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1. Finzer P, Kuntzen C, Soto U, zur Hausen H, Rösl F: Inhibitors of histone deacetylase arrest cell cycle and induce apoptosis in cervical carcinoma cells circumventing human papillomavirus oncogene expression. Oncogene; 2001 Aug 9;20(35):4768-76
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  • [Title] Inhibitors of histone deacetylase arrest cell cycle and induce apoptosis in cervical carcinoma cells circumventing human papillomavirus oncogene expression.
  • Histone deacetylase (HDAC) inhibitors sodium butyrate and trichostatin A arrest human papillomavirus (HPV)-positive carcinoma cells in G1 to S transition of the cell cycle, which is paralleled by an up-regulation of the cyclin-dependent kinase inhibitors (CKIs) p21CIP1 and p27KIP1 as well as the complete loss of cdk2 activity.
  • These data provide novel molecular insights into how the transforming potential of HPV can be bypassed and open new therapeutical perspectives for the treatment of cervical cancer.
  • [MeSH-major] Apoptosis / drug effects. CDC2-CDC28 Kinases. Cell Transformation, Neoplastic. DNA-Binding Proteins. Enzyme Inhibitors / pharmacology. Histone Deacetylase Inhibitors. Muscle Proteins. Oncogene Proteins, Viral / physiology. Uterine Cervical Neoplasms / drug therapy
  • [MeSH-minor] Cell Cycle / drug effects. Cyclin-Dependent Kinase 2. Cyclin-Dependent Kinase Inhibitor p21. Cyclin-Dependent Kinases / antagonists & inhibitors. Cyclins / analysis. Cyclins / physiology. Female. HeLa Cells. Humans. Microfilament Proteins / physiology. Protein-Serine-Threonine Kinases / antagonists & inhibitors. Retinoblastoma Protein / metabolism

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  • (PMID = 11521189.001).
  • [ISSN] 0950-9232
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / CDKN1A protein, human; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / Cyclins; 0 / DNA-Binding Proteins; 0 / E7 protein, Human papillomavirus type 18; 0 / Enzyme Inhibitors; 0 / Histone Deacetylase Inhibitors; 0 / Microfilament Proteins; 0 / Muscle Proteins; 0 / Oncogene Proteins, Viral; 0 / Retinoblastoma Protein; 0 / Tagln protein, mouse; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.22 / CDC2-CDC28 Kinases; EC 2.7.11.22 / CDK2 protein, human; EC 2.7.11.22 / Cyclin-Dependent Kinase 2; EC 2.7.11.22 / Cyclin-Dependent Kinases
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2. Liu T, Ding Y, Xie W, Li Z, Bai X, Li X, Fang W, Ren C, Wang S, Hoffman RM, Yao K: An imageable metastatic treatment model of nasopharyngeal carcinoma. Clin Cancer Res; 2007 Jul 1;13(13):3960-7
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  • [Title] An imageable metastatic treatment model of nasopharyngeal carcinoma.
  • PURPOSE: Nasopharyngeal carcinoma is highly prevalent in southern China and is often resistant to current treatment options.
  • EXPERIMENTAL DESIGN: Clinically relevant mouse models are necessary for further understanding and drug discovery in this disease.
  • Two nasopharyngeal carcinoma cell lines, stably expressing green fluorescent protein (GFP), 5-8F-GFP and 6-10B-GFP, were established.
  • Orthotopic implantation of highly metastatic 5-8F cells resulted in brain invasion, cervical lymph node metastases, and pulmonary metastases similar to what is often observed in patients.
  • These results indicated that, in addition to the cancer cell type, the host microenvironment was critical for metastasis to occur consistent with the "seed-and-soil" hypothesis.
  • CONCLUSIONS: The imageable orthotopic model should play a critical role in elucidating the mechanisms involved in the growth, progression, metastasis, and angiogenesis of nasopharyngeal carcinoma and for evaluation of novel compounds with potential efficacy.
  • [MeSH-major] Carcinoma / pathology. Carcinoma / therapy. Disease Models, Animal. Nasopharyngeal Neoplasms / pathology. Nasopharyngeal Neoplasms / therapy
  • [MeSH-minor] Animals. Antineoplastic Agents / therapeutic use. Cell Line, Tumor. Green Fluorescent Proteins / metabolism. Humans. Mice. Mice, Nude. Microscopy, Fluorescence. Models, Anatomic. Neoplasm Metastasis. Neoplasm Transplantation. Neovascularization, Pathologic

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  • (PMID = 17606730.001).
  • [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 / Antineoplastic Agents; 147336-22-9 / Green Fluorescent Proteins
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3. Rajaram S, Gupta G, Agarwal S, Goel N, Singh KC: High-risk human papillomavirus, tumor suppressor protein p53 and mitomycin-C in invasive squamous cell carcinoma cervix. Indian J Cancer; 2006 Oct-Dec;43(4):156-62
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  • [Title] High-risk human papillomavirus, tumor suppressor protein p53 and mitomycin-C in invasive squamous cell carcinoma cervix.
  • BACKGROUND: Clinical data relating to human papillomavirus (HPV) infection and p53 status in cervical cancer has been sparse and confusing.
  • AIM: To evaluate high-risk HPV and expression of tumor suppressor protein p53 in squamous cell carcinoma of cervix and to assess response to mitomycin-C in neo-adjuvant chemotherapy.
  • MATERIALS AND METHODS: Expression of p53 protein was assessed, using immunohistochemistry with mouse monoclonal antibody in 30 consecutive patients undergoing radical hysterectomy or admitted for neo-adjuvant chemotherapy.
  • Patients eligible for chemotherapy were randomized into vincristine, bleomycin and cisplatin (VBP) group and VBP with mitomycin C group.
  • Analysis of p53 protein in cervical carcinoma patient showed expression in 50% of cancer specimens (P value < 0.001).
  • McNemar's and Fischer's exact test showed no change in p53 status post-chemotherapy; however 66% of stage II B patients in VBP-M group became operable.
  • More studies using mitomycin-C in cervical cancer treatment protocols are needed.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Carcinoma, Squamous Cell / virology. Papillomaviridae. Papillomavirus Infections / metabolism. Tumor Suppressor Protein p53 / metabolism. Uterine Cervical Neoplasms / virology
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Bleomycin / administration & dosage. Chemotherapy, Adjuvant. Child. Cisplatin / administration & dosage. DNA, Viral / genetics. DNA, Viral / metabolism. Female. Humans. Immunoenzyme Techniques. Middle Aged. Mitomycin / administration & dosage. Neoadjuvant Therapy. Polymerase Chain Reaction. Prospective Studies. Vincristine / administration & dosage. Viral Load

