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1. Kast RE: Evidence that amphotericin B mediates reactivation of latent Epstein-Barr virus in Hodgkin's lymphoma allowing cytotoxicity by acyclovir. Yonsei Med J; 2006 Apr 30;47(2):287-90
Hazardous Substances Data Bank. GANCICLOVIR .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Evidence that amphotericin B mediates reactivation of latent Epstein-Barr virus in Hodgkin's lymphoma allowing cytotoxicity by acyclovir.
  • This brief communication focuses on aspects of a recent case report (Yonsei Med J 2005;46:425-30) on a full and sustained remission of Hodgkin's lymphoma (HL) after a single day of chemotherapy.
  • A septic episode required stopping chemotherapy and starting amphotericin B and acyclovir.
  • A review of research supporting the notion that amphotericin B can reactivate latent Epstein-Barr virus and thus allow acyclovir to kill infected HL cells is given.
  • If successful, amphotericin B and acyclovir treatment could be extended to other EBV-driven cancers such as Burkitt's lymphoma, nasopharyngeal carcinoma and the occasional EBV-related epithelial cancer of the breast, colon, prostate, and others.
  • [MeSH-major] Acyclovir / therapeutic use. Amphotericin B / pharmacology. Drug Synergism. Herpesvirus 4, Human / metabolism. Hodgkin Disease / drug therapy. Hodgkin Disease / virology
  • [MeSH-minor] Anti-Bacterial Agents / pharmacology. Burkitt Lymphoma / virology. Ganciclovir / therapeutic use. Humans. Remission Induction. Tumor Necrosis Factor-alpha / metabolism. Virus Activation

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  • Hazardous Substances Data Bank. AMPHOTERICIN B .
  • Hazardous Substances Data Bank. ACYCLOVIR .
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  • (PMID = 16642564.001).
  • [ISSN] 0513-5796
  • [Journal-full-title] Yonsei medical journal
  • [ISO-abbreviation] Yonsei Med. J.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Korea (South)
  • [Chemical-registry-number] 0 / Anti-Bacterial Agents; 0 / Tumor Necrosis Factor-alpha; 7XU7A7DROE / Amphotericin B; P9G3CKZ4P5 / Ganciclovir; X4HES1O11F / Acyclovir
  • [Other-IDs] NLM/ PMC2687644
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2. Weeraratna AT, Dalrymple SL, Lamb JC, Denmeade SR, Miknyoczki S, Dionne CA, Isaacs JT: Pan-trk inhibition decreases metastasis and enhances host survival in experimental models as a result of its selective induction of apoptosis of prostate cancer cells. Clin Cancer Res; 2001 Aug;7(8):2237-45
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  • [Title] Pan-trk inhibition decreases metastasis and enhances host survival in experimental models as a result of its selective induction of apoptosis of prostate cancer cells.
  • During the progression of prostate cancer, molecular changes occur resulting in the autocrine production of a series of neurotrophins by the malignant cells.
  • This is coupled with expression of high-affinity cognate receptors for these ligands, termed trk receptors, by these cancer cells.
  • The binding of the neurotrophins to their trk receptors activates the receptor's latent tyrosine kinase activity inducing a series of signal transduction pathways within these prostate cancer cells.
  • These molecular changes result in the acquisition by prostate cancer cells of a restricted requirement for these trk signaling pathways for optimal survival.
  • In the present studies, the consequences of CEP-701 inhibition of these trk signaling survival pathways were tested in vivo using both rat (R3327 AT 6.3 and H) and human (TSU-pr1 and CWR-22Rv1) prostatic cancer models.
  • These in vivo studies demonstrated that treatment with CEP-701 inhibits the growth of both rodent and human prostate cancers, without being toxic to the normal tissue including the host prostate.
  • Because of this selective effect, CEP-701 inhibits metastasis and growth of both primary and metastatic sites of prostate cancer.
  • Based upon this profile, long-term survival studies were performed using the slow-growing Dunning H rat prostate cancer model.
  • This regimen maintains CEP-701 tumor tissue concentrations of 25-50 nM.
  • Such chronic dosing increased (P < 0.001) the median survival of rats bearing the slow growing H prostate cancers from 408 days (395-432 days, 95% confidence interval) for the vehicle group (n = 18) to 566 days (497-598 days, 95% confidence interval) for the CEP-701-treated group (n = 24).
  • [MeSH-major] Apoptosis / drug effects. Indoles. Neoplasm Metastasis / prevention & control. Prostatic Neoplasms / drug therapy. Receptor, trkA / antagonists & inhibitors
  • [MeSH-minor] Administration, Oral. Animals. Antineoplastic Agents / pharmacology. Carbazoles / pharmacology. Cell Division / drug effects. Cell Line. Disease Models, Animal. Humans. Male. Mice. Mice, Nude. Prostate-Specific Antigen / blood. Prostate-Specific Antigen / drug effects. Rats. Survival Analysis. Tumor Cells, Cultured. Xenograft Model Antitumor Assays

