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1. Yang YM, Jhanwar-Uniyal M, Schwartz J, Conaway CC, Halicka HD, Traganos F, Chung FL: N-acetylcysteine conjugate of phenethyl isothiocyanate enhances apoptosis in growth-stimulated human lung cells. Cancer Res; 2005 Sep 15;65(18):8538-47
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  • [Title] N-acetylcysteine conjugate of phenethyl isothiocyanate enhances apoptosis in growth-stimulated human lung cells.
  • We previously showed that dietary treatment with the N-acetylcysteine conjugate of phenethyl isothiocyanate (PEITC-NAC) inhibited benzo(a)pyrene-induced lung tumorigenesis in A/J mice, and that tumor inhibition was associated with induction of activator protein-1 (AP-1) activity and stimulation of apoptosis in the lungs of mice.
  • In the present study, we show that PEITC-NAC also induces apoptosis and AP-1 activity in human lung adenocarcinoma A549 cells, and that activation of AP-1 is important in PEITC-NAC induced apoptosis in these cells.
  • PEITC-NAC induced AP-1 binding activity in A549 cells in a dose- and time-dependent manner; peak activity appeared at 10 micromol/L after 24 hours.
  • At that time, flow cytometric analysis showed a sub-G1 peak, indicating that approximately 4.5% of the cells had undergone apoptosis.
  • When wild-type c-jun cDNA was transfected into A549 cells, PEITC-NAC-mediated apoptosis was greatly increased in the c-jun-transfected cells compared with the control vector-transfected cells, based on cell morphology and analysis of DNA fragmentation.
  • Furthermore, cells that were pretreated with 100 nmol/L 12-O-tetradecanoyl phorbol-13-acetate, and then treated with 25 micromol/L PEITC-NAC, underwent enhanced apoptosis compared with cells that were treated with PEITC-NAC alone; cells treated with 12-O-tetradecanoyl phorbol-13-acetate alone showed active cell growth without apoptosis.
  • Bivariate flow cytometric analysis of DNA strand breaks versus DNA content showed that apoptosis induced by PEITC-NAC occurred predominantly in the G2-M phase.
  • These findings suggest that growth-stimulated cells with an elevated basal AP-1 activity, i.e., A549 cells transfected with wild-type c-jun or treated with a tumor promoter, were more sensitive to PEITC-NAC-mediated apoptosis.
  • [MeSH-major] Adenocarcinoma / drug therapy. Apoptosis / drug effects. Cysteine / analogs & derivatives. Lung Neoplasms / drug therapy. Thiocarbamates / pharmacology
  • [MeSH-minor] Animals. Cell Line, Tumor. Dose-Response Relationship, Drug. Enzyme Activation. Humans. JNK Mitogen-Activated Protein Kinases / biosynthesis. JNK Mitogen-Activated Protein Kinases / genetics. JNK Mitogen-Activated Protein Kinases / metabolism. Lung / drug effects. Mice. Mice, Inbred A. Tetradecanoylphorbol Acetate. Transcription Factor AP-1 / physiology. Transfection. Tumor Suppressor Protein p53 / biosynthesis. Tumor Suppressor Protein p53 / genetics

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  • (PMID = 16166335.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / 1R03CA110057-01; United States / NCI NIH HHS / CA / CA46535
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / N-acetyl-S-(N-2-phenethylthiocarbamoyl)-L-cysteine; 0 / TP53 protein, human; 0 / Thiocarbamates; 0 / Transcription Factor AP-1; 0 / Tumor Suppressor Protein p53; EC 2.7.11.24 / JNK Mitogen-Activated Protein Kinases; K848JZ4886 / Cysteine; NI40JAQ945 / Tetradecanoylphorbol Acetate
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2. Padar S, van Breemen C, Thomas DW, Uchizono JA, Livesey JC, Rahimian R: Differential regulation of calcium homeostasis in adenocarcinoma cell line A549 and its Taxol-resistant subclone. Br J Pharmacol; 2004 May;142(2):305-16
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  • [Title] Differential regulation of calcium homeostasis in adenocarcinoma cell line A549 and its Taxol-resistant subclone.
  • Drug resistance is a fundamental problem in cancer chemotherapy.
  • We investigated the regulatory role of [Ca2+](i) in Taxol resistance in the non-small-cell lung cancer cell line A549 and its chemoresistant subclone A549-T24.
  • Measurement of cytosolic calcium ([Ca2+](c)) in single cells and cell populations revealed similar levels of basal calcium in the two cell lines.
  • However, a reduced response to thapsigargin (a sarcoplasmic/endoplasmic reticulum Ca2+-ATPase (SERCA) inhibitor) in A549-T24 cells compared to the parent cell line suggested a lower ER Ca2+ content in these cells. mRNA expression of SERCA2b and SERCA3, major Ca2+ pumps involved in ER Ca2+ homeostasis, did not significantly differ between the two cell lines, as revealed by RT-PCR.
  • An altered calcium influx pathway in the Taxol-resistant cell line was observed.
  • Modulation of the ER calcium pools using CMC (4-chloro-m-cresol) and ATP revealed lower ryanodine receptor (RyR) and IP(3) receptor (IP(3)R)-sensitive Ca2+ stores in the chemoresistant cell line.
  • Western blot and RT-PCR studies suggested that A549-T24 cells expressed higher levels of the antiapoptotic protein Bcl-2 and the calcium-binding protein sorcin, respectively, in comparison to the parent cell line.

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  • (PMID = 15066902.001).
  • [ISSN] 0007-1188
  • [Journal-full-title] British journal of pharmacology
  • [ISO-abbreviation] Br. J. Pharmacol.
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / R15 HL071520; United States / NHLBI NIH HHS / HL / R15 HL 071520
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] P88XT4IS4D / Paclitaxel; SY7Q814VUP / Calcium
  • [Other-IDs] NLM/ PMC1574945
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3. Trejo-Becerril C, Pérez-Cárdenas E, Treviño-Cuevas H, Taja-Chayeb L, García-López P, Segura-Pacheco B, Chávez-Blanco A, Lizano-Soberon M, González-Fierro A, Mariscal I, Wegman-Ostrosky T, Dueñas-González A: Circulating nucleosomes and response to chemotherapy: an in vitro, in vivo and clinical study on cervical cancer patients. Int J Cancer; 2003 May 10;104(6):663-8
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  • [Title] Circulating nucleosomes and response to chemotherapy: an in vitro, in vivo and clinical study on cervical cancer patients.
  • It is known that cell-free DNA circulates in plasma/serum of patients with cancer and that part of this DNA circulates as nucleosomes that can be quantified by ELISA.
  • We analyzed the effect of tumor and chemotherapy upon the levels of nucleosomes in vitro, in vivo and in cervical cancer patients.
  • The levels of nucleosomes pre- and post-treatment were correlated with response in 11 patients receiving chemotherapy.
  • Nucleosomes were determined in nude mice treated with or without cisplatin and carrying tumors generated with HeLa cells, and in the cell lysate and supernatant of HeLa cells exposed to cisplatin in culture.
  • In addition, nucleosomes were determined at different time points in patients and in rats receiving chemotherapy.
  • After 24 hr of treatment with oxaliplatin and gemcitabine, the levels decreased in 6 patients of whom 5 had response.
  • Nucleosome levels differed between mice xenografted and not xenografted (765 vs. 378, p = 0.001) and between xenografted treated with or without cisplatin (650 vs. 765, p = 0.010), but not in tumor-free animals treated and untreated with cisplatin (378 vs. 379, p = 0.99).
  • In vitro, nucleosomes reached at peak 8 hr in cell lysates to decrease thereafter, whereas in supernatant, levels continued to increase up to 24 hr.
  • Serial determination of nucleosomes in patients showed a rise within 6-12 hr and then a reduction to below the basal at 24 hr.
  • An overdose of this triple combination produced a transient elevation of almost 1,000 AU over the basal.
  • Our results demonstrate that most of circulating nucleosomes originate from the tumor and that chemotherapy produces an early rise most likely due to tumor apoptosis and that nucleosomes are rapidly cleared from circulation.
  • On the contrary, chemotherapy within the therapeutic range of doses has no effect on nucleosome levels in healthy mice and rats.
  • This data suggests that the determination of circulating nucleosomes pre- and post-treatment could be a useful test to predict response to chemotherapy in cancer patients.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. DNA, Neoplasm / blood. DNA, Viral / blood. Deoxycytidine / analogs & derivatives. Neoplastic Cells, Circulating / metabolism. Nucleosomes / metabolism. Uterine Cervical Neoplasms / blood. Uterine Cervical Neoplasms / drug therapy
  • [MeSH-minor] Adenocarcinoma / blood. Adenocarcinoma / drug therapy. Adult. Aged. Animals. Carcinoma, Adenosquamous / blood. Carcinoma, Adenosquamous / drug therapy. Carcinoma, Squamous Cell / blood. Carcinoma, Squamous Cell / drug therapy. Case-Control Studies. Cisplatin / therapeutic use. Enzyme-Linked Immunosorbent Assay. Female. HeLa Cells. Humans. In Vitro Techniques. Mice. Mice, Nude. Middle Aged. Neoadjuvant Therapy. Organoplatinum Compounds / administration & dosage. Paclitaxel / administration & dosage. Papillomaviridae / pathogenicity. Papillomavirus Infections / blood. Papillomavirus Infections / drug therapy. Prognosis. Rats. Rats, Wistar. Tumor Virus Infections / blood. Tumor Virus Infections / drug therapy

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  • [Copyright] Copyright 2003 Wiley-Liss, Inc.
  • (PMID = 12640671.001).
  • [ISSN] 0020-7136
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA, Neoplasm; 0 / DNA, Viral; 0 / Nucleosomes; 0 / Organoplatinum Compounds; 04ZR38536J / oxaliplatin; 0W860991D6 / Deoxycytidine; B76N6SBZ8R / gemcitabine; P88XT4IS4D / Paclitaxel; Q20Q21Q62J / Cisplatin
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4. Zeng Y, Yokohira M, Saoo K, Takeuchi H, Chen Y, Yamakawa K, Matsuda Y, Kakehi Y, Imaida K: Inhibition of prostate carcinogenesis in probasin/SV40 T antigen transgenic rats by raloxifene, an antiestrogen with anti-androgen action, but not nimesulide, a selective cyclooxygenase-2 inhibitor. Carcinogenesis; 2005 Jun;26(6):1109-16
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  • [Title] Inhibition of prostate carcinogenesis in probasin/SV40 T antigen transgenic rats by raloxifene, an antiestrogen with anti-androgen action, but not nimesulide, a selective cyclooxygenase-2 inhibitor.
  • The chemopreventive efficacies of raloxifene and nimesulide, an anti-estrogen but with anti-androgen action and a cyclooxygenase-2 (COX-2) selective inhibitor, respectively, were evaluated in probasin/SV40 T antigen (Tag) transgenic (TG) rats.
  • The treatment groups were placebo, nimesulide (400 p.p.m. in basal diet p.o.
  • ), raloxifene (slow-release pellets implanted s.c., 5 mg/kg/day), raloxifene (5 mg/kg/day) plus nimesulide (400 p.p.m.
  • ), and raloxifene (10 mg/kg/day) plus nimesulide (400 p.p.m.).
  • Animals were killed at 17 weeks of age, and prostate tissues were harvested and weighed by lobes.
  • Tissues were evaluated by histology, immunohistochemistry, and western blot analyses and blood was collected to measure the testosterone levels.
  • All the animals in the placebo group had tumors in each lobe compared with only 43% each in the dorsolateral (DLP) and anterior prostate (AP) of the animals treated with raloxifene (10 mg/kg/day) plus nimesulide.
  • The total prostate weights and adenocarcinoma portions were significantly reduced in the three raloxifene-treated groups, whereas atrophic glands were increased.
  • There were no significant differences between the nimesulide alone and placebo groups or between the raloxifene (5 mg/kg/day) alone and raloxifene (5 mg/kg/day) plus nimesulide group, suggesting a lack of cancer preventive effects of the COX-2 inhibitor in this animal model.
  • Furthermore, circulating testosterone was decreased after raloxifene (10 mg/kg/day) plus nimesulide treatment.
  • These results demonstrate that raloxifene, but not nimesulide, inhibits prostate carcinogenesis in SV40 Tag TG rats associated with a decline in circulating testosterone levels and a loss of AR expression, as well as an inhibition of cell proliferation.
  • [MeSH-major] Adenocarcinoma / prevention & control. Androgen Antagonists / therapeutic use. Cyclooxygenase Inhibitors / therapeutic use. Prostatic Neoplasms / prevention & control. Raloxifene Hydrochloride / therapeutic use. Sulfonamides / therapeutic use
  • [MeSH-minor] Androgen-Binding Protein / genetics. Animals. Animals, Genetically Modified. Antigens, Polyomavirus Transforming / genetics. Apoptosis / drug effects. Cell Proliferation / drug effects. Cyclooxygenase 2. Cyclooxygenase 2 Inhibitors. Drug Therapy, Combination. Male. Prostaglandin-Endoperoxide Synthases / metabolism. Rats. Rats, Sprague-Dawley. Receptors, Androgen / biosynthesis. Testosterone / blood

