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1. Cook JL, Miura TA, Iklé DN, Lewis AM Jr, Routes JM: E1A oncogene-induced sensitization of human tumor cells to innate immune defenses and chemotherapy-induced apoptosis in vitro and in vivo. Cancer Res; 2003 Jun 15;63(12):3435-43
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  • [Title] E1A oncogene-induced sensitization of human tumor cells to innate immune defenses and chemotherapy-induced apoptosis in vitro and in vivo.
  • Expression of the adenoviral E1A oncogene induces susceptibility of neoplastic cells from different species to both immune-mediated and chemotherapy-induced cell death.
  • E1A expression in p53 mutant human breast carcinoma cells sensitized them in vitro to diverse immunological injuries and apoptosis triggered by chemotherapeutic agents, as predicted from studies of rodent tumor cells.
  • Two distinct, E1A-induced breast cancer cell traits could be measured in nude mice: (a) increased tumor latency and (b) reduced efficiency of tumor induction.
  • These results were confirmed in studies of E1A-expressing human fibrosarcoma cells.
  • This experimental approach should be useful for studies of the effects of other oncogene-related tumor cell traits on tumorigenicity and could be used for preclinical studies of different treatment strategies for human tumors.
  • [MeSH-major] Adenovirus E1A Proteins / physiology. Apoptosis / physiology. Bone Neoplasms / pathology. Breast Neoplasms / pathology. Carcinoma, Ductal, Breast / pathology. Drug Resistance, Neoplasm / physiology. Osteosarcoma / pathology
  • [MeSH-minor] Adenoviruses, Human / genetics. Adenoviruses, Human / physiology. Animals. Antineoplastic Agents / therapeutic use. Cell Line / transplantation. Cytotoxicity, Immunologic. Etoposide / therapeutic use. Female. Fibrosarcoma / immunology. Fibrosarcoma / pathology. Genes, p53. Humans. Immunologic Surveillance. Kidney. Killer Cells, Natural / immunology. Mice. Mice, Nude. Oncogenes. Rats. Rats, Nude. Time Factors. Tumor Cells, Cultured / drug effects. Tumor Cells, Cultured / immunology. Tumor Suppressor Protein p53 / deficiency. Xenograft Model Antitumor Assays

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  • (PMID = 12810682.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA76491; United States / NCI NIH HHS / CA / CA86727
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adenovirus E1A Proteins; 0 / Antineoplastic Agents; 0 / Tumor Suppressor Protein p53; 6PLQ3CP4P3 / Etoposide
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2. Kirova YM, Vilcoq JR, Asselain B, Sastre-Garau X, Fourquet A: Radiation-induced sarcomas after radiotherapy for breast carcinoma: a large-scale single-institution review. Cancer; 2005 Aug 15;104(4):856-63
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  • [Title] Radiation-induced sarcomas after radiotherapy for breast carcinoma: a large-scale single-institution review.
  • BACKGROUND: Sarcomas are a rare complication of radiotherapy for breast carcinoma and patients have a poor prognosis.
  • METHODS: The authors reviewed the records of 16,705 patients with breast carcinoma.
  • Median doses of 50-55 grays (Gy) in 25-27 fractions were delivered to the whole breast over a period of 5-5.5 weeks (2 Gy/day, 5 weekly fractions) followed, when indicated, by a 16-26-Gy boost to the tumor or tumor bed.
  • Treatment of radiation-induced sarcomas (RIS) consisted mostly of radical surgery and chemotherapy.
  • RESULTS: Overall, 35 patients developed sarcomas.
  • Thirteen sarcomas were located in the breast, 5- in the chest wall, 3 in the sternum, 2 in the supraclavicle, 1 in the scapula, and 3 in the axilla.
  • Histologic evaluation identified 13 angiosarcomas, 3 osteosarcomas, 5 undifferentiated sarcomas, 1 malignant fibrous histiocytoma, 2 leiomyosarcomas, 1 fibrosarcoma, 1 rhabdomyosarcoma, and 1 myosarcoma.
  • The 5-year actuarial survival rate after diagnosis of RIS was 36% (+/- 0.11).
  • However, it showed that the risk increased with time.
  • Therefore, careful, long-term follow-up of patients treated with radiotherapy is needed for early detection and efficacious treatment of these malignancies.
  • [MeSH-major] Breast Neoplasms / radiotherapy. Neoplasms, Radiation-Induced / epidemiology. Sarcoma / epidemiology. Sarcoma / etiology
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Antineoplastic Agents / therapeutic use. Breast / surgery. Female. Humans. Incidence. Middle Aged. Neoplasms, Second Primary / epidemiology. Neoplasms, Second Primary / etiology. Neoplasms, Second Primary / therapy. Retrospective Studies. Risk Factors

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  • (PMID = 15981282.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents
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3. Aung L, Gorlick RG, Shi W, Thaler H, Shorter NA, Healey JH, Huvos AG, Meyers PA: Second malignant neoplasms in long-term survivors of osteosarcoma: Memorial Sloan-Kettering Cancer Center Experience. Cancer; 2002 Oct 15;95(8):1728-34
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  • All study patients received chemotherapy and/or surgery on one of six different protocols (T4, 5, 7, 10, 12, and CCG-7921/POG-9351).
  • Chemotherapy was scheduled for up to 40 weeks with some variations in the actual treatment period and consisted of various combinations of the following agents: high-dose methotrexate, doxorubicin, bleomycin, cyclophosphamide, dactinomycin, vincristine, cisplatin, and ifosfamide.
  • Only one had pulmonary metastasis at diagnosis and subsequent multiple recurrences that required thoracotomies and further modification of the chemotherapy regimen.
  • The median age at diagnosis for osteosarcoma was 16.6 years (range, 3.1-74.4 years).
  • The time interval from diagnosis of the primary osteosarcoma to the development of SMN was 1.3-13.1 years (median, 5.5; 95% confidence interval [CI], 3.6-9.6).
  • There were two cases of acute myeloid leukemia and one case each of myelodysplastic syndrome, non-Hodgkin lymphoma, high-grade pleomorphic sarcoma, leiomyosarcoma, fibrosarcoma, breast carcinoma, and mucoepidermoid carcinoma.
  • Although additional follow-up is warranted, the successes of current treatment regimens consisting of intensive, high-dose chemotherapy in combination with topoisomerase II inhibitors outweigh the risks.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Neoplasms, Second Primary / epidemiology. Neoplasms, Second Primary / etiology. Osteosarcoma / complications. Osteosarcoma / drug therapy
  • [MeSH-minor] Adolescent. Adult. Aged. Child. Child, Preschool. Female. Follow-Up Studies. Humans. Incidence. Male. Middle Aged. Time Factors

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  • [Copyright] Copyright 2002 American Cancer Society.
  • (PMID = 12365021.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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4. Muralikrishnan G, Amalan Stanley V, Sadasivan Pillai K: Dual role of vitamin C on lipid profile and combined application of cyclophosphamide, methotrexate and 5-fluorouracil treatment in fibrosarcoma-bearing rats. Cancer Lett; 2001 Aug 28;169(2):115-20
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  • [Title] Dual role of vitamin C on lipid profile and combined application of cyclophosphamide, methotrexate and 5-fluorouracil treatment in fibrosarcoma-bearing rats.
  • Combined application of cyclophosphamide, methotrexate, 5-fluorouracil (CMF) has been followed in the treatment of breast cancer.
  • Hence, the study was launched to appraise the salubrious role of vitamin C in CMF administered fibrosarcoma-bearing rats.
  • Fibrosarcoma cell line-induced rats were treated with CMF (cyclophosphamide 10 mg/kg b.w., methotrexate 1 mg/kg b.w., 5-fluorouracil 10 mg/kg b.w. and vitamin C 200 mg/kg b.w.) individually and in combination for 120 days.
  • The untreated as well as CMF administered fibrosarcoma-bearing rats divulged significantly in increased levels of plasma total cholesterol, triglycerides, phospholipids, very low density lipoprotein (VLDL) and low density lipoprotein (LDL) cholesterol, as compared with their respective control animals.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Ascorbic Acid / physiology. Ascorbic Acid / therapeutic use. Breast Neoplasms / drug therapy. Cyclophosphamide / administration & dosage. Fluorouracil / administration & dosage. Methotrexate / administration & dosage
  • [MeSH-minor] Animals. Cholesterol / metabolism. Female. Fibrosarcoma / metabolism. Lipid Metabolism. Lipids / blood. Neoplasm Transplantation. Neoplasms, Experimental / drug therapy. Rats. Rats, Wistar

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  • (PMID = 11431099.001).
  • [ISSN] 0304-3835
  • [Journal-full-title] Cancer letters
  • [ISO-abbreviation] Cancer Lett.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Lipids; 8N3DW7272P / Cyclophosphamide; 97C5T2UQ7J / Cholesterol; PQ6CK8PD0R / Ascorbic Acid; U3P01618RT / Fluorouracil; YL5FZ2Y5U1 / Methotrexate; CMF regimen
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5. Lage H, Aki-Sener E, Yalcin I: High antineoplastic activity of new heterocyclic compounds in cancer cells with resistance against classical DNA topoisomerase II-targeting drugs. Int J Cancer; 2006 Jul 1;119(1):213-20
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  • [Title] High antineoplastic activity of new heterocyclic compounds in cancer cells with resistance against classical DNA topoisomerase II-targeting drugs.
  • In parental, drug-sensitive cells merely the compounds BD3 and G35 showed efficacies, in terms of microM, which were similar to that of the classical Topo II inhibitor etoposide.
  • On the other hand, most of the tested heterocyclic compounds were found more effective in drug-resistant cells than in the parental, drug-sensitive ones, and some of the compounds showed high antineoplastic efficacy in several drug-resistant cell models.
  • Compounds BD13, BD14 and BD16 exhibited high antineoplastic activities against the drug-resistant sublines EPG85-257RNOV and EPG85-257RDB derived from gastric carcinoma, EPP85-181RNOV and EPP85-181RDB derived from pancreatic carcinoma, MCF-7/Adr derived from breast cancer, D79/86RNOV derived from fibrosarcoma, and MeWoETO1 derived from melanoma.
  • Furthermore, compound D23 was found highly efficient in the multidrug-resistant variants HT-29RNOV and HT-29RDB derived from colon carcinoma, and compound D24 exhibited the highest antineoplastic activity among the tested compounds in the drug-resistant subline MDA-MB-231ROV derived from breast cancer.
  • In conclusion, compounds BD 13, BD 14, BD 16, D 23 and D 24 may be useful for the treatment of different multidrug-resistant cancer cells with cross resistance against "classical" Topo II-targeting drugs.
  • [MeSH-major] Antineoplastic Agents / pharmacology. DNA Topoisomerases, Type II / drug effects. Heterocyclic Compounds / pharmacology. Neoplasms / drug therapy
  • [MeSH-minor] Blotting, Western. Breast Neoplasms / drug therapy. Cell Line, Tumor. Cell Proliferation / drug effects. Colonic Neoplasms / drug therapy. Drug Resistance, Multiple. Drug Resistance, Neoplasm. Female. Fibrosarcoma / drug therapy. Humans. Male. Melanoma / drug therapy. Pancreatic Neoplasms / drug therapy. Reverse Transcriptase Polymerase Chain Reaction. Stomach Neoplasms / drug therapy. Uterine Cervical Neoplasms / drug therapy

