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1. Bhatnagar N, Li X, Padi SK, Zhang Q, Tang MS, Guo B: Downregulation of miR-205 and miR-31 confers resistance to chemotherapy-induced apoptosis in prostate cancer cells. Cell Death Dis; 2010 Dec 09;1:e105
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  • [Title] Downregulation of miR-205 and miR-31 confers resistance to chemotherapy-induced apoptosis in prostate cancer cells.
  • Advanced prostate cancers are known to acquire not only invasive capabilities but also significant resistance to chemotherapy-induced apoptosis.
  • To understand how microRNAs (miRNAs) may contribute to prostate cancer resistance to apoptosis, we compared microRNA expression profiles of a benign prostate cancer cell line WPE1-NA22 and a highly malignant WPE1-NB26 cell line (derived from a common lineage).
  • We found that miR-205 and miR-31 are significantly downregulated in WPE1-NB26 cells, as well as in other cell lines representing advanced-stage prostate cancers.
  • By downregulating Bcl-w and E2F6, miR-205 and miR-31 promote chemotherapeutic agents-induced apoptosis in prostate cancer cells.
  • The promoter region of the miR-205 gene was cloned and was found to be hypermethylated in cell lines derived from advanced prostate cancers, contributing to the downregulation of the gene.
  • Treatment with DNA methylation inhibitor 5-aza-2'-deoxycytidine induced miR-205 expression, downregulated Bcl-w, and sensitized prostate cancer cells to chemotherapy-induced apoptosis.
  • Thus, downregulation of miR-205 and miR-31 has an important role in apoptosis resistance in advanced prostate cancer.

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  • (PMID = 21368878.001).
  • [ISSN] 2041-4889
  • [Journal-full-title] Cell death & disease
  • [ISO-abbreviation] Cell Death Dis
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R03 CA130062; United States / NCRR NIH HHS / RR / P20 RR015566-10; United States / NCI NIH HHS / CA / R03 CA130062-02; United States / NIGMS NIH HHS / GM / P30 GM103332; United States / NCRR NIH HHS / RR / P20 RR015566; United States / NCI NIH HHS / CA / CA130062; United States / NCRR NIH HHS / RR / RR015566; United States / NCI NIH HHS / CA / CA130062-02
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0 / Apoptosis Regulatory Proteins; 0 / BCL2L2 protein, human; 0 / E2F6 Transcription Factor; 0 / E2F6 protein, human; 0 / MIRN205 microRNA, human; 0 / MIRN31 microRNA, human; 0 / MicroRNAs; 776B62CQ27 / decitabine; EC 2.1.1.- / DNA Modification Methylases; M801H13NRU / Azacitidine
  • [Other-IDs] NLM/ NIHMS257670; NLM/ PMC3004480
  • [Keywords] NOTNLM ; Bcl-w / E2F6 / apoptosis / miR-205 / miR-31 / prostate cancer
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2. Nakata S, Takahashi H, Takezawa Y, Kobayashi M, Matumoto K, Kosaku N, Kawashima K: [PSA doubling time in prostate cancer relapsed after endocrine therapy]. Nihon Hinyokika Gakkai Zasshi; 2000 Jul-Aug;91(7-8):584-8
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  • [Title] [PSA doubling time in prostate cancer relapsed after endocrine therapy].
  • PURPOSE: The PSA level of prostate cancer patients generally declines after endocrine therapy, but elevates when the cancer relapses in most cases.
  • We investigated the PSA doubling time (PSA-DT) of the prostate cancer patients whose PSA declined after endocrine therapy and later re-elevated, and investigated the relationship with other parameters.
  • PATIENTS AND METHODS: We investigated 55 prostate cancer patients who underwent endocrine therapy between 1991 and 1998.
  • Their PSA re-elevated continuously after their PSA fell below 10 ng/ml after the endocrine therapy as the first line treatment.
  • First, the correlation coefficients with time and PSA were calculated in order to decide whether their PSA elevation was exponential or linear.
  • PSA-DT was calculated thereafter, and compared with the clinical stage, pathological differentiation, clinical relapse style, time from the beginning of the therapy to PSA relapse, pre-treatment PSA value, and prognosis.
  • The relationship between PSA-DT and each clinical parameter was tested using the Kruskal-Wallis test.
  • Differences in survival rates and PSA-DT were calculated using the log-rank test.
  • RESULTS: PSA elevated exponentially after cancer relapsed.
  • PSA-DT in all cases ranged from 0.5 to 26.3 months, with an average of 4.4 +/- 4.8 (S.D.) months and the median was 2.5 months.
  • PSA-DT was significantly (p < 0.01) short when the pre-treatment clinical stage was high, the time from the beginning of the therapy to PSA relapse was short, or the pre-treatment PSA value was high.
  • PSA-DT tended to be short when the pre-treatment pathological differentiation was low, but not significantly.
  • PSA-DT tended to be short when the cancer relapsed as distant metastasis rather than regional relapse, but not significantly.
  • Prognosis from the initial treatment and PSA relapse was significantly poor when the PSA-DT was short.
  • CONCLUSIONS: PSA elevated exponentially in the relapsed prostate cancer patients after the endocrine therapy.
  • PSA-DT was distributed in a very wide range, and this value was considered to reflect the malignant potential and prognosis of the cancer.
  • PSA-DT may be useful for determining the strategy after relapse.
  • [MeSH-major] Biomarkers, Tumor / blood. Neoplasm Recurrence, Local. Prostate-Specific Antigen / blood. Prostatic Neoplasms / diagnosis
  • [MeSH-minor] Aged. Aged, 80 and over. Antineoplastic Agents, Hormonal / therapeutic use. Humans. Male. Middle Aged. Neoplasm Staging. Prognosis. Time Factors

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  • (PMID = 10965743.001).
  • [ISSN] 0021-5287
  • [Journal-full-title] Nihon Hinyōkika Gakkai zasshi. The japanese journal of urology
  • [ISO-abbreviation] Nippon Hinyokika Gakkai Zasshi
  • [Language] jpn
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] JAPAN
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 0 / Biomarkers, Tumor; EC 3.4.21.77 / Prostate-Specific Antigen
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3. Kinouchi T, Kinoshita T, Kobayashi M, Ueda T, Inoue H, Takada T, Hara T: [A case of primary malignant lymphoma of the prostate presenting as urinary retention]. Hinyokika Kiyo; 2010 Oct;56(10):589-92
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  • [Title] [A case of primary malignant lymphoma of the prostate presenting as urinary retention].
  • We report a case of primary malignant lymphoma of the prostate.
  • Histological and immunocytochemical studies of transperineal biopsy of the prostate showed diffuse large B-cell non-Hogkin's lymphoma.
  • Radiological assessment of the disease confirmed stage IV according to the Ann Arbor classification.
  • Although the tumor was markedly reduced in size after four cycles of combination chemotherapy with cyclophosphamide, adriamycin, vincristine, and prednisolone, he died with brain metastasis 4 months after the diagnosis.
  • [MeSH-major] Lymphoma, Large B-Cell, Diffuse / complications. Prostatic Neoplasms / complications. Urinary Retention / etiology
  • [MeSH-minor] Aged, 80 and over. Antibiotics, Antineoplastic / administration & dosage. Antineoplastic Agents, Alkylating / administration & dosage. Antineoplastic Agents, Hormonal / administration & dosage. Antineoplastic Agents, Phytogenic / administration & dosage. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cyclophosphamide / administration & dosage. Doxorubicin / administration & dosage. Humans. Male. Prednisolone / administration & dosage. Vincristine / administration & dosage