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  • (PMID = 15731164.001).
  • [ISSN] 0143-3334
  • [Journal-full-title] Carcinogenesis
  • [ISO-abbreviation] Carcinogenesis
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Androgen Antagonists; 0 / Androgen-Binding Protein; 0 / Antigens, Polyomavirus Transforming; 0 / Cyclooxygenase 2 Inhibitors; 0 / Cyclooxygenase Inhibitors; 0 / Receptors, Androgen; 0 / Sulfonamides; 0 / probasin; 3XMK78S47O / Testosterone; 4F86W47BR6 / Raloxifene Hydrochloride; EC 1.14.99.1 / Cyclooxygenase 2; EC 1.14.99.1 / Prostaglandin-Endoperoxide Synthases; V4TKW1454M / nimesulide
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5. Arlt A, Gehrz A, Müerköster S, Vorndamm J, Kruse ML, Fölsch UR, Schäfer H: Role of NF-kappaB and Akt/PI3K in the resistance of pancreatic carcinoma cell lines against gemcitabine-induced cell death. Oncogene; 2003 May 22;22(21):3243-51
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  • [Title] Role of NF-kappaB and Akt/PI3K in the resistance of pancreatic carcinoma cell lines against gemcitabine-induced cell death.
  • Pancreatic cancer is resistant to almost all cytotoxic drugs.
  • Currently, gemcitabine appears to be the only clinically active drug but, because of pre-existing or acquired chemoresistance of most of the tumor cells, it failed to significantly improve the outcome of pancreatic carcinoma patients.
  • The current study examined the relevance of nuclear factor kappaB (NF-kappaB) and PI3K/Akt in the resistance of five pancreatic carcinoma cell lines towards gemcitabine.
  • Treatment for 24 h with gemcitabine (0.04-20 micro M) led to a strong induction of apoptosis in PT45-P1 and T3M4 cells but not in BxPc-3, Capan-1 and PancTu-1 cells.
  • These resistant cell lines exhibited a high basal NF-kappaB activity in contrast to the sensitive cell lines.
  • At a dose of 0.04 micro M, gemcitabine still induced apoptosis in the sensitive cell lines, but did not induce NF-kappaB.
  • In contrast to this obvious correlation between basal NF-kappaB activity and gemcitabine resistance, PI3K/Akt seems not to be involved in gemcitabine resistance of these cell lines.
  • Neither did the basal Akt activity correlate with the sensitivity towards gemcitabine treatment, nor did the inhibition of PI3K/Akt by LY294002 alter gemcitabine-induced apoptosis.
  • These results indicate that constitutive NF-kappaB activity confers resistance against gemcitabine and that modulation of this activity by pharmacological or genetic approaches may have therapeutical potential when combined with gemcitabine in the treatment of pancreatic carcinoma.
  • [MeSH-major] Adenocarcinoma / drug therapy. Antimetabolites, Antineoplastic / toxicity. Deoxycytidine / analogs & derivatives. Deoxycytidine / toxicity. NF-kappa B / physiology. Pancreatic Neoplasms / drug therapy. Phosphatidylinositol 3-Kinases / physiology. Protein-Serine-Threonine Kinases. Proto-Oncogene Proteins / physiology
  • [MeSH-minor] Apoptosis. Chromones / pharmacology. Dose-Response Relationship, Drug. Drug Resistance, Neoplasm. Enzyme Inhibitors / pharmacology. Etoposide / therapeutic use. Etoposide / toxicity. Humans. Morpholines / pharmacology. Proto-Oncogene Proteins c-akt. Tumor Cells, Cultured

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  • (PMID = 12761494.001).
  • [ISSN] 0950-9232
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0 / Chromones; 0 / Enzyme Inhibitors; 0 / Morpholines; 0 / NF-kappa B; 0 / Proto-Oncogene Proteins; 0W860991D6 / Deoxycytidine; 154447-36-6 / 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one; 6PLQ3CP4P3 / Etoposide; B76N6SBZ8R / gemcitabine; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; 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
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6. Ramchandani M, Brown AM, Rippin JW, Murray PI: Labial adenocarcinoma after treatment with cyclosporin a in a patient with panuveitis. Am J Ophthalmol; 2000 Jul;130(1):127-8
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  • [Title] Labial adenocarcinoma after treatment with cyclosporin a in a patient with panuveitis.
  • PURPOSE: To report a case of labial basal cell adenocarcinoma in a patient with uveitis on treatment with cyclosporin A.
  • METHOD: Case report.
  • A 73-year-old woman with panuveitis and retinal vasculitis presented with a lump on her lip after 52 months of treatment with cyclosporin A.
  • RESULT: Excision biopsy showed a labial adenocarcinoma.
  • CONCLUSION: Malignancy can occur after long-term cyclosporin A treatment for uveitis.
  • [MeSH-major] Adenocarcinoma / chemically induced. Cyclosporine / adverse effects. Immunosuppressive Agents / adverse effects. Lip Neoplasms / chemically induced. Panuveitis / drug therapy
  • [MeSH-minor] Aged. Female. Humans. Prednisolone / therapeutic use. Retinal Diseases / drug therapy. Retinal Vessels / drug effects. Vasculitis / drug therapy

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  • (PMID = 11004277.001).
  • [ISSN] 0002-9394
  • [Journal-full-title] American journal of ophthalmology
  • [ISO-abbreviation] Am. J. Ophthalmol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] UNITED STATES
  • [Chemical-registry-number] 0 / Immunosuppressive Agents; 83HN0GTJ6D / Cyclosporine; 9PHQ9Y1OLM / Prednisolone
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7. Wong NA, Brett L, Stewart M, Leitch A, Longley DB, Dunlop MG, Johnston PG, Lessells AM, Jodrell DI: Nuclear thymidylate synthase expression, p53 expression and 5FU response in colorectal carcinoma. Br J Cancer; 2001 Dec 14;85(12):1937-43
The Lens. Cited by Patents in .

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  • Nuclear expression of TS in human tissue in vivo has not been characterised and its clinicopathological correlates in malignancy are unknown.
  • 52 cases of primary colorectal carcinoma (CRC) and 24 cases of matched metastatic carcinoma were studied immunohistochemically using the monoclonal antibody TS106.
  • The degree of nuclear TS immunostaining correlated closely with levels of TS mRNA expression amongst 10 CRCs studied.
  • Strong nuclear immunostaining was seen in normal basal crypt colonocytes and germinal centre cells, and in a varying proportion of adenocarcinoma cells.
  • Amongst the primary carcinomas, higher TS nuclear expression was associated with prominent extracellular mucin production and right-sided location.
  • Higher TS nuclear expression also showed a significant association with poorer response to protracted venous infusional 5FU therapy.
  • There was no clear association between TS nuclear expression and Ki67 or p53 expression assessed immunohistochemically.
  • There was a strong positive correlation between TS nuclear expression in primary and metastatic CRC but the latter generally showed higher expression than matched primary tumour tissue.
  • These findings confirm the nuclear expression of TS protein in human cells in vivo and provide new insight into how such expression may relate to the behaviour of CRCs.
  • [MeSH-major] Adenocarcinoma / genetics. Antimetabolites, Antineoplastic / therapeutic use. Cell Nucleus / enzymology. Colorectal Neoplasms / genetics. Enzyme Inhibitors / therapeutic use. Fluorouracil / therapeutic use. Neoplasm Proteins / biosynthesis. Thymidylate Synthase / biosynthesis. Tumor Suppressor Protein p53 / biosynthesis
  • [MeSH-minor] Adult. Aged. Cell Differentiation. Drug Resistance, Neoplasm / genetics. Enzyme Induction. Female. Gene Expression Profiling. Genes, p53. Humans. Ki-67 Antigen / biosynthesis. Ki-67 Antigen / genetics. Male. Middle Aged. Neoplasm Metastasis. RNA, Messenger / biosynthesis. RNA, Neoplasm / biosynthesis. Reproducibility of Results. Survival Analysis. Treatment Outcome

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  • (PMID = 11747337.001).
  • [ISSN] 0007-0920
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Scotland
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0 / Enzyme Inhibitors; 0 / Ki-67 Antigen; 0 / Neoplasm Proteins; 0 / RNA, Messenger; 0 / RNA, Neoplasm; 0 / Tumor Suppressor Protein p53; EC 2.1.1.45 / Thymidylate Synthase; U3P01618RT / Fluorouracil
  • [Other-IDs] NLM/ PMC2364004
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8. Shieh JJ, Liu KT, Huang SW, Chen YJ, Hsieh TY: Modification of alternative splicing of Mcl-1 pre-mRNA using antisense morpholino oligonucleotides induces apoptosis in basal cell carcinoma cells. J Invest Dermatol; 2009 Oct;129(10):2497-506
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  • [Title] Modification of alternative splicing of Mcl-1 pre-mRNA using antisense morpholino oligonucleotides induces apoptosis in basal cell carcinoma cells.
  • Myeloid cell leukemia-1 (Mcl-1, Mcl-1L) is an anti-apoptotic protein of the Bcl-2 family that acts as a critical molecule in apoptosis control.
  • Mcl-1 pre-mRNA can undergo alternative splicing to yield the short isoform, Mcl-1S, which resembles BH3-only pro-apoptotic proteins and induces apoptosis.
  • Overexpression of Mcl-1 may play a role in various human tumors, and Mcl-1 may serve as a target in cancer therapy.
  • In this study, we found an imbalance between the expression levels of Mcl-1L and Mcl-1S in the skin basal cell carcinoma (BCC) cell line when compared with primary keratinocytes.
  • This shift increases the level of pro-apoptotic Mcl-1S and reduces the level of anti-apoptotic Mcl-1L, which induces apoptosis in BCC cells and AGS cells, a human gastric adenocarcinoma epithelial cell line.
  • Thus, this report provides a strategy for cancer therapy in which AMOs change the alternative splicing pattern of Mcl-1 pre-mRNA and thereby induce apoptosis.
  • [MeSH-major] Alternative Splicing / drug effects. Apoptosis / drug effects. Carcinoma, Basal Cell / pathology. Oligonucleotides, Antisense / pharmacology. Proto-Oncogene Proteins c-bcl-2 / genetics. RNA, Messenger / genetics. Skin Neoplasms / pathology
  • [MeSH-minor] Adenocarcinoma / metabolism. Adenocarcinoma / pathology. Cell Line, Tumor. Humans. Keratinocytes / metabolism. Keratinocytes / pathology. Myeloid Cell Leukemia Sequence 1 Protein. Stomach Neoplasms / metabolism. Stomach Neoplasms / pathology

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  • (PMID = 19369967.001).
  • [ISSN] 1523-1747
  • [Journal-full-title] The Journal of investigative dermatology
  • [ISO-abbreviation] J. Invest. Dermatol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Myeloid Cell Leukemia Sequence 1 Protein; 0 / Oligonucleotides, Antisense; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / RNA, Messenger
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9. Catino A, Crucitta E, Latorre A, Sambiasi D, Calabrese P, Lorusso V: Amifostine as chemoprotectant in metastatic breast cancer patients treated with doxorubicin. Oncol Rep; 2003 Jan-Feb;10(1):163-7
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  • Amifostine has shown to selectively protect normal tissues against cytotoxic and mutagenic effects of several anti-neoplastic drugs, such as alkylating agents, organoplatinum compounds, anthracyclines, taxanes, and ionising radiation.
  • This cytoprotection is broad-spectrum and selective, without loss of therapeutic efficacy.
  • In this study we have treated 31 patients affected with inoperable or metastatic breast cancer, not previously submitted to chemotherapy for advanced disease, with amifostine 910 mg/m(2) followed by doxorubicin 75 mg/m(2).
  • The overall response rate was 52% with a median response duration of 13 months (range 6-53+) and a median overall survival of 21 months (range 3-59+).
  • With regard to toxicity, 14 patients (45%) experienced transient g4 neutropenia which was febrile only in one case (3%).
  • Grade 3-4 thrombocytopenia was not recorded.
  • Grade 3 mucositis was observed in only 1 patient, whereas 2 patients (6%) developed an asymptomatic drop of left ventricular ejection fraction (LVEF) >10% below basal value.
  • In conclusion, this study suggests that amifostine can reduce doxorubicin related toxicity, thus improving the patients' quality of life and the efficacy/toxicity ratio of this drug.
  • [MeSH-major] Adenocarcinoma / drug therapy. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Breast Neoplasms / drug therapy
  • [MeSH-minor] Adult. Aged. Amifostine / administration & dosage. Blood Cell Count. Bone Neoplasms / drug therapy. Bone Neoplasms / secondary. Doxorubicin / administration & dosage. Female. Hematologic Diseases / chemically induced. Humans. Middle Aged. Soft Tissue Neoplasms / drug therapy. Soft Tissue Neoplasms / secondary. Survival Rate

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  • (PMID = 12469164.001).
  • [ISSN] 1021-335X
  • [Journal-full-title] Oncology reports
  • [ISO-abbreviation] Oncol. Rep.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 80168379AG / Doxorubicin; M487QF2F4V / Amifostine
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10. Tsutsumi M, Kitada H, Shiraiwa K, Takahama M, Tsujiuchi T, Sakitani H, Sasaki Y, Murakawa K, Yoshimoto M, Konishi Y: Inhibitory effects of combined administration of antibiotics and anti-inflammatory drugs on lung tumor development initiated by N-nitrosobis(2-hydroxypropyl)amine in rats. Carcinogenesis; 2000 Feb;21(2):251-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Inhibitory effects of combined administration of antibiotics and anti-inflammatory drugs on lung tumor development initiated by N-nitrosobis(2-hydroxypropyl)amine in rats.
  • The effects of antibiotics and anti-inflammatory drugs on the promotion stage of lung carcinogenesis initiated with N-nitrosobis(2-hydroxypropyl)amine (BHP) in rats were investigated in two experiments with a similar protocol.
  • BHP for 12 weeks followed by basal diet or basal diet containing 0.02% erythromycin (EM), 0.
  • The development of adenocarcinomas (AC), squamous cell carcinomas (SqC) and adenosquamous carcinomas (ASqC) was completely inhibited in rats given ABPC plus sho-saiko-to and the numbers of lung lesions including alveolar hyperplasias, adenomas and carcinomas were decreased in rats given EM plus sho-saiko-to or ABPC plus sho-saiko-to.
  • In experiment 2, rats received BHP in the same manner as in experiment 1 and basal diet or basal diet containing 0.04% ABPC, 0.006% piroxicam, 0.04% ABPC plus 0.006% piroxicam and 0.04% ABPC plus 0.75% ougon for 8 weeks.
  • [MeSH-major] Adenocarcinoma / prevention & control. Ampicillin / administration & dosage. Anti-Bacterial Agents / administration & dosage. Anti-Inflammatory Agents, Non-Steroidal / administration & dosage. Carcinogens / toxicity. Carcinoma, Adenosquamous / prevention & control. Carcinoma, Squamous Cell / prevention & control. Cocarcinogenesis. Drugs, Chinese Herbal / administration & dosage. Erythromycin / administration & dosage. Lung Neoplasms / prevention & control. Nitrosamines / toxicity. Penicillins / administration & dosage. Piroxicam / administration & dosage. Pneumonia, Bacterial / drug therapy
  • [MeSH-minor] Animals. Bronchoalveolar Lavage Fluid / microbiology. Disease Progression. Drug Evaluation, Preclinical. Drug Synergism. Gene Expression Regulation / drug effects. Inflammation. Macrophages / drug effects. Macrophages / physiology. Male. Neutrophils / drug effects. Neutrophils / physiology. Rats. Rats, Sprague-Dawley. Specific Pathogen-Free Organisms