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  • (PMID = 11489797.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / 2P50-CA58236-07
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Carbazoles; 0 / Indoles; DO989GC5D1 / lestaurtinib; EC 2.7.10.1 / Receptor, trkA; EC 3.4.21.77 / Prostate-Specific Antigen
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3. Fujimoto N, Suzuki T, Honda H, Kitamura S: Estrogen enhancement of androgen-responsive gene expression in hormone-induced hyperplasia in the ventral prostate of F344 rats. Cancer Sci; 2004 Sep;95(9):711-5
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  • [Title] Estrogen enhancement of androgen-responsive gene expression in hormone-induced hyperplasia in the ventral prostate of F344 rats.
  • It has been postulated that, in addition to the crucial role of androgens, estrogens may be involved in development of prostate hyperplasia and cancer.
  • In rats, combined administration of estrogen and androgen synergistically increases ventral prostate weight, and continued treatment results in the development of glandular hyperplasia.
  • Prostate adenocarcinoma can be induced by chemical carcinogens in rats, and estrogen given together with an androgen generally shortens the latent period or increases the incidence and/or multiplicity of carcinomas.
  • In the present study, we examined the combined effects of 17beta-estradiol (E2) and testosterone (T) on gene expression in an early stage of prostate hyperplasia in an F344 rat model.
  • ERalpha expression, which has been suggested to contribute to development of prostatic hyperplasia, was increased by the combined treatment with T and E2, while it was suppressed by T alone.
  • Expression levels of two androgen-responsive genes, probasin and kallikrein S3, were increased in the ventral prostate of rats treated with T plus E2 for 4 weeks in a dose-dependent manner, while short-term treatment did not alter the expression.
  • These results suggested that enhancing effects of E2 on transcription of androgen-responsive genes, as well as an increased level of ERalpha may play roles in the synergistic effects of E2 on T-induced prostate hyperplasia.
  • [MeSH-minor] Androgen-Binding Protein / genetics. Androgen-Binding Protein / metabolism. Animals. Antineoplastic Combined Chemotherapy Protocols. Body Weight / drug effects. Carrier Proteins. Cell Division / drug effects. Drug Synergism. Drug Therapy, Combination. LIM Domain Proteins. Male. Proteins / metabolism. RNA, Messenger / metabolism. Rats. Rats, Inbred F344. Reverse Transcriptase Polymerase Chain Reaction. Tissue Kallikreins / genetics. Tissue Kallikreins / metabolism

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  • (PMID = 15471555.001).
  • [ISSN] 1347-9032
  • [Journal-full-title] Cancer science
  • [ISO-abbreviation] Cancer Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Androgen-Binding Protein; 0 / CRIP1 protein, human; 0 / Carrier Proteins; 0 / Estrogen Receptor alpha; 0 / Estrogen Receptor beta; 0 / LIM Domain Proteins; 0 / Proteins; 0 / RNA, Messenger; 0 / Receptors, Androgen; 0 / probasin; 3XMK78S47O / Testosterone; 4TI98Z838E / Estradiol; EC 3.4.21.35 / Tissue Kallikreins
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4. Benekli M, Baumann H, Wetzler M: Targeting signal transducer and activator of transcription signaling pathway in leukemias. J Clin Oncol; 2009 Sep 10;27(26):4422-32
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  • Signal transducer and activator of transcription (STAT) proteins comprise a seven-member family of latent cytoplasmic transcription factors that are activated through tyrosine phosphorylation by a variety of cytokines and growth factors.
  • A better understanding of the mechanisms of dysregulation of the STAT pathway and understanding of the cause and effect relationship in leukemogenesis may serve as a basis for designing novel therapeutic strategies directed against STATs.
  • Mechanisms of STAT activation, the potential role of STAT signaling in leukemogenesis, and recent advances in drug discovery targeting the STAT pathway are the focus of this review.

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  • (PMID = 19667270.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P30 CA016056; United States / NCI NIH HHS / CA / CA16056; United States / NCI NIH HHS / CA / CA85580; United States / NCI NIH HHS / CA / CA99238; United States / NCI NIH HHS / CA / R01 CA085580; United States / NCI NIH HHS / CA / R21 CA099238
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / STAT Transcription Factors; 0 / STAT1 Transcription Factor; 0 / STAT3 Transcription Factor
  • [Number-of-references] 118
  • [Other-IDs] NLM/ PMC2744278
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5. Amanatullah DF, Reutens AT, Zafonte BT, Fu M, Mani S, Pestell RG: Cell-cycle dysregulation and the molecular mechanisms of prostate cancer. Front Biosci; 2000 Apr 1;5:D372-90
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cell-cycle dysregulation and the molecular mechanisms of prostate cancer.
  • Prostate cancer is the most common cause of non-cutaneous cancer in men and although frequently latent is the second commonest cause of death.
  • Screening for the disease was historically based on symptoms of urethral obstruction, clinical examination of the prostate gland and serum measurements of prostate specific antigen.
  • As prostate cancer growth in the early stages is enhanced by androgens, the mainstay of therapy has been androgen ablation by pharmaco-therapeutic or surgical means.
  • The subsequent development of androgen therapy resistant prostate cancer in many patients, for whom therapeutic options remain limited, has led researchers to focus attention on understanding the molecular genetics of prostate cancer.
  • The array of genetic abnormalities observed in prostate tumors, which include changes in components of the cell cycle, suggest the disease is quite heterogeneous and may require further sub-classification based on genetic markers.
  • Such analyses may lead to identification of relevant new prognostic and therapeutic indicators.
  • The advent of transgenic mouse models of prostate cancer may provide a critical tool for the implementation of rational genetic based therapeutics and alternate drug design.

