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1. Wang L, Bonorden MJ, Li GX, Lee HJ, Hu H, Zhang Y, Liao JD, Cleary MP, Lü J: Methyl-selenium compounds inhibit prostate carcinogenesis in the transgenic adenocarcinoma of mouse prostate model with survival benefit. Cancer Prev Res (Phila); 2009 May;2(5):484-95
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Methyl-selenium compounds inhibit prostate carcinogenesis in the transgenic adenocarcinoma of mouse prostate model with survival benefit.
  • Here we used the transgenic adenocarcinoma mouse prostate (TRAMP) model to establish the efficacy of methylseleninic acid (MSeA) and methylselenocysteine (MSeC) against prostate carcinogenesis and to characterize potential mechanisms.
  • Eight-week-old male TRAMP mice (C57B/6 background) were given a daily oral dose of water, MSeA, or MSeC at 3 mg Se/kg body weight and were euthanized at either 18 or 26 weeks of age.
  • At 26 weeks, 4 of 10 control mice had genitourinary weight >2 g, and only 1 of 10 in each of the Se groups did.
  • The efficacy was accompanied by delayed lesion progression, increased apoptosis, and decreased proliferation without appreciable changes of T-antigen expression in the dorsolateral prostate of Se-treated mice and decreased serum insulin-like growth factor I when compared with control mice.
  • In another experiment, giving MSeA to TRAMP mice from 10 or 16 weeks of age increased their survival to 50 weeks of age, and delayed the death due to synaptophysin-positive neuroendocrine carcinomas and synaptophysin-negative prostate lesions and seminal vesicle hypertrophy.
  • Wild-type mice receiving MSeA from 10 weeks did not exhibit decreased body weight or genitourinary weight or increased serum alanine aminotransferase compared with the control mice.

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  • (PMID = 19401524.001).
  • [ISSN] 1940-6215
  • [Journal-full-title] Cancer prevention research (Philadelphia, Pa.)
  • [ISO-abbreviation] Cancer Prev Res (Phila)
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA095642-04; United States / NCI NIH HHS / CA / R01 CA126880-02; United States / NCI NIH HHS / CA / R01 CA095642-04; United States / NCI NIH HHS / CA / R01 CA126880; United States / NCI NIH HHS / CA / CA 95642; United States / NCI NIH HHS / CA / R01 CA095642; United States / NCI NIH HHS / CA / CA126880-02; United States / NCI NIH HHS / CA / CA 126880
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Organoselenium Compounds; 0CH9049VIS / Selenocysteine; 67763-96-6 / Insulin-Like Growth Factor I; 964MRK2PEL / Selenomethionine; K848JZ4886 / Cysteine; TWK220499Z / selenomethylselenocysteine
  • [Other-IDs] NLM/ NIHMS118689; NLM/ PMC2822708
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2. Singh RP, Raina K, Sharma G, Agarwal R: Silibinin inhibits established prostate tumor growth, progression, invasion, and metastasis and suppresses tumor angiogenesis and epithelial-mesenchymal transition in transgenic adenocarcinoma of the mouse prostate model mice. Clin Cancer Res; 2008 Dec 1;14(23):7773-80
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  • [Title] Silibinin inhibits established prostate tumor growth, progression, invasion, and metastasis and suppresses tumor angiogenesis and epithelial-mesenchymal transition in transgenic adenocarcinoma of the mouse prostate model mice.
  • Herein, for the first time, we investigated the effect and associated mechanisms of silibinin phosphatidylcholine (silybin-phytosome) on established prostate tumors in transgenic adenocarcinoma of the mouse prostate (TRAMP) model.
  • RESULTS: Dietary silibinin inhibited the growth of prostate tumors (up to 60%, P < 0.001) and suppressed tumor progression from prostatic intraepithelial neoplasia to differentiated adenocarcinoma and poorly differentiated adenocarcinoma, with a complete absence of poorly differentiated adenocarcinoma at higher doses.
  • It also inhibited the incidence of tumor invasion of seminal vesicle (up to 81%, P < 0.001) with complete absence of distant metastasis.
  • CONCLUSIONS: Overall, silibinin treatment of TRAMP mice bearing prostate tumor inhibited tumor growth, progression, local invasion, and distant metastasis involving suppression of tumor angiogenesis and epithelial-mesenchymal transition.

