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1. Mabuchi S, Kawase C, Altomare DA, Morishige K, Sawada K, Hayashi M, Tsujimoto M, Yamoto M, Klein-Szanto AJ, Schilder RJ, Ohmichi M, Testa JR, Kimura T: mTOR is a promising therapeutic target both in cisplatin-sensitive and cisplatin-resistant clear cell carcinoma of the ovary. Clin Cancer Res; 2009 Sep 1;15(17):5404-13
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  • [Title] mTOR is a promising therapeutic target both in cisplatin-sensitive and cisplatin-resistant clear cell carcinoma of the ovary.
  • PURPOSE: Mammalian target of rapamycin (mTOR) plays a central role in cell proliferation and is regarded as a promising target in cancer therapy, including for ovarian cancer.
  • This study aimed to examine the role of mTOR as a therapeutic target in clear cell carcinoma of the ovary, which is regarded as an aggressive, chemoresistant histologic subtype.
  • EXPERIMENTAL DESIGN: Using tissue microarrays of 98 primary ovarian cancers (52 clear cell carcinomas and 46 serous adenocarcinomas), the expression of phospho-mTOR was assessed by immunohistochemistry.
  • Then, the growth-inhibitory effect of mTOR inhibition by RAD001 (everolimus) was examined using two pairs of cisplatin-sensitive parental (RMG1 and KOC7C) and cisplatin-resistant human clear cell carcinoma cell lines (RMG1-CR and KOC7C-CR) both in vitro and in vivo.
  • RESULTS: Immunohistochemical analysis showed that mTOR was more frequently activated in clear cell carcinomas than in serous adenocarcinomas (86.6% versus 50%).
  • Treatment with RAD001 markedly inhibited the growth of both RMG1 and KOC7C cells both in vitro and in vivo.
  • CONCLUSION: mTOR is frequently activated in clear cell carcinoma and can be a promising therapeutic target in the management of clear cell carcinoma.
  • Moreover, mTOR inhibition by RAD001 may be efficacious as a second-line treatment of recurrent disease in patients previously treated with cisplatin.

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  • (PMID = 19690197.001).
  • [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 / CA06927; United States / NCI NIH HHS / CA / CA083638-10; United States / NCI NIH HHS / CA / CA077429-02; United States / NCI NIH HHS / CA / P30 CA006927-45; United States / NCI NIH HHS / CA / CA83638; United States / NCI NIH HHS / CA / R01 CA077429; United States / NCI NIH HHS / CA / P50 CA083638-10; United States / NCI NIH HHS / CA / P50 CA083638; United States / NCI NIH HHS / CA / R01 CA077429-02; United States / NCI NIH HHS / CA / CA77429; United States / NCI NIH HHS / CA / P30 CA006927
  • [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 / Antineoplastic Agents; 0 / Immunosuppressive Agents; 9HW64Q8G6G / Everolimus; EC 2.7.- / Protein Kinases; EC 2.7.1.1 / MTOR protein, human; EC 2.7.1.1 / TOR Serine-Threonine Kinases; EC 2.7.1.1 / mTOR protein, mouse; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; Q20Q21Q62J / Cisplatin; W36ZG6FT64 / Sirolimus
  • [Other-IDs] NLM/ NIHMS125079; NLM/ PMC2743856
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2. Azuma H, Takahara S, Ichimaru N, Wang JD, Itoh Y, Otsuki Y, Morimoto J, Fukui R, Hoshiga M, Ishihara T, Nonomura N, Suzuki S, Okuyama A, Katsuoka Y: Marked prevention of tumor growth and metastasis by a novel immunosuppressive agent, FTY720, in mouse breast cancer models. Cancer Res; 2002 Mar 1;62(5):1410-9
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  • [Title] Marked prevention of tumor growth and metastasis by a novel immunosuppressive agent, FTY720, in mouse breast cancer models.
  • In vitro treatment with FTY720 induced dramatic cancer cell apoptosis in a mouse breast cancer cell line, JygMC(A).
  • Electron microscopy revealed distinct changes on the cell surface with decreased filopodias and microvilli in cancer cells treated with FTY720 at 2 microM and clear evidence of apoptosis at 10 microM.
  • We then tested the in vivo effect of FTY720 in a mouse breast cancer model created by inoculating JygMC(A) cells (s.c.) in the flank region of BALB/c-nu/nu mice at three different dosages (2, 5, and 10 mg/kg/day; n = 30/group).
  • FTY720 treatment at 2 microM caused a remarkable cytoskeletal change with deformed and decreased filopodias in cancer cells.
  • In addition, it significantly decreased the ability of cancer cells to adhere and migrate to extracellular matrix components, and markedly reduced the expression of integrins on the cancer cell surface.
  • These results indicate that FTY720 is a potent anticancer agent that induces cancer cell apoptosis and is markedly effective for prevention of metastasis.
  • [MeSH-major] Immunosuppressive Agents / therapeutic use. Mammary Neoplasms, Experimental / drug therapy. Neoplasm Metastasis / prevention & control. Propylene Glycols / pharmacology
  • [MeSH-minor] Actins / metabolism. Animals. Apoptosis / drug effects. Cell Adhesion / drug effects. Cell Movement / drug effects. Cytoskeleton / drug effects. Female. Fingolimod Hydrochloride. Integrins / analysis. Mice. Mice, Inbred BALB C. Microscopy, Electron. Sphingosine / analogs & derivatives. Tumor Cells, Cultured

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  • (PMID = 11888913.001).
  • [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 / Actins; 0 / Immunosuppressive Agents; 0 / Integrins; 0 / Propylene Glycols; G926EC510T / Fingolimod Hydrochloride; NGZ37HRE42 / Sphingosine
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3. Zellweger T, Miyake H, July LV, Akbari M, Kiyama S, Gleave ME: Chemosensitization of human renal cell cancer using antisense oligonucleotides targeting the antiapoptotic gene clusterin. Neoplasia; 2001 Jul-Aug;3(4):360-7
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  • [Title] Chemosensitization of human renal cell cancer using antisense oligonucleotides targeting the antiapoptotic gene clusterin.
  • BACKGROUND: Renal cell cancer (RCC) is a chemoresistant disease with no active chemotherapeutic agent achieving objective response rates higher than 15%.
  • Clusterin is a cell survival gene that increases in human renal tubular epithelial cells after various states of injury and disease.
  • The objectives in this study were to evaluate clusterin expression levels in human RCC and normal kidney tissue, and to test whether clusterin ASO could also enhance chemosensitivity in human RCC Caki-2 cells both in vitro and in vivo.
  • METHODS: Immunohistochemical staining was used to characterize clusterin expression in 67 RCC and normal kidney tissues obtained from radical nephrectomy specimens.
  • Northern blot analysis was used to assess changes in clusterin mRNA expression after ASO and paclitaxel treatment.
  • The effects of combined clusterin ASO and paclitaxel treatment on Caki-2 cell growth was examined using an MTT assay.
  • RESULTS: Immunohistochemistry of normal and malignant kidney tissue sections of 67 patients demonstrated positive clusterin staining for almost all RCC (98%) and an overexpression, compared to normal tissue, in a majority of RCC (69%).
  • Characteristic apoptotic DNA laddering was observed after combined treatment with ASO plus paclitaxel, but not with either agent alone.
  • In addition, TUNEL staining revealed increased apoptotic cells in tumors treated with clusterin ASO plus paclitaxel compared to treatment with either clusterin ASO or paclitaxel alone.
  • [MeSH-major] Antineoplastic Agents, Phytogenic / therapeutic use. Glycoproteins / genetics. Kidney Neoplasms / drug therapy. Molecular Chaperones / genetics. Neoplasm Proteins / genetics. Oligonucleotides, Antisense / therapeutic use. Paclitaxel / therapeutic use
  • [MeSH-minor] Adenocarcinoma, Clear Cell / drug therapy. Adenocarcinoma, Clear Cell / metabolism. Animals. Apoptosis. Blotting, Northern. Carcinoma, Renal Cell / drug therapy. Carcinoma, Renal Cell / metabolism. Clusterin. DNA Primers / chemistry. Down-Regulation. Humans. Immunoenzyme Techniques. In Situ Nick-End Labeling. Kidney / drug effects. Kidney / metabolism. Male. Mice. Mice, Inbred BALB C. Mice, Nude. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 11571636.001).
  • [ISSN] 1522-8002
  • [Journal-full-title] Neoplasia (New York, N.Y.)
  • [ISO-abbreviation] Neoplasia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 0 / CLU protein, human; 0 / Clu protein, mouse; 0 / Clusterin; 0 / DNA Primers; 0 / Glycoproteins; 0 / Molecular Chaperones; 0 / Neoplasm Proteins; 0 / Oligonucleotides, Antisense; 0 / RNA, Messenger; P88XT4IS4D / Paclitaxel
  • [Other-IDs] NLM/ PMC1505861
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4. Cocco E, Casagrande F, Bellone S, Richter CE, Bellone M, Todeschini P, Holmberg JC, Fu HH, Montagna MK, Mor G, Schwartz PE, Arin-Silasi D, Azoudi M, Rutherford TJ, Abu-Khalaf M, Pecorelli S, Santin AD: Clostridium perfringens enterotoxin carboxy-terminal fragment is a novel tumor-homing peptide for human ovarian cancer. BMC Cancer; 2010 Jul 02;10:349
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  • BACKGROUND: Development of innovative, effective therapies against recurrent/chemotherapy-resistant ovarian cancer remains a high priority.
  • METHODS: Because claudin-3 and -4 are the epithelial receptors for Clostridium perfringens enterotoxin (CPE), and are sufficient to mediate CPE binding, in this study we evaluated the in vitro and in vivo bioactivity of the carboxy-terminal fragment of CPE (i.e., CPE290-319 binding peptide) as a carrier for tumor imaging agents and intracellular delivery of therapeutic drugs.
  • Claudin-3 and -4 expression was examined with rt-PCR and flow cytometry in multiple primary ovarian carcinoma cell lines.
  • Cell binding assays were used to assess the accuracy and specificity of the CPE peptide in vitro against primary chemotherapy-resistant ovarian carcinoma cell lines.
  • Confocal microscopy and biodistribution assays were performed to evaluate the localization and uptake of the FITC-conjugated CPE peptide in established tumor tissue.
  • RESULTS: Using a FITC-conjugated CPE peptide we show specific in vitro and in vivo binding to multiple primary chemotherapy resistant ovarian cancer cell lines.
  • Bio-distribution studies in SCID mice harboring clinically relevant animal models of chemotherapy resistant ovarian carcinoma showed higher uptake of the peptide in tumor cells than in normal organs.
  • Imunofluorescence was detectable within discrete accumulations (i.e., tumor spheroids) or even single chemotherapy resistant ovarian cancer cells floating in the ascites of xenografted animals while a time-dependent internalization of the FITC-conjugated CPE peptide was consistently noted in chemotherapy-resistant ovarian tumor cells by confocal microscopy.
  • CONCLUSIONS: Based on the high levels of claudin-3 and -4 expression in chemotherapy-resistant ovarian cancer and other highly aggressive human epithelial tumors including breast, prostate and pancreatic cancers, CPE peptide holds promise as a lead peptide for the development of new diagnostic tracers or alternative anticancer agents.