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  • (PMID = 17192686.001).
  • [ISSN] 0019-509X
  • [Journal-full-title] Indian journal of cancer
  • [ISO-abbreviation] Indian J Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Randomized Controlled Trial
  • [Publication-country] India
  • [Chemical-registry-number] 0 / DNA, Viral; 0 / Tumor Suppressor Protein p53; 11056-06-7 / Bleomycin; 50SG953SK6 / Mitomycin; 5J49Q6B70F / Vincristine; Q20Q21Q62J / Cisplatin
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4. Kawashiri S, Noguchi N, Tanaka A, Nakaya H, Kato K, Yamamoto E: Inhibitory effect of neoadjuvant chemotherapy on metastasis of oral squamous cell carcinoma in a mouse model. Oral Oncol; 2009 Sep;45(9):794-7
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  • [Title] Inhibitory effect of neoadjuvant chemotherapy on metastasis of oral squamous cell carcinoma in a mouse model.
  • Neoadjuvant chemotherapy has become widely employed as an initial treatment.
  • However, the actual effectiveness of neoadjuvant chemotherapy on metastasis is still unestablished.
  • Therefore, using an orthotopic implantation model in which cervical lymph node metastasis of oral squamous cell carcinoma can be reproduced, we investigated the inhibitory effect of neoadjuvant chemotherapy on metastasis.
  • A highly invasive and metastatic human oral squamous cell carcinoma cell line, OSC-19 cells, was implanted into the tongues of nude mice.
  • After implantation, the mice were divided into four groups: S (surgery), C+S (preoperative chemotherapy+surgery), S+C (surgery+postoperative chemotherapy), and a control (nontreatment) groups.
  • The treatment (tumor resection or chemotherapy) was started 7 days postimplantation.
  • The effects of each treatment on cervical lymph node metastasis were investigated by examining the rate of lymph node metastasis formation at 28 days postimplantation.
  • The cervical lymph node metastasis rates were 81.8% in S, 18.1% in C+S, 63.6% in S+C, and 100% in control groups.
  • Thus, metastasis to the cervical lymph node was markedly inhibited by the combination of neoadjuvant chemotherapy and tumor resection.
  • The findings of this study indicate that neoadjuvant chemotherapy is effective for inhibiting metastasis, and that it is necessary to begin chemotherapy as early as possible to achieve an inhibitory effect on metastasis.
  • Considering these effects, if anticancer drugs are used, better therapeutic results can be expected.
  • [MeSH-major] Carcinoma, Squamous Cell / drug therapy. Carcinoma, Squamous Cell / secondary. Tongue Neoplasms / drug therapy
  • [MeSH-minor] Animals. Antibiotics, Antineoplastic / therapeutic use. Antineoplastic Agents / therapeutic use. Cisplatin / therapeutic use. Disease Models, Animal. Female. Humans. Lymphatic Metastasis. Mice. Mice, Inbred BALB C. Mice, Nude. Neck. Neoadjuvant Therapy / methods. Peplomycin / therapeutic use. Treatment Outcome

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  • (PMID = 19200774.001).
  • [ISSN] 1879-0593
  • [Journal-full-title] Oral oncology
  • [ISO-abbreviation] Oral Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / Antineoplastic Agents; 56H9L80NIZ / Peplomycin; Q20Q21Q62J / Cisplatin
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5. Yazici YD, Kim S, Jasser SA, Wang Z, Carter KB Jr, Bucana CD, Myers JN: Antivascular therapy of oral tongue squamous cell carcinoma with PTK787. Laryngoscope; 2005 Dec;115(12):2249-55
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  • [Title] Antivascular therapy of oral tongue squamous cell carcinoma with PTK787.
  • We investigated whether blockade of the VEGF receptor (VEGF-R) signaling pathway by the tyrosine kinase inhibitor PTK787 combined with CPT-11, a semisynthetic camptothecin analogue, can inhibit the tumor growth and angiogenesis of squamous cell carcinoma of the oral tongue in an orthotopic nude mouse model.
  • METHODS: JMAR human oral squamous cell carcinoma cells were injected into the tongues of nude mice.
  • After 4 weeks of treatment, the mice underwent necropsy, and the tongue tumors, cervical lymph nodes, and lungs were removed for immunohistochemical analyses.
  • The combination treatment group had the most significant decrease in volume and increase in survival.
  • PTK787 alone or the combination therapy resulted in apoptosis of both tumor cells and tumor-associated endothelial cells.
  • CONCLUSIONS: These results suggest that targeting VEGF-R tyrosine kinase activity can be an effective therapeutic approach in squamous cell carcinoma of the oral tongue.
  • [MeSH-major] Carcinoma, Squamous Cell / drug therapy. Phthalazines / therapeutic use. Protein Kinase Inhibitors / therapeutic use. Pyridines / therapeutic use. Tongue Neoplasms / drug therapy
  • [MeSH-minor] Animals. Camptothecin / analogs & derivatives. Camptothecin / therapeutic use. Cell Line, Tumor. Drug Therapy, Combination. Follow-Up Studies. In Vitro Techniques. Male. Mice. Mice, Nude. Neoplasm Transplantation. Neoplasms, Experimental. Neovascularization, Pathologic / drug therapy. Neovascularization, Pathologic / pathology. Prodrugs / therapeutic use. Treatment Outcome

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  • (PMID = 16369175.001).
  • [ISSN] 0023-852X
  • [Journal-full-title] The Laryngoscope
  • [ISO-abbreviation] Laryngoscope
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Phthalazines; 0 / Prodrugs; 0 / Protein Kinase Inhibitors; 0 / Pyridines; 5DX9U76296 / vatalanib; 7673326042 / irinotecan; XT3Z54Z28A / Camptothecin
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6. Bisht KS, Bradbury CM, Mattson D, Kaushal A, Sowers A, Markovina S, Ortiz KL, Sieck LK, Isaacs JS, Brechbiel MW, Mitchell JB, Neckers LM, Gius D: Geldanamycin and 17-allylamino-17-demethoxygeldanamycin potentiate the in vitro and in vivo radiation response of cervical tumor cells via the heat shock protein 90-mediated intracellular signaling and cytotoxicity. Cancer Res; 2003 Dec 15;63(24):8984-95
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  • [Title] Geldanamycin and 17-allylamino-17-demethoxygeldanamycin potentiate the in vitro and in vivo radiation response of cervical tumor cells via the heat shock protein 90-mediated intracellular signaling and cytotoxicity.
  • Treatment of two human cervical carcinoma cell lines (HeLa and SiHa) with geldanamycin and 17-AAG resulted in cytotoxicity and, when combined with IR, enhanced the radiation response, each effect with a temporal range from 6 to 48 h after drug exposure.
  • In addition, mouse in vivo models using 17-AAG at clinically achievable concentrations yielded results that paralleled the in vitro radiosensitization studies of both single and fractioned courses of irradiation.
  • Akt1, extracellular signal-regulated kinase-1, Glut-1, HER-2/neu, Lyn, cAMP-dependent protein kinase, Raf-1, and vascular endothelial growth factor expression were down-regulated in 17-AAG-treated cells, identifying these factors as molecular markers and potential therapeutic targets.
  • This work shows that altered HSP90 function induces significant tumor cytotoxicity and radiosensitization, suggesting a potential therapeutic utility.
  • [MeSH-major] Antibiotics, Antineoplastic / pharmacology. HSP90 Heat-Shock Proteins / physiology. Quinones / pharmacology. Radiation-Sensitizing Agents / pharmacology. Rifabutin / analogs & derivatives. Rifabutin / pharmacology. Uterine Cervical Neoplasms / drug therapy. Uterine Cervical Neoplasms / radiotherapy
  • [MeSH-minor] Animals. Benzoquinones. Combined Modality Therapy. Dose-Response Relationship, Drug. Drug Synergism. Female. HeLa Cells. Humans. Lactams, Macrocyclic. Mice. Mice, Inbred C3H. Mice, Nude. Signal Transduction / drug effects. Xenograft Model Antitumor Assays


7. Santin AD, Bellone S, Marizzoni M, Palmieri M, Siegel ER, McKenney JK, Hennings L, Comper F, Bandiera E, Pecorelli S: Overexpression of claudin-3 and claudin-4 receptors in uterine serous papillary carcinoma: novel targets for a type-specific therapy using Clostridium perfringens enterotoxin (CPE). Cancer; 2007 Apr 1;109(7):1312-22
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  • [Title] Overexpression of claudin-3 and claudin-4 receptors in uterine serous papillary carcinoma: novel targets for a type-specific therapy using Clostridium perfringens enterotoxin (CPE).
  • BACKGROUND: Uterine serous papillary carcinoma (USPC) represents a highly aggressive variant of endometrial cancer.
  • The potential for targeting this pathway in the treatment of USPC was explored.
  • METHODS: Claudin-3 and claudin-4 receptor expression was analyzed at the mRNA and protein levels in flash-frozen and formalin-fixed, paraffin-embedded tissue from 20 consecutive USPC patients.
  • The potential of recombinant CPE as a novel therapy against primary, metastatic, and chemotherapy-resistant USPC cell lines was also investigated in vitro.
  • Finally, the in vivo therapeutic effect of sublethal doses of CPE was studied in SCID mouse xenografts harboring subcutaneous and intraperitoneal USPC that expressed claudin-3 and claudin-4.
  • Membranous immunoreactivity for claudin-4 protein expression was documented in the majority of USPC specimens tested by immunohistochemistry, whereas only a low level of membranous staining was found in normal endometrial control tissue samples.
  • In vivo, intratumoral injections of well-tolerated doses of CPE in large subcutaneous USPC xenografts led to large areas of tumor cell necrosis and tumor disappearance in all the treated animals, whereas sublethal intraperitoneal injections of CPE had a significant inhibitory effect on tumor progression, with extended survival of animals harboring chemotherapy-resistant intra-abdominal USPC carcinomatosis.
  • CONCLUSIONS: Claudin-3 and claudin-4 receptors may offer promising targets for the use of CPE as a novel type-specific therapy against this highly aggressive and chemotherapy-resistant variant of endometrial cancer.
  • [MeSH-major] Cystadenocarcinoma, Papillary / drug therapy. Cystadenocarcinoma, Serous / drug therapy. Enterotoxins / therapeutic use. Membrane Proteins / genetics. Uterine Cervical Neoplasms / drug therapy
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Animals. Claudin-3. Claudin-4. Clostridium perfringens. Drug Resistance, Neoplasm. Female. Gene Expression. Humans. Injections, Intraperitoneal. Mice. Mice, SCID. Middle Aged. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Tumor Cells, Cultured. Up-Regulation. Xenograft Model Antitumor Assays