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  • (PMID = 19047104.001).
  • [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 / CA102514-05; United States / NCI NIH HHS / CA / R01 CA102514; United States / NCI NIH HHS / CA / R01 CA102514-05
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Cadherins; 0 / Silymarin; 0 / Vimentin; 0 / silybin-phytosome; EC 3.4.24.- / Matrix Metalloproteinases
  • [Other-IDs] NLM/ NIHMS82719; NLM/ PMC2639624
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3. Garcia GE, Wisniewski HG, Lucia MS, Arevalo N, Slaga TJ, Kraft SL, Strange R, Kumar AP: 2-Methoxyestradiol inhibits prostate tumor development in transgenic adenocarcinoma of mouse prostate: role of tumor necrosis factor-alpha-stimulated gene 6. Clin Cancer Res; 2006 Feb 1;12(3 Pt 1):980-8
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  • [Title] 2-Methoxyestradiol inhibits prostate tumor development in transgenic adenocarcinoma of mouse prostate: role of tumor necrosis factor-alpha-stimulated gene 6.
  • PURPOSE: 2-Methoxyestradiol, an estrogenic metabolite, is in clinical trials for the treatment of hormone-refractory prostate cancer.
  • EXPERIMENTAL DESIGN: Eight- and 24-week-old transgenic adenocarcinoma of mouse prostate (TRAMP) mice were fed a diet containing 50 mg 2-methoxyestradiol/kg body weight for 16 and 8 weeks, respectively.
  • Chemopreventive efficacy was evaluated by magnetic resonance imaging, determining the prostate-seminal vesicle complex volume and histologic analysis of prostate tumor or tissue.
  • Expression of TSG-6 was analyzed in a human tissue array containing different grades of prostate tumors.
  • [MeSH-major] Adenocarcinoma / drug therapy. Adenocarcinoma / prevention & control. Cell Adhesion Molecules / physiology. Estradiol / analogs & derivatives. Prostatic Neoplasms / drug therapy. Prostatic Neoplasms / prevention & control
  • [MeSH-minor] Animals. Cell Line, Tumor. Diet. Disease Models, Animal. Gene Expression Regulation, Neoplastic / drug effects. Humans. Male. Mice. Mice, Inbred C57BL. Mice, Transgenic. Oligonucleotide Array Sequence Analysis

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  • (PMID = 16467113.001).
  • [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 / P30 CA-054174-16; United States / NCI NIH HHS / CA / R21 CA 98744
  • [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 / Cell Adhesion Molecules; 0 / TNFAIP6 protein, human; 0 / Tnfaip6 protein, mouse; 4TI98Z838E / Estradiol; 6I2QW73SR5 / 2-methoxyestradiol
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4. Neubauer BL, McNulty AM, Chedid M, Chen K, Goode RL, Johnson MA, Jones CD, Krishnan V, Lynch R, Osborne HE, Graff JR: The selective estrogen receptor modulator trioxifene (LY133314) inhibits metastasis and extends survival in the PAIII rat prostatic carcinoma model. Cancer Res; 2003 Sep 15;63(18):6056-62
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The PAIII rat prostatic adenocarcinoma (PCa) is an androgen receptor-negative, ERalpha- and ERbeta-positive, spontaneously metastatic rodent tumor cell line.
  • PAIII metastasis to the lungs was significantly inhibited by trioxifene treatment.
  • In PAIII-tumor-bearing animals, trioxifene administration produced a maximal regression of 76% for ventral prostate and 64% for seminal vesicle (P < 0.05 for both).
  • Our data support the contention that trioxifene represents a SERM with potential antimetastatic efficacy for the treatment of androgen-independent, metastatic PCa.
  • [MeSH-major] Adenocarcinoma / drug therapy. Prostatic Neoplasms / drug therapy. Pyrrolidines / pharmacology. Selective Estrogen Receptor Modulators / pharmacology
  • [MeSH-minor] Animals. Body Weight / drug effects. Cell Division / drug effects. Disease Models, Animal. Estrogen Receptor alpha. Estrogen Receptor beta. Genitalia, Male / drug effects. Luciferases / antagonists & inhibitors. Luciferases / metabolism. Lung Neoplasms / prevention & control. Lung Neoplasms / secondary. Lymphatic Metastasis. Male. Organ Size / drug effects. Rats. Receptors, Androgen / biosynthesis. Receptors, Estrogen / biosynthesis. Receptors, Estrogen / metabolism. Testis / anatomy & histology. Testis / drug effects

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  • (PMID = 14522935.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Estrogen Receptor alpha; 0 / Estrogen Receptor beta; 0 / Pyrrolidines; 0 / Receptors, Androgen; 0 / Receptors, Estrogen; 0 / Selective Estrogen Receptor Modulators; EC 1.13.12.- / Luciferases; R0130F043H / trioxifene
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5. Möhring C, Bach P, Kosciesza S, Goepel M: [A primary adenocarcinoma of the seminal vesicles. Case report of a rare malignancy]. Urologe A; 2008 May;47(5):616-9

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [A primary adenocarcinoma of the seminal vesicles. Case report of a rare malignancy].
  • Primary malignancies of the seminal vesicles are extremely rare.
  • They must be strictly differentiated from surrounding malignancies that may infiltrate the seminal vesicles from outside (e.g. prostate, rectum, and bladder carcinoma).
  • MEDLINE and CANCERLIT review showed about 50 documented cases of primary seminal vesicle carcinoma so far worldwide in men between 19 and 90 years of age.
  • Additionally, CT and MRT scans show tumour masses corresponding to the seminal vesicles.
  • Adenocarcinoma of seminal vesicles shows no expression of prostate-specific antigen or prostate-specific acid phosphatase, but there may be expression of carcinoembryonic antigen and cancer antigen 125.
  • Radical surgery including radical prostatectomy and/or cystoprostatectomy including pelvic lymph node dissection offers a curative treatment pathway.
  • Adjuvant or inductive medical treatment is of unproven worth, but a combination of hormonal deprivation and radiotherapy seems to be more effective than any chemotherapy.
  • [MeSH-major] Adenocarcinoma, Mucinous / diagnosis. Genital Neoplasms, Male / diagnosis. Seminal Vesicles