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  • (PMID = 20598131.001).
  • [ISSN] 1471-2407
  • [Journal-full-title] BMC cancer
  • [ISO-abbreviation] BMC Cancer
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA-16359; United States / NCI NIH HHS / CA / R01 CA122728-01A2
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / CLDN3 protein, human; 0 / CLDN4 protein, human; 0 / Claudin-3; 0 / Claudin-4; 0 / Cldn3 protein, mouse; 0 / Cldn4 protein, mouse; 0 / Enterotoxins; 0 / Membrane Proteins; 0 / Peptide Fragments; 0 / RNA, Messenger; 0 / enterotoxin, Clostridium
  • [Other-IDs] NLM/ PMC2908101
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5. Happo L, Cragg MS, Phipson B, Haga JM, Jansen ES, Herold MJ, Dewson G, Michalak EM, Vandenberg CJ, Smyth GK, Strasser A, Cory S, Scott CL: Maximal killing of lymphoma cells by DNA damage-inducing therapy requires not only the p53 targets Puma and Noxa, but also Bim. Blood; 2010 Dec 9;116(24):5256-67
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  • [Title] Maximal killing of lymphoma cells by DNA damage-inducing therapy requires not only the p53 targets Puma and Noxa, but also Bim.
  • DNA-damaging chemotherapy is the backbone of cancer treatment, although it is not clear how such treatments kill tumor cells.
  • In Eμ-Myc lymphomas, however, lack of both Puma and Noxa resulted in no greater drug resistance than lack of Puma alone.
  • A third B-cell lymphoma-2 homology domain (BH)3-only gene, Bim, although not a direct p53 target, was up-regulated in Eμ-Myc lymphomas incurring DNA damage, and knockdown of Bim levels markedly increased the drug resistance of Eμ-Myc/Puma(-/-)Noxa(-/-) lymphomas both in vitro and in vivo.
  • Remarkably, c-MYC-driven lymphoma cell lines from Noxa(-/-)Puma(-/-)Bim(-/-) mice were as resistant as those lacking p53.
  • Thus, the combinatorial action of Puma, Noxa, and Bim is critical for optimal apoptotic responses of lymphoma cells to 2 commonly used DNA-damaging chemotherapeutic agents, identifying Bim as an additional biomarker for treatment outcome in the clinic.

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  • (PMID = 20829369.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA043540-22; United States / NCI NIH HHS / CA / R01 CA043540; United States / NCI NIH HHS / CA / CA 43540; United States / NCI NIH HHS / CA / CA 80188; United States / NCI NIH HHS / CA / R01 CA080188
  • [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 / Apoptosis Regulatory Proteins; 0 / Bcl-2-like protein 11; 0 / Membrane Proteins; 0 / PUMA protein, mouse; 0 / Pmaip1 protein, mouse; 0 / Proto-Oncogene Proteins; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Tumor Suppressor Proteins; 6PLQ3CP4P3 / Etoposide; 8N3DW7272P / Cyclophosphamide
  • [Other-IDs] NLM/ PMC3012543
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6. Meredith RF, Buchsbaum DJ, Alvarez RD, LoBuglio AF: Brief overview of preclinical and clinical studies in the development of intraperitoneal radioimmunotherapy for ovarian cancer. Clin Cancer Res; 2007 Sep 15;13(18 Pt 2):5643s-5645s
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Due to the generally slow and incomplete transit of i.p. infused agents into the circulation, treating disease confined to the peritoneal cavity with chemotherapy, biologics, and/or radionuclides provides a pharmacologic advantage.
  • A recent phase III Gynecologic Oncology Group chemotherapy trial has confirmed a survival advantage for i.p. delivery among women undergoing initial therapy for advanced ovarian cancer (3).
  • Although the therapy was more difficult to tolerate such that 60% of patients randomized to the i.p. arm did not complete the entire regimen, there was a 16-month survival advantage. I.p. radionuclide therapy has been used in treatment of ovarian cancer for more than three decades, but side effects have been problematic in non-tumor-targeted 32P therapy (4).
  • Mouse models and cell culture have been prominent for preclinical study of agents and strategies in the development of i.p. targeted radionuclide therapy for ovarian cancer.
  • Animal studies, which have directed clinical trials, have shown clear improvement in survival with various modifications including combination chemotherapy, pretargeting, and combination of antibodies over simply delivery of a radiolabeled antibody via i.p. route.
  • [MeSH-major] Antibodies, Neoplasm / therapeutic use. Antigens, Neoplasm / immunology. Clinical Trials as Topic. Ovarian Neoplasms / therapy. Peritoneal Neoplasms / therapy. Radioimmunotherapy. Radioisotopes / therapeutic use
  • [MeSH-minor] Animals. Disease Models, Animal. Drug Administration Routes. Drug Evaluation, Preclinical. Female. Humans

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  • (PMID = 17875801.001).
  • [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 / NCRR NIH HHS / RR / M01 RR00032; United States / NCI NIH HHS / CM / N01 CM97611; United States / NCI NIH HHS / CA / P50 CA83591-03; United States / NCI NIH HHS / CA / P50 CA89019-03; United States / NCI NIH HHS / CA / R01 CA62250; United States / NCI NIH HHS / CA / R01 CA73636; United States / NCI NIH HHS / CA / R01 CA78505
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Neoplasm; 0 / Antigens, Neoplasm; 0 / Radioisotopes
  • [Number-of-references] 23
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7. Lonberg N: Fully human antibodies from transgenic mouse and phage display platforms. Curr Opin Immunol; 2008 Aug;20(4):450-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Fully human antibodies from transgenic mouse and phage display platforms.
  • These fully human MAbs provide an alternative to re-engineered, or de-immunized, rodent MAbs as a source of low immunogenicity therapeutic antibodies.
  • There are now two marketed fully human therapeutic MAbs, adalimumab and panitumumab, and several dozen more in various stages of human clinical testing.
  • Most of the drugs, including adalimumab and panitumumab, were generated using either phage display or transgenic mouse platforms.
  • The reported clinical experience with fully human MAbs demonstrates that these two platforms are, and should continue to be, a significant source of active and well tolerated experimental therapeutics.
  • While this body of reported clinical data does not yet provide a clear distinction between the platforms, the available descriptions of the drug discovery processes used to identify the clinical candidates highlight one difference.
  • It appears that lead optimization is more commonly applied to phage display derived leads than transgenic mouse derived leads.
  • [MeSH-major] Antibodies, Monoclonal / immunology. Antibodies, Monoclonal / therapeutic use. Autoimmune Diseases / drug therapy. Neoplasms / drug therapy
  • [MeSH-minor] Animals. Antigens, CD / immunology. Antigens, CD / metabolism. Antigens, CD20 / immunology. Antigens, CD20 / metabolism. Antigens, CD4 / immunology. Antigens, CD4 / metabolism. Antigens, Neoplasm / immunology. Antigens, Neoplasm / metabolism. CTLA-4 Antigen. Cell Adhesion Molecules / immunology. Cell Adhesion Molecules / metabolism. Humans. Interleukin-12 / immunology. Interleukin-12 / metabolism. Interleukin-23 / immunology. Interleukin-23 / metabolism. Mice. Mice, Transgenic. Peptide Library. Protein Engineering. RANK Ligand / immunology. RANK Ligand / metabolism. Receptor, Epidermal Growth Factor / immunology. Receptor, Epidermal Growth Factor / metabolism. TNF-Related Apoptosis-Inducing Ligand / immunology. TNF-Related Apoptosis-Inducing Ligand / metabolism. Tumor Necrosis Factor-alpha / immunology. Tumor Necrosis Factor-alpha / metabolism