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  • (PMID = 10657965.001).
  • [ISSN] 0143-3334
  • [Journal-full-title] Carcinogenesis
  • [ISO-abbreviation] Carcinogenesis
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] ENGLAND
  • [Chemical-registry-number] 0 / Anti-Bacterial Agents; 0 / Anti-Inflammatory Agents, Non-Steroidal; 0 / Carcinogens; 0 / Drugs, Chinese Herbal; 0 / Nitrosamines; 0 / Penicillins; 0 / ougon; 13T4O6VMAM / Piroxicam; 53609-64-6 / diisopropanolnitrosamine; 63364-01-2 / saiko-keishi-to; 63937KV33D / Erythromycin; 7C782967RD / Ampicillin
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11. Schmidt CM, Wang Y, Wiesenauer C: Novel combination of cyclooxygenase-2 and MEK inhibitors in human hepatocellular carcinoma provides a synergistic increase in apoptosis. J Gastrointest Surg; 2003 Dec;7(8):1024-33
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  • [Title] Novel combination of cyclooxygenase-2 and MEK inhibitors in human hepatocellular carcinoma provides a synergistic increase in apoptosis.
  • Cyclooxygenase-2 (COX-2) and ERK-MAPK mitogenic signaling pathways are important in human hepatocellular carcinoma.
  • We investigated the effect of COX-2 inhibition on ERK-MAPK signaling and the effect of combining MEK (MAPK kinase) and COX-2 inhibitors in human hepatocellular carcinoma in vitro.
  • COX-2 and MEK activity were determined by prostaglandin E(2) assay and phosphospecific immunoblot, respectively.
  • Cell growth was determined by cell proliferation and cell counts.
  • Cell cycle was determined by flow cytometry.
  • HepG2 and Hep3B cells do not express COX-1 or COX-2.
  • Correspondingly, basal and agonist (arachidonic acid, lipopolysaccharide)-stimulated COX-2 activity is undetectable.
  • Treatment of HepG2 and Hep3B cells with NS398 resulted in an increase in ERK1/2 phosphorylation (MEK activity) in a concentration-dependent fashion (NS398, 1 to 100 micromol/L).
  • Treatment with the COX-2 inhibitor NS398 in the presence of U0126 (MEK inhibitor) effectively suppressed ERK1/2 phosphorylation as determined by phosphospecific ERK1/2 immunoblot.
  • Total ERK1/2 and COX-2 were unchanged with NS398 and U0126 treatments.
  • Relative apoptosis was increased with U0126 alone or in combination with NS398 (9 to 10 times the control value), eliminating the anti-apoptotic effect of NS398.
  • In Hep3B cells, apoptosis was unchanged with NS398 (1 to 50 micromol/L) or U0126 (1 to 10 micromol/L) alone.
  • The combination of NS398 and U0126 in Hep3B cells resulted in a synergistic increase in apoptosis (10 times the control value).
  • Relative apoptosis in both cell lines strongly correlated with changes in the expression of the antiapoptotic protein Bcl-xL.
  • Cellular growth was assessed by colorimetric proliferation assay and cell counts.
  • HepG2 and Hep3B cells had concentration-dependent inhibition of cell growth with NS398 or U0126 treatment alone.
  • Growth inhibitory effects in HepG2 and Hep3B cells with combination treatment appear to be, in part, secondary to the induction of G(0)/G(1) and G(2)/M cell cycle arrest, respectively, as determined by flow cytometry.
  • [MeSH-major] Apoptosis / drug effects. Carcinoma, Hepatocellular / drug therapy. Enzyme Inhibitors / pharmacology. Isoenzymes / antagonists & inhibitors. Liver Neoplasms / drug therapy. Mitogen-Activated Protein Kinase Kinases / antagonists & inhibitors
  • [MeSH-minor] Adenocarcinoma / drug therapy. Butadienes / pharmacology. Cell Cycle / drug effects. Cell Division / drug effects. Cell Line, Tumor. Cyclooxygenase 1. Cyclooxygenase 2. Dinoprostone / metabolism. Drug Synergism. Humans. Membrane Proteins. Mitogen-Activated Protein Kinases / drug effects. Nitriles / pharmacology. Nitrobenzenes / pharmacology. Pancreatic Neoplasms / drug therapy. Prostaglandin-Endoperoxide Synthases / drug effects. Signal Transduction / drug effects. Sulfonamides / pharmacology

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  • [Cites] Oncogene. 1999 Nov 18;18(48):6635-40 [10597268.001]
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  • (PMID = 14675712.001).
  • [ISSN] 1091-255X
  • [Journal-full-title] Journal of gastrointestinal surgery : official journal of the Society for Surgery of the Alimentary Tract
  • [ISO-abbreviation] J. Gastrointest. Surg.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Butadienes; 0 / Enzyme Inhibitors; 0 / Isoenzymes; 0 / Membrane Proteins; 0 / Nitriles; 0 / Nitrobenzenes; 0 / Sulfonamides; 0 / U 0126; 123653-11-2 / N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide; EC 1.14.99.1 / Cyclooxygenase 1; EC 1.14.99.1 / Cyclooxygenase 2; EC 1.14.99.1 / PTGS1 protein, human; EC 1.14.99.1 / PTGS2 protein, human; EC 1.14.99.1 / Prostaglandin-Endoperoxide Synthases; EC 2.7.11.24 / Mitogen-Activated Protein Kinases; EC 2.7.12.2 / Mitogen-Activated Protein Kinase Kinases; K7Q1JQR04M / Dinoprostone
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14. Vesely DL: Cardiac and renal hormones: anticancer effects in vitro and in vivo. J Investig Med; 2009 Jan;57(1):22-8
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  • BACKGROUND: Four cardiovascular hormones, ie, vessel dilator, long-acting natriuretic peptide, kaliuretic peptide, and atrial natriuretic peptide each at 1 mmol/L, decrease up to 97% of human breast, ovarian, pancreatic, colon, kidney, and prostate adenocarcinoma cells, as well as small cell and squamous cell lung cancer cells within 24 hours.
  • METHODS: Vessel dilator, long-acting natriuretic peptide, and kaliuretic peptide were investigated in vivo.
  • RESULTS: These cardiac hormones completely stop the growth of human pancreatic adenocarcinomas in athymic mice and decrease their tumor volume by 49%, 28%, and 11%, respectively, in 1 week.
  • When these cardiac hormones are given subcutaneously for 1 month via osmotic pumps with the pumps changed weekly, up to 80% of the human pancreatic adenocarcinomas growing in athymic mice can be completely eliminated.
  • Similarly, two thirds of human breast cancers in athymic mice can be eliminated without surgery with these cardiac hormones.
  • Natriuretic peptide receptors A-, B-, and C- are present on the cancer cells to mediate atrial natriuretic peptide's effects.
  • CONCLUSIONS: The cardiac hormones' anticancer mechanism of action(s) include a strong inhibition of mitogen (epidermal growth factor and insulin) activated extracellular signal-regulated kinases (ERK) 1/2 and as well as inhibition of basal extracellular-signal regulated kinase 1/2 and upstream MEK 1/2 phosphorylation.
  • [MeSH-major] Natriuretic Peptides / therapeutic use. Neoplasms / drug therapy

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  • (PMID = 19092678.001).
  • [ISSN] 1081-5589
  • [Journal-full-title] Journal of investigative medicine : the official publication of the American Federation for Clinical Research
  • [ISO-abbreviation] J. Investig. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.; Review
  • [Publication-country] Canada
  • [Chemical-registry-number] 0 / Natriuretic Peptides
  • [Number-of-references] 76
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15. Uphoff J, Woziwodzki J, Schattka SO, Kollias A: [Loss of differentiation of a prostate adenocarcinoma after hormone therapy: the example of a metastasis in the spongy body of the penis]. Aktuelle Urol; 2008 Sep;39(5):373-7
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  • [Title] [Loss of differentiation of a prostate adenocarcinoma after hormone therapy: the example of a metastasis in the spongy body of the penis].
  • [Transliterated title] Differenzierungsverlust eines Adenokarzinoms der Prostata nach Hormontherapie: am Beispiel einer Schwellkörpermetastase des Penis.
  • Prostate cancer as the most frequent malignoma of the male is the main primary lesion.
  • Metastases in the penis only occur at an advanced state of the tumour and with a high dedifferentiation, e. g., ductal adenocarcinoma.
  • Changes in the morphology of the prostate carcinoma are specially known for the occurrence of small-cell neuroendocrine and undifferentiated carcinomas.
  • Often prior to the transformation an anti-androgen therapy has been undertaken.
  • At this state of the disease, there is only the possibility of a palliative therapy with a poor prognosis.
  • The increasing histological dedifferentiation of the tumour tissue can make it difficult or even impossible to identify the primary lesion.
  • [MeSH-major] Adenocarcinoma / secondary. Androgen Antagonists / therapeutic use. Antineoplastic Agents, Hormonal / therapeutic use. Carcinoma, Basal Cell / secondary. Carcinoma, Transitional Cell / secondary. Cell Transformation, Neoplastic / pathology. Diphosphonates / therapeutic use. Gonadotropin-Releasing Hormone / antagonists & inhibitors. Neoplasms, Multiple Primary / drug therapy. Penile Neoplasms / secondary. Prostatic Neoplasms / drug therapy
  • [MeSH-minor] Aged. Biomarkers, Tumor / analysis. Biopsy. Bone Neoplasms / drug therapy. Bone Neoplasms / pathology. Bone Neoplasms / secondary. Bone Neoplasms / surgery. Combined Modality Therapy. Cystectomy. Diagnosis, Differential. Disease Progression. Humans. Lymphatic Metastasis. Male. Neoplasm Staging. Penis / pathology. Penis / surgery. Prostate / pathology. Prostate / surgery. Prostatectomy

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  • (PMID = 18798127.001).
  • [ISSN] 0001-7868
  • [Journal-full-title] Aktuelle Urologie
  • [ISO-abbreviation] Aktuelle Urol
  • [Language] ger
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Androgen Antagonists; 0 / Antineoplastic Agents, Hormonal; 0 / Biomarkers, Tumor; 0 / Diphosphonates; 33515-09-2 / Gonadotropin-Releasing Hormone
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16. Kohno H, Maeda M, Tanino M, Tsukio Y, Ueda N, Wada K, Sugie S, Mori H, Tanaka T: A bitter diterpenoid furanolactone columbin from Calumbae Radix inhibits azoxymethane-induced rat colon carcinogenesis. Cancer Lett; 2002 Sep 26;183(2):131-9

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The modifying effect of dietary administration of a diterpenoid furanolactone columbin isolated from the crude drug Calumbae Radix (the root of Jateorhiza columba MIERS, Menispermacea) on azoxymethane (AOM)-induced was investigated in male F344 rats.
  • Animals were initiated with AOM (three weekly subcutaneous injections of 15 mg/kg body weight) to induce colonic neoplasms.
  • They were fed the experimental diets mixed with columbin (4, 20, and 100 ppm) for 4 weeks, starting 1 week before the first dosing of AOM and thereafter maintained on the basal diet without columbin.
  • Additional experimental groups included the AOM alone group, the columbin alone group (100 ppm in diet for 4 weeks), and the untreated control group.
  • Dietary feeding of columbin (4, 20, and 100 ppm) during the initiation phase of AOM-induced colon carcinogenesis reduced the incidence and multiplicity of colonic adenocarcinoma and the inhibition by feeding of 20 ppm (incidence: 20%, P=0.0242 and multiplicity: 0.20+/-0.40, P<0.02) and 100 ppm (incidence: 10%, P=0.0029 and multiplicity: 0.10+/-0.30, P<0.002) columbin was significant when compared with the AOM alone group (incidence: 55% and multiplicity: 0.55+/-0.50).
  • Also, columbin administration in diet lowered the number of argyrophilic nucleolar organizer regions protein per nucleus in non-lesional colonic crypts and the blood polyamine content, which are reflected in cell proliferation activity.
  • These results indicate chemopreventive ability of dietary columbin against chemically induced colon tumorigenesis when fed during the initiation phase, providing a scientific basis for chemopreventive ability of columbin against human colon cancer.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Azoxymethane. Carcinogens. Colonic Neoplasms / chemically induced. Colonic Neoplasms / drug therapy. Diterpenes / chemistry. Diterpenes / pharmacology. Lactones / chemistry. Lactones / pharmacology. Lactones / therapeutic use. Terpenes / therapeutic use
  • [MeSH-minor] Animals. Cell Nucleus / metabolism. Colon / pathology. Dose-Response Relationship, Drug. Male. Mucous Membrane / pathology. Organ Size. Polyamines / blood. Rats. Rats, Inbred F344. Time Factors

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  • (PMID = 12065087.001).
  • [ISSN] 0304-3835
  • [Journal-full-title] Cancer letters
  • [ISO-abbreviation] Cancer Lett.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Carcinogens; 0 / Diterpenes; 0 / Lactones; 0 / Polyamines; 0 / Terpenes; KKI91P85GE / columbin; MO0N1J0SEN / Azoxymethane
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17. Iwase H, Kurebayashi J, Tsuda H, Ohta T, Kurosumi M, Miyamoto K, Yamamoto Y, Iwase T: Clinicopathological analyses of triple negative breast cancer using surveillance data from the Registration Committee of the Japanese Breast Cancer Society. Breast Cancer; 2010 Apr;17(2):118-24
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  • [Title] Clinicopathological analyses of triple negative breast cancer using surveillance data from the Registration Committee of the Japanese Breast Cancer Society.
  • BACKGROUND: Triple negative (TN) breast cancer is defined as a subtype that is negative for estrogen receptor (ER), progesterone receptor (PgR), and human epidermal growth factor receptor 2 (HER2).
  • This cancer was diagnosed at a slightly advanced stage and with more cases positive for lymph node metastases than other subtypes.
  • Mucinous, tubular, or secretary carcinomas were frequently found in the hormone receptor positive/HER2 negative subtype, while squamous cell carcinoma, spindle cell carcinoma, and metaplastic carcinoma with bone/cartilage metaplasia were very frequently found in the TN group.
  • Apocrine carcinoma was also found very frequently in the TN group.
  • Selection of chemotherapy was not based on receptor subtypes, but was determined by the degree of tumor progression.
  • CONCLUSIONS: Although TN types are similar to basal-like breast tumor, as determined by gene profiling, their diagnosis needs verification by determination of the level of epidermal growth factor receptor or cytokeratin 5/6 expression.
  • TN type should be examined further for immunohistochemical features and analyzed for prognostic details in this cohort.
  • [MeSH-minor] Adenocarcinoma / metabolism. Adenocarcinoma / pathology. Adenocarcinoma, Scirrhous / metabolism. Adenocarcinoma, Scirrhous / pathology. Adult. Aged. Aged, 80 and over. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Biomarkers, Tumor / metabolism. Carcinoma / metabolism. Carcinoma / pathology. Carcinoma, Intraductal, Noninfiltrating / metabolism. Carcinoma, Intraductal, Noninfiltrating / pathology. Carcinoma, Lobular / metabolism. Carcinoma, Lobular / pathology. Female. Humans. Japan. Middle Aged. Prognosis. Receptor, ErbB-2 / metabolism. Registries. Societies, Medical / statistics & numerical data. Young Adult