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  • [Copyright] (c) 2007 American Cancer Society.
  • (PMID = 17326053.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 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 / RNA, Messenger; 0 / enterotoxin, Clostridium
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8. Santin AD, Cané S, Bellone S, Palmieri M, Siegel ER, Thomas M, Roman JJ, Burnett A, Cannon MJ, Pecorelli S: Treatment of chemotherapy-resistant human ovarian cancer xenografts in C.B-17/SCID mice by intraperitoneal administration of Clostridium perfringens enterotoxin. Cancer Res; 2005 May 15;65(10):4334-42
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  • [Title] Treatment of chemotherapy-resistant human ovarian cancer xenografts in C.B-17/SCID mice by intraperitoneal administration of Clostridium perfringens enterotoxin.
  • Although many patients with advanced-stage disease initially respond to standard combinations of surgical and cytotoxic therapy, nearly 90% develop recurrence and inevitably die from the development of chemotherapy-resistant disease.
  • The discovery of novel and effective therapy against chemotherapy-resistant/recurrent ovarian cancer remains a high priority.
  • Because these tight junction proteins have been described as the low- and high-affinity receptors, respectively, for the cytotoxic Clostridium perfringens enterotoxin (CPE), in this study we investigated the level of expression of claudin-3 and/or claudin-4 in chemotherapy-naive and chemotherapy-resistant primary human ovarian cancers as well as their sensitivity to CPE treatment in vitro.
  • Importantly, chemotherapy-resistant/recurrent ovarian tumors were found to express claudin-3 and claudin-4 genes at significantly higher levels when compared with chemotherapy-naive ovarian cancers.
  • CPE therapy in SCID mouse xenografts in a highly relevant clinical model of chemotherapy-resistant freshly explanted human ovarian cancer (i.e., OVA-1).
  • Our findings suggest that CPE may have potential as a novel treatment for chemotherapy-resistant/recurrent ovarian cancer.
  • [MeSH-major] Enterotoxins / pharmacology. Ovarian Neoplasms / drug therapy
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Animals. Carcinoma, Papillary / drug therapy. Carcinoma, Papillary / genetics. Carcinoma, Papillary / metabolism. Cell Line, Tumor. Claudin-3. Claudin-4. Cystadenocarcinoma, Serous / drug therapy. Cystadenocarcinoma, Serous / genetics. Cystadenocarcinoma, Serous / metabolism. Drug Resistance, Neoplasm. Female. Humans. Injections, Intraperitoneal. Membrane Proteins. Mice. Mice, SCID. Middle Aged. Receptors, Cell Surface / biosynthesis. Receptors, Cell Surface / genetics. Uterine Cervical Neoplasms / drug therapy. Xenograft Model Antitumor Assays

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  • (PMID = 15899825.001).
  • [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 / 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 / Receptors, Cell Surface; 0 / enterotoxin, Clostridium
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9. Noguchi N, Kawashiri S, Tanaka A, Kato K, Nakaya H: Effects of fibroblast growth inhibitor on proliferation and metastasis of oral squamous cell carcinoma. Oral Oncol; 2003 Apr;39(3):240-7
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  • [Title] Effects of fibroblast growth inhibitor on proliferation and metastasis of oral squamous cell carcinoma.
  • Development of a new therapeutic approach to improve the prognosis of high grade invasion of oral squamous cell carcinoma is needed.
  • To elucidate the effect of a fibroblast inhibitor (tranilast), we investigated the proliferation and metastasis of oral squamous cell carcinoma in a mouse model.
  • The effect of tranilast on tumour growth, lymph node metastases, microvessel density, and the proliferating cell nuclear antigen (PCNA) labelling index of oral squamous cell carcinoma implanted into the tongue of nude mice was evaluated.
  • Tumour growth and the incidence of cervical lymph node metastases were significantly suppressed by the administration of tranilast.
  • The amount of fibrous tissue, the microvessel density, and the PCNA labelling index of tumour were also significantly reduced.
  • Administration of a fibroblast inhibitor may well be clinically effective for the treatment of oral squamous cell carcinoma.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Carcinoma, Squamous Cell / drug therapy. Fibroblasts / drug effects. Mouth Neoplasms / drug therapy. ortho-Aminobenzoates / therapeutic use
  • [MeSH-minor] Animals. Body Weight / drug effects. Cell Division / drug effects. Female. Humans. Lymphatic Metastasis. Male. Mice. Mice, Inbred BALB C. Mice, Nude. Middle Aged. Neoplasm Transplantation. Neovascularization, Pathologic / pathology. Tumor Cells, Cultured


10. Shaw RJ: Tumor suppression by LKB1: SIK-ness prevents metastasis. Sci Signal; 2009;2(86):pe55
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  • The LKB1 serine-threonine kinase is a tumor suppressor that is inactivated in a large number of sporadic human lung non-small cell carcinomas (NSCLCs) and cervical cancers.
  • Genetic deletion of LKB1 in various mouse tissues results in tumorigenesis, and loss of LKB1 increases metastasis in a mouse model of NSCLC.
  • [MeSH-major] Neoplasm Metastasis / prevention & control. Protein-Serine-Threonine Kinases / genetics. Protein-Serine-Threonine Kinases / therapeutic use
  • [MeSH-minor] AMP-Activated Protein Kinases / metabolism. Animals. Carcinoma, Non-Small-Cell Lung / drug therapy. Carcinoma, Non-Small-Cell Lung / pathology. Chromosome Mapping. Chromosomes, Human, Pair 19. Enzyme Activation. Female. Gene Deletion. Humans. Lung Neoplasms / drug therapy. Lung Neoplasms / pathology. Mice. Mice, Knockout. Peutz-Jeghers Syndrome / genetics. Uterine Cervical Neoplasms / drug therapy. Uterine Cervical Neoplasms / pathology

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  • (PMID = 19724060.001).
  • [ISSN] 1937-9145
  • [Journal-full-title] Science signaling
  • [ISO-abbreviation] Sci Signal
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] EC 2.7.1.- / STK11 protein, human; EC 2.7.1.- / Stk11 protein, mouse; EC 2.7.11.1 / AMP-Activated Protein Kinases; EC 2.7.11.1 / Protein-Serine-Threonine Kinases
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11. Kobayashi H, Yagyu T, Inagaki K, Kondo T, Suzuki M, Kanayama N, Terao T: Therapeutic efficacy of once-daily oral administration of a Kunitz-type protease inhibitor, bikunin, in a mouse model and in human cancer. Cancer; 2004 Feb 15;100(4):869-77
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  • [Title] Therapeutic efficacy of once-daily oral administration of a Kunitz-type protease inhibitor, bikunin, in a mouse model and in human cancer.
  • BACKGROUND: Bikunin, a Kunitz-type protease inhibitor, specifically inhibits tumor invasion and metastasis.
  • METHODS: The authors initially evaluated the therapeutic efficacy of once-daily oral administration of different doses of bikunin against human ovarian carcinoma HRA cells growing in the peritonea of nude mice.
  • On Day 9, the abdominal cavity was examined by two observers who were blinded to treatment.
  • RESULTS: After oral administration, intact bikunin was detectable in mouse serum specimens at 3 and 6 hours.
  • The current study was the first to report the potent activity of once-daily oral administration of bikunin against ovarian carcinoma.
  • The indication was locally advanced uterine cervical carcinoma after definitive treatment.
  • The authors also obtained preliminary data on its effect on urokinase-type plasminogen activator expression at the highest dose level.
  • [MeSH-major] Carcinoma / drug therapy. Membrane Glycoproteins / pharmacology. Ovarian Neoplasms / drug therapy. Serine Proteinase Inhibitors / pharmacology. Trypsin Inhibitor, Kunitz Soybean / pharmacology
  • [MeSH-minor] Administration, Oral. Adolescent. Adult. Animals. Body Weight. Disease Models, Animal. Drug Administration Schedule. Female. Humans. Maximum Tolerated Dose. Mice. Mice, Inbred BALB C. Mice, Nude. Middle Aged. Transplantation, Heterologous