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  • (PMID = 21063166.001).
  • [ISSN] 0018-1994
  • [Journal-full-title] Hinyokika kiyo. Acta urologica Japonica
  • [ISO-abbreviation] Hinyokika Kiyo
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article; Review
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / Antineoplastic Agents, Alkylating; 0 / Antineoplastic Agents, Hormonal; 0 / Antineoplastic Agents, Phytogenic; 5J49Q6B70F / Vincristine; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; 9PHQ9Y1OLM / Prednisolone
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4. Stevens MC, Rey A, Bouvet N, Ellershaw C, Flamant F, Habrand JL, Marsden HB, Martelli H, Sanchez de Toledo J, Spicer RD, Spooner D, Terrier-Lacombe MJ, van Unnik A, Oberlin O: Treatment of nonmetastatic rhabdomyosarcoma in childhood and adolescence: third study of the International Society of Paediatric Oncology--SIOP Malignant Mesenchymal Tumor 89. J Clin Oncol; 2005 Apr 20;23(12):2618-28
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  • [Title] Treatment of nonmetastatic rhabdomyosarcoma in childhood and adolescence: third study of the International Society of Paediatric Oncology--SIOP Malignant Mesenchymal Tumor 89.
  • PURPOSE: To improve outcome for children with nonmetastatic rhabdomyosarcoma and to reduce systematic use of local therapy.
  • PATIENTS AND METHODS: Five hundred three previously untreated patients aged from birth to 18 years, recruited between 1989 and 1995, were allocated to one of six treatment schedules by site and stage.
  • Primary site, T-stage, and pathologic subtype were independent factors in predicting OS by multivariate analysis.
  • Differences between EFS and OS reflected local treatment strategy and successful re-treatment for some patients after relapse.
  • Patients with genitourinary nonbladder prostate tumors had the most favorable outcome (5-year OS, 94%): the majority were boys with paratesticular tumors treated successfully without alkylating agents.
  • Patients with stage III disease treated with a novel six-drug combination showed improved survival compared with the Malignant Mesenchymal Tumor 84 study (MMT 84; 5-year OS, 60% v 42%, respectively).
  • OS was not significantly better than that achieved in the previous MMT 84 study, but 49% of survivors were cured without significant local therapy.
  • CONCLUSION: Selective avoidance of local therapy is justified in some patients, though further work is required to prospectively identify those for whom this is most applicable.
  • The value of the new six-drug chemotherapy combination is being evaluated further in a randomized study (MMT 95).
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Rhabdomyosarcoma / drug therapy. Rhabdomyosarcoma / pathology
  • [MeSH-minor] Adolescent. Carboplatin / administration & dosage. Child. Child, Preschool. Dactinomycin / administration & dosage. Disease-Free Survival. Drug Administration Schedule. Epirubicin / administration & dosage. Etoposide / administration & dosage. Female. Humans. Ifosfamide / administration & dosage. Infant. Infant, Newborn. Male. Multivariate Analysis. Neoplasm Recurrence, Local. Neoplasm Staging. Prognosis. Teniposide / administration & dosage. Treatment Outcome. Vincristine / administration & dosage

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  • [CommentIn] J Clin Oncol. 2005 Apr 20;23(12):2586-7 [15728222.001]
  • (PMID = 15728225.001).
  • [ISSN] 0732-183X
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Multicenter Study; Randomized Controlled Trial
  • [Publication-country] United States
  • [Chemical-registry-number] 1CC1JFE158 / Dactinomycin; 3Z8479ZZ5X / Epirubicin; 5J49Q6B70F / Vincristine; 6PLQ3CP4P3 / Etoposide; 957E6438QA / Teniposide; BG3F62OND5 / Carboplatin; UM20QQM95Y / Ifosfamide; IVA protocol; VCE protocol
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5. Pinthus JH, Sheffer Y, Nagler A, Fridman E, Mor Y, Genina O, Pines M: Inhibition of Wilms tumor xenograft progression by halofuginone is accompanied by activation of WT-1 gene expression. J Urol; 2005 Oct;174(4 Pt 2):1527-31
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  • [Title] Inhibition of Wilms tumor xenograft progression by halofuginone is accompanied by activation of WT-1 gene expression.
  • PURPOSE: Wilms tumor (WT) is the most common malignant neoplasm of the urinary tract in children.
  • Although it is curable with long-term survival, the combination of surgery, chemotherapy and often radiotherapy in some cases results in severe complications in adulthood.
  • Therefore, novel therapeutic strategies that would decrease treatment burden and improve outcome for high risk patients are required.
  • We evaluated the efficacy of halofuginone, an inhibitor of collagen type I synthesis and angiogenesis, to inhibit WT development in xenografts models.
  • RESULTS: Independent of disease stage, tumor location or administration route, halofuginone caused a decrease in angiogenesis that resulted in marked inhibition of tumor development.
  • This result was accompanied by a reduction in collagen synthesis, reduced levels of hepatocyte growth factor receptor MET and increased levels of the tumor suppressor protein WT1.
  • In culture halofuginone increased the synthesis of WT1 in the human WT cell-line SK-NEP-1 and in other cancer cell lines such as hepatocellular carcinoma and prostate cancer.
  • Because of its unique mode of action, halofuginone may decrease the treatment burden when combined with chemotherapy.
  • [MeSH-major] Angiogenesis Inhibitors / pharmacology. Kidney Neoplasms / drug therapy. Quinazolines / pharmacology. WT1 Proteins / biosynthesis. Wilms Tumor / drug therapy

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  • (PMID = 16148645.001).
  • [ISSN] 0022-5347
  • [Journal-full-title] The Journal of urology
  • [ISO-abbreviation] J. Urol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Piperidines; 0 / Quinazolines; 0 / Quinazolinones; 0 / WT1 Proteins; 9007-34-5 / Collagen; EC 2.7.10.1 / Proto-Oncogene Proteins c-met; EC 2.7.10.1 / Receptor, ErbB-2; L31MM1385E / halofuginone
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6. Singh RK, Lokeshwar BL: Depletion of intrinsic expression of Interleukin-8 in prostate cancer cells causes cell cycle arrest, spontaneous apoptosis and increases the efficacy of chemotherapeutic drugs. Mol Cancer; 2009 Jul 31;8:57
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  • [Title] Depletion of intrinsic expression of Interleukin-8 in prostate cancer cells causes cell cycle arrest, spontaneous apoptosis and increases the efficacy of chemotherapeutic drugs.
  • The androgen-independent prostate cancer (AIPC) is the terminal stage of the disease.
  • Many chemokines and cytokines are suspects to cause this increased tumor cell survival that ultimately leads to resistance to therapy and demise of the host.
  • The mechanism of IL-8 mediated survival and therapeutic resistance in AIPC cells is unclear at present.
  • The purpose of this report is to show the pervasive role of IL-8 in malignant progression of androgen-independent prostate cancer (AIPC) and to provide a potential new therapeutic avenue, using RNA interference.
  • More significantly, depletion of intracellular IL-8 increased the cytotoxic activity of multiple chemotherapeutic drugs.
  • CONCLUSION: These results show the pervasive role of IL-8 in promoting tumor cell survival, and resistance to cytotoxic drugs, regardless of the cytotoxic mechanism of antiproliferative drugs, and point to potential therapeutic significance of IL-8 depletion in men with AIPC.