18. Donadelli M, Costanzo C, Beghelli S, Scupoli MT, Dandrea M, Bonora A, Piacentini P, Budillon A, Caraglia M, Scarpa A, Palmieri M: Synergistic inhibition of pancreatic adenocarcinoma cell growth by trichostatin A and gemcitabine. Biochim Biophys Acta; 2007 Jul;1773(7):1095-106
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  • [Title] Synergistic inhibition of pancreatic adenocarcinoma cell growth by trichostatin A and gemcitabine.
  • We investigated the ability of the histone deacetylase (HDAC) inhibitor trichostatin A (TSA) to interact with gemcitabine (GEM) in inducing pancreatic cancer cell death.
  • The combined treatment with TSA and GEM synergistically inhibited growth of four pancreatic adenocarcinoma cell lines and induced apoptosis.
  • This effect was associated with the induction of reactive oxygen species (ROS) by GEM, increased expression of the pro-apoptotic BIM gene by both TSA and GEM and downregulation of the 5'-nucleotidase UMPH type II gene by TSA.
  • The expression of other genes critical for GEM resistance (nucleoside transporters, deoxycytidine kinase, cytidine deaminase, and ribonucleotide reductase genes) was not affected by TSA.
  • The functional role of ROS in cell growth inhibition by GEM was supported by (i) a significantly reduced GEM-associated growth inhibition by the free radical scavenger N-acetyl-L-cysteine, and (ii) a positive correlation between the basal level of ROS and sensitivity to GEM in 10 pancreatic cancer cell lines.
  • The functional role of both Bim and 5'-nucleotidase UMPH type II in cell growth inhibition by TSA and GEM was assessed by RNA interference assays.
  • In vivo studies on xenografts of pancreatic adenocarcinoma cells in nude mice showed that the association of TSA and GEM reduced to 50% the tumour mass and did not cause any apparent form of toxicity, while treatments with TSA or GEM alone were ineffective.
  • In conclusion, the present study demonstrates a potent anti-tumour activity of TSA/GEM combination against pancreatic cancer cells in vitro and in vivo, strongly supporting the use of GEM in combination with an HDAC inhibitor for pancreatic cancer therapy.
  • [MeSH-major] Adenocarcinoma / metabolism. Cell Proliferation / drug effects. Deoxycytidine / analogs & derivatives. Enzyme Inhibitors. Hydroxamic Acids. Pancreatic Neoplasms / metabolism
  • [MeSH-minor] 5'-Nucleotidase / genetics. 5'-Nucleotidase / metabolism. Animals. Apoptosis / physiology. Apoptosis Regulatory Proteins / metabolism. Cell Cycle / physiology. Cell Line, Tumor. Glycoproteins / genetics. Glycoproteins / metabolism. Histone Deacetylase Inhibitors. Humans. Membrane Proteins / metabolism. Mice. Proto-Oncogene Proteins / metabolism. Reactive Oxygen Species / metabolism

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  • (PMID = 17555830.001).
  • [ISSN] 0006-3002
  • [Journal-full-title] Biochimica et biophysica acta
  • [ISO-abbreviation] Biochim. Biophys. Acta
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Apoptosis Regulatory Proteins; 0 / Bcl-2-like protein 11; 0 / Enzyme Inhibitors; 0 / Glycoproteins; 0 / Histone Deacetylase Inhibitors; 0 / Hydroxamic Acids; 0 / Membrane Proteins; 0 / Proto-Oncogene Proteins; 0 / Reactive Oxygen Species; 0W860991D6 / Deoxycytidine; 3X2S926L3Z / trichostatin A; B76N6SBZ8R / gemcitabine; EC 3.1.3.5 / 5'-Nucleotidase; EC 3.1.3.5 / NT5C3 protein, human
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19. Fahy BN, Schlieman M, Virudachalam S, Bold RJ: AKT inhibition is associated with chemosensitisation in the pancreatic cancer cell line MIA-PaCa-2. Br J Cancer; 2003 Jul 21;89(2):391-7
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  • [Title] AKT inhibition is associated with chemosensitisation in the pancreatic cancer cell line MIA-PaCa-2.
  • Activation of the serine/threonine kinase AKT is common in pancreatic cancer; inhibition of which sensitises cells to the apoptotic effect of chemotherapy.
  • Inhibiting this pathway had little effect on the basal level of apoptosis in pancreatic cancer cells, but increased the apoptotic effect of chemotherapy.
  • The antiapoptotic effect of AKT activation in pancreatic cancer cells may involve transcriptional induction of a profile of BCL-2 proteins that confer resistance to apoptosis; alteration of this balance allows sensitisation to the apoptotic effect of chemotherapy.
  • [MeSH-major] Adenocarcinoma / genetics. Adenocarcinoma / physiopathology. Apoptosis. Gene Expression Regulation, Neoplastic. NF-kappa B / pharmacology. Pancreatic Neoplasms / genetics. Pancreatic Neoplasms / physiopathology. Proto-Oncogene Proteins / biosynthesis. Proto-Oncogene Proteins c-bcl-2 / pharmacology
  • [MeSH-minor] Humans. Protein-Serine-Threonine Kinases. Protein-Tyrosine Kinases. Proto-Oncogene Proteins c-akt. Transcription, Genetic. Tumor Cells, Cultured

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  • (PMID = 12865934.001).
  • [ISSN] 0007-0920
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / NF-kappa B; 0 / Proto-Oncogene Proteins; 0 / Proto-Oncogene Proteins c-bcl-2; EC 2.7.10.1 / Protein-Tyrosine Kinases; 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
  • [Other-IDs] NLM/ PMC2394257
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20. Johansen P, Berg K, Selbo PK, Hofbauer GF: [Photochemical internalisation (PCI): a further development of photodynamic therapy for the treatment of skin cancer]. Praxis (Bern 1994); 2010 Nov 17;99(23):1423-8
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  • [Title] [Photochemical internalisation (PCI): a further development of photodynamic therapy for the treatment of skin cancer].
  • [Transliterated title] Photochemische Internalisierung (PCI): eine Weiterentwicklung der photodynamischen Therapie zur Behandlung von Hautkrebs.
  • Recently, several new and non-invasive methods have been introduced for the treatment of skin cancers.
  • Topical creams using the immune modulator imiquimod or the COX inhibitor diclofenac (with hyaluronic acid) are now registered for use against neoplasms such as basal or squamous cell carcinoma.
  • Another modern treatment option is photodynamic therapy (PDT).
  • A refined version of PDT, namely photochemical internalisation, is currently subject to a first clinical trial in patients with osteosarcoma, squamous cell carcinoma, head and neck cancer as well as adenocarcinoma of the breast.
  • Preliminary results from this trial suggest that PCI seems to be a promising treatment.
  • [MeSH-major] Carcinoma, Basal Cell / drug therapy. Carcinoma, Squamous Cell / drug therapy. Melanoma / drug therapy. Photochemotherapy / methods. Skin Neoplasms / drug therapy
  • [MeSH-minor] Animals. Antineoplastic Agents / pharmacokinetics. Antineoplastic Agents / therapeutic use. Cytosol / drug effects. Endocytosis. Endosomes / drug effects. Humans. Melanoma, Experimental / drug therapy. Mice. Neoplasm Transplantation

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  • (PMID = 21082595.001).
  • [ISSN] 1661-8157
  • [Journal-full-title] Praxis
  • [ISO-abbreviation] Praxis (Bern 1994)
  • [Language] ger
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Antineoplastic Agents
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21. Bi S, Liu JR, Li Y, Wang Q, Liu HK, Yan YG, Chen BQ, Sun WG: gamma-Tocotrienol modulates the paracrine secretion of VEGF induced by cobalt(II) chloride via ERK signaling pathway in gastric adenocarcinoma SGC-7901 cell line. Toxicology; 2010 Jul-Aug;274(1-3):27-33
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  • [Title] gamma-Tocotrienol modulates the paracrine secretion of VEGF induced by cobalt(II) chloride via ERK signaling pathway in gastric adenocarcinoma SGC-7901 cell line.
  • These growth factors, such as vascular endothelial growth factor (VEGF), play a major role in the regulation of tumor angiogenesis and metastasis.
  • In this study, the effect of gamma-tocotrienol, a natural product commonly found in palm oil and rice bran, on the accumulation of HIF-1alpha protein and the paracrine secretion of VEGF in human gastric adenocarcinoma SGC-7901 cell line induced by cobalt(II) chloride (as a hypoxia mimic) was investigated.
  • Both basal level and cobalt(II) chloride-induced HIF-1alpha protein accumulation and VEGF paracrine secretion were inhibited in SGC-7901 cells treated with gamma-tocotrienol at 60 micromol/L treatment for 24 h.
  • The mechanism seems to involve in inhibiting hypoxia-mediated activation of p-ERK1/2, it leads to a marked decrease in hypoxia-induced HIF-1alpha protein accumulation and VEGF secretion.
  • These data suggest that HIF-1alpha/VEGF could be a promising target for gamma-tocotrienol in an effective method of chemoprevention and chemotherapy in human gastric cancer.
  • [MeSH-minor] Adenocarcinoma. Cell Line. Chromans. Cobalt / pharmacology. Guanylate Cyclase. Humans. Hypoxia-Inducible Factor 1, alpha Subunit / metabolism. Hypoxia-Inducible Factor 1, alpha Subunit / pharmacology. Mitogen-Activated Protein Kinase 3 / metabolism. Mitogen-Activated Protein Kinase 3 / pharmacology. Neovascularization, Pathologic. Phosphorylation. Receptors, Cytoplasmic and Nuclear. Signal Transduction / drug effects. Vascular Endothelial Growth Factors / metabolism. Vascular Endothelial Growth Factors / pharmacology. Vitamin E / analogs & derivatives

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  • [Copyright] 2010 Elsevier Ireland Ltd. All rights reserved.
  • (PMID = 20452389.001).
  • [ISSN] 1879-3185
  • [Journal-full-title] Toxicology
  • [ISO-abbreviation] Toxicology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Chromans; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / Proteins; 0 / Receptors, Cytoplasmic and Nuclear; 0 / Vascular Endothelial Growth Factor A; 0 / Vascular Endothelial Growth Factors; 1406-18-4 / Vitamin E; 3G0H8C9362 / Cobalt; 4382-43-8 / plastochromanol 8; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 3; EC 4.6.1.2 / Guanylate Cyclase; EC 4.6.1.2 / soluble guanylyl cyclase
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22. Hoffmann S, Wunderlich A, Lingelbach S, Musholt PB, Musholt TJ, von Wasielewski R, Zielke A: Expression and secretion of endostatin in thyroid cancer. Ann Surg Oncol; 2008 Dec;15(12):3601-8
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  • BACKGROUND: In thyroid cancer (TC) endostatin was identified as a powerful negative regulator of tumor angiogenesis in vitro.
  • It is currently being evaluated in phase I trials for antiangiogenic therapy in various solid tumors.
  • The aim of this study was to evaluate endostatin expression in archival TC specimens and its secretion following stimulation with thyrotropin (TSH) and epidermal growth factor (EGF) in TC cell lines.
  • METHODS: Tissue microarrays of 44 differentiated and 7 anaplastic TC and their metastasis were immunostained for endostatin protein expression and compared with corresponding non-neoplastic thyroid tissue (NT).
  • In vitro, six differentiated (FTC133, FTC236, HTC, HTC-TSHr, XTC, and TPC1) and three anaplastic (C643, Hth74, Kat4.0) TC cell lines were evaluated for basal as well as TSH (1-100 mU/ml) and EGF stimulated (1-100 ng/ml) endostatin.
  • In vitro, basal endostatin secretion varied between 33 +/- 5 pg/ml (FTC236) and 549 +/- 65 pg/ml (TPC1) and was doubled in FTC, when the "primary" (FTC133) was compared with the metastasis (FTC236).
  • Some cell lines showed TSH-induced (e.g., 60% in XTC) or EGF-induced (e.g., 120% in TPC1) upregulation of endostatin secretion, while others did not, despite documented receptor expression.
  • CONCLUSION: This study demonstrates endostatin expression in TC, metastasis and--less frequently and intensely--in NT, suggesting a possible association to tumor progression.
  • In vitro, endostatin secretion of some cell lines is regulated by TSH and EGF, however the individual differences deserve further functional studies.
  • These results support rather tumor-specific than histotype-specific expression and regulation of endostatin in TC.
  • [MeSH-major] Adenocarcinoma, Follicular / metabolism. Angiogenesis Inhibitors / metabolism. Carcinoma / metabolism. Carcinoma, Papillary / metabolism. Endostatins / metabolism. Thyroid Gland / metabolism. Thyroid Neoplasms / metabolism
  • [MeSH-minor] Cell Differentiation / drug effects. Enzyme-Linked Immunosorbent Assay. Epidermal Growth Factor / pharmacology. Humans. Immunoenzyme Techniques. Lymphatic Metastasis. Paraffin Embedding. Thyrotropin / pharmacology. Tumor Cells, Cultured

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  • (PMID = 18818971.001).
  • [ISSN] 1534-4681
  • [Journal-full-title] Annals of surgical oncology
  • [ISO-abbreviation] Ann. Surg. Oncol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Endostatins; 62229-50-9 / Epidermal Growth Factor; 9002-71-5 / Thyrotropin
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23. Husain A, Blumenschein G, Esmaeli B: Treatment and outcomes for metastatic sebaceous cell carcinoma of the eyelid. Int J Dermatol; 2008 Mar;47(3):276-9
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  • [Title] Treatment and outcomes for metastatic sebaceous cell carcinoma of the eyelid.
  • OBJECTIVE: To report the management and outcomes in patients with metastatic eyelid sebaceous cell carcinoma.
  • METHODS: The clinical records of four patients with metastatic eyelid sebaceous cell carcinoma treated between January 1999 and August 2006 were reviewed.
  • RESULTS: The study included four women with a mean age of 66 years.
  • Metastatic sites included the lung in three patients, regional lymph nodes in two, liver in two, and bone in one.
  • Time from diagnosis of eyelid carcinoma to metastasis ranged from 0 to 62 months.
  • Treatment of regional nodal metastasis consisted of complete neck dissection followed by radiation therapy.
  • One patient developed lung metastasis 5 years after the diagnosis of eyelid tumor; she was treated with systemic chemotherapy followed by subtotal lung resection.
  • Systemic chemotherapy was considered for two additional patients: in one, chemotherapy was deferred due to poor performance status and ongoing medical problems; and another patient died before chemotherapy could be started.
  • The patient with bony metastasis was treated with radiation therapy to the spine.
  • The follow-up time from diagnosis of metastasis to last contact or death ranged from 1 month to 3 years (median of 21 months).
  • CONCLUSION: Eyelid sebaceous cell carcinoma can result in systemic metastasis and death.
  • Metastasis can be discovered as late as 5 years after treatment of the eyelid carcinoma, warranting continued surveillance.
  • Treatment of metastatic disease may include a combination of chemotherapy, radiation, and surgical neck dissection.
  • [MeSH-major] Adenocarcinoma, Sebaceous / secondary. Bone Neoplasms / secondary. Eyelid Neoplasms / pathology. Liver Neoplasms / secondary. Lung Neoplasms / secondary. Parotid Neoplasms / secondary. Sebaceous Gland Neoplasms / pathology
  • [MeSH-minor] Aged. Aged, 80 and over. Carcinoma, Basal Cell / diagnosis. Chalazion / diagnosis. Diagnostic Errors. Female. Humans. Lymphatic Metastasis / radiotherapy. Middle Aged. Retrospective Studies