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  • [Copyright] Copyright 2004 American Cancer Society.
  • (PMID = 14770446.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Clinical Trial; Clinical Trial, Phase I; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Membrane Glycoproteins; 0 / SPINT2 protein, human; 0 / Serine Proteinase Inhibitors; 9088-41-9 / Trypsin Inhibitor, Kunitz Soybean
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12. Abdulkarim B, Sabri S, Deutsch E, Chagraoui H, Maggiorella L, Thierry J, Eschwege F, Vainchenker W, Chouaïb S, Bourhis J: Antiviral agent Cidofovir restores p53 function and enhances the radiosensitivity in HPV-associated cancers. Oncogene; 2002 Apr 4;21(15):2334-46
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • High-risk human papillomaviruses (HPVs) have been associated to the development of cervical and some other human cancers.
  • Restoration of these pathways by blocking E6 and E7 expression would provide a selective therapeutic effect.
  • Here, we show that a clinically approved antiviral agent Cidofovir reduced E6 and E7 expression in cervical carcinoma Me180 and head and neck squamous cell carcinoma HEP2 cells at the transcriptional level.
  • Cidofovir induced the accumulation of active p53 and pRb associated to induction of cyclin dependent kinase inhibitor p21(WAF1/CIP1) in Me180 and HEP2 cells. p53 induction was also shown in Hela HPV-positive cervical carcinoma cell line.
  • [MeSH-major] Antiviral Agents / pharmacology. Carcinoma / therapy. Cytosine / analogs & derivatives. Cytosine / pharmacology. Organophosphonates. Organophosphorus Compounds / pharmacology. Papillomaviridae. Papillomavirus Infections / therapy. Radiation-Sensitizing Agents / pharmacology. Tumor Virus Infections / therapy
  • [MeSH-minor] Animals. Cell Division / drug effects. Cell Division / radiation effects. Cyclin A / metabolism. Cyclin-Dependent Kinase Inhibitor p21. Cyclins / biosynthesis. Female. Head and Neck Neoplasms / metabolism. Head and Neck Neoplasms / therapy. Head and Neck Neoplasms / virology. Humans. Mice. Mice, Nude. Oncogene Proteins, Viral / metabolism. Radiation, Ionizing. Retinoblastoma Protein / metabolism. Tumor Cells, Cultured. Tumor Suppressor Protein p53 / physiology. Uterine Cervical Neoplasms / metabolism. Uterine Cervical Neoplasms / therapy. Uterine Cervical Neoplasms / virology. Xenograft Model Antitumor Assays

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  • (PMID = 11948417.001).
  • [ISSN] 0950-9232
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antiviral Agents; 0 / CDKN1A protein, human; 0 / Cdkn1a protein, mouse; 0 / Cyclin A; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / Cyclins; 0 / Oncogene Proteins, Viral; 0 / Organophosphonates; 0 / Organophosphorus Compounds; 0 / Radiation-Sensitizing Agents; 0 / Retinoblastoma Protein; 0 / Tumor Suppressor Protein p53; 8J337D1HZY / Cytosine; JIL713Q00N / cidofovir
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13. Pietras K, Pahler J, Bergers G, Hanahan D: Functions of paracrine PDGF signaling in the proangiogenic tumor stroma revealed by pharmacological targeting. PLoS Med; 2008 Jan 29;5(1):e19
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  • [Title] Functions of paracrine PDGF signaling in the proangiogenic tumor stroma revealed by pharmacological targeting.
  • BACKGROUND: Important support functions, including promotion of tumor growth, angiogenesis, and invasion, have been attributed to the different cell types populating the tumor stroma, i.e., endothelial cells, cancer-associated fibroblasts, pericytes, and infiltrating inflammatory cells.
  • The stroma is prominent in cervical carcinoma, and distinguishable from nonmalignant tissue, suggestive of altered (tumor-promoting) functions.
  • We postulated that pharmacological targeting of putative stromal support functions, in particular those of cancer-associated fibroblasts, could have therapeutic utility, and sought to assess the possibility in a pre-clinical setting.
  • METHODS AND FINDINGS: We used a genetically engineered mouse model of cervical carcinogenesis to investigate platelet-derived growth factor (PDGF) receptor signaling in cancer-associated fibroblasts and pericytes.
  • Pharmacological blockade of PDGF receptor signaling with the clinically approved kinase inhibitor imatinib slowed progression of premalignant cervical lesions in this model, and impaired the growth of preexisting invasive carcinomas.
  • Inhibition of stromal PDGF receptors reduced proliferation and angiogenesis in cervical lesions through a mechanism involving suppression of expression of the angiogenic factor fibroblast growth factor 2 (FGF-2) and the epithelial cell growth factor FGF-7 by cancer-associated fibroblasts.
  • Treatment with neutralizing antibodies to the PDGF receptors recapitulated these effects.
  • CONCLUSIONS: This study illustrates the therapeutic benefits in a mouse model of human cervical cancer of mechanism-based targeting of the stroma, in particular cancer-associated fibroblasts.
  • Drugs aimed at stromal fibroblast signals and effector functions may prove complementary to conventional treatments targeting the overt cancer cells for a range of solid tumors, possibly including cervical carcinoma, the second most common lethal malignancy in women worldwide, for which management remains poor.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Carcinoma / blood supply. Neoplasm Proteins / physiology. Neovascularization, Pathologic / drug therapy. Paracrine Communication / physiology. Piperazines / therapeutic use. Platelet-Derived Growth Factor / physiology. Protein Kinase Inhibitors / therapeutic use. Pyrimidines / therapeutic use. Receptors, Platelet-Derived Growth Factor / physiology. Uterine Cervical Neoplasms / blood supply
  • [MeSH-minor] Animals. Benzamides. Epithelial Cells / metabolism. Estradiol / administration & dosage. Estradiol / toxicity. Female. Fibroblast Growth Factor 2 / biosynthesis. Fibroblast Growth Factor 2 / genetics. Fibroblast Growth Factor 2 / physiology. Fibroblast Growth Factor 7 / biosynthesis. Fibroblast Growth Factor 7 / genetics. Fibroblast Growth Factor 7 / physiology. Fibroblasts / drug effects. Fibroblasts / enzymology. Fibroblasts / secretion. Human papillomavirus 16. Humans. Imatinib Mesylate. Mice. Mice, Inbred Strains. Mice, Transgenic. Pericytes / metabolism. Proto-Oncogene Proteins c-kit / biosynthesis. Proto-Oncogene Proteins c-kit / genetics. Stromal Cells / drug effects. Stromal Cells / enzymology. Stromal Cells / secretion

