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6. Krause W: Male breast cancer--an andrological disease: risk factors and diagnosis. Andrologia; 2004 Dec;36(6):346-54
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  • [Title] Male breast cancer--an andrological disease: risk factors and diagnosis.
  • Gynaecomastia, the enlargement of the male breast, is considered as an andrological disease.
  • To date, a review on male breast cancer (MBC) has not been published in an andrological journal.
  • The papers underlying this review were published from authors of different institutions: Clinical Genetics, Dermatology, Gynaecology, Internal Medicine, Oncology, Pathology, Psychiatry, Radiology and Surgery.
  • MBC accounts for approximately 1% of breast cancer patients.
  • A total of 182 men died of breast cancer in 1999, in Germany.
  • MBC accounts for <5% of surgically removed breast lumps.
  • BRCA1 and BRCA2 gene mutations are responsible for approximately 80% of the families with hereditary breast cancer.
  • The diagnosis of MBC is not possible without histological examination.
  • Different diagnostic procedures such as clinical diagnosis, sonography, mammography, fine-needle biopsy and core needle facilitate the decision whether a biopsy is necessary.
  • [MeSH-major] Breast Neoplasms, Male / diagnosis. Breast Neoplasms, Male / etiology
  • [MeSH-minor] Genetic Predisposition to Disease. Germany / epidemiology. Humans. Male. Risk Factors


7. Chen C, Méndez E, Houck J, Fan W, Lohavanichbutr P, Doody D, Yueh B, Futran ND, Upton M, Farwell DG, Schwartz SM, Zhao LP: Gene expression profiling identifies genes predictive of oral squamous cell carcinoma. Cancer Epidemiol Biomarkers Prev; 2008 Aug;17(8):2152-62
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  • [Title] Gene expression profiling identifies genes predictive of oral squamous cell carcinoma.
  • Oral squamous cell carcinoma (OSCC) is associated with substantial mortality and morbidity.
  • To identify potential biomarkers for the early detection of invasive OSCC, we compared the gene expressions of incident primary OSCC, oral dysplasia, and clinically normal oral tissue from surgical patients without head and neck cancer or preneoplastic oral lesions (controls), using Affymetrix U133 2.0 Plus arrays.
  • The best model included LAMC2, encoding laminin-gamma2 chain, and COL4A1, encoding collagen, type IV alpha1 chain.
  • Subsequent modeling without these two markers showed that COL1A1, encoding collagen, type I alpha1 chain, and PADI1, encoding peptidyl arginine deiminase, type 1, could also distinguish OSCC from controls.
  • We validated these two models using an internal independent testing set of 48 invasive OSCC and 10 controls and an external testing set of 42 head and neck squamous cell carcinoma cases and 14 controls (GEO GSE6791), with sensitivity and specificity above 95%.
  • If confirmed in larger studies, the proposed models may hold promise for monitoring local recurrence at surgical margins and the development of second primary oral cancer in patients with OSCC.

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  • (PMID = 18669583.001).
  • [ISSN] 1055-9965
  • [Journal-full-title] Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology
  • [ISO-abbreviation] Cancer Epidemiol. Biomarkers Prev.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA095419-05; United States / NIDCD NIH HHS / DC / DC000018-26; United States / NCRR NIH HHS / RR / K12 RR023265-04; United States / NIDCD NIH HHS / DC / T32 DC000018; United States / NCRR NIH HHS / RR / K12RR023265; United States / NCRR NIH HHS / RR / RR023265-04; United States / NIDCD NIH HHS / DC / T32DC00018; United States / NCI NIH HHS / CA / R01CA095419; United States / NCI NIH HHS / CA / CA095419-05; United States / NIDCD NIH HHS / DC / T32 DC000018-26; United States / NCRR NIH HHS / RR / K12 RR023265; United States / NCI NIH HHS / CA / R01 CA095419
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Validation Studies
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Collagen Type I; 0 / Collagen Type IV; 0 / LAMC2 protein, human; 0 / Laminin; 0 / collagen type I, alpha 1 chain; EC 3.- / Hydrolases; EC 3.5.3.- / peptidylarginine deiminase type I
  • [Other-IDs] NLM/ NIHMS69787; NLM/ PMC2575803
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8. Okuno S, Harada M, Yano T, Yano S, Kiuchi S, Tsuda N, Sakamura Y, Imai J, Kawaguchi T, Tsujihara K: Complete regression of xenografted human carcinomas by camptothecin analogue-carboxymethyl dextran conjugate (T-0128). Cancer Res; 2000 Jun 1;60(11):2988-95
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  • Clinically available camptothecins (CPTs), such as irinotecan (CPT-11) and topotecan, represent one of the most promising classes of antitumor agents, despite their toxicity.
  • To improve their pharmacological profiles, a new macromolecular prodrug, denoted T-0128, was synthesized.
  • This study was designed to test the concept that the rational design of a CPT-polymer conjugate would increase the efficacy of the parent drug.
  • The in vivo antitumor study against Walker-256 carcinoma demonstrated that T-0128 was 10 times as active as T-2513, supporting this concept.
  • Even a single i.v. injection of T-0128 at 6 mg/kg (based on the amount of T-2513 bound to CM dextran) induced complete regression of MX-1 mammary carcinoma.
  • T-0128 at 10 mg/kg weekly for 3 weeks (one-tenth of its MTD) cured LX-1 lung carcinoma.
  • Pharmacokinetic studies were performed to correlate the efficacy results obtained for T-0128 with plasma and tissue drug concentrations using Walker-256 tumor-bearing rats.
  • [MeSH-major] Breast Neoplasms / drug therapy. Camptothecin / analogs & derivatives. Dextrans / pharmacology. Lung Neoplasms / drug therapy. Prodrugs / pharmacology. Topotecan / analogs & derivatives
  • [MeSH-minor] Animals. Cell Cycle / drug effects. Chromatography, Gel. Chromatography, High Pressure Liquid. DNA Topoisomerases, Type I / metabolism. Dose-Response Relationship, Drug. Female. HeLa Cells. Humans. Male. Mice. Mice, Nude. Neoplasm Transplantation. Rats. Rats, Wistar. Time Factors. Tissue Distribution. Tumor Cells, Cultured

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  • (PMID = 10850447.001).
  • [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 / Prodrugs; 0 / T 0128; 0 / T 2153; 7M7YKX2N15 / Topotecan; EC 5.99.1.2 / DNA Topoisomerases, Type I; K3R6ZDH4DU / Dextrans; XT3Z54Z28A / Camptothecin
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9. Zha S, Gage WR, Sauvageot J, Saria EA, Putzi MJ, Ewing CM, Faith DA, Nelson WG, De Marzo AM, Isaacs WB: Cyclooxygenase-2 is up-regulated in proliferative inflammatory atrophy of the prostate, but not in prostate carcinoma. Cancer Res; 2001 Dec 15;61(24):8617-23
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  • [Title] Cyclooxygenase-2 is up-regulated in proliferative inflammatory atrophy of the prostate, but not in prostate carcinoma.
  • Cyclooxygenase-2 (COX-2) is the inducible isoform of the rate-limiting enzymes that convert arachidonic acid to proinflammatory prostaglandins as well as a primary target for nonsteroidal anti-inflammatory drugs.
  • Accumulating evidence suggests that up-regulation of COX-2 is associated with carcinogenesis in multiple organ systems including the large bowel, lung, breast, and prostate.
  • In this report, we examine the expression of COX-2 protein and mRNA in prostate tissue containing various lesions and in prostate cancer cell lines.
  • Immunohistochemical analysis of 144 human prostate cancer cases suggested that, in contrast to several previous reports, there was no consistent overexpression of COX-2 in established prostate cancer or high-grade prostatic intraepithelial neoplasia, as compared with adjacent normal prostate tissue.
  • These results suggest that if nonsteroidal anti-inflammatory drugs are indeed chemopreventive and/or chemotherapeutic for prostate cancer, their effects are likely to be mediated by modulating COX-2 activity in non-PCa cells (either inflammatory cells or atrophic epithelial cells) or by affecting a COX-2-independent pathway.
  • [MeSH-minor] Atrophy / enzymology. Blotting, Western. Cyclooxygenase 2. Disease Progression. Epithelium / enzymology. Epithelium / pathology. Humans. Immunohistochemistry. Male. Membrane Proteins. RNA, Messenger / biosynthesis. RNA, Messenger / genetics. Reverse Transcriptase Polymerase Chain Reaction. Stromal Cells / enzymology. Stromal Cells / pathology. Tumor Cells, Cultured. Up-Regulation

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  • (PMID = 11751373.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA58236; United States / NCI NIH HHS / CA / CA78588
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Isoenzymes; 0 / Membrane Proteins; 0 / RNA, Messenger; EC 1.14.99.1 / Cyclooxygenase 2; EC 1.14.99.1 / PTGS2 protein, human; EC 1.14.99.1 / Prostaglandin-Endoperoxide Synthases
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10. Migliorati CA, Schubert MM, Peterson DE, Seneda LM: Bisphosphonate-associated osteonecrosis of mandibular and maxillary bone: an emerging oral complication of supportive cancer therapy. Cancer; 2005 Jul 1;104(1):83-93
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  • [Title] Bisphosphonate-associated osteonecrosis of mandibular and maxillary bone: an emerging oral complication of supportive cancer therapy.
  • BACKGROUND: The current report presented 17 patients with cancer with bone metastases and 1 patient with osteopenia who received treatment with bisphosphonates and who subsequently developed osteonecrosis of the mandible and/or maxilla.
  • METHODS: The authors reviewed information on 18 patients who were referred to oral medicine or oral surgery specialists for evaluation and treatment of mandibular and/or maxillary bone necrosis from June 2002 to September 2004.
  • All patients with cancer had received chemotherapy while receiving bisphosphonate management.
  • RESULTS: The 17 patients with cancer were receiving active medical care for a malignancy.
  • Cancer treatment included a variety of chemotherapeutic agents.
  • Malignancies included breast carcinoma (n = 10), multiple myeloma (n = 3), prostate carcinoma (n = 1), ovarian carcinoma (n = 1), prostate carcinoma/lymphoma (n = 1), and breast/ovarian carcinoma (n = 1).
  • However, 1 patient with cancer healed after discontinuation of bisphosphonate therapy for 4 months.
  • This condition represents a new oral complication in patients with cancer and can be termed bisphosphonate-associated osteonecrosis.
  • [MeSH-major] Bone Neoplasms / drug therapy. Bone Neoplasms / secondary. Diphosphonates / adverse effects. Mandibular Diseases / chemically induced. Maxillary Diseases / chemically induced. Osteonecrosis / chemically induced
  • [MeSH-minor] Adult. Aged. Bone Diseases, Metabolic / drug therapy. Female. Humans. Male. Middle Aged


11. Li QQ, Wang G, Huang F, Banda M, Reed E: Antineoplastic effect of beta-elemene on prostate cancer cells and other types of solid tumour cells. J Pharm Pharmacol; 2010 Aug;62(8):1018-27
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  • [Title] Antineoplastic effect of beta-elemene on prostate cancer cells and other types of solid tumour cells.
  • OBJECTIVES: beta-Elemene, a natural compound extracted from over 50 different Chinese medicinal herbs and plants, has been effective in the treatment of hyperplastic and proliferative disorders such as prostatic hypertrophy, hysteromyoma and neoplasms.
  • Our previous studies have demonstrated that beta-elemene exhibits strong inhibitory activity in ovarian cancer cells.
  • The aim of the present study was to assess the effect of beta-elemene on prostate cancer cells as well as other types of tumour cells and to determine whether the effect of beta-elemene on prostate cancer cell death was mediated through the induction of apoptosis.
  • METHODS: The MTT assay was used to evaluate the ability of beta-elemene to inhibit cellular proliferation in cancer cells.
  • KEY FINDINGS: Here, we showed that beta-elemene had an antiproliferative effect on androgen-insensitive prostate carcinoma DU145 and PC-3 cells.
  • Treatment with beta-elemene also inhibited the growth of brain, breast, cervical, colon and lung carcinoma cells.
  • The effect of beta-elemene on cancer cells was dose dependent, with IC50 values ranging from 47 to 95 microg/ml (230-465 microm).
  • TUNEL assay and flow cytometric analysis using annxin V/propidium iodide staining revealed that the percentage of apoptotic prostate cancer cells was increased by beta-elemene in a dose- and time-dependent manner.
  • Moreover, beta-elemene exposure resulted in a decreased Bcl-2 protein level, increased cytochrome c release, and activated PARP and caspase-3, -7, -9, and -10 in prostate cancer cells.
  • CONCLUSIONS: Overall, these findings suggest that beta-elemene exerts broad-spectrum antitumour activity against many types of solid carcinoma and supports a proposal of beta-elemene as a new potentially therapeutic drug for castration-resistant prostate cancer and other solid tumours.
  • [MeSH-major] Antineoplastic Agents, Phytogenic / pharmacology. Apoptosis / drug effects. Prostatic Neoplasms / pathology. Sesquiterpenes / pharmacology
  • [MeSH-minor] Annexin A5 / metabolism. Blotting, Western. Brain Neoplasms / pathology. Breast Neoplasms / pathology. Caspases / metabolism. Cell Line, Tumor. Cell Proliferation / drug effects. Cell Survival / drug effects. Colonic Neoplasms / pathology. Cytochromes c / metabolism. Dose-Response Relationship, Drug. Enzyme-Linked Immunosorbent Assay. Female. Humans. In Situ Nick-End Labeling. Inhibitory Concentration 50. Lung Neoplasms / pathology. Male. Poly(ADP-ribose) Polymerases / metabolism. Proto-Oncogene Proteins c-bcl-2 / metabolism. Time Factors. Uterine Cervical Neoplasms / pathology

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  • (PMID = 20663036.001).
  • [ISSN] 2042-7158
  • [Journal-full-title] The Journal of pharmacy and pharmacology
  • [ISO-abbreviation] J. Pharm. Pharmacol.
  • [Language] eng
  • [Grant] United States / NCRR NIH HHS / RR / P20RR016440-010003; United States / NCRR NIH HHS / RR / P20RR016440-020003; United States / NCRR NIH HHS / RR / P20RR016440-040003
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Annexin A5; 0 / Antineoplastic Agents, Phytogenic; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Sesquiterpenes; 0 / beta-elemene; 9007-43-6 / Cytochromes c; EC 2.4.2.30 / Poly(ADP-ribose) Polymerases; EC 3.4.22.- / Caspases
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12. Chen L, Hu GF: Angiogenin-mediated ribosomal RNA transcription as a molecular target for treatment of head and neck squamous cell carcinoma. Oral Oncol; 2010 Sep;46(9):648-53
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  • [Title] Angiogenin-mediated ribosomal RNA transcription as a molecular target for treatment of head and neck squamous cell carcinoma.
  • Squamous cell carcinoma of the head and neck (HNSCC) is the eighth most common disease, affecting approximately 640,000 patients worldwide each year.
  • New agents that target molecular and cellular pathways of the disease pathogenesis of HNSCC are promising candidates.
  • One class of these new agents is angiogenesis inhibitors that have been proven effective in the treatment of advanced colorectal, breast, and non-small cell lung cancers.
  • ANG-stimulated rRNA transcription has been shown to be a general requirement for angiogenesis induced by other angiogenic factors.

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  • [Copyright] Copyright 2010 Elsevier Ltd. All rights reserved.
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  • (PMID = 20656548.001).
  • [ISSN] 1879-0593
  • [Journal-full-title] Oral oncology
  • [ISO-abbreviation] Oral Oncol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA105241-05; United States / NCI NIH HHS / CA / R01 CA105241; United States / NCI NIH HHS / CA / R01 CA105241-05
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Neoplasm Proteins; 0 / RNA, Ribosomal; EC 3.1.27.- / angiogenin; EC 3.1.27.5 / Ribonuclease, Pancreatic
  • [Other-IDs] NLM/ NIHMS219339; NLM/ PMC2932836
  • [Keywords] NOTNLM ; Angiogenin / HNSCC / angiogenesis / rRNA transcription
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13. [Very promising phytotherapeutic agent in cancer?]. Praxis (Bern 1994); 2005 Jan 12;94(1-2):48-9
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  • [Title] [Very promising phytotherapeutic agent in cancer?].
  • [Transliterated title] Vielversprechendes Phytotherapeutikum bei Krebs?
  • [MeSH-major] Antineoplastic Agents, Phytogenic / therapeutic use. Drugs, Chinese Herbal / therapeutic use. Isodon. Neoplasms / drug therapy. Phytotherapy
  • [MeSH-minor] Animals. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Breast Neoplasms / drug therapy. Carcinoma / drug therapy. Cell Survival / drug effects. Drug Synergism. Female. Humans. Male. Mice. Neoplasm Transplantation. Prostatic Neoplasms / drug therapy. Transplantation, Heterologous. Tumor Cells, Cultured / drug effects

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  • (PMID = 15697150.001).
  • [ISSN] 1661-8157
  • [Journal-full-title] Praxis
  • [ISO-abbreviation] Praxis (Bern 1994)
  • [Language] ger
  • [Publication-type] Journal Article
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 0 / Drugs, Chinese Herbal; 0 / herbal preparation PC-SPES
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1
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4. Voutsas IF, Baxevanis CN, Gritzapis AD, Missitzis I, Stathopoulos GP, Archodakis G, Banis C, Voelter W, Papamichail M: Synergy between interleukin-2 and prothymosin alpha for the increased generation of cytotoxic T lymphocytes against autologous human carcinomas. Cancer Immunol Immunother; 2000 Oct;49(8):449-58
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  • Peripheral blood mononuclear cells (PBMC) from cancer patients were cultured in vitro with irradiated autologous tumor cells isolated from malignant effusions (mixed lymphocyte tumor cultures, MLTC) and low-dose (50 IU/ml) recombinant interleukin-2 (IL-2).
  • [MeSH-major] Carcinoma / therapy. Interleukin-2 / therapeutic use. Protein Precursors / therapeutic use. T-Lymphocytes, Cytotoxic / immunology. Thymosin / analogs & derivatives. Thymosin / therapeutic use
  • [MeSH-minor] Aged. Animals. Antigens, CD3 / metabolism. Breast Neoplasms / therapy. CD4-Positive T-Lymphocytes / immunology. CD8-Positive T-Lymphocytes / immunology. Cattle. Cell Communication. Cell Division / drug effects. Cell Division / immunology. Cell Separation. Cells, Cultured. Female. Humans. Lung Neoplasms / therapy. Male. Middle Aged. Monocytes / immunology. Monocytes / metabolism. Ovarian Neoplasms / therapy. Phenotype. Thymus Gland / chemistry. Time Factors. Tumor Cells, Cultured

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  • (PMID = 11043852.001).
  • [ISSN] 0340-7004
  • [Journal-full-title] Cancer immunology, immunotherapy : CII
  • [ISO-abbreviation] Cancer Immunol. Immunother.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] GERMANY
  • [Chemical-registry-number] 0 / Antigens, CD3; 0 / Interleukin-2; 0 / Protein Precursors; 0 / prothymosin alpha; 61512-21-8 / Thymosin
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15. Farhana L, Dawson MI, Huang Y, Zhang Y, Rishi AK, Reddy KB, Freeman RS, Fontana JA: Apoptosis signaling by the novel compound 3-Cl-AHPC involves increased EGFR proteolysis and accompanying decreased phosphatidylinositol 3-kinase and AKT kinase activities. Oncogene; 2004 Mar 11;23(10):1874-84
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  • The threonine and serine protein kinase AKT plays a major role in inhibiting apoptosis in a number of malignant cell types including prostate and breast carcinoma.
  • We now report that the novel compound 4-[3-(1-adamantyl)-4-hydroxyphenyl]-3-chlorocinnamic acid (3-Cl-AHPC), induces apoptosis in breast and prostate carcinoma cells and inhibits AKT activity in these cells.
  • [MeSH-major] Adamantane / toxicity. Apoptosis / drug effects. Cinnamates / toxicity. Phosphatidylinositol 3-Kinases / metabolism. Protein-Serine-Threonine Kinases. Proto-Oncogene Proteins / metabolism. Receptor, Epidermal Growth Factor / metabolism
  • [MeSH-minor] Breast Neoplasms. Cell Line, Tumor. Female. Humans. Male. Phosphorylation. Prostatic Neoplasms. Proto-Oncogene Proteins c-akt. Recombinant Proteins / drug effects. Recombinant Proteins / metabolism. Transfection

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  • (PMID = 14981538.001).
  • [ISSN] 0950-9232
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P0 CA51993
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / 4-(3-(1-adamantyl)-4-hydroxyphenyl)-3-chlorocinnamic acid; 0 / Cinnamates; 0 / Proto-Oncogene Proteins; 0 / Recombinant Proteins; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.11.1 / AKT1 protein, human; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; PJY633525U / Adamantane
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21. Kariakin OB, Sviridova TV, Tsodikova LB, Grishin GN, Sergeeva TN, Perekhrest MA, Donichkina EA: [Changes in prostate-specific antigen in casodex (bicalutamide) monotherapy in a dose 150 mg/day given to patients with locally advanced and/or advanced prostatic cancer]. Urologiia; 2001 Jul-Aug;(4):26-9
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  • [Title] [Changes in prostate-specific antigen in casodex (bicalutamide) monotherapy in a dose 150 mg/day given to patients with locally advanced and/or advanced prostatic cancer].
  • Three-month treatment with casodex (150 mg/day) of untreated patients with locally advanced and/or advanced cancer of the prostate is well tolerated.
  • The only side effect encountered in 9(60%) patients was temporary breast painfulness and swelling.
  • [MeSH-major] Adenocarcinoma / drug therapy. Androgen Antagonists / therapeutic use. Anilides / therapeutic use. Antineoplastic Agents / therapeutic use. Prostate-Specific Antigen / blood. Prostatic Neoplasms / drug therapy
  • [MeSH-minor] Aged. Carcinoma, Acinar Cell / blood. Carcinoma, Acinar Cell / drug therapy. Fluorescent Antibody Technique. Humans. Male. Middle Aged. Neoplasm Metastasis. Nitriles. Time Factors. Tosyl Compounds