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  • (PMID = 16450374.001).
  • [ISSN] 0020-7136
  • [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 / Antineoplastic Agents; 0 / Heterocyclic Compounds; EC 5.99.1.3 / DNA Topoisomerases, Type II
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6. Cole PD, Kamen BA, Gorlick R, Banerjee D, Smith AK, Magill E, Bertino JR: Effects of overexpression of gamma-Glutamyl hydrolase on methotrexate metabolism and resistance. Cancer Res; 2001 Jun 1;61(11):4599-604
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  • To clarify the specific role of GGH in determining MTX sensitivity, we investigated the phenotype produced by forced GGH overexpression in two cell types.
  • The full-length cDNA for GGH, subcloned into a constitutive expression vector, was transfected into a human fibrosarcoma (HT-1080) and a human breast carcinoma (MCF-7) cell line.
  • [MeSH-minor] Breast Neoplasms / drug therapy. Breast Neoplasms / enzymology. Drug Resistance, Neoplasm. Fibrosarcoma / drug therapy. Fibrosarcoma / enzymology. Folic Acid / physiology. Humans. RNA, Messenger / biosynthesis. RNA, Messenger / genetics. Reverse Transcriptase Polymerase Chain Reaction. Tetrahydrofolates / pharmacokinetics. Transfection. Tumor Cells, Cultured

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  • (PMID = 11389096.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA09512; United States / NCI NIH HHS / CA / CA25933; United States / NCI NIH HHS / CA / CA82425
  • [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 / Antimetabolites, Antineoplastic; 0 / RNA, Messenger; 0 / Tetrahydrofolates; 134-35-0 / 5-methyltetrahydrofolate; 935E97BOY8 / Folic Acid; EC 3.4.19.9 / gamma-Glutamyl Hydrolase; YL5FZ2Y5U1 / Methotrexate
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7. Watanabe J, Minami M, Kobayashi M: Antitumor activity of TZT-1027 (Soblidotin). Anticancer Res; 2006 May-Jun;26(3A):1973-81
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  • MATERIALS AND METHODS: Cell-killing kinetic analysis was performed by the colony-forming assay and the kinetics of TZT-1027 were compared with those of neocarzinostatin, adriamycin and vincristine, known to be typical concentration-, AUC- and time-dependent agents, respectively.
  • DNA fragmentation was detectable by electrophoresis, cytotoxicity was evaluated by MTT assay and antitumor activity was examined by measuring the tumor weight after treatment.
  • RESULTS: TZT-1027 exhibited its cytocidal and apoptosis-inducing activity in a time-dependent manner.
  • Its growth-inhibitory effect was less affected by overexpression of P-glycoprotein than that of other tubulin inhibitors and was not affected by the overexpression of breast cancer resistance protein or multidrug resistance-associated protein.
  • CONCLUSION: Because its growth-inhibitory and antitumor activities were superior to those of the other drugs tested, including the tubulin inhibitors paclitaxel, docetaxel and vincristine, TZT-1027 should be useful in the chemotherapy of tumors that are not responsive to other tubulin inhibitors.
  • [MeSH-minor] ATP Binding Cassette Transporter, Sub-Family G, Member 2. ATP-Binding Cassette Transporters / biosynthesis. ATP-Binding Cassette Transporters / metabolism. ATP-Binding Cassette, Sub-Family B, Member 1 / biosynthesis. ATP-Binding Cassette, Sub-Family B, Member 1 / metabolism. Animals. Cell Death / drug effects. Cell Death / physiology. Cell Growth Processes / drug effects. Cell Line, Tumor. Colonic Neoplasms / drug therapy. Colonic Neoplasms / metabolism. Colonic Neoplasms / pathology. DNA Fragmentation / drug effects. Drug Resistance, Multiple. Drug Resistance, Neoplasm. Drug Screening Assays, Antitumor. Fibrosarcoma / drug therapy. Fibrosarcoma / metabolism. Fibrosarcoma / pathology. Humans. Male. Mice. Mice, Inbred BALB C. Multidrug Resistance-Associated Proteins / biosynthesis. Multidrug Resistance-Associated Proteins / metabolism. Neoplasm Proteins / biosynthesis. Neoplasm Proteins / metabolism. Xenograft Model Antitumor Assays

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  • (PMID = 16827132.001).
  • [ISSN] 0250-7005
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / ABCG2 protein, human; 0 / ATP Binding Cassette Transporter, Sub-Family G, Member 2; 0 / ATP-Binding Cassette Transporters; 0 / ATP-Binding Cassette, Sub-Family B, Member 1; 0 / Antineoplastic Agents; 0 / Multidrug Resistance-Associated Proteins; 0 / Neoplasm Proteins; 0 / Oligopeptides; DQC51A0WQH / soblidotin
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8. Blanchard DK, Reynolds CA, Grant CS, Donohue JH: Primary nonphylloides breast sarcomas. Am J Surg; 2003 Oct;186(4):359-61
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  • [Title] Primary nonphylloides breast sarcomas.
  • BACKGROUND: The prevalence of primary breast sarcoma is low, occurring in fewer than 1% of women with breast malignancies.
  • The purpose of this study was to examine the presentation, treatment, and prognosis of patients presenting with these neoplasms.
  • METHODS: This was a retrospective review of patients with a primary breast sarcoma treated at Mayo Clinic, Rochester, Minnesota, between 1975 and 2001.
  • RESULTS: Of the 55 patients, 17 had breast-conserving therapy and 38 women had mastectomy.
  • The types of sarcoma included angiosarcoma (18), malignant fibrous histiocytoma (11), stromal sarcoma (8), liposarcoma (4), leiomyosarcoma (4), dermatofibrosarcoma protuberans (4), osteosarcoma (3), fibrosarcoma (2), and rhabdomyosarcoma (1).
  • Twenty-nine of 53 patients (55%) developed recurrent sarcoma, and 23 patients (43%) died of their disease.
  • Overall median survival of patients with breast sarcoma was 58 months.
  • Of 34 patients who did not receive adjuvant chemotherapy or radiation, 13 died of their disease (38%), as compared with 10 of 16 patients (63%) who did receive adjuvant therapy.
  • CONCLUSIONS: While primary nonphylloides breast sarcomas are rare tumors, their treatment and prognosis are poor.
  • Adjuvant chemotherapy and radiation did not improve survival in this report.
  • Surgical extirpation remains the only effective treatment.
  • [MeSH-major] Breast Neoplasms. Sarcoma

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  • (PMID = 14553850.001).
  • [ISSN] 0002-9610
  • [Journal-full-title] American journal of surgery
  • [ISO-abbreviation] Am. J. Surg.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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9. Potrich C, Tomazzolli R, Dalla Serra M, Anderluh G, Malovrh P, Macek P, Menestrina G, Tejuca M: Cytotoxic activity of a tumor protease-activated pore-forming toxin. Bioconjug Chem; 2005 Mar-Apr;16(2):369-76
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  • It is able to kill very unspecifically most cell types by the membrane-perturbing action of an amphiphilic alpha-helix located at its N-terminal.
  • After having measured the enzymatic activity of fibrosarcoma and breast carcinoma cells, we analyzed the cytotoxic effect of the conjugate on the same lines and on human red blood cells (HRBC) as controls.
  • (1) binding occurred normally on all type of cells including HRBC which however were insensitive being devoid of enzymes;.
  • [MeSH-major] Antineoplastic Agents / chemical synthesis. Cnidarian Venoms / administration & dosage. Drug Delivery Systems / methods. Neoplasm Proteins / metabolism. Peptides / metabolism
  • [MeSH-minor] Animals. Breast Neoplasms / drug therapy. Breast Neoplasms / enzymology. Breast Neoplasms / pathology. Cathepsin B / metabolism. Cell Line, Tumor. Cross-Linking Reagents. Cytotoxins / administration & dosage. Cytotoxins / chemistry. Cytotoxins / genetics. Female. Fibrosarcoma / drug therapy. Fibrosarcoma / enzymology. Fibrosarcoma / pathology. Humans. Male. Matrix Metalloproteinases / metabolism. Mutation. Prodrugs / chemical synthesis. Prodrugs / metabolism. Sea Anemones / chemistry

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  • (PMID = 15769091.001).
  • [ISSN] 1043-1802
  • [Journal-full-title] Bioconjugate chemistry
  • [ISO-abbreviation] Bioconjug. Chem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Cnidarian Venoms; 0 / Cross-Linking Reagents; 0 / Cytotoxins; 0 / Neoplasm Proteins; 0 / Peptides; 0 / Prodrugs; 54578-46-0 / equinatoxin; EC 3.4.22.1 / Cathepsin B; EC 3.4.24.- / Matrix Metalloproteinases
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10. Schellens JH, Maliepaard M, Scheper RJ, Scheffer GL, Jonker JW, Smit JW, Beijnen JH, Schinkel AH: Transport of topoisomerase I inhibitors by the breast cancer resistance protein. Potential clinical implications. Ann N Y Acad Sci; 2000;922:188-94
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  • [Title] Transport of topoisomerase I inhibitors by the breast cancer resistance protein. Potential clinical implications.
  • The multidrug resistance protein BCRP (breast cancer resistance protein) is a member of the ATP-binding cassette family of drug transporters.
  • Recently, the BCRP gene has been described in ovarian, breast, colon, and gastric cancer and fibrosarcoma cell lines.
  • Increased energy-dependent efflux of affected drugs was noted.
  • [MeSH-minor] ATP Binding Cassette Transporter, Sub-Family G, Member 2. Animals. Antibodies, Monoclonal / biosynthesis. Biological Transport. Drug Resistance, Multiple. Drug Resistance, Neoplasm. Female. Humans. Mice. Mice, Inbred BALB C. Mitoxantrone / pharmacokinetics. Mitoxantrone / pharmacology. Ovarian Neoplasms / drug therapy. Ovarian Neoplasms / metabolism. Ovarian Neoplasms / pathology. Topotecan / pharmacokinetics. Topotecan / pharmacology. Tumor Cells, Cultured / drug effects. Tumor Cells, Cultured / metabolism