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  • (PMID = 18232728.001).
  • [ISSN] 1549-1676
  • [Journal-full-title] PLoS medicine
  • [ISO-abbreviation] PLoS Med.
  • [Language] eng
  • [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 / Benzamides; 0 / Fgf7 protein, mouse; 0 / Neoplasm Proteins; 0 / Piperazines; 0 / Platelet-Derived Growth Factor; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 103107-01-3 / Fibroblast Growth Factor 2; 126469-10-1 / Fibroblast Growth Factor 7; 4TI98Z838E / Estradiol; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit; EC 2.7.10.1 / Receptors, Platelet-Derived Growth Factor
  • [Other-IDs] NLM/ PMC2214790
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14. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • 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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15. Yin DS, Ge ZQ, Yang WY, Liu CX, Yuan YJ: Inhibition of tumor metastasis in vivo by combination of paclitaxel and hyaluronic acid. Cancer Lett; 2006 Nov 8;243(1):71-9
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  • The aim of present study is to determine whether the combined administration of hyaluronic acid (HA) with paclitaxel can produce additional or synergistic therapeutic effects in the control of Lewis lung carcinoma (LLC) migration and ascites formation of U14 cervical tumor.
  • The anti-metastasis effect of hyaluronic acid alone, paclitaxel alone and paclitaxel-hyaluronic acid combination were examined in a mouse model bearing LLC cells. i.v.
  • We also analyzed the serum proteome of mice with lung neoplasm before and after treatment with paclitaxel-hyaluronic acid.
  • In conclusion, the in vivo anti-metastasis effect was associated with the synergistic therapeutic effects of hyaluronic acid-paclitaxel combination and a significant promotion of immune proteins expression.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Carcinoma, Lewis Lung / drug therapy. Neoplasm Metastasis / prevention & control. Uterine Cervical Neoplasms / drug therapy
  • [MeSH-minor] Amino Acid Sequence. Animals. Ascites / drug therapy. Ascites / pathology. Blood Proteins / analysis. Cell Line, Tumor. Cell Movement / drug effects. Electrophoresis, Gel, Two-Dimensional. Female. Hyaluronic Acid / administration & dosage. Hyaluronic Acid / pharmacology. Injections, Intraperitoneal. Injections, Intravenous. Mice. Mice, Inbred C57BL. Molecular Sequence Data. Paclitaxel / administration & dosage. Paclitaxel / pharmacology. Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization. Survival Analysis. Swine. Treatment Outcome


16. Casana PH, Hernandez H, Arana MJ: Interleukin-2 inhibits proliferation of HPV-associated tumor cells and halts tumor growth in vivo. Biochem Biophys Res Commun; 2002 Dec 20;299(5):818-24
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Previous studies have shown inhibition of cervical cancer cell growth by treatment with high concentrations of IL-2.
  • Treatment of 3T3-16 cells with rhIL-2 for 72 h inhibited cell growth in a dose-dependent manner and this effect was evidenced at nanomolar concentrations.
  • These results indicate the potential adequacy of therapeutic strategies based on local administration of rhIL-2 for cervical carcinoma, not only based on the ability of this cytokine to stimulate cellular-mediated immunity but also because of its direct effects on tumor cells.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Interleukin-2 / therapeutic use. Neoplasms, Experimental / drug therapy. Papillomaviridae. Papillomavirus Infections / drug therapy. Tumor Virus Infections / drug therapy
  • [MeSH-minor] Animals. Cell Division / drug effects. Cell Line, Transformed. Cell Transformation, Viral. Dose-Response Relationship, Drug. Female. Humans. Interleukin-2 Receptor beta Subunit. Mice. Mice, Inbred BALB C. RNA, Messenger / biosynthesis. Receptors, Interleukin / biosynthesis. Receptors, Interleukin / genetics. Receptors, Interleukin-2 / biosynthesis. Receptors, Interleukin-2 / genetics. Uterine Cervical Neoplasms / drug therapy

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  • (PMID = 12470652.001).
  • [ISSN] 0006-291X
  • [Journal-full-title] Biochemical and biophysical research communications
  • [ISO-abbreviation] Biochem. Biophys. Res. Commun.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / IL2RB protein, human; 0 / Il2rb protein, mouse; 0 / Interleukin-2; 0 / Interleukin-2 Receptor beta Subunit; 0 / RNA, Messenger; 0 / Receptors, Interleukin; 0 / Receptors, Interleukin-2
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17. Goon PK, Stanley MA, Ebmeyer J, Steinsträsser L, Upile T, Jerjes W, Bernal-Sprekelsen M, Görner M, Sudhoff HH: HPV & head and neck cancer: a descriptive update. Head Neck Oncol; 2009;1:36
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  • The incidence of head and neck squamous cell carcinoma (HNSCC) has been gradually increasing over the last three decades.
  • The dominance of HPV 16 in HPV+ HNSCC is even greater than that seen in cervical carcinoma of total worldwide cases.
  • These patients are treated with curative intent using single modality treatments either radiation or surgery alone.
  • Cetuximab, a humanized mouse anti-EGFR IgG1 monoclonal antibody, improved locoregional control and overall survival in combination with radiotherapy in locally advanced tumours but at the cost of some increased cardiac morbidity and mortality.
  • Finally, the improved prognosis and treatment responses to chemotherapy and radiotherapy by HPV+ tumours may suggest that HPV status detection is required to better plan and individualize patient treatment regimes.
  • [MeSH-major] Carcinoma, Squamous Cell / etiology. Head and Neck Neoplasms / etiology. Papillomavirus Infections / complications
  • [MeSH-minor] Combined Modality Therapy. Human papillomavirus 16 / isolation & purification. Humans. Neoplasm Recurrence, Local. Receptor, Epidermal Growth Factor / antagonists & inhibitors. Risk Factors. Viral Load. Virus Integration

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  • (PMID = 19828033.001).
  • [ISSN] 1758-3284
  • [Journal-full-title] Head & neck oncology
  • [ISO-abbreviation] Head Neck Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] EC 2.7.10.1 / Receptor, Epidermal Growth Factor
  • [Other-IDs] NLM/ PMC2770444
  • [General-notes] NLM/ Original DateCompleted: 20100629
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18. Vardouli L, Lindqvist C, Vlahou K, Loskog AS, Eliopoulos AG: Adenovirus delivery of human CD40 ligand gene confers direct therapeutic effects on carcinomas. Cancer Gene Ther; 2009 Nov;16(11):848-60
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  • [Title] Adenovirus delivery of human CD40 ligand gene confers direct therapeutic effects on carcinomas.
  • CD40, a tumor necrosis factor receptor family member, is an emerging target for cancer therapy being best appreciated as an important regulator of the anti-tumor immune response.
  • Thus, transduction of CD40-positive bladder, cervical and ovarian carcinoma cell lines with RAd-hCD40L potently inhibits their proliferation in vitro, whereas CD40-negative lines remain unresponsive.
  • RAd-hCD40L is also found to be superior to recombinant CD40L in inducing carcinoma cell death and in amplifying the cytotoxic effects of the chemotherapeutic agents 5-fluorouracil, cis-platin and mitomycin C.
  • Soluble CD40L is produced by RAd-hCD40L transduced carcinoma cells but unlike other soluble tumor necrosis factor family ligands, it does not interfere with the death-promoting activity of its membrane-bound form.
  • In a mouse xenograft tumor model bearing a human bladder carcinoma, intratumoral delivery of RAd-hCD40L suppresses cancer growth.
  • These findings highlight the potential of exploiting the CD40 pathway in carcinomas using CD40L gene transfer alone or in combination with other modalities for cancer therapy.
  • [MeSH-major] Adenoviridae / genetics. CD40 Ligand / genetics. CD40 Ligand / metabolism. CD40 Ligand / physiology. Carcinoma / therapy. Genetic Therapy / methods
  • [MeSH-minor] Animals. Antineoplastic Agents / therapeutic use. Apoptosis / physiology. Cell Line, Tumor. Cell Proliferation / drug effects. Cisplatin / therapeutic use. Flow Cytometry. Fluorouracil / therapeutic use. Humans. Immunoblotting. Mice. Mice, Nude. Mitomycin / therapeutic use. Xenograft Model Antitumor Assays