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  • (PMID = 11569230.001).
  • [ISSN] 1728-2985
  • [Journal-full-title] Urologii︠a︡ (Moscow, Russia : 1999)
  • [ISO-abbreviation] Urologiia
  • [Language] rus
  • [Publication-type] Comparative Study; English Abstract; Journal Article
  • [Publication-country] Russia
  • [Chemical-registry-number] 0 / Androgen Antagonists; 0 / Anilides; 0 / Antineoplastic Agents; 0 / Nitriles; 0 / Tosyl Compounds; A0Z3NAU9DP / bicalutamide; EC 3.4.21.77 / Prostate-Specific Antigen
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22. Yamazaki K, Yoshino T, Boku N: [Bevacizumab (Avastin)]. Gan To Kagaku Ryoho; 2007 Aug;34(8):1183-91
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  • Angiogenesis is one of the hallmarks of cancer.
  • Among the identified angiogenic factors, vascular endothelial growth factor (VEGF) is a crucial regulator of angiogenesis in normal and malignant tissue.
  • The United States Food and Drug Administration approved the use of bevacizumab for patients with unresectable colorectal cancer and unresectable non-squamous, non small cell lung cancer.
  • In April 2007, the Japanese Ministry of Health, Labour and Welfare approved bevacizumab for patients with unresectable colorectal cancer.
  • [MeSH-major] Angiogenesis Inhibitors / administration & dosage. Antibodies, Monoclonal / administration & dosage. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Colonic Neoplasms / drug therapy. Rectal Neoplasms / drug therapy
  • [MeSH-minor] Antibodies, Monoclonal, Humanized. Bevacizumab. Breast Neoplasms / drug therapy. Camptothecin / administration & dosage. Camptothecin / analogs & derivatives. Carcinoma, Non-Small-Cell Lung / drug therapy. Chemotherapy, Adjuvant. Clinical Trials, Phase III as Topic. Drug Administration Schedule. Drug Approval. Female. Fluorouracil / administration & dosage. Humans. Leucovorin / administration & dosage. Lung Neoplasms / drug therapy. Male. Organoplatinum Compounds / administration & dosage. Vascular Endothelial Growth Factor A / biosynthesis

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  • (PMID = 17687199.001).
  • [ISSN] 0385-0684
  • [Journal-full-title] Gan to kagaku ryoho. Cancer & chemotherapy
  • [ISO-abbreviation] Gan To Kagaku Ryoho
  • [Language] jpn
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Organoplatinum Compounds; 0 / Vascular Endothelial Growth Factor A; 04ZR38536J / oxaliplatin; 2S9ZZM9Q9V / Bevacizumab; 7673326042 / irinotecan; Q573I9DVLP / Leucovorin; U3P01618RT / Fluorouracil; XT3Z54Z28A / Camptothecin; Folfox protocol
  • [Number-of-references] 33
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23. Safdie FM, Dorff T, Quinn D, Fontana L, Wei M, Lee C, Cohen P, Longo VD: Fasting and cancer treatment in humans: A case series report. Aging (Albany NY); 2009 Dec;1(12):988-1007
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  • [Title] Fasting and cancer treatment in humans: A case series report.
  • Short-term fasting (48 hours) was shown to be effective in protecting normal cells and mice but not cancer cells against high dose chemotherapy, termed Differential Stress Resistance (DSR), but the feasibility and effect of fasting in cancer patients undergoing chemotherapy is unknown.
  • None of these patients, who received an average of 4 cycles of various chemotherapy drugs in combination with fasting, reported significant side effects caused by the fasting itself other than hunger and lightheadedness.
  • Chemotherapy associated toxicity was graded according to the Common Terminology Criteria for Adverse Events (CTCAE) of the National Cancer Institute (NCI).
  • In those patients whose cancer progression could be assessed, fasting did not prevent the chemotherapy-induced reduction of tumor volume or tumor markers.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Fasting. Neoplasms / drug therapy
  • [MeSH-minor] Adenocarcinoma / drug therapy. Adult. Aged. Breast Neoplasms / drug therapy. Carcinoma, Non-Small-Cell Lung / drug therapy. Carcinoma, Papillary / diet therapy. Cystadenocarcinoma, Serous / drug therapy. Esophageal Neoplasms / drug therapy. Female. Humans. Male. Middle Aged. Prostatic Neoplasms / drug therapy. Uterine Neoplasms / drug therapy

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  • (PMID = 20157582.001).
  • [ISSN] 1945-4589
  • [Journal-full-title] Aging
  • [ISO-abbreviation] Aging (Albany NY)
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  • [Other-IDs] NLM/ PMC2815756
  • [Keywords] NOTNLM ; Cancer / Chemotherapy / IGF-I / Side-effect / Toxicity / fasting
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24. Yang RS, Tang CH, Chuang WJ, Huang TH, Peng HC, Huang TF, Fu WM: Inhibition of tumor formation by snake venom disintegrin. Toxicon; 2005 Apr;45(5):661-9
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  • Breast and prostate cancer cells have predilection for spreading to bone.
  • Here, we found that rhodostomin inhibited the adhesion of breast and prostate carcinoma cells to both unmineralized and mineralized bone extracellular matrices in a dose-dependent manner, without affecting the viability of tumor cells.
  • In addition, rhodostomin also inhibited the migration and invasion of breast and prostate carcinoma cells.
  • As breast cancer cells MDA-MB-231 were locally injected into tibia in nude mice, histological examination of the tibia of control group revealed that most of the cancellous bone had been replaced by the breast cancer cells after 28 days' inoculation.
  • In contrast, co-administration of trigramin with cancer cells markedly inhibited tumor growth and bone destruction.
  • Taken together, disintegrins strongly inhibit the adhesion, migration, invasion of tumor cells and also tumor growth of human breast cancer cells in bone as well.
  • Therefore, disintegrins may be developed as alternate therapy for bone metastasis of cancer cells.
  • [MeSH-major] Bone Neoplasms / secondary. Breast Neoplasms / physiopathology. Cell Adhesion / drug effects. Disintegrins / pharmacology. Prostatic Neoplasms / physiopathology
  • [MeSH-minor] Animals. Antibodies, Monoclonal / metabolism. Apoptosis / drug effects. Cell Movement / drug effects. Dose-Response Relationship, Drug. Extracellular Matrix / metabolism. Female. Flow Cytometry. Fluorescence. Humans. Male. Mice. Mice, Nude. Neoplasm Invasiveness / prevention & control. Peptides / pharmacology. Rats. Tibia / pathology. Tumor Cells, Cultured

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  • (PMID = 15777962.001).
  • [ISSN] 0041-0101
  • [Journal-full-title] Toxicon : official journal of the International Society on Toxinology
  • [ISO-abbreviation] Toxicon
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Disintegrins; 0 / Peptides; 111019-84-2 / trigramin
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25. Gernez Y, Barlesi F, Astoul P, Magnan A: [Hypersensitivity to carboplatin. An effect of generic drugs?]. Rev Mal Respir; 2006 Jun;23(3 Pt 1):269-72
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  • [Title] [Hypersensitivity to carboplatin. An effect of generic drugs?].
  • INTRODUCTION: Carboplatin is a chemotherapeutic agent used frequently in thoracic medicine on account of its relatively good tolerance.
  • CASE REPORTS: We report the cases of 2 patients, treated for undifferentiated bronchial carcinoma and carcinoma of the breast, presenting with hypersensitivity reactions to carboplatin developing after 6 and 8 courses respectively.
  • Both of these reactions occurred when generic carboplatin was substituted for the propriety preparation.
  • In addition a national survey of hypersensitivity to carboplatin should be considered by the regional drug safety centres.
  • [MeSH-major] Antineoplastic Agents / adverse effects. Carboplatin / adverse effects. Drug Hypersensitivity / etiology. Drugs, Generic / adverse effects
  • [MeSH-minor] Female. Humans. Male. Middle Aged

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  • [CommentIn] Rev Mal Respir. 2006 Nov;23(5 Pt 1):487-8 [17314753.001]
  • (PMID = 16788528.001).
  • [ISSN] 0761-8425
  • [Journal-full-title] Revue des maladies respiratoires
  • [ISO-abbreviation] Rev Mal Respir
  • [Language] fre
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Drugs, Generic; BG3F62OND5 / Carboplatin
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26. Peer D, Dekel Y, Melikhov D, Margalit R: Fluoxetine inhibits multidrug resistance extrusion pumps and enhances responses to chemotherapy in syngeneic and in human xenograft mouse tumor models. Cancer Res; 2004 Oct 15;64(20):7562-9
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  • Multidrug resistance (MDR) operated by extrusion pumps such as P-glycoprotein and multidrug-resistance-associated-proteins, is a major reason for poor responses and failures in cancer chemotherapy.
  • MDR modulators (chemosensitizers) were found among drugs approved for noncancer indications and their derivatives.
  • In vitro, fluoxetine enhanced (10- to 100-fold) cytotoxicity of anticancer drugs (doxorubicin, mitomycin C, vinblastine, and paclitaxel) in drug-resistant but not in drug-sensitive cells (5 and 3 lines, respectively).
  • Fluoxetine increased drug accumulation within MDR-cells and inhibited drug efflux from those cells.
  • This low-dose range, together with the findings reported here, indicate that fluoxetine has a high potential to join the arsenal of MDR reversal agents that may reach the clinic.
  • [MeSH-major] Antineoplastic Agents / pharmacokinetics. Fluoxetine / pharmacology. Neoplasms, Experimental / drug therapy. Neoplasms, Experimental / metabolism
  • [MeSH-minor] Animals. Breast Neoplasms / drug therapy. Breast Neoplasms / metabolism. Carcinoma, Lewis Lung / drug therapy. Carcinoma, Lewis Lung / metabolism. Cell Line, Tumor. Disease Progression. Doxorubicin / pharmacokinetics. Doxorubicin / pharmacology. Drug Resistance, Multiple. Drug Resistance, Neoplasm. Drug Synergism. Female. Humans. Lung Neoplasms / drug therapy. Lung Neoplasms / metabolism. Male. Mice. Mice, Inbred C57BL. Mice, Nude. Mitomycin / pharmacokinetics. Mitomycin / pharmacology. Paclitaxel / pharmacokinetics. Paclitaxel / pharmacology. Tissue Distribution. Vinblastine / pharmacokinetics. Vinblastine / pharmacology. Xenograft Model Antitumor Assays

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  • (PMID = 15492283.001).
  • [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 / Antineoplastic Agents; 01K63SUP8D / Fluoxetine; 50SG953SK6 / Mitomycin; 5V9KLZ54CY / Vinblastine; 80168379AG / Doxorubicin; P88XT4IS4D / Paclitaxel
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27. Xie BF, Feng GK, Zhu XF, Su XR, Liu ZC, Yang RZ, Wei XY: [Antitumor effect of anuoning]. Ai Zheng; 2002 Apr;21(4):379-82
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  • METHODS: MTT assay was used to examine the growth inhibition of anuoning on human colon carcinoma cell line (HT-29), human nasopharyngeal carcinoma cell line (SUNE1, CNE2), human liver carcinoma (bel-7402), human breast adenocarcinoma cell line (MCF-7) and human lung adenocarcinoma cell line (GLC-82).
  • [MeSH-major] Antineoplastic Agents, Phytogenic / pharmacology. Furans / pharmacology. Lactones / pharmacology
  • [MeSH-minor] Animals. Disease Models, Animal. Drug Screening Assays, Antitumor. Female. HL-60 Cells. HT29 Cells. Humans. Inhibitory Concentration 50. Male. Mice. Neoplasm Transplantation. Neoplasms, Experimental / drug therapy. Treatment Outcome. Tumor Cells, Cultured

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  • (PMID = 12452015.001).
  • [Journal-full-title] Ai zheng = Aizheng = Chinese journal of cancer
  • [ISO-abbreviation] Ai Zheng
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 0 / Furans; 0 / Lactones; 102989-24-2 / bullatacin; 120298-30-8 / squamocin
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28. Li L, Liang Z, Deng H, Kuang A, Tan T, Luo S: Samarium-153-EDTMP bone uptake rate and its relation to therapeutic effect. Chin Med J (Engl); 2002 Jul;115(7):1096-8
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  • METHODS: Sixty-six patients with painful bony metastases from prostate (n = 15), lung (n = 20), breast (n= 18), nasopharyngeal carcinoma (NPC) (n=5), colon (n=2), kidney (n=2) and unknown cause (n=4) carcinoma were examined with whole-body scintigraphy 10 min and 5 h post administration of (153)Sm-EDTMP.
  • Bone uptake rate was then calculated. (1 ) Complete response (CR): disappearance of > 2 metastases, Karnofsky Performance Score (KPS) increase > 20, moderate or complete remission of bone pain 7 d post injection of (153)Sm-EDTMP. (2) Partial response (PR): disappearance of 1-2 metastases, KPS increase 10-20, moderate remission of bone pain in 3 wk. (3) Non-response (NR): no disappearance or shrinkage of metastases, KPS increase < 10, no or slight remission of bone pain.
  • The bone uptake rate in the CR group (17 cases, 25.7%), PR group (24 cases, 36.4%), and NR group (25 cases, 37.9%) was 52.4% - 86.6% (mean = 68.7%), 43.7% - 70.4% (mean = 58.3%), and 31.9%- 51 .5% (mean = 41 .
  • Statistical analysis showed that there was a significant difference between the CR and PR groups ( t = 4.258, P = 0.001 ) as well as between PR and NR groups ( t = 8.48,P = 0.001 ).
  • This allows nuclear medicine physicians to calculate a safe and effective dose of (153)Sm-EDTMPin individual patients to palliate bone cancer pain without myelotoxicity.
  • [MeSH-major] Bone Neoplasms / drug therapy. Bone Neoplasms / secondary. Bone and Bones / metabolism. Organometallic Compounds / pharmacokinetics. Organophosphorus Compounds / pharmacokinetics
  • [MeSH-minor] Female. Humans. Male

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  • (PMID = 12173602.001).
  • [ISSN] 0366-6999
  • [Journal-full-title] Chinese medical journal
  • [ISO-abbreviation] Chin. Med. J.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Organometallic Compounds; 0 / Organophosphorus Compounds; 122575-21-7 / samarium ethylenediaminetetramethylenephosphonate
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29. Yoshimasu T, Ohta F, Oura S, Tamaki T, Shimizu Y, Naito K, Kiyoi M, Hirai Y, Kawago M, Okamura Y: Histoculture drug response assay for gefitinib in non-small-cell lung cancer. Gen Thorac Cardiovasc Surg; 2009 Mar;57(3):138-43
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  • [Title] Histoculture drug response assay for gefitinib in non-small-cell lung cancer.
  • We evaluated the chemosensitivity for gefitinib in non-small-cell lung cancer (NSCLC) using a histoculture drug response assay (HDRA).
  • There were 13 male and 9 female patients, ranging in age from 49 to 84 (average 70) years old.
  • Small pieces of viable cancer tissue were placed on the collagen gel and then cultured for 7 days in the presence of gefitinib.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Carcinoma, Non-Small-Cell Lung / drug therapy. Lung Neoplasms / drug therapy. Protein Kinase Inhibitors / therapeutic use. Quinazolines / therapeutic use
  • [MeSH-minor] Adenocarcinoma / drug therapy. Aged. Aged, 80 and over. Carcinoma, Squamous Cell / drug therapy. Cell Proliferation / drug effects. Dose-Response Relationship, Drug. Drug Resistance, Neoplasm / genetics. Drug Screening Assays, Antitumor. Female. Gene Expression Regulation, Neoplastic. Genes, ras. Humans. Male. Middle Aged. Mutation. Patient Selection. Receptor, Epidermal Growth Factor / antagonists & inhibitors. Receptor, Epidermal Growth Factor / genetics. Smoking / adverse effects. Tissue Culture Techniques


30. Odhav B, Adam JK, Bhoola KD: Modulating effects of fumonisin B1 and ochratoxin A on leukocytes and messenger cytokines of the human immune system. Int Immunopharmacol; 2008 Jun;8(6):799-809
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  • Although much is known about their cellular toxicity and carcinogenesis in animals, there are no reports of adverse effects on immune cells (leukocytes) or on the immune modulation of the molecular messengers (cytokines) in humans.
  • This study was designed, therefore, to determine and compare the morphological effects of fumonisin B1 and ochratoxin A on lymphocytes and neutrophils harvested from the circulation of healthy volunteer subjects and patients with oesophageal and breast carcinomas.
  • Both fumonisin B1 and ochratoxin A reduced the number of viable lymphocytes and neutrophils harvested from the circulation of volunteer subjects carcinoma patients in a dose-dependent manner.
  • Cytokine levels were determined in the circulation of healthy volunteer subjects and in patients with oesophageal and breast carcinomas since they reflect the status of the immune system in humans.
  • The findings of this study on immunocytes (leukocytes) and the immune molecular messengers (cytokines) suggest that fumonisin B1 and ochratoxin A have an immuno-suppressive effect in humans, in particular patients with cancer by impairing immune surveillance.
  • [MeSH-major] Breast Neoplasms / immunology. Cytokines / blood. Esophageal Neoplasms / immunology. Fumonisins / pharmacology. Leukocytes / drug effects. Ochratoxins / pharmacology
  • [MeSH-minor] Adult. Aged. Female. Granulocyte Colony-Stimulating Factor / blood. Humans. Male. Microscopy, Electron, Transmission. Middle Aged. Neutrophils / drug effects. Neutrophils / immunology. Neutrophils / metabolism. Neutrophils / ultrastructure. Receptors, Chemokine / blood. Receptors, Granulocyte Colony-Stimulating Factor / blood. Receptors, Tumor Necrosis Factor / blood. Tumor Necrosis Factor-alpha / blood

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  • (PMID = 18442783.001).
  • [ISSN] 1567-5769
  • [Journal-full-title] International immunopharmacology
  • [ISO-abbreviation] Int. Immunopharmacol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / CX3CR1 protein, human; 0 / Cytokines; 0 / Fumonisins; 0 / Ochratoxins; 0 / Receptors, Chemokine; 0 / Receptors, Granulocyte Colony-Stimulating Factor; 0 / Receptors, Tumor Necrosis Factor; 0 / Tumor Necrosis Factor-alpha; 116355-83-0 / fumonisin B1; 143011-72-7 / Granulocyte Colony-Stimulating Factor; 1779SX6LUY / ochratoxin A
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31. Suga Y, Hara Y, Hashimoto H, Nishigami J, Shimizu M, Akasaka H, Hayashi K, Yonejima M, Nakamura M, Inokuchi M, Kasahara K, Nishimura G, Miyamoto K: [Consideration of preventive free-flowing IV infusion method for vinorelbine]. Gan To Kagaku Ryoho; 2007 Aug;34(8):1255-7
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  • [Title] [Consideration of preventive free-flowing IV infusion method for vinorelbine].
  • Vinorelbine is administered to treat solid tumors such as non-small cell lung cancer and breast cancer, and good treatment results have been reported.
  • Although this agent is known to cause phlebitis, some studies indicated that its administration over 5 minutes or less decreased the incidence of this adverse effect to approximately 5%.
  • In the present study,we investigated the preventive effects on phlebitis of administering this agent over 5 minutes or less by drip infusion,which is simpler and more useful than intravenous injection.
  • We administered vinorelbine 35 times to 6 patients with breast cancer or non-small cell lung cancer.
  • [MeSH-major] Antineoplastic Agents, Phytogenic / administration & dosage. Breast Neoplasms / drug therapy. Carcinoma, Non-Small-Cell Lung / drug therapy. Infusions, Intravenous / methods. Lung Neoplasms / drug therapy. Phlebitis / prevention & control. Vinblastine / analogs & derivatives
  • [MeSH-minor] Adult. Aged. Antibodies, Monoclonal / administration & dosage. Antibodies, Monoclonal, Humanized. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Deoxycytidine / administration & dosage. Deoxycytidine / analogs & derivatives. Female. Humans. Male. Middle Aged. Trastuzumab

