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1. Chheda N, Bolegave M, Shet T, Tongaonkar H: Recurrent mullerian adenosarcoma like tumor of seminal vesicle. Indian J Pathol Microbiol; 2010 Apr-Jun;53(2):342-4

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Recurrent mullerian adenosarcoma like tumor of seminal vesicle.
  • Adenosarcoma like tumor of the seminal vesicle is reported herein.
  • A 35-year-old male presented with mass in the pelvis between bladder and rectum, involving the seminal vesicle and prostate.
  • Histologically, the tumor was multicystic with bland ciliated lining epithelium and sarcomatous stroma.
  • A wide excision was performed followed with chemotherapy and radiotherapy.
  • [MeSH-major] Adenosarcoma / diagnosis. Adenosarcoma / pathology. Seminal Vesicles / pathology. Urogenital Neoplasms / diagnosis. Urogenital Neoplasms / pathology
  • [MeSH-minor] Adult. Antineoplastic Agents / therapeutic use. Drug Therapy / methods. Histocytochemistry. Humans. Male. Microscopy. Recurrence. Tomography, X-Ray Computed. Urography

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  • (PMID = 20551553.001).
  • [ISSN] 0974-5130
  • [Journal-full-title] Indian journal of pathology & microbiology
  • [ISO-abbreviation] Indian J Pathol Microbiol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] India
  • [Chemical-registry-number] 0 / Antineoplastic Agents
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2. Hamada S, Ito K, Kanbara T, Yoshii T, Sato K, Sumitomo M, Kimura F, Asano T: [A case of malignant lymphoma mimicking a seminal vesicle tumor]. Hinyokika Kiyo; 2010 Jul;56(7):393-6

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [A case of malignant lymphoma mimicking a seminal vesicle tumor].
  • Abdominal computed tomography (CT) showed a mass 7 cm in diameter mimicking a seminal vesicle tumor and magnetic resonance imaging showed a heterogeneously enhanced mass with an unclear borderline to the rectum.
  • The differential diagnosis of the lesion included a tumor arising from a seminal vesicle, a local recurrence of rectal cancer, a rectal GIST, and a mesenchymal tumor.
  • Chest and abdominal CT showed no specific findings except the lesion for the seminal vesicle lesion, but positron emission tomography showed accumulations in the gastrointestinal tract, pleura, and lymph nodes.
  • The patient was thus determined to have stage IV malignant lymphoma and was given two courses of combination chemotherapy including RCHOP.
  • The tumor responded to one course, but the patient died of neutropenic sepsis during the second course.
  • [MeSH-major] Genital Neoplasms, Male / diagnosis. Lymphoma, Large B-Cell, Diffuse / diagnosis. Seminal Vesicles
  • [MeSH-minor] Aged. Diagnosis, Differential. Humans. Male

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  • (PMID = 20724815.001).
  • [ISSN] 0018-1994
  • [Journal-full-title] Hinyokika kiyo. Acta urologica Japonica
  • [ISO-abbreviation] Hinyokika Kiyo
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
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3. Agrawal V, Kumar S, Sharma D, Singh UR, Gupta A: Primary leiomyosarcoma of the seminal vesicle. Int J Urol; 2004 Apr;11(4):253-5
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  • [Title] Primary leiomyosarcoma of the seminal vesicle.
  • A case of leiomyosarcoma of the seminal vesicle detected as a prerectal mass on routine per-rectal examination is described in a 37-year-old man.
  • Computed tomography scan confirmed it to be arising from the right seminal vesicle.
  • Microscopic examination of the resected specimen showed moderately differentiated leiomyosarcoma from the seminal vesicle.
  • The patient received adjuvant chemotherapy and sandwiched radiotherapy.
  • He is well and free of tumor 20 months after surgery.
  • [MeSH-major] Genital Neoplasms, Male / diagnosis. Leiomyosarcoma / diagnosis. Seminal Vesicles / pathology
  • [MeSH-minor] Adult. Chemotherapy, Adjuvant. Cystectomy. Humans. Lymph Node Excision. Male. Prostatectomy. Radiotherapy, Adjuvant