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  • (PMID = 11193894.001).
  • [ISSN] 0077-8923
  • [Journal-full-title] Annals of the New York Academy of Sciences
  • [ISO-abbreviation] Ann. N. Y. Acad. Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / ABCG2 protein, human; 0 / ATP Binding Cassette Transporter, Sub-Family G, Member 2; 0 / ATP-Binding Cassette Transporters; 0 / Antibodies, Monoclonal; 0 / Antineoplastic Agents; 0 / Enzyme Inhibitors; 0 / Neoplasm Proteins; 0 / Topoisomerase I Inhibitors; 5MB77ICE2Q / 9-aminocamptothecin; 7673326042 / irinotecan; 7M7YKX2N15 / Topotecan; BZ114NVM5P / Mitoxantrone; XT3Z54Z28A / Camptothecin
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11. Sartippour MR, Liu C, Shao ZM, Go VL, Heber D, Nguyen M: Livistona extract inhibits angiogenesis and cancer growth. Oncol Rep; 2001 Nov-Dec;8(6):1355-7

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  • The aqueous extract inhibits the in vitro proliferation of endothelial cells and multiple tumor cell lines including mouse fibrosarcoma and human breast and colon cancer.
  • In mouse experiments, this extract suppresses the growth of the subcutaneous fibrosarcoma tumors.
  • Our results suggest that the extract from the shell of Livistona chinensis may be a potential supplemental source for cancer treatment.
  • [MeSH-minor] Animals. Carcinoma / drug therapy. Cell Division / drug effects. Endothelium, Vascular / drug effects. Fibrosarcoma / drug therapy. HT29 Cells / drug effects. Humans. Mice. Mice, Inbred C3H. Seeds. Tumor Cells, Cultured. Xenograft Model Antitumor Assays

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  • [CommentIn] NIH Guide Grants Contracts. 2009 Feb 20;:NOT-OD-09-052 [19241492.001]
  • (PMID = 11605065.001).
  • [ISSN] 1021-335X
  • [Journal-full-title] Oncology reports
  • [ISO-abbreviation] Oncol. Rep.
  • [Language] eng
  • [Grant] United States / NCCIH NIH HHS / AT / P50 AT 00151; United States / NIDDK NIH HHS / DK / T32 DK07688
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Antineoplastic Agents, Phytogenic; 0 / Plant Extracts
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12. Suzuki-Uematsu S, Shiraishi K, Ito T, Adachi N, Inage Y, Taeda Y, Ueki H, Ohtani H: Malignant phyllodes tumor composed almost exclusively of a fibrosarcomatous component: a case report and review of malignant phyllodes tumors with metastases. Breast Cancer; 2010 Jul;17(3):218-24
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  • A 52-year-old Japanese female noted a rapid increase of her right breast tumor.
  • Multiple sectioning revealed that the tumor had only focal occurrence of elongated tubular structures, and the occurrence of a small component of benign phyllodes tumor, leading to the aforementioned final diagnosis.
  • Although the patient received adjuvant chemotherapy, no responsiveness was obtained.
  • The estimated 2.2-year survival rate following detection of metastasis was 11%, thus confirming the aggressiveness of the disease.
  • [MeSH-major] Breast Neoplasms / pathology. Fibrosarcoma / pathology. Lung Neoplasms / secondary. Phyllodes Tumor / secondary
  • [MeSH-minor] Female. Humans. Mastectomy, Simple. Middle Aged. Tomography, X-Ray Computed

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  • (PMID = 19350353.001).
  • [ISSN] 1880-4233
  • [Journal-full-title] Breast cancer (Tokyo, Japan)
  • [ISO-abbreviation] Breast Cancer
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] Japan
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13. Ostenfeld MS, Fehrenbacher N, Høyer-Hansen M, Thomsen C, Farkas T, Jäättelä M: Effective tumor cell death by sigma-2 receptor ligand siramesine involves lysosomal leakage and oxidative stress. Cancer Res; 2005 Oct 1;65(19):8975-83
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  • Acquired resistance to classic caspase-mediated apoptosis is a common problem for the treatment of human cancer.
  • Cathepsin B inhibitors (CA-074-Me and R-2525) conferred similar, but less pronounced protection, whereas ectopic expression of antiapoptotic protein Bcl-2, lack of wild-type p53 as well as pharmacologic inhibitors of caspases (zVAD-fmk, DEVD-CHO, and LEHD-CHO), calpains (PD150606), and serine proteases (N-tosyl-L-phenylalanine chloromethyl ketone and pefabloc) failed to protect cells against siramesine-induced death.
  • Furthermore, p.o. administration of well-tolerated doses of siramesine had a significant antitumorigenic effect in orthotopic breast cancer and s.c. fibrosarcoma models in mice.
  • These results present siramesine as a promising new drug for the treatment of tumors resistant to traditional therapies.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Apoptosis / drug effects. Indoles / pharmacology. Lysosomes / drug effects. Receptors, sigma / metabolism. Spiro Compounds / pharmacology
  • [MeSH-minor] Animals. Breast Neoplasms / drug therapy. Breast Neoplasms / metabolism. Breast Neoplasms / pathology. Caspases / metabolism. Cathepsins / metabolism. Cell Line, Transformed. Cell Line, Tumor. Cytochromes c / metabolism. Female. Fibrosarcoma / drug therapy. Fibrosarcoma / metabolism. Fibrosarcoma / pathology. Humans. Ligands. Mice. Mice, Inbred BALB C. NIH 3T3 Cells. Oxidative Stress / drug effects. Tumor Suppressor Protein p53 / metabolism. Xenograft Model Antitumor Assays

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  • (PMID = 16204071.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Indoles; 0 / Ligands; 0 / Lu 28-179; 0 / Receptors, sigma; 0 / Spiro Compounds; 0 / Tumor Suppressor Protein p53; 0 / sigma-2 receptor; 9007-43-6 / Cytochromes c; EC 3.4.- / Cathepsins; EC 3.4.22.- / Caspases
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14. Hayashi K, Zhao M, Yamauchi K, Yamamoto N, Tsuchiya H, Tomita K, Hoffman RM: Cancer metastasis directly eradicated by targeted therapy with a modified Salmonella typhimurium. J Cell Biochem; 2009 Apr 15;106(6):992-8
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  • [Title] Cancer metastasis directly eradicated by targeted therapy with a modified Salmonella typhimurium.
  • Cancer metastasis is the life-threatening aspect of cancer and is usually resistant to standard treatment.
  • We report here a targeted therapy strategy for cancer metastasis using a genetically-modified strain of Salmonella typhimurium.
  • These mutations preclude growth in normal tissue but do not reduce bacterial virulence in cancer cells.
  • The tumor-targeting strain of S. typhimurium, termed A1-R, and expressing green fluorescent protein (GFP), was administered to both axillary lymph and popliteal lymph node metastasis of human pancreatic cancer and fibrosarcoma, respectively, as well as lung metastasis of the fibrosarcoma in nude mice.
  • The cancer cells expressed red fluorescent protein (RFP) in the cytoplasm and GFP in the nucleus linked to histone H2B, enabling color-coded real-time imaging of the bacteria targeting the metastatic tumors.
  • After 7-21 days of treatment, the metastases were eradicated without the need of chemotherapy or any other treatment.
  • This new strategy demonstrates the clinical potential of targeting and curing cancer metastasis with engineered bacteria without the need of toxic chemotherapy.

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  • [Copyright] Copyright 2009 Wiley-Liss, Inc.
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  • (PMID = 19199339.001).
  • [ISSN] 1097-4644
  • [Journal-full-title] Journal of cellular biochemistry
  • [ISO-abbreviation] J. Cell. Biochem.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R43 CA119841; United States / NCI NIH HHS / CA / R43 CA119841-01A1; United States / NCI NIH HHS / CA / CA119841; None / None / / R43 CA119841-01A1; United States / NCI NIH HHS / CA / CA126023
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Luminescent Proteins
  • [Other-IDs] NLM/ NIHMS137009; NLM/ PMC2779055
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15. Stojkovic R, Karminski-Zamola G, Racane L, Tralic-Kulenovic V, Glavas-Obrovac L, Ivankovic S, Radacic M: Antitumor efficiency of novel fluoro-substituted 6-amino-2-phenylbenzothiazole hydrochloride salts in vitro and in vivo. Methods Find Exp Clin Pharmacol; 2006 Jul-Aug;28(6):347-54
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  • A novel series of hydrochloride or dihydrochloride salts of the novel 2-(fluoro-substituted phenyl)-6-aminobenzothiazoles (5-7) have been prepared in multistep synthesis starting from 3- or 4-fluorobenzaldehydes and 2-amino-5-nitrothiophenol and evaluated for their antiproliferative activity against human cervical (HeLa), breast (MCF-7), colon (CaCO-2), and laryngeal (Hep-2) carcinomas and against fibroblast cell lines (WI-38).
  • Also, antitumor activity of these compounds was evaluated in vitro and in vivo against murine melanoma (B16-F10), fibrosarcoma (FsaR), and squamous cell carcinoma (SCCVII).
  • All examined benzothiazoles had significant antitumor activity in vivo against melanoma B16-F10, fibrosarcoma, and squamous cell carcinoma.
  • The best therapeutic results were achieved when therapy started 7 days after tumor cell implantation and when benzothiazoles were given repeatedly five times every 2 days, i.e., on day 7, 9, 11, 13, and 15 after transplantation of tumor cells.
  • [MeSH-minor] Animals. Carcinoma, Squamous Cell / drug therapy. Carcinoma, Squamous Cell / pathology. Cell Line, Tumor. Cell Proliferation / drug effects. Cell Survival. DNA, Neoplasm / biosynthesis. Drug Screening Assays, Antitumor. Fibroblasts / drug effects. Fibrosarcoma / drug therapy. Fibrosarcoma / pathology. Humans. Indicators and Reagents. Melanoma, Experimental / drug therapy. Melanoma, Experimental / pathology. Mice. Mice, Inbred C3H. Mice, Inbred C57BL. Neoplasm Proteins / biosynthesis. Neoplasm Transplantation. RNA, Neoplasm / biosynthesis

