GEMMs shine a light on resistance to androgen deprivation therapy for prostate cancer.

Abstract:

:Androgen deprivation therapy (ADT) for advanced prostate cancer inexorably leads to resistance, and clinically useful biomarkers are lacking. The value of genetically engineered mice for coclinical studies is clearly demonstrated in a recent publication that reveals XAF1, XIAP, and SRD5A1 as novel predictive biomarkers and therapeutic targets for ADT resistance.

journal_name

Cancer Cell

journal_title

Cancer cell

authors

Karantanos T,Thompson TC

doi

10.1016/j.ccr.2013.06.007

subject

Has Abstract

pub_date

2013-07-08 00:00:00

pages

11-3

issue

1

eissn

1535-6108

issn

1878-3686

pii

S1535-6108(13)00283-3

journal_volume

24

pub_type

杂志文章
  • Successful targeting of ErbB2 receptors-is PTEN the key?

    abstract::Women with ErbB2-positive breast cancer have a poor prognosis, and frequently, chemotherapy treatment is ineffective. The ErbB2-targeted antibody trastuzumab improves survival when given with chemotherapy to patients with ErbB2-overexpressing metastatic disease, but treatment is not curative, and primary resistance is...

    journal_title:Cancer cell

    pub_type: 评论,杂志文章

    doi:10.1016/j.ccr.2004.08.001

    authors: Crowder RJ,Lombardi DP,Ellis MJ

    更新日期:2004-08-01 00:00:00

  • AF10 regulates progressive H3K79 methylation and HOX gene expression in diverse AML subtypes.

    abstract::Homeotic (HOX) genes are dysregulated in multiple malignancies, including several AML subtypes. We demonstrate that H3K79 dimethylation (H3K79me2) is converted to monomethylation (H3K79me1) at HOX loci as hematopoietic cells mature, thus coinciding with a decrease in HOX gene expression. We show that H3K79 methyltrans...

    journal_title:Cancer cell

    pub_type: 杂志文章

    doi:10.1016/j.ccell.2014.10.009

    authors: Deshpande AJ,Deshpande A,Sinha AU,Chen L,Chang J,Cihan A,Fazio M,Chen CW,Zhu N,Koche R,Dzhekieva L,Ibáñez G,Dias S,Banka D,Krivtsov A,Luo M,Roeder RG,Bradner JE,Bernt KM,Armstrong SA

    更新日期:2014-12-08 00:00:00

  • Opening a new GATAway for treating KRAS-driven lung tumors.

    abstract::In a recent issue of Cell, Kumar and colleagues uncovered a synthetic lethal interaction between oncogenic KRAS and the transcription factor GATA2 in non-small cell lung carcinoma. Pharmacological inhibition of GATA2-mediated pathways with bortezomib and fasudil results in dramatic tumor inhibition. These observations...

    journal_title:Cancer cell

    pub_type: 评论,杂志文章

    doi:10.1016/j.ccr.2012.04.032

    authors: Barbacid M

    更新日期:2012-05-15 00:00:00

  • Differential utilization of two ATP-generating pathways is regulated by p53.

    abstract::A fundamental property of cancer cells is the preferential utilization of glycolysis over aerobic respiration to produce ATP. Renewed interest in understanding the mechanism underlying this metabolic shift in energy production is broadening our understanding of the relationship between cancer and cellular metabolism. ...

    journal_title:Cancer cell

    pub_type: 杂志文章

    doi:10.1016/j.ccr.2006.06.014

    authors: Assaily W,Benchimol S

    更新日期:2006-07-01 00:00:00

  • A new TIPE of phosphoinositide regulator in cancer.

    abstract::Specific phosphoinositide lipids promote cell growth and cancer. In this issue of Cancer Cell, Fayngerts and colleagues demonstrate that the TIPE3 protein enhances PtdIns(4,5)P2 and PtdIns(3,4,5)P3, is overexpressed in certain cancers, and promotes tumorigenesis. TIPE3 can act as a lipid transfer protein and may const...

    journal_title:Cancer cell

    pub_type: 杂志文章

    doi:10.1016/j.ccell.2014.09.017

    authors: Moniz LS,Vanhaesebroeck B

    更新日期:2014-10-13 00:00:00

  • Targeted inactivation of Mdm2 RING finger E3 ubiquitin ligase activity in the mouse reveals mechanistic insights into p53 regulation.

    abstract::It is believed that Mdm2 suppresses p53 in two ways: transcriptional inhibition by direct binding, and degradation via its E3 ligase activity. To study these functions physiologically, we generated mice bearing a single-residue substitution (C462A) abolishing the E3 function without affecting p53 binding. Unexpectedly...