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  • (PMID = 15028108.001).
  • [ISSN] 0919-8172
  • [Journal-full-title] International journal of urology : official journal of the Japanese Urological Association
  • [ISO-abbreviation] Int. J. Urol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Australia
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4. 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-minor] Aged. Follow-Up Studies. Humans. Lymph Node Excision. Lymphatic Metastasis. Male. Neoplasm Recurrence, Local. Prognosis. Prostate-Specific Antigen / blood. Prostatectomy. Prostatic Hyperplasia / pathology. Radiotherapy, Conformal. Survival Rate

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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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5. 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).
  • 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-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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6. Taue R, Takigawa H, Sinotou K, Uno S, Mori R, Tatara K, Sano T: A case of pelvic malignant paraganglioma. Int J Urol; 2001 Dec;8(12):715-8
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  • We report a rare case of pelvic malignant paraganglioma that was treated with surgery, combination chemotherapy and radiation.
  • The pelvic mass, which was 6 cm in size, was on the posterior side of the bladder and had invaded the prostate, seminal vesicle and bladder neck.
  • We resected the intrapelvic tumor and lymph nodes using cystoprostatectomy.
  • Adjuvant therapies included six courses of the combination chemotherapy (cyclophosphamide, vincristine and dacarbazine), and 12 courses of VP-16 therapy.
  • Radiation therapy was done for metastasis of the thoracic vertebrae.
  • Local recurrence, progression of bone metastasis and new metastasis have not been detected since these treatments.
  • Chemotherapy of cyclophosphamide, vincristine and dacarbazine and VP-16 with radiation appears to be effective in treating advanced malignant paraganglioma.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols. Paraganglioma / therapy. Pelvic Neoplasms / therapy
  • [MeSH-minor] Combined Modality Therapy. Cyclophosphamide / administration & dosage. Dacarbazine / administration & dosage. Etoposide / administration & dosage. Humans. Magnetic Resonance Imaging. Male. Middle Aged. Vincristine / administration & dosage

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  • (PMID = 11851776.001).
  • [ISSN] 0919-8172
  • [Journal-full-title] International journal of urology : official journal of the Japanese Urological Association
  • [ISO-abbreviation] Int. J. Urol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Australia
  • [Chemical-registry-number] 5J49Q6B70F / Vincristine; 6PLQ3CP4P3 / Etoposide; 7GR28W0FJI / Dacarbazine; 8N3DW7272P / Cyclophosphamide
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7. Lattouf JB, Mc Cormack M, Yelle L, Hadjeres R, Saad F: Recurrence of a non-seminomatous germ cell tumor in the seminal vesicle 20 years after initial diagnosis and treatment. Can J Urol; 2004 Aug;11(4):2350-1
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  • [Title] Recurrence of a non-seminomatous germ cell tumor in the seminal vesicle 20 years after initial diagnosis and treatment.
  • We present a case of a pathologic stage 1, right sided, non-seminomatous germ cell tumor recurrence in the left seminal vesicle, 20 years after initial diagnosis and treatment.
  • At 24 months of follow-up after completion of chemotherapy, digital rectal and TRUS examinations revealed complete resolution of the lesion.
  • We believe that this tumor is a late metastasis to the contralateral seminal vesicle.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Germinoma / drug therapy. Neoplasm Recurrence, Local / drug therapy. Testicular Neoplasms / drug therapy
  • [MeSH-minor] Bleomycin / administration & dosage. Cisplatin / administration & dosage. Etoposide / administration & dosage. Humans. Male. Middle Aged. Seminal Vesicles. Time Factors. Treatment Outcome

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  • (PMID = 15380057.001).
  • [ISSN] 1195-9479
  • [Journal-full-title] The Canadian journal of urology
  • [ISO-abbreviation] Can J Urol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Canada
  • [Chemical-registry-number] 11056-06-7 / Bleomycin; 6PLQ3CP4P3 / Etoposide; Q20Q21Q62J / Cisplatin
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8. Kreiner B, Denzinger S, Ganzer R, Fritsche HM, Burger M, Wieland WF, Otto W: Neuroendocrine carcinoma of the seminal vesicles presenting with Lambert Eaton syndrome: a case report. J Med Case Rep; 2010;4:320