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  • (PMID = 18606226.001).
  • [ISSN] 0952-7915
  • [Journal-full-title] Current opinion in immunology
  • [ISO-abbreviation] Curr. Opin. Immunol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antigens, CD; 0 / Antigens, CD20; 0 / Antigens, CD4; 0 / Antigens, Neoplasm; 0 / CTLA-4 Antigen; 0 / CTLA4 protein, human; 0 / Cell Adhesion Molecules; 0 / Ctla4 protein, mouse; 0 / EPCAM protein, human; 0 / Interleukin-23; 0 / Peptide Library; 0 / RANK Ligand; 0 / TNF-Related Apoptosis-Inducing Ligand; 0 / TNFSF10 protein, human; 0 / TNFSF11 protein, human; 0 / Tumor Necrosis Factor-alpha; 187348-17-0 / Interleukin-12; EC 2.7.10.1 / EGFR protein, human; EC 2.7.10.1 / Receptor, Epidermal Growth Factor
  • [Number-of-references] 76
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8. Roth DR, Roman D, Cozens R, Brandt R, Seewald W, Greiner B, Wenger F, Mamom T, Germann PG: Effects of epithelial growth factor receptor (EGFR) kinase inhibitors on genetically reconstituted mouse mammary glands. Exp Toxicol Pathol; 2003 Nov;55(4):237-45
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Effects of epithelial growth factor receptor (EGFR) kinase inhibitors on genetically reconstituted mouse mammary glands.
  • NeuT-transfected immortalized HC11 epithelial cells and primary mouse mammary epithelial cells have been transplanted into the gland-free mammary fat pad of female BALB/c mice.
  • Mammary tumors developed after a latency period of three to four weeks.
  • RESULTS: Oral Treatment with EGFR-KI in this transgenic organ model showed clear antitumor efficacy in a dose-dependent manner in the range between 38 and 75 mg/kg b.w.
  • For all treatments a strong correlation between the biological behavior of the tumor, histopathology and cell proliferation could be established.
  • In contrast, treatment with Taxol showed no significant reduction of tumor growth or cell proliferation in this model.
  • This new transgenic organ model comprising histopathological evaluation and cell proliferation analysis appears to be a suitable test system for drug candidates that affect specific biochemical pathways.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Enzyme Inhibitors / therapeutic use. Mammary Glands, Animal / transplantation. Mammary Neoplasms, Experimental / drug therapy. Protein-Tyrosine Kinases / antagonists & inhibitors. Receptor, Epidermal Growth Factor / antagonists & inhibitors
  • [MeSH-minor] Administration, Oral. Animals. Cell Line, Transformed. Cell Line, Tumor. Disease Models, Animal. Dose-Response Relationship, Drug. Drug Screening Assays, Antitumor / methods. Female. Image Cytometry. Injections, Intravenous. Ki-67 Antigen / metabolism. Mice. Mice, Inbred BALB C. Neoplasm Transplantation. Paclitaxel / administration & dosage. Paclitaxel / therapeutic use. Treatment Outcome

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  • (PMID = 14703768.001).
  • [ISSN] 0940-2993
  • [Journal-full-title] Experimental and toxicologic pathology : official journal of the Gesellschaft für Toxikologische Pathologie
  • [ISO-abbreviation] Exp. Toxicol. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Enzyme Inhibitors; 0 / Ki-67 Antigen; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; P88XT4IS4D / Paclitaxel
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9. Chiou SH, Kao CL, Lin HT, Tseng WS, Liu RS, Chung CF, Ku HH, Lin CP, Wong TT: Monitoring the growth effect of xenotransplanted human medulloblastoma in an immunocompromised mouse model using in vitro and ex vivo green fluorescent protein imaging. Childs Nerv Syst; 2006 May;22(5):475-80
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Monitoring the growth effect of xenotransplanted human medulloblastoma in an immunocompromised mouse model using in vitro and ex vivo green fluorescent protein imaging.
  • CASE REPORT: In this study, we established xenotransplanted human MB (hMB) cells - isochromosome 17q - in a severe combined immunodeficiency (SCID) mouse model.
  • RESULTS: The result of an ex vivo GFP imaging system showed that a small lesion of the third-week-hMB-transplanted graft presented "green" signals with a clear tumor margin before any tumor-related symptoms were noted.
  • Because MB is sensitive to radiation and also response to chemotherapy, this SCID mouse model will be helpful for preclinical studies in the future.
  • [MeSH-minor] Animals. Cell Proliferation. Diagnostic Imaging. Disease Models, Animal. Glial Fibrillary Acidic Protein / metabolism. Humans. In Vitro Techniques. Mice. Mice, SCID. Neoplasm Transplantation / methods. Time Factors

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  • (PMID = 16541296.001).
  • [ISSN] 0256-7040
  • [Journal-full-title] Child's nervous system : ChNS : official journal of the International Society for Pediatric Neurosurgery
  • [ISO-abbreviation] Childs Nerv Syst
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Glial Fibrillary Acidic Protein; 147336-22-9 / Green Fluorescent Proteins
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10. Azzoli CG, Krug LM, Miller VA, Kris MG, Mass R: Trastuzumab in the treatment of non-small cell lung cancer. Semin Oncol; 2002 Feb;29(1 Suppl 4):59-65
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Trastuzumab in the treatment of non-small cell lung cancer.
  • Trastuzumab is a humanized monoclonal antibody that binds to human epidermal growth factor-2 (HER2) and is approved by the US Food and Drug Administration for the treatment of advanced breast cancer that overexpresses HER2/neu protein.
  • Preclinical data suggests a role for trastuzumab in the treatment of non-small cell lung cancer (NSCLC).
  • Experiments with NSCLC cell lines show that HER2 overexpression increases chemoresistance, invasiveness, and metastatic potential of the cells.
  • In mouse xenograft experiments, trastuzumab halts tumor growth and is synergistic with cytotoxic chemotherapy.
  • Ongoing phase II trials are showing that trastuzumab can be added to standard chemotherapy in the treatment of patients with advanced NSCLC without additional toxicity, and with promising efficacy.
  • Whether trastuzumab will show a clear benefit for patients with NSCLC, either alone or in combination with established chemotherapy, remains to be proven in phase III testing.
  • [MeSH-major] Antibodies, Monoclonal / pharmacology. Antineoplastic Agents / pharmacology. Carcinoma, Non-Small-Cell Lung / drug therapy. Lung Neoplasms / drug therapy. Receptor, ErbB-2 / biosynthesis
  • [MeSH-minor] Antibodies, Monoclonal, Humanized. Clinical Trials as Topic. Drug Resistance, Neoplasm. Humans. Neoplasm Invasiveness. Neoplasm Metastasis. Prognosis. Trastuzumab. Up-Regulation


11. Nagarkatti N: Tumor-derived Fas ligand induces toxicity in lymphoid organs and plays an important role in successful chemotherapy. Cancer Immunol Immunother; 2000 Apr;49(1):46-55
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Tumor-derived Fas ligand induces toxicity in lymphoid organs and plays an important role in successful chemotherapy.
  • However, the effect of growth of FasL+ tumors in vivo, on lymphoid tissues of the host is not clear and therefore was the subject of this investigation.
  • The LSA (FasL+) but not P815(FasL-) tumor cell lysates and culture supernatants induced marked apoptosis in Fas+ thymocytes, when tested both in vitro and in vivo.
  • Chemotherapy of LSA-tumor-bearing C57BL/ 6+/+ mice at advanced stages of tumor growth failed to cure the mice, whereas, more than 80% of LSA-tumor-bearing C57BL/6-lpr/lpr mice, similarly treated, survived.
  • Also, Fas/FasL interactions may play an important role in the successful chemotherapy of FasL-bearing tumor.
  • [MeSH-major] Antigens, Neoplasm / immunology. Apoptosis / immunology. Cytotoxicity, Immunologic. Membrane Glycoproteins / immunology. Neoplasms, Experimental / immunology. Tumor Escape
  • [MeSH-minor] Animals. Fas Ligand Protein. Female. Immunotherapy. Lymphoid Tissue / immunology. Lymphoid Tissue / pathology. Mice. Mice, Inbred C57BL

