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  • 1
    Online Resource
    Online Resource
    Gene silencing for epidermal growth factor receptor variant III induces cell-specific cytotoxicity
    American Association for Cancer Research (AACR) ; 2008
    In:  Molecular Cancer Therapeutics Vol. 7, No. 11 ( 2008-11-01), p. 3586-3597
    Details
    In: Molecular Cancer Therapeutics, American Association for Cancer Research (AACR), Vol. 7, No. 11 ( 2008-11-01), p. 3586-3597
    Abstract: Epidermal growth factor receptor variant III (EGFRvIII) is a constitutively active mutant form of EGFR that is expressed in 40% to 50% of gliomas and several other malignancies. Here, we describe the therapeutic effects of silencing EGFRvIII on glioma cell lines in vitro and in vivo. A small interfering RNA molecule against EGFRvIII was introduced into EGFRvIII-expressing glioma cells (U87Δ) by electroporation resulting in complete inhibition of expression of EGFRvIII as early as 48 h post-treatment. During EGFRvIII silencing, a decrease in the proliferation and invasiveness of U87Δ cells was accompanied by an increase in apoptosis (P & lt; 0.05). Notably, EGFRvIII silencing inhibited the signal transduction machinery downstream of EGFRvIII as evidenced by decreases in the activated levels of Ras and extracellular signal-regulated kinase. A lentivirus capable of expressing anti-EGFRvIII short hairpin RNA was also able to achieve progressive silencing of EGFRvIII in U87Δ cells in addition to inhibiting cell proliferation, invasiveness, and colony formation in a significant manner (P & lt; 0.05). Silencing EGFRvIII in U87Δ cultures with this virus reduced the expression of factors involved in epithelial-mesenchymal transition including N-cadherin, β-catenin, Snail, Slug, and paxillin but not E-cadherin. The anti-EGFRvIII lentivirus also affected the cell cycle progression of U87Δ cells with a decrease in G1 and increase in S and G2 fractions. In an in vivo model, tumor growth was completely inhibited in severe combined immunodeficient mice (n = 10) injected s.c. with U87Δ cells treated with the anti-EGFRvIII lentivirus (P = 0.005). We conclude that gene specific silencing of EGFRvIII is a promising strategy for treating cancers that contain this mutated receptor. [Mol Cancer Ther 2008;7(11):3586–97]
    Type of Medium: Online Resource
    ISSN: 1535-7163 , 1538-8514
    URL: Article
    DOI: 10.1158/1535-7163.MCT-08-0653
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2008
    detail.hit.zdb_id: 2062135-8
    SSG: 12
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  • 2
    Online Resource
    Online Resource
    Decline in the overall incidence of regional‐distant prostate cancer in Olmsted County, MN, 1980–2000
    Wiley ; 2005
    In:  BJU International Vol. 95, No. 7 ( 2005-05), p. 951-955
    Details
    In: BJU International, Wiley, Vol. 95, No. 7 ( 2005-05), p. 951-955
    Abstract: There are many papers in this section covering a wide range of topics relating to prostate, kidney and bladder cancer. Authors from the Mayo Clinic evaluate trends in the incidence of regional‐distant prostate cancer before and after the introduction of PSA screening in 1987 in their residents in Olmsted County. They found a decrease in the overall incidence of this type of disease, regardless of stage at initial diagnosis. Authors from the Royal Marsden describe their policy of active surveillance and contrast it with watchful waiting, differentiating clearly between the policies. These are early results, but they make interesting reading. The authors mention ongoing studies which seek to optimise the active surveillance protocol. OBJECTIVE To describe trends in the incidence of regional‐distant prostate cancer over the entire course of the disease, before and after the introduction of prostate‐specific antigen screening in 1987. PATIENTS AND METHODS All residents of Olmsted County, MN, USA, with a diagnosis of prostate cancer from 1964 to 2000 were identified using the resources of the Rochester Epidemiology Project. Their community medical records were examined to identify men with documented evidence of locally advanced (T3/4 or N+ disease) or metastatic prostate cancer between 1980 and 2000. RESULTS In all, 407 men had regional‐distant prostate cancer, based on clinical or pathological staging at the time of initial diagnosis of prostate cancer and/or on radiological information over the entire course of their illness. The age‐adjusted incidence per 100 000 men increased from 47.4 in 1980–86 to 65.8 in 1987–93, and declined to 33.3 in 1994–2000 ( P   〈  0.001). Based on clinical and radiological information over the entire course of illness (268 men) the age‐adjusted incidence of regional‐distant disease was 42.3 in 1980–86, 41.2 in 1987–93, and declined to 18.1 in 1994–2000 ( P   〈  0.001). These latter rates were 27%, 32% and 47% higher for the three periods, respectively, than rates based on clinical staging at initial diagnosis of prostate cancer. CONCLUSIONS The overall incidence of regional‐distant stages of prostate cancer has declined in recent years, regardless of the stage at initial diagnosis. This may be a result in part of early detection and curative treatments. These findings also indicate that assessing the incidence of regional‐distant prostate cancer only at the initial diagnosis underestimates the full impact of the benefits of early detection and treatment.