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Neuroendocrine carcinoma of the seminal vesicles presenting with Lambert Eaton syndrome: a case report.
  • INTRODUCTION: Primary tumors of seminal vesicles are rare and only a few cases have been reported.
  • Diagnosis is difficult due to the absence of early clinical signs.
  • CASE PRESENTATION: We present the case of a 70-year-old Caucasian man with a seminal vesicle mass and concomitant lymph node metastasis detected by computed tomography and body positron emission tomography/low-dose computed tomography scan carried out for evaluation of Lambert Eaton syndrome.
  • Following chemotherapy the disease was stable and active surveillance was initiated.
  • CONCLUSIONS: Lambert Eaton syndrome may be the initial symptom of a seminal vesicle mass.
  • Diagnosis needs to be obtained by transrectal biopsy and chemotherapy may delay progression of the tumor.

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  • (PMID = 20939874.001).
  • [ISSN] 1752-1947
  • [Journal-full-title] Journal of medical case reports
  • [ISO-abbreviation] J Med Case Rep
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC2964736
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9. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Earlier studies have shown that seminal vesicle mesenchyme (SVM) has the ability to induce Dunning tumor (DT) to undergo morphogenetic changes and cytodifferentiation.
  • The aim of the present study was to investigate the roles of growth factors and their receptors in tumor-mesenchymal interactions.
  • 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.
  • This study suggests that these factors and their receptors may be essential mediators in tumor-mesenchymal interactions.
  • [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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10. Ham WS, Cho NH, Kim WT, Ju HJ, Lee JS, Choi YD: Pathological effects of prostate cancer correlate with neuroendocrine differentiation and PTEN expression after bicalutamide monotherapy. J Urol; 2009 Oct;182(4):1378-84
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  • PURPOSE: Androgen deprivation therapy is the primary treatment for advanced prostate cancer but many patients eventually experience progression to hormone refractory status.
  • Understanding the molecular changes after androgen deprivation therapy would help evaluate the efficacy or failure of second line therapies.
  • Therefore, we analyzed the expression of the tumor suppressor phosphatase and tensin homologue deleted on chromosome 10 (PTEN), the human epidermal receptor-2 and neuroendocrine differentiation after bicalutamide monotherapy, which is emerging as an alternative treatment for locally advanced prostate cancer.
  • RESULTS: Patients with minimal regression effects after bicalutamide therapy had advanced pathological stage disease, and tended to have positive chromogranin A expression and PTEN inactivation.
  • Cox regression analysis revealed that seminal vesicle invasion, PTEN/chromogranin A expression and lymph node invasion were significant variables for time to biochemical recurrence.
  • CONCLUSIONS: PTEN inactivation and neuroendocrine differentiation were related to refractoriness to bicalutamide therapy.
  • [MeSH-major] Androgen Antagonists / therapeutic use. Anilides / therapeutic use. Nitriles / therapeutic use. PTEN Phosphohydrolase / biosynthesis. Prostatic Neoplasms / drug therapy. Prostatic Neoplasms / metabolism. Tosyl Compounds / therapeutic use

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  • (PMID = 19683286.001).
  • [ISSN] 1527-3792
  • [Journal-full-title] The Journal of urology
  • [ISO-abbreviation] J. Urol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Androgen Antagonists; 0 / Anilides; 0 / Nitriles; 0 / Tosyl Compounds; A0Z3NAU9DP / bicalutamide; EC 3.1.3.48 / PTEN protein, human; EC 3.1.3.67 / PTEN Phosphohydrolase
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11. Lee EC, Frolov A, Li R, Ayala G, Greenberg NM: Targeting Aurora kinases for the treatment of prostate cancer. Cancer Res; 2006 May 15;66(10):4996-5002
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  • [Title] Targeting Aurora kinases for the treatment of prostate cancer.
  • Interestingly, expression of Aurora-A in non-neoplastic prostates correlated with seminal vesicle invasion (rho = 0.275, P = 0.0169) and in prostate tumor with positive surgical margins (rho = 0.265, P = 0.0161).
  • In addition, nuclear expression of Aurora-B in prostatic intraepithelial neoplasia lesions correlated with clinical staging of the tumor (rho = -0.4, P = 0.0474) whereas cytoplasmic expression in tumors correlated with seminal vesicle invasion (rho = 0.282, P = 0.0098).
  • VX680 could further reduce cell viability >2-fold when used in combination with the chemotherapy drug doxorubicin.
  • Our findings support a functional relationship between Aurora kinase expression and prostate cancer and the application of small-molecule inhibitors in therapeutic modalities.
  • [MeSH-major] Piperazines / pharmacology. Prostatic Neoplasms / drug therapy. Prostatic Neoplasms / enzymology. Protein Kinase Inhibitors / pharmacology. Protein-Serine-Threonine Kinases / antagonists & inhibitors
  • [MeSH-minor] Animals. Aurora Kinase A. Aurora Kinase B. Aurora Kinases. Cell Line, Tumor. Humans. Male. Mice