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  • (PMID = 16894403.001).
  • [ISSN] 0379-0355
  • [Journal-full-title] Methods and findings in experimental and clinical pharmacology
  • [ISO-abbreviation] Methods Find Exp Clin Pharmacol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Spain
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / DNA, Neoplasm; 0 / Indicators and Reagents; 0 / Neoplasm Proteins; 0 / RNA, Neoplasm; 0 / Thiazoles
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16. Wolf JS, Li D, Taylor RJ, O'Malley BW Jr: Lactoferrin inhibits growth of malignant tumors of the head and neck. ORL J Otorhinolaryngol Relat Spec; 2003 Sep-Oct;65(5):245-9
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  • Lactoferrin, a naturally occurring glycoprotein found in breast milk, has previously been shown to have antimicrobial properties and recently has been demonstrated to inhibit malignant tumor growth, presumably through immunomodulation.
  • Using an orthotopic murine model for both squamous cell carcinoma and fibrosarcoma of the floor of the mouth, we administered lactoferrin directly into the tumors using variable dosing strategies.
  • [MeSH-major] Carcinoma, Squamous Cell / drug therapy. Fibrosarcoma / drug therapy. Head and Neck Neoplasms / drug therapy. Lactoferrin / therapeutic use
  • [MeSH-minor] Animals. Cell Line. Disease Models, Animal. Dose-Response Relationship, Drug. Humans. Immunocompetence. Injections, Intralesional. Mice. Mice, Inbred C3H. Mice, Nude. Tumor Cells, Cultured

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  • [Copyright] Copyright 2003 S. Karger AG, Basel
  • (PMID = 14730178.001).
  • [ISSN] 0301-1569
  • [Journal-full-title] ORL; journal for oto-rhino-laryngology and its related specialties
  • [ISO-abbreviation] ORL J. Otorhinolaryngol. Relat. Spec.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Switzerland
  • [Chemical-registry-number] EC 3.4.21.- / Lactoferrin
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17. Sacchi A, Gasparri A, Gallo-Stampino C, Toma S, Curnis F, Corti A: Synergistic antitumor activity of cisplatin, paclitaxel, and gemcitabine with tumor vasculature-targeted tumor necrosis factor-alpha. Clin Cancer Res; 2006 Jan 1;12(1):175-82
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  • We have examined the antitumor activity of NGR-TNF in combination with various chemotherapeutic drugs acting via different mechanisms, including, besides doxorubicin and melphalan, cisplatin, paclitaxel, and gemcitabine.
  • EXPERIMENTAL DESIGN: Chemotherapeutic drugs were tested alone and in combination with NGR-TNF (0.1 ng) in murine lymphoma, fibrosarcoma, and mammary adenocarcinoma models.
  • RESULTS: Pretreatment with NGR-TNF enhanced the response to all these drugs although to a different extent.
  • The synergistic effect was transient, maximal synergism being observed with a 2-hour delay between NGR-TNF and drug administrations in all models and with all drugs tested.
  • NGR-TNF did not increase the in vitro cytotoxicity of chemotherapeutic drugs against tumor cells, suggesting that the in vivo synergism depends on NGR-TNF effects on host cells rather than on tumor cells.
  • CONCLUSIONS: Targeted delivery of low doses of NGR-TNF to the tumor vasculature can increase the efficacy of various drugs acting via different mechanisms.
  • Optimal administration schedule requires 2 hours of pretreatment with NGR-TNF independently from the mechanism of drug cytotoxicity.
  • This work could provide important information for designing clinical studies with NGR-TNF in combination with chemotherapeutic drugs.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Neoplasms / drug therapy. Tumor Necrosis Factor-alpha / therapeutic use
  • [MeSH-minor] Adenocarcinoma / blood supply. Adenocarcinoma / drug therapy. Animals. Breast Neoplasms / blood supply. Breast Neoplasms / drug therapy. Cisplatin / therapeutic use. Deoxycytidine / analogs & derivatives. Deoxycytidine / therapeutic use. Drug Synergism. Female. Fibrosarcoma / blood supply. Fibrosarcoma / drug therapy. Lymphoma / drug therapy. Mice. Neoplasm Transplantation. Paclitaxel / therapeutic use

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  • (PMID = 16397040.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Tumor Necrosis Factor-alpha; 0W860991D6 / Deoxycytidine; B76N6SBZ8R / gemcitabine; P88XT4IS4D / Paclitaxel; Q20Q21Q62J / Cisplatin
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18. Blackwell KL, Haroon ZA, Shan S, Saito W, Broadwater G, Greenberg CS, Dewhirst MW: Tamoxifen inhibits angiogenesis in estrogen receptor-negative animal models. Clin Cancer Res; 2000 Nov;6(11):4359-64
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  • Inhibition of tumor angiogenesis is a therapeutic strategy that can inhibit tumor growth and metastases.
  • The aim of this study was to determine whether the estrogen receptor (ER) ligand drug tamoxifen has antiangiogenic effects.
  • ER-negative fibrosarcoma tumors in tamoxifen-treated ovariectomized rats had significantly less vessel formation compared with untreated animals (median microvessel density, 53.6 versus 94.3 counts/per x 200 field; P = 0.002).
  • These three animal models all showed significant inhibition of angiogenesis by tamoxifen and suggest a possible contributory mechanism of ER-independent manipulation by tamoxifen in the treatment and prevention of breast cancer.
  • These studies raise the question as to whether or not newer ER ligand drugs might possess even more potent antiangiogenic effects, which in turn could lead to the broadening of the clinical usefulness of these compounds in a number of diseases.
  • [MeSH-minor] Animals. Aorta / drug effects. Breast Neoplasms / drug therapy. Cornea / drug effects. Female. Fibrosarcoma / blood supply. In Vitro Techniques. Models, Animal. Rats. Rats, Inbred F344

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  • (PMID = 11106254.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA-68438; United States / NHLBI NIH HHS / HL / HL-26309; United States / NHLBI NIH HHS / HL / HL-38245
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] UNITED STATES
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Estrogen Receptor Modulators; 0 / Receptors, Estrogen; 094ZI81Y45 / Tamoxifen
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19. Ciocca DR, Rozados VR, Cuello Carrión FD, Gervasoni SI, Matar P, Scharovsky OG: Hsp25 and Hsp70 in rodent tumors treated with doxorubicin and lovastatin. Cell Stress Chaperones; 2003;8(1):26-36
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Heat shock protein 27 (Hsp27) and Hsp70 have been involved in resistance to anticancer drugs in human breast cancer cells growing in vitro and in vivo.
  • In this study, we examined the expression of Hsp25 (the rodent homologue to human Hsp27) and Hsp70 in 3 different rodent tumors (a mouse breast carcinoma, a rat sarcoma, and a rat lymphoma maintained by subcutaneous passages) treated in vivo with doxorubicin (DOX) and lovastatin (LOV).
  • All tumors showed massive cell death under control untreated conditions, and this massive death increased after cytotoxic drug administration.
  • The tumor type that was more resistant to cell death was the sarcoma, and this was found in sarcomas growing both under control conditions and after cytotoxic drug administration.
  • After drug treatment, only sarcoma tumor cells showed a significant increase in Hsp70.
  • In sarcomas, Hsp25 and Hsp70 were found in viable tumor cells located around the blood vessels, and these areas showed the most resistant tumor cell phenotype after chemotherapy.
  • In conclusion, our study shows that each tumor type has unique features regarding the expression of Hsp25 and Hsp70 and that these proteins seem to be implicated in drug resistance mainly in sarcomas, making these model systems important to perform more mechanistic studies on the role of Hsps in resistance to certain cytotoxic drugs.
  • [MeSH-major] Adenocarcinoma / metabolism. Antineoplastic Combined Chemotherapy Protocols / pharmacology. Fibrosarcoma / metabolism. HSP70 Heat-Shock Proteins / biosynthesis. Heat-Shock Proteins. Mammary Neoplasms, Animal / metabolism. Neoplasm Proteins / biosynthesis
  • [MeSH-minor] Animals. Apoptosis. Doxorubicin / administration & dosage. Drug Resistance, Neoplasm. Endothelium, Vascular / metabolism. Female. HSP27 Heat-Shock Proteins. Lovastatin / administration & dosage. Lymphoma, B-Cell / metabolism. Lymphoma, B-Cell / pathology. Mice. Mice, Inbred Strains. Rats. Rats, Inbred Strains

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  • (PMID = 12820652.001).
  • [ISSN] 1355-8145
  • [Journal-full-title] Cell stress & chaperones
  • [ISO-abbreviation] Cell Stress Chaperones
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / HSP27 Heat-Shock Proteins; 0 / HSP70 Heat-Shock Proteins; 0 / Heat-Shock Proteins; 0 / Hspb1 protein, mouse; 0 / Hspb1 protein, rat; 0 / Neoplasm Proteins; 80168379AG / Doxorubicin; 9LHU78OQFD / Lovastatin
  • [Other-IDs] NLM/ PMC514851
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20. Liu S, Netzel-Arnett S, Birkedal-Hansen H, Leppla SH: Tumor cell-selective cytotoxicity of matrix metalloproteinase-activated anthrax toxin. Cancer Res; 2000 Nov 1;60(21):6061-7
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  • Matrix metalloproteinases (MMPs) are overexpressed in a variety of tumor tissues and cell lines, and their expression is highly correlated to tumor invasion and metastasis.
  • The toxicity of the mutated PA proteins for MMP-overexpressing cells was blocked by hydroxamate inhibitors of MMPs, including BB94, and by a tissue inhibitor of matrix metalloproteinases (TIMP-2).
  • This method of achieving cell-type specificity is conceptually distinct from, and potentially synergistic with, the more common strategy of retargeting a protein toxin by fusion to a growth factor, cytokine, or antibody.
  • [MeSH-minor] Amino Acid Sequence. Animals. Binding Sites. Biotransformation. Breast Neoplasms / drug therapy. Breast Neoplasms / enzymology. COS Cells / enzymology. Cercopithecus aethiops. Coculture Techniques. Fibrosarcoma / drug therapy. Fibrosarcoma / enzymology. Humans. Matrix Metalloproteinase 2 / biosynthesis. Matrix Metalloproteinase 2 / metabolism. Matrix Metalloproteinase 9 / biosynthesis. Matrix Metalloproteinase 9 / metabolism. Matrix Metalloproteinases, Membrane-Associated. Melanoma / drug therapy. Melanoma / enzymology. Metalloendopeptidases / biosynthesis. Metalloendopeptidases / metabolism. Mutation. Tumor Cells, Cultured. Vero Cells / enzymology