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  • (PMID = 10762592.001).
  • [ISSN] 1093-9946
  • [Journal-full-title] Frontiers in bioscience : a journal and virtual library
  • [ISO-abbreviation] Front. Biosci.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA77552; United States / NCI NIH HHS / CA / R01CA75503; United States / NCI NIH HHS / CA / R29CA70897; etc
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.; Review
  • [Publication-country] UNITED STATES
  • [Chemical-registry-number] 0 / Cell Adhesion Molecules; 0 / Cyclins; 0 / Cytokines; 0 / Oncogene Proteins; 0 / Receptors, Calcitriol; 0 / Tumor Suppressor Proteins; EC 3.1.3.- / Phosphoric Monoester Hydrolases; EC 3.1.3.48 / PTEN protein, human; EC 3.1.3.67 / PTEN Phosphohydrolase
  • [Number-of-references] 186
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6. Hsieh TC, Wu JM: Cell growth and gene modulatory activities of Yunzhi (Windsor Wunxi) from mushroom Trametes versicolor in androgen-dependent and androgen-insensitive human prostate cancer cells. Int J Oncol; 2001 Jan;18(1):81-8
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  • [Title] Cell growth and gene modulatory activities of Yunzhi (Windsor Wunxi) from mushroom Trametes versicolor in androgen-dependent and androgen-insensitive human prostate cancer cells.
  • The incidence of prostate cancer varies greatly throughout the world; it is highest in African-Americans and lowest in the Asian populations of China, India, and Japan.
  • Geographical differences in both prevalence of latent prostate cancer and mortality have been postulated to be influenced by diverse tumor-promoting and protective factors, both environmental and dietary.
  • Prostate cancer is a tumor with an extremely long latency; the pattern of prostate tumorigenesis, in terms of the display and sequence of appearance of particular molecular or biochemical features, or morphological changes, characterizing different stages of the carcinogenic process, is expected to be heterogeneous.
  • The present study aims to investigate whether hormone-responsive LNCaP and androgen-refractory JCA-1, PC-3, and DU-145 prostate cancer cells are responsive to Yunzhi (YZ), a proprietary dietary supplement prepared from extracts of Trametes versicolor, also known as Coriolus versicolor (a mushroom consumed by Chinese for its purported health benefits), and to elucidate its mechanism of action.
  • In androgen-unresponsive prostate cancer cells, YZ had a much less pronounced suppressive effect on proliferation of PC-3 and DU-145 cells, compared to LNCaP, and was inactive against JCA-1 cells.
  • Western blot analyses show that the expression of Rb, a key regulatory protein in G1/S transition, and PCNA, integrally involved in mammalian cell DNA replication, were significantly reduced by treatment with YZ in PC-3 and DU-145 cells, respectively.
  • In contradiction, none of these biochemical parameters were affected in JCA-1 cells under identical treatment conditions.
  • The greater sensitivity of LNCaP cells to this polysaccharopeptide raises the possibility that YZ may be considered as an adjuvant therapy in the treatment of hormone responsive prostate cancer; additionally, it may have chemopreventive potential to restrict prostate tumorigenic progression from the hormone-dependent to the hormone-refractory state.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Drugs, Chinese Herbal / pharmacology. Gene Expression Regulation, Neoplastic / drug effects. Polyporales / chemistry. Prostatic Neoplasms / drug therapy
  • [MeSH-minor] Androgens / metabolism. Cell Cycle Proteins / biosynthesis. Cell Cycle Proteins / genetics. Cell Division / drug effects. DNA-Binding Proteins / biosynthesis. DNA-Binding Proteins / genetics. Humans. Male. Prostate-Specific Antigen / biosynthesis. Prostate-Specific Antigen / genetics. STAT1 Transcription Factor. Trans-Activators / biosynthesis. Trans-Activators / genetics. Tumor Cells, Cultured


7. Wong SF, Seow HF, Lai LC: Effect of cathepsin D and prostate specific antigen on latent transforming growth factor-beta in breast cancer cell lines. Malays J Pathol; 2003 Dec;25(2):129-34
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  • [Title] Effect of cathepsin D and prostate specific antigen on latent transforming growth factor-beta in breast cancer cell lines.
  • Transforming growth factor-beta (TGFbeta) is present, predominantly in latent forms, in normal and malignant breast tissue.
  • The mechanisms by which latent TGFbeta is activated physiologically remain largely an enigma.
  • The objective of this study was to assess whether the proteases, cathepsin D and prostate specific antigen (PSA) could activate latent TGFbeta1 and TGFbeta2 in conditioned media of the hormone-dependent MCF-7 and hormone-independent MDA-MB-231 human breast cancer cell lines, newly purchased from ATCC.
  • Both of the cell lines were seeded in 6-well plates 2 days prior to treatment with varying concentrations of cathepsin D and PSA.
  • Active TGFbeta1 and TGFbeta2 in the media were then measured by ELISA after 4, 8, 24 and 72 hours of treatment.
  • There was a significant increase in only active TGFbeta2 levels in the MDA-MB-231 cell line with both treatments.
  • Cathepsin D and PSA were unable to activate latent TGFbeta1 and TGFbeta2 in these two breast cancer cell lines.
  • [MeSH-major] Breast Neoplasms / drug therapy. Cathepsin D / pharmacology. Prostate-Specific Antigen / pharmacology. Transforming Growth Factor beta / metabolism
  • [MeSH-minor] Cell Line, Tumor / drug effects. Cell Line, Tumor / metabolism. Culture Media, Conditioned / chemistry. Dose-Response Relationship, Drug. Female. Gene Expression Regulation, Neoplastic / drug effects. Humans. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction


8. Sooriakumaran P: Management of prostate cancer. Part 1: chemoprevention. Expert Rev Anticancer Ther; 2006 Mar;6(3):419-25
MedlinePlus Health Information. consumer health - Prostate Cancer.

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  • [Title] Management of prostate cancer. Part 1: chemoprevention.
  • Numerous agents have been investigated in prostate cancer prevention.
  • Some are postulated to even affect downstream targets, such as cyclooxygenase-2, which has been shown to be elevated in prostate cancer by most investigators.
  • In addition, the current lack of ability to accurately differentiate clinically important prostate cancer from latent disease makes chemoprevention in this setting even more challenging.
  • Currently, no reliable biomarkers that can act as surrogate endpoints for the development of clinically relevant prostate cancer exist, which makes performing large chemoprevention trials expensive.
  • At present, there is little to suggest that the urologist or General Practitioner should be recommending any particular chemopreventive agent to either the general population or those deemed to be at higher risk of contracting prostate cancer.
  • [MeSH-minor] Anti-Inflammatory Agents, Non-Steroidal / pharmacology. Anti-Inflammatory Agents, Non-Steroidal / therapeutic use. Cell Proliferation / drug effects. Clinical Trials as Topic. Cyclooxygenase Inhibitors / pharmacology. Cyclooxygenase Inhibitors / therapeutic use. Dietary Fats. Gonadal Steroid Hormones / antagonists & inhibitors. Gonadal Steroid Hormones / physiology. Humans. Male