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  • (PMID = 16707419.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / U01-CA84296
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Piperazines; 0 / Protein Kinase Inhibitors; 639089-54-6 / VX680; EC 2.7.11.1 / AURKB protein, human; EC 2.7.11.1 / Aurka protein, mouse; EC 2.7.11.1 / Aurkb protein, mouse; EC 2.7.11.1 / Aurora Kinase A; EC 2.7.11.1 / Aurora Kinase B; EC 2.7.11.1 / Aurora Kinases; EC 2.7.11.1 / Protein-Serine-Threonine Kinases
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12. Sella A, Zisman A, Kovel S, Yarom N, Leibovici D, Lindner A: Neoadjuvant chemohormonal therapy in poor-prognosis localized prostate cancer. Urology; 2008 Feb;71(2):323-7
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  • [Title] Neoadjuvant chemohormonal therapy in poor-prognosis localized prostate cancer.
  • OBJECTIVES: To conduct a trial of neoadjuvant chemohormonal therapy and radical prostatectomy for patients with poor-prognosis localized prostate cancer (prostate-specific antigen [PSA] value 20 ng/mL or greater, Gleason score 8 or higher, and clinical stage T2c or greater), who are at high risk for local and systemic relapse.
  • METHODS: Complete androgen blockage and four cycles of docetaxel (70 mg/m2) on day 2 and estramustine (280 mg three times daily) on days 1 to 5 every 21 days were given to 22 patients before radical prostatectomy and nerve preservation.
  • Presurgery characteristics after chemohormonal therapy were as follows: PSA value 0.21 (0.05 to 0.6) ng/mL, clinical stage T1c in 14 patients (63.7%), T2a in 6 (27.3%), and T3a in 2 (9%).
  • The pathologic specimens revealed viable disease in all patients, organ-confined disease in 14 (63.6%), specimen-confined disease in 16 (72.7%), seminal vesicle disease in 9 (40.9%), and lymph node involvement in 4 (18.1%).
  • To date, at a median follow-up of 23.6 (12.1 to 54.7) months, 10 patients (45.4%) relapsed, with PSA doubling time of 1.5 (0.4 to 34.3) months.
  • It leads to clinical tumor downstaging.
  • The pattern of relapse suggests that local therapy, with radiotherapy for patients with surgical or capsular involvement, and additional systemic therapy should be integrated.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Estramustine / therapeutic use. Prostatectomy. Prostatic Neoplasms / drug therapy. Prostatic Neoplasms / surgery. Taxoids / therapeutic use
  • [MeSH-minor] Aged. Antineoplastic Agents, Hormonal / therapeutic use. Humans. Male. Middle Aged. Neoadjuvant Therapy. Preoperative Care. Prognosis. Risk Factors