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  • (PMID = 18231770.001).
  • [ISSN] 0340-2592
  • [Journal-full-title] Der Urologe. Ausg. A
  • [ISO-abbreviation] Urologe A
  • [Language] ger
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Germany
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6. Thyavihally YB, Tongaonkar HB, Gupta S, Gujral S: Primary seminal vesicle adenocarcinoma presenting as isolated metastasis to penis responding to chemotherapy and hormonal therapy. Urology; 2007 Apr;69(4):778.e1-3
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Primary seminal vesicle adenocarcinoma presenting as isolated metastasis to penis responding to chemotherapy and hormonal therapy.
  • We report a rare case of isolated penile metastasis from seminal vesicle adenocarcinoma associated with ipsilateral renal agenesis in a 62-year-old man.
  • Imaging studies confirmed seminal vesicle origin, and biopsy revealed a papillary mucin-secreting adenocarcinoma, with cytokeratin 20 positivity and prostate-specific antigen negativity.
  • The patient received six cycles of 5-fluorouracil, leucovorin, and oxaliplatin chemotherapy and underwent bilateral orchiectomy.
  • The patient was symptomatically better, and the penile swelling and seminal vesicle mass had regressed considerably.
  • He later developed multiple lung metastases and died of the disease.
  • [MeSH-major] Adenocarcinoma / secondary. Adenocarcinoma / therapy. Antineoplastic Agents / therapeutic use. Orchiectomy. Penile Neoplasms / secondary. Penile Neoplasms / therapy. Seminal Vesicles
  • [MeSH-minor] Combined Modality Therapy. Genital Neoplasms, Male / pathology. Humans. Male. Middle Aged

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  • (PMID = 17445672.001).
  • [ISSN] 1527-9995
  • [Journal-full-title] Urology
  • [ISO-abbreviation] Urology
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents
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7. Losa CA, Fernando AB, Lázaro VA, Berlanga FF, Frago PS, López MA, Sanz MJ, Martínez PG, Sanz LA: [Current value of seminal vesicle biopsy in patients with prostate cancer and influence of radical prostatectomy in patients with seminal vesicle invasion]. Arch Esp Urol; 2006 Dec;59(10):977-88
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  • [Title] [Current value of seminal vesicle biopsy in patients with prostate cancer and influence of radical prostatectomy in patients with seminal vesicle invasion].
  • [Transliterated title] Valor actual de la biopsia de vesículas seminales en pacientes con cancer de próstata e influencia de la prostatectomía radical en pacientes con infiltarción seminal.
  • OBJECTIVES: To evaluate if radical prostatectomy may positively influence cancer-specific survival (CSS), hormone-resistance-free time, metastasis-free time, and quality of life(QoL) of patients with prostate adenocarcinoma and seminal vesicle invasion, and also to update our thoughts about seminal vesicle biopsy.
  • Forty-six cases were diagnosed of seminal vesicle invasion after radical prostatectomy; 68 cases were diagnosed of seminal vesicle invasion after biopsy, not undergoing then surgery.
  • Cancer specific survival, time to hormone resistance from the start of hormonal treatment, metastasis free time and QoL, measured as need for hospital care, were compared between groups.
  • Median follow-up time was 52.6 mos.
  • RESULTS: There were not statistically significant differences between groups in CSS, time to hormone resistance, metastasis free time and QoL.
  • Primary grade and Gleason Score were independent predictors for CSS in the Cox regression test; clinical stage was independent predictor for time to hormone resistance.
  • CONCLUSIONS: Radical prostatectomy as monotherapy does not show a statistically significant influence on followup time, CSS, time to hormone resistance, metastasis free time or QoL in patients with prostate cancer and seminal vesicle invasion associated with other bad prognostic factors (unfavourable Gleason and PSA).
  • The value of seminal vesicle biopsy remains for the study of new multimodal treatments, such as chemotherapy + surgery, and it is to be defined in the planning of radio and cryosurgery.
  • [MeSH-major] Adenocarcinoma / pathology. Adenocarcinoma / surgery. Prostatectomy. Prostatic Neoplasms / pathology. Prostatic Neoplasms / surgery. Seminal Vesicles / pathology