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  • (PMID = 16503858.001).
  • [ISSN] 1744-8328
  • [Journal-full-title] Expert review of anticancer therapy
  • [ISO-abbreviation] Expert Rev Anticancer Ther
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents, Non-Steroidal; 0 / Cyclooxygenase Inhibitors; 0 / Dietary Fats; 0 / Gonadal Steroid Hormones
  • [Number-of-references] 96
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9. Denmeade SR, Jakobsen CM, Janssen S, Khan SR, Garrett ES, Lilja H, Christensen SB, Isaacs JT: Prostate-specific antigen-activated thapsigargin prodrug as targeted therapy for prostate cancer. J Natl Cancer Inst; 2003 Jul 2;95(13):990-1000
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  • [Title] Prostate-specific antigen-activated thapsigargin prodrug as targeted therapy for prostate cancer.
  • BACKGROUND: Standard anti-proliferative chemotherapy is relatively ineffective against slowly proliferating androgen-independent prostate cancer cells within metastatic sites.
  • However, thapsigargin's mechanism of action indicates that it is unlikely to be selective for cancer cells or prostate cells.
  • METHODS: We coupled a chemically modified form of thapsigargin, L12ADT, to a peptide carrier that is a substrate for the prostate-specific antigen (PSA) protease to produce a soluble, cell-impermeant latent prodrug that is specifically activated extracellularly within metastatic prostate cancer sites by PSA.
  • We analyzed the kinetics of PSA hydrolysis of the prodrug, the in vitro cytotoxicity of the prodrug against PSA-producing LNCaP human prostate cancer and PSA non-producing HCT-116 human colon cancer cells, and the in vivo pharmacokinetics of the prodrug in mice.
  • We also analyzed antitumor efficacy of the prodrug in nude mice xenograft models of prostate cancer (using LNCaP cells) and renal carcinoma (using human SN12C cells).
  • RESULTS: The L12ADT peptide prodrug was hydrolyzed efficiently by PSA, was selectively toxic to PSA-producing prostate cancer cells in vitro, and was stable in human plasma.
  • Levels of prodrug and liberated L12ADT in prostate cancer xenograft tumors were approximately eightfold and sixfold, respectively, higher than the in vitro LD50s.
  • Prostate cancer xenograft tumors in mice treated with prodrug by intravenous administration were growth-inhibited without substantial host toxicity.
  • Continuous subcutaneous prodrug administration in mice produced complete growth inhibition of established PSA-producing prostate cancer xenograft tumors but had no effect on PSA non-producing renal carcinoma xenograft tumors.
  • CONCLUSION: Further development of PSA-activated thapsigargin prodrugs as therapy for metastatic prostate cancer is warranted.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Prodrugs / therapeutic use. Prostate-Specific Antigen / drug effects. Prostatic Neoplasms / drug therapy. Prostatic Neoplasms / immunology. Thapsigargin / therapeutic use
  • [MeSH-minor] Animals. Disease Models, Animal. Humans. Hydrolysis / drug effects. Male. Mice. Mice, Nude. Transplantation, Heterologous. Treatment Outcome


10. Sternberg CN: Highlights of contemporary issues in the medical management of prostate cancer. Crit Rev Oncol Hematol; 2002 Aug;43(2):105-21
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  • [Title] Highlights of contemporary issues in the medical management of prostate cancer.
  • This paper highlights contemporary issues in the medical management of prostate cancer.
  • Controversies surrounding adjuvant and neo-adjuvant hormonal therapy in localized prostate cancer are reviewed, as well as the use of chemohormonal therapy in high risk localized disease.
  • The latent period of asymptomatic biochemical progression prior to clinical progression is an opportunity to evaluate new non-toxic therapies.
  • In patients with advanced metastatic disease hormonal therapy and new alternatives are discussed.
  • Chemotherapy in hormone refractory prostate cancer (HRPC) is extensively covered as well as the emerging role of molecular-targeted therapies.
  • [MeSH-major] Prostatic Neoplasms / therapy
  • [MeSH-minor] Antineoplastic Agents / therapeutic use. Antineoplastic Agents, Hormonal / therapeutic use. Bone Neoplasms / drug therapy. Bone Neoplasms / secondary. Disease Management. Drug Resistance, Neoplasm. Humans. Male. Palliative Care / methods

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  • (PMID = 12191733.001).
  • [ISSN] 1040-8428
  • [Journal-full-title] Critical reviews in oncology/hematology
  • [ISO-abbreviation] Crit. Rev. Oncol. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Antineoplastic Agents, Hormonal
  • [Number-of-references] 142
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11. Miller GJ, Torkko KC: Natural history of prostate cancer--epidemiologic considerations. Epidemiol Rev; 2001;23(1):14-8
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  • [Title] Natural history of prostate cancer--epidemiologic considerations.
  • Multicentricity, heterogeneity, and sampling error complicate the study of the natural history of prostate cancer.
  • Carcinomas previously termed "latent" are probably similar to those detected clinically.
  • Estimates of grade and stage made at the time of detection are prone to sampling error and are likely to change following examination of radical prostatectomy specimens.
  • In regions with lower life expectancies, the problem of prostate cancer becomes a lower priority due to its association with aging.
  • However, in view of the high worldwide prevalence of the disease, further epidemiologic studies of prostate cancer are warranted.
  • [MeSH-minor] Developed Countries. Epidemiologic Studies. Humans. Male. Precancerous Conditions / epidemiology. Precancerous Conditions / pathology. Prostate / abnormalities. United States / epidemiology