    Type of Medium: Online Resource
    ISSN: 1464-4096 , 1464-410X
    URL: Issue
    URL: Article
    DOI: 10.1111/bju.2005.95.issue-7
    DOI: 10.1111/j.1464-410X.2005.05445.x
    Language: English
    Publisher: Wiley
    Publication Date: 2005
    detail.hit.zdb_id: 2019983-1
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  • 3
    Online Resource
    Online Resource
    Inverse Association between Prostate Cancer and the Use of Calcium Channel Blockers
    American Association for Cancer Research (AACR) ; 2004
    In:  Cancer Epidemiology, Biomarkers & Prevention Vol. 13, No. 2 ( 2004-02-01), p. 255-259
    Details
    In: Cancer Epidemiology, Biomarkers & Prevention, American Association for Cancer Research (AACR), Vol. 13, No. 2 ( 2004-02-01), p. 255-259
    Abstract: Calcium channel blockers block calcium signal-mediated apoptosis. It is hypothesized that the use of these drugs may be associated with the development of cancer. This study investigated the association between daily use of calcium channel blockers and prostate cancer in a community-based cohort of men who participated in a longitudinal study of lower urinary tract symptoms. Study subjects were men ages 40 to 79 years by January 1, 1990, and were randomly selected from Olmsted County in Minnesota. At baseline, participants underwent an interview to determine all medications taken on a daily basis, including calcium channel blockers and to elicit a family history of prostate cancer. During follow-up, all men with a histological diagnosis of prostate cancer were identified through patient self-report and by a review of the complete medical record. Over 12,668 person years of follow-up, 15 (6.8%) of 220 calcium channel blocker users and 120 (10.5%) of 1142 nonusers developed prostate cancer (P = 0.09; odds ratio, 0.62; 95% confidence interval, 0.36–1.10). With adjustment for age and family history of prostate cancer, the risk (odds ratio, 95% confidence interval) of prostate cancer was 0.55 (0.31–0.97) in calcium channel blocker users compared with nonusers. In analyses stratified by family history of prostate cancer, the risk of prostate cancer was 0.45 (0.23–0.88) in men without a family history and 2.64 (0.82–8.47) in men with a family history of prostate cancer (P = 0.006). These findings suggest an association between prostate cancer and daily use of calcium channel blockers that varies by family history of prostate cancer.
    Type of Medium: Online Resource
    ISSN: 1055-9965 , 1538-7755
    URL: Article
    DOI: 10.1158/1055-9965.EPI-03-0093
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2004
    detail.hit.zdb_id: 2036781-8
    detail.hit.zdb_id: 1153420-5
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  • 4
    Online Resource
    Online Resource
    Gluthatione-S-transferase P1 polymorphism I105V in familial and sporadic prostate cancer
    Elsevier BV ; 2004
    In:  Cancer Genetics and Cytogenetics Vol. 155, No. 1 ( 2004-11), p. 82-86
    Details
    In: Cancer Genetics and Cytogenetics, Elsevier BV, Vol. 155, No. 1 ( 2004-11), p. 82-86
    Type of Medium: Online Resource
    ISSN: 0165-4608
    URL: Article
    DOI: 10.1016/j.cancergencyto.2004.03.015
    RVK:
    XA 10000
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2004
    detail.hit.zdb_id: 2004205-X
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  • 5
    Online Resource
    Online Resource
    Truncating Variants in p53AIP1 Disrupting DNA Damage–Induced Apoptosis Are Associated with Prostate Cancer Risk
    American Association for Cancer Research (AACR) ; 2006
    In:  Cancer Research Vol. 66, No. 21 ( 2006-11-01), p. 10302-10307
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 66, No. 21 ( 2006-11-01), p. 10302-10307
    Abstract: Germ line mutations in several genes (BRCA1, BRCA2, and CHEK2) whose products are involved in the DNA damage–signaling pathway have been implicated in prostate cancer risk. To identify additional genes in this pathway that might confer susceptibility to this cancer, we analyzed a recently identified DNA damage–response gene, p53AIP1 (a gene encoding for p53-regulated apoptosis-inducing protein 1), for genetic variants in prostate cancer. Five novel germ line variants were identified. The two truncating variants (Ser32Stop and Arg21insG) were found in 3% (4 of 132) of unselected prostate tumor samples. Genotyping of the two variants in an additional 