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  • (PMID = 17283711.001).
  • [ISSN] 0004-0614
  • [Journal-full-title] Archivos españoles de urología
  • [ISO-abbreviation] Arch. Esp. Urol.
  • [Language] spa
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Spain
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8. Haut MJ, Harryhill JF, Rosenstock J, Warhol MJ, Vitti R: Progressing prostate carcinoma. Oncologist; 2001;6(2):183-96
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  • In the Karnell Cancer Center Grand Rounds, we present a patient who underwent radical prostatectomy with bilateral pelvic lymphadenectomy, but had positive margins and subsequently developed local recurrence and then systemic disease.
  • Therapeutic options at different stages of the disease are examined from the point of view of the urologist, radiation oncologist, and medical oncologist.
  • The surgical portion of the discussion focuses on the selection of initial therapy.
  • Both the selection of surgical candidates and choice of pre- or post-operative therapy in patients can be aided by prognostic tools looking at several variables, including prostate-specific antigen (PSA) level, Gleason score of the tumor, seminal vesicle invasion, extracapsular invasion, and lymph node involvement.
  • Low-risk patients can be treated with monotherapy, such as radical prostatectomy, external beam radiation therapy, prostate brachytherapy, or cryosurgical ablation of the prostate.
  • Higher risk patients may require adjuvant and possibly neoadjuvant therapy in addition.
  • The radiation portion of the discussion focuses on the use of radiation therapy as salvage for relapsing disease.
  • Of particular importance is the point that treating high-risk patients whose PSA levels have started to rise but are less than 1 ng/ml results in a long-term PSA control rate as high as 75%, but that limiting the use of salvage radiation therapy to patients with high PSA levels or biopsy confirmation of local recurrence in the face of a negative bone scan results in biochemical long-term control of less than 40%.
  • In the medical oncology part of the discussion, the major focus is on the use of chemotherapy to treat patients whose disease has become resistant to hormonal therapy.
  • Combination therapy with estramustine plus taxanes, other microtubule inhibitors, or other agents such as topoisomerase II inhibitors, has been found to cause shrinkage of measurable soft tissue disease and diminution of serum PSA levels.
  • The development of effective hormonal and chemotherapeutic drugs for treatment of metastatic disease has led to new interest in adjuvant and neoadjuvant therapy of high-risk patients.
  • [MeSH-major] Adenocarcinoma / secondary. Prostatic Neoplasms / pathology

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  • (PMID = 11306730.001).
  • [ISSN] 1083-7159
  • [Journal-full-title] The oncologist
  • [ISO-abbreviation] Oncologist
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] EC 3.4.21.77 / Prostate-Specific Antigen
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9. Harvey I, Têtu B: [Amyloidosis of the seminal vesicles: a local condition with no systemic impact]. Ann Pathol; 2004 Jun;24(3):236-40; quiz 227
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  • [Title] [Amyloidosis of the seminal vesicles: a local condition with no systemic impact].
  • [Transliterated title] L'amyloïdose des vésicules séminales, une condition localisée sans répercussion systémique.
  • AIM: Localised seminal vesicle amyloidosis is relatively infrequent and we present 9 additional cases.
  • MATERIAL: and methods: Those 9 cases were retrospectively retrieved from 803 radical prostatectomies performed between 1995 and 2000 for prostatic adenocarcinoma.
  • In each case, the type of amyloidosis was characterised by immunohistochemistry.
  • Information regarding a possible concurrent disease or prior hormone therapy has been obtained.
  • RESULTS: The prevalence of amyloidosis of seminal vesicles is lower in our study (1.1%) than in unselected autopsy cases.
  • The prevalence of amyloidosis in patients exposed to prior hormone therapy (LHRH agonist and anti-androgen) was 2% while it reached only 0.9% in those who received no hormone therapy (p>0.3).
  • No patient had systemic amyloidosis and all cases were of non A-A type.
  • Lactoferrin, a glycoprotein produced by normal seminal vesicles, was detected in more than a half of them (5/9).
  • CONCLUSION: No association was found between the occurrence of seminal vesicle amyloidosis and occurrence of a prostatic adenocarcinoma, corcomitant systemic disease or exposure to prior hormone therapy.
  • Seminal vesicle amyloidosis is a localised condition without systemic involvement and amyloid deposition is composed mostly of lactoferrin.
  • [MeSH-major] Amyloidosis / pathology. Genital Diseases, Male / pathology. Seminal Vesicles / pathology
  • [MeSH-minor] Adenocarcinoma / complications. Adenocarcinoma / drug therapy. Adenocarcinoma / surgery. Adult. Aged. Amyloid / chemistry. Androgen Antagonists / pharmacology. Androgen Antagonists / therapeutic use. Antineoplastic Agents, Hormonal / pharmacology. Antineoplastic Agents, Hormonal / therapeutic use. Combined Modality Therapy. France / epidemiology. Gonadotropin-Releasing Hormone / agonists. Humans. Lactoferrin / analysis. Male. Middle Aged. Neoadjuvant Therapy. Prevalence. Prostatectomy. Prostatic Neoplasms / complications. Prostatic Neoplasms / drug therapy. Prostatic Neoplasms / surgery. Retrospective Studies