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  • (PMID = 18308112.001).
  • [ISSN] 1527-9995
  • [Journal-full-title] Urology
  • [ISO-abbreviation] Urology
  • [Language] eng
  • [Publication-type] Journal Article; Randomized Controlled Trial
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Antineoplastic Agents, Hormonal; 0 / Taxoids; 15H5577CQD / docetaxel; 35LT29625A / Estramustine
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13. Shimada K, Matsuyoshi S, Nakamura M, Ishida E, Konishi N: Phosphorylation status of Fas-associated death domain-containing protein (FADD) is associated with prostate cancer progression. J Pathol; 2005 Aug;206(4):423-32
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  • It has recently been demonstrated that phosphorylation of FADD at serine 194 plays an important role in the induction of apoptosis by anti-cancer drugs in human prostate cancer cells.
  • The positivity for phosphorylated FADD was significantly lower for patients with a Gleason score greater than or equal to 7, a positive surgical margin, extracapsular or seminal vesicle invasion.
  • In addition, a relationship was also apparent in cancer cells refractory to neoadjuvant hormonal therapy.
  • Interestingly, in Gleason score 3 + 4 tumours, the positivity for FADD phosphorylation was statistically increased by neoadjuvant hormonal therapy, resulting in a reduced percentage of cases with a positive surgical margin and extracapsular invasion.
  • These results clearly demonstrate that transition from phosphorylated FADD to the non-phosphorylated form might be associated with carcinogenesis and that induction of FADD phosphorylation could therefore be a target for chemohormonal therapy of human prostate cancer.
  • [MeSH-minor] Aged. Androgen Antagonists / therapeutic use. Anilides / therapeutic use. Apoptosis / physiology. Biomarkers, Tumor / analysis. Cell Division. Cell Line, Tumor. Cell Survival / physiology. Cells, Cultured. Disease Progression. Drug Therapy, Combination. Epithelial Cells / metabolism. Gonadotropin-Releasing Hormone / agonists. Humans. Immunohistochemistry / methods. Male. Middle Aged. Neoplasm Proteins / metabolism. Nitriles. Phosphorylation. Prostate-Specific Antigen / analysis. Tosyl Compounds

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  • [Copyright] Copyright 2005 Pathological Society of Great Britain and Ireland
  • (PMID = 15906275.001).
  • [ISSN] 0022-3417
  • [Journal-full-title] The Journal of pathology
  • [ISO-abbreviation] J. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Androgen Antagonists; 0 / Anilides; 0 / Arabidopsis Proteins; 0 / Biomarkers, Tumor; 0 / Neoplasm Proteins; 0 / Nitriles; 0 / Tosyl Compounds; 33515-09-2 / Gonadotropin-Releasing Hormone; A0Z3NAU9DP / bicalutamide; EC 1.14.19.- / Fatty Acid Desaturases; EC 1.14.99.- / Fad7 protein, Arabidopsis; EC 3.4.21.77 / Prostate-Specific Antigen
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14. Magi-Galluzzi C, Zhou M, Reuther AM, Dreicer R, Klein EA: Neoadjuvant docetaxel treatment for locally advanced prostate cancer: a clinicopathologic study. Cancer; 2007 Sep 15;110(6):1248-54
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  • [Title] Neoadjuvant docetaxel treatment for locally advanced prostate cancer: a clinicopathologic study.
  • BACKGROUND: The objective of the current study was to determine the histologic and molecular changes that occurred in patients with high-risk, localized prostate cancer (PCa) after neoadjuvant docetaxel chemotherapy.
  • RESULTS: Twenty-eight patients completed chemotherapy and underwent RP at the Cleveland Clinic; none achieved a pathologic complete response.
  • Pretreatment diagnostic prostate biopsies (PBx) were reviewed in all patients, and unstained sections of formalin-fixed tissue were available from 11 patients.
  • At a median follow-up of 49.5 months (range, 23-72 months), 12 patients (43%) remained clinically and biochemically free of disease with no additional therapy, and 16 patients (57%) had biochemical failure.
  • Four patients (14.3%) had positive lymph nodes, and 11 patients (39.3%) had seminal vesicle involvement.
  • Immunohistochemical (IHC) staining for a panel of markers involved in various cellular functions (alpha-methylacyl-coenzyme A racemase [AMACR], beta-tubulin I, beta-tubulin III, cyclin D1, p27, p21, Ki-67, p53, Bcl-2, and an apoptosis detection kit [ApopTag]) was performed on a tissue microarray that contained the posttreatment (RP) tissue specimens and on the PBx specimens, if available.
  • When the IHC staining patterns were compared between PBx and RP specimens using the Wilcoxon signed-rank test, only p53 expression (P = .017) and Bcl-2 expression (P = .014) were found to be increased significantly after neoadjuvant docetaxel treatment.
  • Ki-67, ApopTag, beta-tubulin I, and beta-tubulin III expression levels also were increased after treatment; however, the differences were not found to be statistically significant.
  • CONCLUSIONS: The current results indicated that, although it will require longer follow-up studies and larger numbers of patients to ascertain the value of neoadjuvant treatment, the negative findings of the current study may explain the lack of clinical response in patients who received neoadjuvant docetaxel for PCa.
  • Although the results were subject to interpretation limits based on the study size, the increased expression of p53 and Bcl-2 that was detected after treatment using the Wilcoxon signed-rank test suggested that the apoptotic pathway may be an important target for this drug, and further investigation is warranted.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Neoadjuvant Therapy / methods. Prostatectomy. Prostatic Neoplasms / drug therapy. Prostatic Neoplasms / pathology. Taxoids / therapeutic use
  • [MeSH-minor] Aged. Biomarkers, Tumor / analysis. Humans. Immunohistochemistry. Male. Microarray Analysis. Middle Aged. Patient Selection. Prostate-Specific Antigen / blood. Treatment Outcome