    journal_title:Cancer cell

    pub_type: 杂志文章

    doi:10.1016/j.ccr.2007.09.007

    authors: Itahana K,Mao H,Jin A,Itahana Y,Clegg HV,Lindström MS,Bhat KP,Godfrey VL,Evan GI,Zhang Y

    更新日期:2007-10-01 00:00:00

  • Undifferentiated Sarcomas Develop through Distinct Evolutionary Pathways.

    abstract::Undifferentiated sarcomas (USARCs) of adults are diverse, rare, and aggressive soft tissue cancers. Recent sequencing efforts have confirmed that USARCs exhibit one of the highest burdens of structural aberrations across human cancer. Here, we sought to unravel the molecular basis of the structural complexity in USARC...

    journal_title:Cancer cell

    pub_type: 杂志文章

    doi:10.1016/j.ccell.2019.02.002

    authors: Steele CD,Tarabichi M,Oukrif D,Webster AP,Ye H,Fittall M,Lombard P,Martincorena I,Tarpey PS,Collord G,Haase K,Strauss SJ,Berisha F,Vaikkinen H,Dhami P,Jansen M,Behjati S,Amary MF,Tirabosco R,Feber A,Campbell PJ,

    更新日期:2019-03-18 00:00:00

  • Normal Somatic Mutations in Cancer Transformation.

    abstract::Gene alterations play a prominent role in driving cancer initiation and progression. However, the genetic events that occur in normal cells prior to tumorigenesis are still unknown. Recent studies have started to map somatic mutations in normal human tissues, and here we discuss their implications for our understandin...

    journal_title:Cancer cell

    pub_type: 杂志文章

    doi:10.1016/j.ccell.2020.11.002

    authors: Wijewardhane N,Dressler L,Ciccarelli FD

    更新日期:2020-11-17 00:00:00

  • Oncogenic BRAF regulates oxidative metabolism via PGC1α and MITF.

    abstract::Activating mutations in BRAF are the most common genetic alterations in melanoma. Inhibition of BRAF by small molecules leads to cell-cycle arrest and apoptosis. We show here that BRAF inhibition also induces an oxidative phosphorylation gene program, mitochondrial biogenesis, and the increased expression of the mitoc...

    journal_title:Cancer cell

    pub_type: 杂志文章

    doi:10.1016/j.ccr.2013.02.003

    authors: Haq R,Shoag J,Andreu-Perez P,Yokoyama S,Edelman H,Rowe GC,Frederick DT,Hurley AD,Nellore A,Kung AL,Wargo JA,Song JS,Fisher DE,Arany Z,Widlund HR

    更新日期:2013-03-18 00:00:00

  • Nilotinib and MEK inhibitors induce synthetic lethality through paradoxical activation of RAF in drug-resistant chronic myeloid leukemia.

    abstract::We show that imatinib, nilotinib, and dasatinib possess weak off-target activity against RAF and, therefore, drive paradoxical activation of BRAF and CRAF in a RAS-dependent manner. Critically, because RAS is activated by BCR-ABL, in drug-resistant chronic myeloid leukemia (CML) cells, RAS activity persists in the pre...

    journal_title:Cancer cell

    pub_type: 杂志文章

    doi:10.1016/j.ccr.2011.11.004

    authors: Packer LM,Rana S,Hayward R,O'Hare T,Eide CA,Rebocho A,Heidorn S,Zabriskie MS,Niculescu-Duvaz I,Druker BJ,Springer C,Marais R

    更新日期:2011-12-13 00:00:00

  • MLL-GAS7 transforms multipotent hematopoietic progenitors and induces mixed lineage leukemias in mice.

    abstract::A specific association with mixed lineage leukemias suggests that MLL oncoproteins may selectively target early multipotent hematopoietic progenitors or stem cells. We demonstrate here that a representative MLL fusion protein, MLL-GAS7, impairs the differentiation and enhances the in vitro growth of murine hematopoiet...

    journal_title:Cancer cell

    pub_type: 杂志文章

    doi:10.1016/s1535-6108(03)00019-9

    authors: So CW,Karsunky H,Passegué E,Cozzio A,Weissman IL,Cleary ML

    更新日期:2003-02-01 00:00:00

  • Hyper-Editing of Cell-Cycle Regulatory and Tumor Suppressor RNA Promotes Malignant Progenitor Propagation.