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  • (PMID = 15480258.001).
  • [ISSN] 0242-6498
  • [Journal-full-title] Annales de pathologie
  • [ISO-abbreviation] Ann Pathol
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Amyloid; 0 / Androgen Antagonists; 0 / Antineoplastic Agents, Hormonal; 33515-09-2 / Gonadotropin-Releasing Hormone; EC 3.4.21.- / Lactoferrin
  • [Number-of-references] 8
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10. Kasibhatla M, Peterson B, Anscher MS: What is the best postoperative treatment for patients with pT3bN0M0 adenocarcinoma of the prostate? Prostate Cancer Prostatic Dis; 2005;8(2):167-73
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  • [Title] What is the best postoperative treatment for patients with pT3bN0M0 adenocarcinoma of the prostate?
  • The purpose of this paper to identify the optimal therapy after radical prostatectomy (RP) for patients with adenocarcinoma of the prostate invading the seminal vesicles (pT3bN0M0 or SVI).
  • A PubMed search using the keywords 'prostate', 'seminal vesicle', 'prostatectomy', 'radiotherapy', 'androgen blockade' was performed to identify literature regarding rates of disease failure in patients with SVI who are observed or treated with androgen blockade (AB), radiotherapy (RT) or RT + AB after RP.
  • Seminal vesicle invasion confers a poor prognosis after RP.
  • [MeSH-major] Adenocarcinoma / drug therapy. Adenocarcinoma / radiotherapy. Androgen Antagonists / therapeutic use. Prostatic Neoplasms / drug therapy. Prostatic Neoplasms / radiotherapy
  • [MeSH-minor] Aged. Chemotherapy, Adjuvant. Combined Modality Therapy. Humans. Male. Middle Aged. Neoplasm Invasiveness. Neoplasm Staging. Radiotherapy, Adjuvant. Seminal Vesicles / pathology. Treatment Outcome

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  • (PMID = 15711603.001).
  • [ISSN] 1365-7852
  • [Journal-full-title] Prostate cancer and prostatic diseases
  • [ISO-abbreviation] Prostate Cancer Prostatic Dis.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Androgen Antagonists
  • [Number-of-references] 33
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11. Lu XF, Tam NC, Wong YC: Roles of growth factors in mediating mesenchymal influence on the cytodifferentiation of the Dunning prostatic adenocarcinoma. Tumour Biol; 2000 Jan-Feb;21(1):21-32
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  • [Title] Roles of growth factors in mediating mesenchymal influence on the cytodifferentiation of the Dunning prostatic adenocarcinoma.
  • Earlier studies have shown that seminal vesicle mesenchyme (SVM) has the ability to induce Dunning tumor (DT) to undergo morphogenetic changes and cytodifferentiation.
  • Small pieces of DT were combined with SVM (0-day neonatal SD rat) and the tissue recombinants (SVM + DT) were grafted under the renal capsule of male athymic nude mice and allowed to grow for 4 weeks.
  • Histopathological examination confirmed that SVM can induce DT to express apparently more normal morphological features, with the formation of large tubules lined by highly differentiated columnar epithelial cells and the reappearance of a fibromuscular stroma.
  • Using immunohistochemistry, the results demonstrated that the tissue recombinants typically exhibited an overexpression of EGF, EGF-R, bFGF, TGF-beta(1) together with a concurrent downregulation of TGF-alpha, IGF-I, IGF-II, and VEGF receptors (flk-1, flt-1).
  • The levels of these growth factors and their receptors in DT + SVM tissue recombinants were more similar to those of the normal prostate.
  • These findings reaffirmed that SVM has the ability to reprogram DT toward a more normal direction on one hand, while implicating the importance of cytokines in mesenchyme-induced DT phenotypic changes under in vivo condition on the other hand.
  • [MeSH-major] Adenocarcinoma / metabolism. Adenocarcinoma / pathology. Growth Substances / physiology. Mesoderm / physiology. Prostatic Neoplasms / metabolism. Prostatic Neoplasms / pathology
  • [MeSH-minor] Animals. Cell Differentiation. Endothelial Growth Factors / metabolism. Endothelial Growth Factors / physiology. Epidermal Growth Factor / physiology. Fibroblast Growth Factor 2 / physiology. Immunohistochemistry. Insulin-Like Growth Factor I / physiology. Insulin-Like Growth Factor II / physiology. Lymphokines / metabolism. Lymphokines / physiology. Male. Mice. Mice, Nude. Rats. Rats, Sprague-Dawley. Receptor Protein-Tyrosine Kinases / physiology. Receptor, Epidermal Growth Factor / physiology. Receptor, IGF Type 1 / physiology. Receptors, Growth Factor / physiology. Receptors, Vascular Endothelial Growth Factor. Transforming Growth Factor alpha / physiology. Transforming Growth Factor beta / physiology. Vascular Endothelial Growth Factor A. Vascular Endothelial Growth Factors

