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https://www.readbyqxmd.com/read/29786791/protocols-for-studies-on-tmprss2-erg-in-prostate-cancer
#1
Hubert Pakula, Douglas E Linn, Daniel R Schmidt, Marit Van Gorsel, Matthew G Vander Heiden, Zhe Li
TMPRSS2/ERG is the most common type of gene fusions found in human prostate cancer. There are two important features of TMPRSS2/ERG fusions. One is that these gene fusions lead to ectopic expression of ERG, an ETS family transcription factor, in prostate epithelial cells from the 5' control region of an androgen/estrogen dual-responsive gene, TMPRSS2; the other is that ~60% of these fusions are generated via intrachromosomal deletion of the interstitial region between TMPRSS2 and ERG. To recapitulate these important aspects of TMPRSS2/ERG fusions, we generated several TMPRSS2/ERG knockin mouse models based on the endogenous Tmprss2 locus...
2018: Methods in Molecular Biology
https://www.readbyqxmd.com/read/29782499/tgf%C3%AE-signaling-limits-lineage-plasticity-in-prostate-cancer
#2
Yi Hao, Glen A Bjerke, Karolina Pietrzak, Tiffany A Melhuish, Yu Han, Stephen D Turner, Henry F Frierson, David Wotton
Although treatment options for localized prostate cancer (CaP) are initially effective, the five-year survival for metastatic CaP is below 30%. Mutation or deletion of the PTEN tumor suppressor is a frequent event in metastatic CaP, and inactivation of the transforming growth factor (TGF) ß signaling pathway is associated with more advanced disease. We previously demonstrated that mouse models of CaP based on inactivation of Pten and the TGFß type II receptor (Tgfbr2) rapidly become invasive and metastatic...
May 21, 2018: PLoS Genetics
https://www.readbyqxmd.com/read/29776955/high-fat-diet-induced-inflammation-accelerates-prostate-cancer-growth-via-il6-signaling
#3
Takuji Hayashi, Kazutoshi Fujita, Satoshi Nojima, Yujiro Hayashi, Kosuke Nakano, Yu Ishizuya, Cong Wang, Yoshiyuki Yamamoto, Toshiro Kinouchi, Kyosuke Matsuzaki, Kentaro Jingushi, Taigo Kato, Atsunari Kawashima, Akira Nagahara, Takeshi Ujike, Motohide Uemura, Maria Del Carmen Rodriguez Pena, Jennifer B Gordetsky, Eiichi Morii, Kazutake Tsujikawa, George J Netto, Norio Nonomura
OBJECTIVE: High-fat diet (HFD) could induce prostate cancer progression. The aim of this study is to identify mechanisms of HFD-induced prostate cancer progression, focusing on inflammation. MATERIALS AND METHODS: We administered HFD and celecoxib to autochthonous immunocompetent Pb-Cre+; Pten(fl/fl) model mice for prostate cancer. Tumor growth was evaluated by tumor weight and Ki67 stain, and local immune cells were assessed by flow cytometry at 22 weeks of age...
May 18, 2018: Clinical Cancer Research: An Official Journal of the American Association for Cancer Research
https://www.readbyqxmd.com/read/29765153/cox-2-mediates-pro-tumorigenic-effects-of-pkc%C3%AE%C2%B5-in-prostate-cancer
#4
Rachana Garg, Jorge M Blando, Carlos J Perez, Priti Lal, Michael D Feldman, Emer M Smyth, Emanuela Ricciotti, Tilo Grosser, Fernando Benavides, Marcelo G Kazanietz
The pro-oncogenic kinase PKCε is overexpressed in human prostate cancer and cooperates with loss of the tumor suppressor Pten for the development of prostatic adenocarcinoma. However, the effectors driving PKCε-mediated phenotypes remain poorly defined. Here, using cellular and mouse models, we showed that PKCε overexpression acts synergistically with Pten loss to promote NF-κB activation and induce cyclooxygenase-2 (COX-2) expression, phenotypic traits which are also observed in human prostate tumors. Targeted disruption of PKCε from prostate cancer cells impaired COX-2 induction and PGE2 production...