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  • (PMID = 19646263.001).
  • [ISSN] 1476-4598
  • [Journal-full-title] Molecular cancer
  • [ISO-abbreviation] Mol. Cancer
  • [Language] ENG
  • [Grant] United States / NCCIH NIH HHS / AT / R01 AT003544; United States / NCI NIH HHS / CA / R01 CA061038; United States / NCCIH NIH HHS / AT / 1 R01 AT 003544; United States / NCI NIH HHS / CA / 5R01 CA 061038
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Apoptosis Regulatory Proteins; 0 / Interleukin-8; 0 / RNA, Small Interfering; 0 / Recombinant Proteins; 0 / VEGFA protein, human; 0 / Vascular Endothelial Growth Factor A
  • [Other-IDs] NLM/ PMC2729725
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7. Morgan TM, Koreckij TD, Corey E: Targeted therapy for advanced prostate cancer: inhibition of the PI3K/Akt/mTOR pathway. Curr Cancer Drug Targets; 2009 Mar;9(2):237-49
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  • [Title] Targeted therapy for advanced prostate cancer: inhibition of the PI3K/Akt/mTOR pathway.
  • A large number of novel therapeutics is currently undergoing clinical evaluation for the treatment of prostate cancer, and small molecule signal transduction inhibitors are a promising class of agents.
  • These inhibitors have recently become a standard therapy in renal cell carcinoma and offer significant promise in prostate cancer.
  • Through an understanding of the key pathways involved in prostate cancer progression, a rational drug design can be aimed at the molecules critical to cellular signaling.
  • This may enable administration of selective therapies based on the expression of molecular targets, more appropriately individualizing treatment for prostate cancer patients.
  • One pathway with a prominent role in prostate cancer is the PI3K/Akt/mTOR pathway.
  • Current estimates suggest that PI3K/Akt/mTOR signaling is upregulated in 30-50% of prostate cancers, often through loss of PTEN.
  • Molecular changes in the PI3K/Akt/mTOR signaling pathway have been demonstrated to differentiate benign from malignant prostatic epithelium and are associated with increasing tumor stage, grade, and risk of biochemical recurrence.
  • Multiple inhibitors of this pathway have been developed and are being assessed in the laboratory and in clinical trials, with much attention focusing on mTOR inhibition.
  • Current clinical trials in prostate cancer are assessing efficacy of mTOR inhibitors in combination with multiple targeted or traditional chemotherapies, including bevacizumab, gefitinib, and docetaxel.
  • Completion of these trials will provide substantial information regarding the importance of this pathway in prostate cancer and the clinical implications of its targeted inhibition.
  • In this article we review the data surrounding PI3K/Akt/mTOR inhibition in prostate cancer and their clinical implications.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Oncogene Protein v-akt / antagonists & inhibitors. Phosphatidylinositol 3-Kinases / antagonists & inhibitors. Prostatic Neoplasms / drug therapy. Protein Kinases / drug effects. Signal Transduction / drug effects

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  • (PMID = 19275762.001).
  • [ISSN] 1873-5576
  • [Journal-full-title] Current cancer drug targets
  • [ISO-abbreviation] Curr Cancer Drug Targets
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P50 CA097186; United States / NCI NIH HHS / CA / P50 CA 097186; United States / NCI NIH HHS / CA / R01 CA125395; United States / NCI NIH HHS / CA / P01 CA085859; United States / NCI NIH HHS / CA / P01 CA 85859-01A1; United States / NCI NIH HHS / CA / 5R01 CA 125395-02; United States / NCI NIH HHS / CA / R01 CA125395-02
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Androgen Receptor Antagonists; 0 / Antineoplastic Agents; EC 2.7.- / Protein Kinases; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.1.1 / MTOR protein, human; EC 2.7.1.1 / TOR Serine-Threonine Kinases; EC 2.7.11.1 / Oncogene Protein v-akt
  • [Number-of-references] 139
  • [Other-IDs] NLM/ NIHMS224512; NLM/ PMC2921605
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8. Luchman HA, Benediktsson H, Villemaire ML, Peterson AC, Jirik FR: The pace of prostatic intraepithelial neoplasia development is determined by the timing of Pten tumor suppressor gene excision. PLoS One; 2008;3(12):e3940
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  • [Title] The pace of prostatic intraepithelial neoplasia development is determined by the timing of Pten tumor suppressor gene excision.
  • Loss of the PTEN tumor suppressor is a common occurrence in human prostate cancer, particularly in advanced disease.
  • In keeping with its role as a pivotal upstream regulator of the phosphatidylinositol 3-kinase signaling pathway, experimentally-induced deletion of Pten in the murine prostate invariably results in neoplasia.
  • However, and unlike humans where prostate tumorigenesis likely evolves over decades, disease progression in the constitutively Pten deficient mouse prostate is relatively rapid, culminating in invasive cancer within several weeks post-puberty.
  • Given that the prostate undergoes rapid androgen-dependent growth at puberty, and that Pten excisions during this time might be especially tumorigenic, we hypothesized that delaying prostate-specific Pten deletions until immediately after puberty might alter the pace of tumorigenesis.
  • To this end we generated mice with a tamoxifen-inducible Cre recombinase transgene enabling temporal control over prostate-specific gene alterations.
  • Despite evidence of increased Akt/mTOR/S6K axis activity at early time points in Pten-deficient epithelial cells, excisions induced in the post-pubertal (6 wk-old) prostate yielded gradual acquisition of a range of lesions.
  • These progressed from pre-malignant changes (nuclear atypia, focal hyperplasia) and low grade prostatic intraepithelial neoplasia (PIN) at 16-20 wks post-tamoxifen exposure, to overtly malignant lesions by approximately 1 yr of age, characterized by high-grade PIN and microinvasive carcinoma.
  • In contrast, when Pten excisions were triggered in the pre-pubertal (2 week-old) prostate, neoplasia evolved over a more abbreviated time-frame, with a spectrum of premalignant lesions, as well as overt PIN and microinvasive carcinoma by 10-12 wks post-tamoxifen exposure.
  • These results indicate that the developmental stage at which Pten deletions are induced dictates the pace of PIN development.
  • [MeSH-major] Gene Deletion. Genes, Tumor Suppressor. PTEN Phosphohydrolase / genetics. Prostatic Intraepithelial Neoplasia / enzymology. Prostatic Intraepithelial Neoplasia / pathology. Prostatic Neoplasms / enzymology. Prostatic Neoplasms / pathology
  • [MeSH-minor] Androgen-Binding Protein / genetics. Animals. Apoptosis. Arrestins / metabolism. Cell Proliferation. Crosses, Genetic. Disease Progression. Epithelium / enzymology. Epithelium / pathology. Female. Humans. Integrases / metabolism. Male. Mice. Neoplasm Invasiveness. Phosphatidylinositol 3-Kinases / metabolism. Precancerous Conditions / drug therapy. Precancerous Conditions / enzymology. Precancerous Conditions / genetics. Precancerous Conditions / pathology. Rats. Ribosomal Protein S6 / metabolism. Tamoxifen / analogs & derivatives. Tamoxifen / therapeutic use. Time Factors. Up-Regulation