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  • [Copyright] Copyright 2000 S. Karger AG, Basel
  • (PMID = 10601838.001).
  • [ISSN] 1010-4283
  • [Journal-full-title] Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine
  • [ISO-abbreviation] Tumour Biol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Endothelial Growth Factors; 0 / Growth Substances; 0 / Lymphokines; 0 / Receptors, Growth Factor; 0 / Transforming Growth Factor alpha; 0 / Transforming Growth Factor beta; 0 / Vascular Endothelial Growth Factor A; 0 / Vascular Endothelial Growth Factors; 103107-01-3 / Fibroblast Growth Factor 2; 62229-50-9 / Epidermal Growth Factor; 67763-96-6 / Insulin-Like Growth Factor I; 67763-97-7 / Insulin-Like Growth Factor II; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.10.1 / Receptor, IGF Type 1; EC 2.7.10.1 / Receptors, Vascular Endothelial Growth Factor
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12. Anscher MS, Clough R, Robertson CN, Prosnitz LR, Dahm P, Walther P, Donatucci CF, Albala DM, Febbo P, George DJ, Sun L, Moul JW: Timing and patterns of recurrences and deaths from prostate cancer following adjuvant pelvic radiotherapy for pathologic stage T3/4 adenocarcinoma of the prostate. Prostate Cancer Prostatic Dis; 2006;9(3):254-60
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  • [Title] Timing and patterns of recurrences and deaths from prostate cancer following adjuvant pelvic radiotherapy for pathologic stage T3/4 adenocarcinoma of the prostate.
  • Between 1970 and 1983, 159 patients underwent RP for newly diagnosed adenocarcinoma of the prostate and were found to have positive surgical margins, extracapsular extension and/or seminal vesicle invasion.
  • The RT group generally received 45-50 Gy to the whole pelvis, then a boost to the prostate bed (total dose of 55-65 Gy).
  • The median time to failure in the surgery group was 7.5 vs 14.7 years in the RT group (P=0.1).
  • In contrast to recurrences, nearly half of deaths from prostate cancer occurred more than 10 years after treatment.
  • Despite its long natural history, death from prostate cancer was the most common cause of mortality in this population with locally advanced tumors, reflecting the need for more effective therapy.
  • [MeSH-major] Adenocarcinoma / pathology. Adenocarcinoma / radiotherapy. Prostatic Neoplasms / pathology. Prostatic Neoplasms / radiotherapy
  • [MeSH-minor] Adult. Aged. Antineoplastic Agents, Hormonal / therapeutic use. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Disease-Free Survival. Humans. Male. Middle Aged. Neoplasm Recurrence, Local / drug therapy. Neoplasm Recurrence, Local / mortality. Neoplasm Recurrence, Local / radiotherapy. Neoplasm Staging. Pelvis / radiation effects. Prostatectomy / methods. Radiation Dosage. Radiotherapy, Adjuvant. Retrospective Studies. Survival Analysis. Time Factors. Treatment Failure

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  • (PMID = 16880828.001).
  • [ISSN] 1365-7852
  • [Journal-full-title] Prostate cancer and prostatic diseases
  • [ISO-abbreviation] Prostate Cancer Prostatic Dis.
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal
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13. Oh WK, Kaplan ID, Febbo P, Prisby J, Manola J, Kaufman DS, Kantoff PW: Neoadjuvant doxil chemotherapy prior to androgen ablation plus radiotherapy for high-risk localized prostate cancer: feasibility and toxicity. Am J Clin Oncol; 2003 Jun;26(3):312-6
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  • [Title] Neoadjuvant doxil chemotherapy prior to androgen ablation plus radiotherapy for high-risk localized prostate cancer: feasibility and toxicity.
  • Patients with clinical T3 or T4 prostate cancer or with elevated serum prostate-specific antigen (PSA) levels greater than 40 ng/ml are at high risk of failure with primary treatment.
  • Chemotherapy administered at the time of diagnosis may decrease the risk of recurrence.
  • Patients were then treated with androgen ablative therapy and prostate radiotherapy.
  • Three patients had T3 disease, and 4 patients had T2b disease with either PSA greater than 40 ng/ml or erMRI evidence of seminal vesicle involvement or extracapsular disease.
  • All seven patients responded to androgen ablative therapy and prostate irradiation.
  • [MeSH-major] Adenocarcinoma / drug therapy. Antibiotics, Antineoplastic / therapeutic use. Doxorubicin / therapeutic use. Prostatic Neoplasms / drug therapy
  • [MeSH-minor] Androgen Antagonists / therapeutic use. Anilides / therapeutic use. Antineoplastic Agents, Hormonal / therapeutic use. Humans. Leuprolide / therapeutic use. Magnetic Resonance Imaging. Male. Middle Aged. Neoadjuvant Therapy. Nitriles. Pilot Projects. Prostate-Specific Antigen / blood. Tosyl Compounds