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  • (PMID = 17687207.001).
  • [ISSN] 0385-0684
  • [Journal-full-title] Gan to kagaku ryoho. Cancer & chemotherapy
  • [ISO-abbreviation] Gan To Kagaku Ryoho
  • [Language] jpn
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antineoplastic Agents, Phytogenic; 0W860991D6 / Deoxycytidine; 5V9KLZ54CY / Vinblastine; B76N6SBZ8R / gemcitabine; P188ANX8CK / Trastuzumab; Q6C979R91Y / vinorelbine
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32. Kee K, Vujcic S, Merali S, Diegelman P, Kisiel N, Powell CT, Kramer DL, Porter CW: Metabolic and antiproliferative consequences of activated polyamine catabolism in LNCaP prostate carcinoma cells. J Biol Chem; 2004 Jun 25;279(26):27050-8
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  • [Title] Metabolic and antiproliferative consequences of activated polyamine catabolism in LNCaP prostate carcinoma cells.
  • Although this is usually accomplished by inhibiting polyamine biosynthesis, we reasoned that this might be more effectively achieved by activation of polyamine catabolism at the level of spermidine/spermine N(1)-acetyltransferase (SSAT); a strategy first validated in MCF-7 breast carcinoma cells.
  • Thus, SSAT was conditionally overexpressed in LNCaP prostate carcinoma cells via a tetracycline-regulatable (Tet-off) system.
  • SSAT products N(1)-acetylspermidine, N(1)-acetylspermine, and N(1),N(12)-diacetylspermine accumulated intracellularly and extracellularly.
  • Thus, flux-induced growth inhibition appears to derive from overaccumulation of metabolic products and/or from depletion of metabolic precursors.
  • [MeSH-major] Carcinoma / metabolism. Polyamines / metabolism. Prostatic Neoplasms / metabolism. Putrescine / analogs & derivatives
  • [MeSH-minor] Acetyl Coenzyme A / metabolism. Acetyltransferases / genetics. Acetyltransferases / metabolism. Adenosylmethionine Decarboxylase / metabolism. Cell Division / drug effects. Cell Division / physiology. Deoxyadenosines / metabolism. Eflornithine / pharmacology. Enzyme Inhibitors / pharmacology. Humans. Male. Methionine / pharmacology. Ornithine / pharmacology. Ornithine Decarboxylase / metabolism. Ornithine Decarboxylase Inhibitors. Oxidoreductases Acting on CH-NH Group Donors / antagonists & inhibitors. RNA, Messenger / biosynthesis. S-Adenosylmethionine / analogs & derivatives. S-Adenosylmethionine / metabolism. Tetracyclines / pharmacology. Thionucleosides / metabolism. Tumor Cells, Cultured

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  • (PMID = 15096507.001).
  • [ISSN] 0021-9258
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA-09072-30; United States / NCI NIH HHS / CA / CA-16056; United States / NCI NIH HHS / CA / CA-22153; United States / NCI NIH HHS / CA / CA-72648
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Deoxyadenosines; 0 / Enzyme Inhibitors; 0 / Ornithine Decarboxylase Inhibitors; 0 / Polyamines; 0 / RNA, Messenger; 0 / Tetracyclines; 0 / Thionucleosides; 634Z2VK3UQ / 5'-methylthioadenosine; 72-89-9 / Acetyl Coenzyme A; 7LP2MPO46S / S-Adenosylmethionine; 93565-01-6 / MDL 72527; AE28F7PNPL / Methionine; E524N2IXA3 / Ornithine; EC 1.5.- / Oxidoreductases Acting on CH-NH Group Donors; EC 1.5.3.- / polyamine oxidase; EC 2.3.1.- / Acetyltransferases; EC 2.3.1.57 / diamine N-acetyltransferase; EC 4.1.1.17 / Ornithine Decarboxylase; EC 4.1.1.50 / Adenosylmethionine Decarboxylase; V10TVZ52E4 / Putrescine; ZQN1G5V6SR / Eflornithine
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33. Chang HJ, Yoo BC, Lim SB, Jeong SY, Kim WH, Park JG: Metabotropic glutamate receptor 4 expression in colorectal carcinoma and its prognostic significance. Clin Cancer Res; 2005 May 1;11(9):3288-95
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  • [Title] Metabotropic glutamate receptor 4 expression in colorectal carcinoma and its prognostic significance.
  • Recently, we reported that mGluR4 mediates 5-fluorouracil resistance in a human colon cancer cell line.
  • EXPERIMENTAL DESIGN: mGluR4 expression was investigated in 21 normal and 312 malignant tissues from various organs using immunohistochemistry.
  • RESULTS: Expression of mGluR4 was identified in the normal epithelia of the upper respiratory tract, gastrointestinal tracts, breast, uterine cervix, urinary bladder, and skin, whereas it was not detected in the thyroid, lung alveoli, liver, testis, or prostate.
  • In the corresponding malignant tissues, mGluR4 expression was frequently identified in colorectal carcinoma (68%), followed by malignant melanoma, laryngeal carcinoma, and breast carcinomas.
  • [MeSH-minor] Aminobutyrates / pharmacology. Blotting, Western. Cell Line, Tumor. Cell Movement / drug effects. Cell Proliferation / drug effects. Female. Humans. Immunohistochemistry. Male. Prognosis. Survival Analysis

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  • (PMID = 15867225.001).
  • [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
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Aminobutyrates; 0 / Receptors, Metabotropic Glutamate; 0 / metabotropic glutamate receptor 4; 6323-99-5 / 2-amino-4-phosphonobutyric acid
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34. Drucker L, Ciobotaro P, Kimchi O, Tohami T, Yarkoni S, Radnay J, Shapira H, Lishner M: Initial exposed phosphatidylserine levels correlate with cellular response to cytotoxic drugs. Eur J Haematol; 2003 Feb;70(2):98-105
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  • [Title] Initial exposed phosphatidylserine levels correlate with cellular response to cytotoxic drugs.
  • Phosphatidylserine's (PS) membranal distribution is associated with an expanding variety of biological processes.
  • We studied the relevance of preliminarily exposed membranal PS levels to cellular effects of cytotoxic agents.
  • PBL of normal controls (n = 18) and patients with doxorubicin-treated breast carcinoma (n = 27) or 5'-fluorouracil-treated colorectal cancer (n = 32) were assayed before and after drug infusion.
  • Membranal expression levels of PS, adhesion molecules (CD18, CD11a-c, CD63) and Fas-R of leukocyte subtypes were assessed by flow cytometer.
  • Several distinct features were observed of which the more prominent were: leukocyte subtypes each display characteristic PS levels; cancer patients' PBL display higher preliminary PS levels than normal controls in all cell groups; and existence of negative correlations between initial membranal PS levels and drug-induced changes in its expression.
  • Our findings underscore the complex involvement of PS in PBL apoptosis and possibly drug resistance.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Cell Membrane / chemistry. Leukocytes / drug effects. Phosphatidylserines / metabolism
  • [MeSH-minor] Aged. Analysis of Variance. Apoptosis. Biomarkers / blood. Breast Neoplasms / blood. Breast Neoplasms / complications. Breast Neoplasms / drug therapy. Case-Control Studies. Cell Adhesion Molecules / metabolism. Colorectal Neoplasms / blood. Colorectal Neoplasms / complications. Colorectal Neoplasms / drug therapy. Female. Humans. Leukopenia / etiology. Male. Middle Aged

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  • (PMID = 12581191.001).
  • [ISSN] 0902-4441
  • [Journal-full-title] European journal of haematology
  • [ISO-abbreviation] Eur. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Biomarkers; 0 / Cell Adhesion Molecules; 0 / Phosphatidylserines
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35. Qi H, Ma J, Liu YM, Yang L, Peng L, Wang H, Chen HZ: Allostatic tumor-burden induces depression-associated changes in hepatoma-bearing mice. J Neurooncol; 2009 Sep;94(3):367-72
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  • The high incidence of depression among cancer patients has created the need for deeper insights into its underlying pathophysiological mechanism.
  • Taken together, these data indicate that tumor-burden might induce depressive-related behavior and brain changes, and suggest that antidepressants might not only palliate depression symptoms but also modify disease processes in the auxiliary treatment of cancer.
  • [MeSH-major] Carcinoma, Hepatocellular / complications. Depression / etiology. Liver Neoplasms / complications. Tumor Burden
  • [MeSH-minor] Analysis of Variance. Animals. Antidepressive Agents, Second-Generation / therapeutic use. Brain-Derived Neurotrophic Factor / genetics. Brain-Derived Neurotrophic Factor / metabolism. Cerebral Cortex / drug effects. Cerebral Cortex / metabolism. Disease Models, Animal. Fluoxetine / therapeutic use. Gene Expression Regulation, Neoplastic / drug effects. Gene Expression Regulation, Neoplastic / physiology. Glia Maturation Factor / genetics. Glia Maturation Factor / metabolism. Hindlimb Suspension / methods. Hippocampus / drug effects. Hippocampus / metabolism. Male. Mice. Mice, Inbred BALB C. Motor Activity / drug effects. Neoplasm Transplantation. RNA, Messenger / metabolism. Superoxide Dismutase / metabolism. Time Factors. Tumor Cells, Cultured

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  • (PMID = 19381448.001).
  • [ISSN] 1573-7373
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antidepressive Agents, Second-Generation; 0 / Brain-Derived Neurotrophic Factor; 0 / Glia Maturation Factor; 0 / RNA, Messenger; 01K63SUP8D / Fluoxetine; EC 1.15.1.1 / Superoxide Dismutase
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36. Ampil FL, Heldmann M, Ibrahim AM, Balfour EL: Involvement of the cavernous sinus by malignant (extracranial) tumour: palliation in six cases without surgery. J Craniomaxillofac Surg; 2000 Jun;28(3):161-4
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  • [Title] Involvement of the cavernous sinus by malignant (extracranial) tumour: palliation in six cases without surgery.
  • Involvement of the cavernous sinus region due to haematogenous spread or by local extension of a malignant head and neck tumour does not occur frequently.
  • [MeSH-minor] Adult. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Breast Neoplasms / pathology. Carcinoma, Squamous Cell / drug therapy. Carcinoma, Squamous Cell / radiotherapy. Carcinoma, Squamous Cell / secondary. Carcinoma, Squamous Cell / therapy. Chemotherapy, Adjuvant. Female. Humans. Male. Maxillary Sinus Neoplasms / pathology. Middle Aged. Nasopharyngeal Neoplasms / pathology. Prostatic Neoplasms / pathology. Retrospective Studies

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  • [Copyright] Copyright 2000 European Association for Cranio-Maxillofacial Surgery.
  • (PMID = 10964552.001).
  • [ISSN] 1010-5182
  • [Journal-full-title] Journal of cranio-maxillo-facial surgery : official publication of the European Association for Cranio-Maxillo-Facial Surgery
  • [ISO-abbreviation] J Craniomaxillofac Surg
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] SCOTLAND
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37. Zhang T, Ma SL, Yue JH: [Clinical observation on treatment of radiation pneumonia by Qingjin Runfei Decoction combined with hormone and antibiotic]. Zhongguo Zhong Xi Yi Jie He Za Zhi; 2007 Mar;27(3):254-6
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  • [Title] [Clinical observation on treatment of radiation pneumonia by Qingjin Runfei Decoction combined with hormone and antibiotic].
  • OBJECTIVE: To observe the curative effect of Qingjin Runfei Decoction (QRD) combined with hormone and antibiotic in treating radiation pneumonia (RP).
  • METHODS: Patients were randomly assigned to two groups, the control group (51 cases) treated with hormone and antibiotic and the treated group (53 cases) with the above therapy plus QRD.
  • The curative effects on RP, quality of life (QOL), chest radiography and TCM symptoms were observed.
  • RESULTS: The curative effects on the above items in the treated group were all significantly better than those in the control group (P < 0.05).
  • CONCLUSION: QRD could enhance the effects of hormone and antibiotic in treating RP, as well as improve QOL of the patients.

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  • (PMID = 17432692.001).
  • [ISSN] 1003-5370
  • [Journal-full-title] Zhongguo Zhong xi yi jie he za zhi Zhongguo Zhongxiyi jiehe zazhi = Chinese journal of integrated traditional and Western medicine
  • [ISO-abbreviation] Zhongguo Zhong Xi Yi Jie He Za Zhi
  • [Language] CHI
  • [Publication-type] English Abstract; Journal Article; Randomized Controlled Trial
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Anti-Bacterial Agents; 0 / Drugs, Chinese Herbal; 0 / Glucocorticoids; 0 / qingjin runfei; VB0R961HZT / Prednisone
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38. Régina A, Demeule M, Ché C, Lavallée I, Poirier J, Gabathuler R, Béliveau R, Castaigne JP: Antitumour activity of ANG1005, a conjugate between paclitaxel and the new brain delivery vector Angiopep-2. Br J Pharmacol; 2008 Sep;155(2):185-97
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  • BACKGROUND AND PURPOSE: Paclitaxel is highly efficacious in the treatment of breast, head and neck, non-small cell lung cancers and ovarian carcinoma.
  • For malignant gliomas, paclitaxel is prevented from reaching its target by the presence of the efflux pump P-glycoprotein (P-gp) at the blood-brain barrier.
  • We investigated the utilization of a new drug delivery system to increase brain delivery of paclitaxel.
  • KEY RESULTS: We show by in situ brain perfusion that ANG1005 enters the brain to a greater extent than paclitaxel and bypasses the P-gp.
  • ANG1005 has an antineoplastic potency similar to that of paclitaxel against human cancer cell lines.
  • Finally, ANG1005 administration led to a significant increase in the survival of mice with intracerebral implantation of U87 MG glioblastoma cells or NCI-H460 lung carcinoma cells.
  • CONCLUSIONS AND IMPLICATIONS: These results demonstrate the antitumour potential of a new drug, ANG1005, and establish that conjugation of anticancer agents with the Angiopep-2 peptide vector could increase their efficacy in the treatment of brain cancer.
  • [MeSH-major] Antineoplastic Agents, Phytogenic / administration & dosage. Brain Neoplasms / drug therapy. Drug Carriers / metabolism. Drug Delivery Systems. Paclitaxel / administration & dosage
  • [MeSH-minor] Animals. Disease Models, Animal. Female. Humans. Male. Mice. Mice, Nude. Neoplasm Transplantation. Peptides / chemistry. Tumor Cells, Cultured / transplantation. Xenograft Model Antitumor Assays

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  • (PMID = 18574456.001).
  • [ISSN] 0007-1188
  • [Journal-full-title] British journal of pharmacology
  • [ISO-abbreviation] Br. J. Pharmacol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Angiopep-2; 0 / Antineoplastic Agents, Phytogenic; 0 / Drug Carriers; 0 / Peptides; 0 / paclitaxel-Angiopep-2 conjugate; P88XT4IS4D / Paclitaxel
  • [Other-IDs] NLM/ PMC2538693
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39. Ong DC, Ho YM, Rudduck C, Chin K, Kuo WL, Lie DK, Chua CL, Tan PH, Eu KW, Seow-Choen F, Wong CY, Hong GS, Gray JW, Lee AS: LARG at chromosome 11q23 has functional characteristics of a tumor suppressor in human breast and colorectal cancer. Oncogene; 2009 Nov 26;28(47):4189-200
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  • [Title] LARG at chromosome 11q23 has functional characteristics of a tumor suppressor in human breast and colorectal cancer.
  • Deletion of 11q23-q24 is frequent in a diverse variety of malignancies, including breast and colorectal carcinoma, implicating the presence of a tumor suppressor gene at that chromosomal region.
  • LARG (leukemia-associated Rho guanine-nucleotide exchange factor) (also called ARHGEF12), identified from the analysed region, is frequently underexpressed in breast and colorectal carcinomas with a reduced expression observed in all breast cancer cell lines (n=11), in 12 of 38 (32%) primary breast cancers, 5 of 10 (50%) colorectal cell lines and in 20 of 37 (54%) primary colorectal cancers.
  • Hypermethylation of the LARG promoter was not detected in either breast or colorectal cancer, and treatment of four breast and four colorectal cancer cell lines with 5-aza-2'-deoxycytidine and/or trichostatin A did not result in a reactivation of LARG.
  • Enforced expression of LARG in breast and colorectal cancer cells by stable transfection resulted in reduced cell proliferation and colony formation, as well as in a markedly slower cell migration rate in colorectal cancer cells, providing functional evidence for LARG as a candidate tumor suppressor gene.

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  • (PMID = 19734946.001).
  • [ISSN] 1476-5594
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P30 CA082103-05; United States / NCI NIH HHS / CA / P01 CA064602; United States / NCI NIH HHS / CA / CA058207-14; United States / NCI NIH HHS / CA / CA083639-100013; United States / NCI NIH HHS / CA / U24 CA126551; United States / NCI NIH HHS / CA / P50 CA 83639; United States / NCI NIH HHS / CA / U24 CA 126477; United States / NCI NIH HHS / CA / P30 CA082103; United States / NCI NIH HHS / CA / CA126477-01; United States / NCI NIH HHS / CA / CA112970-05S2; United States / NCI NIH HHS / CA / U54 CA 112970; United States / NCI NIH HHS / CA / U54 CA112970-05S2; United States / NCI NIH HHS / CA / P01 CA64602; United States / NCI NIH HHS / CA / U24 CA126477; United States / NCI NIH HHS / CA / P30 CA 82103; United States / NCI NIH HHS / CA / P50 CA 58207; United States / NCI NIH HHS / CA / P50 CA058207; United States / NCI NIH HHS / CA / P50 CA058207-14; United States / NCI NIH HHS / CA / U54 CA112970; United States / NCI NIH HHS / CA / P50 CA083639-100013; United States / NCI NIH HHS / CA / CA082103-05; United States / NCI NIH HHS / CA / P01 CA064602-04; United States / NCI NIH HHS / CA / U24 CA126477-01; United States / NCI NIH HHS / CA / P50 CA083639; United States / NCI NIH HHS / CA / CA064602-04
  • [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] England
  • [Chemical-registry-number] 0 / ARHGEF12 protein, human; 0 / Antimetabolites, Antineoplastic; 0 / Guanine Nucleotide Exchange Factors; 0 / Hydroxamic Acids; 0 / Protein Synthesis Inhibitors; 0 / Rho Guanine Nucleotide Exchange Factors; 0 / Tumor Suppressor Proteins; 3X2S926L3Z / trichostatin A; 776B62CQ27 / decitabine; M801H13NRU / Azacitidine
  • [Other-IDs] NLM/ NIHMS185870; NLM/ PMC2844776
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40. Chen T, Hwang H, Rose ME, Nines RG, Stoner GD: Chemopreventive properties of black raspberries in N-nitrosomethylbenzylamine-induced rat esophageal tumorigenesis: down-regulation of cyclooxygenase-2, inducible nitric oxide synthase, and c-Jun. Cancer Res; 2006 Mar 1;66(5):2853-9
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  • Our laboratory has used a rodent model of human esophageal squamous cell carcinoma to identify putative chemopreventive agents for this disease and to determine their mechanisms of action.
  • The expression and enzymatic activities of cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS) as well as the expression of c-Jun in the esophagi, were evaluated to investigate the mechanism(s) by which black raspberries modulate tumorigenesis.
  • At week 25, BRB inhibited tumor multiplicity, the standard end point in this tumor model, from 3.78 +/- 0.41 tumors per rat in NMBA-treated animals to 2.23 +/- 0.21 tumors per rat in animals treated with NMBA plus BRB (P < 0.005).

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  • (PMID = 16510608.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA096130; United States / NCI NIH HHS / CA / R01 CA103180-03; United States / NCI NIH HHS / CA / CA103180; United States / NCI NIH HHS / CA / R01 CA96130; United States / NCI NIH HHS / CA / CA103180-03; United States / NCI NIH HHS / CA / R01 CA103180
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Carcinogens; 0 / Nitrites; 0 / RNA, Messenger; 937-40-6 / nitrosobenzylmethylamine; EC 1.14.13.39 / Nitric Oxide Synthase Type II; EC 1.14.99.1 / Cyclooxygenase 2; EC 2.7.11.24 / JNK Mitogen-Activated Protein Kinases; K7Q1JQR04M / Dinoprostone; M43H21IO8R / Dimethylnitrosamine
  • [Other-IDs] NLM/ NIHMS258981; NLM/ PMC3015097
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41. Moffat DF, Oien KA, Dickson J, Habeshaw T, McLellan DR: Hepatocellular carcinoma after long-term tamoxifen therapy. Ann Oncol; 2000 Sep;11(9):1195-6
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  • [Title] Hepatocellular carcinoma after long-term tamoxifen therapy.
  • We describe a case of hepatocellular carcinoma (HCC) after long term tamoxifen therapy in a 71-year-old woman.
  • The patient was prescribed tamoxifen for 12 years following right mastectomy and axillary node clearance for breast carcinoma in 1985.
  • In addition, HCC in tamoxifen treated patients may be under-reported since there may be reluctance to biopsy liver tumours which are assumed to be secondary carcinoma of the breast.