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  • (PMID = 11085528.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] UNITED STATES
  • [Chemical-registry-number] 0 / Antigens, Bacterial; 0 / Bacterial Toxins; 0 / anthrax toxin; EC 3.4.24.- / Matrix Metalloproteinases; EC 3.4.24.- / Matrix Metalloproteinases, Membrane-Associated; EC 3.4.24.- / Metalloendopeptidases; EC 3.4.24.24 / Matrix Metalloproteinase 2; EC 3.4.24.35 / Matrix Metalloproteinase 9
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21. Metwally K, Khalil A, Pratsinis H, Kletsas D: Synthesis, in-vitro cytotoxicity, and a preliminary structure-activity relationship investigation of pyrimido[4,5-c]quinoline-1(2H)-ones. Arch Pharm (Weinheim); 2010 Aug;343(8):465-72
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  • The effect of several quinoline-ring substituents was examined and the new compounds were evaluated in vitro for cytotoxicity against three human cancer cell lines namely, lung fibrosarcoma HT-1080, colon adenocarcinoma HT-29, and breast carcinoma MDA-MB-231.
  • Flow cytometric cell cycle analysis performed on HT-1080 cells revealed that the most cytotoxic compounds 48, 50, 54, 59, and 63 inhibit the S-phase and arrest the cells in the G2/M phase of the cell cycle suggesting an antimitotic action of these compounds.
  • [MeSH-minor] Breast Neoplasms / drug therapy. Breast Neoplasms / pathology. Cell Cycle / drug effects. Colonic Neoplasms / drug therapy. Colonic Neoplasms / pathology. Humans. Lung Neoplasms / drug therapy. Lung Neoplasms / pathology. Pyrimidines / chemical synthesis. Pyrimidines / pharmacology. Structure-Activity Relationship. Tumor Cells, Cultured

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  • (PMID = 20803623.001).
  • [ISSN] 1521-4184
  • [Journal-full-title] Archiv der Pharmazie
  • [ISO-abbreviation] Arch. Pharm. (Weinheim)
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antimitotic Agents; 0 / Pyrimidines; 0 / Quinolines
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22. Zanzonico P, O'Donoghue J, Chapman JD, Schneider R, Cai S, Larson S, Wen B, Chen Y, Finn R, Ruan S, Gerweck L, Humm J, Ling C: Iodine-124-labeled iodo-azomycin-galactoside imaging of tumor hypoxia in mice with serial microPET scanning. Eur J Nucl Med Mol Imaging; 2004 Jan;31(1):117-28
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  • Tumor hypoxia, present in many human cancers, can lead to resistance to radiation and chemotherapy, is associated with a more aggressive tumor phenotype and is an independent prognostic factor of clinical outcome.
  • In the current study, serial microPET imaging was used to evaluate iodine-124-labeled iodo-azomycin-galactoside ((124)I-IAZG) (4.2-day physical half-life) as a hypoxia imaging agent in 17 MCa breast tumors and six FSaII fibrosarcomas implanted in mice.
  • Region-of-interest analysis was performed as a function of time p.i. and indicated a tumor uptake of 5-10% (of total-body activity) for FMISO at 3-6 h p.i., and of ~17% for IAZG at 48 h p.i.
  • This was corroborated by biodistribution data in that the tumor-to-normal tissue (T/N, normal tissues of blood, heart, lung, liver, spleen, kidney, intestine, and muscle) activity ratios of IAZG at 24 h p.i. was 1.5-2 times higher than those of FMISO at 3 h p.i., with the exception of stomach.
  • [MeSH-major] Cell Hypoxia. Fibrosarcoma / diagnostic imaging. Fibrosarcoma / metabolism. Mammary Neoplasms, Animal / diagnostic imaging. Mammary Neoplasms, Animal / metabolism. Misonidazole / analogs & derivatives. Monosaccharides / pharmacokinetics. Nitroimidazoles / pharmacokinetics. Tomography, Emission-Computed / methods
  • [MeSH-minor] Animals. Cell Line, Tumor. Female. Metabolic Clearance Rate. Mice. Mice, Inbred C3H. Organ Specificity. Tissue Distribution

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  • [Cites] Radiother Oncol. 1993 Jan;26(1):45-50 [8438086.001]
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  • (PMID = 14523586.001).
  • [ISSN] 1619-7070
  • [Journal-full-title] European journal of nuclear medicine and molecular imaging
  • [ISO-abbreviation] Eur. J. Nucl. Med. Mol. Imaging
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA84596; United States / NCI NIH HHS / CA / R24 CA83084
  • [Publication-type] Comparative Study; Evaluation Studies; Journal Article; Research Support, U.S. Gov't, P.H.S.; Validation Studies
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Monosaccharides; 0 / Nitroimidazoles; 0 / iodinated azomycin galactopyranoside; 082285VIDF / fluoromisonidazole; 8FE7LTN8XE / Misonidazole
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23. Lee FY, Borzilleri R, Fairchild CR, Kim SH, Long BH, Reventos-Suarez C, Vite GD, Rose WC, Kramer RA: BMS-247550: a novel epothilone analog with a mode of action similar to paclitaxel but possessing superior antitumor efficacy. Clin Cancer Res; 2001 May;7(5):1429-37
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  • BMS-247550, a novel epothilone derivative, is being developed by Bristol-Myers Squibb Company (BMS) as an anticancer agent for the treatment of patients with malignant tumors.
  • Importantly, BMS-247550 retains its antineoplastic activity against human cancers that are naturally insensitive to paclitaxel or that have developed resistance to paclitaxel, both in vitro and in vivo.
  • Tumors for which BMS-247550 demonstrated significant antitumor activity encompass both paclitaxel-sensitive and -refractory categories, i.e., (a) paclitaxel-resistant: HCT116/VM46 colorectal (multidrug resistant), Pat-21 breast and Pat-7 ovarian carcinoma (clinical isolates; mechanisms of resistance not fully known), and A2780Tax ovarian carcinoma (tubulin mutation);.
  • (b) paclitaxel-insensitive: Pat-26 human pancreatic carcinoma (clinical isolate) and M5076 murine fibrosarcoma; and (c) paclitaxel sensitive: A2780 ovarian, LS174T, and HCT116 human colon carcinoma.
  • These efficacy data demonstrate that BMS-247550 has the potential to surpass Taxol in both clinical efficacy and ease of use (i.e., less frequent treatment schedule and/or oral administration).
  • [MeSH-minor] Administration, Oral. Animals. Breast Neoplasms / drug therapy. Cell Cycle / drug effects. Cell Survival / drug effects. Colonic Neoplasms / drug therapy. Disease Models, Animal. Drug Resistance, Neoplasm. Female. Humans. Infusions, Parenteral. Mice. Mice, Inbred BALB C. Mice, Inbred C57BL. Mice, Inbred DBA. Neoplasm Transplantation. Ovarian Neoplasms / drug therapy. Pancreatic Neoplasms / drug therapy. Sarcoma / drug therapy. Tubulin / genetics. Tubulin / metabolism. Tumor Cells, Cultured. Tumor Stem Cell Assay. Xenograft Model Antitumor Assays

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  • (PMID = 11350914.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Epothilones; 0 / Epoxy Compounds; 0 / Thiazoles; 0 / Tubulin; K27005NP0A / ixabepilone; P88XT4IS4D / Paclitaxel; UEC0H0URSE / epothilone B
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24. Fang Z, Matsumoto S, Ae K, Kawaguchi N, Yoshikawa H, Ueda T, Ishii T, Araki N, Kito M: Postradiation soft tissue sarcoma: a multiinstitutional analysis of 14 cases in Japan. J Orthop Sci; 2004;9(3):242-6
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  • [Title] Postradiation soft tissue sarcoma: a multiinstitutional analysis of 14 cases in Japan.
  • Radiation therapy (RT) is commonly used to treat malignant tumors, but it leads to side effects and complications.
  • This article focuses on the clinical manifestations, pathological characteristics, and therapeutic effects concerning postradiation soft tissue sarcomas (PRSTSs).
  • Their histological types were malignant fibrous histiocytoma (eight cases), extraskeletal osteosarcoma (four cases), fibrosarcoma (one case), and leiomyosarcoma (one case).
  • The primary diagnoses, RT history, latent period, and outcome of treatment were studied retrospectively.
  • The original tumors included uterine cancer (seven cases), breast cancer (four cases), synovial sarcoma (one case), squamous cell carcinoma (one case), and Hodgkin's disease (one case).
  • There were 13 women and 1 man, with ages ranging from 23 to 77 years (mean 58 years) at the time of the appearance of the PRSTS.
  • RT doses ranged from 48 to 91 Gy (mean 62 Gy).
  • One of three who underwent RT and one of five who underwent chemotherapy (CT) responded.
  • Because adjuvant therapies including RT and CT had a poor effect on PRSTSs, the primary treatment of PRSTSs should be radical resection with a wide margin.
  • [MeSH-major] Neoplasms, Second Primary / surgery. Sarcoma / surgery. Soft Tissue Neoplasms / surgery
  • [MeSH-minor] Adult. Aged. Breast Neoplasms / radiotherapy. Female. Histiocytoma, Benign Fibrous / etiology. Histiocytoma, Benign Fibrous / surgery. Humans. Japan. Male. Middle Aged. Neoplasm Recurrence, Local. Radiotherapy / adverse effects. Radiotherapy Dosage. Uterine Neoplasms / radiotherapy

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  • [Copyright] The Japanese Orthopaedic Association
  • (PMID = 15168177.001).
  • [ISSN] 0949-2658
  • [Journal-full-title] Journal of orthopaedic science : official journal of the Japanese Orthopaedic Association
  • [ISO-abbreviation] J Orthop Sci
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study
  • [Publication-country] Japan
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25. Qayum N, Muschel RJ, Im JH, Balathasan L, Koch CJ, Patel S, McKenna WG, Bernhard EJ: Tumor vascular changes mediated by inhibition of oncogenic signaling. Cancer Res; 2009 Aug 01;69(15):6347-54
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  • Many inhibitors of the epidermal growth factor receptor (EGFR)-RAS-phosphatidylinositol 3-kinase (PI3K)-AKT signaling pathway are in clinical use or under development for cancer therapy.
  • Here, we show that treatment of mice bearing human tumor xenografts with inhibitors that block EGFR, RAS, PI3K, or AKT resulted in prolonged and durable enhancement of tumor vascular flow, perfusion, and decreased tumor hypoxia.
  • Inhibition of tumor growth cannot account for these results, as the drugs were given at doses that did not alter tumor growth.
  • These changes are similar to the vascular normalization that has been described after the antiangiogenic treatment of xenografts.
  • One difficulty in the use of vascular normalization as a therapeutic strategy has been its limited duration.
  • These results indicate that vascular alterations must be considered as a consequence of signaling inhibition in cancer therapy.
  • [MeSH-major] Enzyme Inhibitors / pharmacology. Fibrosarcoma / blood supply. Fibrosarcoma / drug therapy
  • [MeSH-minor] Animals. Cell Hypoxia / physiology. Cell Line, Tumor. Female. Humans. Mice. Mice, SCID. Mice, Transgenic. Neovascularization, Pathologic / drug therapy. Neovascularization, Pathologic / metabolism. Oxygen / metabolism. Phosphatidylinositol 3-Kinases / antagonists & inhibitors. Phosphatidylinositol 3-Kinases / metabolism. Proto-Oncogene Proteins c-akt / antagonists & inhibitors. Proto-Oncogene Proteins c-akt / metabolism. Receptor, Epidermal Growth Factor / antagonists & inhibitors. Receptor, Epidermal Growth Factor / metabolism. Signal Transduction / drug effects. Xenograft Model Antitumor Assays. ras Proteins / antagonists & inhibitors. ras Proteins / metabolism