393 men with sporadic prostate cancer showed a frequency of 3.1% (12 of 393) in contrast to 0.6% (2 of 327) in 327 unaffected men (Fisher's exact test, P = 0.018), with an odds ratio (OR) of 5.1 [95% confidence interval (95% CI), 1.1-23.0]. In addition, two of six tumors carrying the truncating variants were associated with loss of heterozygosity of the wild-type alleles, suggesting that p53AIP1 may act as a tumor suppressor. We also showed that the truncated p53AIP1 was unable to induce apoptosis and suppress cell growth in HeLa and COS-7 cells. These results suggest that loss-of-function variants in p53AIP1 associated with the risk of sporadic prostate cancer and further support the concept that the genetic defects in the DNA damage–response genes play an important role in the development of prostate cancer. (Cancer Res 2006; 66(21): 10302-7)
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/0008-5472.CAN-06-0638
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2006
    detail.hit.zdb_id: 2036785-5
    detail.hit.zdb_id: 1432-1
    detail.hit.zdb_id: 410466-3
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  • 6
    Online Resource
    Online Resource
    Mutations in CHEK2 Associated with Prostate Cancer Risk
    Elsevier BV ; 2003
    In:  The American Journal of Human Genetics Vol. 72, No. 2 ( 2003-02), p. 270-280
    Details
    In: The American Journal of Human Genetics, Elsevier BV, Vol. 72, No. 2 ( 2003-02), p. 270-280
    Type of Medium: Online Resource
    ISSN: 0002-9297
    URL: Article
    DOI: 10.1086/346094
    RVK:
    XA 10000
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2003
    detail.hit.zdb_id: 1473813-2
    SSG: 12
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  • 7
    Online Resource
    Online Resource
    Noninvasive Imaging and Radiovirotherapy of Prostate Cancer Using an Oncolytic Measles Virus Expressing the Sodium Iodide Symporter
    Elsevier BV ; 2009
    In:  Molecular Therapy Vol. 17, No. 12 ( 2009-12), p. 2041-2048
    Details
    In: Molecular Therapy, Elsevier BV, Vol. 17, No. 12 ( 2009-12), p. 2041-2048
    Type of Medium: Online Resource
    ISSN: 1525-0016
    URL: Article
    DOI: 10.1038/mt.2009.218
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2009
    detail.hit.zdb_id: 2001818-6
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  • 8
    Online Resource
    Online Resource
    Expression and significance of androgen receptor coactivators in urothelial carcinoma of the bladder
    Bioscientifica ; 2009
    In:  Endocrine-Related Cancer Vol. 16, No. 1 ( 2009-03), p. 123-137
    Details
    In: Endocrine-Related Cancer, Bioscientifica, Vol. 16, No. 1 ( 2009-03), p. 123-137
    Abstract: Urothelial carcinoma (UC) of the bladder is approximately three times more common in men than women. While the etiology for this gender difference in incidence remains unknown, a role for androgen receptor (AR) signaling has been suggested. The mechanisms by which AR activity is regulated in UC cells, however, are largely elusive. Here, we explore the significance of coregulators that are critical for the formation of a functional AR transcriptional complex, in UC cells. Using two AR-positive UC cell lines, TCC-SUP and UMUC3, we demonstrate the expression of the coactivators NCOA1, NCOA2, NCOA3, CREBBP, and EP300 in UC cells. small interfering RNA-mediated knockdown of the AR or any of these coactivators markedly impacted cell viability and abrogated androgen-dependent cell proliferation. Noteworthy, contrary to AR-positive prostate cancer cells, expression of these AR-associated coactivators was not androgen regulated in UC cells. To assess the clinical relevance of coactivator expression, we performed immunohistochemistry on paraffin-embedded sections from 55 patients with UC of the bladder. We found that while 24 out of 55 (44%) of tumors expressed the AR, each of the coactivators was expressed by 85–100% of the bladder cancers. Moreover, we noted a significant downregulation of NCOA1 expression in tumors versus adjacent, non-tumor bladder urothelium, with a mean of 68% (range 0–100) of tumor cells demonstrating NCOA1 staining versus a mean of 81% (range 0–90) of non-tumor cells ( P =0.03). Taken together, our data suggest an important role for AR-associated coactivators in UC and point toward differences in the regulation of AR activity between bladder and prostate cancer cells.