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  • (PMID = 18289332.001).
  • [ISSN] 1365-4632
  • [Journal-full-title] International journal of dermatology
  • [ISO-abbreviation] Int. J. Dermatol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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24. Lovrić E, Gatalica Z, Eyzaguirre E, Kruslin B: Expression of maspin and glutathionine-S-transferase-pi in normal human prostate and prostatic carcinomas. Appl Immunohistochem Mol Morphol; 2010 Oct;18(5):429-32
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  • [Title] Expression of maspin and glutathionine-S-transferase-pi in normal human prostate and prostatic carcinomas.
  • BACKGROUND: Maspin and glutathionine-S-transferase-pi (GST-pi) are both involved in tumor suppression activity.
  • Maspin expression functions as an inhibitor of tumor progression preventing the local invasion and etastatic spread of prostate cancer cells.
  • GST-pi has an essential role in the inactivation of xenobiotic agents and protection from oxidative stress and in resistance to chemotherapy.
  • DESIGN: Maspin and GST-pi expression were assessed in needle core and transurethral resection prostatic biopsies from 42 patients (34 with carcinoma, and 8 with normal prostate gland) using immunohistochemical methods.
  • RESULTS: Maspin and GST-pi were strongly and consistently coexpressed in the cytoplasm of basal cells of normal prostatic glands, whereas normal luminal cells were inconsistently weakly positive.
  • Prostatic adenocarcinomas overexpressed maspin in 27/34 cases (79%).
  • In contrast, only 1 case of prostatic carcinoma expressed GST-pi.
  • CONCLUSION: Consistent coexpression of maspin and GST-pi was observed in basal cells of the prostatic glands, which could be used as an additional immunohistochemical test in the evaluation of prostatic malignancy.
  • Prostatic adenocarcinomas express maspin in an aberrant nuclear distribution without coexpresion of GST-pi.
  • These results indicate a deregulation of expression of maspin and GST-pi in prostatic adenocarcinomas.

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  • (PMID = 20453817.001).
  • [ISSN] 1533-4058
  • [Journal-full-title] Applied immunohistochemistry & molecular morphology : AIMM
  • [ISO-abbreviation] Appl. Immunohistochem. Mol. Morphol.
  • [Language] ENG
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / SERPIN-B5; 0 / Serpins; EC 2.5.1.18 / Glutathione S-Transferase pi
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25. McCormick DL, Rao KV, Johnson WD, Bosland MC, Lubet RA, Steele VE: Null activity of selenium and vitamin e as cancer chemopreventive agents in the rat prostate. Cancer Prev Res (Phila); 2010 Mar;3(3):381-92
Hazardous Substances Data Bank. N-NITROSO-N-METHYLUREA .

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  • [Title] Null activity of selenium and vitamin e as cancer chemopreventive agents in the rat prostate.
  • After stimulation of prostate epithelial cell proliferation by a sequential regimen of cyproterone acetate followed by testosterone propionate, male Wistar-Unilever rats received a single i.v. injection of N-methyl-N-nitrosourea (MNU) followed by chronic androgen stimulation via subcutaneous implantation of testosterone pellets.
  • At 1 week post-MNU, groups of carcinogen-treated rats (39-44/group) were fed either a basal diet or a basal diet supplemented with l-selenomethionine (3 or 1.5 mg/kg diet; study 1), dl-alpha-tocopherol (vitamin E, 4,000 or 2,000 mg/kg diet; study 2), l-selenomethionine + vitamin E (3 + 2,000 mg/kg diet or 3 + 500 mg/kg diet; study 3), or selenized yeast (target selenium levels of 9 or 3 mg/kg diet; study 4).
  • No statistically significant reductions in prostate cancer incidence were identified in any group receiving dietary supplementation with selenium and/or vitamin E.
  • These data do not support the hypotheses that selenium and vitamin E are potent cancer chemopreventive agents in the prostate, and when considered with the recent clinical data reported in the Selenium and Vitamin E Cancer Prevention Trial (SELECT), show the predictive nature of this animal model for human prostate cancer chemoprevention.

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  • (PMID = 20145190.001).
  • [ISSN] 1940-6215
  • [Journal-full-title] Cancer prevention research (Philadelphia, Pa.)
  • [ISO-abbreviation] Cancer Prev Res (Phila)
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CN / N01-CN-95113; United States / NCI NIH HHS / CA / P30 CA016087; United States / NCI NIH HHS / CN / N01 CN095113; United States / NIEHS NIH HHS / ES / P30-ES-00260; United States / NCI NIH HHS / CN / N01 CN065120; United States / NIEHS NIH HHS / ES / P30 ES000260; United States / NCI NIH HHS / CA / P30-CA-16087; United States / NCI NIH HHS / CA / N01 CN35566; United States / NCI NIH HHS / CN / CN35566-02; United States / NCI NIH HHS / CN / N01-CN-65120; United States / NCI NIH HHS / CN / N01 CN35566-02; United States / NCI NIH HHS / CN / N01-CN-35566-02
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Alkylating Agents; 0 / Androgens; 0 / Antioxidants; 0 / Selenium Compounds; 1406-18-4 / Vitamin E; 3XMK78S47O / Testosterone; 4KM2BN5JHF / Cyproterone Acetate; 684-93-5 / Methylnitrosourea; 964MRK2PEL / Selenomethionine; H4N855PNZ1 / alpha-Tocopherol
  • [Other-IDs] NLM/ NIHMS161245; NLM/ PMC2945242
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26. Burrows N, Resch J, Cowen RL, von Wasielewski R, Hoang-Vu C, West CM, Williams KJ, Brabant G: Expression of hypoxia-inducible factor 1 alpha in thyroid carcinomas. Endocr Relat Cancer; 2010 Mar;17(1):61-72
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  • We evaluated the regulation of HIF-1 alpha and target gene expression in primary thyroid carcinomas and thyroid carcinoma cell lines (BcPAP, WRO, FTC-133 and 8505c).
  • HIF-1 alpha was not detectable in normal tissue but was expressed in thyroid carcinomas.
  • The HIF-1 target glucose transporter 1 was expressed to a similar level in all tumour types, whereas carbonic anhydrase-9 was significantly elevated in ATCs.
  • In vitro studies revealed a functionally active HIF-1 alpha pathway in thyroid cells with transcriptional activation observed after graded hypoxia (1% O(2), anoxia) or treatment with a hypoxia mimetic cobalt chloride.
  • High basal and hypoxia-induced expression of HIF-1 alpha in FTC-133 cells that harbour a phosphatase and tensin homologue (PTEN) mutation was reduced by introduction of wild-type PTEN.
  • Similarly, pharmacological inhibition of the phosphoinositide 3-kinase (PI3K) pathway using LY294002 inhibited HIF-1 alpha and HIF-1 alpha targets in all cell lines, including those with B-RAF mutations (BcPAP and 8505c).
  • HIF-1 is functionally expressed in thyroid carcinomas and is regulated not only by hypoxia but also via growth factor signalling pathways and, in particular, the PI3K pathway.
  • Given the strong association of HIF-1 alpha with an aggressive disease phenotype and therapeutic resistance, this pathway may be an attractive target for improved therapy in thyroid carcinomas.

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  • (PMID = 19808899.001).
  • [ISSN] 1479-6821
  • [Journal-full-title] Endocrine-related cancer
  • [ISO-abbreviation] Endocr. Relat. Cancer
  • [Language] ENG
  • [Grant] United Kingdom / Cancer Research UK / / C7820/A8696
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Chromones; 0 / Glucose Transporter Type 1; 0 / HIF1A protein, human; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / Morpholines; 0 / Neoplasm Proteins; 0 / RNA, Small Interfering; 154447-36-6 / 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one; 3G0H8C9362 / Cobalt; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.11.1 / BRAF protein, human; EC 2.7.11.1 / Proto-Oncogene Proteins B-raf; EC 3.1.3.48 / PTEN protein, human; EC 3.1.3.67 / PTEN Phosphohydrolase; EC 4.2.1.1 / CA9 protein, human; EC 4.2.1.1 / Carbonic Anhydrases; EVS87XF13W / cobaltous chloride
  • [Other-IDs] NLM/ PMC2828807
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27. Martinez VG, Williams KJ, Stratford IJ, Clynes M, O'Connor R: Overexpression of cytochrome P450 NADPH reductase sensitises MDA 231 breast carcinoma cells to 5-fluorouracil: possible mechanisms involved. Toxicol In Vitro; 2008 Apr;22(3):582-8
Hazardous Substances Data Bank. VINCRISTINE .

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  • Activity of cytochromes P450 is highly dependent on cytochrome P450 NADPH reductase (P450R), but this enzyme can also metabolise drugs on its own.
  • MDA 231 breast adenocarcinoma cells transfected with human P450R (MDA R4) or an empty vector (MDA EV) were exposed to a series of commonly used chemotherapeutic drugs.
  • Overexpression of P450R did not affect cell sensitivity to cisplatin, mitoxantrone, paclitaxel, docetaxel, vincristine or etoposide.
  • However, MDA R4 cells showed increased sensitivity to mitomycin C (6.6-fold) and also to 5-fluorouracil (2.8-fold).
  • In vitro toxicity assays where mitomycin C, 5-fluorouracil and vincristine were preincubated with microsomes expressing recombinant P450R showed that this effect was not a result of direct metabolism by P450R.
  • Levels of NADPH were considerably decreased in MDA R4 as compared to MDA EV cells, while reactive oxygen species (ROS) production was increased in MDA R4 cells in basal conditions, showing no significant further increase after treatment with mitomycin C or 5-fluorouracil.
  • P450R overexpression appears therefore to be detrimental to MDA 231 cells, depleting NADPH and increasing ROS levels; the increased oxidative stress observed in MDA R4 cells might explain the enhanced sensitivity to 5-fluorouracil.
  • Expression of this enzyme in tumour cells might therefore modulate response to 5-fluorouracil.
  • [MeSH-major] Antimetabolites, Antineoplastic / pharmacology. Breast Neoplasms / drug therapy. Fluorouracil / pharmacology. NADPH-Ferrihemoprotein Reductase / biosynthesis
  • [MeSH-minor] Antibiotics, Antineoplastic / metabolism. Antibiotics, Antineoplastic / pharmacology. Antineoplastic Agents, Phytogenic / metabolism. Antineoplastic Agents, Phytogenic / pharmacology. Blotting, Western. Cell Line, Tumor. Cell Survival. Female. Glutathione / metabolism. Humans. Microsomes / metabolism. Mitomycin / metabolism. Mitomycin / pharmacology. NADP / metabolism. Reactive Oxygen Species / metabolism. Transfection. Vincristine / metabolism. Vincristine / pharmacology

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  • (PMID = 18191533.001).
  • [ISSN] 0887-2333
  • [Journal-full-title] Toxicology in vitro : an international journal published in association with BIBRA
  • [ISO-abbreviation] Toxicol In Vitro
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / G0500366; United Kingdom / Medical Research Council / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / Antimetabolites, Antineoplastic; 0 / Antineoplastic Agents, Phytogenic; 0 / Reactive Oxygen Species; 50SG953SK6 / Mitomycin; 53-59-8 / NADP; 5J49Q6B70F / Vincristine; EC 1.6.2.4 / NADPH-Ferrihemoprotein Reductase; GAN16C9B8O / Glutathione; U3P01618RT / Fluorouracil
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28. Tanaka T, de Azevedo MB, Durán N, Alderete JB, Epifano F, Genovese S, Tanaka M, Tanaka T, Curini M: Colorectal cancer chemoprevention by 2 beta-cyclodextrin inclusion compounds of auraptene and 4'-geranyloxyferulic acid. Int J Cancer; 2010 Feb 15;126(4):830-40
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  • The inhibitory effects of novel prodrugs, inclusion complexes of 3-(4'-geranyloxy-3'-methoxyphenyl)-2-trans propenoic acid (GOFA) and auraptene (AUR) with beta-cyclodextrin (CD), on colon carcinogenesis were investigated using an azoxymethane (AOM)/dextran sodium sulfate (DSS) model.
  • Male CD-1 (ICR) mice initiated with a single intraperitoneal injection of AOM (10 mg/kg body weight) were promoted by the addition of 1.5% (w/v) DSS to their drinking water for 7 days.
  • They were then given a basal diet containing 2 dose levels (100 and 500 ppm) of GOFA/beta-CD or AUR/beta-CD for 15 weeks.
  • At Week 18, the development of colonic adenocarcinoma was significantly inhibited by feeding with GOFA/beta-CD at dose levels of 100 ppm (63% reduction in multiplicity, p < 0.05) and 500 ppm (83% reduction in the multiplicity, p < 0.001), when compared with the AOM/DSS group (multiplicity: 3.36 +/- 3.34).
  • In addition, feeding with 100 and 500 ppm (p < 0.01) of AUR/beta-CD suppressed the development of colonic adenocarcinomas.
  • The dietary administration with GOFA/beta-CD and AUR/beta-CD inhibited colonic inflammation and also modulated proliferation, apoptosis and the expression of several proinflammatory cytokines, such as nuclear factor-kappaB, tumor necrosis factor-alpha, Stat3, NF-E2-related factor 2, interleukin (IL)-6 and IL-1beta, which were induced in the adenocarcinomas.
  • [MeSH-major] Colorectal Neoplasms / drug therapy. Colorectal Neoplasms / prevention & control. Coumarins / therapeutic use. beta-Cyclodextrins / therapeutic use
  • [MeSH-minor] Animals. Colonic Neoplasms / drug therapy. Colonic Neoplasms / pathology. Diterpenes / therapeutic use. Humans. Immunohistochemistry. Incidence. Inflammation / drug therapy. Inflammation / etiology. Inflammation / pathology. Inflammatory Bowel Diseases / complications. Inhibitor of Apoptosis Proteins. Interleukin-1beta / metabolism. Interleukin-6 / metabolism. Male. Mice. Mice, Inbred ICR. Microtubule-Associated Proteins / metabolism. NF-kappa B / metabolism. Proliferating Cell Nuclear Antigen / metabolism. Propionates / therapeutic use. Repressor Proteins. Tumor Necrosis Factor-alpha / metabolism