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  • (PMID = 19622766.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / G0700730(82363); United States / NCI NIH HHS / CA / R01 CA73820; United Kingdom / Medical Research Council / / ; United States / NCI NIH HHS / CA / P01 CA75138; United Kingdom / Medical Research Council / / G0700730; United States / NCI NIH HHS / CA / R01 CA073820; United States / NCI NIH HHS / CA / P01 CA075138; United Kingdom / Cancer Research UK / / ; United States / NCI NIH HHS / CA / R01 CA073820-10; United States / NCI NIH HHS / CA / P01 CA075138-060001
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Enzyme Inhibitors; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 3.6.5.2 / ras Proteins; S88TT14065 / Oxygen
  • [Other-IDs] NLM/ NIHMS120198; NLM/ PMC2825046
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26. Wang J, Sheppard GS, Lou P, Kawai M, BaMaung N, Erickson SA, Tucker-Garcia L, Park C, Bouska J, Wang YC, Frost D, Tapang P, Albert DH, Morgan SJ, Morowitz M, Shusterman S, Maris JM, Lesniewski R, Henkin J: Tumor suppression by a rationally designed reversible inhibitor of methionine aminopeptidase-2. Cancer Res; 2003 Nov 15;63(22):7861-9
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  • Methionine aminopeptidase (MetAP)-2 has been suggested as a novel target for cancer therapy because the anticancer agent TNP-470 irreversibly inactivates the catalytic activity of this enzyme.
  • We have synthesized this bestatin-type MetAP2 inhibitor with the aid of crystal structures of the enzyme-inhibitor complexes and parallel synthesis.
  • A-357300 induces cytostasis by cell cycle arrest at the G(1) phase selectively in endothelial cells and in a subset of tumor cells, but not in most primary cells of nonendothelial type.
  • These data affirm that MetAP2 plays a pivotal role in cell growth and establish that reversible MetAP2 inhibitors are promising novel cancer therapeutic agents.
  • [MeSH-minor] Animals. Breast Neoplasms / drug therapy. Breast Neoplasms / enzymology. Cell Cycle / drug effects. Cell Division / drug effects. Cornea / blood supply. Cyclohexanes. Drug Design. Endothelium, Vascular / cytology. Endothelium, Vascular / drug effects. Endothelium, Vascular / enzymology. Female. Fibrosarcoma / drug therapy. Fibrosarcoma / enzymology. Humans. Mice. Mice, SCID. Models, Molecular. Neovascularization, Physiologic / drug effects. Neuroblastoma / drug therapy. Neuroblastoma / enzymology. Sesquiterpenes / chemistry. Sesquiterpenes / pharmacology. Sesquiterpenes / toxicity. Xenograft Model Antitumor Assays

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  • (PMID = 14633714.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / A357300; 0 / Antineoplastic Agents; 0 / Chlorobenzenes; 0 / Cyclohexanes; 0 / Protease Inhibitors; 0 / Sesquiterpenes; 129298-91-5 / O-(chloroacetylcarbamoyl)fumagillol; EC 3.4.11.- / Aminopeptidases; EC 3.4.11.18 / methionine aminopeptidase 2; EC 3.4.24.- / Metalloendopeptidases
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27. Lynch RA, Etchin J, Battle TE, Frank DA: A small-molecule enhancer of signal transducer and activator of transcription 1 transcriptional activity accentuates the antiproliferative effects of IFN-gamma in human cancer cells. Cancer Res; 2007 Feb 1;67(3):1254-61
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  • Thus, enhancing gene transcription mediated by STAT1 may be an effective approach to cancer therapy.
  • A high-throughput screen was developed to identify molecules that could enhance STAT1-dependent gene expression.
  • Reflecting the fact that STAT1 can exert tumor-suppressive effects, 2-NP enhanced the ability of IFN-gamma to inhibit the proliferation of human breast cancer and fibrosarcoma cells.
  • These findings indicate that enhancement of STAT1 transcriptional activity may have utility in anticancer therapies, and that cell-based screens for modulators of transcription factor function can be a useful approach for drug discovery.
  • [MeSH-major] Interferon-gamma / pharmacology. STAT1 Transcription Factor / biosynthesis. Transcription, Genetic / drug effects
  • [MeSH-minor] Animals. Cell Growth Processes / drug effects. Cell Line, Tumor. Drug Synergism. Gene Expression Regulation / drug effects. Humans. Mice. NIH 3T3 Cells. Naphthyridines. Phosphorylation / drug effects. Transcriptional Activation

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  • (PMID = 17283162.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 2-(1-,8-naphthyridin-2-yl)phenol; 0 / Naphthyridines; 0 / STAT1 Transcription Factor; 82115-62-6 / Interferon-gamma
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28. Hine CM, Seluanov A, Gorbunova V: Use of the Rad51 promoter for targeted anti-cancer therapy. Proc Natl Acad Sci U S A; 2008 Dec 30;105(52):20810-5
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  • [Title] Use of the Rad51 promoter for targeted anti-cancer therapy.
  • Here we propose to exploit the overexpression of Rad51 in cancer cells to design a Rad51 promoter-based anticancer therapy.
  • This dramatic difference in activity has high therapeutic potential.
  • We demonstrate that the fusion of Rad51 promoter to diphtheria toxin A (DTA) gene kills a variety of cancer cell types, including breast cancer, fibrosarcoma, and cervical cancer cells, with minimal effect on normal breast epithelial cells and normal fibroblasts.
  • Our results suggest that therapies based on the Rad51 promoter will be highly tumor specific and open new avenues for targeting a broad range of cancers.
  • [MeSH-major] Diphtheria Toxin / biosynthesis. Genetic Therapy. Neoplasm Proteins / metabolism. Neoplasms / metabolism. Neoplasms / therapy. Peptide Fragments / biosynthesis. Promoter Regions, Genetic. Rad51 Recombinase / metabolism

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  • (PMID = 19106292.001).
  • [ISSN] 1091-6490
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] eng
  • [Grant] United States / NIA NIH HHS / AG / R01 AG027237
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Diphtheria Toxin; 0 / Neoplasm Proteins; 0 / Peptide Fragments; 0 / RNA, Messenger; 0 / RNA, Neoplasm; 0 / diphtheria toxin fragment A; EC 2.7.7.- / RAD51 protein, human; EC 2.7.7.- / Rad51 Recombinase
  • [Other-IDs] NLM/ PMC2634908
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29. Brasch R, Turetschek K: MRI characterization of tumors and grading angiogenesis using macromolecular contrast media: status report. Eur J Radiol; 2000 Jun;34(3):148-55
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  • The utility of MMCM-enhanced MRI for tumor characterizations has been established experimentally in a range of cancer types including breast, ovary, fibrosarcoma, and prostate.
  • Suppression of microvascular permeability (up to 98%) induced by this inhibitor of angiogenesis was detected and quantified as soon as 24 h after initiation of therapy.
  • Thus, MRI assays of tumor microvascular characteristics, particularly macromolecular permeability, provide a means to non-invasively characterize tumors for prognostication, for individualization and optimization of treatment, and for monitoring therapeutic response.
  • Pending successful completion of drug trials, now in progress, the availability of MMCM should permit the immediate application of these powerful techniques in clinical practice.

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  • (PMID = 10927157.001).
  • [ISSN] 0720-048X
  • [Journal-full-title] European journal of radiology
  • [ISO-abbreviation] Eur J Radiol
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA5827; United States / NCI NIH HHS / CA / R01CA82923-01
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.; Review
  • [Publication-country] IRELAND
  • [Chemical-registry-number] 0 / Contrast Media
  • [Number-of-references] 29
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30. Miettinen M: From morphological to molecular diagnosis of soft tissue tumors. Adv Exp Med Biol; 2006;587:99-113
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  • [Title] From morphological to molecular diagnosis of soft tissue tumors.
  • Cytogenetic discoveries of balanced translocations in soft tissue tumors have opened the way to molecular genetic definition of these translocations as gene fusions from the late 1980s.
  • Many sarcomas are known to have such fusions, and the demonstration of the fusion transcripts in tumor tissue is of great value in specific diagnosis of synovial sarcoma (SYT-SSX), Ewing sarcoma (EWS-Fli1), clear cell sarcoma (EWS-ATF1), myxoid liposarcoma (FUS-CHOP), and other sarcomas.
  • Demonstration of SYT-SSX and EWS-ATF1 fusion assists in the diagnosis of synovial and clear cell sarcomas in unusual locations, such as the gastrointestinal tract, where these tumors occur with low frequency.
  • In two exceptional instances, the same translocation and gene fusion occurs in two unrelated diseases: ETV6-NTRK fusion in infantile fibrosarcoma and secretory carcinoma of the breast, and ALK-TPM3 fusion in inflammatory myofibroblastic tumor and large cell anaplastic lymphoma.
  • Activating mutations in two related receptor tyrosine kinases (RTKs), KIT, and platelet-derived growth factor receptor alpha (PDGFRA) is central to the pathogenesis of gastrointestinal stromal tumors (GISTs), and countering the mutational activation by specific tyrosine kinase inhibitors, such as Imatinib mesylate, is now standard treatment for metastatic GISTs.
  • Mutation type influences therapy responsiveness, but fortunately very few GISTs carry primarily Imatinib-resistant mutations.
  • Secondary drug resistance acquired during Imatinib treatment based on new, Imatinib-resistant mutations is a major problem limiting treatment success.
  • Schwannoma types may differ in their pathogenesis: gastrointestinal schwannomas lack NF2 changes suggesting a different pathogenesis.
  • [MeSH-major] Genetic Testing. Soft Tissue Neoplasms / genetics. Soft Tissue Neoplasms / pathology