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  • (PMID = 11061618.001).
  • [ISSN] 0923-7534
  • [Journal-full-title] Annals of oncology : official journal of the European Society for Medical Oncology
  • [ISO-abbreviation] Ann. Oncol.
  • [Language] ENG
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 094ZI81Y45 / Tamoxifen
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42. Mueller BA, Chow EJ, Kamineni A, Daling JR, Fraser A, Wiggins CL, Mineau GP, Hamre MR, Severson RK, Drews-Botsch C: Pregnancy outcomes in female childhood and adolescent cancer survivors: a linked cancer-birth registry analysis. Arch Pediatr Adolesc Med; 2009 Oct;163(10):879-86
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  • [Title] Pregnancy outcomes in female childhood and adolescent cancer survivors: a linked cancer-birth registry analysis.
  • OBJECTIVE: To compare birth outcomes among female survivors of childhood and adolescent cancer who subsequently bear children, relative to those of women without a history of cancer.
  • PARTICIPANTS: Cancer registries identified girls younger than 20 years who were diagnosed as having cancer from 1973 through 2000.
  • Linked birth records identified the first live births after diagnosis (n = 1898).
  • MAIN EXPOSURE: Cancer diagnosis at younger than 20 years.
  • RESULTS: Infants born to childhood cancer survivors were more likely to be preterm (relative risk [RR], 1.54; 95% confidence interval [CI], 1.30-1.83) and to weigh less than 2500 g (1.31; 1.10-1.57).
  • For the offspring of genital tract carcinoma survivors, RRs were 1.33 (95% CI, 1.13-1.56) and 1.29 (1.10-1.53), respectively.
  • In exploratory analysis, bone cancer survivors had an increased risk of diabetes (RR, 4.92; 95% CI, 1.60-15.13), and anemia was more common among brain tumor survivors (3.05; 1.16-7.98) and childhood cancer survivors whose initial treatment was chemotherapy only (2.45; 1.16-5.17).
  • CONCLUSIONS: Infants born to female survivors of childhood and adolescent cancer were not at increased risk of malformations or death.

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  • (PMID = 19805705.001).
  • [ISSN] 1538-3628
  • [Journal-full-title] Archives of pediatrics & adolescent medicine
  • [ISO-abbreviation] Arch Pediatr Adolesc Med
  • [Language] ENG
  • [Grant] None / None / / N01 CN067000-003; United States / NCI NIH HHS / CN / N01 CN067000-003; United States / NCI NIH HHS / PC / N01-PC-35141; United States / NCI NIH HHS / CA / N01PC35141; United States / NCI NIH HHS / CN / N01 CN065064; United States / NCI NIH HHS / PC / PC005016-20; United States / NCI NIH HHS / PC / N01 PC067006-009; United States / NCI NIH HHS / PC / N01-PC-67006; United States / NCI NIH HHS / PC / N01 PC035141; United States / NCI NIH HHS / CN / N01-CN-05230; United States / NCI NIH HHS / PC / PC067006-009; United States / NCI NIH HHS / CN / N01 CN067000; United States / NCI NIH HHS / PC / N01 PC067006; United States / NCI NIH HHS / PC / N01-PC-05016-20; United States / NCI NIH HHS / PC / N01 PC005016-20; United States / NCI NIH HHS / PC / N01 PC005016; United States / NCI NIH HHS / CN / N01 CN005230; United States / NCI NIH HHS / CN / N01-CN-67000; United States / NCI NIH HHS / CN / N01-CN-65064
  • [Publication-type] Journal Article; Multicenter Study; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  • [Other-IDs] NLM/ NIHMS92713; NLM/ PMC2758647
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43. Shao G, Berenguer J, Borczuk AC, Powell CA, Hei TK, Zhao Y: Epigenetic inactivation of Betaig-h3 gene in human cancer cells. Cancer Res; 2006 May 1;66(9):4566-73
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  • [Title] Epigenetic inactivation of Betaig-h3 gene in human cancer cells.
  • It has been shown previously that Betaig-h3 gene, which encodes an extracellular matrix protein involved in cell adhesion and tumorigenesis, is down-regulated or silenced in a variety of human cancer cell lines.
  • To unravel the underlying molecular mechanism(s) for this phenomenon, DNA methylation patterns of Betaig-h3 CpG island were examined in normal, immortalized, and cancer cell lines derived from lung, prostate, mammary, and kidney.
  • [MeSH-major] DNA Methylation. Extracellular Matrix Proteins / genetics. Gene Silencing. Neoplasms / genetics. Transforming Growth Factor beta / genetics
  • [MeSH-minor] Azacitidine / analogs & derivatives. Azacitidine / pharmacology. Breast Neoplasms / genetics. Breast Neoplasms / metabolism. Carcinoma, Non-Small-Cell Lung / genetics. Carcinoma, Non-Small-Cell Lung / metabolism. Cell Line, Tumor. CpG Islands. Epigenesis, Genetic. Female. Gene Expression Regulation, Neoplastic / drug effects. Genes, Reporter. Humans. Luciferases / biosynthesis. Luciferases / genetics. Lung Neoplasms / genetics. Lung Neoplasms / metabolism. Male. Promoter Regions, Genetic. Prostatic Neoplasms / genetics. Prostatic Neoplasms / metabolism

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  • (PMID = 16651406.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NIEHS NIH HHS / ES / ES 11804
  • [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 / Extracellular Matrix Proteins; 0 / Transforming Growth Factor beta; 148710-76-3 / betaIG-H3 protein; 776B62CQ27 / decitabine; EC 1.13.12.- / Luciferases; M801H13NRU / Azacitidine
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44. Xue LY, Chiu SM, Oleinick NL: Photochemical destruction of the Bcl-2 oncoprotein during photodynamic therapy with the phthalocyanine photosensitizer Pc 4. Oncogene; 2001 Jun 7;20(26):3420-7
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  • It was accompanied by a trace of a 23-kDa cleavage product as well as high-molecular weight products that may result from photochemical crosslinking.
  • [MeSH-major] Apoptosis / drug effects. Indoles / therapeutic use. Photochemotherapy. Photosensitizing Agents / therapeutic use. Proto-Oncogene Proteins c-bcl-2 / radiation effects
  • [MeSH-minor] Adenocarcinoma / pathology. Animals. Breast Neoplasms / pathology. CHO Cells / drug effects. CHO Cells / radiation effects. Carcinoma, Squamous Cell / pathology. Cricetinae. Cricetulus. Female. Free Radical Scavengers / pharmacology. Histidine / pharmacology. Humans. Intracellular Membranes / chemistry. Intracellular Membranes / drug effects. Intracellular Membranes / radiation effects. Laryngeal Neoplasms / pathology. Male. Membrane Proteins / drug effects. Membrane Proteins / radiation effects. Molecular Weight. Neoplasm Proteins / drug effects. Neoplasm Proteins / radiation effects. Oxidative Stress. Oxygen / metabolism. Photochemistry. Prostatic Neoplasms / pathology. Singlet Oxygen. Tumor Cells, Cultured / drug effects. Tumor Cells, Cultured / radiation effects

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  • (PMID = 11423992.001).
  • [ISSN] 0950-9232
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P01 CA48735; United States / NCI NIH HHS / CA / P30 CA43703; United States / NCI NIH HHS / CA / R01 CA83917
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Free Radical Scavengers; 0 / Indoles; 0 / Membrane Proteins; 0 / Neoplasm Proteins; 0 / Photosensitizing Agents; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / phthalocyanine Pc 4; 17778-80-2 / Singlet Oxygen; 4QD397987E / Histidine; S88TT14065 / Oxygen
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45. Mercader M, Bodner BK, Moser MT, Kwon PS, Park ES, Manecke RG, Ellis TM, Wojcik EM, Yang D, Flanigan RC, Waters WB, Kast WM, Kwon ED: T cell infiltration of the prostate induced by androgen withdrawal in patients with prostate cancer. Proc Natl Acad Sci U S A; 2001 Dec 4;98(25):14565-70
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  • [Title] T cell infiltration of the prostate induced by androgen withdrawal in patients with prostate cancer.
  • The induction of T cell infiltration in prostate tissues treated with androgen ablation may have implications for the immunotherapeutic treatment of prostate cancer as well as other hormone-sensitive malignancies, including breast carcinoma.

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  • (PMID = 11734652.001).
  • [ISSN] 0027-8424
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA 82185
  • [Publication-type] Clinical Trial; Journal Article; Randomized Controlled Trial; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Androgen Antagonists; 0 / Antineoplastic Agents, Hormonal; 76W6J0943E / Flutamide
  • [Other-IDs] NLM/ PMC64722
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46. Damyanov C, Radoslavova M, Gavrilov V, Stoeva D: Low dose chemotherapy in combination with insulin for the treatment of advanced metastatic tumors. Preliminary experience. J BUON; 2009 Oct-Dec;14(4):711-5
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  • Toxic effects and chemoresistance are serious problems concerning chemotherapy administration.
  • It combines standard chemotherapy schemes, using lower doses of anticancer drugs and the hormone insulin which is administered intravenously (i.v.).
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Bone Neoplasms / drug therapy. Breast Neoplasms / drug therapy. Carcinoma, Ductal, Breast / drug therapy. Hypoglycemic Agents / therapeutic use. Insulin / therapeutic use. Prostatic Neoplasms / drug therapy
  • [MeSH-minor] Adult. Drug Therapy, Combination. Female. Humans. Lymphatic Metastasis. Male. Middle Aged. Prognosis. Treatment Outcome


47. Aderca I, Moser CD, Veerasamy M, Bani-Hani AH, Bonilla-Guerrero R, Ahmed K, Shire A, Cazanave SC, Montoya DP, Mettler TA, Burgart LJ, Nagorney DM, Thibodeau SN, Cunningham JM, Lai JP, Roberts LR: The JNK inhibitor SP600129 enhances apoptosis of HCC cells induced by the tumor suppressor WWOX. J Hepatol; 2008 Sep;49(3):373-83
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  • The c-jun N-terminal kinase JNK1 interacts with WWOX and inhibits apoptosis.
  • We investigated the function of WWOX in human hepatocellular carcinoma (HCC) and the effect of JNK inhibition on WWOX-mediated apoptosis.

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  • (PMID = 18620777.001).
  • [ISSN] 0168-8278
  • [Journal-full-title] Journal of hepatology
  • [ISO-abbreviation] J. Hepatol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA082862-01; United States / NCI NIH HHS / CA / K08 CA082862-02; United States / NCI NIH HHS / CA / CA100882; United States / NCI NIH HHS / CA / K08 CA082862-04; United States / NCI NIH HHS / CA / K08 CA082862-01; United States / NCI NIH HHS / CA / R01 CA100882; United States / NCI NIH HHS / CA / R01 CA100882-01A1; United States / NCI NIH HHS / CA / K08 CA082862-05; United States / NCI NIH HHS / CA / CA082862-05; United States / NCI NIH HHS / CA / CA082862-02; United States / NCI NIH HHS / CA / K08 CA082862-03; United States / NCI NIH HHS / CA / CA082862-04; United States / NCI NIH HHS / CA / CA82862; United States / NCI NIH HHS / CA / K08 CA082862; United States / NCI NIH HHS / CA / CA082862-03; United States / NCI NIH HHS / CA / R56 CA100882
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Enzyme Inhibitors; 0 / RNA, Messenger; 0 / Tumor Suppressor Proteins; EC 1.- / Oxidoreductases; EC 1.1.1.- / WWOX protein, human; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 8; H88EPA0A3N / Staurosporine
  • [Other-IDs] NLM/ NIHMS59493; NLM/ PMC2574998
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48. Lorenzen S, Duyster J, Lersch C, von Delius S, Hennig M, Bredenkamp R, Peschel C, Lordick F: Capecitabine plus docetaxel every 3 weeks in first- and second-line metastatic oesophageal cancer: final results of a phase II trial. Br J Cancer; 2005 Jun 20;92(12):2129-33
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  • [Title] Capecitabine plus docetaxel every 3 weeks in first- and second-line metastatic oesophageal cancer: final results of a phase II trial.
  • Capecitabine and docetaxel have single-agent activity in upper gastrointestinal tumours, and have together demonstrated preclinical synergy and a survival benefit in breast cancer, and high response rates in first-line metastatic gastric cancer.
  • This trial assessed the efficacy, safety and feasibility of capecitabine in combination with docetaxel in patients with metastatic oesophageal cancer.
  • In all, 24 patients with advanced disease (17 squamous cell carcinoma and seven adenocarcinoma) received oral capecitabine (1000 mg m(-2) twice daily on days 1-14) plus intravenous docetaxel (75 mg m(-2) on day 1) every 3 weeks as first- (n = 16) or second-line (n = 8) therapy.
  • Capecitabine plus docetaxel has a manageable adverse event profile and very promising activity in metastatic oesophageal cancer, at least comparable to other doublet regimens.
  • [MeSH-major] Adenocarcinoma / drug therapy. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Carcinoma, Squamous Cell / drug therapy. Esophageal Neoplasms / drug therapy
  • [MeSH-minor] Aged. Capecitabine. Deoxycytidine / administration & dosage. Deoxycytidine / analogs & derivatives. Drug Administration Schedule. Feasibility Studies. Female. Fluorouracil / analogs & derivatives. Humans. Male. Middle Aged. Survival Analysis. Taxoids / administration & dosage. Treatment Outcome

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  • (PMID = 15942631.001).
  • [ISSN] 0007-0920
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] eng
  • [Publication-type] Clinical Trial; Clinical Trial, Phase II; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Taxoids; 0W860991D6 / Deoxycytidine; 15H5577CQD / docetaxel; 6804DJ8Z9U / Capecitabine; U3P01618RT / Fluorouracil
  • [Other-IDs] NLM/ PMC2361804
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49. Wang-Rodriguez J, Dreilinger AD, Alsharabi GM, Rearden A: The signaling adapter protein PINCH is up-regulated in the stroma of common cancers, notably at invasive edges. Cancer; 2002 Sep 15;95(6):1387-95
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  • Because no information is available regarding its expression in vivo in human tissues, this study evaluated the distribution and abundance of PINCH in patients with breast, prostate, lung, colon, and skin carcinomas.
  • METHODS: A polyclonal antibody was raised to a purified 6-histidine PINCH fusion protein and used to evaluate 74 cases comprising 33 breast carcinomas (21 ductal carcinomas, 6 lobular carcinomas, 4 ductal carcinomas in situ, 2 lobular carcinomas in situ), 22 prostate carcinomas, 5 colon carcinomas, 6 lung carcinomas (3 adenocarcinomas and 3 squamous carcinomas), and 8 skin carcinomas (4 basal cell carcinomas and 4 squamous cell carcinomas) by immunoperoxidase histochemistry of formalin-fixed, paraffin-embedded tissues.
  • Lysates of frozen tissue from the epithelium of two normal breasts and six breast carcinomas were evaluated by immunoblotting.
  • The most intense stromal immunostaining for PINCH was noted at invasive edges, particularly in breast carcinomatous tissue.
  • Immunoblotting of lysates from normal breast and breast carcinomatous tissue confirmed that PINCH protein expression was markedly increased in breast carcinomatous tissues.
  • Because of this and because PINCH functions as a "molecular switch" in signal transduction, PINCH may be a new target for drug discovery aimed at the tumor-associated stroma.
  • [MeSH-major] DNA-Binding Proteins / metabolism. Neoplasms / metabolism
  • [MeSH-minor] Adaptor Proteins, Signal Transducing. Adenocarcinoma / metabolism. Breast Neoplasms / metabolism. Carcinoma in Situ / metabolism. Carcinoma, Basal Cell / metabolism. Carcinoma, Ductal, Breast / metabolism. Carcinoma, Lobular / metabolism. Carcinoma, Squamous Cell / metabolism. Colonic Neoplasms / metabolism. Female. Humans. Immunoblotting. Immunohistochemistry. LIM Domain Proteins. Lung Neoplasms / metabolism. Male. Membrane Proteins. Neoplasm Invasiveness. Paraffin Embedding. Prostatic Neoplasms / metabolism. Skin Neoplasms / metabolism. Tissue Distribution. Up-Regulation

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  • [Copyright] Copyright 2002 American Cancer Society.
  • (PMID = 12216108.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / DNA-Binding Proteins; 0 / LIM Domain Proteins; 0 / LIMS1 protein, human; 0 / Membrane Proteins
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50. Modica-Napolitano JS, Nalbandian R, Kidd ME, Nalbandian A, Nguyen CC: The selective in vitro cytotoxicity of carcinoma cells by AZT is enhanced by concurrent treatment with delocalized lipophilic cations. Cancer Lett; 2003 Jul 30;198(1):59-68
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  • [Title] The selective in vitro cytotoxicity of carcinoma cells by AZT is enhanced by concurrent treatment with delocalized lipophilic cations.
  • This study assessed the selective growth inhibitory effect on cultured carcinoma cells by 3'-azido-3'-deoxythymidine (AZT), as a single agent, and in combination with delocalized lipophilic cations (DLCs) that are known to inhibit mitochondrial function.
  • In cytotoxicity assays, treatment of cells with varying concentrations of AZT induced a dose-dependent inhibition of cell growth of the human carcinoma lines DU-145 (prostate; IC50 at 24 microM), MCF-7 (breast; IC50 at 22 microM), and CX-1 (colon; IC50 at 23 microM), yet caused no significant effect on the growth of the control epithelial cell line CV-1 (monkey kidney) at a concentration as high as 50 microM AZT.
  • Combination treatment employing a constant concentration (1.25 microM) of the DLC dequalinium chloride (DECA) plus varying concentrations of AZT (0-50 microM) enhanced the AZT-induced cytotoxicity of carcinoma cells at least fourfold for MCF-7 and CX-1 cells (IC50 at 5 microM AZT), and twofold for DU-145 cells (IC50 at 11 microM AZT).
  • Similar results were obtained in DU-145 cells using a constant concentration of the DLC MKT-077 (1.0 microM) and varying concentrations of AZT (IC50 at 12.5 microM).
  • As expected, the drug combination of constant DLC and varying AZT had no significant effect on the growth of CV-1 cells.
  • Clonogenic assays demonstrated up to 20-fold enhancement of selective carcinoma cell killing by combination vs. single agent treatment, depending on the specific drug combination and concentrations used.
  • It is hypothesized that the efficacy of the AZT/DLC drug combination in carcinoma cell killing may be based on a dual selectivity involving inhibition of mitochondrial energy metabolism and inhibition of DNA synthesis due to limited deoxythymidine monophosphate availability.
  • [MeSH-major] Carcinoma / drug therapy. Cations / administration & dosage. Zidovudine / pharmacology
  • [MeSH-minor] Adenosine Triphosphate / analysis. Cell Survival / drug effects. Colony-Forming Units Assay. Humans. Male. Pyridines / administration & dosage. Thiazoles / administration & dosage. Thymidine / metabolism. Tumor Cells, Cultured

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  • (PMID = 12893431.001).
  • [ISSN] 0304-3835
  • [Journal-full-title] Cancer letters
  • [ISO-abbreviation] Cancer Lett.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / 1R15CA78323-01
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Cations; 0 / MKT 077; 0 / Pyridines; 0 / Thiazoles; 4B9XT59T7S / Zidovudine; 8L70Q75FXE / Adenosine Triphosphate; VC2W18DGKR / Thymidine
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51. Gennatas C, Michalaki V, Carvounis E, Psychogios J, Poulakaki N, Katsiamis G, Voros D, Kouloulias V, Mouratidou D, Tsavaris N: Third-line hormonal treatment with exemestane in postmenopausal patients with advanced breast cancer progressing on letrozole or anastrozole. A phase II trial conducted by the Hellenic Group of Oncology (HELGO). Tumori; 2006 Jan-Feb;92(1):13-7
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  • [Title] Third-line hormonal treatment with exemestane in postmenopausal patients with advanced breast cancer progressing on letrozole or anastrozole. A phase II trial conducted by the Hellenic Group of Oncology (HELGO).
  • AIMS AND BACKGROUND: The understanding of hormonal therapies in postmenopausal women with metastatic breast cancer has advanced greatly in the past several decades.
  • With the introduction of orally active, potent and selective third-generation aromatase inhibitors (anastrozole, letrozole and exemestane), approaches to the treatment of hormone-sensitive advanced breast cancer are undergoing reevaluation.
  • For treatment of advanced or metastatic disease that has progressed on tamoxifen, all three agents are active.
  • The purpose of the study was to assess the antitumor efficacy and tolerance of exemestane administered as third-line hormonal therapy to postmenopausal women with metastatic breast cancer refractory to letrozole and anastrozole.
  • STUDY DESIGN: Sixty postmenopausal women with stage IV hormone receptor-positive carcinoma of the breast were enrolled in the study.
  • CONCLUSIONS: Exemestane represents an active and well-tolerated treatment option in pretreated patients with advanced breast cancer who have received standard first- and second line hormonal therapies.
  • [MeSH-major] Androstadienes / therapeutic use. Antineoplastic Agents, Hormonal / therapeutic use. Aromatase Inhibitors / therapeutic use. Breast Neoplasms / drug therapy. Breast Neoplasms / pathology. Postmenopause
  • [MeSH-minor] Aged. Disease Progression. Female. Greece. Humans. Middle Aged. Neoplasm Staging. Neoplasms, Hormone-Dependent / drug therapy. Neoplasms, Hormone-Dependent / pathology. Nitriles / therapeutic use. Treatment Failure. Treatment Outcome. Triazoles / therapeutic use