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  • (PMID = 19688830.001).
  • [ISSN] 1097-0215
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 3-(4'-geranyloxy-3'-methoxyphenyl)-2-trans-propenoic acid; 0 / Birc5 protein, mouse; 0 / Coumarins; 0 / Diterpenes; 0 / Inhibitor of Apoptosis Proteins; 0 / Interleukin-1beta; 0 / Interleukin-6; 0 / Microtubule-Associated Proteins; 0 / NF-kappa B; 0 / Proliferating Cell Nuclear Antigen; 0 / Propionates; 0 / Repressor Proteins; 0 / Tumor Necrosis Factor-alpha; 0 / beta-Cyclodextrins; 495-02-3 / aurapten
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29. Casas A, Battah S, Di Venosa G, Dobbin P, Rodriguez L, Fukuda H, Batlle A, MacRobert AJ: Sustained and efficient porphyrin generation in vivo using dendrimer conjugates of 5-ALA for photodynamic therapy. J Control Release; 2009 Apr 17;135(2):136-43
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  • [Title] Sustained and efficient porphyrin generation in vivo using dendrimer conjugates of 5-ALA for photodynamic therapy.
  • The use of endogenous protoporphyrin IX (PpIX) after administration of 5-aminolaevulinic acid (ALA) has led to many applications in photodynamic therapy (PDT).
  • However the efficacy of ALA-PDT is sub-optimal for thicker tumours and improved ALA delivery and therapeutic response are required.
  • We have investigated the conjugation of ALA to a second-generation dxcendrimer for enhancing porphyrin synthesis in vitro and in vivo in a murine tumour model using systemic i.p. administration.
  • In vivo, the porphyrin kinetics from ALA exhibited an early peak between 3 and 4 h in most tissues, whereas the dendrimer induced sustained porphyrin production for over 24 h and basal values were not reached until 48 h after administration.
  • ALA dendrimers may be useful for metronomic PDT, and multiple low-dose ALA-PDT treatments.
  • [MeSH-major] Aminolevulinic Acid / pharmacology. Dendrimers / chemistry. Photochemotherapy. Photosensitizing Agents / therapeutic use. Porphyrins / metabolism
  • [MeSH-minor] Adenocarcinoma / drug therapy. Animals. Cell Line, Tumor. Cell Survival / drug effects. Coloring Agents / metabolism. Dose-Response Relationship, Drug. Injections, Subcutaneous. Male. Mammary Neoplasms, Experimental / drug therapy. Mice. Mice, Inbred BALB C. Molecular Structure. Molecular Weight. Protoporphyrins / biosynthesis. Structure-Activity Relationship. Tetrazolium Salts / metabolism. Thiazoles / metabolism. Time Factors. Xenograft Model Antitumor Assays

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  • (PMID = 19168101.001).
  • [ISSN] 1873-4995
  • [Journal-full-title] Journal of controlled release : official journal of the Controlled Release Society
  • [ISO-abbreviation] J Control Release
  • [Language] eng
  • [Grant] United Kingdom / Biotechnology and Biological Sciences Research Council / / BB/D011329/1; United Kingdom / Wellcome Trust / / 067062/Z/029/Z; United Kingdom / Biotechnology and Biological Sciences Research Council / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Coloring Agents; 0 / Dendrimers; 0 / Photosensitizing Agents; 0 / Porphyrins; 0 / Protoporphyrins; 0 / Tetrazolium Salts; 0 / Thiazoles; 88755TAZ87 / Aminolevulinic Acid; C2K325S808 / protoporphyrin IX; EUY85H477I / thiazolyl blue
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30. Lisovsky M, Patel K, Cymes K, Chase D, Bhuiya T, Morgenstern N: Immunophenotypic characterization of anal gland carcinoma: loss of p63 and cytokeratin 5/6. Arch Pathol Lab Med; 2007 Aug;131(8):1304-11
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  • [Title] Immunophenotypic characterization of anal gland carcinoma: loss of p63 and cytokeratin 5/6.
  • Anal gland carcinoma (AGC) is a rare perianal invasive cancer composed of tubular glands lined by cuboidal epithelium.
  • The clinical features and histogenesis of AGC are not well understood and its origin from anal glands is often difficult to prove.
  • Little is known about immunophenotypic features of AGC that could be useful in establishing the diagnosis.
  • In case 1 of AGC, radiation and chemotherapy preceded an abdominoperineal resection.
  • In biopsies from this case, the neoplastic anal glands had a tubular pattern, whereas most glands in the resection specimen exhibited mucinous features.
  • The histologic pattern in case 2 was tubular.
  • Normal anal glands showed immunoreactivity for myoepithelial and basal cell markers CK5/6 and p63 in basal and parabasal cell layers and for CK7 in superficial cell layers.
  • Anal gland carcinoma shares negativity for CDX2 and CK7+/CK20- profile with normal anal glands.
  • These data may be useful in establishing the diagnosis of AGC.
  • [MeSH-major] Adenocarcinoma / pathology. Anus Neoplasms / pathology. Biomarkers, Tumor / metabolism. Keratin-5 / metabolism. Keratin-6 / metabolism. Membrane Proteins / metabolism
  • [MeSH-minor] Anal Canal / metabolism. Anal Canal / pathology. Fluorescent Antibody Technique, Indirect. Hemorrhoids / pathology. Hemorrhoids / surgery. Humans. Immunoenzyme Techniques. Immunophenotyping. Male. Middle Aged

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  • [CommentIn] Arch Pathol Lab Med. 2008 Oct;132(10):1547-8 [18834205.001]
  • (PMID = 17683193.001).
  • [ISSN] 1543-2165
  • [Journal-full-title] Archives of pathology & laboratory medicine
  • [ISO-abbreviation] Arch. Pathol. Lab. Med.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / CKAP4 protein, human; 0 / Keratin-5; 0 / Keratin-6; 0 / Membrane Proteins
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31. Forest V, Campos L, Péoc'h M, Guyotat D, Vergnon JM: [Development of an experimental model for the study of the effects of cryotherapy on lung tumours]. Pathol Biol (Paris); 2005 May;53(4):199-203
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  • [Transliterated title] Mise au point d'un modèle d'étude des effets d'une cryothérapie sur des tumeurs pulmonaires.
  • Adenocarcinomas are today the most frequent lung cancers.
  • They are mainly treated by surgery or by chemotherapy, but for the most advanced stages a local cryotherapy can be proposed as a palliative option for bronchial desobstruction.
  • AIM OF THE STUDY: The aim of this work was to establish an experimental model to study in vivo the biological effects of this technique to propose it as a neoadjuvant treatment.
  • MATERIALS AND METHODS: A xenograft system was used: cells from the A549 cell line were injected subcutaneously into SCID mice.
  • Tumour nodes could be treated after seven weeks.
  • The histological study showed that these tumours faithfully reproduced the morphological features of adenocarcinoma, and developed an intratumoral neovascularization.
  • RESULTS: The basal expression of cleaved caspase-3 in untreated tumours (23%) increased after cryotherapy.
  • The increase was maximal eight hours after treatment (up to 47% of positive cells) and was less important with the first protocol, suggesting a lesser efficiency in the induction of apoptosis.
  • CONCLUSION: The establishment of this model, which is faithful to physiological features, allowed us to demonstrate in vivo time and dose-dependent effects of cryotherapy.
  • [MeSH-major] Adenocarcinoma / therapy. Cryotherapy. Lung Neoplasms / therapy. Neoadjuvant Therapy. Neoplasms, Experimental / therapy
  • [MeSH-minor] Animals. Cell Line, Tumor / transplantation. Humans. Male. Mice. Mice, SCID. Neoplasm Transplantation. Xenograft Model Antitumor Assays

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  • (PMID = 15850952.001).
  • [ISSN] 0369-8114
  • [Journal-full-title] Pathologie-biologie
  • [ISO-abbreviation] Pathol. Biol.
  • [Language] fre
  • [Publication-type] English Abstract; Evaluation Studies; Journal Article
  • [Publication-country] France
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32. Sohn TA, Su GH, Ryu B, Yeo CJ, Kern SE: High-throughput drug screening of the DPC4 tumor-suppressor pathway in human pancreatic cancer cells. Ann Surg; 2001 May;233(5):696-703
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  • [Title] High-throughput drug screening of the DPC4 tumor-suppressor pathway in human pancreatic cancer cells.
  • OBJECTIVE: To screen a library of small chemicals for compounds that activate the DPC4 signal transduction pathway in a human pancreatic cancer cell line.
  • SUMMARY BACKGROUND DATA: Various tumor-suppressor genes are mutated in all human cancers.
  • Specifically, DPC4 (deleted in pancreatic carcinoma, locus 4 or MADH4/SMAD4) is a tumor-suppressor gene mutated in approximately 50% of human pancreatic adenocarcinomas.
  • It would be useful to identify therapies that augment or restore the downstream functions of this critical signal transduction pathway, in hopes that such therapy would have a rational role in anticancer therapy.
  • METHODS: Using a commercially available plasmid vector with a luciferase reporter gene already incorporated, a DPC4-specific reporter construct was genetically engineered.
  • This construct was then stably integrated into the genome of a human pancreatic cancer cell line (PANC-1) that has wild-type DPC4.
  • Several stably transfected clones were tested for basal luciferase expression and inducibility with TGFbeta, which is known to activate the DPC4 signal transduction pathway.
  • A single transfected clone was chosen for the drug screen based on basal luciferase (reporter) expression and TGFbeta inducibility.
  • A systematic screen of the chemical library was then performed, using luciferase activity to detect DPC4 activity and induction of the signaling pathway.
  • Of the 16,320 compounds screened, 11 were associated with a 2- to 5-fold induction of luciferase activity, and one with a 12-fold activation.
  • CONCLUSIONS: These results confirm the feasibility of a specific high-throughput reporter system to screen a large compound library in human cells efficiently.
  • The screening identified several compounds capable of augmenting DPC4-specific luciferase reporter activity, and a specific mechanism for one compound was identified.
  • The discovery of such agents will aid our understanding of complex tumor-suppressive signaling pathways and may identify other potential therapeutic targets within this critical signaling pathway.
  • In addition, random drug screening provides an unbiased method for identifying drugs or lead compounds for potential therapeutic use.

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  • (PMID = 11323508.001).
  • [ISSN] 0003-4932
  • [Journal-full-title] Annals of surgery
  • [ISO-abbreviation] Ann. Surg.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01-CA62694
  • [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 / DNA-Binding Proteins; 0 / SMAD4 protein, human; 0 / Smad4 Protein; 0 / Trans-Activators; 0 / Transforming Growth Factor beta; 0 / Tumor Suppressor Protein p53
  • [Other-IDs] NLM/ PMC1421310
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33. Watson S, Serrate C, Vignot S: [Sonic Hedgehog signaling pathway: from embryology to molecular targeted therapies]. Bull Cancer; 2010 Dec;97(12):1477-83
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  • [Title] [Sonic Hedgehog signaling pathway: from embryology to molecular targeted therapies].
  • [Transliterated title] Voie de signalisation Sonic Hedgehog : du développement embryonnaire aux thérapies moléculaires ciblées.
  • During the past few years its implication in carcinogenesis has become clear and today it is acknowledged that this pathway plays a role in the malignant transformation of multiple cell types, either owing to the mutation of some of its components or to its erratic activation.
  • New molecular targeted therapies that inhibit the pathway have shown their unquestionable efficiency in several tumours -among which basal cell carcinoma, medulloblastoma, or pancreatic adenocarcinoma.
  • The assessment of these inhibitors in other types of tumours is currently underway with promising results, suggesting that the Sonic hedgehog signalling pathway may become one of the therapeutic targets of the future.
  • [MeSH-major] Embryonic Development / physiology. Hedgehog Proteins / antagonists & inhibitors. Hedgehog Proteins / physiology. Molecular Targeted Therapy / methods. Neoplasms / drug therapy. Neoplasms / genetics
  • [MeSH-minor] Anilides / therapeutic use. Animals. Carcinoma, Basal Cell / drug therapy. Carcinoma, Basal Cell / genetics. Cerebellar Neoplasms / genetics. Embryonic Induction / physiology. Humans. Lung Neoplasms / genetics. Medulloblastoma / genetics. Mutation / physiology. Neoplastic Stem Cells / physiology. Pancreatic Neoplasms / genetics. Patient Selection. Pyridines / therapeutic use. Receptors, Cell Surface / physiology. Signal Transduction / drug effects. Signal Transduction / physiology. Skin Neoplasms / drug therapy. Skin Neoplasms / genetics. Small Cell Lung Carcinoma / genetics