May 16, 2018: Oncogene
https://www.readbyqxmd.com/read/29762619/isolation-and-genome-sequencing-of-individual-circulating-tumor-cells-using-hydrogel-encapsulation-and-laser-capture-microdissection
#5
Emily S Park, Justin P Yan, Richard A Ang, Jeong Hyun Lee, Xiaoyan Deng, Simon P Duffy, Kevin Beja, Matti Annala, Peter C Black, Kim N Chi, Alexander W Wyatt, Hongshen Ma
Circulating tumor cells (CTCs) are malignant cells released into the bloodstream with the potential to form metastases in secondary sites. These cells, acquired non-invasively, represent a sample of highly relevant tumor tissue that is an alternative to difficult and low-yield tumor biopsies. In recent years, there has been growing interest in genomic profiling of CTCs to enable longitudinal monitoring of the tumor's adaptive response to therapy. However, due to their extreme rarity, genotyping CTCs has proved challenging...
May 15, 2018: Lab on a Chip
https://www.readbyqxmd.com/read/29748904/androgen-receptor-signaling-in-castration-resistant-prostate-cancer-alters-hyperpolarized-pyruvate-to-lactate-conversion-and-lactate-levels-in-vivo
#6
Niki Zacharias, Jaehyuk Lee, Sumankalai Ramachandran, Sriram Shanmugavelandy, James McHenry, Prasanta Dutta, Steven Millward, Seth Gammon, Eleni Efstathiou, Patricia Troncoso, Daniel E Frigo, David Piwnica-Worms, Christopher J Logothetis, Sankar N Maity, Mark A Titus, Pratip Bhattacharya
PURPOSE: Androgen receptor (AR) signaling affects prostate cancer (PCa) growth, metabolism, and progression. Often, PCa progresses from androgen-sensitive to castration-resistant prostate cancer (CRPC) following androgen-deprivation therapy. Clinicopathologic and genomic characterizations of CRPC tumors lead to subdividing CRPC into two subtypes: (1) AR-dependent CRPC containing dysregulation of AR signaling alterations in AR such as amplification, point mutations, and/or generation of splice variants in the AR gene; and (2) an aggressive variant PCa (AVPC) subtype that is phenotypically similar to small cell prostate cancer and is defined by chemotherapy sensitivity, gain of neuroendocrine or pro-neural marker expression, loss of AR expression, and combined alterations of PTEN, TP53, and RB1 tumor suppressors...
May 10, 2018: Molecular Imaging and Biology: MIB: the Official Publication of the Academy of Molecular Imaging
https://www.readbyqxmd.com/read/29743291/-pten-deletion-in-luminal-cells-of-mature-prostate-induces-replication-stress-and-senescence-in-vivo
#7
Maxime Parisotto, Elise Grelet, Rana El Bizri, Yongyuan Dai, Julie Terzic, Doriane Eckert, Laetitia Gargowitsch, Jean-Marc Bornert, Daniel Metzger
Genetic ablation of the tumor suppressor PTEN in prostatic epithelial cells (PECs) induces cell senescence. However, unlike oncogene-induced senescence, no hyperproliferation phase and no signs of DNA damage response (DDR) were observed in PTEN -deficient PECs; PTEN loss-induced senescence (PICS) was reported to be a novel type of cellular senescence. Our study reveals that PTEN ablation in prostatic luminal epithelial cells of adult mice stimulates PEC proliferation, followed by a progressive growth arrest with characteristics of cell senescence...
May 9, 2018: Journal of Experimental Medicine
https://www.readbyqxmd.com/read/29720450/er-stress-in-prostate-cancer-a-therapeutically-exploitable-vulnerability
#8
REVIEW
Christopher Logothetis, Ana Aparicio, Timothy C Thompson
Cooperative oncogenic effects resulting from the loss of PTEN and overexpression of MYC overcome the deleterious effects of endoplasmic reticulum stress not only to promote the growth of aggressive prostate cancer but also to expose a new therapy target for this disease (Nguyen et al , this issue).