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  • (PMID = 19461675.001).
  • [ISSN] 1476-5500
  • [Journal-full-title] Cancer gene therapy
  • [ISO-abbreviation] Cancer Gene Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 147205-72-9 / CD40 Ligand; 50SG953SK6 / Mitomycin; Q20Q21Q62J / Cisplatin; U3P01618RT / Fluorouracil
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19. Sharma RK, Schabowsky RH, Srivastava AK, Elpek KG, Madireddi S, Zhao H, Zhong Z, Miller RW, Macleod KJ, Yolcu ES, Shirwan H: 4-1BB ligand as an effective multifunctional immunomodulator and antigen delivery vehicle for the development of therapeutic cancer vaccines. Cancer Res; 2010 May 15;70(10):3945-54
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  • [Title] 4-1BB ligand as an effective multifunctional immunomodulator and antigen delivery vehicle for the development of therapeutic cancer vaccines.
  • Therapeutic subunit vaccines based on tumor-associated antigens (TAA) represent an attractive approach for the treatment of cancer.
  • However, poor immunogenicity of TAAs requires potent adjuvants for therapeutic efficacy.
  • We recently proposed the tumor necrosis factor family costimulatory ligands as potential adjuvants for therapeutic vaccines and, hence, generated a soluble form of 4-1BBL chimeric with streptavidin (SA-4-1BBL) that has pleiotropic effects on cells of innate, adaptive, and regulatory immunity.
  • Conjugate vaccines containing human papillomavirus 16 E7 oncoprotein or survivin as a self-TAA had potent therapeutic efficacy against TC-1 cervical and 3LL lung carcinoma tumors, respectively.
  • Therapeutic efficacy of the vaccines was associated with increased CD4(+) T and CD8(+) T-cell effector and memory responses and higher intratumoral CD8(+) T effector/CD4(+)CD25(+)Foxp3(+) T regulatory cell ratio.
  • Thus, potent pleiotropic immune functions of SA-4-1BBL combined with its ability to serve as a vehicle to increase the delivery of antigens to DCs in vivo endow this molecule with the potential to serve as an effective immunomodulatory component of therapeutic vaccines against cancer and chronic infections.

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  • [Copyright] (c)2010 AACR.
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  • (PMID = 20406989.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R41 CA121665; United States / NIAID NIH HHS / AI / R43 AI074176-01A2; United States / NIAID NIH HHS / AI / AI074176-01A2; United States / NIAID NIH HHS / AI / R44 AI071618; United States / NIAID NIH HHS / AI / R43AI074176; United States / NIAID NIH HHS / AI / AI071618-02; United States / NIAID NIH HHS / AI / R43 AI071618; United States / NCI NIH HHS / CA / CA121665-01A2; United States / NIAID NIH HHS / AI / AI071618-01A1; United States / NIAID NIH HHS / AI / R44 AI071618-02; United States / NIAID NIH HHS / AI / R43 AI074176; United States / NIAID NIH HHS / AI / R43 AI071618-01A1; United States / NCI NIH HHS / CA / R41 CA121665-01A2
  • [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 / 4-1BB Ligand; 0 / Birc5 protein, mouse; 0 / Cancer Vaccines; 0 / Immunologic Factors; 0 / Inhibitor of Apoptosis Proteins; 0 / Microtubule-Associated Proteins; 0 / Papillomavirus E7 Proteins; 0 / Repressor Proteins; 0 / oncogene protein E7, Human papillomavirus type 16
  • [Other-IDs] NLM/ NIHMS187631; NLM/ PMC2872136
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20. Lu WZ, Geng GX, Li QW, Li J, Liu FZ, Han ZS: Antitumor activity of polysaccharides isolated from Patrinia heterophylla. Pharm Biol; 2010 Sep;48(9):1012-7
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  • The number of apoptotic tumor cells was significantly increased in the mice by treatment of PHB-P1 (30, 60 mg/kgbw).
  • By the immunohistochemical analysis, PHB-P1 (30, 60 mg/kgbw) might up-regulate the expression of p53 and Bax, and significantly inhibited the expression of Bcl-2 in tumor tissues.
  • [MeSH-major] Antineoplastic Agents, Phytogenic / therapeutic use. Carcinoma / drug therapy. Patrinia / chemistry. Phytotherapy. Plant Extracts / therapeutic use. Polysaccharides / therapeutic use. Uterine Cervical Neoplasms / drug therapy
  • [MeSH-minor] Animals. Apoptosis / drug effects. Cell Cycle / drug effects. Cell Line, Tumor. Dose-Response Relationship, Drug. Down-Regulation / drug effects. Drug Screening Assays, Antitumor. Female. Mice. Proto-Oncogene Proteins c-bcl-2 / metabolism. Random Allocation. Tumor Burden / drug effects. Tumor Suppressor Protein p53 / metabolism. Up-Regulation / drug effects. bcl-2-Associated X Protein / metabolism

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  • (PMID = 20731553.001).
  • [ISSN] 1744-5116
  • [Journal-full-title] Pharmaceutical biology
  • [ISO-abbreviation] Pharm Biol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 0 / Bax protein, mouse; 0 / Plant Extracts; 0 / Polysaccharides; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Tumor Suppressor Protein p53; 0 / bcl-2-Associated X Protein
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21. Ogbourne SM, Suhrbier A, Jones B, Cozzi SJ, Boyle GM, Morris M, McAlpine D, Johns J, Scott TM, Sutherland KP, Gardner JM, Le TT, Lenarczyk A, Aylward JH, Parsons PG: Antitumor activity of 3-ingenyl angelate: plasma membrane and mitochondrial disruption and necrotic cell death. Cancer Res; 2004 Apr 15;64(8):2833-9
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  • Options for skin cancer treatment currently include surgery, radiotherapy, topical chemotherapy, cryosurgery, curettage, and electrodessication.
  • Radiotherapy can leave a poor cosmetic effect, and current chemotherapy is limited by low cure rates and extended treatment schedules.
  • Here, we describe the preclinical activity of a novel topical chemotherapeutic agent for the treatment of skin cancer, 3-ingenyl angelate (PEP005), a hydrophobic diterpene ester isolated from the plant Euphorbia peplus.
  • Three daily topical applications of 42 nmol (18 micro g) of PEP005 cured a series of s.c. mouse tumors (B16 melanoma, LK2 UV-induced squamous cell carcinoma, and Lewis lung carcinoma; n = >14 tumors/group) and human tumors (DO4 melanoma, HeLa cervical carcinoma, and PC3 and DU145 prostate carcinoma; n = >4 tumors/group) previously established (5-10 mm(3)) on C57BL/6 or Foxn1(nu) mice.
  • The treatment produced a mild, short-term erythema and eschar formation but, ultimately, resulted in excellent skin cosmesis.
  • Electron microscopy showed that treatment with PEP005 both in vitro (230 micro M) and in vivo (42 nmol) rapidly caused swelling of mitochondria and cell death by primary necrosis. (51)Cr release, uptake of propidium iodide, and staining with the mitochondria dye JC1, revealed that PEP005 (230 micro M) treatment of tumor cells in vitro resulted in a rapid plasma membrane perturbation and loss of mitochondrial membrane potential.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Diterpenes / pharmacology. Esters / pharmacology. Mitochondria / drug effects
  • [MeSH-minor] Administration, Topical. Animals. Cell Death / drug effects. Cell Line, Tumor. Cell Membrane / drug effects. Female. Humans. Intracellular Membranes / drug effects. Intracellular Membranes / physiology. Membrane Potentials / drug effects. Mice. Mice, Inbred BALB C. Mice, Inbred C57BL. Neoplasms, Experimental / drug therapy