15. Völkel T, Heidtmann HH, Müller R, Kontermann RE: Engineering of human coagulation factor x variants activated by prostate-specific antigen. Mol Biotechnol; 2005 Jan;29(1):19-30
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  • In this study, we present a novel approach for the induction of tumor vessel thrombosis using genetically modified coagulation factor X.
  • Human factor X was engineered in its activation peptide in a way that it can be specifically activated by prostate-specific antigen (PSA), a tumor-specific proteinase secreted into the bloodstream by prostate cancer cells.
  • These FX variants should be useful for site-specific induction of blood coagulation in the tumor vasculature.
  • [MeSH-major] Factor X / genetics. Prostate-Specific Antigen / genetics. Protein Engineering. Seminal Vesicle Secretory Proteins / genetics
  • [MeSH-minor] Animals. Enzyme Activation / genetics. Humans. Male. Neovascularization, Pathologic / drug therapy. Neovascularization, Pathologic / genetics. Prostatic Neoplasms / blood supply. Prostatic Neoplasms / drug therapy. Recombinant Fusion Proteins / genetics. Recombinant Fusion Proteins / therapeutic use. Thrombosis / chemically induced

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  • (PMID = 15668516.001).
  • [ISSN] 1073-6085
  • [Journal-full-title] Molecular biotechnology
  • [ISO-abbreviation] Mol. Biotechnol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Recombinant Fusion Proteins; 0 / Seminal Vesicle Secretory Proteins; 0 / seminal vesicle-specific antigen; 9001-29-0 / Factor X; EC 3.4.21.77 / Prostate-Specific Antigen
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16. 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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  • The PAIII rat prostatic adenocarcinoma (PCa) is an androgen receptor-negative, ERalpha- and ERbeta-positive, spontaneously metastatic rodent tumor cell line.
  • After s.c. implantation of 10(6) PAIII cells in the tail, s.c. administration of trioxifene (2.0, 4.0, 20.0, or 40.0 mg/kg-day) for 30 days produced significant (P < 0.05) inhibition of PAIII metastasis from the primary tumor in the tail to the gluteal and iliac lymph nodes (maximum nodal weight decreases, 86% and 88% from control values, respectively).
  • PAIII metastasis to the lungs was significantly inhibited by trioxifene treatment.
  • Trioxifene inhibited the proliferation of PAIII cells at micromolar levels in vitro but did not slow growth of the primary tumor growth in the tail.
  • 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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17. Hachiya T, Minei S, Hirano D, Ishida H, Okada K, Takimoto Y: [Adjuvant hormone therapy in patients with positive surgical margins after radical prostatectomy]. Nihon Hinyokika Gakkai Zasshi; 2002 Mar;93(3):469-75
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Adjuvant hormone therapy in patients with positive surgical margins after radical prostatectomy].
  • BACKGROUND: We carried out a retrospective study comparing radical prostatectomy plus adjuvant hormone therapy with radical prostatectomy plus surveillance in patients with positive surgical margins to evaluate whether adjuvant hormone therapy is beneficial for disease free survival.
  • Twenty-six patients received adjuvant hormone therapy.
  • Thirty-nine patients underwent surveillance with salvage hormone therapy at PSA failure.
  • Treatment outcomes were measured in terms of progression free survival.
  • RESULTS: Five year clinical progression free survival rates for the patients with positive surgical margins in the adjuvant therapy group and surveillance group were 85.9% and 80.0% respectively (p = 0.85).
  • Clinical progression free survival between the groups was not statistically different in terms of seminal vesicle involvement and tumor grade.
  • The difference of clinical progression free survival between the two groups approached statistical significance in poorly differentiated tumor (p = 0.08).
  • CONCLUSIONS: We conclude that adjuvant hormone therapy is not beneficial in terms of progression free survival in patients with positive surgical margins.
  • Nevertheless, adjuvant hormone therapy could be beneficial in patients with poorly differentiated prostate cancer.
  • [MeSH-major] Gonadotropin-Releasing Hormone / agonists. Postoperative Care. Prostatectomy. Prostatic Neoplasms / drug therapy. Prostatic Neoplasms / surgery
  • [MeSH-minor] Aged. Chemotherapy, Adjuvant. Humans. Male. Middle Aged. Retrospective Studies. Survival Rate