May 2, 2018: Science Translational Medicine
https://www.readbyqxmd.com/read/29706654/the-essential-role-of-wd-repeat-domain-77-in-prostate-tumor-initiation-induced-by-pten-loss
#9
Deon O'Bryant, Zhengxin Wang
Prostate cancer is the most commonly diagnosed malignancy among men, but few genetic factors that drive prostate cancer initiation have been identified. The WD repeat domain 77 (Wdr77) protein is essential for cellular proliferation when localizes in the cytoplasm of epithelial cells at the early stage of prostate development. In the adult prostate, it is transported into the nucleus and functions as a co-regulator of the androgen receptor to promote cellular differentiation and prostate function. This developmental process is reversed during prostate tumorigenesis, i...
April 30, 2018: Oncogene
https://www.readbyqxmd.com/read/29690565/prostate-cancer-genomics-recent-advances-and-the-prevailing-underrepresentation-from-racial-and-ethnic-minorities
#10
REVIEW
Shyh-Han Tan, Gyorgy Petrovics, Shiv Srivastava
Prostate cancer (CaP) is the most commonly diagnosed non-cutaneous cancer and the second leading cause of male cancer deaths in the United States. Among African American (AA) men, CaP is the most prevalent malignancy, with disproportionately higher incidence and mortality rates. Even after discounting the influence of socioeconomic factors, the effect of molecular and genetic factors on racial disparity of CaP is evident. Earlier studies on the molecular basis for CaP disparity have focused on the influence of heritable mutations and single-nucleotide polymorphisms (SNPs)...
April 22, 2018: International Journal of Molecular Sciences
https://www.readbyqxmd.com/read/29687779/selective-eradication-of-cancer-displaying-hyperactive-akt-by-exploiting-the-metabolic-consequences-of-akt-activation
#11
Veronique Nogueira, Krushna Chandra Patra, Nissim Hay
Akt activation in human cancers exerts chemoresistance, but pan-Akt inhibition elicits adverse consequences. We exploited the consequences of Akt-mediated mitochondrial and glucose metabolism to selectively eradicate and evade chemoresistance of prostate cancer displaying hyperactive Akt. PTEN-deficient prostate cancer cells that display hyperactivated Akt have high intracellular reactive oxygen species (ROS) levels, which are due, in part, to Akt-dependent increase of oxidative phosphorylation. High intracellular ROS levels selectively sensitize cells displaying hyperactive Akt to ROS-induced cell death enabling a therapeutic strategy combining a ROS inducer and rapamycin in PTEN-deficient prostate tumors in mouse models...
April 24, 2018: ELife
https://www.readbyqxmd.com/read/29686284/multi-faceted-immunomodulatory-and-tissue-tropic-clinical-bacterial-isolate-potentiates-prostate-cancer-immunotherapy
#12
Jonathan F Anker, Anum F Naseem, Hanlin Mok, Anthony J Schaeffer, Sarki A Abdulkadir, Praveen Thumbikat
Immune checkpoint inhibitors have not been effective for immunologically "cold" tumors, such as prostate cancer, which contain scarce tumor infiltrating lymphocytes. We hypothesized that select tissue-specific and immunostimulatory bacteria can potentiate these immunotherapies. Here we show that a patient-derived prostate-specific microbe, CP1, in combination with anti-PD-1 immunotherapy, increases survival and decreases tumor burden in orthotopic MYC- and PTEN-mutant prostate cancer models. CP1 administered intra-urethrally specifically homes to and colonizes tumors without causing any systemic toxicities...