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  • (PMID = 11588839.001).
  • [ISSN] 0193-936X
  • [Journal-full-title] Epidemiologic reviews
  • [ISO-abbreviation] Epidemiol Rev
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA 53520; United States / NCI NIH HHS / CA / CA 66161
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, P.H.S.; Review
  • [Publication-country] United States
  • [Number-of-references] 52
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12. Mathé G: Impotence-free hormonal treatment of prostate cancer. Biomed Pharmacother; 2001 Apr;55(3):127-9
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  • [Title] Impotence-free hormonal treatment of prostate cancer.
  • Since the protein-specific antigen (PSA) test is systematically used in some countries for cancer detection, many asymptomatic and latent cancer patients are uselessly victims of anxiety, hormonotherapy, and impotence, when they are not demolished by surgery and/or radiotherapy's local and/or regional complications.
  • We propose to conduct a study of dexamethasone as treatment of such latent, small and even wrongly diagnosed cases.
  • But it has an anti-growth factor effect, which may explain its often beneficial action on prostate cancer with resistance to androgen inhibitors.
  • [MeSH-major] Dexamethasone / therapeutic use. Erectile Dysfunction / etiology. Iatrogenic Disease / prevention & control. Prostatic Neoplasms / drug therapy
  • [MeSH-minor] Aged. Humans. Male. Middle Aged. Prostate-Specific Antigen

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  • (PMID = 11325208.001).
  • [ISSN] 0753-3322
  • [Journal-full-title] Biomedicine & pharmacotherapy = Biomédecine & pharmacothérapie
  • [ISO-abbreviation] Biomed. Pharmacother.
  • [Language] eng
  • [Publication-type] Editorial
  • [Publication-country] France
  • [Chemical-registry-number] 7S5I7G3JQL / Dexamethasone; EC 3.4.21.77 / Prostate-Specific Antigen
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13. Tokar EJ, Ancrile BB, Ablin RJ, Webber MM: Cholecalciferol (vitamin D3) and the retinoid N-(4-hydroxyphenyl)retinamide (4-HPR) are synergistic for chemoprevention of prostate cancer. J Exp Ther Oncol; 2006;5(4):323-33
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  • [Title] Cholecalciferol (vitamin D3) and the retinoid N-(4-hydroxyphenyl)retinamide (4-HPR) are synergistic for chemoprevention of prostate cancer.
  • Prostate cancer, the most commonly diagnosed cancer among American men, develops slowly over many years.
  • The long latent period of 20 to 30 years, involved in the multistep process of carcinogenesis, provides an important opportunity to block or reverse progression to a malignant state.
  • Vitamin A (retinoids) and vitamin D not only have the ability to block steps in the process of carcinogenesis but they can also modulate or reverse some malignant characteristics of cancer cells.
  • Therefore, combination treatment at low doses, to increase efficacy and avoid toxicity, is of special interest.
  • This study examines the effects of the synthetic retinoid N-(4-hydroxyphenyl)retinamide (4-HPR) in combination with cholecalciferol (vitamin D3) on growth, and on the expression of vimentin, matrix metalloproteinase-2 (MMP-2), and retinoid and vitamin D receptor expression, using the non-tumorigenic, human prostate epithelial cell line RWPE-1.
  • Treatment with 4-HPR and cholecalciferol resulted in synergistic growth inhibition when compared to that caused by each agent alone.
  • These results suggest that combined treatment with 4-HPR and cholecalciferol, at doses lower than what might be effective with single agents, increases their efficacy and suggest that this may serve as an effective strategy for chemoprevention and treatment of prostate cancer.
  • [MeSH-major] Anticarcinogenic Agents / pharmacology. Cholecalciferol / pharmacology. Drug Synergism. Fenretinide / pharmacology. Gene Expression Regulation, Neoplastic. Prostatic Neoplasms / drug therapy

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  • (PMID = 17024972.001).
  • [ISSN] 1359-4117
  • [Journal-full-title] Journal of experimental therapeutics & oncology
  • [ISO-abbreviation] J. Exp. Ther. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anticarcinogenic Agents; 0 / Retinoids; 0 / Vimentin; 0 / Vitamins; 187EJ7QEXL / Fenretinide; 1C6V77QF41 / Cholecalciferol; EC 3.4.24.24 / Matrix Metalloproteinase 2
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14. Rusu D, Rusu V, Răileanu I, Stefănescu C: [PSA as a marker for prostate cancer progression]. Rev Med Chir Soc Med Nat Iasi; 2010 Jul-Sep;114(3):792-7
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  • [Title] [PSA as a marker for prostate cancer progression].
  • Monitoring the evolution of prostate cancer has crucial importance since this tip of neoplasia has a variable biology, ranging from latent cancers to extremely aggressive tumors.
  • At the moment, PSA (prostate specific antigen) values point out to either successful or unsuccessful prostate cancer therapy.
  • Depending on therapeutic strategies, biochemical recurrence (BCR) is differently defined.
  • After external beam therapy, PSA is slowly decreasing reaching up the nadir of 0.2-0.5 ng/mL in months or years; BCR: PSA = nadir + 2 ng/mL.
  • After hormonal therapy, PSA declines in 3-6 months, maintains low values for 18-24 months, then increases, settling for hormone independency.
  • After chemotherapy, PSA is considered normal at values < 2 ng/mL; the response of PSA represents a confirmed decreasing from the second test at 4 or more weeks after the initial decline; the length of the response is the period between first decline with 50 % of PSA to 50 % increase from nadir; the progression of PSA is shown in the increase with 25 % in comparison to the basic level.
  • [MeSH-major] Biomarkers, Tumor / blood. Prostate-Specific Antigen / blood. Prostatic Neoplasms / diagnosis
  • [MeSH-minor] Chemotherapy, Adjuvant. Disease Progression. Humans. Male. Predictive Value of Tests. Prostatectomy. Radiotherapy, Adjuvant. Sensitivity and Specificity. Severity of Illness Index