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  • (PMID = 16683378.001).
  • [ISSN] 0300-8916
  • [Journal-full-title] Tumori
  • [ISO-abbreviation] Tumori
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase II; Journal Article; Multicenter Study
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Androstadienes; 0 / Antineoplastic Agents, Hormonal; 0 / Aromatase Inhibitors; 0 / Nitriles; 0 / Triazoles; 2Z07MYW1AZ / anastrozole; 7LKK855W8I / letrozole; NY22HMQ4BX / exemestane
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52. Bayet-Robert M, Kwiatkowski F, Leheurteur M, Gachon F, Planchat E, Abrial C, Mouret-Reynier MA, Durando X, Barthomeuf C, Chollet P: Phase I dose escalation trial of docetaxel plus curcumin in patients with advanced and metastatic breast cancer. Cancer Biol Ther; 2010 Jan;9(1):8-14
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  • [Title] Phase I dose escalation trial of docetaxel plus curcumin in patients with advanced and metastatic breast cancer.
  • Eight patients out of 14 had measurable lesions according to RECIST criteria, with five PR and three SD.
  • Some improvements as biological and clinical responses were observed in most patients.
  • PATIENTS AND METHODS: Patients with advanced or metastatic breast cancer were eligible.
  • The primary endpoint of this study was to determine the maximal tolerated dose of the combination of dose-escalating curcumin and standard dose of docetaxel chemotherapy in advanced and metastatic breast cancer patients.
  • From the encouraging efficacy results, a comparative phase II trial of this regimen plus docetaxel versus docetaxel alone is ongoing in advanced and metastatic breast cancer patients.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Breast Neoplasms / drug therapy. Breast Neoplasms, Male / drug therapy. Carcinoma / drug therapy. Curcumin / administration & dosage
  • [MeSH-minor] Aged. Aged, 80 and over. Diarrhea / chemically induced. Dose-Response Relationship, Drug. Drug Administration Schedule. Feasibility Studies. Female. Follow-Up Studies. Humans. Leukopenia / chemically induced. Male. Maximum Tolerated Dose. Middle Aged. Neoplasm Metastasis / drug therapy. Neoplasm Metastasis / pathology. Neutropenia / chemically induced. Taxoids / administration & dosage. Time Factors. Treatment Outcome

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  • (PMID = 19901561.001).
  • [ISSN] 1555-8576
  • [Journal-full-title] Cancer biology & therapy
  • [ISO-abbreviation] Cancer Biol. Ther.
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase I; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Taxoids; 15H5577CQD / docetaxel; IT942ZTH98 / Curcumin
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53. Lissoni P, Messina G, Vaghi M, Bartolacelli E, Massarenti LL, Trabattoni P, Meregalli P, Meregalli M, Gavazzeni C, Rovelli F, Tancini G, Gardani GS: A psychoneuroendocrine study of brain dopaminergic sensitivity in locally limited or metastatic cancer patients. In Vivo; 2003 Nov-Dec;17(6):647-50
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  • [Title] A psychoneuroendocrine study of brain dopaminergic sensitivity in locally limited or metastatic cancer patients.
  • In addition to the occurrence of pain, the evidence of a diminished capacity to feel pleasure is one of the most common cancer-related symptoms.
  • Moreover, it has also been demonstrated that the brain dopaminergic sensitivity may be clinically explored by evaluating the endocrine response to the administration of dopaminergic agents, such as apomorphine, which consists of a decline in PRL concentrations and an increase in GH and cortisol levels.
  • The present study was performed to evaluate dopaminergic sensitivity by the administration of apomorphine in cancer patients in an attempt to document possible cancer-related neuroendocrine anomalies, which could explain the psychological status of the patients.
  • The study included 24 cancer patients (breast cancer: 12; colorectal cancer: 7; non-small cell lung cancer: 5), 12 of whom showed distant organ metastases.
  • A normal decline in PRL levels was seen in both non-metastatic and metastatic cancer patients.
  • No GH rise occurred in either metastatic or non-metastatic cancer patients.
  • Therefore, the psychological condition of cancer patients would not depend only on psychological factors, but it could be due at least in part to cancer-related neuroendocrine alterations involving the dopaminergic system.
  • [MeSH-major] Brain Chemistry / physiology. Breast Neoplasms / physiopathology. Breast Neoplasms / psychology. Colorectal Neoplasms / physiopathology. Colorectal Neoplasms / psychology. Dopamine / physiology
  • [MeSH-minor] Adult. Aged. Carcinoma, Non-Small-Cell Lung / physiopathology. Carcinoma, Non-Small-Cell Lung / psychology. Carcinoma, Non-Small-Cell Lung / secondary. Female. Happiness. Human Growth Hormone / blood. Humans. Hydrocortisone / blood. Lung Neoplasms / physiopathology. Lung Neoplasms / psychology. Lung Neoplasms / secondary. Male. Middle Aged. Perception. Prolactin / blood


54. Tassi R, Muto A, Rangan S, Vannini A, Politi L, Neri B: Response and safety of sunitinib in a heavily pre-treated metastatic non-small cell lung carcinoma patient. Anticancer Res; 2010 Dec;30(12):5169-73
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  • [Title] Response and safety of sunitinib in a heavily pre-treated metastatic non-small cell lung carcinoma patient.
  • BACKGROUND: The activity of sunitinib, a multitargeted tyrosine kinase inhibitor with antiangiogenic and antitumor activities, has been explored in several solid malignancies such as breast, lung, prostate and pancreatic cancer.
  • Currently it is approved for the treatment of metastatic renal cell carcinoma and gastrointestinal stromal tumors.
  • Non-small cell lung cancer usually presents at an advanced or metastatic stage at diagnosis.
  • CASE REPORT: We describe the case of a patient (male, 67 years old) with heavily pre-treated metastatic non-small cell lung carcinoma who received sunitinib according to the following 3-week schedule: 50 mg daily for 2 weeks followed by a 1-week rest.
  • CONCLUSION: In this case, sunitinib shows promising single-agent activity in pretreated non-small cell lung cancer, with a good toxicity profile and flexible administration schedule.
  • [MeSH-major] Antineoplastic Agents / administration & dosage. Carcinoma, Non-Small-Cell Lung / drug therapy. Indoles / administration & dosage. Lung Neoplasms / drug therapy. Pyrroles / administration & dosage
  • [MeSH-minor] Aged. Drug Administration Schedule. Humans. Male

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  • (PMID = 21187507.001).
  • [ISSN] 1791-7530
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Indoles; 0 / Pyrroles; 0 / sunitinib
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55. Edovitsky E, Elkin M, Zcharia E, Peretz T, Vlodavsky I: Heparanase gene silencing, tumor invasiveness, angiogenesis, and metastasis. J Natl Cancer Inst; 2004 Aug 18;96(16):1219-30
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  • Expression of the heparanase gene is associated with the invasive, angiogenic, and metastatic potential of diverse malignant tumors and cell lines.
  • Human breast carcinoma (MDA-MB-435) and mouse lymphoma (Eb) and melanoma (B16-BL6) tumor cell lines, which have naturally high levels of endogenous heparanase or have been genetically engineered to overexpress heparanase, were transfected with anti-heparanase ribozyme or siRNA.
  • RESULTS: Compared with cells transfected with control constructs, cells transfected with the anti-heparanase ribozyme or siRNA vectors had profoundly reduced invasion and adhesion in vitro, regardless of cell type, and expressed less heparanase.
  • CONCLUSIONS: The association of reduced levels of heparanase and altered tumorigenic properties in cells with anti-heparanase ribozyme- or siRNA-mediated gene-silencing vectors suggests that heparanase is important in cancer progression.
  • Heparanase gene silencing has potential use as a target for anticancer drug development.
  • [MeSH-major] Angiogenesis Inhibitors / pharmacology. Enzyme Inhibitors / pharmacology. Gene Silencing. Glucuronidase / antagonists & inhibitors. Glucuronidase / genetics. Neoplasm Invasiveness. Neoplasm Metastasis. Neovascularization, Pathologic. RNA, Catalytic / pharmacology. RNA, Small Interfering
  • [MeSH-minor] Angiogenesis Inducing Agents / metabolism. Animals. Basement Membrane / enzymology. Basement Membrane / pathology. Disease Progression. Gene Expression Regulation, Enzymologic. Gene Expression Regulation, Neoplastic. Genetic Vectors. Growth Substances / metabolism. Heparitin Sulfate / metabolism. Humans. Immunohistochemistry. Lung Neoplasms / enzymology. Lung Neoplasms / genetics. Lung Neoplasms / secondary. Male. Melanoma, Experimental / enzymology. Melanoma, Experimental / genetics. Mice. Mice, Inbred C57BL. Plasmids. RNA, Neoplasm / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Transfection

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  • [CommentIn] J Natl Cancer Inst. 2004 Aug 18;96(16):1194-5 [15316047.001]
  • (PMID = 15316057.001).
  • [ISSN] 1460-2105
  • [Journal-full-title] Journal of the National Cancer Institute
  • [ISO-abbreviation] J. Natl. Cancer Inst.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01-CA106456-01
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Angiogenesis Inducing Agents; 0 / Angiogenesis Inhibitors; 0 / Enzyme Inhibitors; 0 / Growth Substances; 0 / RNA, Catalytic; 0 / RNA, Neoplasm; 0 / RNA, Small Interfering; 9050-30-0 / Heparitin Sulfate; EC 3.2.1.- / heparanase; EC 3.2.1.31 / Glucuronidase
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56. de la Haba Rodríguez JR, Porras Quintela I, Pulido Cortijo G, Berciano Guerrero M, Aranda E: Fulvestrant in advanced male breast cancer. Ann Oncol; 2009 Nov;20(11):1896-7
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  • [Title] Fulvestrant in advanced male breast cancer.


57. Lee MG, Kim HY, Byun DS, Lee SJ, Lee CH, Kim JI, Chang SG, Chi SG: Frequent epigenetic inactivation of RASSF1A in human bladder carcinoma. Cancer Res; 2001 Sep 15;61(18):6688-92
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  • [Title] Frequent epigenetic inactivation of RASSF1A in human bladder carcinoma.
  • Allelic deletion or transcriptional silencing of RASSF1, a putative tumor suppressor at 3p21.3, has been found in a considerable proportion of lung, breast, and ovarian cancers.
  • In this study, we analyzed the expression and mutation status of three RASSF1 isoforms (-A, -B, and -C) in 55 primary bladder carcinomas and 10 bladder and prostate cancer cell lines.
  • Expression of RASSF1A and RASSF1B was reactivated in all nonexpressor cell lines by treatment with the demethylating agent 5-aza-2'-deoxycytidine.
  • Together, our data suggest that RASSF1A inactivation may play a critical role in the malignant progression of human bladder carcinomas.
  • [MeSH-major] Gene Silencing. Neoplasm Proteins / genetics. Tumor Suppressor Proteins. Urinary Bladder Neoplasms / genetics
  • [MeSH-minor] Adult. Base Sequence. Chromosomes, Human, Pair 3. CpG Islands / genetics. DNA Methylation. Down-Regulation. Female. Gene Expression Regulation, Neoplastic. Genes, Tumor Suppressor / genetics. Humans. Loss of Heterozygosity. Male. Middle Aged. Molecular Sequence Data. Promoter Regions, Genetic. RNA, Messenger / biosynthesis. RNA, Messenger / genetics. Tumor Cells, Cultured

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  • (PMID = 11559536.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Neoplasm Proteins; 0 / RASSF1 protein, human; 0 / RNA, Messenger; 0 / Tumor Suppressor Proteins
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58. Pawlicki M, Rolski J, Zaluski J, Siedlecki P, Ramlau C, Tomzak P: A phase II study of intravenous navelbine and doxorubicin combination in previously untreated advanced breast carcinoma. Oncologist; 2002;7(3):205-9
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  • [Title] A phase II study of intravenous navelbine and doxorubicin combination in previously untreated advanced breast carcinoma.
  • PURPOSE: The combination of vinorelbine and doxorubicin, two very active drugs in metastatic breast cancer, has demonstrated impressive results in terms of efficacy, at the price of cardiac toxicity (10% grades 2-4) due to the cumulative dose of doxorubicin delivered.
  • PATIENTS AND METHODS: Thirty-eight chemotherapy-naïve metastatic breast cancer patients entered into the study and were treated with vinorelbine, 25 mg/m(2), and doxorubicin, 25 mg/m(2), both on days 1 and 8, every 3 weeks.
  • RESULTS: Patients received a median of seven cycles and 94.9% of the intended dose intensity of both drugs.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Breast Neoplasms / drug therapy. Breast Neoplasms, Male / drug therapy. Carcinoma / drug therapy. Vinblastine / analogs & derivatives
  • [MeSH-minor] Adult. Aged. Alopecia / chemically induced. Doxorubicin / administration & dosage. Doxorubicin / adverse effects. Drug Administration Schedule. Female. Humans. Infusions, Intravenous. Male. Middle Aged. Nausea / chemically induced. Neoplasm Metastasis. Neutropenia / chemically induced. Survival Analysis. Treatment Outcome. Vomiting / chemically induced

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  • (PMID = 12065792.001).
  • [ISSN] 1083-7159
  • [Journal-full-title] The oncologist
  • [ISO-abbreviation] Oncologist
  • [Language] eng
  • [Publication-type] Clinical Trial; Clinical Trial, Phase II; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 5V9KLZ54CY / Vinblastine; 80168379AG / Doxorubicin; Q6C979R91Y / vinorelbine
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59. Korman DB, Mikaélian SG, Boronovskaia LE, Maslova IA: [Results of a phase I-II clinical trial of Emoxyl, a novel antineoplastic anthracycline]. Vopr Onkol; 2004;50(2):202-7
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  • Emoxyl (ruboxyl) is a product of chemical modification of daunorubicin mediated by a stable free radical.
  • The drug was given to 63 patients with different malignancies stages I-II.
  • Out of 55 cases evaluated for immediate effect, complete remission (breast cancer, small-cell cancer of the lung, Kaposi's sarcoma)--3; partial remission (breast cancer--2; non-Hodgkin's lymphoma--1)--3, and stabilization--26.
  • [MeSH-major] Anthracyclines / therapeutic use. Antibiotics, Antineoplastic / therapeutic use. Daunorubicin / analogs & derivatives. Daunorubicin / therapeutic use. Neoplasms / drug therapy
  • [MeSH-minor] Aged. Breast Neoplasms / drug therapy. Carcinoma, Small Cell / drug therapy. Drug Administration Schedule. Female. Humans. Lung Neoplasms / drug therapy. Lymphoma, Non-Hodgkin / drug therapy. Male. Middle Aged. Sarcoma, Kaposi / drug therapy. Treatment Outcome

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  • (PMID = 15176224.001).
  • [ISSN] 0507-3758
  • [Journal-full-title] Voprosy onkologii
  • [ISO-abbreviation] Vopr Onkol
  • [Language] rus
  • [Publication-type] Clinical Trial; Clinical Trial, Phase I; Clinical Trial, Phase II; English Abstract; Journal Article
  • [Publication-country] Russia
  • [Chemical-registry-number] 0 / Anthracyclines; 0 / Antibiotics, Antineoplastic; 84412-94-2 / Emoxyl; ZS7284E0ZP / Daunorubicin
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60. Li YC, Park MJ, Ye SK, Kim CW, Kim YN: Elevated levels of cholesterol-rich lipid rafts in cancer cells are correlated with apoptosis sensitivity induced by cholesterol-depleting agents. Am J Pathol; 2006 Apr;168(4):1107-18; quiz 1404-5
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  • [Title] Elevated levels of cholesterol-rich lipid rafts in cancer cells are correlated with apoptosis sensitivity induced by cholesterol-depleting agents.
  • To better understand the role of rafts in tumor progression and therapeutics, we investigated the effect of raft disruption on cell viability and compared raft levels in human cancer cell lines versus their normal counterparts.
  • Moreover, the breast cancer and the prostate cancer cell lines contained more lipid rafts and were more sensitive to cholesterol depletion-induced cell death than their normal counterparts.
  • These results indicate that cancer cells contain increased levels of rafts and suggest a potential use of raft-modulating agents as anti-cancer drugs.
  • [MeSH-minor] Breast Neoplasms. Carcinoma, Squamous Cell. Caspase 3. Caspases / metabolism. Cell Line, Tumor. Cell Survival. Down-Regulation. Enzyme Activation. Female. Humans. Hydroxymethylglutaryl-CoA Reductase Inhibitors / pharmacology. Male. Prostatic Neoplasms. Proto-Oncogene Proteins c-akt / metabolism. Receptor, Epidermal Growth Factor / metabolism. Signal Transduction. Simvastatin / pharmacology. bcl-X Protein / metabolism

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  • (PMID = 16565487.001).
  • [ISSN] 0002-9440
  • [Journal-full-title] The American journal of pathology
  • [ISO-abbreviation] Am. J. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Hydroxymethylglutaryl-CoA Reductase Inhibitors; 0 / bcl-X Protein; 0 / beta-Cyclodextrins; 0 / methyl-beta-cyclodextrin; 97C5T2UQ7J / Cholesterol; AGG2FN16EV / Simvastatin; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 3.4.22.- / CASP3 protein, human; EC 3.4.22.- / Caspase 3; EC 3.4.22.- / Caspases
  • [Other-IDs] NLM/ PMC1606567
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61. Musch E, Gremmler B, Nitsch J, Rieger J, Malek M, Chrissafidou A: Intrapericardial instillation of mitoxantrone in palliative therapy of malignant pericardial effusion. Onkologie; 2003 Apr;26(2):135-9
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  • [Title] Intrapericardial instillation of mitoxantrone in palliative therapy of malignant pericardial effusion.
  • For long-term therapy success, the intrapericardial instillation of anti-neoplastic agents is an alternative to surgical methods, which are stressful for the patient.
  • Following our positive experiences with mitoxantrone in the treatment of malignant pleural effusions, we applied this substance for the therapy of malignant pericardial effusions.
  • PATIENTS AND METHODS: 16 patients with cytologically verified malignant pericardial effusions (8 with bronchial carcinoma, 7 with carcinoma of the breast, 1 with adenocarcinoma of the stomach) received an intrapericardial instillation of mitoxantrone 1-3 x10-20 mg.
  • 3 patients showed a partial remission (recurrence of non-drainage-dependent effusion) (CR + PR = 94%).
  • CONCLUSION: Intrapericardial instillation of mitoxantrone is a feasible and effective palliative method for the control of malignant pericardial effusions with little strain on the patients, short duration of hospital stay, cytotoxic characteristics of the substance with a correspondingly high rate of response and low side effects.
  • [MeSH-major] Antineoplastic Agents / administration & dosage. Breast Neoplasms / drug therapy. Heart Neoplasms / secondary. Mitoxantrone / administration & dosage. Palliative Care. Pericardial Effusion / drug therapy
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Dose-Response Relationship, Drug. Drug Administration Schedule. Echocardiography. Feasibility Studies. Female. Follow-Up Studies. Humans. Instillation, Drug. Lung Neoplasms / diagnostic imaging. Lung Neoplasms / drug therapy. Male. Middle Aged. Pericardium / drug effects. Stomach Neoplasms / diagnostic imaging. Stomach Neoplasms / drug therapy. Treatment Outcome

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  • [Copyright] Copyright 2003 S. Karger GmbH, Freiburg
  • (PMID = 12771521.001).
  • [ISSN] 0378-584X
  • [Journal-full-title] Onkologie
  • [ISO-abbreviation] Onkologie
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Antineoplastic Agents; BZ114NVM5P / Mitoxantrone
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62. Moreira JN, Santos A, Simões S: Bcl-2-targeted antisense therapy (Oblimersen sodium): towards clinical reality. Rev Recent Clin Trials; 2006 Sep;1(3):217-35
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  • The identification of activated oncogenes, such as the bcl-2, in several types of cancer has made it possible to consider such genes as targets for antitumor therapy.
  • Bcl-2 is an anti-apoptotic protein, whose overexpression is associated with chemotherapy resistant cancer, aggressive clinical course and poor survival.
  • The development of novel targeted gene-silencing strategies, such as those based on the use of antisense oligonucleotides, represents a renewed hope in the treatment of cancer.
  • Randomized phase III trials are currently underway to evaluate whether the combined use of Oblimersen with standard treatment is superior to standard treatment alone in chronic lymphocytic leukaemia, malignant melanoma and multiple myeloma.
  • [MeSH-minor] Breast Neoplasms. Carcinoma, Small Cell / drug therapy. Clinical Trials as Topic. Colorectal Neoplasms / secondary. Down-Regulation / drug effects. Drug Therapy, Combination. Female. Humans. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy. Leukemia, Myeloid, Acute / drug therapy. Lymphoma, Non-Hodgkin / drug therapy. Male. Melanoma / drug therapy. Prostatic Neoplasms / drug therapy. Proto-Oncogene Proteins c-bcl-2 / metabolism

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  • (PMID = 18473975.001).
  • [ISSN] 1574-8871
  • [Journal-full-title] Reviews on recent clinical trials
  • [ISO-abbreviation] Rev Recent Clin Trials
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United Arab Emirates
  • [Chemical-registry-number] 0 / Oligonucleotides, Antisense; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Thionucleotides; 85J5ZP6YSL / oblimersen
  • [Number-of-references] 86
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63. Tatchum-Talom R, Martel C, Labrie F, Marette A: Acute vascular effects of the selective estrogen receptor modulator EM-652 (SCH 57068) in the rat mesenteric vascular bed. Cardiovasc Res; 2003 Feb;57(2):535-43
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  • SERMs exert beneficial effects on bone and lipids but are not associated with an increased risk of breast or uterine carcinoma.
  • RESULTS: EM-652 and E2 relaxed MVBs removed from intact and gonadectomized female and male rats.
  • [MeSH-major] Piperidines / pharmacology. Selective Estrogen Receptor Modulators / pharmacology. Splanchnic Circulation / drug effects. Vasodilator Agents / pharmacology
  • [MeSH-minor] Animals. Cyclic GMP / physiology. Dose-Response Relationship, Drug. Endothelium, Vascular / drug effects. Endothelium, Vascular / physiology. Estradiol / pharmacology. Female. Male. Methoxamine / pharmacology. Nitric Oxide / physiology. Potassium Channels / physiology. Rats. Reactive Oxygen Species / metabolism. Receptors, Estrogen / physiology. Vasoconstriction / drug effects. Vasoconstrictor Agents / pharmacology