April 23, 2018: Nature Communications
https://www.readbyqxmd.com/read/29679140/comparison-of-cell-cycle-progression-score-with-two-immunohistochemical-markers-pten-and-ki-67-for-predicting-outcome-in-prostate-cancer-after-radical-prostatectomy
#13
Priscilla Léon, Geraldine Cancel-Tassin, Sara Drouin, Marie Audouin, Justine Varinot, Eva Comperat, Xavier Cathelineau, François Rozet, Christophe Vaessens, Steven Stone, Julia Reid, Zaina Sangale, Patrick Korman, Morgan Rouprêt, Gaelle Fromond-Hankard, Olivier Cussenot
PURPOSE: Previous studies of the cell cycle progression (CCP) score in surgical specimens of prostate cancer (PCa) in patients treated by radical prostatectomy (RP) demonstrated significant association with time to biochemical recurrence (BCR). In this study, we compared the ability of the CCP score and the expression of PTEN or Ki-67 to predict BCR in a cohort of patients treated by RP. Finally, we constructed the best predictive model for BCR, incorporating biomarkers and relevant clinical variables...
April 20, 2018: World Journal of Urology
https://www.readbyqxmd.com/read/29665325/a-gene-signature-associated-with-pten-activation-defines-good-prognosis-intermediate-risk-prostate-cancer-cases
#14
Chee W Ong, Pamela Maxwell, Muhammad A Alvi, Stephen McQuaid, David Waugh, Ian Mills, Manuel Salto-Tellez
Accurate identification of intermediate risk (Gleason 3 + 4 = 7) prostate cancer patients with low risk of disease progression is an unmet challenge in treatment decision making. Here we describe a gene signature that could guide clinicians in the selection of patients with intermediate stage clinically localized prostate cancer for active surveillance. We examined six major drivers of aggressive disease - PTEN, MYC, RB1, TP53, AURKA, AR - by immunohistochemistry in a focused (N = 69) cohort predominantly consisting of intermediate risk prostate cancer...
April 2018: Journal of Pathology. Clinical Research
https://www.readbyqxmd.com/read/29650325/improving-the-genetic-signature-of-prostate-cancer-the-somatic-mutations
#15
Luis Javier Martinez-Gonzalez, Manrique Pascual Geler, Inmaculada Robles Fernandez, Jose Manuel Cozar, Jose Antonio Lorente, Maria Jesus Alvarez Cubero
BACKGROUND: Somatic mutations have been related to the highest incidence of metastatic disease and different treatment responses. The molecular cause of prostate cancer (PC) is still unclear; however, its progression involves alterations in oncogenes and tumor suppressor genes as well as somatic mutations such as the ones in PIK3CA gene. A high percentage of PC is considered sporadic, which means that the damage to the genes occurs by chance after birth (mainly somatic mutations will drive the cancer event)...
April 9, 2018: Urologic Oncology
https://www.readbyqxmd.com/read/29621096/pten-expression-in-mucinous-prostatic-adenocarcinoma-prostatic-adenocarcinoma-with-mucinous-features-and-adjacent-conventional-prostatic-adenocarcinoma-a-multi-institutional-study-of-92-cases
#16
Elizabeth C Bertsch, Cristina Magi-Galluzzi, Liang Cheng, Adeboye O Osunkoya
Recent studies have demonstrated that most patients with mucinous prostatic adenocarcinoma may have a better prognosis than those with conventional prostatic adenocarcinoma; however, the mechanism remains unclear. Loss of phosphatase and tensin homolog (PTEN) expression is known to occur in aggressive high-grade prostatic adenocarcinoma, but expression in mucinous prostatic adenocarcinoma has not been well characterized. In this study, we sought to analyze PTEN expression in mucinous prostatic adenocarcinoma, prostatic adenocarcinoma with mucinous features, and the adjacent conventional prostatic adenocarcinoma...