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  • (PMID = 21243806.001).
  • [ISSN] 0048-7848
  • [Journal-full-title] Revista medico-chirurgicală̆ a Societă̆ţ̜ii de Medici ş̧i Naturaliş̧ti din Iaş̧i
  • [ISO-abbreviation] Rev Med Chir Soc Med Nat Iasi
  • [Language] rum
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Romania
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; EC 3.4.21.77 / Prostate-Specific Antigen
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15. Howard EW, Leung SC, Yuen HF, Chua CW, Lee DT, Chan KW, Wang X, Wong YC: Decreased adhesiveness, resistance to anoikis and suppression of GRP94 are integral to the survival of circulating tumor cells in prostate cancer. Clin Exp Metastasis; 2008;25(5):497-508
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  • [Title] Decreased adhesiveness, resistance to anoikis and suppression of GRP94 are integral to the survival of circulating tumor cells in prostate cancer.
  • The presence of circulating tumor cells (CTC) is common in prostate cancer patients, however until recently their clinical significance was unknown.
  • The CTC stage is essential for the formation of distant metastases, and their continuing presence after radical prostatectomy has been shown to predict recurrent or latent disease.
  • A novel CTC cell line from the bloodstream of an orthotopic mouse model of castration-resistant prostate cancer was established and compared with the primary tumor using attachment assays, detachment culture, Western blot, flow cytometry and 2D gel electrophoresis.
  • Decreased adhesiveness and expression of adhesion molecules E-cadherin, beta4-integrin and gamma-catenin, together with resistance to detachment and drug-induced apoptosis and upregulation of Bcl-2 were integral to the development of CTC and their survival.
  • GRP94 was also shown to be suppressed in a tissue microarray study of 79 prostate cancer patients, indicating its possible role in prostate cancer progression.
  • Overall, this study suggests molecular alterations accounting for the release and survival of CTC, which may be used as drug targets for either anti-metastatic therapy or the suppression of latent disease.
  • We also indicate the novel involvement of GRP94 suppression in prostate cancer metastasis.
  • [MeSH-minor] Animals. Blotting, Western. Cell Adhesion / physiology. Cell Line, Tumor. Cell Survival / physiology. Flow Cytometry. Humans. Immunohistochemistry. Male. Mice. Reverse Transcriptase Polymerase Chain Reaction. Tissue Array Analysis

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  • (PMID = 18340425.001).
  • [ISSN] 0262-0898
  • [Journal-full-title] Clinical & experimental metastasis
  • [ISO-abbreviation] Clin. Exp. Metastasis
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / HSP70 Heat-Shock Proteins; 0 / Membrane Proteins; 0 / glucose-regulated proteins
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16. Jankun J, Aleem AM, Specht Z, Keck RW, Lysiak-Szydlowska W, Selman SH, Skrzypczak-Jankun E: PAI-1 induces cell detachment, downregulates nucleophosmin (B23) and fortilin (TCTP) in LnCAP prostate cancer cells. Int J Mol Med; 2007 Jul;20(1):11-20
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  • [Title] PAI-1 induces cell detachment, downregulates nucleophosmin (B23) and fortilin (TCTP) in LnCAP prostate cancer cells.
  • In low concentrations it could induce cancer cell motility by interacting with urokinase (uPA), its receptor (uPAR), vitronectin and integrins.
  • Active PAI-1 binds to uPA forming a complex with uPAR, while the latent form of PAI-1 does not.
  • Both VLHL PAI-1s convert into the latent form when treated with a reducing agent (DTT) that breaks disulfide bridges.
  • Further investigation showed that treatment of cancer cells with VLHL PAI-1 downregulated nucleophosmin, while all forms of PAI-1 downregulated fortilin.
  • We hope that by exploring PAI-1's structure and function we might be able to understand and separate the different effects of PAI-1 on cancer cells and develop more effective therapeutic strategies in cancer treatment.
  • [MeSH-major] Biomarkers, Tumor / metabolism. Cell Movement / drug effects. Nuclear Proteins / metabolism. Plasminogen Activator Inhibitor 1 / metabolism. Plasminogen Activator Inhibitor 1 / pharmacology. Prostatic Neoplasms / drug therapy
  • [MeSH-minor] Amino Acid Sequence. Cell Line, Tumor. Cell Proliferation / drug effects. Cell Survival / drug effects. Dose-Response Relationship, Drug. Down-Regulation. Half-Life. Humans. Male. Models, Molecular. Molecular Weight. Protein Conformation. Protein Structure, Secondary. Recombinant Proteins / chemistry. Recombinant Proteins / metabolism. Recombinant Proteins / pharmacology