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  • (PMID = 12796607.001).
  • [ISSN] 1537-453X
  • [Journal-full-title] American journal of clinical oncology
  • [ISO-abbreviation] Am. J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Clinical Trial; Clinical Trial, Phase II; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Androgen Antagonists; 0 / Anilides; 0 / Antibiotics, Antineoplastic; 0 / Antineoplastic Agents, Hormonal; 0 / Nitriles; 0 / Tosyl Compounds; 80168379AG / Doxorubicin; A0Z3NAU9DP / bicalutamide; EC 3.4.21.77 / Prostate-Specific Antigen; EFY6W0M8TG / Leuprolide
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14. Tollefson MK, Slezak JM, Leibovich BC, Zincke H, Blute ML: Stratification of patient risk based on prostate-specific antigen doubling time after radical retropubic prostatectomy. Mayo Clin Proc; 2007 Apr;82(4):422-7
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  • [Title] Stratification of patient risk based on prostate-specific antigen doubling time after radical retropubic prostatectomy.
  • OBJECTIVE: To assess the risk of local recurrence, systemic progression, and death from cancer among patients who experience biochemical relapse after radical retropubic prostatectomy and to stratify those patients by prostate-specific antigen (PSA) doubling time (DT).
  • PATIENTS AND METHODS: We identified patients who experienced biochemical recurrence (defined as a PSA level < or =0.4 ng/mL) after radical prostatectomy from January 1, 1990, to December 31, 1999, for prostate adenocarcinoma.
  • The PSA-DT was calculated by log linear regression using all PSA values within 2 years of biochemical recurrence.
  • Of the 1064 patients with a calculable PSA-DT, 322 (30%) had a PSA-DT of less than 1 year, 357 (34%) had a PSA-DT of 1 to 9.9 years, and 385 (36%) had a PSA-DT of 10 years or more.
  • Patients with a PSA-DT of 10 years or more were less likely to have a higher preoperative PSA level, Gleason score, advanced pathologic stage, and seminal vesicle invasion.
  • Patients with a PSA-DT of 10 years or more were at low risk of local recurrence (hazard ratio [HR], 0.09; 95% confidence interval [CI], 0.06-0.14; compared with patients with a PSA-DT of <1 year), systemic progression (HR, 0.05; 95% CI, 0.02-0.13), or death from cancer (HR, 0.15; 95% CI, 0.05-0.43).
  • CONCLUSIONS: Prostate-specific antigen DT is an independent predictor of clinical disease recurrence and mortality after surgical biochemical failure.
  • Risk stratification into high-, intermediate-, and low-risk categories based on the PSA-DT provides helpful clinical information and assists in the development of salvage therapy trials.
  • [MeSH-major] Adenocarcinoma / surgery. Prostate-Specific Antigen / biosynthesis. Prostatectomy. Prostatic Neoplasms / surgery
  • [MeSH-minor] Adult. Aged. Biomarkers, Tumor / blood. Disease Progression. Disease-Free Survival. Follow-Up Studies. Humans. Male. Middle Aged. Neoplasm Recurrence, Local. Time Factors

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  • (PMID = 17418069.001).
  • [ISSN] 0025-6196
  • [Journal-full-title] Mayo Clinic proceedings
  • [ISO-abbreviation] Mayo Clin. Proc.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; EC 3.4.21.77 / Prostate-Specific Antigen
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15. Suckow MA, Rosen ED, Wolter WR, Sailes V, Jeffrey R, Tenniswood M: Prevention of human PC-346C prostate cancer growth in mice by a xenogeneic tissue vaccine. Cancer Immunol Immunother; 2007 Aug;56(8):1275-83
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  • [Title] Prevention of human PC-346C prostate cancer growth in mice by a xenogeneic tissue vaccine.
  • To examine if a xenogeneic tissue vaccine could stimulate protective immunity in a human prostate cancer cell line, a vaccine was produced by glutaraldehyde fixation of harvested PAIII prostate cancer cells tumors (GFT cell vaccine) from Lobund-Wistar rats.
  • Immunocompetent Ncr-Foxn1<nu> mice were vaccinated with the GFT cell vaccine four times, 7 days apart.
  • Results showed that vaccination with GFT cells resulted in increased serum antibody to a PAIII cell lysate; reduced weight of the prostate/seminal vesicle complex and reduced incidence of prostate cancer in nude mice; increased splenocyte supernatant levels of TNF-alpha, IL-2, IFN-gamma and IL-12, cytokines associated with Th1 immunity; and increased splenocyte supernatant levels of IL-4 and IL-10, cytokines associated with Th2 immunity.
  • In summary, the results suggest that use of a xenogeneic tissue vaccine can stimulate protective immunity against human prostate cancer cells.
  • [MeSH-major] Adenocarcinoma / therapy. Cancer Vaccines / therapeutic use. Immunotherapy, Active. Prostatic Neoplasms / therapy
  • [MeSH-minor] Animals. Antibodies, Neoplasm / blood. Cell Line, Tumor / immunology. Cells, Cultured / immunology. Cells, Cultured / secretion. Coculture Techniques. Cytokines / secretion. Disease Progression. Drug Screening Assays, Antitumor. Humans. Male. Mice. Mice, Inbred BALB C. Mice, Nude. Organ Size. Spleen / immunology. T-Lymphocyte Subsets / immunology. T-Lymphocyte Subsets / secretion. Tumor Burden. Vaccination. Xenograft Model Antitumor Assays