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  • (PMID = 11968803.001).
  • [ISSN] 0021-5287
  • [Journal-full-title] Nihon Hinyōkika Gakkai zasshi. The japanese journal of urology
  • [ISO-abbreviation] Nippon Hinyokika Gakkai Zasshi
  • [Language] jpn
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 33515-09-2 / Gonadotropin-Releasing Hormone
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18. Singh RP, Raina K, Deep G, Chan D, Agarwal R: Silibinin suppresses growth of human prostate carcinoma PC-3 orthotopic xenograft via activation of extracellular signal-regulated kinase 1/2 and inhibition of signal transducers and activators of transcription signaling. Clin Cancer Res; 2009 Jan 15;15(2):613-21
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  • RESULTS: Silibinin treatment reduced the lower urogenital weight (including tumor, prostate, and seminal vesicle) by 40% (P < 0.05) without any toxicity in mice.
  • Silibinin decreased proliferating cell nuclear antigen expression and proliferating cells (P < 0.001) but increased cleaved caspase-3-positive cells (P < 0.01) and apoptotic cells (P < 0.001) and suppressed tumor microvessel density (P < 0.001) and vascular endothelial growth factor expression (P = 0.02).
  • CONCLUSIONS: These findings provide evidence for antitumor efficacy of silibinin against orthotopically growing prostate tumor in mice with multitargeted mechanistic insights and support its clinical investigation in prostate cancer.

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  • (PMID = 19147767.001).
  • [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 / 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 / Antigens, CD31; 0 / Antioxidants; 0 / Silymarin; 0 / Vascular Endothelial Growth Factor A; 4RKY41TBTF / silybin; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 1; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 3; EC 3.4.22.- / Caspase 3
  • [Other-IDs] NLM/ NIHMS81817; NLM/ PMC2629529
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19. 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.
  • Chemopreventive efficacy was evaluated by magnetic resonance imaging, determining the prostate-seminal vesicle complex volume and histologic analysis of prostate tumor or tissue.
  • Tumor invasion assays were used to show the role of tumor necrosis factor-alpha-stimulated gene (TSG-6), a 2-methoxyestradiol-up-regulated gene identified by DNA array analysis.
  • Expression of TSG-6 was analyzed in a human tissue array containing different grades of prostate tumors.
  • Immunohistochemistry of the human prostate tumor array showed a decrease in TSG-6-positive cells with increasing grade relative to normal prostate (P = 0.0001).
  • We have also identified TSG-6 as a potential marker that could be used for early diagnosis and prognosis of cancerous or precancerous lesions.
  • [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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20. Pilepich MV, Winter K, Lawton CA, Krisch RE, Wolkov HB, Movsas B, Hug EB, Asbell SO, Grignon D: Androgen suppression adjuvant to definitive radiotherapy in prostate carcinoma--long-term results of phase III RTOG 85-31. Int J Radiat Oncol Biol Phys; 2005 Apr 1;61(5):1285-90
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  • [Title] Androgen suppression adjuvant to definitive radiotherapy in prostate carcinoma--long-term results of phase III RTOG 85-31.
  • PURPOSE: Radiation Therapy Oncology Group protocol 85-31 was designed to evaluate the effectiveness of adjuvant androgen suppression, using goserelin, in unfavorable prognosis carcinoma of the prostate treated with definitive radiotherapy (RT).
  • METHODS AND MATERIALS: Eligible patients were those with palpable primary tumor extending beyond the prostate (clinical Stage T3) or those with regional lymphatic involvement.
  • Patients who had undergone prostatectomy were eligible if penetration through the prostatic capsule to the margin of resection and/or seminal vesicle involvement was documented histologically.
  • In Arm I, the drug was to be started during the last week of RT and was to be continued indefinitely or until signs of progression.
  • CONCLUSION: In a population of patients with unfavorable prognosis carcinoma of the prostate, androgen suppression applied as an adjuvant after definitive RT was associated not only with a reduction in disease progression but in a statistically significant improvement in absolute survival.
  • [MeSH-major] Antineoplastic Agents, Hormonal / therapeutic use. Goserelin / therapeutic use. Prostatic Neoplasms / drug therapy. Prostatic Neoplasms / radiotherapy
  • [MeSH-minor] Aged. Androgen Antagonists. Chemotherapy, Adjuvant. Combined Modality Therapy. Humans. Male. Multivariate Analysis. Prostatectomy. Survival Rate