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  • (PMID = 12566126.001).
  • [ISSN] 0008-6363
  • [Journal-full-title] Cardiovascular research
  • [ISO-abbreviation] Cardiovasc. Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Piperidines; 0 / Potassium Channels; 0 / Reactive Oxygen Species; 0 / Receptors, Estrogen; 0 / Selective Estrogen Receptor Modulators; 0 / Vasoconstrictor Agents; 0 / Vasodilator Agents; 31C4KY9ESH / Nitric Oxide; 37607-02-6 / ritetronium; 4TI98Z838E / Estradiol; H2D2X058MU / Cyclic GMP; HUQ1KC1YLI / Methoxamine
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64. Eisen TG: Thalidomide in solid tumors: the London experience. Oncology (Williston Park); 2000 Dec;14(12 Suppl 13):17-20
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  • In the phase II low-dose study, responses were disappointing in patients with melanoma, ovarian cancer, and breast cancer.
  • Results for patients with renal-cell carcinoma were more encouraging.
  • A case study of a patient with metastatic renal-cell carcinoma in the lung and lymph nodes in the low-dose thalidomide study illustrates that (1) responses may be very slow;.
  • [MeSH-minor] Adult. Breast Neoplasms / drug therapy. Carcinoma, Renal Cell / drug therapy. Clinical Trials, Phase II as Topic. Female. Humans. Kidney Neoplasms / drug therapy. Male. Melanoma / drug therapy. Middle Aged. Models, Biological. Ovarian Neoplasms / drug therapy

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  • (PMID = 11204668.001).
  • [ISSN] 0890-9091
  • [Journal-full-title] Oncology (Williston Park, N.Y.)
  • [ISO-abbreviation] Oncology (Williston Park, N.Y.)
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 4Z8R6ORS6L / Thalidomide
  • [Number-of-references] 12
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65. Malingré MM, Beijnen JH, Rosing H, Koopman FJ, van Tellingen O, Duchin K, ten Bokkel Huinink WW, Swart M, Lieverst J, Schellens JH: The effect of different doses of cyclosporin A on the systemic exposure of orally administered paclitaxel. Anticancer Drugs; 2001 Apr;12(4):351-8
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  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / pharmacokinetics. Cyclosporine / administration & dosage. Neoplasms / drug therapy. Paclitaxel / administration & dosage
  • [MeSH-minor] Adenocarcinoma / drug therapy. Administration, Oral. Adult. Aged. Area Under Curve. Breast Neoplasms / drug therapy. Carcinoma, Small Cell / drug therapy. Dose-Response Relationship, Drug. Drug Administration Schedule. Female. Gastrointestinal Diseases / chemically induced. Hematologic Diseases / chemically induced. Humans. Infusions, Intravenous. Lung Neoplasms / drug therapy. Male. Middle Aged. Premedication. Stomach Neoplasms / drug therapy. Uterine Cervical Neoplasms / drug therapy. Uterine Neoplasms / drug therapy

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  • (PMID = 11335792.001).
  • [ISSN] 0959-4973
  • [Journal-full-title] Anti-cancer drugs
  • [ISO-abbreviation] Anticancer Drugs
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 83HN0GTJ6D / Cyclosporine; P88XT4IS4D / Paclitaxel
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66. Subramaniam M, Hawse JR, Rajamannan NM, Ingle JN, Spelsberg TC: Functional role of KLF10 in multiple disease processes. Biofactors; 2010 Jan-Feb;36(1):8-18
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  • Overall, KLF10 has been implicated in cell differentiation, as a target gene for a variety of signaling pathways, and in serving as a potential marker for human diseases such as breast cancer, cardiac hypertrophy, and osteoporosis.
  • Overall, KLF10 has been shown to play a major role in the TGFbeta inhibition of cell proliferation and inflammation and induction of apoptosis, and its overexpression in human osteoblasts and pancreatic carcinoma cells mimics the actions of TGFbeta.

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  • (PMID = 20087894.001).
  • [ISSN] 1872-8081
  • [Journal-full-title] BioFactors (Oxford, England)
  • [ISO-abbreviation] Biofactors
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / R01 HL085591-03; United States / NIDCR NIH HHS / DE / R01 DE014036-09; United States / NHLBI NIH HHS / HL / R01 HL085591-02S1; United States / NIDCR NIH HHS / DE / R01 DE-14036; United States / NHLBI NIH HHS / HL / R01 HL085591-04; United States / NHLBI NIH HHS / HL / R01 HL085591; United States / NHLBI NIH HHS / HL / R01 HL085591-02; United States / NIAMS NIH HHS / AR / AR52004; United States / NIDCR NIH HHS / DE / R01 DE014036; United States / NHLBI NIH HHS / HL / R01 HL085591-01A1; United States / NIAMS NIH HHS / AR / R01 AR052004
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Early Growth Response Transcription Factors; 0 / KLF10 protein, human; 0 / Kruppel-Like Transcription Factors; 0 / Smad Proteins; 0 / Transforming Growth Factor beta
  • [Number-of-references] 78
  • [Other-IDs] NLM/ NIHMS294484; NLM/ PMC3104724
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67. Otten HM, Prins MH, Smorenburg SM, Hutten BA: Risk assessment and prophylaxis of venous thromboembolism in non-surgical patients: cancer as a risk factor. Haemostasis; 2000;30 Suppl 2:72-6; discussion 63
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  • [Title] Risk assessment and prophylaxis of venous thromboembolism in non-surgical patients: cancer as a risk factor.
  • It is well documented that cancer patients undergoing surgery are at a sufficiently high risk of developing venous thromboembolism (VTE) to justify the routine use of prophylactic anticoagulant therapy.
  • However, despite many studies showing an increased incidence of VTE associated with the use of chemotherapy in patients with breast carcinoma and with the use of indwelling venous access catheters in patients with various kinds of cancer, thromboprophylactic strategies are not yet widely used.
  • [MeSH-minor] Antineoplastic Agents / adverse effects. Antineoplastic Agents, Hormonal / adverse effects. Brain Neoplasms / complications. Brain Neoplasms / drug therapy. Brain Neoplasms / surgery. Breast Neoplasms / complications. Breast Neoplasms / drug therapy. Catheterization, Central Venous / adverse effects. Combined Modality Therapy. Female. Glioma / complications. Glioma / drug therapy. Glioma / surgery. Humans. Incidence. Lymphoma / complications. Lymphoma / drug therapy. Male. Prospective Studies. Risk Assessment

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  • [Copyright] Copyright 2001 S. Karger AG, Basel
  • (PMID = 11251345.001).
  • [ISSN] 0301-0147
  • [Journal-full-title] Haemostasis
  • [ISO-abbreviation] Haemostasis
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Antineoplastic Agents, Hormonal
  • [Number-of-references] 37
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68. Engebraaten O, Sivam G, Juell S, Fodstad O: Systemic immunotoxin treatment inhibits formation of human breast cancer metastasis and tumor growth in nude rats. Int J Cancer; 2000 Dec 15;88(6):970-6
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  • [Title] Systemic immunotoxin treatment inhibits formation of human breast cancer metastasis and tumor growth in nude rats.
  • Adjuvant chemotherapy in breast cancer patients has had limited success, which is possibly because of lack of effect on non-proliferating cells accompanied by the emergence of drug-resistant cell clones.
  • Since immunotoxins (ITs) are known to exert proliferation-independent cytotoxicity, we investigated the efficacy of systemically administered anti-carcinoma ITs in nude rat models, simulating micrometastatic disease.
  • The monoclonal antibodies MOC31, BM7 and 425.3, which recognize epithelial glycoprotein 2, MUC-1 mucin and the epidermal growth factor receptor, chemically conjugated to Pseudomonas exotoxin A (PE), inhibited protein synthesis of the 2 breast cancer cell lines at concentrations of 0.3-0.4 ng/ml, except for BM7-PE, which was less efficacious (65 ng/ml).
  • In the MA-11 model in nude rats, a single i. v. dose of 20 microg MOC31-PE prevented development of metastasis in the spinal cord in 11/19 (58%) of the animals.
  • The results demonstrate that systemic short-term treatment with non-toxic doses of the 3 ITs tested can effectively inhibit the development of experimental breast cancer metastasis and/or local tumor growth in bone.
  • [MeSH-major] ADP Ribose Transferases. Antibodies, Monoclonal / therapeutic use. Bacterial Toxins. Breast Neoplasms / therapy. Exotoxins / therapeutic use. Immunotoxins / therapeutic use. Receptor, Epidermal Growth Factor / immunology. Virulence Factors
  • [MeSH-minor] Animals. Antineoplastic Agents / therapeutic use. Bone Neoplasms / prevention & control. Bone Neoplasms / secondary. Cisplatin / therapeutic use. Doxorubicin / therapeutic use. Female. Injections, Intravenous. Male. Rats. Rats, Nude. Specific Pathogen-Free Organisms. Spinal Neoplasms / prevention & control. Spinal Neoplasms / secondary. Tibia. Tumor Cells, Cultured

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  • [Copyright] Copyright 2000 Wiley-Liss, Inc.
  • (PMID = 11093823.001).
  • [ISSN] 0020-7136
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] UNITED STATES
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antineoplastic Agents; 0 / Bacterial Toxins; 0 / Exotoxins; 0 / Immunotoxins; 0 / Virulence Factors; 80168379AG / Doxorubicin; EC 2.4.2.- / ADP Ribose Transferases; EC 2.4.2.31 / toxA protein, Pseudomonas aeruginosa; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; Q20Q21Q62J / Cisplatin
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69. Valentini V, Massaccesi M, Balducci M, Mantini G, Micciché F, Mattiucci GC, Dinapoli N, Meduri B, D'Agostino GR, Salvi G, Nardone L: Low-dose hyperradiosensitivity: is there a place for future investigation in clinical settings? Int J Radiat Oncol Biol Phys; 2010 Feb 1;76(2):535-9
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  • RESULTS: Between June 2006 and October 2007, 12 patients with lung cancer, 7 patients with head-and-neck tumors, 2 patients with breast cancer, and 1 patient with esophageal carcinoma, for a total patient population of 22, underwent concomitant LD-FRT and chemotherapy.
  • All patients but 3 (86%) had received previous treatments for their cancer.
  • [MeSH-major] Neoplasms / drug therapy. Neoplasms / radiotherapy. Palliative Care / methods. Radiation Tolerance. Radiotherapy Dosage
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Antineoplastic Combined Chemotherapy Protocols / adverse effects. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Breast Neoplasms / drug therapy. Breast Neoplasms / radiotherapy. Capecitabine. Cisplatin / administration & dosage. Combined Modality Therapy / methods. Deoxycytidine / administration & dosage. Deoxycytidine / analogs & derivatives. Disease Progression. Esophageal Neoplasms / drug therapy. Esophageal Neoplasms / radiotherapy. Female. Fluorouracil / administration & dosage. Fluorouracil / analogs & derivatives. Follow-Up Studies. Glutamates / administration & dosage. Guanine / administration & dosage. Guanine / analogs & derivatives. Head and Neck Neoplasms / drug therapy. Head and Neck Neoplasms / radiotherapy. Humans. Lung Neoplasms / drug therapy. Lung Neoplasms / radiotherapy. Male. Middle Aged. Neoplasm Recurrence, Local / drug therapy. Neoplasm Recurrence, Local / radiotherapy. Pemetrexed. Prospective Studies. Young Adult

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  • [Copyright] Copyright 2010 Elsevier Inc. All rights reserved.
  • (PMID = 19540061.001).
  • [ISSN] 1879-355X
  • [Journal-full-title] International journal of radiation oncology, biology, physics
  • [ISO-abbreviation] Int. J. Radiat. Oncol. Biol. Phys.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Glutamates; 04Q9AIZ7NO / Pemetrexed; 0W860991D6 / Deoxycytidine; 5Z93L87A1R / Guanine; 6804DJ8Z9U / Capecitabine; Q20Q21Q62J / Cisplatin; U3P01618RT / Fluorouracil
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70. Wang YM, Huang GS, Hui YP, Zhang J: [Expression of breast cancer resistance protein in liver cirrhosis, hepatocellular carcinoma and peritumoral tissues]. Zhonghua Gan Zang Bing Za Zhi; 2009 Mar;17(3):227-9
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  • [Title] [Expression of breast cancer resistance protein in liver cirrhosis, hepatocellular carcinoma and peritumoral tissues].
  • [MeSH-major] ATP-Binding Cassette Transporters / metabolism. Carcinoma, Hepatocellular / metabolism. Liver / metabolism. Liver Cirrhosis / metabolism. Liver Neoplasms / metabolism. Neoplasm Proteins / metabolism. RNA, Messenger / metabolism
  • [MeSH-minor] ATP Binding Cassette Transporter, Sub-Family G, Member 2. Adult. Aged. Biomarkers, Tumor / metabolism. Drug Resistance, Multiple. Female. Humans. Immunohistochemistry. Male. Middle Aged. Neoplasm Staging. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 19335991.001).
  • [ISSN] 1007-3418
  • [Journal-full-title] Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology
  • [ISO-abbreviation] Zhonghua Gan Zang Bing Za Zhi
  • [Language] chi
  • [Publication-type] Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / ABCG2 protein, human; 0 / ATP Binding Cassette Transporter, Sub-Family G, Member 2; 0 / ATP-Binding Cassette Transporters; 0 / Biomarkers, Tumor; 0 / Neoplasm Proteins; 0 / RNA, Messenger
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71. Kim SW, Park SS, Ahn SJ, Chung KW, Moon WK, Im JG, Yeo JS, Chung JK, Noh DY: Identification of angiogenesis in primary breast carcinoma according to the image analysis. Breast Cancer Res Treat; 2002 Jul;74(2):121-9
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  • [Title] Identification of angiogenesis in primary breast carcinoma according to the image analysis.
  • Tumor angiogenesis may be an independent prognostic factor for breast cancer survival.
  • However, we can get the angiogenic property of the breast cancer only after the removal of breast tissue.
  • To get this information before surgical resection of the tumor, we evaluated 29 breast carcinoma patients with Tc-99m MIBI scintimammography and power Doppler ultrasound (US) with a microbubble contrast agent preoperatively and compare their results with intratumoral microvessel density (IMD) and reverse transcriptase-polymerase chain reaction (RT-PCR) of VEGF mRNA.
  • In conclusion, the preoperative evaluation of breast cancer with power Doppler US with a microbubble contrast agent could predict tumor angiogenesis.
  • [MeSH-major] Breast Neoplasms / blood supply. Breast Neoplasms / pathology. Neovascularization, Pathologic / radiography. Neovascularization, Pathologic / radionuclide imaging. Radiopharmaceuticals. Technetium Tc 99m Sestamibi
  • [MeSH-minor] Adult. Aged. Endothelial Growth Factors / analysis. Endothelial Growth Factors / biosynthesis. Female. Humans. Intercellular Signaling Peptides and Proteins / analysis. Intercellular Signaling Peptides and Proteins / biosynthesis. Lymphokines / analysis. Lymphokines / biosynthesis. Male. Mammography / methods. Middle Aged. Predictive Value of Tests. Prognosis. RNA, Messenger / analysis. Radionuclide Imaging. Reverse Transcriptase Polymerase Chain Reaction. Ultrasonography, Doppler. Vascular Endothelial Growth Factor A. Vascular Endothelial Growth Factors

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  • (PMID = 12186372.001).
  • [ISSN] 0167-6806
  • [Journal-full-title] Breast cancer research and treatment
  • [ISO-abbreviation] Breast Cancer Res. Treat.
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Endothelial Growth Factors; 0 / Intercellular Signaling Peptides and Proteins; 0 / Lymphokines; 0 / RNA, Messenger; 0 / Radiopharmaceuticals; 0 / VEGFA protein, human; 0 / Vascular Endothelial Growth Factor A; 0 / Vascular Endothelial Growth Factors; 971Z4W1S09 / Technetium Tc 99m Sestamibi
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72. Ishida T, Kiba T, Takeda M, Matsuyama K, Teramukai S, Ishiwata R, Masuda N, Takatsuka Y, Noguchi S, Ishioka C, Fukushima M, Ohuchi N: Phase II study of capecitabine and trastuzumab combination chemotherapy in patients with HER2 overexpressing metastatic breast cancers resistant to both anthracyclines and taxanes. Cancer Chemother Pharmacol; 2009 Jul;64(2):361-9
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  • [Title] Phase II study of capecitabine and trastuzumab combination chemotherapy in patients with HER2 overexpressing metastatic breast cancers resistant to both anthracyclines and taxanes.
  • PURPOSE: The purpose of this study was to investigate the activity of capecitabine and trastuzumab in patients with HER2-overexpressing metastatic breast cancer resistant to both anthracyclines and taxanes.
  • METHOD: From June 2003 and May 2006, 40 female patients with measurable or assessable metastatic breast cancer were enrolled and data from 38 patients were reviewed extramurally and analyzed.
  • All evaluable patients have responded with two CR (5.3%), 5 PR (13.2%), 20 SD (52.6%), 8 PD (21.1%) and 3 NE (7.9%).
  • CONCLUSION: The combination of capecitabine and trastuzumab is active and well-tolerated in patients with HER2-overexpressing breast caner resistant to both anthracyclines and taxanes.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Breast Neoplasms / drug therapy. Carcinoma, Ductal, Breast / drug therapy. Drug Resistance, Neoplasm. Receptor, ErbB-2 / metabolism. Salvage Therapy
  • [MeSH-minor] Adult. Aged. Anthracyclines / administration & dosage. Antibodies, Monoclonal / administration & dosage. Antibodies, Monoclonal, Humanized. Capecitabine. Deoxycytidine / administration & dosage. Deoxycytidine / analogs & derivatives. Female. Fluorouracil / administration & dosage. Fluorouracil / analogs & derivatives. Humans. Immunoenzyme Techniques. Lymphatic Metastasis. Male. Maximum Tolerated Dose. Middle Aged. Neoplasm Staging. Prognosis. Survival Rate. Taxoids / administration & dosage. Trastuzumab. Treatment Outcome. Young Adult

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  • (PMID = 19082596.001).
  • [ISSN] 1432-0843
  • [Journal-full-title] Cancer chemotherapy and pharmacology
  • [ISO-abbreviation] Cancer Chemother. Pharmacol.
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase II; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Anthracyclines; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Taxoids; 0W860991D6 / Deoxycytidine; 6804DJ8Z9U / Capecitabine; EC 2.7.10.1 / Receptor, ErbB-2; P188ANX8CK / Trastuzumab; U3P01618RT / Fluorouracil
  • [Other-IDs] NLM/ PMC2688618
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73. Trafalis DT, Geromichalos GD, Koukoulitsa C, Papageorgiou A, Karamanakos P, Camoutsis C: Lactandrate: a D-homo-aza-androsterone alkylator in the treatment of breast cancer. Breast Cancer Res Treat; 2006 May;97(1):17-31
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  • [Title] Lactandrate: a D-homo-aza-androsterone alkylator in the treatment of breast cancer.
  • The sensitivity of breast neoplasms to hormonal control provides the basis of novel investigational treatments with steroidal alkylators.
  • An androsterone D-lactam steroidal ester, the 3beta-hydroxy-13alpha-amino-13,17-seco- 5alpha-androstan-17-oic-13,17-lactam, p-bis(2-chloroethyl)amino phenyl acetate (lactandrate) was synthesized and tested for antitumor activity against six human breast cancer cell lines in vitro and against two murine and one xenograft mammary tumors in vivo.
  • In vitro testing of lactandrate cytostatic and cytotoxic activity was performed on T47D, MCF7, MDA-MB-231, BT-549, Hs578T, MDA-MB-435 breast adenocarcinoma human cell lines.
  • In vivo testing was performed on two murine mammary tumors, the MXT tumor and CD8F1 adenocarcinoma, as well as on human mammary carcinoma MX-1 xenograft.
  • Lactandrate produced important anticancer activity on breast cancer in vitro and in vivo.
  • [MeSH-major] Alkylating Agents / therapeutic use. Antineoplastic Agents / therapeutic use. Azasteroids / therapeutic use. Homosteroids / therapeutic use. Mammary Neoplasms, Experimental / drug therapy. Secosteroids / therapeutic use
  • [MeSH-minor] Adenocarcinoma / drug therapy. Androsterone / therapeutic use. Animals. Cell Proliferation / drug effects. Estrogen Receptor alpha / metabolism. Female. Humans. Male. Mice. Mice, Inbred C57BL. Mice, Inbred DBA. Molecular Structure. Tumor Cells, Cultured / drug effects