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  • (PMID = 17242926.001).
  • [ISSN] 0340-7004
  • [Journal-full-title] Cancer immunology, immunotherapy : CII
  • [ISO-abbreviation] Cancer Immunol. Immunother.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antibodies, Neoplasm; 0 / Cancer Vaccines; 0 / Cytokines
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16. Valicenti RK, Winter K, Cox JD, Sandler HM, Bosch W, Vijayakumar S, Michalski J, Purdy J: RTOG 94-06: is the addition of neoadjuvant hormonal therapy to dose-escalated 3D conformal radiation therapy for prostate cancer associated with treatment toxicity? Int J Radiat Oncol Biol Phys; 2003 Nov 1;57(3):614-20
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  • [Title] RTOG 94-06: is the addition of neoadjuvant hormonal therapy to dose-escalated 3D conformal radiation therapy for prostate cancer associated with treatment toxicity?
  • PURPOSE: This study determines the effect on toxicity of adding neoadjuvant hormonal therapy (NHT) to three-dimensional conformal radiation therapy (3D-CRT) in RTOG 94-06.
  • Two hundred and seven men initiated hormonal therapy (HT) between 2 to 3 months before 3D-CRT, and completed all HT no longer than 3 months after radiotherapy.
  • The 547 patients were treated at dose level I (68.4 Gy), level II (73.8 Gy), or level III (79.2 Gy).
  • Men were stratified into three risk groups according to their relative risk of seminal vesicle invasion: <15% (Group 1) vs. >15% (Group 2), or to T stage (T1, 2 vs. T3 tumors [Group 3]).
  • In Group 2 patients, there was a clinical target volume reduction to treat only the prostate after delivery of 55.8 Gy to a planning target volume including the seminal vesicles.
  • Hormonal therapy did not have a significant univariate effect on any other acute or late toxicity.
  • On multivariate analysis, the percent of the bladder (< or =30% vs. >30%) receiving > or = the reference dose (68.4 Gy, 73.8 Gy, or 79.2 Gy) (p = 0.0009, relative risk = 2.07, confidence interval: 1.88-2.28) was a significant predictor of acute GU effects.
  • However, this combined modality therapy significantly increased the risk of acute GU effects compared to 3D-CRT alone in men with poor baseline urinary function.
  • [MeSH-major] Hormones / therapeutic use. Prostatic Neoplasms / drug therapy. Prostatic Neoplasms / radiotherapy. Radiotherapy Planning, Computer-Assisted / methods. Radiotherapy, Conformal / adverse effects
  • [MeSH-minor] Adenocarcinoma. Aged. Combined Modality Therapy. Follow-Up Studies. Humans. Male. Maximum Tolerated Dose. Multivariate Analysis. Neoadjuvant Therapy. Prostate-Specific Antigen / blood. Radiation Injuries / prevention & control. Radiotherapy Dosage

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  • (PMID = 14529764.001).
  • [ISSN] 0360-3016
  • [Journal-full-title] International journal of radiation oncology, biology, physics
  • [ISO-abbreviation] Int. J. Radiat. Oncol. Biol. Phys.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA21661; United States / NCI NIH HHS / CA / CA60267; United States / NCI NIH HHS / CA / U10CA32115; United States / NCI NIH HHS / CA / U24 CA 81647
  • [Publication-type] Clinical Trial; Clinical Trial, Phase I; Clinical Trial, Phase II; 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 / Hormones; EC 3.4.21.77 / Prostate-Specific Antigen
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17. Rubin MA, Mucci NR, Figurski J, Fecko A, Pienta KJ, Day ML: E-cadherin expression in prostate cancer: a broad survey using high-density tissue microarray technology. Hum Pathol; 2001 Jul;32(7):690-7
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  • [Title] E-cadherin expression in prostate cancer: a broad survey using high-density tissue microarray technology.
  • To address these variations, we undertook a study to systematically evaluate E-cadherin expression in a broad range of prostate tissue.
  • Benign prostate, clinically localized prostate cancer, and hormone-refractory metastatic prostate cancer were analyzed under uniform conditions using high-density tissue microarrays (TMA).
  • Benign and atrophic prostate tissue and high-grade prostatic intraepithelial neoplasia (PIN) were also included from the clinically localized cases.
  • No significant associations were seen with extraprostatic extension and seminal vesicle invasion.
  • [MeSH-major] Adenocarcinoma / metabolism. Cadherins / metabolism. Prostatic Neoplasms / metabolism
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Antineoplastic Agents, Hormonal / therapeutic use. Drug Resistance, Neoplasm. Humans. Immunohistochemistry. Male. Middle Aged. Neoplasm Metastasis / drug therapy. Neoplasm Metastasis / pathology






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