    abstract::Adenosine deaminase associated with RNA1 (ADAR1) deregulation contributes to therapeutic resistance in many malignancies. Here we show that ADAR1-induced hyper-editing in normal human hematopoietic progenitors impairs miR-26a maturation, which represses CDKN1A expression indirectly via EZH2, thereby accelerating cell-...

    journal_title:Cancer cell

    pub_type: 杂志文章

    doi:10.1016/j.ccell.2018.11.017

    authors: Jiang Q,Isquith J,Zipeto MA,Diep RH,Pham J,Delos Santos N,Reynoso E,Chau J,Leu H,Lazzari E,Melese E,Ma W,Fang R,Minden M,Morris S,Ren B,Pineda G,Holm F,Jamieson C

    更新日期:2019-01-14 00:00:00

  • Is NF-kappaB2/p100 a direct activator of programmed cell death?

    abstract::Transcription factor NF-kappaB has been implicated in cancer development due to its ability to upregulate expression of genes with potentially prooncogenic functions, such as cell cycle regulators and antiapoptotic proteins (Karin et al., 2002). A recent report by suggests that a structural motif, a death domain (DD),...

    journal_title:Cancer cell

    pub_type: 杂志文章,评审

    doi:10.1016/s1535-6108(02)00213-1

    authors: Häcker H,Karin M

    更新日期:2002-12-01 00:00:00

  • Cross-species regulatory network analysis identifies a synergistic interaction between FOXM1 and CENPF that drives prostate cancer malignancy.

    abstract::To identify regulatory drivers of prostate cancer malignancy, we have assembled genome-wide regulatory networks (interactomes) for human and mouse prostate cancer from expression profiles of human tumors and of genetically engineered mouse models, respectively. Cross-species computational analysis of these interactome...

    journal_title:Cancer cell

    pub_type: 杂志文章

    doi:10.1016/j.ccr.2014.03.017

    authors: Aytes A,Mitrofanova A,Lefebvre C,Alvarez MJ,Castillo-Martin M,Zheng T,Eastham JA,Gopalan A,Pienta KJ,Shen MM,Califano A,Abate-Shen C

    更新日期:2014-05-12 00:00:00

  • Developmental biology informs cancer: the emerging role of the hedgehog signaling pathway in upper gastrointestinal cancers.

    abstract::The hedgehog (Hh) signaling pathway plays many roles in invertebrate and vertebrate development. For example, specific inhibition of sonic Hh expression is critical during early stages of pancreas organogenesis, but an active Hh pathway appears to be required for maintenance of adult endocrine functions. Mutational in...

    journal_title:Cancer cell

    pub_type: 杂志文章,评审

    doi:10.1016/s1535-6108(03)00246-0

    authors: Xie K,Abbruzzese JL

    更新日期:2003-10-01 00:00:00

  • The histone demethylase KDM1A sustains the oncogenic potential of MLL-AF9 leukemia stem cells.

    abstract::Using a mouse model of human MLL-AF9 leukemia, we identified the lysine-specific demethylase KDM1A (LSD1 or AOF2) as an essential regulator of leukemia stem cell (LSC) potential. KDM1A acts at genomic loci bound by MLL-AF9 to sustain expression of the associated oncogenic program, thus preventing differentiation and a...

    journal_title:Cancer cell

    pub_type: 杂志文章

    doi:10.1016/j.ccr.2012.03.014

    authors: Harris WJ,Huang X,Lynch JT,Spencer GJ,Hitchin JR,Li Y,Ciceri F,Blaser JG,Greystoke BF,Jordan AM,Miller CJ,Ogilvie DJ,Somervaille TC

    更新日期:2012-04-17 00:00:00

  • Tobacco smoke promotes lung tumorigenesis by triggering IKKbeta- and JNK1-dependent inflammation.

    abstract::Chronic exposure to tobacco smoke, which contains over 60 tumor-initiating carcinogens, is the major risk factor for development of lung cancer, accounting for a large portion of cancer-related deaths worldwide. It is well established that tobacco smoke is a tumor initiator, but we asked whether it also acts as a tumo...

    journal_title:Cancer cell

    pub_type: 杂志文章

    doi:10.1016/j.ccr.2009.12.008

    authors: Takahashi H,Ogata H,Nishigaki R,Broide DH,Karin M

    更新日期:2010-01-19 00:00:00

  • CD4(+) T cells regulate pulmonary metastasis of mammary carcinomas by enhancing protumor properties of macrophages.

    abstract::During breast cancer development, increased presence of leukocytes in neoplastic stroma parallels disease progression; however, the functional significance of leukocytes in regulating protumor versus antitumor immunity in the breast remains poorly understood. Utilizing the MMTV-PyMT model of mammary carcinogenesis, we...