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  • (PMID = 10782865.001).
  • [ISSN] 0340-7004
  • [Journal-full-title] Cancer immunology, immunotherapy : CII
  • [ISO-abbreviation] Cancer Immunol. Immunother.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] GERMANY
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Fas Ligand Protein; 0 / Fasl protein, mouse; 0 / Membrane Glycoproteins
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12. Cardarelli PM, Quinn M, Buckman D, Fang Y, Colcher D, King DJ, Bebbington C, Yarranton G: Binding to CD20 by anti-B1 antibody or F(ab')(2) is sufficient for induction of apoptosis in B-cell lines. Cancer Immunol Immunother; 2002 Mar;51(1):15-24
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Binding to CD20 by anti-B1 antibody or F(ab')(2) is sufficient for induction of apoptosis in B-cell lines.
  • CD20 is a B-cell-specific cell surface protein expressed on mature B lymphocytes and is a target for monoclonal antibody therapy for non-Hodgkin's lymphoma (NHL).
  • Though clear clinical efficacy has been demonstrated with several anti-CD20 antibodies, the mechanisms by which the antibodies activate CD20 and kill cells remain unclear.
  • Proposed mechanisms of action include complement-dependent cytotoxicity (CDC), antibody-dependent cell-mediated cytotoxicity (ADCC), and induction of apoptosis.
  • In this report we compared the activity of two anti-CD20 antibodies, Anti-B1 Antibody (tositumomab) and rituximab (C2B8), in a variety of cellular assays using a panel of B-cell lines.
  • Anti-B1 Antibody showed a low level of activity in a CDC assay against complement-sensitive B-cell lines, Ramos and Daudi.
  • In addition, Anti-B1 Antibody showed direct induction of apoptosis in all B-cell lines tested.
  • In general, crosslinking Anti-B1 Antibody with a goat anti-mouse Ig did not further enhance the percentage of cells undergoing apoptosis.
  • In contrast, rituximab, which binds to an overlapping epitope on CD20 with a three-fold lower affinity than Anti-B1 Antibody, did not efficiently induce apoptosis in the cell lines tested in the absence of crosslinking.
  • In conclusion, these two anti-CD20 antibodies have overlapping, but distinct mechanisms of action on B-cell lines.
  • [MeSH-major] Antibodies, Monoclonal / pharmacology. Antigens, CD20 / physiology. Apoptosis / drug effects. B-Lymphocytes / drug effects. Immunoglobulin Fab Fragments / pharmacology
  • [MeSH-minor] Animals. Annexin A5 / analysis. Antibodies, Monoclonal, Murine-Derived. Antibody Specificity. Antibody-Dependent Cell Cytotoxicity / drug effects. Antigens, CD55 / analysis. Antigens, CD59 / analysis. Antigens, Neoplasm / analysis. Burkitt Lymphoma / immunology. Burkitt Lymphoma / pathology. Complement System Proteins / immunology. Cytotoxicity, Immunologic / drug effects. Dimerization. Goats. Humans. Immunoglobulin Fc Fragments / immunology. Immunoglobulin G / immunology. Immunoglobulin G / pharmacology. Lymphoma, B-Cell / immunology. Lymphoma, B-Cell / pathology. Mice. Neoplasm Proteins / analysis. Rituximab. Tumor Cells, Cultured / drug effects. Tumor Cells, Cultured / immunology

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  • (PMID = 11845256.001).
  • [ISSN] 0340-7004
  • [Journal-full-title] Cancer immunology, immunotherapy : CII
  • [ISO-abbreviation] Cancer Immunol. Immunother.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Annexin A5; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / Antigens, CD20; 0 / Antigens, CD55; 0 / Antigens, CD59; 0 / Antigens, Neoplasm; 0 / Immunoglobulin Fab Fragments; 0 / Immunoglobulin Fc Fragments; 0 / Immunoglobulin G; 0 / Neoplasm Proteins; 0 / iodine-131 anti-B1 antibody; 4F4X42SYQ6 / Rituximab; 9007-36-7 / Complement System Proteins
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13. Yuki K, Takahashi A, Ota I, Ohnishi K, Yasumoto J, Kanata H, Yane K, Hosoi H, Ohnishi T: Glycerol enhances CDDP-induced growth inhibition of thyroid anaplastic carcinoma tumor carrying mutated p53 gene. Oncol Rep; 2004 Apr;11(4):821-4
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  • To increase the chemo-sensitivity of anaplastic thyroid carcinoma, we examined the effects of glycerol on the tumor growth after CDDP treatment.
  • The cultured cells of an anaplastic thyroid carcinoma cell line (8305c) carrying a mutated p53 gene (mp53) were transplanted into the thighs of nude mice.
  • When we treated the mice with the combination of glycerol and CDDP at these concentrations, however, a clear delay of the tumor growth was observed.
  • Therefore, glycerol might be useful for chemotherapy in patients with mp53 cancer cells.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Carcinoma / drug therapy. Cisplatin / therapeutic use. Genes, p53. Glycerol / therapeutic use. Thyroid Neoplasms / drug therapy
  • [MeSH-minor] Animals. Apoptosis / drug effects. Caspase 3. Caspases / metabolism. Cell Culture Techniques. Drug Synergism. Humans. Immunohistochemistry. Male. Mice. Mice, Inbred BALB C. Models, Animal. Neoplasm Transplantation. Point Mutation / genetics

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  • (PMID = 15010879.001).
  • [ISSN] 1021-335X
  • [Journal-full-title] Oncology reports
  • [ISO-abbreviation] Oncol. Rep.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] EC 3.4.22.- / CASP3 protein, human; EC 3.4.22.- / Casp3 protein, mouse; EC 3.4.22.- / Caspase 3; EC 3.4.22.- / Caspases; PDC6A3C0OX / Glycerol; Q20Q21Q62J / Cisplatin
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14. Sellar GC, Watt KP, Li L, Nelkin BD, Rabiasz GJ, Porteous DJ, Smyth JF, Gabra H: The homeobox gene BARX2 can modulate cisplatin sensitivity in human epithelial ovarian cancer. Int J Oncol; 2002 Nov;21(5):929-33
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  • Resistance to platinum chemotherapy is a major reason for treatment failure and poor prognosis.
  • BARX2 is a transcription factor known to regulate transcription of specific cell adhesion molecules in the mouse.
  • We have previously shown that BARX2 expression is low in clear cell/endometrioid and high in serous adenocarcinomas of the ovary, histologic variants that are less and more sensitive, respectively to platinum chemotherapy.
  • In two cell line series sequentially derived from ovarian cancer patients pre- and post-cisplatin chemotherapy, BARX2 expression was downregulated in the cell lines established upon tumor recurrence after platinum therapy.
  • Transfection of BARX2 into a platinum resistant cell line significantly reversed cisplatin resistance compared with its isogenic platinum sensitive parent, in both growth inhibition and clonogenic assays.
  • [MeSH-major] Cisplatin / pharmacology. Genes, Homeobox / physiology. Homeodomain Proteins / genetics. Neoplasms, Glandular and Epithelial / drug therapy. Ovarian Neoplasms / drug therapy
  • [MeSH-minor] Blotting, Northern. Drug Resistance, Neoplasm. Female. Humans. Transfection. Tumor Cells, Cultured


15. Kubo H, Matsumoto K, Funahashi M, Takagi H, Kitajima Y, Taniguchi S, Saida T: Sequential chemoimmunotherapy with cisplatin, interferon-beta and interleukin-2 inhibits the growth of B16-F1 melanoma in syngeneic mice. Melanoma Res; 2000 Jun;10(3):223-9
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  • Sequential combinations of chemotherapy with biological response modifiers has recently been evaluated as systemic treatment for patients with advanced melanoma.
  • The response rates of the chemoimmunotherapy were reported to be higher than conventional treatment using chemotherapy or biological agents alone.
  • To investigate the effectiveness of such chemoimmunotherapy, we evaluated the antitumour effect of sequential chemoimmunotherapy in vivo using a B16 mouse melanoma system.
  • This combination therapy synergistically inhibited the growth of B16-F1 melanoma and prolonged the survival of mice bearing B16-F1.
  • In contrast, this therapy did not show any antitumour effect on B16-F10 melanoma.
  • The exact mechanism of the antitumour effect is not clear, but the following results were noted: no synergistic effect of this therapy was detected in nude mice, neutralizing anti-IFNgamma antibody significantly blocked the antitumour effect of this therapy, and the number of apoptotic melanoma cells was significantly increased in melanoma tissues removed from mice treated with this therapy.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Immunotherapy. Interleukin-2 / therapeutic use. Melanoma, Experimental / therapy. Skin Neoplasms / therapy
  • [MeSH-minor] Animals. Cell Division / drug effects. Cell Survival / drug effects. Cell Survival / immunology. Cisplatin / administration & dosage. Female. Interferon-beta / administration & dosage. Mice. Mice, Inbred BALB C. Mice, Inbred C57BL. Mice, Nude. Neoplasm Metastasis. Survival Rate. Tumor Cells, Cultured