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  • (PMID = 17549383.001).
  • [ISSN] 1107-3756
  • [Journal-full-title] International journal of molecular medicine
  • [ISO-abbreviation] Int. J. Mol. Med.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA109625; United States / NCI NIH HHS / CA / CA90524
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Nuclear Proteins; 0 / Plasminogen Activator Inhibitor 1; 0 / Recombinant Proteins; 0 / tumor protein, translationally-controlled 1; 117896-08-9 / nucleophosmin
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17. Sun LC, Luo J, Mackey LV, Fuselier JA, Coy DH: A conjugate of camptothecin and a somatostatin analog against prostate cancer cell invasion via a possible signaling pathway involving PI3K/Akt, alphaVbeta3/alphaVbeta5 and MMP-2/-9. Cancer Lett; 2007 Feb 8;246(1-2):157-66
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A conjugate of camptothecin and a somatostatin analog against prostate cancer cell invasion via a possible signaling pathway involving PI3K/Akt, alphaVbeta3/alphaVbeta5 and MMP-2/-9.
  • It was found that, in addition to blocking migration and invasion of highly invasive prostate cancer PC-3 cells, this conjugate also inhibited in vitro capillary-like tube formation of endothelial cells and in vivo angiogenesis in C57B1/6N female mice.
  • This conjugate also inactivated phosphorylation of protein kinase B (PKB/Akt), down-regulated the expression of latent matrix metalloproteinase (MMP) -2 and MMP-9, but had little effect on MMP-3/-10.
  • Meanwhile, membrane type-1 matrix metalloproteinase (MT1-MMP) and the tissue inhibitor of matrix metalloproteinase-2 (TIMP-2) were not detectable in PC-3 cells. alphaVbeta3/alphaVbeta5 and MMP-2/-9 are known to be highly expressed in many tumor cells and play an important role in tumor progression.
  • Our results support that this conjugate could possibly inhibit prostate cancer PC-3 cell invasion through a signaling pathway involving PI3K/Akt, alphaVbeta3/alphaVbeta5 and MMP-2/-9, and this SSA could be used as an efficient vector to deliver CPT or other cytotoxic agents to target sites for cancer therapy.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Camptothecin / pharmacology. Cell Movement / drug effects. Signal Transduction / drug effects. Somatostatin / pharmacology
  • [MeSH-minor] Amino Acid Sequence. Animals. Blotting, Western. Cell Adhesion / drug effects. Cell Line, Tumor. Female. Humans. Integrin alphaVbeta3 / metabolism. Integrins / metabolism. Male. Matrix Metalloproteinase 2 / metabolism. Matrix Metalloproteinase 9 / metabolism. Mice. Mice, Inbred C57BL. Neoplasm Invasiveness. Neovascularization, Pathologic / pathology. Neovascularization, Pathologic / prevention & control. Phosphatidylinositol 3-Kinases / metabolism. Phosphorylation / drug effects. Prostatic Neoplasms / metabolism. Prostatic Neoplasms / pathology. Prostatic Neoplasms / physiopathology. Proto-Oncogene Proteins c-akt / metabolism. Receptors, Vitronectin / metabolism

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  • (PMID = 16644105.001).
  • [ISSN] 0304-3835
  • [Journal-full-title] Cancer letters
  • [ISO-abbreviation] Cancer Lett.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Integrin alphaVbeta3; 0 / Integrins; 0 / JF-10-81; 0 / Receptors, Vitronectin; 0 / integrin alphaVbeta5; 51110-01-1 / Somatostatin; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 3.4.24.24 / Matrix Metalloproteinase 2; EC 3.4.24.35 / Matrix Metalloproteinase 9; XT3Z54Z28A / Camptothecin
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18. Quader ST, Bello-DeOcampo D, Williams DE, Kleinman HK, Webber MM: Evaluation of the chemopreventive potential of retinoids using a novel in vitro human prostate carcinogenesis model. Mutat Res; 2001 Sep 20;496(1-2):153-61
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Evaluation of the chemopreventive potential of retinoids using a novel in vitro human prostate carcinogenesis model.
  • The prevalence of prostatic intraepithelial neoplasia (PIN) and latent prostatic carcinoma, representing multiple steps in carcinogenesis and progression to invasive carcinoma, makes them relevant targets for prevention.
  • A unique family of human prostate epithelial cell lines, which mimic steps in prostate carcinogenesis and progression, were used to evaluate the chemopreventive potential of all-trans-retinoic acid (RA) and N-(4-hydroxyphenyl)retinamide (4-HPR).
  • Both RA and 4-HPR inhibited anchorage-dependent growth of all cell lines and anchorage-independent growth of WPE1-NB14 and WPE1-NB11 cells, in a dose-dependent manner, however, 10 times more RA than 4-HPR was required to produce the same effect.
  • These three cell lines mimic progressive steps in carcinogenesis and progression, from immortalized, non-tumorigenic RWPE-1 cells, to the less malignant WPE1-NB14 to the more malignant WPE1-NB11 cells, and provide powerful models for studies on secondary and tertiary prevention, i.e. promotion and progression stages, respectively, of prostate cancer.
  • [MeSH-major] Anticarcinogenic Agents / therapeutic use. Prostatic Neoplasms / drug therapy. Retinoids / therapeutic use
  • [MeSH-minor] Animals. Cell Adhesion / drug effects. Cell Line, Transformed / drug effects. Cell Transformation, Neoplastic. Chemoprevention. Dose-Response Relationship, Drug. Epithelial Cells / drug effects. Humans. Male. Methylnitrosourea / pharmacology. Mice. Mice, Nude. Mutagenicity Tests. Neoplasm Transplantation. Phenotype. Tumor Cells, Cultured / drug effects

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  • (PMID = 11551491.001).
  • [ISSN] 0027-5107
  • [Journal-full-title] Mutation research
  • [ISO-abbreviation] Mutat. Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Anticarcinogenic Agents; 0 / Retinoids; 684-93-5 / Methylnitrosourea
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19. Sharma G, Singh RP, Agarwal R: Growth inhibitory and apoptotic effects of inositol hexaphosphate in transgenic adenocarcinoma of mouse prostate (TRAMP-C1) cells. Int J Oncol; 2003 Nov;23(5):1413-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Growth inhibitory and apoptotic effects of inositol hexaphosphate in transgenic adenocarcinoma of mouse prostate (TRAMP-C1) cells.
  • Inositol hexaphosphate (IP6), a dietary agent, has been extensively studied for its cancer chemopreventive and anti-cancer efficacy in several different animal models, but not in prostate cancer (PCA) possibly because the known PCA models are both expensive and highly time-consuming.
  • One such PCA model is transgenic adenocarcinoma of mouse prostate (TRAMP), which reproduces the spectrum of benign latent, aggressive and metastatic forms of human PCA.
  • In this study, we investigated the anti-cancer effects of IP6 in TRAMP-derived established TRAMP-C1 cell line.
  • IP6 (0.5-4.0 mM) treatment of cells for 24-72 h resulted in 17-76% cell growth inhibition and 6-35% cell death, in a dose- and time-dependent manner.
  • In the studies assessing whether cell growth inhibition by IP6 is associated with an alteration in cell cycle progression, IP6 treatment resulted in up to 92% cells in G0-G1 phase as compared to controls.
  • [MeSH-major] Adenocarcinoma / drug therapy. Phytic Acid / pharmacology. Prostatic Neoplasms / drug therapy. Prostatic Neoplasms / pathology
  • [MeSH-minor] Animals. Antineoplastic Agents / pharmacology. Apoptosis. Caspase Inhibitors. Caspases / metabolism. Cell Cycle. Cell Death. Cell Division. Cell Line, Tumor. Cell Survival. Dose-Response Relationship, Drug. Enzyme Inhibitors / pharmacology. Flow Cytometry. G0 Phase. G1 Phase. Male. Mice. Mice, Transgenic. Polymerase Chain Reaction. Time Factors. Transgenes