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  • (PMID = 21220225.001).
  • [ISSN] 1769-6917
  • [Journal-full-title] Bulletin du cancer
  • [ISO-abbreviation] Bull Cancer
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Anilides; 0 / Hedgehog Proteins; 0 / HhAntag691; 0 / Pyridines; 0 / Receptors, Cell Surface; 0 / patched receptors
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34. Darash-Yahana M, Pikarsky E, Abramovitch R, Zeira E, Pal B, Karplus R, Beider K, Avniel S, Kasem S, Galun E, Peled A: Role of high expression levels of CXCR4 in tumor growth, vascularization, and metastasis. FASEB J; 2004 Aug;18(11):1240-2
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  • [Title] Role of high expression levels of CXCR4 in tumor growth, vascularization, and metastasis.
  • Hormone refractory metastatic prostate cancer remains an incurable disease.
  • We found that high expression levels of the chemokine receptor CXCR4 correlated with the presence of metastatic disease in prostate cancer patients.
  • Positive staining for CXCL12, the ligand for CXCR4, was mainly present in the tumor-associated blood vessels and basal cell hyperplasia.
  • Moreover, blood vessel density, functionality, invasiveness of tumors into the surrounding tissues, and metastasis to the lymph node and lung were significantly increased in these tumors.
  • Neutralizing the interactions of CXCL12/CXCR4 in vivo with CXCR4 specific antibodies inhibited the CXCR4-dependent tumor growth and vascularization.
  • In vitro, CXCL12 induced the proliferation and VEGF secretion but not migration of PC3 and 22Rv1 cells overexpressing CXCR4.
  • Similar effects of CXCR4 overexpression on tumor growth in vivo were also noted in two breast cancer lines, suggesting that the observed effect of CXCR4 is not unique to prostate tumor cells.
  • Thus high levels of the chemokine receptor CXCR4 induce a more aggressive phenotype in prostate cancer cells and identify CXCR4 as a potential therapeutic target in advanced cases of metastatic prostate cancer.
  • [MeSH-major] Adenocarcinoma / metabolism. Neoplasm Metastasis / genetics. Neoplasm Proteins / physiology. Neovascularization, Pathologic / genetics. Prostatic Neoplasms / metabolism. Receptors, CXCR4 / physiology
  • [MeSH-minor] Animals. Bone Marrow / pathology. Bone Neoplasms / secondary. Breast Neoplasms / pathology. Cell Adhesion / drug effects. Cell Line, Tumor / drug effects. Cell Line, Tumor / metabolism. Cell Line, Tumor / pathology. Cell Movement / drug effects. Chemokine CXCL12. Chemokines, CXC / analysis. Chemokines, CXC / pharmacology. Female. Humans. Hyperplasia. Lung Neoplasms / secondary. Lymphatic Metastasis. Magnetic Resonance Imaging. Male. Mice. Mice, Inbred NOD. Mice, SCID. Organ Specificity. Ovarian Neoplasms / pathology. Phenotype. Recombinant Fusion Proteins / physiology. Transplantation, Heterologous. Vascular Endothelial Growth Factor A / secretion

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  • (PMID = 15180966.001).
  • [ISSN] 1530-6860
  • [Journal-full-title] FASEB journal : official publication of the Federation of American Societies for Experimental Biology
  • [ISO-abbreviation] FASEB J.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CXCL12 protein, human; 0 / Chemokine CXCL12; 0 / Chemokines, CXC; 0 / Cxcl12 protein, mouse; 0 / Neoplasm Proteins; 0 / Receptors, CXCR4; 0 / Recombinant Fusion Proteins; 0 / Vascular Endothelial Growth Factor A
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35. Gupta S, Adhami VM, Subbarayan M, MacLennan GT, Lewin JS, Hafeli UO, Fu P, Mukhtar H: Suppression of prostate carcinogenesis by dietary supplementation of celecoxib in transgenic adenocarcinoma of the mouse prostate model. Cancer Res; 2004 May 1;64(9):3334-43
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  • [Title] Suppression of prostate carcinogenesis by dietary supplementation of celecoxib in transgenic adenocarcinoma of the mouse prostate model.
  • Epidemiological studies and clinical observations suggest that nonsteroidal anti-inflammatory drugs and certain selective cyclooxygenase (COX)-2 inhibitors may reduce the relative risk of clinically evident prostate cancer.
  • This prompted us to investigate the chemopreventive potential of celecoxib, a selective COX-2 inhibitor, against prostate carcinogenesis in a transgenic adenocarcinoma of the mouse prostate (TRAMP) model.
  • Similar to prostate cancer in humans, prostate malignancies in TRAMP mice progress from precursor intraepithelial lesions, to invasive carcinoma that metastasizes to lymph nodes, liver, lungs, and occasionally to bone.
  • The basal enzyme activity and protein expression of COX-2 is significantly higher (>4-fold) in the dorsolateral prostate of TRAMP mice up to 24 weeks of age compared with their nontransgenic littermates.
  • Eight-week-old TRAMP mice were randomly divided and fed either control diet (AIN 76A) or a custom prepared AIN 76A diet containing 1500-ppm celecoxib ad libitum for 24 weeks, a dosage that would compare with the normal recommended dose for the treatment of human disease.
  • Studies from two independent experiments, each consisting of 10 mice on test, showed that the cumulative incidence of prostate cancer development at 32 weeks of age in animals fed with AIN 76A diet was 100% (20 of 20) as observed by tumor palpation, whereas 65% (13 of 20), 35% (7 of 20), and 20% (4 of 20) of the animals exhibited distant site metastases to lymph nodes, lungs, and liver.
  • Celecoxib supplementation to TRAMP mice from 8-32 weeks of age exhibited significant reduction in tumor development (5 of 20) with no signs of metastasis.
  • Sequential magnetic resonance imaging analysis of celecoxib-fed mice documented lower prostate volume compared with the AIN 76A-fed group.
  • These results correlated with retention of antimetastasis markers, viz E-cadherin, and alpha- and beta-catenin, along with a significant decrease in vascular endothelial growth factor protein expression.
  • One striking observation in an additional study was that celecoxib feeding to mice with established tumors (16 weeks of age) significantly improved their overall survival (P = 0.014), compared with AIN 76A-fed group.
  • [MeSH-major] Adenocarcinoma / prevention & control. Anticarcinogenic Agents / pharmacology. Cyclooxygenase Inhibitors / pharmacology. Prostatic Neoplasms / prevention & control. Sulfonamides / pharmacology
  • [MeSH-minor] Animals. Biomarkers, Tumor / metabolism. Celecoxib. Cell Division / drug effects. Cyclooxygenase 2. Cyclooxygenase 2 Inhibitors. Dietary Supplements. Dinoprostone / blood. Female. Immunohistochemistry. Isoenzymes / biosynthesis. Isoenzymes / genetics. Isoenzymes / metabolism. Male. Mice. Mice, Inbred C57BL. Mice, Transgenic. Neoplasm Metastasis. Neovascularization, Pathologic / drug therapy. Neovascularization, Pathologic / metabolism. Proliferating Cell Nuclear Antigen / biosynthesis. Prostaglandin-Endoperoxide Synthases / biosynthesis. Prostaglandin-Endoperoxide Synthases / genetics. Prostaglandin-Endoperoxide Synthases / metabolism. Pyrazoles. RNA, Messenger / biosynthesis. RNA, Messenger / genetics

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  • (PMID = 15126378.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA 89739
  • [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 / Anticarcinogenic Agents; 0 / Biomarkers, Tumor; 0 / Cyclooxygenase 2 Inhibitors; 0 / Cyclooxygenase Inhibitors; 0 / Isoenzymes; 0 / Proliferating Cell Nuclear Antigen; 0 / Pyrazoles; 0 / RNA, Messenger; 0 / Sulfonamides; EC 1.14.99.1 / Cyclooxygenase 2; EC 1.14.99.1 / Prostaglandin-Endoperoxide Synthases; JCX84Q7J1L / Celecoxib; K7Q1JQR04M / Dinoprostone
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36. Roy JW, Cowley EA, Blay J, Linsdell P: The intermediate conductance Ca2+-activated K+ channel inhibitor TRAM-34 stimulates proliferation of breast cancer cells via activation of oestrogen receptors. Br J Pharmacol; 2010 Feb 1;159(3):650-8
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  • [Title] The intermediate conductance Ca2+-activated K+ channel inhibitor TRAM-34 stimulates proliferation of breast cancer cells via activation of oestrogen receptors.
  • We have investigated the effects of specific K(+) channel inhibitors on basal and oestrogen-stimulated proliferation of breast cancer cells.
  • EXPERIMENTAL APPROACH: Using the mammary adenocarcinoma cell line MCF-7 we assayed cell proliferation by radiolabelled thymidine incorporation in the absence or presence of various K(+) channel inhibitors with or without 17beta-oestradiol.
  • KEY RESULTS: Inhibitors of K(v)10.1 and K(Ca)3.1 K(+) channels suppressed basal proliferation of MCF-7 cells, but not oestrogen-stimulated proliferation.
  • TRAM-34, a specific inhibitor of K(Ca)3.1 channels increased or decreased cell proliferation depending on the concentration.
  • At intermediate concentrations (3-10 microM) TRAM-34 increased cell proliferation, whereas at higher concentrations (20-100 microM) TRAM-34 decreased cell proliferation.
  • The enhancement of cell proliferation caused by TRAM-34 was blocked by the oestrogen receptor antagonists ICI182,780 and tamoxifen.
  • TRAM-34 also increased progesterone receptor mRNA expression, decreased oestrogen receptor-alpha mRNA expression and reduced the binding of radiolabelled oestrogen to MCF-7 oestrogen receptor, in each case mimicking the effects of 17beta-oestradiol.
  • CONCLUSIONS AND IMPLICATIONS: Our results demonstrate that K(+) channels K(v)10.1 and K(Ca)3.1 play a role in basal, but not oestrogen-stimulated MCF-7 cell proliferation.
  • TRAM-34, as well as inhibiting K(Ca)3.1, directly interacts with the oestrogen receptor and mimics the effects of 17beta-oestradiol on MCF-7 cell proliferation and gene modulation.
  • Our finding that TRAM-34 is able to activate the oestrogen receptor suggests a novel action of this supposedly specific K(+) channel inhibitor and raises concerns of interpretation in its use.
  • [MeSH-major] Breast Neoplasms / drug therapy. Breast Neoplasms / metabolism. Estradiol / pharmacology. Potassium Channels, Calcium-Activated. Tamoxifen / pharmacology
  • [MeSH-minor] Calcium / metabolism. Calcium / pharmacology. Calcium / therapeutic use. Cell Line, Tumor. Cells / metabolism. Cells / pathology. Cellular Structures / metabolism. Cellular Structures / pathology. Estrogen Receptor alpha / metabolism. Estrogens / metabolism. Estrogens / pharmacology. Estrogens / therapeutic use. Female. Gene Expression / drug effects. Humans. Ion Transport / drug effects. Pyrazoles. RNA, Messenger / metabolism. RNA, Messenger / pharmacology. Receptors, Estrogen / metabolism. Receptors, Progesterone / metabolism

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  • (PMID = 20050851.001).
  • [ISSN] 1476-5381
  • [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 / Estrogen Receptor alpha; 0 / Estrogens; 0 / Potassium Channels, Calcium-Activated; 0 / Pyrazoles; 0 / RNA, Messenger; 0 / Receptors, Estrogen; 0 / Receptors, Progesterone; 0 / TRAM 34; 0 / estrogen receptor alpha, human; 094ZI81Y45 / Tamoxifen; 4TI98Z838E / Estradiol; SY7Q814VUP / Calcium
  • [Other-IDs] NLM/ PMC2828028
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37. Mukherjee S, Bhattacharya RK, Roy M: Targeting protein kinase C (PKC) and telomerase by phenethyl isothiocyanate (PEITC) sensitizes PC-3 cells towards chemotherapeutic drug-induced apoptosis. J Environ Pathol Toxicol Oncol; 2009;28(4):269-82
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  • [Title] Targeting protein kinase C (PKC) and telomerase by phenethyl isothiocyanate (PEITC) sensitizes PC-3 cells towards chemotherapeutic drug-induced apoptosis.
  • Protein kinase C (PKC), an enzyme, gets overexpressed in prostate cancer and results in a resistance to chemotherapy.
  • Telomerase, a reverse transcriptase, is highly activated in prostate cancer cells.
  • Both of these enzymes can be considered as potential molecular markers for prostate cancer.
  • The present study investigates the effects of natural isothiocyanate phenethyl isothiocyanate (PEITC) in modulating the activities of PKC and telomerase in the androgen-independent human prostate adenocarcinoma (PC-3) cell line.
  • Basal level of PKC delta, a proapoptotic form, was very poor and its modulation was not significant.
  • PEITC also inhibited the activity of telomerase.
  • Studies were conducted to measure the degree of apoptotic cell death induced either by PEITC alone or in combination with adriamycin or etoposide.
  • PEITC exhibited remarkable efficacy in sensitizing PC-3 cells to undergo cell death by adriamycin and etoposide, which might prove to be of considerable value in synergistic therapy of cancer.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Apoptosis / drug effects. Isothiocyanates / pharmacology. Prostatic Neoplasms / enzymology. Protein Kinase C / antagonists & inhibitors. Telomerase / antagonists & inhibitors
  • [MeSH-minor] Antineoplastic Combined Chemotherapy Protocols / pharmacology. Biomarkers, Tumor / metabolism. Caspases / metabolism. Cell Line, Tumor. Cytochromes c / metabolism. Down-Regulation / drug effects. Doxorubicin / pharmacology. Drug Resistance, Neoplasm. Etoposide / pharmacology. Humans. Male

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  • (PMID = 20102325.001).
  • [ISSN] 2162-6537
  • [Journal-full-title] Journal of environmental pathology, toxicology and oncology : official organ of the International Society for Environmental Toxicology and Cancer
  • [ISO-abbreviation] J. Environ. Pathol. Toxicol. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Biomarkers, Tumor; 0 / Isothiocyanates; 6PLQ3CP4P3 / Etoposide; 6U7TFK75KV / phenethyl isothiocyanate; 80168379AG / Doxorubicin; 9007-43-6 / Cytochromes c; EC 2.7.11.13 / Protein Kinase C; EC 2.7.7.49 / Telomerase; EC 3.4.22.- / Caspases
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38. Angelucci A, Muzi P, Cristiano L, Millimaggi D, Cimini A, Dolo V, Miano R, Vicentini C, Cerù MP, Bologna M: Neuroendocrine transdifferentiation induced by VPA is mediated by PPARgamma activation and confers resistance to antiblastic therapy in prostate carcinoma. Prostate; 2008 May 1;68(6):588-98
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  • [Title] Neuroendocrine transdifferentiation induced by VPA is mediated by PPARgamma activation and confers resistance to antiblastic therapy in prostate carcinoma.
  • When prostatectomy fails to eradicate the primary tumor, PCa is generally refractory to all therapeutic approaches.
  • However molecular mechanisms underlying VPA action in PCa cells are largely unknown and further experimental validation to prove its potential application in clinic practice is needed.
  • NET was an early event detectable through the expression of neuro-endocrine (NE) markers within 72 hr after VPA treatment and it was associated to a reduction in the overall cell proliferation.
  • When we interrupted VPA treatment we observed the recovery in residual cells of the basal proliferation rate both in vitro and in a xenograft model.
  • In order to counteract the VPA-induced NET, the inhibition of PPARgamma may represent a suitable adjuvant treatment strategy and awaits further experimental validation.
  • [MeSH-major] Adenocarcinoma / drug therapy. Cell Transdifferentiation / drug effects. Enzyme Inhibitors / pharmacology. Neurosecretory Systems / drug effects. PPAR gamma / metabolism. Prostatic Neoplasms / drug therapy. Valproic Acid / pharmacology
  • [MeSH-minor] Anilides / pharmacology. Animals. Cell Line, Tumor. Cell Proliferation / drug effects. Cell Transformation, Neoplastic / drug effects. Cell Transformation, Neoplastic / pathology. Drug Combinations. Histone Deacetylase Inhibitors. Humans. Male. Mice. Mice, Nude. Proto-Oncogene Proteins c-bcl-2 / metabolism. Xenograft Model Antitumor Assays