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  • (PMID = 10890375.001).
  • [ISSN] 0960-8931
  • [Journal-full-title] Melanoma research
  • [ISO-abbreviation] Melanoma Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] ENGLAND
  • [Chemical-registry-number] 0 / Interleukin-2; 77238-31-4 / Interferon-beta; Q20Q21Q62J / Cisplatin
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16. Büchler P, Gukovskaya AS, Mouria M, Büchler MC, Büchler MW, Friess H, Pandol SJ, Reber HA, Hines OJ: Prevention of metastatic pancreatic cancer growth in vivo by induction of apoptosis with genistein, a naturally occurring isoflavonoid. Pancreas; 2003 Apr;26(3):264-73
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  • INTRODUCTION: The critical need for novel therapeutic approaches to pancreatic cancer treatment is clear.
  • METHODOLOGY: The effect of intraperitoneal genistein administration on local tumor growth and metastatic disease was determined in an orthotopic nude mouse model.
  • In vitro, the effect of genistein on cell growth was assessed by cell count and MTT (3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyl tetrazolium bromide) colorimetric assay.
  • Caspase-3 and nuclear factor-kappaB activity were measured following genistein treatment.
  • In vitro genistein treatment resulted in apoptosis in all pancreatic cancer cell lines tested, and this appeared to be mediated by activation of caspase-3.
  • CONCLUSION: These findings suggest that the antimetastatic effect of genistein treatment in vivo is mediated by induction of apoptosis.
  • Genistein may have a therapeutic benefit for patients with pancreatic cancer, in particular after surgery, to prevent recurrence of metastatic disease.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Apoptosis. Genistein / therapeutic use. Pancreatic Neoplasms / drug therapy
  • [MeSH-minor] Animals. Carcinoma / drug therapy. Carcinoma / metabolism. Carcinoma / pathology. Caspase 3. Caspases / metabolism. Cell Division / drug effects. Cell Line, Tumor. Humans. Male. Mice. Mice, Inbred BALB C. Mice, Nude. NF-kappa B / metabolism. Neoplasm Metastasis

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  • (PMID = 12657953.001).
  • [ISSN] 1536-4828
  • [Journal-full-title] Pancreas
  • [ISO-abbreviation] Pancreas
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / NF-kappa B; DH2M523P0H / Genistein; EC 3.4.22.- / CASP3 protein, human; EC 3.4.22.- / Casp3 protein, mouse; EC 3.4.22.- / Caspase 3; EC 3.4.22.- / Caspases
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17. Jiang T, Chen N, Zhao F, Wang XJ, Kong B, Zheng W, Zhang DD: High levels of Nrf2 determine chemoresistance in type II endometrial cancer. Cancer Res; 2010 Jul 1;70(13):5486-96
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  • [Title] High levels of Nrf2 determine chemoresistance in type II endometrial cancer.
  • Type II endometrial cancer, which mainly presents as serous and clear cell types, has proved to be the most malignant and recurrent carcinoma among various female genital malignancies.
  • Nrf2 is constitutively upregulated in several types of human cancer tissues and cancer cell lines.
  • Furthermore, inhibition of Nrf2 expression sensitizes cancer cells to chemotherapeutic drugs.
  • In this study, the constitutive level of Nrf2 was compared in different types of human endometrial tumors.
  • Likewise, the ESC-derived SPEC-2 cell line had a higher level of Nrf2 expression and was more resistant to the toxic effects of cisplatin and paclitaxel than the Ishikawa cell line, which was generated from EEC.
  • Silencing of Nrf2 rendered SPEC-2 cells more susceptible to chemotherapeutic drugs, whereas it had a limited effect on Ishikawa cells.
  • Inhibition of Nrf2 expression by overexpressing Keap1 sensitized SPEC-2 cells or SPEC-2-derived xenografts to chemotherapeutic treatments using both cell culture and severe combined immunodeficient mouse models.
  • Collectively, we provide a molecular basis for the use of Nrf2 inhibitors to increase the efficacy of chemotherapeutic drugs and to combat chemoresistance, the biggest obstacle in chemotherapy.

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  • [Copyright] Copyright 2010 AACR.
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  • (PMID = 20530669.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P30 CA23074; United States / NCI NIH HHS / CA / P30 CA023074; United States / NIEHS NIH HHS / ES / ES015010-04; United States / NIEHS NIH HHS / ES / R01 ES015010-04; United States / NIEHS NIH HHS / ES / ES015010; United States / NIEHS NIH HHS / ES / R01 ES015010
  • [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 / Intracellular Signaling Peptides and Proteins; 0 / KEAP1 protein, human; 0 / NF-E2-Related Factor 2; 0 / NFE2L2 protein, human; 0 / RNA, Messenger; 0 / RNA, Small Interfering; P88XT4IS4D / Paclitaxel; Q20Q21Q62J / Cisplatin
  • [Other-IDs] NLM/ NIHMS203767; NLM/ PMC2896449
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18. Moyle PM, Olive C, Ho MF, Pandey M, Dyer J, Suhrbier A, Fujita Y, Toth I: Toward the development of prophylactic and therapeutic human papillomavirus type-16 lipopeptide vaccines. J Med Chem; 2007 Sep 20;50(19):4721-7
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  • [Title] Toward the development of prophylactic and therapeutic human papillomavirus type-16 lipopeptide vaccines.
  • Four lipid-core peptide systems were synthesized using stepwise solid-phase peptide synthesis, incorporating a sequence from the human papillomavirus type-16 (HPV-16) E7 protein (E744-62), for the purpose of developing vaccines against HPV-16 associated cervical cancer. d-Mannose was conjugated to the vaccine in order to investigate whether the targeting of dendritic cell mannose receptors would improve vaccine efficacy.
  • The ability of the vaccines to clear or reduce the size of HPV-16 associated tumors was assessed in C57BL/6 (H-2b) mice using the TC-1 HPV-16 tumor model.
  • Overall, significant reductions in the size of TC-1 tumors were observed in the mouse model, with the conjugation of mannose to these vaccines demonstrated to clear or reduce the size of TC-1 tumors to a greater extent than non-mannose-containing vaccines (37 out of 40 versus 21 out of 30 tumors cleared, respectively).
  • [MeSH-minor] Animals. Dendritic Cells / metabolism. Epitopes. Female. Glucose / chemistry. Lectins, C-Type / metabolism. Mannose / chemistry. Mannose-Binding Lectins / metabolism. Mice. Mice, Inbred C57BL. Neoplasm Transplantation. Oncogene Proteins, Viral / chemistry. Papillomavirus E7 Proteins. Papillomavirus Infections / drug therapy. Papillomavirus Infections / immunology. Papillomavirus Infections / prevention & control. Peptide Fragments / chemistry. Receptors, Cell Surface / metabolism. Transplantation, Heterologous. Uterine Cervical Neoplasms / drug therapy. Uterine Cervical Neoplasms / immunology. Uterine Cervical Neoplasms / prevention & control. Vaccines, Synthetic / immunology. Vaccines, Synthetic / therapeutic use

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  • (PMID = 17705361.001).
  • [ISSN] 0022-2623
  • [Journal-full-title] Journal of medicinal chemistry
  • [ISO-abbreviation] J. Med. Chem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cancer Vaccines; 0 / Epitopes; 0 / Lectins, C-Type; 0 / Lipoproteins; 0 / Mannose-Binding Lectins; 0 / Oncogene Proteins, Viral; 0 / Papillomavirus E7 Proteins; 0 / Papillomavirus Vaccines; 0 / Peptide Fragments; 0 / Peptides; 0 / Receptors, Cell Surface; 0 / Vaccines, Synthetic; 0 / mannose receptor; 0 / oncogene protein E7, Human papillomavirus type 16; IY9XDZ35W2 / Glucose; PHA4727WTP / Mannose
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19. Raguénez G, Mühlethaler-Mottet A, Meier R, Duros C, Bénard J, Gross N: Fenretinide-induced caspase-8 activation and apoptosis in an established model of metastatic neuroblastoma. BMC Cancer; 2009;9:97
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  • BACKGROUND: Resistance of high-risk metastatic neuroblastoma (HR-NB) to high dose chemotherapy (HD-CT) raises a major therapeutic challenge in pediatric oncology.
  • For some patients, an adjuvant retinoid therapy is proposed, such as the synthetic retinoid fenretinide (4-HPR), an apoptotic inducer.
  • METHODS: We used the human IGR-N-91 MYCN-amplified NB experimental model, able to disseminate in vivo from the primary nude mouse tumor xenograft (PTX) into myocardium (Myoc) and bone marrow (BM) of the animal.
  • NB cell lines, i.e., IGR-N-91 and SH-EP, were treated with various doses of Fenretinide (4-HPR), then cytotoxicity was analyzed by MTS proliferation assay, apoptosis by the propidium staining method, gene or protein expressions by RT-PCR and immunoblotting and caspases activity by colorimetric protease assays.
  • However the PTX cells established from the primary tumor in the mouse, are caspase-8 positive.
  • In contrast, metastatic BM and Myoc cells show a clear down-regulation of the caspase-8 expression.
  • Our data show that in BM, compared to PTX cells, 4-HPR up-regulates caspase-8 expression that parallels a higher sensitivity to apoptotic cell death.
  • Stable caspase-8-silenced SH-EP cells appear more resistant to 4-HPR-induced cell death compared to control SH-EP cells.
  • Moreover, 4-HPR synergizes with drugs since apoptosis is restored in VP16- or TRAIL-resistant-BM cells.
  • These results demonstrate that 4-HPR in up-regulating caspase-8 expression, restores and induces apoptotic cell death in metastatic neuroblasts through caspase-8 activation.
  • CONCLUSION: This study provides basic clues for using fenretinide in clinical treatment of HR-NB patients.
  • Moreover, since 4-HPR induces cell death in caspase-8 negative NB, it also challenges the concept of including 4-HPR in the induction of CT of these patients.
  • [MeSH-major] Apoptosis / drug effects. Caspase 8 / metabolism. Fenretinide / pharmacology. Neuroblastoma / drug therapy. Xenograft Model Antitumor Assays / methods
  • [MeSH-minor] Animals. Antineoplastic Agents / pharmacology. Blotting, Western. Bone Marrow / drug effects. Bone Marrow / metabolism. Bone Marrow / pathology. Caspase Inhibitors. Cell Line, Tumor. Cell Survival / drug effects. Cysteine Proteinase Inhibitors / pharmacology. Drug Resistance, Neoplasm. Enzyme Activation / drug effects. Etoposide / pharmacology. Gene Expression Regulation, Enzymologic / drug effects. Gene Expression Regulation, Neoplastic / drug effects. Humans. Mice. Mice, Nude. Neoplasm Metastasis. Reverse Transcriptase Polymerase Chain Reaction. TNF-Related Apoptosis-Inducing Ligand / pharmacology