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  • (PMID = 19081794.001).
  • [ISSN] 1932-6203
  • [Journal-full-title] PloS one
  • [ISO-abbreviation] PLoS ONE
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Androgen-Binding Protein; 0 / Arrestins; 0 / Ribosomal Protein S6; 0 / beta-arrestin; 094ZI81Y45 / Tamoxifen; 17197F0KYM / afimoxifene; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.7.- / Cre recombinase; EC 2.7.7.- / Integrases; EC 3.1.3.48 / Pten protein, mouse; EC 3.1.3.67 / PTEN Phosphohydrolase
  • [Other-IDs] NLM/ PMC2597775
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9. Cavarretta IT, Neuwirt H, Zaki MH, Steiner H, Hobisch A, Nemeth JA, Culig Z: Mcl-1 is regulated by IL-6 and mediates the survival activity of the cytokine in a model of late stage prostate carcinoma. Adv Exp Med Biol; 2008;617:547-55
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Mcl-1 is regulated by IL-6 and mediates the survival activity of the cytokine in a model of late stage prostate carcinoma.
  • The proinflammatory cytokine interleukin-6 (IL-6) has been considered a positive growth factor in late stage prostate cancer (PC) cells and a potential target for therapeutic interference.
  • Dysregulation of Bcl-2 family members could be implicated in the acquisition of resistance to apoptosis in malignant cell lines.
  • These data support the concept of anti-IL-6 therapy in human PC.
  • [MeSH-major] Apoptosis / drug effects. Gene Expression Regulation, Neoplastic / drug effects. Interleukin-6 / pharmacology. Neoplasms, Hormone-Dependent / drug therapy. Prostatic Neoplasms / drug therapy. Proto-Oncogene Proteins c-bcl-2 / genetics
  • [MeSH-minor] Antibodies, Monoclonal / pharmacology. Disease Progression. Humans. Male. Mitogen-Activated Protein Kinase 1 / antagonists & inhibitors. Mitogen-Activated Protein Kinase 1 / metabolism. Mitogen-Activated Protein Kinase 3 / antagonists & inhibitors. Mitogen-Activated Protein Kinase 3 / metabolism. Myeloid Cell Leukemia Sequence 1 Protein. RNA, Small Interfering / pharmacology. Tumor Cells, Cultured. p38 Mitogen-Activated Protein Kinases / antagonists & inhibitors. p38 Mitogen-Activated Protein Kinases / metabolism

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  • (PMID = 18497081.001).
  • [ISSN] 0065-2598
  • [Journal-full-title] Advances in experimental medicine and biology
  • [ISO-abbreviation] Adv. Exp. Med. Biol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Interleukin-6; 0 / Myeloid Cell Leukemia Sequence 1 Protein; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / RNA, Small Interfering; 0 / siltuximab; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 1; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 3; EC 2.7.11.24 / p38 Mitogen-Activated Protein Kinases
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10. Kurokawa K, Suzuki K, Yamanaka H: [Treatment strategy for locally advanced prostate cancer]. Gan To Kagaku Ryoho; 2003 Jan;30(1):38-42
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  • [Title] [Treatment strategy for locally advanced prostate cancer].
  • With the increasing aged population, prostate cancer has become one of the commonest malignant tumors in the United States.
  • The incidence of prostate cancer is the highest among malignant tumors in males, and the mortality rate is the second highest following lung cancer.
  • Even when prostate cancer is diagnosed to be in the early stage preoperatively, its excised lesions are often judged pathohistologically to be locally advanced tumor (staging error).
  • Therefore, to estimate the exact pathological stage of excised lesions by preoperative parameters such as clinical T, PSA and biopsy Gleason Score, Partin's nomogram is generally used in the United States.
  • Currently, the standard methods for the treatment of locally advanced prostate cancer may be external beam radiotherapy and brachytherapy with neoadjuvant hormonal therapy and intraprostate 125I and 103Pd seeds with neoadjuvant hormonal therapy, although the long-term results are unknown.
  • In our study, similar to a report by Messing et al., adjuvant hormonal therapy might be effective in patients in whom the tumor was diagnosed as being in the early stage but was later found to be N (+) after its operation.
  • [MeSH-major] Brachytherapy. Gonadotropin-Releasing Hormone / agonists. Prostatic Neoplasms / drug therapy. Prostatic Neoplasms / radiotherapy
  • [MeSH-minor] Chemotherapy, Adjuvant. Combined Modality Therapy. Humans. Male. Neoadjuvant Therapy. Neoplasm Staging. Prognosis. Prostate-Specific Antigen / blood. Survival Rate

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  • (PMID = 12557703.001).
  • [ISSN] 0385-0684
  • [Journal-full-title] Gan to kagaku ryoho. Cancer & chemotherapy
  • [ISO-abbreviation] Gan To Kagaku Ryoho
  • [Language] jpn
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 33515-09-2 / Gonadotropin-Releasing Hormone; EC 3.4.21.77 / Prostate-Specific Antigen
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11. Berruti A, Dogliotti L, Mosca A, Gorzegno G, Bollito E, Mari M, Tarabuzzi R, Poggio M, Torta M, Fontana D, Angeli A: Potential clinical value of circulating chromogranin A in patients with prostate carcinoma. Ann Oncol; 2001;12 Suppl 2:S153-7
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  • [Title] Potential clinical value of circulating chromogranin A in patients with prostate carcinoma.
  • BACKGROUND: Neuroendocrine (NE) differentiation of prostate adenocarcinoma has received increasing attention in recent years as a result of possible implications for prognosis and therapy.
  • The presence of NE tumor subpopulation can be gauged non invasively by measuring circulating levels of secretory products, primarily chromogranin A (CgA).
  • METHODS: This article provides a review on published papers evaluating circulating CgA in prostate cancer patients.
  • RESULTS: Circulating CgA levels were found to be higher in prostate cancer patients than in patients with benign or pre-malignant prostatic diseases.
  • In patients with malignancy, they correlated either to the stage of disease or to the condition of hormone refractoriness.
  • CgA levels did not correlate with serum prostate specific antigen (PSA) and were supranormal in the majority of advanced patients with PSA within normality.
  • CgA values were not substantially affected by either endocrine therapy or chemotherapy.
  • CONCLUSIONS: Present data suggest a potential role of circulating CgA in the management of prostate cancer patients.
  • Serial evaluation of circulating CgA could provide information on changes in the NE phenotype expression as a consequence of tumor progression and/or treatment administration.

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  • (PMID = 11762344.001).
  • [ISSN] 0923-7534
  • [Journal-full-title] Annals of oncology : official journal of the European Society for Medical Oncology
  • [ISO-abbreviation] Ann. Oncol.
  • [Language] ENG
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Androgen Antagonists; 0 / Biomarkers, Tumor; 0 / CHGA protein, human; 0 / Chromogranin A; 0 / Chromogranins; EC 3.4.21.77 / Prostate-Specific Antigen
  • [Number-of-references] 42
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12. Huang J, Yao JL, di Sant'Agnese PA, Yang Q, Bourne PA, Na Y: Immunohistochemical characterization of neuroendocrine cells in prostate cancer. Prostate; 2006 Sep 15;66(13):1399-406
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  • [Title] Immunohistochemical characterization of neuroendocrine cells in prostate cancer.
  • BACKGROUND: Neuroendocrine (NE) cells increase in high grade/stage prostate cancer (PC) and may contribute to androgen-independent cancer.
  • METHODS: PC tissue was stained immunohistochemically for luminal secretory cell-associated cytokeratin, basal cell markers, ki-67, androgen receptor (AR), PSA, prostate acid phosphatase (PAP), and alpha-methylacyl coenzyme A racemase (AMACR).
  • The benign NE cells are negative for AMACR while the malignant NE cells are positive for AMACR.
  • CONCLUSIONS: NE cells of PC constitute a unique subset of cancer cells, which have a unique immunohistochemical profile.
  • They do not express AR, consistent with their resistance to hormonal therapy.
  • They are post-mitotic cells but are malignant and part of the tumor.
  • [MeSH-major] Neuroendocrine Tumors / metabolism. Neuroendocrine Tumors / pathology. Prostatic Neoplasms / metabolism. Prostatic Neoplasms / pathology
  • [MeSH-minor] Acid Phosphatase / genetics. Acid Phosphatase / metabolism. Androgen Antagonists / pharmacology. Drug Resistance, Neoplasm. Gene Expression Regulation, Neoplastic. Humans. Immunohistochemistry. Keratins / genetics. Keratins / metabolism. Ki-67 Antigen / genetics. Ki-67 Antigen / metabolism. Male. Phenotype. Prostate-Specific Antigen / genetics. Prostate-Specific Antigen / metabolism. Racemases and Epimerases / genetics. Racemases and Epimerases / metabolism. Receptors, Androgen / genetics. Receptors, Androgen / metabolism