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  • (PMID = 16319980.001).
  • [ISSN] 0167-6806
  • [Journal-full-title] Breast cancer research and treatment
  • [ISO-abbreviation] Breast Cancer Res. Treat.
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / /
  • [Publication-type] Journal Article; Research Support, N.I.H., Intramural
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / 3-hydroxy-13-amino-13,17-secoandrostan-17-oic-13,17-lactam p-bis(2-chloroethyl)amino phenyl acetate; 0 / Alkylating Agents; 0 / Antineoplastic Agents; 0 / Azasteroids; 0 / Estrogen Receptor alpha; 0 / Homosteroids; 0 / Secosteroids; C24W7J5D5R / Androsterone
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74. Hollingshead M, Alley M, Burger AM, Borgel S, Pacula-Cox C, Fiebig HH, Sausville EA: In vivo antitumor efficacy of 17-DMAG (17-dimethylaminoethylamino-17-demethoxygeldanamycin hydrochloride), a water-soluble geldanamycin derivative. Cancer Chemother Pharmacol; 2005 Aug;56(2):115-25
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  • METHODS: In vitro proliferation assays, and in vivo model studies in metastatic pancreatic carcinoma and subcutaneous xenograft melanoma and small-cell lung carcinoma models.
  • RESULTS: 17-DMAG emerged from screening studies as a potent geldanamycin analog, with the average concentration inhibiting the growth of the NCI anticancer cell line drug screen by 50% being 0.053 microM.
  • "Head to head" comparison with 17-allylamino-17-demethoxygeldanamycin (17-AAG, NSC 330507) revealed 17-DMAG to possess potent activity against certain cell types, e.g., MDA-MB-231 breast carcinoma and HL60-TB leukemia which were relatively insensitive to 17-AAG.
  • 17-DMAG inhibited the growth of the AsPC-1 pancreatic carcinoma xenografts growing as intrahepatic metastases at doses of 6.7-10 mg/kg twice daily for 5 days administered orally under conditions where 17-AAG was without activity.
  • 17-DMAG in an aqueous vehicle at 7.5-15 mg/kg per day for 3 days on days 1-3, 8-10 and 13-17, or 1-5 and 8-12 showed evidence of antitumor activity by the parenteral and oral routes in the MEXF 276 and MEXF 989 melanomas and by the parenteral route in the LXFA 629 and LXFS 650 adenocarcinoma and small-cell carcinoma models.
  • [MeSH-major] Carcinoma, Non-Small-Cell Lung / pathology. Lung Neoplasms / pathology. Melanoma / pathology. Quinones / pharmacology. Skin Neoplasms / pathology
  • [MeSH-minor] Animals. Benzoquinones. Cell Proliferation. Drug Screening Assays, Antitumor. Lactams, Macrocyclic. Liver Neoplasms / drug therapy. Liver Neoplasms / secondary. Liver Neoplasms / veterinary. Male. Mice. Mice, Nude. Solubility. Transplantation, Heterologous. Tumor Cells, Cultured

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  • (PMID = 15791458.001).
  • [ISSN] 0344-5704
  • [Journal-full-title] Cancer chemotherapy and pharmacology
  • [ISO-abbreviation] Cancer Chemother. Pharmacol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CM / N01-CM-270; United States / NCI NIH HHS / CM / N01-CM-97017; United States / NCI NIH HHS / CO / N01-CO 12400
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Benzoquinones; 0 / Lactams, Macrocyclic; 0 / Quinones; 001L2FE0M3 / 17-(dimethylaminoethylamino)-17-demethoxygeldanamycin
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75. Politi PM: [Thalidomide. Clinical trials in cancer]. Medicina (B Aires); 2000;60 Suppl 2:61-5
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  • [Title] [Thalidomide. Clinical trials in cancer].
  • This drug also down-regulates TNF alpha.
  • Thalidomide has shown clinical antitumor activity in single-agent, phase II clinical trials in AIDS-related Kaposi sarcoma, glioma, multiple myeloma refractory to chemotherapy, and hormone-refractory prostate cancer.
  • In contrast, thalidomide was inactive in breast, lung and kidney cancer.
  • Other adverse effects include skin rash, constipation, dry mouth and liver function abnormalities, along with peripheral neuropathy and the drug's well-known teratogenic potential.
  • The advantages of thalidomide include the convenience of the oral route of administration, the drug's toxicity profile--substantially milder than that of chemotherapy--and its low cost.
  • [MeSH-major] Angiogenesis Inhibitors / therapeutic use. Neoplasms / drug therapy. Thalidomide / therapeutic use
  • [MeSH-minor] Carcinoma, Hepatocellular / drug therapy. Humans. Liver Neoplasms / drug therapy. Male. Multiple Myeloma / drug therapy. Prostatic Neoplasms / drug therapy. Sarcoma, Kaposi / drug therapy

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  • (PMID = 11188934.001).
  • [ISSN] 0025-7680
  • [Journal-full-title] Medicina
  • [ISO-abbreviation] Medicina (B Aires)
  • [Language] spa
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Argentina
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 4Z8R6ORS6L / Thalidomide
  • [Number-of-references] 10
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76. Dumont P, Ingrassia L, Rouzeau S, Ribaucour F, Thomas S, Roland I, Darro F, Lefranc F, Kiss R: The Amaryllidaceae isocarbostyril narciclasine induces apoptosis by activation of the death receptor and/or mitochondrial pathways in cancer cells but not in normal fibroblasts. Neoplasia; 2007 Sep;9(9):766-76
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  • [Title] The Amaryllidaceae isocarbostyril narciclasine induces apoptosis by activation of the death receptor and/or mitochondrial pathways in cancer cells but not in normal fibroblasts.
  • Our study has shown that the Amaryllidaceae isocarbostyril narciclasine induces marked apoptosis-mediated cytotoxic effects in human cancer cells but not in normal fibroblasts by triggering the activation of the initiator caspases of the death receptor pathway (caspase-8 and caspase-10) at least in human MCF-7 breast and PC-3 prostate carcinoma cells.
  • The formation of the Fas and death receptor 4 (DR4) death-inducing signaling complex was clearly evidenced in MCF-7 and PC-3 cancer cells.
  • It is postulated that the high selectivity of narciclasine to cancer cells might be linked, at least in part, to this activation of the death receptor pathway.
  • [MeSH-major] Amaryllidaceae Alkaloids / pharmacology. Antineoplastic Agents, Phytogenic / pharmacology. Apoptosis / drug effects. Breast Neoplasms / pathology. Carcinoma / pathology. Mitochondria / physiology. Phenanthridines / pharmacology. Prostatic Neoplasms / pathology. Receptors, Tumor Necrosis Factor / physiology
  • [MeSH-minor] Antigens, CD95 / drug effects. Antigens, CD95 / physiology. BH3 Interacting Domain Death Agonist Protein / physiology. Caspases / physiology. Cytochromes c / analysis. DNA Fragmentation. Drug Resistance, Neoplasm. Enzyme Activation / drug effects. Female. Fibroblasts / drug effects. Humans. Male. Narcissus / chemistry. Neoplasm Proteins / drug effects. Neoplasm Proteins / physiology. Receptors, TNF-Related Apoptosis-Inducing Ligand

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  • (PMID = 17898872.001).
  • [ISSN] 1476-5586
  • [Journal-full-title] Neoplasia (New York, N.Y.)
  • [ISO-abbreviation] Neoplasia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Canada
  • [Chemical-registry-number] 0 / Amaryllidaceae Alkaloids; 0 / Antigens, CD95; 0 / Antineoplastic Agents, Phytogenic; 0 / BH3 Interacting Domain Death Agonist Protein; 0 / BID protein, human; 0 / Neoplasm Proteins; 0 / Phenanthridines; 0 / Receptors, TNF-Related Apoptosis-Inducing Ligand; 0 / Receptors, Tumor Necrosis Factor; 0 / TNFRSF10A protein, human; 29477-83-6 / narciclasine; 9007-43-6 / Cytochromes c; EC 3.4.22.- / Caspases
  • [Other-IDs] NLM/ PMC1993861
  • [Keywords] NOTNLM ; Apoptosis / cancer cells / death receptor pathway / fibroblasts / narciclasine
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77. Pittock SJ, Lennon VA: Aquaporin-4 autoantibodies in a paraneoplastic context. Arch Neurol; 2008 May;65(5):629-32
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  • Its antigen is the astrocytic water channel aquaporin-4; NMO-IgG has not been described in a cancer context.
  • OBJECTIVES: To report (1) neurologic and oncologic correlates for patients incidentally identified as NMO-IgG seropositive in a blinded evaluation for paraneoplastic autoantibodies and (2) the frequency of cancer in NMO-IgG-seropositive patients.
  • SETTING: Neuroimmunology Laboratory and Neurology Clinical Practice, Mayo Clinic College of Medicine.
  • (1) 31 patients (88% female) identified incidentally among 180 000 patients evaluated for paraneoplastic autoantibodies and (2) 141 patients identified through physician-requested serological evaluation for a suspected NMO-spectrum disorder.
  • An NMO-spectrum disorder was diagnosed in 26 patients (93%), of whom 6 had a neoplasm (5 carcinomas [2 breast, 1 lung, 1 thymic, and 1 uterine cervical] and 1 B-cell lymphoma) and 1 had monoclonal gammopathy.
  • Two patients had carcinoma (1 breast and 1 lung) without neurological evidence of an NMO-spectrum disorder.
  • In the second group, neoplasms were recorded in 7 seropositive patients (5.0%) with a clinically diagnosed NMO-spectrum disorder: 3 carcinomas (all breast), 1 thyroid Hürthle cell, 1 carcinoid, 1 pituitary somatotropinoma, and 1 B-cell lymphoma.
  • The clinical utility of this autoantibody as a cancer marker warrants prospective investigation.
  • [MeSH-minor] Adolescent. Adult. Aged. Biomarkers / analysis. Comorbidity. Female. Humans. Immunoglobulin G / blood. Immunoglobulin G / immunology. Male. Middle Aged. Neuromyelitis Optica / immunology. Paraproteinemias / epidemiology. Paraproteinemias / immunology. Paraproteinemias / physiopathology. Predictive Value of Tests. Retrospective Studies

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  • [ErratumIn] Arch Neurol. 2008 Oct;65(10):1394
  • (PMID = 18474738.001).
  • [ISSN] 1538-3687
  • [Journal-full-title] Archives of neurology
  • [ISO-abbreviation] Arch. Neurol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Aquaporin 4; 0 / Autoantibodies; 0 / Biomarkers; 0 / Immunoglobulin G
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78. Ross JS, Gray GS: Targeted therapy for cancer: the HER-2/neu and Herceptin story. Clin Leadersh Manag Rev; 2003 Nov-Dec;17(6):333-40
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  • [Title] Targeted therapy for cancer: the HER-2/neu and Herceptin story.
  • In this article, the association of HER-2/neu gene and protein abnormalities with prognosis and response to therapy with Herceptin and other therapies in breast cancer is presented.
  • The significance of HER-2/neu overexpression in ductal carcinoma in situ and the HER-2/neu status in uncommon female breast conditions and male breast cancer also are considered.
  • The role of HER-2/neu testing for the prediction of response to Herceptin therapy in breast cancer is presented as well as its potential impact on responses to standard and newer hormonal therapies, cytotoxic chemotherapy, and radiation.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Antineoplastic Agents / therapeutic use. Breast Neoplasms / drug therapy. Breast Neoplasms / genetics. Genes, erbB-2 / genetics. Receptor, ErbB-2 / analysis
  • [MeSH-minor] Antibodies, Monoclonal, Humanized. Biomarkers, Tumor. Combined Modality Therapy. Drug Delivery Systems. Female. Gene Expression Regulation, Neoplastic. Humans. Immunohistochemistry. Trastuzumab

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  • (PMID = 14692077.001).
  • [ISSN] 1527-3954
  • [Journal-full-title] Clinical leadership & management review : the journal of CLMA
  • [ISO-abbreviation] Clin Leadersh Manag Rev
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antineoplastic Agents; 0 / Biomarkers, Tumor; EC 2.7.10.1 / Receptor, ErbB-2; P188ANX8CK / Trastuzumab
  • [Number-of-references] 70
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79. Friboulet L, Gourzones C, Tsao SW, Morel Y, Paturel C, Témam S, Uzan C, Busson P: Poly(I:C) induces intense expression of c-IAP2 and cooperates with an IAP inhibitor in induction of apoptosis in cancer cells. BMC Cancer; 2010;10:327
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  • [Title] Poly(I:C) induces intense expression of c-IAP2 and cooperates with an IAP inhibitor in induction of apoptosis in cancer cells.
  • BACKGROUND: There is increasing evidence that the toll-like receptor 3 (TLR3) is an interesting target for anti-cancer therapy.
  • Unfortunately, most laboratory investigations about the impact of TLR3 stimulation on human malignant cells have been performed with very high concentrations--5 to 100 microg/ml--of the prototype TLR3 ligand, poly(I:C).
  • In a previous study focused on a specific type of human carcinoma - nasopharyngeal carcinoma - we have shown that concentrations of poly(I:C) as low as 100 ng/ml are sufficient to induce apoptosis of malignant cells when combined to a pharmacological antagonist of the IAP family based on Smac mimicry.
  • METHODS: This observation prompted us to investigate the contribution of the IAP family in cell response to poly(I:C) in a variety of human malignant cell types.
  • RESULTS: We report a rapid, intense and selective increase in c-IAP2 protein expression observed under stimulation by poly(I:C)(500 ng/ml) in all types of human malignant cells.
  • When poly(I:C) is combined to the IAP inhibitor RMT 5265, a cooperative effect in apoptosis induction and/or inhibition of clonogenic growth is obtained in a large fraction of carcinoma and melanoma cell lines.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / pharmacology. Apoptosis / drug effects. Inhibitor of Apoptosis Proteins / antagonists & inhibitors. Neoplasms / pathology
  • [MeSH-minor] Adaptor Proteins, Vesicular Transport / metabolism. Adult. Cell Line, Tumor. Cell Proliferation / drug effects. Dose-Response Relationship, Drug. Female. Gene Expression Regulation, Neoplastic. Humans. Male. Middle Aged. Poly I-C / pharmacology. RNA Interference. RNA, Messenger / metabolism. Time Factors. Toll-Like Receptor 3 / agonists. Toll-Like Receptor 3 / metabolism. Tumor Cells, Cultured. Ubiquitin-Protein Ligases. Up-Regulation

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  • (PMID = 20576118.001).
  • [ISSN] 1471-2407
  • [Journal-full-title] BMC cancer
  • [ISO-abbreviation] BMC Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Adaptor Proteins, Vesicular Transport; 0 / BIRC3 protein, human; 0 / Inhibitor of Apoptosis Proteins; 0 / RNA, Messenger; 0 / TICAM1 protein, human; 0 / TLR3 protein, human; 0 / Toll-Like Receptor 3; 24939-03-5 / Poly I-C; EC 6.3.2.19 / Ubiquitin-Protein Ligases
  • [Other-IDs] NLM/ PMC2928000
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80. Crawshaw A: Carcinoma of the breast and hormone replacement therapy for osteoporosis. Int J Clin Pract; 2000 Mar;54(2):99-103
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  • [Title] Carcinoma of the breast and hormone replacement therapy for osteoporosis.
  • It is still not clear whether oestrogen replacement therapy can be given safely to women with breast cancer.
  • The incidence and survival of breast cancer is rising in the UK and increasing numbers of young women with breast cancer treated systemically experience an early menopause and are at prolonged risk of osteoporosis.
  • This review discusses the risk/benefit analysis of oestrogen replacement therapy for breast cancer patients, and alternative therapies: SERMs, phyto-oestrogens and bisphosphonates.
  • A schedule for monitoring osteoporosis for breast cancer patients with a therapeutic early menopause is suggested.
  • [MeSH-major] Breast Neoplasms. Carcinoma / drug therapy. Estrogen Replacement Therapy. Osteoporosis / prevention & control
  • [MeSH-minor] Adult. Aged. Algorithms. Female. Great Britain. Humans. Incidence. Menopause / drug effects. Middle Aged. Risk Assessment. Selective Estrogen Receptor Modulators / therapeutic use. Survival Rate

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  • (PMID = 10824364.001).
  • [ISSN] 1368-5031
  • [Journal-full-title] International journal of clinical practice
  • [ISO-abbreviation] Int. J. Clin. Pract.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] ENGLAND
  • [Chemical-registry-number] 0 / Selective Estrogen Receptor Modulators
  • [Number-of-references] 45
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81. Koda T, Morita M, Imai H: Retinoic acid inhibits uterotrophic activity of bisphenol A in adult ovariectomized rats. J Nutr Sci Vitaminol (Tokyo); 2007 Oct;53(5):432-6
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  • Retinal acetate has been reported to inhibit the adverse effects of BPA on male mice reproduction.
  • All-trans-retinoic acid (ATRA) is a potent natural derivative of vitamin A and is reported to inhibit the estrogen-induced proliferation of human breast carcinoma cells.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Free Radical Scavengers / pharmacology. Phenols / pharmacology. Tretinoin / pharmacology. Uterus / drug effects
  • [MeSH-minor] Animals. Apoptosis / drug effects. Benzhydryl Compounds. Bromodeoxyuridine. Cell Proliferation / drug effects. Dietary Supplements. Female. In Situ Nick-End Labeling. Organ Size / drug effects. Ovariectomy. Rats. Rats, Sprague-Dawley

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  • (PMID = 18079610.001).
  • [ISSN] 0301-4800
  • [Journal-full-title] Journal of nutritional science and vitaminology
  • [ISO-abbreviation] J. Nutr. Sci. Vitaminol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzhydryl Compounds; 0 / Free Radical Scavengers; 0 / Phenols; 5688UTC01R / Tretinoin; G34N38R2N1 / Bromodeoxyuridine; MLT3645I99 / bisphenol A
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82. Singer CF, Hudelist G, Lamm W, Mueller R, Handl C, Kubista E, Czerwenka K: Active (p)CrkL is overexpressed in human malignancies: potential role as a surrogate parameter for therapeutic tyrosine kinase inhibition. Oncol Rep; 2006 Feb;15(2):353-9
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  • CrkL is a nuclear adaptor and transcriptional activator in Bcr-Abl expressing cells and constitutes the major tyrosine phosphorylated protein in CML, but the expression and biological function of CrkL in other malignancies is largely unknown.
  • Using immunohistochemistry, we have analyzed the protein expression of activated (p)CrkL in normal and malignant tissues.
  • We then treated K562 leukemia cells with imatinib to analyze the effect of tyrosine kinase inhibition on CrkL activation. pCrkL expression was predominantly epithelial and detected in the majority of non-malignant prostate (79%), 49% of colon biopsies, 36% of skin biopsies, and 41% of samples obtained from normal brain.
  • Protein expression was, however, considerably less frequent in normal breast (18%), lung (16%) and ovarian (12%) tissues.
  • In contrast to their corresponding benign tissues, pCrkL expression was significantly more common in breast cancer samples (49%, p<0.0001; Fisher's exact test), lung carcinomas (55%, p=0.0002), lymphatic tissues (80% vs. 10%, p=0.012), skin cancer (67%, p=0.020), ovarian malignomas (50%, p<0.0001) and colon carcinomas (63%, p<0.03).
  • By contrast, activated CrkL was significantly less frequent in prostate carcinoma samples when compared to corresponding non-malignant prostatic tissues (14% vs. 79%, p<0.0001).
  • We hypothesize that pCrkL is selectively up-regulated in a number of malignant tumor entities and involved in malignant transformation.
  • [MeSH-major] Adaptor Proteins, Signal Transducing / biosynthesis. Biomarkers, Tumor / analysis. Neoplasms / drug therapy. Neoplasms / metabolism. Nuclear Proteins / biosynthesis. Protein Kinase Inhibitors / therapeutic use. Protein-Tyrosine Kinases / drug effects
  • [MeSH-minor] Benzamides. Blotting, Western. Cell Line, Tumor. Enzyme Activation / drug effects. Female. Humans. Imatinib Mesylate. Immunohistochemistry. Male. Piperazines / therapeutic use. Pyrimidines / therapeutic use. Up-Regulation

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  • (PMID = 16391854.001).
  • [ISSN] 1021-335X
  • [Journal-full-title] Oncology reports
  • [ISO-abbreviation] Oncol. Rep.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / Benzamides; 0 / Biomarkers, Tumor; 0 / CRKL protein; 0 / Nuclear Proteins; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Protein-Tyrosine Kinases
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83. Gu LQ, Li FY, Zhao L, Liu Y, Chu Q, Zang XX, Liu JM, Ning G, Zhao YJ: Association of XIAP and P2X7 receptor expression with lymph node metastasis in papillary thyroid carcinoma. Endocrine; 2010 Oct;38(2):276-82
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  • [Title] Association of XIAP and P2X7 receptor expression with lymph node metastasis in papillary thyroid carcinoma.
  • The purpose of the present study was to investigate the associations of XIAP and P2X7 receptor expression with the clinicopathological features of patients with papillary thyroid carcinoma (PTC).
  • [MeSH-major] Carcinoma, Papillary / metabolism. Carcinoma, Papillary / secondary. Receptors, Purinergic P2X7 / metabolism. Thyroid Neoplasms / metabolism. Thyroid Neoplasms / pathology. X-Linked Inhibitor of Apoptosis Protein / metabolism
  • [MeSH-minor] Adult. Biomarkers, Tumor / metabolism. Female. Goiter, Nodular / metabolism. Goiter, Nodular / pathology. Humans. Lymphatic Metastasis / pathology. Male. Middle Aged. Predictive Value of Tests. Prognosis

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  • (PMID = 20972735.001).
  • [ISSN] 1559-0100
  • [Journal-full-title] Endocrine
  • [ISO-abbreviation] Endocrine
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Receptors, Purinergic P2X7; 0 / X-Linked Inhibitor of Apoptosis Protein; 0 / XIAP protein, human
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84. Schallier D, Decoster L, Fontaine C, De Grève J: Pemetrexed-induced eyelid edema: incidence and clinical manifestations. Anticancer Res; 2010 Dec;30(12):5185-8
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  • RESULTS: Eighty-six patients received pemetrexed-containing chemotherapy either as a single agent (45 patients) or in combination with cis- or carboplatin (41 patients).
  • Two patients (2.3%) with stage IV non-small cell lung cancer (NSCLC) presented the edema typically localized in the lower eyelid after first-line treatment with carboplatin-pemetrexed.
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Breast Neoplasms / drug therapy. Carboplatin / administration & dosage. Carcinoma, Non-Small-Cell Lung / drug therapy. Eyelids / drug effects. Female. Humans. Lung Neoplasms / drug therapy. Male. Mesothelioma / drug therapy. Middle Aged. Pemetrexed. Retrospective Studies

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  • (PMID = 21187510.001).
  • [ISSN] 1791-7530
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Glutamates; 04Q9AIZ7NO / Pemetrexed; 5Z93L87A1R / Guanine; BG3F62OND5 / Carboplatin
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85. Singh G, Thulkar S, Seith A, Parshad R, Kumar P: An approach for assessment of tumor volume from mammography in locally advanced breast cancer. Malays J Med Sci; 2008 Jan;15(1):37-41
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  • [Title] An approach for assessment of tumor volume from mammography in locally advanced breast cancer.
  • Tumor size is an important independent indicator in patients with carcinoma of the breast.
  • Measurement of tumor burden with ultrasonography and computed tomography is being used with increasing frequency to assess the effectiveness of cytotoxic anticancer drugs.