April 2018: Applied Immunohistochemistry & Molecular Morphology: AIMM
https://www.readbyqxmd.com/read/29617673/mitochondrial-complex-i-inhibitors-expose-a-vulnerability-for-selective-killing-of-pten-null-cells
#17
Adam Naguib, Grinu Mathew, Colleen R Reczek, Kaitlin Watrud, Alexandra Ambrico, Tali Herzka, Irene Casanova Salas, Matthew F Lee, Nour El-Amine, Wu Zheng, M Emilia Di Francesco, Joseph R Marszalek, Darryl J Pappin, Navdeep S Chandel, Lloyd C Trotman
A hallmark of advanced prostate cancer (PC) is the concomitant loss of PTEN and p53 function. To selectively eliminate such cells, we screened cytotoxic compounds on Pten-/- ;Trp53-/- fibroblasts and their Pten-WT reference. Highly selective killing of Pten-null cells can be achieved by deguelin, a natural insecticide. Deguelin eliminates Pten-deficient cells through inhibition of mitochondrial complex I (CI). Five hundred-fold higher drug doses are needed to obtain the same killing of Pten-WT cells, even though deguelin blocks their electron transport chain equally well...
April 3, 2018: Cell Reports
https://www.readbyqxmd.com/read/29611022/a-phase-i-open-label-two-stage-study-to-investigate-the-safety-tolerability-pharmacokinetics-and-pharmacodynamics-of-the-oral-akt-inhibitor-gsk2141795-in-patients-with-solid-tumors
#18
Carol Aghajanian, Katherine M Bell-McGuinn, Howard A Burris, Lillian L Siu, Lee-Ann Stayner, Jennifer J Wheler, David S Hong, Carla Kurkjian, Shubham Pant, Ademi Santiago-Walker, Jennifer L Gauvin, Joyce M Antal, Joanna B Opalinska, Shannon R Morris, Jeffrey R Infante
Background We sought to determine the recommended phase II dose (RP2D) and schedule of GSK2141795, an oral pan-AKT kinase inhibitor. Patients and Methods Patients with solid tumors were enrolled in the dose-escalation phase. Pharmacokinetic (PK) analysis after a single dose (Cycle 0) informed dose escalation using accelerated dose titration. Once one grade 2 toxicity or dose-limiting toxicity was observed in Cycle 1, the accelerated dose titration was terminated and a 3 + 3 dose escalation was started. Continuous daily dosing was evaluated along with two intermittent regimens (7 days on/7 days off and 3 times per week)...
April 3, 2018: Investigational New Drugs
https://www.readbyqxmd.com/read/29600194/function-of-tumor-suppressors-in-resistance-to-antiandrogen-therapy-and-luminal-epithelial-plasticity-of-aggressive-variant-neuroendocrine-prostate-cancers
#19
REVIEW
Rama Soundararajan, Ana M Aparicio, Christopher J Logothetis, Sendurai A Mani, Sankar N Maity
Combined loss of tumor suppressors (TSPs), PTEN, TP53, and RB1, is highly associated with small cell carcinoma of prostate phenotype. Recent genomic studies of human tumors as well as analyses in mouse genetic models have revealed a unique role for these TSPs in dictating epithelial lineage plasticity-a phenomenon that plays a critical role in the development of aggressive variant prostate cancer (PCa) and associated androgen therapy resistance. Here, we summarize recently published key observations on this topic and hypothesize a possible mechanism by which concurrent loss of TSPs could potentially regulate the PCa disease phenotype...
2018: Frontiers in Oncology
https://www.readbyqxmd.com/read/29581856/fibroblast-growth-factor-receptor-signaling-plays-a-key-role-in-transformation-induced-by-the-tmprss2-erg-fusion-gene-and-decreased-pten
#20
Longjiang Shao, Jianghua Wang, Omer Faruk Karatas, Shu Feng, Yiqun Zhang, Chad J Creighton, Michael Ittmann
Prostate cancer is the most common visceral malignancy and the second leading cause of cancer deaths in US men. Correlative studies in human prostate cancers reveal a frequent association of the TMPRSS2/ERG (TE) fusion gene with loss of PTEN and studies in mouse models reveal that ERG expression and PTEN loss synergistically promote prostate cancer progression. To determine the mechanism by which ERG overexpression and PTEN loss leads to transformation, we overexpressed the TE fusion gene and knocked down PTEN in an immortalized but non-transformed prostate epithelial cell line...
March 6, 2018: Oncotarget
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