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  • (PMID = 16865726.001).
  • [ISSN] 0270-4137
  • [Journal-full-title] The Prostate
  • [ISO-abbreviation] Prostate
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Androgen Antagonists; 0 / Ki-67 Antigen; 0 / Receptors, Androgen; 68238-35-7 / Keratins; EC 3.1.3.2 / Acid Phosphatase; EC 3.4.21.77 / Prostate-Specific Antigen; EC 5.1.- / Racemases and Epimerases; EC 5.1.99.4 / alpha-methylacyl-CoA racemase
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13. Qiu YQ, Leuschner I, Braun PM: Androgen receptor expression in clinically localized prostate cancer: immunohistochemistry study and literature review. Asian J Androl; 2008 Nov;10(6):855-63
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  • [Title] Androgen receptor expression in clinically localized prostate cancer: immunohistochemistry study and literature review.
  • AIM: To evaluate androgen receptor (AR) expression in clinically localized prostate cancer (PCa).
  • METHODS: Specimens were studied from 232 patients who underwent radical prostatectomy for clinically localized prostatic adenocarcinoma without neoadjuvant hormonal therapy or chemotherapy at our institution between November 2001 and June 2005.
  • The mean AR density in the hot spots of different histological areas within the same sections were compared and the correlation of malignant epithelial AR density with clinicopathological parameters such as Gleason score, tumor, nodes and metastases (TNM) stage and pre-treatment prostate-specific antigen (PSA) value was assessed.
  • RESULTS: AR immunoreactivity was almost exclusively nuclear and was observed in tumor cells, non-neoplastic glandular epithelial cells and a proportion of peritumoral and interglandular stromal cells.
  • Mean percentage of AR-positive epithelial cells was significantly higher in cancer tissues than that in normal prostate tissues (mean +/- SD, 90.0% +/- 9.3% vs. 85.3 +/- ?9.7%, P < 0.001).
  • The percentage of AR immunoreactive prostatic cancer nuclei and histological score were not correlated with existing parameters such as Gleason score, tumor, nodes and metastases stage and pre-treatment PSA value in this surgically treated cohort.
  • [MeSH-major] Adenocarcinoma / genetics. Prostatic Neoplasms / genetics. Receptors, Androgen / biosynthesis. Receptors, Androgen / genetics
  • [MeSH-minor] Aged. Humans. Immunohistochemistry. Male. Middle Aged. Neoplasm Metastasis. Neoplasm Staging. Paraffin Embedding. Prostate-Specific Antigen / analysis. Prostate-Specific Antigen / metabolism. Prostatectomy

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  • [Copyright] (c) 2008, Asian Journal of Andrology, SIMM and SJTU. All rights reserved.
  • (PMID = 18958349.001).
  • [ISSN] 1008-682X
  • [Journal-full-title] Asian journal of andrology
  • [ISO-abbreviation] Asian J. Androl.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Receptors, Androgen; EC 3.4.21.77 / Prostate-Specific Antigen
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14. Bullock MJ, Srigley JR, Klotz LH, Goldenberg SL: Pathologic effects of neoadjuvant cyproterone acetate on nonneoplastic prostate, prostatic intraepithelial neoplasia, and adenocarcinoma: a detailed analysis of radical prostatectomy specimens from a randomized trial. Am J Surg Pathol; 2002 Nov;26(11):1400-13
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  • [Title] Pathologic effects of neoadjuvant cyproterone acetate on nonneoplastic prostate, prostatic intraepithelial neoplasia, and adenocarcinoma: a detailed analysis of radical prostatectomy specimens from a randomized trial.
  • Neoadjuvant hormonal therapy (NHT; androgen ablation) is used prior to radical prostatectomy (RP) in an attempt to pathologically "downstage" prostatic adenocarcinoma and ultimately to improve disease-free survival.
  • This study describes the pathologic effects of NHT with the antiandrogen cyproterone acetate, 300 mg/day for 12 weeks, on the RP specimens from men with clinically localized (stage T1 or T2) prostatic adenocarcinoma.
  • The prevalence and extent of morphologic effects were recorded for the nonneoplastic prostate, high-grade prostatic intraepithelial neoplasia, and invasive adenocarcinoma.
  • The commonest effects on the nonneoplastic prostate were atrophy and basal cell hyperplasia and prominence.
  • High-grade prostatic intraepithelial neoplasia was more commonly identified in the surgery alone group than the CPA group (p <0.01).
  • In the CPA group, flat and low tufted patterns of high-grade prostatic intraepithelial neoplasia predominated.
  • In many cases there was prominence of collagenous stroma, obscuring malignant glands.
  • Compared with the surgery alone group, the CPA group RP specimens had a significantly lower mean specimen weight (40.3 g vs 46.5 g, p = 0.025) and less tumor extent by several measures.
  • Organ-confined tumor (stage pT2, margin negative) was found in 41.6% of the CPA group compared with 19.8% of the surgery alone group (p = 0.0017).
  • We consider that the difference in margin positivity is the result of tumor shrinkage with a decreased likelihood of sampling in routine sections.
  • The higher rate of elevation in the CPA group largely resulted from an increase in primary or secondary Gleason score 5 tumor, a morphologic artifact introduced by NHT.
  • Monotherapy with CPA has similar pathologic effects on benign and malignant prostate tissue as does dual agent androgen blockade.
  • [MeSH-major] Adenocarcinoma / drug therapy. Antineoplastic Agents / therapeutic use. Cyproterone Acetate / therapeutic use. Prostate / drug effects. Prostatic Intraepithelial Neoplasia / drug therapy. Prostatic Neoplasms / drug therapy
  • [MeSH-minor] Humans. Male. Middle Aged. Neoadjuvant Therapy. Treatment Outcome