    Type of Medium: Online Resource
    ISSN: 1351-0088 , 1479-6821
    URL: Article
    DOI: 10.1677/ERC-08-0124
    Language: Unknown
    Publisher: Bioscientifica
    Publication Date: 2009
    detail.hit.zdb_id: 2010895-3
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  • 9
    Online Resource
    Online Resource
    Androgen Receptor Upregulation Mediates Radioresistance after Ionizing Radiation
    American Association for Cancer Research (AACR) ; 2015
    In:  Cancer Research Vol. 75, No. 22 ( 2015-11-15), p. 4688-4696
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 75, No. 22 ( 2015-11-15), p. 4688-4696
    Abstract: Clinical trials have established the benefit of androgen deprivation therapy (ADT) combined with radiotherapy in prostate cancer. ADT sensitizes prostate cancer to radiotherapy-induced death at least in part through inhibition of DNA repair machinery, but for unknown reasons, adjuvant ADT provides further survival benefits. Here, we show that androgen receptor (AR) expression and activity are durably upregulated following radiotherapy in multiple human prostate cancer models in vitro and in vivo. Moreover, the degree of AR upregulation correlates with survival in vitro and time to tumor progression in animal models. We also provide evidence of AR pathway upregulation, measured by a rise in serum levels of AR-regulated hK2 protein, in nearly 20% of patients after radiotherapy. Furthermore, these men were three-fold more likely to experience subsequent biochemical failure. Collectively, these data demonstrate that radiotherapy can upregulate AR signaling after therapy to an extent that negatively affects disease progression and/or survival. Cancer Res; 75(22); 4688–96. ©2015 AACR.
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/0008-5472.CAN-15-0892
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2015
    detail.hit.zdb_id: 2036785-5
    detail.hit.zdb_id: 1432-1
    detail.hit.zdb_id: 410466-3
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  • 10
    Online Resource
    Online Resource
    RhoA as a Mediator of Clinically Relevant Androgen Action in Prostate Cancer Cells
    The Endocrine Society ; 2012
    In:  Molecular Endocrinology Vol. 26, No. 5 ( 2012-05-01), p. 716-735
    Details
    In: Molecular Endocrinology, The Endocrine Society, Vol. 26, No. 5 ( 2012-05-01), p. 716-735
    Abstract: Recently, we have identified serum response factor (SRF) as a mediator of clinically relevant androgen receptor (AR) action in prostate cancer (PCa). Genes that rely on SRF for androgen responsiveness represent a small fraction of androgen-regulated genes, but distinguish benign from malignant prostate, correlate with aggressive disease, and are associated with biochemical recurrence. Thus, understanding the mechanism(s) by which SRF conveys androgen regulation to its target genes may provide novel opportunities to target clinically relevant androgen signaling. Here, we show that the small GTPase ras homolog family member A (RhoA) mediates androgen-responsiveness of more than half of SRF target genes. Interference with expression of RhoA, activity of the RhoA effector Rho-associated coiled-coil containing protein kinase 1 (ROCK), and actin polymerization necessary for nuclear translocation of the SRF cofactor megakaryocytic acute leukemia (MAL) prevented full androgen regulation of SRF target genes. Androgen treatment induced RhoA activation, increased the nuclear content of MAL, and led to MAL recruitment to the promoter of the SRF target gene FHL2. In clinical specimens RhoA expression was higher in PCa cells than benign prostate cells, and elevated RhoA expression levels were associated with aggressive disease features and decreased disease-free survival after radical prostatectomy. Overexpression of RhoA markedly increased the androgen-responsiveness of select SRF target genes, in a manner that depends on its GTPase activity. The use of isogenic cell lines and a xenograft model that mimics the transition from androgen-stimulated to castration-recurrent PCa indicated that RhoA levels are not altered during disease progression, suggesting that RhoA expression levels in the primary tumor determine disease aggressiveness. Androgen-responsiveness of SRF target genes in castration-recurrent PCa cells continued to rely on AR, RhoA, SRF, and MAL and the presence of intact SRF binding sites. Silencing of RhoA, use of Rho-associated coiled-coil containing protein kinase 1 inhibitors, or an inhibitor of SRF-MAL interaction attenuated (androgen-regulated) cell viability and blunted PCa cell migration. Taken together, these studies demonstrate that the RhoA signaling axis mediates clinically relevant AR action in PCa.
    Type of Medium: Online Resource
    ISSN: 0888-8809 , 1944-9917
    URL: Article
    DOI: 10.1210/me.2011-1130
    Language: English
    Publisher: The Endocrine Society
    Publication Date: 2012
    detail.hit.zdb_id: 1492112-1
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