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  • [CommentIn] Nat Clin Pract Urol. 2005 Nov;2(11):536-7 [16474596.001]
  • (PMID = 15817329.001).
  • [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 / CA-21661; United States / NCI NIH HHS / CA / CA-32115
  • [Publication-type] Clinical Trial; Clinical Trial, Phase III; Journal Article; Randomized Controlled Trial; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Androgen Antagonists; 0 / Antineoplastic Agents, Hormonal; 0F65R8P09N / Goserelin
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21. Ahmed SU, Meklat F, Shahriar M, Zhang J, Mastulov S, Giannakouros T, Jewell A, Zhang Y, Lim SH: SEMG-1 expression in early stage chronic lymphocytic leukemia. Cytotherapy; 2009;11(2):238-44
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  • These patients are, therefore, a suitable group for testing immunotherapeutic approaches to avoid problems of immunosuppression as a result of disease progression and chemotherapy.
  • In this study, we investigated the expression of SEMG-1 in early CLL to determine the suitability of SEMG-1 as a target for further development of tumor vaccines for early CLL.
  • [MeSH-major] Antigens, Neoplasm / metabolism. Biomarkers, Tumor / metabolism. Leukemia, Lymphocytic, Chronic, B-Cell / immunology. Seminal Vesicle Secretory Proteins / metabolism
  • [MeSH-minor] Antibody Formation. Cancer Vaccines. Enzyme-Linked Immunosorbent Assay. Gene Expression Regulation, Neoplastic. Humans. Immunoglobulin G / blood. Immunoglobulin M / blood. Immunohistochemistry. Neoplasm Staging. Reverse Transcriptase Polymerase Chain Reaction. ZAP-70 Protein-Tyrosine Kinase / genetics. ZAP-70 Protein-Tyrosine Kinase / immunology. ZAP-70 Protein-Tyrosine Kinase / metabolism

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  • (PMID = 19241194.001).
  • [ISSN] 1477-2566
  • [Journal-full-title] Cytotherapy
  • [ISO-abbreviation] Cytotherapy
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA 088434; United States / NCI NIH HHS / CA / R01 CA 106283
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Biomarkers, Tumor; 0 / Cancer Vaccines; 0 / Immunoglobulin G; 0 / Immunoglobulin M; 0 / Seminal Vesicle Secretory Proteins; 0 / seminal vesicle-specific antigen; EC 2.7.10.2 / ZAP-70 Protein-Tyrosine Kinase
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22. 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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23. 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.
  • EXPERIMENTAL DESIGN: Twenty-week-old TRAMP male mice having palpable prostate tumor were fed with control or 0.5% and 1%, w/w, silybin-phytosome diets for 11 weeks and then sacrificed.
  • 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.
  • Silibinin moderately inhibited tumor cell proliferation and induced apoptosis, but strongly suppressed tumor microvessel density (up to 60%, P < 0.001), vascular endothelial growth factor, and vascular endothelial growth factor receptor-2 expression.
  • 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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24. 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.
  • There was a statistically significant association between aberrant E-cadherin expression and larger tumor size (P =.01).
  • No significant associations were seen with extraprostatic extension and seminal vesicle invasion.
  • A statically significant association between aberrant E-cadherin expression and larger tumor size was identified.
  • [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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