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  • (PMID = 12409716.001).
  • [ISSN] 0147-5185
  • [Journal-full-title] The American journal of surgical pathology
  • [ISO-abbreviation] Am. J. Surg. Pathol.
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Multicenter Study; Randomized Controlled Trial
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 4KM2BN5JHF / Cyproterone Acetate
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15. Yashi M, Nukui A, Kurokawa S, Ochi M, Ishikawa S, Goto K, Kobayashi Y, Muraishi O, Tokue A: Elevated serum progastrin-releasing peptide (31-98) level is a predictor of short response duration after hormonal therapy in metastatic prostate cancer. Prostate; 2003 Sep 1;56(4):305-12
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  • [Title] Elevated serum progastrin-releasing peptide (31-98) level is a predictor of short response duration after hormonal therapy in metastatic prostate cancer.
  • BACKGROUND: The neuroendocrine (NE) pathway has been attracting attention as a mechanism for the androgen-independent progression because the neuropeptide provokes tumor growth and inhibits apoptosis under androgen-deprived milieu in prostate cancer cells.
  • On the basis that serum progastrin-releasing peptide (ProGRP) is elevated in patients with advanced disease stage, we examined the prognostic value of the neuropeptide.
  • METHODS: Serum ProGRP status was determined with an enzyme-linked immunosorbent assay (ELISA) in 460 men with benign and malignant prostatic diseases, chronic renal failure, and healthy controls.
  • Seventy patients with metastatic prostate cancer including four patients (5.7%) with NE carcinoma who underwent hormonal therapy were enrolled in the prognostic analyses by Cox proportional hazards model.
  • RESULTS: The serum status steadily shifted toward predominant expression of ProGRP with the progression of prostate cancer into metastatic and androgen-independent stages.
  • Univariate analysis revealed that the deteriorated performance status (PS) and extent of bony disease (EOD), and high serum alkaline phosphatase (ALP), serum ProGRP, and nadir prostate-specific antigen (PSA) levels were associated with a lower progression-free survival (PFS) rate (P < 0.005).
  • Serum ProGRP was the most significant predictor among pre-treatment factors in this model (P = 0.0094).
  • CONCLUSIONS: The neuropeptide precursor ProGRP is a distinct serum marker that is useful to know the NE milieu and provides prognostic information in patients with advanced prostate cancer.
  • Standard therapy for metastatic prostate cancer may make progress when further studies will clarify the causative link between serum ProGRP level and androgen-independent disease progression.
  • [MeSH-major] Biomarkers, Tumor / analysis. Gastrointestinal Hormones / analysis. Neoplasm Metastasis. Neoplasm Staging / methods. Peptide Fragments / analysis. Peptides / analysis. Prostatic Neoplasms / drug therapy. Prostatic Neoplasms / pathology. Recombinant Proteins / analysis
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Androgens / pharmacology. Antineoplastic Agents, Hormonal / pharmacology. Drug Resistance, Neoplasm. Enzyme-Linked Immunosorbent Assay. Humans. Male. Middle Aged. Predictive Value of Tests. Prognosis. Prostate-Specific Antigen / analysis. Treatment Outcome

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  • [Copyright] Copyright 2003 Wiley-Liss, Inc.
  • (PMID = 12858359.001).
  • [ISSN] 0270-4137
  • [Journal-full-title] The Prostate
  • [ISO-abbreviation] Prostate
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Androgens; 0 / Antineoplastic Agents, Hormonal; 0 / Biomarkers, Tumor; 0 / Gastrointestinal Hormones; 0 / Peptide Fragments; 0 / Peptides; 0 / Recombinant Proteins; 0 / pro-gastrin-releasing peptide (31-98); EC 3.4.21.77 / Prostate-Specific Antigen
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16. Gray A, Raff AB, Chiriva-Internati M, Chen SY, Kast WM: A paradigm shift in therapeutic vaccination of cancer patients: the need to apply therapeutic vaccination strategies in the preventive setting. Immunol Rev; 2008 Apr;222:316-27
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  • [Title] A paradigm shift in therapeutic vaccination of cancer patients: the need to apply therapeutic vaccination strategies in the preventive setting.
  • An extraordinary variety of potential therapeutic vaccine strategies directed against a wide variety of tumor antigens has been explored in clinical trials.
  • To date, none of these cancer immunotherapies have been approved by the Food and Drug Administration for use in humans.
  • A significant problem is that the vast majority of such clinical trials are carried out in patients with advanced or metastatic cancer.
  • The immune systems of these patients are considerably compromised as a result of tumor- and treatment-mediated immunosuppression.
  • Even in cases where patients are immunized in the adjuvant setting, where there is minimal residual disease, vaccines directed against tumor-associated antigens have failed to mediate eradication of tumors in the overwhelming majority of cases.
  • Recently, we and others have experimented with administering therapeutic cancer vaccines in the preventive setting.
  • This is achieved by vaccinating at the earliest possible stage of carcinogenesis.
  • These studies have demonstrated that early vaccination is extremely effective in eliciting an anti-tumor immune response that leads to unprecedented improvements in the survival of mice that spontaneously develop cancer.
  • Certain human cancers, notably prostate adenocarcinoma and cervical cancer, can currently be detected at very early stages of carcinogenesis.
  • Therapeutic vaccines are available for these diseases, opening up the possibility of administering vaccinations early to patients diagnosed with pre-malignant lesions to halt disease progression.
  • Earlier detection of these cancers, combined with existing vaccines directed against them, will soon make them targets for therapeutic vaccination in the preventive setting.
  • The ability to immunize patients at the very earliest stages of carcinogenesis, when they have fully competent immune systems, has the potential to cause a paradigm shift in how therapeutic cancer vaccines are tested and used clinically.
  • [MeSH-major] Cancer Vaccines / therapeutic use. Immunotherapy / methods. Neoplasms / immunology
  • [MeSH-minor] Animals. Antigens, Neoplasm / immunology. Female. Gene Expression Regulation, Neoplastic. Humans. Immune Tolerance / immunology. Immunocompromised Host. Immunotherapy, Adoptive. Male. Mice. Papillomaviridae / immunology. Papillomavirus Infections / immunology. Papillomavirus Infections / therapy. Papillomavirus Vaccines / immunology. Viral Vaccines / immunology

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  • (PMID = 18364011.001).
  • [ISSN] 1600-065X
  • [Journal-full-title] Immunological reviews
  • [ISO-abbreviation] Immunol. Rev.
  • [Language] eng
  • [Grant] United States / NIGMS NIH HHS / GM / T32 GM 067587
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Cancer Vaccines; 0 / Papillomavirus Vaccines; 0 / Viral Vaccines
  • [Number-of-references] 90
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17. Thors L, Bergh A, Persson E, Hammarsten P, Stattin P, Egevad L, Granfors T, Fowler CJ: Fatty acid amide hydrolase in prostate cancer: association with disease severity and outcome, CB1 receptor expression and regulation by IL-4. PLoS One; 2010 Aug 19;5(8):e12275
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  • [Title] Fatty acid amide hydrolase in prostate cancer: association with disease severity and outcome, CB1 receptor expression and regulation by IL-4.
  • BACKGROUND: Recent data have indicated that there may be a dysregulation of endocannabinoid metabolism in cancer.
  • Here we have investigated the expression of the endocannabinoid metabolising enzyme fatty acid amide hydrolase (FAAH) in a well characterised tissue microarray from patients diagnosed with prostate cancer at transurethral resection for voiding problems.
  • METHODOLOGY/PRINCIPAL FINDINGS: FAAH immunoreactivity (FAAH-IR) was assessed in formalin-fixed paraffin-embedded non-malignant and tumour cores from 412 patients with prostate cancer.
  • Tumour epithelial FAAH-IR was positively correlated with the disease severity at diagnosis (Gleason score, tumour stage, % of the specimen that contained tumour) for cases with mid-range CB(1)IR scores, but not for those with high CB(1)IR scores.
  • For the 281 cases who only received palliative therapy at the end stages of the disease, a high tumour epithelial FAAH-IR was associated with a poor disease-specific survival.
  • Interleukin-4 (IL-4) receptor IR was found on tumour epithelial cells and incubation of prostate cancer PC-3 and R3327 AT1 cells with IL-4 increased their FAAH activity.
  • CONCLUSIONS/SIGNIFICANCE: Tumour epithelial FAAH-IR is associated with prostate cancer severity and outcome at mid-range, but not high, CB(1)IR scores.
  • The correlation with CB(1)IR in the tumour tissue may be related to a common local dysregulation by a component of the tumour microenvironment.