    journal_title:Cancer cell

    pub_type: 杂志文章

    doi:10.1016/j.ccr.2009.06.018

    authors: DeNardo DG,Barreto JB,Andreu P,Vasquez L,Tawfik D,Kolhatkar N,Coussens LM

    更新日期:2009-08-04 00:00:00

  • A high-frequency regulatory polymorphism in the p53 pathway accelerates tumor development.

    abstract::MDM2, a negative regulator of p53, is elevated in many cancers that retain wild-type p53. A single nucleotide polymorphism (SNP) in the human MDM2 promoter increases the affinity of Sp1 resulting in elevated MDM2 levels. We generated mice carrying either the MDM2(SNP309T) or the MDM2(SNP309G) allele to address the imp...

    journal_title:Cancer cell

    pub_type: 评论,杂志文章

    doi:10.1016/j.ccr.2010.07.010

    authors: Post SM,Quintás-Cardama A,Pant V,Iwakuma T,Hamir A,Jackson JG,Maccio DR,Bond GL,Johnson DG,Levine AJ,Lozano G

    更新日期:2010-09-14 00:00:00

  • Alternative and aberrant splicing of MDM2 mRNA in human cancer.

    abstract::MDM2 has been characterized as a protein that binds to and facilitates degradation of the tumor suppressor p53. Interestingly, more than 40 different splice variants of MDM2 transcripts have been identified both in tumors and normal tissues, and the majority of these variants do not contain sequence encoding the p53 b...

    journal_title:Cancer cell

    pub_type: 杂志文章,评审

    doi:10.1016/s1535-6108(02)00091-0

    authors: Bartel F,Taubert H,Harris LC

    更新日期:2002-07-01 00:00:00

  • It's the peptide-MHC affinity, stupid.

    abstract::Adoptively transferred T cells can reject large established tumors, but recurrence due to escape variants frequently occurs. In this issue of Cancer Cell, Engels et al. demonstrate that the affinity of the target peptide to the MHC molecule determines whether large tumors will relapse following adoptive T cell therapy...

    journal_title:Cancer cell

    pub_type: 评论,杂志文章

    doi:10.1016/j.ccr.2013.04.004

    authors: Kammertoens T,Blankenstein T

    更新日期:2013-04-15 00:00:00

  • Structural Design of Engineered Costimulation Determines Tumor Rejection Kinetics and Persistence of CAR T Cells.

    abstract::T cell engineering is a powerful means to rapidly generate anti-tumor T cells. The costimulatory properties of second-generation chimeric antigen receptors (CARs) determine the overall potency of adoptively transferred T cells. Using an in vivo "stress test" to challenge CD19-targeted T cells, we studied the functiona...

    journal_title:Cancer cell

    pub_type: 杂志文章

    doi:10.1016/j.ccell.2015.09.004

    authors: Zhao Z,Condomines M,van der Stegen SJC,Perna F,Kloss CC,Gunset G,Plotkin J,Sadelain M

    更新日期:2015-10-12 00:00:00

  • Large-Scale Characterization of Drug Responses of Clinically Relevant Proteins in Cancer Cell Lines.

    abstract::Perturbation biology is a powerful approach to modeling quantitative cellular behaviors and understanding detailed disease mechanisms. However, large-scale protein response resources of cancer cell lines to perturbations are not available, resulting in a critical knowledge gap. Here we generated and compiled perturbed...

    journal_title:Cancer cell

    pub_type: 杂志文章

    doi:10.1016/j.ccell.2020.10.008

    authors: Zhao W,Li J,Chen MM,Luo Y,Ju Z,Nesser NK,Johnson-Camacho K,Boniface CT,Lawrence Y,Pande NT,Davies MA,Herlyn M,Muranen T,Zervantonakis IK,von Euw E,Schultz A,Kumar SV,Korkut A,Spellman PT,Akbani R,Slamon DJ,Gray

    更新日期:2020-12-14 00:00:00

  • Glutathione and thioredoxin antioxidant pathways synergize to drive cancer initiation and progression.

    abstract::Controversy over the role of antioxidants in cancer has persisted for decades. Here, we demonstrate that synthesis of the antioxidant glutathione (GSH), driven by GCLM, is required for cancer initiation. Genetic loss of Gclm prevents a tumor's ability to drive malignant transformation. Intriguingly, these findings can...