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  • (PMID = 15087400.001).
  • [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 / 3-ingenyl angelate; 0 / Antineoplastic Agents; 0 / Diterpenes; 0 / Esters
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22. Hambek M, Solbach C, Schnuerch HG, Roller M, Stegmueller M, Sterner-Kock A, Kiefer J, Knecht R: Tumor necrosis factor alpha sensitizes low epidermal growth factor receptor (EGFR)-expressing carcinomas for anti-EGFR therapy. Cancer Res; 2001 Feb 1;61(3):1045-9
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  • [Title] Tumor necrosis factor alpha sensitizes low epidermal growth factor receptor (EGFR)-expressing carcinomas for anti-EGFR therapy.
  • Analysis of 1,060 xenotransplants derived from cancer cell lines as wel as spontaneously occurring tumors from the larynx, pharynx, mammary gland, uterine cervix, and vulva revealed that tumor regression induced by treatment with monoclonal antibodies (EMD 55900 and EMD 72000 against the epidermal growth factor receptor (EGFR) could be enhanced by tumor necrosis factor alpha (TNF-alpha) treatment in vivo.
  • Moreover, tumor that primarily do not respond to antibody treatment can be made suscep tible by additional TNF-alpha treatment.
  • To investigate the in vivo effects of monoclonal antibodies, we treated tumors derived from cell lines (A431 and Detroit 562) as well as spontaneously occurring squamous cell carci nomas and adenocarcinomas (transplanted on NMRI-nu/nu mice) gener ally with EMD 55900 (40 microg/g mouse) and its humanized version EMD 72000 (40 microg/g mouse).
  • In mice treated with TNF-alpha (0.5 microg/g mouse) and EMD 55900 72000 simultaneously, we observed enhanced antitumor effects up to complete tumor eradication.
  • Carcinomas with an EGFR concentration <70 fmol/mg protein could be made susceptible to treatment with EMD 55900 and EMD 72000 by simultaneous treatment with TNF-alpha, resulting in a significant reduction in tumor size.
  • [MeSH-major] Adenocarcinoma / therapy. Antibodies, Monoclonal / pharmacology. Carcinoma, Squamous Cell / therapy. Receptor, Epidermal Growth Factor / immunology. Tumor Necrosis Factor-alpha / pharmacology
  • [MeSH-minor] Animals. Breast Neoplasms / immunology. Breast Neoplasms / metabolism. Breast Neoplasms / therapy. Cell Division / drug effects. Drug Synergism. Female. Humans. Laryngeal Neoplasms / immunology. Laryngeal Neoplasms / metabolism. Laryngeal Neoplasms / therapy. Mice. Mice, Inbred BALB C. Mice, Nude. Pharyngeal Neoplasms / immunology. Pharyngeal Neoplasms / metabolism. Pharyngeal Neoplasms / therapy. Tumor Cells, Cultured. Uterine Cervical Neoplasms / immunology. Uterine Cervical Neoplasms / metabolism. Uterine Cervical Neoplasms / therapy. Xenograft Model Antitumor Assays

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  • (PMID = 11221831.001).
  • [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 / Antibodies, Monoclonal; 0 / Tumor Necrosis Factor-alpha; EC 2.7.10.1 / Receptor, Epidermal Growth Factor
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23. Bernt KM, Steinwaerder DS, Ni S, Li ZY, Roffler SR, Lieber A: Enzyme-activated Prodrug Therapy Enhances Tumor-specific Replication of Adenovirus Vectors. Cancer Res; 2002 Nov 1;62(21):6089-98
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  • [Title] Enzyme-activated Prodrug Therapy Enhances Tumor-specific Replication of Adenovirus Vectors.
  • Adenoviruses (Ads) that selectively replicate in tumor cells have shown promising preliminary results in clinical trials, especially in combination with chemotherapy.
  • Here, we describe a system that combines the antitumor synergy of Ads and chemotherapeutic agents with the benefits of enzyme-activated prodrug therapy.
  • Furthermore, exposure of cells to activated prodrug or drug at subtoxic concentrations enhanced viral DNA replication.
  • Characteristically, these agents induced changes in the cell cycle status of exposed cells (G(2) arrest), which closely resembled the effect of wild-type Ad infection, and are thought to be favorable for viral replication.
  • We tested a number of cytostatic drugs (camptothecin, etoposide, daunorubicin, cisplatin, 5-fluorouracil, hydroxyurea, Taxol, and actinomycin D) for their effect on viral DNA replication and found considerable differences between individual agents.
  • Finally, we show that the combination of viral and prodrug therapy enhances viral replication and spread in liver metastases derived from human colon carcinoma or cervical carcinoma in a mouse model.
  • Our data indicate that specific vector/drug combinations tailored to be synergistic may have the potential to improve the potency of either therapeutic approach.
  • [MeSH-major] Adenoviridae / physiology. Camptothecin / analogs & derivatives. Genetic Therapy / methods. Glucuronidase / metabolism. Nucleoside Deaminases / metabolism. Pentosyltransferases / metabolism. Prodrugs / pharmacokinetics
  • [MeSH-minor] Biotransformation. Cell Cycle / drug effects. Combined Modality Therapy. Cytopathogenic Effect, Viral / drug effects. Cytosine Deaminase. DNA Replication / drug effects. Flucytosine / pharmacokinetics. Fluorouracil / pharmacology. Glucuronides / pharmacokinetics. HeLa Cells. Humans. Transgenes. Virus Replication / drug effects

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  • (PMID = 12414633.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA 80192
  • [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 / 9-aminocamptothecin glucuronide; 0 / Glucuronides; 0 / Prodrugs; 5MB77ICE2Q / 9-aminocamptothecin; D83282DT06 / Flucytosine; EC 2.4.2.- / Pentosyltransferases; EC 2.4.2.9 / uracil phosphoribosyltransferase; EC 3.2.1.31 / Glucuronidase; EC 3.5.4.- / Nucleoside Deaminases; EC 3.5.4.1 / Cytosine Deaminase; U3P01618RT / Fluorouracil; XT3Z54Z28A / Camptothecin
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24. Lukashev M, LePage D, Wilson C, Bailly V, Garber E, Lukashin A, Ngam-ek A, Zeng W, Allaire N, Perrin S, Xu X, Szeliga K, Wortham K, Kelly R, Bottiglio C, Ding J, Griffith L, Heaney G, Silverio E, Yang W, Jarpe M, Fawell S, Reff M, Carmillo A, Miatkowski K, Amatucci J, Crowell T, Prentice H, Meier W, Violette SM, Mackay F, Yang D, Hoffman R, Browning JL: Targeting the lymphotoxin-beta receptor with agonist antibodies as a potential cancer therapy. Cancer Res; 2006 Oct 1;66(19):9617-24
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  • [Title] Targeting the lymphotoxin-beta receptor with agonist antibodies as a potential cancer therapy.
  • In a syngeneic colon carcinoma tumor model, treatment of the tumor-bearing mice with an agonistic antibody against murine LT beta R caused increased lymphocyte infiltration and necrosis of the tumor.
  • A pattern of differential gene expression predictive of cellular and xenograft response to LT beta R activation was identified in a panel of colon carcinoma cell lines and when applied to a panel of clinical colorectal tumor samples indicated 35% likelihood a tumor response to CBE11.
  • Consistent with this estimate, CBE11 decreased tumor size and/or improved long-term animal survival with two of six independent orthotopic xenografts prepared from surgical colorectal carcinoma samples.
  • Targeting of LT beta R with agonistic mAbs offers a novel approach to the treatment of colorectal and potentially other types of cancers.
  • [MeSH-major] Adenocarcinoma / therapy. Antibodies, Monoclonal / therapeutic use. Colonic Neoplasms / therapy. Lymphotoxin beta Receptor / agonists. Uterine Cervical Neoplasms / therapy
  • [MeSH-minor] Animals. Camptothecin / analogs & derivatives. Camptothecin / therapeutic use. Cell Line, Tumor. Combined Modality Therapy. Drug Synergism. Female. Gene Expression Regulation, Neoplastic / drug effects. Humans. Immunoglobulin G / immunology. Immunoglobulin G / therapeutic use. Immunoglobulin M / immunology. Immunoglobulin M / therapeutic use. Lymphocytes, Tumor-Infiltrating / immunology. Mice. Mice, Inbred BALB C. Mice, Nude. Random Allocation. Recombinant Fusion Proteins / immunology. Recombinant Fusion Proteins / therapeutic use. Single-Blind Method. Xenograft Model Antitumor Assays