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  • (PMID = 20808855.001).
  • [ISSN] 1932-6203
  • [Journal-full-title] PloS one
  • [ISO-abbreviation] PLoS ONE
  • [Language] ENG
  • [Grant] United States / NIDA NIH HHS / DA / R01 DA011322; United States / NIDA NIH HHS / DA / DA11322
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Receptor, Cannabinoid, CB1; 207137-56-2 / Interleukin-4; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 3.5.- / Amidohydrolases; EC 3.5.1.- / fatty-acid amide hydrolase
  • [Other-IDs] NLM/ PMC2924377
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18. Santini D, Galluzzo S, Vincenzi B, Schiavon G, Fratto E, Pantano F, Tonini G: New developments of aminobisphosphonates: the double face of Janus. Ann Oncol; 2007 Jun;18 Suppl 6:vi164-7
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  • BACKGROUND: Bisphosphonate (BP) therapy has become a standard of therapy for patients with malignant bone disease.
  • In vivo preclinical and preliminary clinical data indicate that BPs may prevent cancer treatment-induced bone loss and the onset of malignant bone disease in patients with early-stage cancer.
  • DESIGN: This review will describe the preclinical evidences of action of BPs on osteoclasts and tumor cells.
  • In addition, the effects of principal BPs on skeletal disease progression in patients with breast cancer, prostate cancer, non-small-cell lung cancer and other cancers will be reported.
  • CONCLUSIONS: This review will describe the preliminary clinical evidences from prospective studies on the effect of ZA treatment on the prevention of bone metastasis.

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  • (PMID = 17591815.001).
  • [ISSN] 0923-7534
  • [Journal-full-title] Annals of oncology : official journal of the European Society for Medical Oncology
  • [ISO-abbreviation] Ann. Oncol.
  • [Language] ENG
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Bone Density Conservation Agents; 0 / Diphosphonates; 0 / Imidazoles; 6XC1PAD3KF / zoledronic acid
  • [Number-of-references] 45
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19. Tomobe M, Miyanaga N, Kawai K, Kikuchi K, Uchida K, Takeshima H, Hasegawa Y, Nagasawa T, Akaza H: [Intrascrotal tumors: a clinicopathologic study of 15 cases]. Nihon Hinyokika Gakkai Zasshi; 2000 Sep;91(9):618-22

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  • Tumor weight ranged from 2 to 200 g, with an average of 104.6 g.
  • The histological diagnoses of 15 patients were 8 malignant lymphomas, 2 paratesticular rhabdomyosarcomas, 2 metastatic tumors (origin; stomach and prostate), 1 epidermoid cyst, 1 cyst of tunica testis, and 1 adenomatoid tumor.
  • As for the cases with malignant lymphoma, all of them were non-Hodgkin's lymphoma whose clinical stages were stage I in 2 cases and stage IV in 6 cases.
  • Five 8 patients died in spite of systemic chemotherapy after an orchiectomy, whereas 2 cases with metastatic tumors died of primary cancer, and two cases with paratesticular rhabdomyosarcoma are still alive and have had no evidence of disease.
  • In particular, some kinds of malignant lymphoma mimic anaplastic seminoma histopathologically.
  • Therefore, accurate diagnosis and precise treatment is important in the patient with intrascrotal tumors.
  • [MeSH-minor] Adolescent. Adult. Aged. Child. Diagnosis, Differential. Humans. Infant. Male. Middle Aged. Prognosis

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  • (PMID = 11068425.001).
  • [ISSN] 0021-5287
  • [Journal-full-title] Nihon Hinyōkika Gakkai zasshi. The japanese journal of urology
  • [ISO-abbreviation] Nippon Hinyokika Gakkai Zasshi
  • [Language] jpn
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] JAPAN
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20. Kumi-Diaka J, Hassanhi M, Brown J, Merchant K, Garcia C, Jimenez W: CytoregR inhibits growth and proliferation of human adenocarcinoma cells via induction of apoptosis. J Carcinog; 2006;5:1
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  • BACKGROUND: Cancer is one of the devastating neovascular diseases that incapacitate so many people the world over.
  • Recent reports from the National Cancer Institute indicate some significant gain therapy and cancer management as seen in the increase in the 5-year survival rate over the past two decades.
  • Although near-perfect cure rate have been reported in the early-stage disease, these data reveal high recurrence rate and serious side effects including second malignancies and fatalities.
  • Most of the currently used anticancer agents are only effective against proliferating cancer cells.
  • Thus attention has been focused on potential anti-cancer agents capable of killing cancer cells independent of the cell cycle state, to ensure effective elimination of most cancer cells.
  • The objective of this study was to test the chemosensitivity and potential mechanism of action of a novel cancer drug, CytoregR, in a panel of human cancer cells.
  • RESULTS: CytoregR induced significant dose- and time-dependent inhibition of growth in all the cells; with significant differences in chemosensitivity (P < 0.05) between the target cells becoming more apparent at 48 hr exposure.
  • CytoregR showed no significant effect on normal cells relative to the tumor cells.
  • CONCLUSION: CytoregR exerted a dose-and time-dependent growth inhibitory effect in all the target cells through induction of apoptosis via the CPP32 death pathway, independent of hormonal sensitivity of the cells.
  • The present data indicate that not only could CPP32 provide a potential target for regulation of cytoregR-induced apoptosis but also that cytoregR could play a significant role in chemotherapeutic regimen in many human malignant tumors.

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  • [ISSN] 1477-3163
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  • [Other-IDs] NLM/ PMC1343545
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21. Djeu JY, Wei S: Clusterin and chemoresistance. Adv Cancer Res; 2009;105:77-92
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  • Resistance to anticancer agents is one of the primary impediments to effective cancer therapy.
  • Chemoresistance occurs not only to clinically established therapeutic agents but also to novel targeted therapeutics.
  • Both intrinsic and acquired mechanisms have been implicated in drug resistance but it remains controversial which mechanisms are responsible that lead to failure of therapy in cancer patients.
  • Its role has been documented in prostate cancer for paclitaxel/docetaxel resistance as well as in renal, breast, and lung tumor cells.
  • Moreover, it is abnormally upregulated in numerous advanced stage and metastatic cancers spanning prostate, renal, bladder, breast, head and neck, colon, cervical, pancreatic, lung carcinomas, melanoma, and lymphoma.
  • It is noteworthy that only the cytoplasmic/secretory clusterin form (sCLU), and not the nuclear form, is expressed in aggressive late stage tumors, which is in line with its antiapoptotic function.
  • Resistance to targeted death-inducing molecules, tumor necrosis factor, Fas and TRAIL, or histone deacetylase inhibitors can also be mediated by sCLU.
  • Expression of sCLU may be an adaptive response to genotoxic and oxidative stresses but this adaptive response could pose a threat in malignant cells being treated with cytotoxic agents by enhancing their survival potential.
  • The actual mechanisms for sCLU induction are unclear but STAT1 is required for its constitutive upregulation in docetaxel-resistant tumor cells.
  • Thus, sCLU has a key role in preventing apoptosis induced by cytotoxic agents and has the potential to be targeted for cancer therapy.
  • [MeSH-major] Clusterin / physiology. Drug Resistance, Neoplasm. Neoplasms / drug therapy
  • [MeSH-minor] Drug Resistance, Multiple. Humans. Oxidative Stress