    journal_title:Cancer cell

    pub_type: 杂志文章

    doi:10.1016/j.ccell.2014.11.019

    authors: Harris IS,Treloar AE,Inoue S,Sasaki M,Gorrini C,Lee KC,Yung KY,Brenner D,Knobbe-Thomsen CB,Cox MA,Elia A,Berger T,Cescon DW,Adeoye A,Brüstle A,Molyneux SD,Mason JM,Li WY,Yamamoto K,Wakeham A,Berman HK,Khokha R,

    更新日期:2015-02-09 00:00:00

  • Context-dependent transformation of adult pancreatic cells by oncogenic K-Ras.

    abstract::Pancreatic ductal adenocarcinoma (PDAC) is one of the most lethal human malignancies. To investigate the cellular origin(s) of this cancer, we determined the effect of PDAC-relevant gene mutations in distinct cell types of the adult pancreas. We show that a subpopulation of Pdx1-expressing cells is susceptible to onco...

    journal_title:Cancer cell

    pub_type: 杂志文章

    doi:10.1016/j.ccr.2009.09.027

    authors: Gidekel Friedlander SY,Chu GC,Snyder EL,Girnius N,Dibelius G,Crowley D,Vasile E,DePinho RA,Jacks T

    更新日期:2009-11-06 00:00:00

  • A radical role for p38 MAPK in tumor initiation.

    abstract::It is established that p38 MAPK can negatively regulate tumorigenesis, but the mechanism is incompletely understood. A new study in this issue of Cancer Cell shows that p38 MAP kinase plays a selective role in tumor initiation mediated by oxidative stress. ...

    journal_title:Cancer cell

    pub_type: 评论,杂志文章

    doi:10.1016/j.ccr.2007.01.009

    authors: Kennedy NJ,Cellurale C,Davis RJ

    更新日期:2007-02-01 00:00:00

  • Wild-type RAS: keeping mutant RAS in CHK.

    abstract::Mutant RAS-driven tumorigenesis was thought for decades to arise independently of wild-type RAS isoforms, but recent evidence indicates wild-type isoforms are involved. In this issue of Cancer Cell, Grabocka and colleagues report how the loss of wild-type RAS alters oncogenic signaling and dampens the DNA-damage respo...

    journal_title:Cancer cell

    pub_type: 评论,杂志文章

    doi:10.1016/j.ccr.2014.01.029

    authors: Anastassiadis T,Brown EJ

    更新日期:2014-02-10 00:00:00

  • ALK inhibition for non-small cell lung cancer: from discovery to therapy in record time.

    abstract::It was only 3 years ago that an acquired translocation of EML4 with ALK leading to the expression of an EML4-ALK oncoprotein in non-small cell lung cancer (NSCLC) was reported. Tumor cells expressing EML4-ALK are "addicted" to its continued function. Now, crizotinib, an oral ALK inhibitor, is demonstrated to provide d...

    journal_title:Cancer cell

    pub_type: 杂志文章,评审

    doi:10.1016/j.ccr.2010.11.033

    authors: Gerber DE,Minna JD

    更新日期:2010-12-14 00:00:00

  • Proteogenomic Characterization of Human Early-Onset Gastric Cancer.

    abstract::We report proteogenomic analysis of diffuse gastric cancers (GCs) in young populations. Phosphoproteome data elucidated signaling pathways associated with somatic mutations based on mutation-phosphorylation correlations. Moreover, correlations between mRNA and protein abundances provided potential oncogenes and tumor ...

    journal_title:Cancer cell

    pub_type: 杂志文章

    doi:10.1016/j.ccell.2018.12.003

    authors: Mun DG,Bhin J,Kim S,Kim H,Jung JH,Jung Y,Jang YE,Park JM,Kim H,Jung Y,Lee H,Bae J,Back S,Kim SJ,Kim J,Park H,Li H,Hwang KB,Park YS,Yook JH,Kim BS,Kwon SY,Ryu SW,Park DY,Jeon TY,Kim DH,Lee JH,Han SU,

    更新日期:2019-01-14 00:00:00

  • Inhibition of NF-kappaB in cancer cells converts inflammation- induced tumor growth mediated by TNFalpha to TRAIL-mediated tumor regression.

    abstract::We used an experimental murine cancer metastasis model in which a colon adenocarcinoma cell line generates lung metastases, whose growth is stimulated in response to injection of bacterial lipopolysaccharide (LPS), to investigate the role of NF-kappaB in inflammation-induced tumor growth. We found that LPS-induced met...

    journal_title:Cancer cell

    pub_type: 杂志文章

    doi:10.1016/j.ccr.2004.08.012

    authors: Luo JL,Maeda S,Hsu LC,Yagita H,Karin M

    更新日期:2004-09-01 00:00:00