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  • (PMID = 17163160.001).
  • [ISSN] 0065-2598
  • [Journal-full-title] Advances in experimental medicine and biology
  • [ISO-abbreviation] Adv. Exp. Med. Biol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 70
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31. Li WW, Takahashi N, Jhanwar S, Cordon-Cardo C, Elisseyeff Y, Jimeno J, Faircloth G, Bertino JR: Sensitivity of soft tissue sarcoma cell lines to chemotherapeutic agents: identification of ecteinascidin-743 as a potent cytotoxic agent. Clin Cancer Res; 2001 Sep;7(9):2908-11
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  • [Title] Sensitivity of soft tissue sarcoma cell lines to chemotherapeutic agents: identification of ecteinascidin-743 as a potent cytotoxic agent.
  • The cytotoxic effects of ecteinascidin-743(ET-743), a novel marine natural product, were evaluated and compared with that of clinically used anticancer agents methotrexate, doxorubicin, etoposide, and paclitaxel in eight human soft tissue sarcoma (STS) cell lines.
  • HT-1080, a fibrosarcoma cell line, and HS-42, a malignant mesodermal cell line, were the most sensitive of the cell lines to methotrexate, doxorubicin, etoposide, and paclitaxel.
  • Cytotoxicity of ET-743 was dose- and time-related (4-72 h exposure).
  • Three colon adenocarcinoma cell lines, HCT-8, HT-29, and HCT-116, and one breast cancer cell line, MCF-7, were 1-2 logs less sensitive to ET-743 than the STS cell lines.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Dioxoles / pharmacology. Isoquinolines / pharmacology. Sarcoma / drug therapy
  • [MeSH-minor] Blotting, Western. Cell Cycle / drug effects. Cell Survival / drug effects. Dose-Response Relationship, Drug. Doxorubicin / pharmacology. Etoposide / pharmacology. Humans. Inhibitory Concentration 50. Methotrexate / pharmacology. P-Glycoprotein / drug effects. P-Glycoprotein / metabolism. Proto-Oncogene Proteins c-bcl-2 / drug effects. Proto-Oncogene Proteins c-bcl-2 / metabolism. Retinoblastoma Protein / drug effects. Retinoblastoma Protein / metabolism. Sensitivity and Specificity. Tetrahydroisoquinolines. Tumor Cells, Cultured. Tumor Suppressor Protein p53 / drug effects. Tumor Suppressor Protein p53 / metabolism

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  • (PMID = 11555609.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P01-CA-47179
  • [Publication-type] Comparative Study; Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Dioxoles; 0 / Isoquinolines; 0 / P-Glycoprotein; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Retinoblastoma Protein; 0 / Tetrahydroisoquinolines; 0 / Tumor Suppressor Protein p53; 114899-77-3 / trabectedin; 6PLQ3CP4P3 / Etoposide; 80168379AG / Doxorubicin; YL5FZ2Y5U1 / Methotrexate
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32. Lee Y, Vassilakos A, Feng N, Lam V, Xie H, Wang M, Jin H, Xiong K, Liu C, Wright J, Young A: GTI-2040, an antisense agent targeting the small subunit component (R2) of human ribonucleotide reductase, shows potent antitumor activity against a variety of tumors. Cancer Res; 2003 Jun 1;63(11):2802-11
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  • In vivo studies have shown that GTI-2040 significantly inhibits growth of human colon tumors (adenocarcinoma), pancreatic tumors (adenocarcinoma), liver tumors, lung tumors, breast tumors (adenocarcinoma), renal tumors, ovarian tumors (adenocarcinoma), melanoma, brain glioblastoma-astrocytoma, prostatic tumors, and cervical tumors in nude and/or severe combined immunodeficient mice.
  • Treatment of severe combined immunodeficient mice bearing Burkitt's lymphoma with GTI-2040, but not control oligonucleotides, greatly extended the survival of mice, and survival extended well beyond the treatment period.
  • [MeSH-major] Neoplasms / drug therapy. Oligonucleotides, Antisense / pharmacology. Ribonucleotide Reductases / antagonists & inhibitors
  • [MeSH-minor] Animals. Burkitt Lymphoma / drug therapy. Burkitt Lymphoma / enzymology. Burkitt Lymphoma / immunology. CpG Islands / drug effects. Dose-Response Relationship, Drug. Down-Regulation / drug effects. Female. Fibrosarcoma / drug therapy. Fibrosarcoma / enzymology. Fibrosarcoma / secondary. Humans. Lung Neoplasms / drug therapy. Lung Neoplasms / enzymology. Lung Neoplasms / secondary. Melanoma / drug therapy. Melanoma / enzymology. Melanoma / secondary. Mice. Mice, Inbred BALB C. Mice, Nude. Mice, SCID. Oligodeoxyribonucleotides. RNA, Messenger / antagonists & inhibitors. RNA, Messenger / biosynthesis. RNA, Messenger / genetics. Tumor Cells, Cultured. Xenograft Model Antitumor Assays

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  • (PMID = 12782585.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Oligodeoxyribonucleotides; 0 / Oligonucleotides, Antisense; 0 / RNA, Messenger; 236391-66-5 / GTI2040; EC 1.17.4.- / Ribonucleotide Reductases; EC 1.17.4.- / ribonucleotide reductase R2 subunit
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33. Atkinson JM, Falconer RA, Edwards DR, Pennington CJ, Siller CS, Shnyder SD, Bibby MC, Patterson LH, Loadman PM, Gill JH: Development of a novel tumor-targeted vascular disrupting agent activated by membrane-type matrix metalloproteinases. Cancer Res; 2010 Sep 01;70(17):6902-12
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  • [Title] Development of a novel tumor-targeted vascular disrupting agent activated by membrane-type matrix metalloproteinases.
  • Several VDAs have progressed into early clinical trials, but their therapeutic value seems to be compromised by systemic toxicity.
  • In this report, we describe the design and characterization of a novel VDA, ICT2588, that is nontoxic until activated specifically in the tumor by membrane-type 1 matrix metalloproteinase (MT1-MMP).
  • The antitumor activity of ICT2588 was superior to its active metabolite, exhibiting reduced toxicity, improved therapeutic index, enhanced pharmacodynamic effect, and greater efficacy.
  • [MeSH-major] Angiogenesis Inhibitors / pharmacology. Breast Neoplasms / drug therapy. Colchicine / analogs & derivatives. Fibrosarcoma / drug therapy. Matrix Metalloproteinases / metabolism. Matrix Metalloproteinases, Membrane-Associated / metabolism. Oligopeptides / pharmacology. Thiourea / analogs & derivatives
  • [MeSH-minor] Animals. Doxorubicin / pharmacology. Female. Humans. Mice. Mice, Inbred BALB C. Mice, Nude. Neovascularization, Pathologic / drug therapy. Neovascularization, Pathologic / enzymology. Neovascularization, Pathologic / pathology. Tissue Distribution. Xenograft Model Antitumor Assays

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  • (PMID = 20663911.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United Kingdom / Cancer Research UK / / A5953; United Kingdom / Cancer Research UK / / A8706; United Kingdom / Cancer Research UK / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / ICT 2552; 0 / Oligopeptides; 80168379AG / Doxorubicin; EC 3.4.24.- / Matrix Metalloproteinases; EC 3.4.24.- / Matrix Metalloproteinases, Membrane-Associated; GYV9AM2QAG / Thiourea; SML2Y3J35T / Colchicine
  • [Other-IDs] NLM/ PMC2933508; NLM/ UKMS31558
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34. Hoffman RM: Tumor-targeting amino acid auxotrophic Salmonella typhimurium. Amino Acids; 2009 Sep;37(3):509-21
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  • We have developed an effective bacterial cancer therapy strategy by targeting viable tumor tissue using Salmonella typhimurium auxotrophs that we have generated which grow in viable as well as necrotic areas of tumors.
  • However, the auxotrophy severely restricts growth of these bacteria in normal tissue.
  • The S. typhimurium A1-R mutant, which is auxotrophic for leu-arg and has high anti-tumor virulence, was developed in our laboratory.
  • A1-R was initially used to treat metastatic human prostate and breast tumors that had been orthotopically implanted in nude mice.
  • A1-R was also targeted to both axillary lymph and popliteal lymph node metastasis of human pancreatic cancer and fibrosarcoma, respectively, as well as lung metastasis of the fibrosarcoma in nude mice.
  • The metastases were cured without the need of chemotherapy or any other treatment.
  • The primary pancreatic cancer regressed without additional chemotherapy or any other treatment.
  • The approach described here, where bacterial monotherapy effectively treats primary and metastatic tumors, is a significant improvement over previous bacterial tumor-therapy strategies that require combination with toxic chemotherapy.
  • The expression of therapeutics in Salmonella under the regulation of one or more promoters that are activated preferentially in tumors has the potential to improve the efficacy of Salmonella tumor therapy.
  • Exploitation of the tumor-killing capability of Salmonella has great promise for a new paradigm of cancer therapy.
  • [MeSH-major] Amino Acids / metabolism. Biological Therapy / methods. Neoplasms, Experimental / microbiology. Neoplasms, Experimental / therapy. Salmonella Infections, Animal. Salmonella typhimurium / growth & development

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  • (PMID = 19291366.001).
  • [ISSN] 1438-2199
  • [Journal-full-title] Amino acids
  • [ISO-abbreviation] Amino Acids
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Austria
  • [Chemical-registry-number] 0 / Amino Acids; 94ZLA3W45F / Arginine; GMW67QNF9C / Leucine
  • [Number-of-references] 30
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35. Petrova EE, Valyakina TI, Simonova MA, Komaleva RL, Khaidukov SV, Makarov EA, Blokhin DY, Ivanov PK, Andronova TM, Nesmeyanov VA: Muramyl peptides augment cytotoxic effect of tumor necrosis factor-alpha in combination with cytotoxic drugs on tumor cells. Int Immunopharmacol; 2006 Sep;6(9):1377-86
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  • [Title] Muramyl peptides augment cytotoxic effect of tumor necrosis factor-alpha in combination with cytotoxic drugs on tumor cells.
  • We have demonstrated that biologically active muramyl peptides, in particular, glucosaminylmuramyl dipeptide (GMDP), augmented in vitro cytotoxic activity of tumor necrosis factor-alpha (TNF-alpha) against murine fibrosarcoma L929 cells.
  • GMDP also enhanced cytotoxicity of TNF-alpha and cisplatin against human breast carcinoma MCF7 and histiocytic lymphoma U937 cells.
  • [MeSH-major] Acetylmuramyl-Alanyl-Isoglutamine / analogs & derivatives. Adjuvants, Immunologic / toxicity. Antineoplastic Agents / toxicity. Cytotoxicity, Immunologic / drug effects. Neoplasms / pathology. Tumor Necrosis Factor-alpha / toxicity
  • [MeSH-minor] Animals. Cell Death / drug effects. Cells, Cultured. Cisplatin / toxicity. Dactinomycin / toxicity. Drug Therapy, Combination. Humans. L Cells (Cell Line). Mice. U937 Cells

