- Dong Wang
- , Ivan Garcia-Bassets
- & Xiang-Dong Fu
-
Article
| Open Access
The genomic complexity of primary human prostate cancer
Prostate cancer is a common cause of male cancer-related deaths. Complete sequencing of prostate cancer genomes now reveals previously unknown balanced rearrangements. Single-nucleotide resolution afforded by sequencing indicates that complex rearrangements may arise from transcriptional or chromatin aberrancies and engage prostate tumorigenic mechanisms.
- Michael F. Berger
- , Michael S. Lawrence
- & Levi A. Garraway
-
Letter |
LRRC26 auxiliary protein allows BK channel activation at resting voltage without calcium
Here the authors show that in non-excitable LNCaP prostate cancer cells, the large-conductance, voltage- and calcium-activated potassium (BK) channel can be activated at negative voltages without rises in intracellular Ca2+ concentration, by interacting with an auxiliary protein, the leucine-rich repeat containing protein 26. This auxiliary protein modulates BK channel gating by enhancing the allosteric coupling between voltage-sensor activation and the channel's closed–open transition.
- Jiusheng Yan
- & Richard W. Aldrich
-
Research Highlights |
Cancer genomics: Probing prostate cancer
-
Research Highlights |
Cancer detection: Tracking roving cancer cells
-
Letter |
B-cell-derived lymphotoxin promotes castration-resistant prostate cancer
In a mouse model of prostate cancer it is shown that infiltrating B cells promote tumorigenesis by secreting lymphotoxin. Lymphotoxin accelerates the emergence of castration-resistant prostate tumours in this model. Interfering with this pathway may offer therapeutic strategies for androgen-independent prostate cancer.
- Massimo Ammirante
- , Jun-Li Luo
- & Michael Karin
-
News |
Blame it on the B cells
Immune cells seem to spark recurrent prostate cancer in mice.
- Brian Vastag
Targeting myeloid chemotaxis to reverse prostate cancer therapy resistance