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  • (PMID = 19331667.001).
  • [ISSN] 1471-2407
  • [Journal-full-title] BMC cancer
  • [ISO-abbreviation] BMC Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Caspase Inhibitors; 0 / Cysteine Proteinase Inhibitors; 0 / TNF-Related Apoptosis-Inducing Ligand; 187EJ7QEXL / Fenretinide; 6PLQ3CP4P3 / Etoposide; EC 3.4.22.- / Caspase 8
  • [Other-IDs] NLM/ PMC2670318
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20. Bu X, Khankaldyyan V, Gonzales-Gomez I, Groshen S, Ye W, Zhuo S, Pons J, Stratton JR, Rosenberg S, Laug WE: Species-specific urokinase receptor ligands reduce glioma growth and increase survival primarily by an antiangiogenesis mechanism. Lab Invest; 2004 Jun;84(6):667-78
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  • The ligands blocked endothelial cell tube formation in Matrigel in a species-specific manner and reduced both baseline and uPA amino-terminal fragment-stimulated cell migration on vitronectin gradients.
  • Treatment of U87MG gliomas implanted orthotopically in mice with single species-specific or combination uPAR ligands resulted in significant decreases in tumor size, which translated to increases in survival time, and which were most significant when the murine-specific ligand was included.
  • Further analysis of tumors showed that the reduced sizes were correlated with a decrease in tumor cell proliferation and mean vessel density and an increase in tumor cell apoptosis.
  • Statistical analysis showed that the combination therapy demonstrated a clear synergy as compared to the individual agent treatments.
  • [MeSH-major] Brain Neoplasms / drug therapy. Glioma / drug therapy. Receptors, Cell Surface / metabolism
  • [MeSH-minor] Animals. Cell Line, Tumor. Cells, Cultured. Endothelium, Vascular / cytology. Endothelium, Vascular / drug effects. Humans. Ligands. Mice. Mice, Nude. Neoplasm Transplantation. Neovascularization, Pathologic. Peptide Fragments / chemistry. Peptide Fragments / genetics. Peptide Fragments / pharmacology. Polyethylene Glycols / pharmacology. Receptors, Urokinase Plasminogen Activator. Species Specificity. Transplantation, Heterologous. Urokinase-Type Plasminogen Activator / chemistry. Urokinase-Type Plasminogen Activator / genetics. Urokinase-Type Plasminogen Activator / pharmacology

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  • (PMID = 15094713.001).
  • [ISSN] 0023-6837
  • [Journal-full-title] Laboratory investigation; a journal of technical methods and pathology
  • [ISO-abbreviation] Lab. Invest.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA 82989
  • [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 / Ligands; 0 / PLAUR protein, human; 0 / Peptide Fragments; 0 / Plaur protein, mouse; 0 / Receptors, Cell Surface; 0 / Receptors, Urokinase Plasminogen Activator; 30IQX730WE / Polyethylene Glycols; EC 3.4.21.73 / Urokinase-Type Plasminogen Activator
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21. Lin SH, Nishino M, Luo W, Aumais JP, Galfione M, Kuang J, Yu-Lee LY: Inhibition of prostate tumor growth by overexpression of NudC, a microtubule motor-associated protein. Oncogene; 2004 Apr 1;23(14):2499-506
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  • Anticancer drugs that target microtubule dynamics have been shown to be effective in cancer treatment.
  • However, the effect of microtubule motor-associated molecules on cancer cell proliferation is not clear.
  • At the cellular level, expression of NudC in DU145 and PC-3 cells inhibited cell proliferation at 48 h after Ad-NudC infection.
  • FACS analysis of cell cycle distribution showed that 50-60% of Ad-NudC-infected PC-3 cells have a G2/M-phase DNA content compared to about 16-19% in Ad-Luciferase (Ad-Luc)-infected control cells, suggesting that NudC overexpression resulted in aberrant cell cycle progression.
  • Immunofluorescence microscopy revealed a significant increase in cells with a single enlarged nucleus and cells exhibiting multiple nuclei, along with a concomitant increase in cell size in Ad-NudC-infected cells.
  • These results suggest that NudC overexpression led to a block in cell division of prostate cancer cells, and that Ad-NudC may provide a new anticancer drug approach targeting the function of a microtubule motor-associated protein.
  • [MeSH-major] Microtubule-Associated Proteins / metabolism. Prostatic Neoplasms / etiology. Prostatic Neoplasms / therapy. Proteins / metabolism. Proteins / therapeutic use
  • [MeSH-minor] Adenoviridae / genetics. Animals. Cell Adhesion. Cell Cycle Proteins. Cell Division. Cell Line, Tumor. Cell Size. DNA / analysis. Dyneins / metabolism. G2 Phase. Gene Expression. Gene Transfer Techniques. Humans. Male. Mice. Mice, Nude. Models, Biological. Neoplasm Transplantation. Nuclear Proteins. Recombinant Proteins / metabolism. Transplantation, Heterologous

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  • (PMID = 14676831.001).
  • [ISSN] 0950-9232
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA86342; United States / NIDDK NIH HHS / DK / R01 DK53176
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cell Cycle Proteins; 0 / Microtubule-Associated Proteins; 0 / NUDC protein, human; 0 / Nuclear Proteins; 0 / Nudc protein, mouse; 0 / Proteins; 0 / Recombinant Proteins; 9007-49-2 / DNA; EC 3.6.4.2 / Dyneins
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22. Hofer T, Desbaillets I, Höpfl G, Gassmann M, Wenger RH: Dissecting hypoxia-dependent and hypoxia-independent steps in the HIF-1alpha activation cascade: implications for HIF-1alpha gene therapy. FASEB J; 2001 Dec;15(14):2715-7
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  • [Title] Dissecting hypoxia-dependent and hypoxia-independent steps in the HIF-1alpha activation cascade: implications for HIF-1alpha gene therapy.
  • The heterodimeric hypoxia-inducible factor (HIF)-1 is a master transcriptional regulator of oxygen homeostasis and a possible target for gene therapy of ischemic disease.
  • Although the role of oxygen concentration in HIF-1a protein stabilization is well established, it is less clear whether and how oxygen-regulated mechanisms contribute to HIF-1a protein modifications, nuclear translocation, heterodimerization with the b-subunit, recruitment of cofactors, and gene trans-activation.
  • Because the HIF-1a protein is proteolytically degraded under normoxic conditions, we established two HeLa Tet-Off cell lines (HT42 and HT43), which inducibly overexpress high levels of HIF-1a under normoxic conditions, allowing to distinguish hypoxia-dependent from hypoxia-independent activation mechanisms.
  • [MeSH-major] Cell Hypoxia / physiology. Transcription Factors / genetics
  • [MeSH-minor] Animals. Biological Transport. Cell Nucleus / metabolism. Endothelial Growth Factors / genetics. Endothelial Growth Factors / metabolism. Enzyme Inhibitors / pharmacology. Flavonoids / pharmacology. Gene Expression. Gene Expression Regulation. Genetic Therapy / methods. Glucose Transporter Type 1. HeLa Cells. Humans. Hypoxia-Inducible Factor 1, alpha Subunit. Lymphokines / genetics. Lymphokines / metabolism. MAP Kinase Kinase 1. Mice. Mice, Nude. Mitogen-Activated Protein Kinase Kinases / antagonists & inhibitors. Monosaccharide Transport Proteins / genetics. Monosaccharide Transport Proteins / metabolism. Neoplasm Transplantation. Protein-Serine-Threonine Kinases / antagonists & inhibitors. RNA, Messenger / genetics. RNA, Messenger / metabolism. Transcriptional Activation / drug effects. Transplantation, Heterologous. Tumor Suppressor Protein p53 / genetics. Tumor Suppressor Protein p53 / metabolism. Vascular Endothelial Growth Factor A. Vascular Endothelial Growth Factors