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  • (PMID = 19879424.001).
  • [ISSN] 0065-230X
  • [Journal-full-title] Advances in cancer research
  • [ISO-abbreviation] Adv. Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA098080
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CLU protein, human; 0 / Clusterin
  • [Number-of-references] 78
  • [Other-IDs] NLM/ NIHMS539156; NLM/ PMC3889866
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22. Zamir G, Zeira E, Gelman AE, Shaked A, Olthoff KM, Eid A, Galun E: Replication-deficient adenovirus induces host topoisomerase I activity: implications for adenovirus-mediated gene expression. Mol Ther; 2007 Apr;15(4):772-81
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  • Replication-deficient adenoviruses are useful vectors for the transfer of therapeutic transgenes to malignant and non-malignant tissues.
  • Although transgene expression from adenovirus vectors is initially higher than expression of transgenes transduced by other viral or non-viral vectors, it is often insufficient to generate a significant therapeutic effect.
  • Consequently, the inhibition of topoisomerase I by the anti-cancer drug topotecan greatly enhanced transgene expression in adenovirus-infected hepatic cells, colon cancer and prostate cancer cell cultures, mouse liver, human ex vivo tumor specimens, and mouse tumor in vivo.
  • These findings are significant for gene therapy as they reveal novel aspects of the host anti-adenovirus response and set the stage for the development of a rational molecular-pharmacological approach to increase the effectiveness, and safety, of adenovirus-mediated cancer therapeutics.
  • [MeSH-major] Adenoviridae / genetics. DNA Topoisomerases, Type I / biosynthesis. Defective Viruses / genetics. Genetic Vectors
  • [MeSH-minor] Animals. Base Sequence. Cell Line. DNA Primers / genetics. Enzyme Inhibitors / pharmacology. Female. Gene Expression / drug effects. Genetic Therapy / methods. Humans. In Vitro Techniques. Liver / drug effects. Liver / enzymology. Liver / virology. Mice. Mice, Inbred BALB C. Neoplasms / enzymology. Neoplasms / genetics. Neoplasms / therapy. Rats. Rats, Inbred Lew. Topoisomerase I Inhibitors. Topotecan / pharmacology. Transduction, Genetic

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  • (PMID = 17299399.001).
  • [ISSN] 1525-0016
  • [Journal-full-title] Molecular therapy : the journal of the American Society of Gene Therapy
  • [ISO-abbreviation] Mol. Ther.
  • [Language] eng
  • [Grant] United States / NIAID NIH HHS / AI / R01 AI144554
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA Primers; 0 / Enzyme Inhibitors; 0 / Topoisomerase I Inhibitors; 7M7YKX2N15 / Topotecan; EC 5.99.1.2 / DNA Topoisomerases, Type I
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23. Zhang J, Chen YH, Lu Q: Pro-oncogenic and anti-oncogenic pathways: opportunities and challenges of cancer therapy. Future Oncol; 2010 Apr;6(4):587-603
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  • [Title] Pro-oncogenic and anti-oncogenic pathways: opportunities and challenges of cancer therapy.
  • Carcinogenesis is the uncontrolled growth of cells gaining the potential to invade and disrupt vital tissue functions.
  • This malignant process includes the occurrence of 'unwanted' gene mutations that induce the transformation of normal cells, for example, by overactivation of pro-oncogenic pathways and inactivation of tumor-suppressive or anti-oncogenic pathways.
  • It is now recognized that the number of major signaling pathways that control oncogenesis is not unlimited; therefore, suppressing these pathways can conceivably lead to a cancer cure.
  • However, the clinical application of cancer intervention has not matched up to scientific expectations.
  • Increasing numbers of studies have revealed that many oncogenic-signaling elements show double faces, in which they can promote or suppress cancer pathogenesis depending on tissue type, cancer stage, gene dosage and their interaction with other players in carcinogenesis.
  • This complexity of oncogenic signaling poses challenges to traditional cancer therapy and calls for considerable caution when designing an anticancer drug strategy.
  • We propose future oncology interventions with the concept of integrative cancer therapy.

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  • (PMID = 20373871.001).
  • [ISSN] 1744-8301
  • [Journal-full-title] Future oncology (London, England)
  • [ISO-abbreviation] Future Oncol
  • [Language] ENG
  • [Grant] United States / NIEHS NIH HHS / ES / R03 ES016888; United States / NCI NIH HHS / CA / R01 CA111891-03; United States / NCI NIH HHS / CA / R01 CA111891-04; United States / NCI NIH HHS / CA / R01 CA111891; United States / NIEHS NIH HHS / ES / ES016888; United States / NCI NIH HHS / CA / CA111891; United States / NIA NIH HHS / AG / AG026630; United States / NIA NIH HHS / AG / R03 AG026630
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  • [Number-of-references] 271
  • [Other-IDs] NLM/ NIHMS206895; NLM/ PMC2886915
  •  go-up   go-down


24. Dietel M, Sers C: Personalized medicine and development of targeted therapies: The upcoming challenge for diagnostic molecular pathology. A review. Virchows Arch; 2006 Jun;448(6):744-55

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Personalized medicine and development of targeted therapies: The upcoming challenge for diagnostic molecular pathology. A review.
  • Due to continuous technical developments and new insights into the high complexity of many diseases, molecular pathology is a rapidly growing field gaining center stage in the clinical management of tumors as well as in the pharmaceutical development of new anti-cancer drugs.
  • The application of novel compounds in clinical trials has revealed promising results; however, the current diagnostic procedures available for determining which patients will primarily benefit from rational tumor therapy are insufficient.
  • To read a patient's tissue as "deeply" as possible, in the future, gaining information on the morphology and on genetic, proteomic, and epigenetic alterations will be the upcoming task of surgical pathologists experienced in molecular diagnostics to provide the clinicians with information relevant for an individualized medicine.
  • Technically advanced and well-established microarray platforms can nowadays be evaluated by distinct bioinformatic tools capable of identifying both novel genes associated with disease development and clusters of genes predicting clinical outcome of an individual tumor.
  • The automatic, highly parallel analysis of proteins and complex proteins lysates for early detection of cancers such as breast, prostate and ovary as proteomic patterns in the serum also appears at the horizon.
  • In addition, an improved analysis of tumor samples via antibody or reverse-phase protein arrays is likely to provide the pathologist in the future with information about activated oncogenic signaling pathways and other cell functions, such as drug response or the potential to metastasize.
  • While expression microarrays and proteomic analysis rely on relatively unstable material incompatible with paraffin-embedded tissue samples, an investigation of DNA methylation using specialized high-throughput platforms has revealed the potential of being used in future diagnostics.
  • Therefore, a "multiplex approach" combining the different biological levels DNA, RNA, and protein, may be necessary to functionally classify malignant tumors.
  • [MeSH-major] Drug Design. Molecular Biology. Molecular Diagnostic Techniques / methods. Pathology / methods. Personal Health Services

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  • (PMID = 16736190.001).
  • [ISSN] 0945-6317
  • [Journal-full-title] Virchows Archiv : an international journal of pathology
  • [ISO-abbreviation] Virchows Arch.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Germany
  • [Number-of-references] 95
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25. Brassens S, Chevalier JM, Leblainvaux M: [A strange case of phlebitis]. Ann Cardiol Angeiol (Paris); 2003 Dec;52(6):375-8

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • This sarcoma developed from the smooth muscle of a leg vessel, probably a vein.
  • Leiomyosarcoma is a malignant mesenchymal tumor of specialized connective tissue, with a strong potential for local proliferation and metastatic spread.
  • It usually involves the uterine muscle or the wall of the digestive tract, as well as the large vessels of the abdomen and thorax, the prostate very seldom, and only exceptionally a peripheral vein as in this case.
  • The diagnosis suggested by imaging techniques (in particular MRI) is first and foremost immunohistochemical.
  • The treatment is surgical when possible, associated with radiotherapy and chemotherapy as appropriate.
  • The prognosis is especially poor when the diagnosis is made at the metastatic stage.
  • [MeSH-major] Leiomyosarcoma / diagnosis. Popliteal Vein / pathology. Thrombophlebitis / diagnosis

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  • (PMID = 14752921.001).
  • [ISSN] 0003-3928
  • [Journal-full-title] Annales de cardiologie et d'angéiologie
  • [ISO-abbreviation] Ann Cardiol Angeiol (Paris)
  • [Language] fre
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] France
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