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  • (PMID = 16846831.001).
  • [ISSN] 1567-5769
  • [Journal-full-title] International immunopharmacology
  • [ISO-abbreviation] Int. Immunopharmacol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Adjuvants, Immunologic; 0 / Antineoplastic Agents; 0 / Tumor Necrosis Factor-alpha; 1CC1JFE158 / Dactinomycin; 53678-77-6 / Acetylmuramyl-Alanyl-Isoglutamine; 97590-38-0 / glucosaminylmuramyl-2-alanine-D-isoglutamine; Q20Q21Q62J / Cisplatin
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36. Sun XY, Zheng YP, Lin DH, Zhang H, Zhao F, Yuan CS: Potential anti-cancer activities of Furanodiene, a Sesquiterpene from Curcuma wenyujin. Am J Chin Med; 2009;37(3):589-96
International Agency for Research on Cancer - Screening Group. diagnostics - Histopathology and cytopathology of the uterine cervix - digital atlas .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [MeSH-major] Curcuma. Drugs, Chinese Herbal / pharmacology. Furans / pharmacology. Heterocyclic Compounds, 2-Ring / pharmacology. Sesquiterpenes / pharmacology. Uterine Cervical Neoplasms / drug therapy
  • [MeSH-minor] Adenocarcinoma. Animals. Breast Neoplasms. Carcinoma, Hepatocellular. Cell Division / drug effects. Female. Fibrosarcoma / drug therapy. Fibrosarcoma / pathology. HL-60 Cells. HeLa Cells. Humans. K562 Cells. Leukemia. Liver Neoplasms. Lung Neoplasms. Mice. Mice, Inbred Strains. Organ Size. Spleen / pathology. Thymus Gland / pathology. Xenograft Model Antitumor Assays

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  • (PMID = 19606517.001).
  • [ISSN] 0192-415X
  • [Journal-full-title] The American journal of Chinese medicine
  • [ISO-abbreviation] Am. J. Chin. Med.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Singapore
  • [Chemical-registry-number] 0 / Drugs, Chinese Herbal; 0 / Furans; 0 / Heterocyclic Compounds, 2-Ring; 0 / Sesquiterpenes; 19912-61-9 / furanodiene
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37. Ying H, Biroc SL, Li WW, Alicke B, Xuan JA, Pagila R, Ohashi Y, Okada T, Kamata Y, Dinter H: The Rho kinase inhibitor fasudil inhibits tumor progression in human and rat tumor models. Mol Cancer Ther; 2006 Sep;5(9):2158-64
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  • In the orthotopic breast cancer model with MDA-MB-231, there were 3-fold more tumor-free mice in the fasudil-treated group versus saline control group (P < 0.01).
  • Fasudil has been approved for the treatment of cerebral vasospasm and associated cerebral ischemic symptoms.
  • Therefore, the concept of Rho kinase inhibition as an antimetastatic therapy for cancer can now be clinically explored.
  • [MeSH-major] 1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine / analogs & derivatives. Breast Neoplasms / drug therapy. Fibrosarcoma / drug therapy. Intracellular Signaling Peptides and Proteins / antagonists & inhibitors. Protein Kinase Inhibitors / pharmacology. Protein-Serine-Threonine Kinases / antagonists & inhibitors. rho-Associated Kinases / antagonists & inhibitors
  • [MeSH-minor] Animals. Cell Adhesion / drug effects. Cell Adhesion / physiology. Cell Growth Processes / drug effects. Cell Line, Tumor. Cell Movement / drug effects. Disease Progression. Female. Humans. Male. Mice. Mice, Nude. Rats. Xenograft Model Antitumor Assays

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  • (PMID = 16985048.001).
  • [ISSN] 1535-7163
  • [Journal-full-title] Molecular cancer therapeutics
  • [ISO-abbreviation] Mol. Cancer Ther.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Intracellular Signaling Peptides and Proteins; 0 / Protein Kinase Inhibitors; 0 / ROCK1 protein, human; 0 / ROCK2 protein, human; 0 / Rock1 protein, mouse; 0 / Rock2 protein, mouse; 103745-39-7 / fasudil; 84477-87-2 / 1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.1 / ROCK2 protein, rat; EC 2.7.11.1 / rho-Associated Kinases
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38. Li L, Huang YH, Li Y, Wang FQ, Shang BY, Zhen YS: Antitumor activity of anti-type IV collagenase monoclonal antibody and its lidamycin conjugate against colon carcinoma. World J Gastroenterol; 2005 Aug 7;11(29):4478-83
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  • [Title] Antitumor activity of anti-type IV collagenase monoclonal antibody and its lidamycin conjugate against colon carcinoma.
  • AIM: Type IV collagenase including MMP-2 and -9 plays an important role in cancer cell invasion and metastasis and is an attractive target for mAb-directed therapy.
  • The immunoreactivity of mAb 3G11, a mAb directed against type IV collagenase in human colorectal carcinomas, was studied by immuno-histochemical (IHC) staining. mAb 3G11 was conjugated to an antitumor antibiotic lidamycin (LDM).
  • The therapeutic effect of conjugate 3G11-LDM was evaluated with colon carcinoma 26 in mice.
  • RESULTS: As shown in ELISA, mAb 3G11 reacted specifically with type IV collagenase, while 3G11-LDM conjugate also recognized specifically its respective antigen.
  • In IHC assay, mAb 3G11 showed positive immunoreactivity in most cases of colorectal carcinoma, and negative immunoreactivity in the adjacent non-malignant tissues.
  • By gelatin zymography, the inhibition effect of mAb 3G11 on the secretion activity of type IV collagenase was proved.
  • [MeSH-major] Aminoglycosides / pharmacology. Antibiotics, Antineoplastic / pharmacology. Antibodies, Monoclonal / pharmacology. Collagen Type IV / immunology. Colonic Neoplasms / drug therapy
  • [MeSH-minor] Animals. Breast Neoplasms. Carcinoma, Hepatocellular. Enediynes. Fibrosarcoma. HT29 Cells. Humans. Immunoconjugates / pharmacology. In Vitro Techniques. Liver Neoplasms. Mice. Mice, Inbred BALB C

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  • (PMID = 16052675.001).
  • [ISSN] 1007-9327
  • [Journal-full-title] World journal of gastroenterology
  • [ISO-abbreviation] World J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Aminoglycosides; 0 / Antibiotics, Antineoplastic; 0 / Antibodies, Monoclonal; 0 / Collagen Type IV; 0 / Enediynes; 0 / Immunoconjugates; 120177-69-7 / C 1027
  • [Other-IDs] NLM/ PMC4398695
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39. Adeniyi BA, Robert MF, Chai H, Fong HH: In vitro cytotoxicity activity of Diosquinone, a naphthoquinone epoxide. Phytother Res; 2003 Mar;17(3):282-4
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  • The ethno-pharmacological claim of this plant and the previously observed good antibacterial activity of this compound among the others isolated from this plant suggest its probable cytotoxicity activity.
  • [MeSH-minor] Breast Neoplasms / drug therapy. Colonic Neoplasms / drug therapy. Drug Resistance, Multiple. Female. Fibrosarcoma / drug therapy. Humans. Lung Neoplasms / drug therapy. Male. Nasopharyngeal Neoplasms / drug therapy. Neoplasms, Hormone-Dependent / drug therapy. Plant Extracts / administration & dosage. Plant Extracts / pharmacology. Plant Extracts / therapeutic use. Prostatic Neoplasms / drug therapy. Tumor Cells, Cultured / drug effects

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  • [Copyright] Copyright 2003 John Wiley & Sons, Ltd.
  • (PMID = 12672163.001).
  • [ISSN] 0951-418X
  • [Journal-full-title] Phytotherapy research : PTR
  • [ISO-abbreviation] Phytother Res
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Naphthoquinones; 0 / Plant Extracts; 50886-69-6 / diosquinone
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40. Pavón Jiménez R, García Rubira JC, García Martínez JT, Sánchez Escribano R, Calvo Jambrina R, Cruz Fernández JM: [Intrapericardial cisplatin for malignant tamponade]. Rev Esp Cardiol; 2000 Apr;53(4):587-9
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  • The choice therapy of malignant pericardial effusion is controversial.
  • There were 6 patients, and the primary tumor was breast carcinoma in 2, lung in 1, ovary in 1, mediastinal fibrosarcoma in 1, and unknown in 1.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Cardiac Tamponade / drug therapy. Cardiac Tamponade / etiology. Cisplatin / therapeutic use. Heart Neoplasms / complications. Heart Neoplasms / drug therapy. Pericardial Effusion / drug therapy. Pericardial Effusion / etiology

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  • (PMID = 10758038.001).
  • [ISSN] 0300-8932
  • [Journal-full-title] Revista española de cardiología
  • [ISO-abbreviation] Rev Esp Cardiol
  • [Language] spa
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] SPAIN
  • [Chemical-registry-number] 0 / Antineoplastic Agents; Q20Q21Q62J / Cisplatin
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41. Palmer K, Hitt M, Emtage PC, Gyorffy S, Gauldie J: Combined CXC chemokine and interleukin-12 gene transfer enhances antitumor immunity. Gene Ther; 2001 Feb;8(4):282-90
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  • It has been shown that intratumor administration of an adenovirus vector expressing IL-12 produces a potent T cell-mediated response that leads to significant tumor regression in a murine breast cancer model.
  • Adenovirus vectors expressing IP-10 or MIG and/or IL-12 were administered intratumorally in a murine model of mammary adenocarcinoma and fibrosarcoma.
  • Administration of IP-10 or MIG in combination with IL-12 resulted in considerable tumor regression and increased survival time of tumor-bearing animals as compared with IP-10, MIG, IL-12 alone or control-treated animals, with the IP-10 IL-12 combination being most effective.
  • [MeSH-major] Adenoviridae / genetics. Chemokines, CXC / genetics. Genetic Therapy / methods. Genetic Vectors / administration & dosage. Interleukin-12 / genetics. Mammary Neoplasms, Experimental / therapy
  • [MeSH-minor] Animals. Antigens, CD3 / analysis. Blotting, Northern. CD4-Positive T-Lymphocytes / immunology. CD8-Positive T-Lymphocytes / immunology. Collagen. Cytotoxicity Tests, Immunologic. Drug Combinations. Endothelium, Vascular / pathology. Female. Fibroblast Growth Factor 2 / pharmacology. Injections, Intralesional. Interferon-gamma / analysis. Interleukin-4 / analysis. Laminin. Mice. Mice, Inbred C57BL. Mice, Inbred Strains. Mice, Nude. Neovascularization, Pathologic. Proteoglycans. T-Lymphocytes / immunology. Xenograft Model Antitumor Assays

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  • (PMID = 11313802.001).
  • [ISSN] 0969-7128
  • [Journal-full-title] Gene therapy
  • [ISO-abbreviation] Gene Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD3; 0 / Chemokines, CXC; 0 / Drug Combinations; 0 / Laminin; 0 / Proteoglycans; 103107-01-3 / Fibroblast Growth Factor 2; 119978-18-6 / matrigel; 187348-17-0 / Interleukin-12; 207137-56-2 / Interleukin-4; 82115-62-6 / Interferon-gamma; 9007-34-5 / Collagen
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