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  • (PMID = 11606485.001).
  • [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
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one; 0 / Endothelial Growth Factors; 0 / Enzyme Inhibitors; 0 / Flavonoids; 0 / Glucose Transporter Type 1; 0 / HIF1A protein, human; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / Lymphokines; 0 / Monosaccharide Transport Proteins; 0 / RNA, Messenger; 0 / SLC2A1 protein, human; 0 / Transcription Factors; 0 / Tumor Suppressor Protein p53; 0 / Vascular Endothelial Growth Factor A; 0 / Vascular Endothelial Growth Factors; EC 2.7.1.- / MAP2K1 protein, human; EC 2.7.1.- / Map2k1 protein, mouse; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.12.2 / MAP Kinase Kinase 1; EC 2.7.12.2 / Mitogen-Activated Protein Kinase Kinases
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23. Guo K, Li J, Tang JP, Koh V, Gan BQ, Zeng Q: Catalytic domain of PRL-3 plays an essential role in tumor metastasis: formation of PRL-3 tumors inside the blood vessels. Cancer Biol Ther; 2004 Oct;3(10):945-51
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  • Our studies provide clear evidence for a causative role of PRL-3 phosphatase activity in cancer metastasis and tumor-related angiogenesis events.
  • The catalytic domain of PRL-3 could serve as an ideal therapeutic target for drug development to block the spread of colorectal cancer.
  • [MeSH-minor] Animals. CHO Cells. Catalytic Domain. Cricetinae. Female. Green Fluorescent Proteins / metabolism. Mice. Mice, Nude. Neoplasm Invasiveness / pathology. Transplantation, Heterologous

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  • [CommentIn] Cancer Biol Ther. 2004 Oct;3(10):952-3 [15467431.001]
  • (PMID = 15326366.001).
  • [ISSN] 1538-4047
  • [Journal-full-title] Cancer biology & therapy
  • [ISO-abbreviation] Cancer Biol. Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Immediate-Early Proteins; 0 / Ptp4a3 protein, mouse; 0 / enhanced green fluorescent protein; 147336-22-9 / Green Fluorescent Proteins; EC 3.1.3.48 / Protein Tyrosine Phosphatases
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24. Rojo J, Díaz V, de la Fuente JM, Segura I, Barrientos AG, Riese HH, Bernad A, Penadés S: Gold glyconanoparticles as new tools in antiadhesive therapy. Chembiochem; 2004 Mar 5;5(3):291-7
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  • [Title] Gold glyconanoparticles as new tools in antiadhesive therapy.
  • Gold glyconanoparticles (GNPs) have been prepared as new multivalent tools that mimic glycosphingolipids on the cell surface.
  • A mouse melanoma model was selected to test glyconanoparticles as possible inhibitors of experimental lung metastasis.
  • This result shows for the first time a clear biological effect of lacto-GNPs, demonstrating the potential application of this glyconanotechnology in biological processes.
  • [MeSH-major] Gold / therapeutic use. Lactose / therapeutic use. Nanotechnology / methods. Neoplasm Metastasis / drug therapy
  • [MeSH-minor] Animals. Cell Adhesion / drug effects. Cell Line, Tumor. Glycosphingolipids. Lung Neoplasms / prevention & control. Lung Neoplasms / secondary. Melanoma, Experimental / drug therapy. Melanoma, Experimental / pathology. Mice. Molecular Mimicry. Neoplasm Invasiveness / prevention & control. Particle Size. Treatment Outcome

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  • (PMID = 14997521.001).
  • [ISSN] 1439-4227
  • [Journal-full-title] Chembiochem : a European journal of chemical biology
  • [ISO-abbreviation] Chembiochem
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Glycosphingolipids; 7440-57-5 / Gold; J2B2A4N98G / Lactose
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25. Koshikawa N, Mizushima H, Minegishi T, Iwamoto R, Mekada E, Seiki M: Membrane type 1-matrix metalloproteinase cleaves off the NH2-terminal portion of heparin-binding epidermal growth factor and converts it into a heparin-independent growth factor. Cancer Res; 2010 Jul 15;70(14):6093-103
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  • [Title] Membrane type 1-matrix metalloproteinase cleaves off the NH2-terminal portion of heparin-binding epidermal growth factor and converts it into a heparin-independent growth factor.
  • Epidermal growth factor (EGF) receptors (ErbB) and EGF family members represent promising targets for cancer therapy.
  • Heparin-binding EGF (HB-EGF) is a member of the EGF family and is an important target for therapy in some types of human cancers.
  • Although heparin potentiates HB-EGF activity in vitro, it is not clear how the heparin-binding activity of HB-EGF is regulated.
  • Here, we show that membrane type 1-matrix metalloproteinase (MT1-MMP; MMP14), a potent invasion-promoting protease, markedly enhances HB-EGF-dependent tumor formation in mice.
  • Consequently, the processing of HB-EGF by MT1-MMP converts HB-EGF into a heparin-independent growth factor with enhanced mitogenic activity, and thereby, expression of both proteins costimulates tumor cell growth in vitro and in vivo.
  • The ErbB family of receptors expressed in human gastric carcinoma cells play a role in mediating enhanced HB-EGF activity by MT1-MMP during invasive cell growth in collagen.
  • Thus, we shed light on a new mechanism whereby HB-EGF activity is regulated that should be considered when designing HB-EGF-targeted cancer therapy.
  • [MeSH-minor] Amino Acid Sequence. Animals. Cell Growth Processes / drug effects. Cell Growth Processes / physiology. Cell Line. Cell Line, Tumor. Dogs. Fibroblasts / cytology. Fibroblasts / drug effects. Gene Knockdown Techniques. Heparin-binding EGF-like Growth Factor. Humans. Mice. Molecular Sequence Data. Neoplasm Invasiveness. RNA, Messenger / biosynthesis. RNA, Messenger / genetics. RNA, Small Interfering / genetics. Rats. Rats, Inbred BUF. Stomach Neoplasms / metabolism. Stomach Neoplasms / pathology. Transfection

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  • [Copyright] (c)2010 AACR.
  • (PMID = 20587521.001).
  • [ISSN] 1538-7445
  • [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 / HBEGF protein, human; 0 / Hbegf protein, mouse; 0 / Hbegf protein, rat; 0 / Heparin-binding EGF-like Growth Factor; 0 / Intercellular Signaling Peptides and Proteins; 0 / RNA, Messenger; 0 / RNA, Small Interfering; EC 3.4.24.80 / Matrix Metalloproteinase 14
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26. Sasaki CY, Lin Hc, Passaniti A: Expression of E-cadherin reduces bcl-2 expression and increases sensitivity to etoposide-induced apoptosis. Int J Cancer; 2000 Jun 1;86(5):660-6
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  • Expression of Bcl-2 is important in determining cancer cell resistance to chemotherapy.
  • However, it is not clear whether cell-cell interactions regulate Bcl-2 expression.
  • To determine whether re-expression of E-cadherin in F cells would restore etoposide sensitivity, F cells were transfected with an expression vector coding for the mouse E-cadherin gene.
  • Cad) showed increased sensitivity to etoposide treatment compared with control clones (F.Neo).
  • Unlike F cells, F.Cad transfectants were not able to express Bcl-2, but transient transfection of bcl-2 resulted in re-expression and resistance to etoposide treatment.
  • Loss of E-cadherin in invasive tumor cells may lead to increased Bcl-2 expression and resistance to chemotherapeutic drugs.
  • [MeSH-minor] Animals. Gene Expression. Mice. Neoplasm Invasiveness / genetics. Rats. Transfection. Tumor Cells, Cultured

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  • (PMID = 10797287.001).
  • [ISSN] 0020-7136
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] UNITED STATES
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 0 / Cadherins; 0 / Proto-Oncogene Proteins c-bcl-2; 6PLQ3CP4P3 / Etoposide
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27. Kalani AD, Jack A, Montenegro G, Degliuomini J, Wallack MK: Immunotherapy as an adjuvant therapy in the management of advanced, surgically resected, melanoma. G Ital Dermatol Venereol; 2008 Feb;143(1):59-70
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  • [Title] Immunotherapy as an adjuvant therapy in the management of advanced, surgically resected, melanoma.
  • It is a heterogeneous solid tumor whose treatment is challenging and difficult.
  • It afflicts thousands of otherwise healthy patients annually, and clinicians have yet to discover an effective treatment for locally advanced disease.
  • Over the years, much attention has been devoted to the development of an effective adjuvant treatment for patients with resected melanoma who remain at high risk for recurrence.
  • The new advances in the understanding of melanoma's microenvironment and the complexity of its disease process, makes it clear that the treatment approach to this disease needs to be multi-directional.
  • Numerous studies have tested various immunotherapeutic strategies in the treatment of advanced melanoma, in particular.
  • These strategies include melanoma vaccines, interferon-alpha, interleukin-2 (IL-2), and dendritic cell vaccines. The Dr.
  • Recently, the same Laboratory has produced a second generation melanoma vaccine (DC-Melvac) that consists of five human melanoma cell lines, a recombinant vaccinia virus that encodes for IL-2, as well as dendritic cells that have been programmed to recognize certain melanoma associated antigens.
  • DC-MelVac was recently approved by the Food and Drug Administration for its use in Phase I clinical trials.
  • The ensuing review discusses many of the immunotherapeutic strategies that have been studied in the treatment of melanoma, including DC-MelVac.
  • [MeSH-major] Immunotherapy. Melanoma / therapy. Skin Neoplasms / therapy
  • [MeSH-minor] Animals. Antibodies, Monoclonal / therapeutic use. Antigens, CD / immunology. CTLA-4 Antigen. Cancer Vaccines / therapeutic use. Clinical Trials as Topic / statistics & numerical data. Combined Modality Therapy. Dendritic Cells / immunology. Dendritic Cells / transplantation. Humans. Immunologic Factors / therapeutic use. Immunotherapy, Active. Immunotherapy, Adoptive. Interferon-alpha / therapeutic use. Interleukin-2 / therapeutic use. Melanoma, Experimental / therapy. Mice. Neoplasm Staging