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  • (PMID = 18288684.001).
  • [ISSN] 0270-4137
  • [Journal-full-title] The Prostate
  • [ISO-abbreviation] Prostate
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 2-chloro-5-nitrobenzanilide; 0 / Anilides; 0 / Drug Combinations; 0 / Enzyme Inhibitors; 0 / Histone Deacetylase Inhibitors; 0 / PPAR gamma; 0 / Proto-Oncogene Proteins c-bcl-2; 614OI1Z5WI / Valproic Acid
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39. Verma A, Wang H, Manavathi B, Fok JY, Mann AP, Kumar R, Mehta K: Increased expression of tissue transglutaminase in pancreatic ductal adenocarcinoma and its implications in drug resistance and metastasis. Cancer Res; 2006 Nov 1;66(21):10525-33
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  • [Title] Increased expression of tissue transglutaminase in pancreatic ductal adenocarcinoma and its implications in drug resistance and metastasis.
  • Pancreatic ductal adenocarcinoma (PDAC) is one of the most aggressive neoplastic diseases and is virtually incurable.
  • The molecular mechanisms that contribute to the intrinsic resistance of PDAC to various anticancer therapies are not well understood.
  • Recently, we have observed that several drug-resistant and metastatic tumors and tumor cell lines expressed elevated levels of tissue transglutaminase (TG2).
  • Because PDAC exhibits inherent resistance to various drugs, we determined the constitutive expression of TG2 in 75 PDAC and 12 PDAC cell lines.
  • Our results showed that 42 of 75 (56%) PDAC tumor samples expressed higher basal levels of TG2 compared with the normal pancreatic ducts [odds ratio (OR), 2.439; P = 0.012].
  • The increased expression of TG2 in PDAC was strongly associated with nodal metastasis (OR, 3.400; P = 0.017) and lymphovascular invasion (OR, 3.055; P = 0.045).
  • Increased expression of TG2 was also evident in all 12 cell lines examined.
  • The elevated expression of TG2 in PDAC cell lines was associated with gemcitabine resistance and increased invasive potential.
  • Overexpression of catalytically active or inactive (C(277)S mutant) TG2 induced focal adhesion kinase (FAK) activation and augmented invasive functions in the BxPC-3 cell line.
  • Immunoprecipitation and confocal microscopy data revealed that TG2 was associated with FAK protein in PDAC cells.
  • The activated FAK colocalized with TG2 at focal adhesion points.
  • These results show for the first time that elevated expression of TG2 can induce constitutive activation of FAK and thus may contribute to the development of drug resistance and invasive phenotypes in PDAC.
  • [MeSH-major] Carcinoma, Pancreatic Ductal / enzymology. Pancreatic Neoplasms / drug therapy. Pancreatic Neoplasms / enzymology. Transglutaminases / physiology
  • [MeSH-minor] Cell Line, Tumor. Deoxycytidine / analogs & derivatives. Deoxycytidine / pharmacology. Drug Resistance, Neoplasm. Focal Adhesion Protein-Tyrosine Kinases / physiology. GTP-Binding Proteins. Humans. Neoplasm Invasiveness. Neoplasm Metastasis. Phosphatidylinositol 3-Kinases / physiology. Proto-Oncogene Proteins c-akt / physiology. RNA, Small Interfering / pharmacology. Signal Transduction

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  • (PMID = 17079475.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA092115; United States / NCI NIH HHS / CA / CA098823; United States / NCI NIH HHS / CA / P20CA101936
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / RNA, Small Interfering; 0W860991D6 / Deoxycytidine; B76N6SBZ8R / gemcitabine; EC 2.3.2.- / transglutaminase 2; EC 2.3.2.13 / Transglutaminases; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.10.2 / Focal Adhesion Protein-Tyrosine Kinases; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 3.6.1.- / GTP-Binding Proteins
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40. Eriksson SE, Prast-Nielsen S, Flaberg E, Szekely L, Arnér ES: High levels of thioredoxin reductase 1 modulate drug-specific cytotoxic efficacy. Free Radic Biol Med; 2009 Dec 1;47(11):1661-71
Hazardous Substances Data Bank. 1-CHLORO-2,4-DINITROBENZENE .

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  • [Title] High levels of thioredoxin reductase 1 modulate drug-specific cytotoxic efficacy.
  • The selenoprotein thioredoxin reductase 1 (TrxR1) is currently recognized as a plausible anticancer drug target.
  • Here we analyzed the effects of TrxR1 targeting in the human A549 lung carcinoma cell line, having a very high basal TrxR1 expression.
  • We determined the total cellular TrxR activity to be 271.4 +/- 39.5 nmol min(-1) per milligram of total protein, which by far exceeded the total thioredoxin activity (39.2 +/- 3.5 nmol min(-1) per milligram of total protein).
  • Knocking down TrxR1 by approx 90% using siRNA gave only a slight effect on cell growth, irrespective of concurrent glutathione depletion (> or = 98% decrease), and no increase in cell death or distorted cell cycle phase distributions.
  • This apparent lack of phenotype could probably be explained by Trx functions being maintained by the remaining TrxR1 activity.
  • TrxR1 knockdown nonetheless yielded drug-specific modulation of cytotoxic efficacy in response to various chemotherapeutic agents.
  • No changes in response upon exposure to auranofin or juglone were seen after TrxR1 knockdown, whereas sensitivity to 1-chloro-2,4-dinitrobenzene or menadione became markedly increased.
  • The results suggest that high overexpression of TrxR has an impact not necessarily linked to Trx function that nonetheless modulates drug-specific cytotoxic responses.
  • [MeSH-major] Adenocarcinoma / drug therapy. Lung Neoplasms / drug therapy. Thioredoxin Reductase 1 / metabolism
  • [MeSH-minor] Apoptosis / drug effects. Apoptosis / genetics. Auranofin / pharmacology. Cell Cycle / drug effects. Cell Cycle / genetics. Cell Growth Processes / drug effects. Cell Growth Processes / genetics. Cell Line, Tumor. Cisplatin / pharmacology. Dinitrochlorobenzene / pharmacology. Drug Resistance, Neoplasm / drug effects. Drug Resistance, Neoplasm / genetics. Humans. Naphthoquinones / pharmacology. RNA, Small Interfering / genetics. Vitamin K 3 / pharmacology

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  • (PMID = 19766715.001).
  • [ISSN] 1873-4596
  • [Journal-full-title] Free radical biology & medicine
  • [ISO-abbreviation] Free Radic. Biol. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Naphthoquinones; 0 / RNA, Small Interfering; 3H04W2810V / Auranofin; 723JX6CXY5 / Vitamin K 3; EC 1.8.1.9 / Thioredoxin Reductase 1; GE3IBT7BMN / Dinitrochlorobenzene; Q20Q21Q62J / Cisplatin; W6Q80SK9L6 / juglone
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41. Degrate L, Nobili C, Franciosi C, Caprotti R, Brivio F, Romano F, Leone BE, Trezzi R, Uggeri F: Interleukin-2 immunotherapy action on innate immunity cells in peripheral blood and tumoral tissue of pancreatic adenocarcinoma patients. Langenbecks Arch Surg; 2009 Jan;394(1):115-21
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  • [Title] Interleukin-2 immunotherapy action on innate immunity cells in peripheral blood and tumoral tissue of pancreatic adenocarcinoma patients.
  • This study aims to evaluate the toxicity of pre- and postoperative rIL-2 treatment and the effects on innate immunity both in peripheral blood and in cancer tissue of patients with resectable pancreatic adenocarcinoma.
  • We evaluated NK cell and eosinophil count in blood and in pancreatic surgical specimens.
  • In the early postoperative period, blood NK cells and eosinophils significantly increased compared to basal values (p < 0.02).
  • Histopathological analysis did not find significant intratumoral infiltration of NK cells nor of eosinophils.
  • CONCLUSIONS: Preoperative high dose rIL-2 administration is able to counteract surgery-induced deficiency of NK cells and eosinophils in peripheral blood in the early postoperative period, although it cannot overcome local mechanisms of immune tumor escape in cancer tissue.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Carcinoma, Pancreatic Ductal / drug therapy. Carcinoma, Pancreatic Ductal / immunology. Immunity, Innate / drug effects. Immunity, Innate / immunology. Immunotherapy / methods. Interleukin-2 / analogs & derivatives. Pancreatic Neoplasms / drug therapy. Pancreatic Neoplasms / immunology
  • [MeSH-minor] Aged. Aged, 80 and over. Chemotherapy, Adjuvant. Combined Modality Therapy. Dose-Response Relationship, Drug. Eosinophils / drug effects. Eosinophils / immunology. Female. Humans. Injections, Subcutaneous. Killer Cells, Natural / drug effects. Killer Cells, Natural / immunology. Leukocyte Count. Male. Middle Aged. Neoadjuvant Therapy. Pancreatectomy. Pancreaticoduodenectomy. Recombinant Proteins / adverse effects. Recombinant Proteins / therapeutic use

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  • (PMID = 18670745.001).
  • [ISSN] 1435-2451
  • [Journal-full-title] Langenbeck's archives of surgery
  • [ISO-abbreviation] Langenbecks Arch Surg
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Interleukin-2; 0 / Recombinant Proteins; M89N0Q7EQR / aldesleukin
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42. Candelaria M, Cetina L, Dueñas-González A: Anemia in cervical cancer patients: implications for iron supplementation therapy. Med Oncol; 2005;22(2):161-8
Hazardous Substances Data Bank. IRON, ELEMENTAL .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Anemia in cervical cancer patients: implications for iron supplementation therapy.
  • Iron deficiency and tumor bleeding are common causes of anemia in cervical cancer.
  • At present little is known about the value of iron stores replenishment to increase hemoglobin levels in this setting.
  • Untreated cervical cancer patients with a hemoglobin <12 g/dL were randomized to intramuscular iron or to transfusion.
  • In both arms, patients who did not achieve at least 10 g/dL hemoglobin before or during chemoradiation were transfused.
  • Mean basal hemoglobin levels were 9.9 and 9.5 g/dL respectively.
  • Two weeks after randomization, hemoglobin increased to 10.9 and 10.2 g/dL respectively.
  • At wk 1 of treatment and thereafter, levels were higher in the iron arm, in whom the values were close or higher than 12 g/dL (p=0.03).
  • The median number of units transfused were 0 in the iron group and 2 in the transfusion (p=0.02) arm.
  • [MeSH-major] Anemia, Iron-Deficiency / drug therapy. Dietary Supplements. Iron / administration & dosage. Uterine Cervical Neoplasms / radiotherapy
  • [MeSH-minor] Adenocarcinoma / drug therapy. Adenocarcinoma / radiotherapy. Adult. Aged. Carcinoma, Adenosquamous / drug therapy. Carcinoma, Adenosquamous / radiotherapy. Carcinoma, Squamous Cell / drug therapy. Carcinoma, Squamous Cell / radiotherapy. Female. Hemoglobins / drug effects. Humans. Infusions, Intravenous. Middle Aged. Pilot Projects. Treatment Outcome

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  • (PMID = 15965279.001).
  • [ISSN] 1357-0560
  • [Journal-full-title] Medical oncology (Northwood, London, England)
  • [ISO-abbreviation] Med. Oncol.
  • [Language] eng
  • [Publication-type] Clinical Trial; Comparative Study; Journal Article; Randomized Controlled Trial
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Hemoglobins; E1UOL152H7 / Iron
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43. Arancia G, Calcabrini A, Marra M, Crateri P, Artico M, Martone A, Martelli F, Agostinelli E: Mitochondrial alterations induced by serum amine oxidase and spermine on human multidrug resistant tumor cells. Amino Acids; 2004 Jun;26(3):273-82
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Mitochondrial alterations induced by serum amine oxidase and spermine on human multidrug resistant tumor cells.
  • Multidrug resistance (MDR) has been studied extensively because it is one of major problems in cancer chemotherapy.
  • The MDR phenotype is often due to overexpression of P-glycoprotein (P-gp), that acting as an energy-dependent drug efflux pump exports various anticancer drugs out of cells.
  • The major goal of our investigation is to establish whether bovine serum amine oxidase (BSAO), which generates the products H(2)O(2) and aldehyde(s), from the polyamine spermine, is able to overcome MDR of human cancer cells.
  • The cytotoxicity of the products was evaluated in both drug-sensitive (LoVo WT) and drug-resistant (LoVo DX) colon adenocarcinoma cells.
  • A clonogenic cell survival assay demonstrated that LoVo DX cells were more sensitive than LoVo WT cells.
  • The mitochondrial activity was checked by flow cytometry studies, labelling cells with the probe JC1, that displayed a basal hyperpolarized status of the mitochondria in multidrug-resistant cells.
  • After treatment with amine oxidase in the presence of polyamine-spermine, the cells showed a marked increase in mitochondrial membrane depolarization higher in LoVo DX than in LoVo WT cells.
  • Our findings suggest that toxic oxidation products formed from spermine and BSAO could be a powerful tool in the development of new anticancer treatments, mainly against MDR tumor cells.
  • [MeSH-major] Amine Oxidase (Copper-Containing) / pharmacology. Drug Resistance, Neoplasm / genetics. Mitochondria / metabolism. Spermine / pharmacology
  • [MeSH-minor] Adenocarcinoma / drug therapy. Adenocarcinoma / ultrastructure. Animals. Cattle. Cell Line, Tumor. Cell Survival / drug effects. Colonic Neoplasms / drug therapy. Colonic Neoplasms / ultrastructure. Drug Screening Assays, Antitumor. Humans. Hydrogen Peroxide / pharmacology. Reactive Oxygen Species / metabolism. Time Factors. Tumor Stem Cell Assay

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  • (PMID = 15221508.001).
  • [ISSN] 0939-4451
  • [Journal-full-title] Amino acids
  • [ISO-abbreviation] Amino Acids
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Austria
  • [Chemical-registry-number] 0 / Reactive Oxygen Species; 2FZ7Y3VOQX / Spermine; BBX060AN9V / Hydrogen Peroxide; EC 1.4.3.21 / Amine Oxidase (Copper-Containing)
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