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  • (PMID = 14532984.001).
  • [ISSN] 1019-6439
  • [Journal-full-title] International journal of oncology
  • [ISO-abbreviation] Int. J. Oncol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA83741
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Caspase Inhibitors; 0 / Enzyme Inhibitors; 7IGF0S7R8I / Phytic Acid; EC 3.4.22.- / Caspases
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20. Moinpour CM, Donaldson GW, Redman MW: Do general dimensions of quality of life add clinical value to symptom data? J Natl Cancer Inst Monogr; 2007;(37):31-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Since global health-related quality of life (GHRQL) reflects broad impacts of treatment, its assessment in an advanced-stage disease trial should add valuable clinical information beyond that of a targeted symptom.
  • Using latent trajectory modeling that allowed for individual trends as well as overall relationships, we reanalyzed three repeated assessments of the present pain intensity from the McGill Pain Questionnaire and the European Organization for Research and Treatment of Cancer Quality of life Questionnaire- Core 30 (QLQ-C30) GHRQL score from a hormone-refractory prostate cancer trial.
  • Within- and between-treatment differences not detected in the original S9916 report of pain palliation and GHRQL suggested substantial individual variation in GHRQL level and change after controlling for within-assessment pain.
  • The treatment had a differential effect on the relationship between GHRQL and pain; we observed an approximately threefold stronger association of reported pain with GHRQL in the docetaxel plus estramustine (D + E) arm compared with the mitoxantrone plus prednisone (M + P) arm (P = .02).
  • In addition, the treatment had an effect, on average, on the rate of change in GHRQL, after controlling for pain level.
  • In addition, identifying the rate at which a person's GHRQL changes or responds to treatment provides clinically relevant information.
  • [MeSH-major] Outcome Assessment (Health Care). Prostatic Neoplasms / drug therapy. Prostatic Neoplasms / psychology. Quality of Life

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  • (PMID = 17951229.001).
  • [ISSN] 1052-6773
  • [Journal-full-title] Journal of the National Cancer Institute. Monographs
  • [ISO-abbreviation] J. Natl. Cancer Inst. Monographs
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA03096; United States / NCI NIH HHS / CA / CA04919; United States / NCI NIH HHS / CA / CA11083; United States / NCI NIH HHS / CA / CA12213; United States / NCI NIH HHS / CA / CA12644; United States / NCI NIH HHS / CA / CA13612; United States / NCI NIH HHS / CA / CA14028; United States / NCI NIH HHS / CA / CA16385; United States / NCI NIH HHS / CA / CA20319; United States / NCI NIH HHS / CA / CA22433; United States / NCI NIH HHS / CA / CA25224; United States / NCI NIH HHS / CA / CA27057; United States / NCI NIH HHS / CA / CA32102; United States / NCI NIH HHS / CA / CA35090; United States / NCI NIH HHS / CA / CA35119; United States / NCI NIH HHS / CA / CA35128; United States / NCI NIH HHS / CA / CA35176; United States / NCI NIH HHS / CA / CA35178; United States / NCI NIH HHS / CA / CA35192; United States / NCI NIH HHS / CA / CA35261; United States / NCI NIH HHS / CA / CA35281; United States / NCI NIH HHS / CA / CA35431; United States / NCI NIH HHS / CA / CA35996; United States / NCI NIH HHS / CA / CA37135; United States / NCI NIH HHS / CA / CA37981; United States / NCI NIH HHS / CA / CA38926; United States / NCI NIH HHS / CA / CA42777; United States / NCI NIH HHS / CA / CA45377; United States / NCI NIH HHS / CA / CA45450; United States / NCI NIH HHS / CA / CA45461; United States / NCI NIH HHS / CA / CA45807; United States / NCI NIH HHS / CA / CA45808; United States / NCI NIH HHS / CA / CA46113; United States / NCI NIH HHS / CA / CA46136; United States / NCI NIH HHS / CA / CA46282; United States / NCI NIH HHS / CA / CA46368; United States / NCI NIH HHS / CA / CA46441; United States / NCI NIH HHS / CA / CA46462; United States / NCI NIH HHS / CA / CA58416; United States / NCI NIH HHS / CA / CA58658; United States / NCI NIH HHS / CA / CA58686; United States / NCI NIH HHS / CA / CA58723; United States / NCI NIH HHS / CA / CA58861; United States / NCI NIH HHS / CA / CA58882; United States / NCI NIH HHS / CA / CA63844; United States / NCI NIH HHS / CA / CA63845; United States / NCI NIH HHS / CA / CA63848; United States / NCI NIH HHS / CA / CA63850; United States / NCI NIH HHS / CA / CA67575; United States / NCI NIH HHS / CA / CA67663; United States / NCI NIH HHS / CA / CA68183; United States / NCI NIH HHS / CA / CA74647; United States / NCI NIH HHS / CA / CA74811; United States / NCI NIH HHS / CA / CA76129; United States / NCI NIH HHS / CA / CA76132; United States / NCI NIH HHS / CA / CA76447; United States / NCI NIH HHS / CA / CA86780
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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