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  • (PMID = 18833052.001).
  • [ISSN] 0392-0488
  • [Journal-full-title] Giornale italiano di dermatologia e venereologia : organo ufficiale, Società italiana di dermatologia e sifilografia
  • [ISO-abbreviation] G Ital Dermatol Venereol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antigens, CD; 0 / CTLA-4 Antigen; 0 / CTLA4 protein, human; 0 / Cancer Vaccines; 0 / Canvaxin; 0 / Ctla4 protein, mouse; 0 / DC-MelVac; 0 / Immunologic Factors; 0 / Interferon-alpha; 0 / Interleukin-2; 0 / Melacine
  • [Number-of-references] 131
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28. De Milito A, Fais S: Tumor acidity, chemoresistance and proton pump inhibitors. Future Oncol; 2005 Dec;1(6):779-86
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  • Acidity, in particular, has been shown to have a role in resistance to chemotherapy, proliferation and metastatic behavior.
  • In fact, a mechanism of resistance to cytotoxic drugs may be the alteration of the tumor microenvironment through changes of the pH gradient between the extracellular environment and cell cytoplasm.
  • The extracellular pH of solid tumors is significantly more acidic than that of normal tissues, thus impairing the uptake of weakly basic chemotherapeutic drugs and reducing their effect on tumors.
  • It appears clear that a complex framework of protein-protein, protein-lipid and lipid-lipid interactions underlay the pH homeostasis in mammalian cells.
  • Recent data suggest that vacuolar-type (V-type) H(+)-ATPases, that pump protons across the plasma membrane, may have a key role in the acidification of the tumor microenvironment.
  • Some human tumor cells are characterized by an increased V-type H(+)-ATPase expression and activity, and pretreatment with proton pump inhibitors -- a class of H(+)-ATPase inhibitors -- sensitized tumor cell lines to the effect of a variety of anticancer drugs.
  • Proton pump inhibitor pretreatment has been associated with inhibition of V-type H(+)-ATPase activity and increase in both extracellular pH and pH of lysosomal organelles.
  • In vivo experiments in human/mouse xenografts have shown that oral pretreatment with proton pump inhibitors is able to sensitize human solid tumors to anticancer drugs.
  • [MeSH-major] Acid-Base Equilibrium. Antineoplastic Agents / therapeutic use. Drug Resistance, Neoplasm. Proton Pump Inhibitors

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  • (PMID = 16556057.001).
  • [ISSN] 1479-6694
  • [Journal-full-title] Future oncology (London, England)
  • [ISO-abbreviation] Future Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Proton Pump Inhibitors
  • [Number-of-references] 71
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29. Gupta S, Wang Y, Ramos-Garcia R, Shevrin D, Nelson JB, Wang Z: Inhibition of 5alpha-reductase enhances testosterone-induced expression of U19/Eaf2 tumor suppressor during the regrowth of LNCaP xenograft tumor in nude mice. Prostate; 2010 Oct 1;70(14):1575-85
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  • BACKGROUND: Intermittent androgen deprivation therapy (IADT) was developed to improve the quality of life and retard prostate cancer progression to castration resistance.
  • However, it is not clear if the same phenomenon would occur during androgen-induced regrowth of prostate tumors.
  • The expression of five androgen-responsive genes, including the tumor suppressor U19/Eaf2, was determined using real-time RT-PCR, 3 days after randomization.
  • RESULTS: In LNCaP tumors, the expression of U19/Eaf2 was higher in the T+D group as compared with T alone (2.87-fold, P < 0.05).
  • In contrast, dutasteride treatment in testes-intact animals inhibited the expression of U19/Eaf2.

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  • [Copyright] (c) 2010 Wiley-Liss, Inc.
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  • (PMID = 20564326.001).
  • [ISSN] 1097-0045
  • [Journal-full-title] The Prostate
  • [ISO-abbreviation] Prostate
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA090386-03; United States / NIDDK NIH HHS / DK / R37 DK51193; United States / NIDDK NIH HHS / DK / R37 DK051193; United States / NCI NIH HHS / CA / CA90386; United States / NCI NIH HHS / CA / P50 CA090386; United States / NIDDK NIH HHS / DK / R37 DK051193-16; United States / NIDDK NIH HHS / DK / DK051193-16; United States / NCI NIH HHS / CA / P50 CA090386-03
  • [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 / Androgens; 0 / Azasteroids; 0 / Enzyme Inhibitors; 0 / FESTA protein, mouse; 0 / Nuclear Proteins; 0 / Trans-Activators; 0 / Tumor Suppressor Proteins; 08J2K08A3Y / Dihydrotestosterone; 3XMK78S47O / Testosterone; 57GNO57U7G / Finasteride; EC 1.3.1.22 / Cholestenone 5 alpha-Reductase; EC 3.4.21.77 / Prostate-Specific Antigen; O0J6XJN02I / Dutasteride
  • [Other-IDs] NLM/ NIHMS273341; NLM/ PMC3076187
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30. Francis RJ, Sharma SK, Springer C, Green AJ, Hope-Stone LD, Sena L, Martin J, Adamson KL, Robbins A, Gumbrell L, O'Malley D, Tsiompanou E, Shahbakhti H, Webley S, Hochhauser D, Hilson AJ, Blakey D, Begent RH: A phase I trial of antibody directed enzyme prodrug therapy (ADEPT) in patients with advanced colorectal carcinoma or other CEA producing tumours. Br J Cancer; 2002 Sep 9;87(6):600-7
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  • [Title] A phase I trial of antibody directed enzyme prodrug therapy (ADEPT) in patients with advanced colorectal carcinoma or other CEA producing tumours.
  • Antibody-directed enzyme prodrug therapy is a targeted therapy in which a prodrug is activated selectively at the tumour site by an enzyme, which has been targeted to the tumour by an antibody (antibody-enzyme conjugate).
  • Previous clinical trials have shown evidence of tumour response, however, the activated drug had a long half-life, which resulted in dose-limiting myelosuppression.
  • Twenty-seven patients were treated with antibody-directed enzyme prodrug therapy using A5CP antibody-enzyme conjugate and ZD2767P prodrug, in a dose-escalating phase I trial.
  • Human anti-mouse antibody and human anti-carboxypeptidase G2 antibody were produced in response to the antibody enzyme conjugate (A5CP).
  • The antibody-enzyme conjugate localisation data (carboxypeptidase G2 enzyme levels by HPLC on tumour and normal tissue samples, and gamma camera analysis of I-131 radiolabelled conjugate) are consistent with inadequate tumour localisation (median tumour: normal tissue ratios of antibody-enzyme conjugate of less than 1).
  • ZD2767P was shown to clear rapidly from the circulation and activated drug was not measurable in the blood.
  • ZD2767P has potential for use in future antibody-directed enzyme prodrug therapy systems.
  • [MeSH-major] Antibodies, Monoclonal / administration & dosage. Colorectal Neoplasms / therapy. Nitrogen Mustard Compounds / therapeutic use. Prodrugs / therapeutic use. gamma-Glutamyl Hydrolase / administration & dosage. gamma-Glutamyl Hydrolase / metabolism
  • [MeSH-minor] Adult. Aged. Animals. Antibodies, Neoplasm. Antineoplastic Agents / adverse effects. Antineoplastic Agents / pharmacokinetics. Antineoplastic Agents / therapeutic use. Carcinoembryonic Antigen / immunology. Colon / metabolism. Comet Assay. Enzyme-Linked Immunosorbent Assay. Female. Humans. Immunity, Cellular. Male. Maximum Tolerated Dose. Mice. Middle Aged. Quality of Life. Rectum / metabolism. Surveys and Questionnaires

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  • (PMID = 12237768.001).
  • [ISSN] 0007-0920
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] eng
  • [Publication-type] Clinical Trial; Clinical Trial, Phase I; Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Scotland
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Neoplasm; 0 / Antineoplastic Agents; 0 / Carcinoembryonic Antigen; 0 / Nitrogen Mustard Compounds; 0 / Prodrugs; 0 / ZD 2767; EC 3.4.19.9 / gamma-Glutamyl Hydrolase
  • [Other-IDs] NLM/ PMC2364249
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