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  • [ErratumIn] Malays J Med Sci. 2008 Apr;15(4):71. Thulkar, Sanjay [added]; Seith, Ashu [added]; Parshad, Rajinder [added]; Kumar, Pratik [added]
  • (PMID = 22589613.001).
  • [ISSN] 1394-195X
  • [Journal-full-title] The Malaysian journal of medical sciences : MJMS
  • [ISO-abbreviation] Malays J Med Sci
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Malaysia
  • [Other-IDs] NLM/ PMC3341896
  • [Keywords] NOTNLM ; Mammography / locally advanced breast cancer / magnification / prognosis / tumor volume
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86. Piao BK, Wang YX, Xie GR, Mansmann U, Matthes H, Beuth J, Lin HS: Impact of complementary mistletoe extract treatment on quality of life in breast, ovarian and non-small cell lung cancer patients. A prospective randomized controlled clinical trial. Anticancer Res; 2004 Jan-Feb;24(1):303-9
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  • [Title] Impact of complementary mistletoe extract treatment on quality of life in breast, ovarian and non-small cell lung cancer patients. A prospective randomized controlled clinical trial.
  • Standardized aqueous mistletoe extracts have been applied to cancer patients for several decades as complementary medicine.
  • Two hundred and thirty-three patients with breast (n=68), ovarian (n=71) and non-small cell lung cancer (NSCLC; n=94) were enrolled into this study.
  • Quality of life (QoL) was significantly (p<0.05) improved for patients who were complementarily treated with sME, as determined by the questionnaires FLIC (Functional Living Index-Cancer), TCM (Traditional Chinese Medicine Index) and the KPI (Karnofsky Performance Index) in comparison to the control group.
  • This study showed that complementary treatment with sME can beneficially reduce the side-effects of chemotherapy in cancer patients and thus improve quality of life.
  • [MeSH-major] Breast Neoplasms / drug therapy. Carcinoma, Non-Small-Cell Lung / drug therapy. Lung Neoplasms / drug therapy. Ovarian Neoplasms / drug therapy. Phytotherapy. Plant Extracts / therapeutic use. Plant Preparations / therapeutic use. Plant Proteins. Toxins, Biological / therapeutic use
  • [MeSH-minor] Antineoplastic Agents / therapeutic use. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Female. Humans. Male. Mistletoe / chemistry. Prospective Studies. Quality of Life. Ribosome Inactivating Proteins, Type 2


87. Wangsaturaka P, Asavamongkolkul A, Waikakul S, Phimolsarnti R: The results of surgical management of bone metastasis involving the periacetabular area: Siriraj experience. J Med Assoc Thai; 2007 May;90(5):1006-13
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  • Non-operative treatment including medication or radiation therapy is the first treatment modality.
  • The primary tumors were breast carcinoma in five patients, thyroid carcinoma in three, kidney carcinoma in two, and one each of cervix carcinoma, urinary bladder carcinoma, lung carcinoma, and multiple myeloma.
  • Type of periacetabular metastases by Harrington 's classification, age of patients, blood loss, unit of blood transfusion, and postoperative complication were reviewed.
  • The mean time from diagnosis of primary tumor to periacetabular metastatic surgery was 32.5 months (range 0-84 months).
  • [MeSH-minor] Adult. Aged. Female. Humans. Male. Middle Aged. Palliative Care. Prognosis. Prospective Studies. Quality of Life. Survival. Thailand

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  • (PMID = 17596060.001).
  • [ISSN] 0125-2208
  • [Journal-full-title] Journal of the Medical Association of Thailand = Chotmaihet thangphaet
  • [ISO-abbreviation] J Med Assoc Thai
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Thailand
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88. Huh JW, Park YA, Lee KY, Sohn SK: Heterogeneity of adenosine triphosphate-based chemotherapy response assay in colorectal cancer--secondary publication. Yonsei Med J; 2009 Oct 31;50(5):697-703
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  • [Title] Heterogeneity of adenosine triphosphate-based chemotherapy response assay in colorectal cancer--secondary publication.
  • PURPOSE: Adenosine triphosphate-based chemotherapy response assay (ATP-CRA) is a well-documented and validated technology that can individualize chemotherapy for patients with lung, stomach, or breast cancer.
  • This study explored the feasibility of ATP-CRA as a chemosensitivity test in patients with colorectal cancer.
  • MATERIALS AND METHODS: A total of 118 patients who underwent surgical resection for colorectal adenocarcinoma were analyzed for chemosensitivity to 6 anticancer drugs using ATP-CRA.
  • We calculated the cell death rate (CDR) by measuring intracellular ATP levels of drug-exposed cells and untreated controls.
  • Irinotecan had the greatest responsiveness in patients with well differentiated and moderately differentiated carcinoma.
  • CONCLUSION: Our study suggests that ATP-CRA could be used to identify patients with colorectal cancer who might benefit from treatment with a specific chemotherapeutic agent.
  • [MeSH-major] Adenocarcinoma / drug therapy. Adenosine Triphosphate / metabolism. Antineoplastic Agents / pharmacology. Colorectal Neoplasms / drug therapy. Drug Screening Assays, Antitumor / methods
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Female. Humans. Male. Middle Aged. Precision Medicine. Tumor Cells, Cultured

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  • (PMID = 19881975.001).
  • [ISSN] 1976-2437
  • [Journal-full-title] Yonsei medical journal
  • [ISO-abbreviation] Yonsei Med. J.
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article
  • [Publication-country] Korea (South)
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 8L70Q75FXE / Adenosine Triphosphate
  • [Other-IDs] NLM/ PMC2768246
  • [Keywords] NOTNLM ; Adenosine triphosphate / chemotherapy response assay / colorectal cancer
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89. Kakadiya R, Dong H, Kumar A, Narsinh D, Zhang X, Chou TC, Lee TC, Shah A, Su TL: Potent DNA-directed alkylating agents: Synthesis and biological activity of phenyl N-mustard-quinoline conjugates having a urea or hydrazinecarboxamide linker. Bioorg Med Chem; 2010 Mar 15;18(6):2285-99
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  • [Title] Potent DNA-directed alkylating agents: Synthesis and biological activity of phenyl N-mustard-quinoline conjugates having a urea or hydrazinecarboxamide linker.
  • A series of N-mustard-quinoline conjugates bearing a urea or hydrazinecarboxamide linker was synthesized for antitumor evaluation.
  • It was shown that complete tumor remission in nude mice bearing human breast carcinoma MX-1 xenograft by 17a, i and 18c, d was achieved.
  • [MeSH-major] Antineoplastic Agents, Alkylating / pharmacology. DNA / chemistry. DNA / drug effects. Hydrazines / chemistry. Neoplasms, Experimental / drug therapy. Quinolines / pharmacology. Urea / chemistry
  • [MeSH-minor] Animals. Cell Proliferation / drug effects. Drug Screening Assays, Antitumor. Humans. Male. Mice. Mice, Nude. Molecular Structure. Neoplasm Transplantation. Rats. Stereoisomerism. Structure-Activity Relationship. Tumor Cells, Cultured

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  • [Copyright] Copyright 2010 Elsevier Ltd. All rights reserved.
  • (PMID = 20181487.001).
  • [ISSN] 1464-3391
  • [Journal-full-title] Bioorganic & medicinal chemistry
  • [ISO-abbreviation] Bioorg. Med. Chem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 0 / Hydrazines; 0 / Quinolines; 8W8T17847W / Urea; 9007-49-2 / DNA; E66400VT9R / quinoline
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90. Masuelli L, Marzocchella L, Focaccetti C, Lista F, Nardi A, Scardino A, Mattei M, Turriziani M, Modesti M, Forni G, Schlom J, Modesti A, Bei R: Local delivery of recombinant vaccinia virus encoding for neu counteracts growth of mammary tumors more efficiently than systemic delivery in neu transgenic mice. Cancer Immunol Immunother; 2010 Aug;59(8):1247-58
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  • Recombinant vaccinia virus has been widely employed as a cancer vaccine in several clinical trials.
  • In this study we explored, employing BALB/c mice transgenic for the rat neu oncogene, the ability of the recombinant vaccinia virus neu (rV-neuT) vaccine to inhibit growth of neu+ mammary carcinomas and whether the efficacy of vaccination was dependent on: (a) carcinogenesis stage at which the vaccination was initiated;.
  • BALB-neuT mice were vaccinated one, two and three times by subcutaneous (s.c.) and intramammary gland (im.g.) injection with rV-neuT or V-wt (wild-type vaccinia virus) starting at the stage in which mouse mammary gland displays atypical hyperplasia, carcinoma in situ or invasive carcinoma.
  • The im.g. vaccination was more effective than the s.c. vaccination in inhibiting mammary carcinogenesis, eliciting anti-Neu antibodies, increasing anti-Neu IgG2a/G3 isotypes and inducing antibodies able to trigger mammary tumor cells apoptosis and antibody-dependent cellular cytotoxicity.
  • The better protective ability of rV-neuT im.g. vaccination was associated with its capacity to induce a superior degree of in vivo mammary cancer cells apoptosis.
  • Our research suggests that intratumoral vaccination using recombinant vaccinia virus could be employed to increase the activity of a genetic cancer vaccine.
  • This study may have important implications for the design of cancer vaccine protocols for the treatment of breast cancer and of accessible tumors using recombinant vaccinia virus.
  • [MeSH-major] Cancer Vaccines. Mammary Glands, Animal / metabolism. Mammary Neoplasms, Experimental / immunology. Receptor, ErbB-2 / immunology
  • [MeSH-minor] Animals. Antigens, Neoplasm / genetics. Antigens, Neoplasm / immunology. Antigens, Neoplasm / metabolism. Cell Proliferation. Female. Gene Transfer Techniques. Male. Mice. Mice, Inbred BALB C. Mice, Transgenic. NIH 3T3 Cells. Rats. Vaccines, Synthetic. Vaccinia virus / genetics

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  • (PMID = 20364378.001).
  • [ISSN] 1432-0851
  • [Journal-full-title] Cancer immunology, immunotherapy : CII
  • [ISO-abbreviation] Cancer Immunol. Immunother.
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / / ZIA BC010944-05
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Cancer Vaccines; 0 / Erbb2 protein, rat; 0 / Vaccines, Synthetic; EC 2.7.10.1 / Receptor, ErbB-2
  • [Other-IDs] NLM/ NIHMS426706; NLM/ PMC3561760
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91. Zabel-du Bois A, Milker-Zabel S, Wannenmacher M, Debus J: [Postoperative radiotherapy of the chest wall in patients with male breast cancer]. Zentralbl Chir; 2007 Oct;132(5):391-5
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  • [Title] [Postoperative radiotherapy of the chest wall in patients with male breast cancer].
  • [Transliterated title] Postoperative Strahlentherapie der Thoraxwand beim Mammakarzinom des Mannes.
  • INTRODUCTION: We analysed our long-term results with postoperative radiotherapy of the chest wall in male breast cancer patients with respect to local control and survival.
  • METHODS: Twenty-five patients with 26 histological proven carcinomas of the male breast underwent postoperative radiotherapy of the chest wall with (n = 15) or without regional lymphatics after mastectomy.
  • Survival was significantly affected by the presence of lymph node metastases (p < 0.01) and localisation of the tumor in the right breast (p < 0.04).
  • CONCLUSION: Postoperative radiotherapy is an important part of the management of male breast cancer to improve local control and progression-free survival.
  • [MeSH-major] Breast Neoplasms, Male / radiotherapy
  • [MeSH-minor] Actuarial Analysis. Aged. Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Chemotherapy, Adjuvant. Combined Modality Therapy. Cyclophosphamide / administration & dosage. Disease-Free Survival. Fluorouracil / administration & dosage. Follow-Up Studies. Humans. Lymph Node Excision. Lymphatic Metastasis. Male. Mastectomy, Modified Radical. Mastectomy, Segmental. Methotrexate / administration & dosage. Middle Aged. Neoplasm Recurrence, Local / drug therapy. Neoplasm Recurrence, Local / mortality. Neoplasm Recurrence, Local / radiotherapy. Neoplasm Recurrence, Local / surgery. Prognosis. Radioisotope Teletherapy. Radiotherapy, Adjuvant. Tamoxifen / therapeutic use. Thoracic Wall / radiation effects

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  • (PMID = 17907080.001).
  • [ISSN] 0044-409X
  • [Journal-full-title] Zentralblatt für Chirurgie
  • [ISO-abbreviation] Zentralbl Chir
  • [Language] ger
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 094ZI81Y45 / Tamoxifen; 8N3DW7272P / Cyclophosphamide; U3P01618RT / Fluorouracil; YL5FZ2Y5U1 / Methotrexate; CMF regimen
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92. Engels FK, Sparreboom A, Mathot RA, Verweij J: Potential for improvement of docetaxel-based chemotherapy: a pharmacological review. Br J Cancer; 2005 Jul 25;93(2):173-7
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  • [Title] Potential for improvement of docetaxel-based chemotherapy: a pharmacological review.
  • This review discusses the pharmacological attempts at treatment optimisation, which include reducing interindividual pharmacokinetic and pharmacodynamic variability, optimising schedule, route of administration, reversing drug resistance and the development of structurally related second-generation taxanes.
  • [MeSH-major] Antineoplastic Agents, Phytogenic / pharmacokinetics. Antineoplastic Agents, Phytogenic / pharmacology. Antineoplastic Agents, Phytogenic / therapeutic use. Breast Neoplasms / drug therapy. Carcinoma, Non-Small-Cell Lung / drug therapy. Lung Neoplasms / drug therapy. Prostatic Neoplasms / drug therapy. Taxoids / pharmacokinetics. Taxoids / pharmacology
  • [MeSH-minor] Drug Administration Schedule. Drug Resistance, Neoplasm. Female. Humans. Male

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  • (PMID = 16012521.001).
  • [ISSN] 0007-0920
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 0 / Taxoids; 15H5577CQD / docetaxel
  • [Number-of-references] 30
  • [Other-IDs] NLM/ PMC2361544
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93. Yang M, Baranov E, Li XM, Wang JW, Jiang P, Li L, Moossa AR, Penman S, Hoffman RM: Whole-body and intravital optical imaging of angiogenesis in orthotopically implanted tumors. Proc Natl Acad Sci U S A; 2001 Feb 27;98(5):2616-21
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  • The development of drugs for the control of tumor angiogenesis requires a simple, accurate, and economical assay for tumor-induced vascularization.
  • The orthotopic implantation model of human cancer has been well characterized, and fluorescence shadowing replaces the laborious histological techniques for determining blood vessel density.
  • Whole-body optical imaging of tumor angiogenesis was demonstrated by injecting fluorescent Lewis lung carcinoma cells into the s.c. site of the footpad of nude mice.
  • Similarly, the green fluorescent protein-expressing human breast tumor MDA-MB-435 was orthotopically transplanted to the mouse fat pad, where whole-body optical imaging showed that blood vessel density increased linearly over a 20-week period.
  • These powerful and clinically relevant angiogenesis mouse models can be used for real-time in vivo evaluation of agents inhibiting or promoting tumor angiogenesis in physiological microenvironments.
  • [MeSH-minor] Animals. Female. Fluorescence. Green Fluorescent Proteins. Humans. Luminescent Proteins / genetics. Male. Mice. Mice, Inbred BALB C. Mice, Nude. Neoplasm Transplantation. Tumor Cells, Cultured

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  • (PMID = 11226288.001).
  • [ISSN] 0027-8424
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Luminescent Proteins; 147336-22-9 / Green Fluorescent Proteins
  • [Other-IDs] NLM/ PMC30187
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94. Lara PN Jr, Meyers FJ, Gray CR, Edwards RG, Gumerlock PH, Kauderer C, Tichauer G, Twardowski P, Doroshow JH, Gandara DR: HER-2/neu is overexpressed infrequently in patients with prostate carcinoma. Results from the California Cancer Consortium Screening Trial. Cancer; 2002 May 15;94(10):2584-9
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  • [Title] HER-2/neu is overexpressed infrequently in patients with prostate carcinoma. Results from the California Cancer Consortium Screening Trial.
  • BACKGROUND: The overexpression of HER-2/neu is found in 20-30% of patients with breast carcinoma and is an adverse prognostic factor.
  • HER-2 overexpression also has been reported in up to 60% of patients with hormone-refractory prostate carcinoma (HRPC) and was correlated with shortened survival.
  • Trastuzumab (Herceptin) is a humanized monoclonal antibody that binds to the HER-2 receptor and has antitumor activity in patients with HER-2-overexpressing breast carcinoma.
  • The authors report the results of HER-2 screening from a Phase II trial of chemotherapy with trastuzumab and docetaxel in patients with HER-2-overexpressing prostate carcinoma.
  • CONCLUSIONS: Unlike breast carcinoma and contrary to prior reports, HER-2 overexpression by IHC in archival prostate tissue from patients who eventually developed hormone-refractory disease was infrequent.
  • There did not appear to be any correlation between HER-2 overexpression by IHC and shed HER-2 antigen levels in serum by ELISA in this tumor type.
  • Whether trastuzumab possesses single-agent activity or modulates chemotherapy response in tumor types other than breast carcinoma remains to be determined.
  • [MeSH-minor] Aged. Aged, 80 and over. Enzyme-Linked Immunosorbent Assay. Humans. Immunohistochemistry. In Situ Hybridization. Male. Middle Aged

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  • (PMID = 12173324.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA62505; United States / NCI NIH HHS / CA / CA63265; United States / NCI NIH HHS / CM / N01-CM17101
  • [Publication-type] Clinical Trial; 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] EC 2.7.10.1 / Receptor, ErbB-2
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95. Whatley WS, Thompson JW, Rao B: Salivary gland tumors in survivors of childhood cancer. Otolaryngol Head Neck Surg; 2006 Mar;134(3):385-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Salivary gland tumors in survivors of childhood cancer.
  • BACKGROUND: There is an increased incidence of second malignant neoplasms in survivors of childhood cancers.
  • The most common second malignancies are acute leukemia, bone and soft tissue tumors, and carcinoma of the skin, breast, and thyroid.
  • Although, ionizing radiation has been demonstrated to increase the risk of developing a salivary gland neoplasm, there are few reports of salivary gland neoplasms occurring in patients treated for cancer in childhood.
  • RESULTS: Twelve survivors of childhood cancer developed a salivary gland neoplasm after completion of treatment.
  • The pathology of the salivary gland tumors were mucoepidermoid carcinoma (10), adenoid cystic carcinoma (1) , and pleomorphic adenoma (1).
  • CONCLUSION: Radiation and chemotherapy used to treat patients with childhood malignancies increases the risk of developing a second neoplasm of salivary gland origin.
  • The majority of these neoplasms are malignant; mucoepidermoid carcinoma occurs most frequently.
  • [MeSH-major] Neoplasms, Second Primary / diagnosis. Salivary Gland Neoplasms / diagnosis. Survivors
  • [MeSH-minor] Adenoma, Pleomorphic / diagnosis. Adenoma, Pleomorphic / surgery. Carcinoma, Adenoid Cystic / diagnosis. Carcinoma, Adenoid Cystic / surgery. Carcinoma, Mucoepidermoid / diagnosis. Carcinoma, Mucoepidermoid / surgery. Child. Disease-Free Survival. Female. Follow-Up Studies. Humans. Lung Neoplasms / secondary. Lymphatic Metastasis / diagnosis. Male. Neck Dissection. Neoplasms / drug therapy. Neoplasms / radiotherapy. Radiotherapy, Adjuvant. Registries. Retrospective Studies. Risk Factors


96. Tejeda M, Gaal D, Barna K, Csuka O, Kéri G: The antitumor activity of the somatos