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  • (PMID = 17018619.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Immunoglobulin G; 0 / Immunoglobulin M; 0 / Ltbr protein, mouse; 0 / Lymphotoxin beta Receptor; 0 / Recombinant Fusion Proteins; 7673326042 / irinotecan; XT3Z54Z28A / Camptothecin
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25. Kirikoshi H, Katoh M: Expression and regulation of WNT10B in human cancer: up-regulation of WNT10B in MCF-7 cells by beta-estradiol and down-regulation of WNT10B in NT2 cells by retinoic acid. Int J Mol Med; 2002 Oct;10(4):507-11
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  • We have previously cloned and characterized the human orthologue of mouse proto-oncogene Wnt-10b using bioinformatics and cDNA-PCR.
  • WNT10B mRNA was expressed in the majority of squamous cell carcinoma cell lines derived from esophageal cancer and cervical cancer.
  • WNT10B mRNA was relatively highly expressed in TE3, TE6, TE10, TE11 (esophageal cancer), Hs700T (pancreatic cancer), SKG-IIIa, HeLa S3 (cervical cancer), and T-47D (breast cancer).
  • [MeSH-major] Estradiol / pharmacology. Gene Expression Regulation, Neoplastic / drug effects. Proto-Oncogene Proteins / genetics. Tretinoin / pharmacology
  • [MeSH-minor] Breast Neoplasms / drug therapy. Cell Line. Down-Regulation. Humans. Neoplasms, Germ Cell and Embryonal / drug therapy. Up-Regulation. Wnt Proteins

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  • (PMID = 12239602.001).
  • [ISSN] 1107-3756
  • [Journal-full-title] International journal of molecular medicine
  • [ISO-abbreviation] Int. J. Mol. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Proto-Oncogene Proteins; 0 / WNT10B protein, human; 0 / Wnt Proteins; 4TI98Z838E / Estradiol; 5688UTC01R / Tretinoin
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26. Zhou S, Kestell P, Baguley BC, Paxton JW: 5,6-dimethylxanthenone-4-acetic acid (DMXAA): a new biological response modifier for cancer therapy. Invest New Drugs; 2002 Aug;20(3):281-95
The Lens. Cited by Patents in .

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  • [Title] 5,6-dimethylxanthenone-4-acetic acid (DMXAA): a new biological response modifier for cancer therapy.
  • The investigational anti-cancer drug 5,6-dimethylxanthenone-4-acetic acid (DMXAA) was developed by the Auckland Cancer Society Research Centre (ACSRC).
  • As a biological response modifier, pharmacological and toxicological properties of DMXAA are remarkably different from most conventional chemotherapeutic agents.
  • In contrast to FAA that did not show anti-tumour activity in cancer patients, DMXAA (22 mg/kg by intravenous infusion over 20 min) resulted in partial response in one patient with metastatic cervical squamous carcinoma in a Phase I study where 65 cancer patients were enrolled in New Zealand.
  • The maximum tolerated dose (MTD) in mouse, rabbit, rat and human was 30, 99, 330, and 99 mg/kg respectively.
  • The plasma protein binding and distribution into blood cells of DMXAA are dependent on species and drug concentration.
  • Species differences in DMXAA plasma pharmacokinetics have been observed, with the rabbit having the greatest plasma clearance, followed by the human, rat and mouse.
  • Co-administration of DMXAA with other drugs has been shown to result in enhanced anti-tumour activity and alterations in pharmacokinetics, as reported for the combination of DMXAA with melphalan, thalidomide, cyproheptadine, and the bioreductive agent tirapazamine, in mouse models.
  • Co-administration of thalidomide significantly increased the plasma area of the plasma concentration-time curve (AUC) of DMXAA in mice, but had no effect on DMXAA's pharmacokinetics in the rat.
  • It appears that the pharmacological and toxicological properties of DMXAA as a new biological response modifier are unlikely to be predicted based on preclinical studies.
  • However, preclinical studies of DMXAA-drug combinations indicate that DMXAA may have a potential role in cancer treatment when co-administered with other drugs.
  • Further studies are required to explore the molecular targets of DMXAA and mechanisms for the interactions with other drugs co-administered during combination treatment, which may allow for the optimisation of DMXAA-based chemotherapy.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Immunologic Factors / pharmacology. Neoplasms / drug therapy. Xanthenes / pharmacology. Xanthones
  • [MeSH-minor] Animals. Drug Interactions. Humans

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  • (PMID = 12201491.001).
  • [ISSN] 0167-6997
  • [Journal-full-title] Investigational new drugs
  • [ISO-abbreviation] Invest New Drugs
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Immunologic Factors; 0 / Xanthenes; 0 / Xanthones; 0829J8133H / vadimezan
  • [Number-of-references] 75
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27. Morré DM, Morré DJ: Anticancer activity of grape and grape skin extracts alone and combined with green tea infusions. Cancer Lett; 2006 Jul 18;238(2):202-9
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

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  • Grapes and grape extracts were compared for inhibition of a growth-related and cancer-specific form of cell surface NADH oxidase with protein disulfide-thiol interchange activity designated tNOX from human cervical carcinoma (HeLa) cells and growth of HeLa and mouse mammary 4T1 cells in culture and transplanted tumors in mice.
  • [MeSH-minor] Animals. Female. HeLa Cells. Humans. Mammary Neoplasms, Experimental / drug therapy. Mice. Mice, Inbred BALB C. NADH, NADPH Oxidoreductases / antagonists & inhibitors

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  • (PMID = 16129553.001).
  • [ISSN] 0304-3835
  • [Journal-full-title] Cancer letters
  • [ISO-abbreviation] Cancer Lett.
  • [Language] eng
  • [Grant] United States / NCCIH NIH HHS / AT / P50 AT00477
  • [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] Ireland
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 0 / Plant Extracts; 0 / Tea; EC 1.6.- / NADH, NADPH Oxidoreductases; EC 1.6.- / tumor-associated NADH oxidase
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28. Wiewrodt R, Amin K, Kiefer M, Jovanovic VP, Kapoor V, Force S, Chang M, Lanuti M, Black ME, Kaiser LR, Albelda SM: Adenovirus-mediated gene transfer of enhanced Herpes simplex virus thymidine kinase mutants improves prodrug-mediated tumor cell killing. Cancer Gene Ther; 2003 May;10(5):353-64
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  • The Herpes simplex virus 1 (HSV) thymidine kinase (tk) suicide gene together with ganciclovir (GCV) have been successfully used for the in vivo treatment of various solid tumors and for the ablation of unwanted transfused stem cells in recent clinical trials.
  • With the aim of improving this therapeutic system, we compared the potential efficacy of adenoviral (Ad) vectors expressing enhanced tk mutants in vitro and in vivo.
  • Cells expressing the two TK mutants were two-to-five-fold more sensitive to GCV when compared with Ad.HSV-tk transduced cells in all cell lines tested (five human mesotheliomas, one human lung cancer, a human cervical carcinoma, a mouse fibrosarcoma, and a rat glioma line) at equal TK expression levels.
  • The use of adenovirus-mediated gene transfer of both tk mutants dm30-tk and sr39-tk for cancer suicide gene therapy should provide a more effective and safer alternative to wild-type HSV-tk.
  • [MeSH-major] Adenoviridae / genetics. Herpesvirus 1, Human / enzymology. Neoplasms / pathology. Prodrugs / therapeutic use. Thymidine Kinase / genetics
  • [MeSH-minor] Animals. Antiviral Agents / pharmacology. Apoptosis / drug effects. Binding Sites. Female. Ganciclovir / pharmacology. Gene Transfer Techniques. Genes, Transgenic, Suicide. Genetic Vectors. Humans. Mice. Mice, Inbred BALB C. Mice, SCID. Mutagenesis. Rats. Transfection. Tumor Cells, Cultured. Xenograft Model Antitumor Assays

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  • (PMID = 12719705.001).
  • [ISSN] 0929-1903
  • [Journal-full-title] Cancer gene therapy
  • [ISO-abbreviation] Cancer Gene Ther.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA85939; United States / PHS HHS / / P01 66726; United States / NCI NIH HHS / CA / P50-CA-83638
  • [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 / Antiviral Agents; 0 / Prodrugs; EC 2.7.1.21 / Thymidine Kinase; P9G3CKZ4P5 / Ganciclovir
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29. Hausner SH, Abbey CK, Bold RJ, Gagnon MK, Marik J, Marshall JF, Stanecki CE, Sutcliffe JL: Targeted in vivo imaging of integrin alphavbeta6 with an improved radiotracer and its relevance in a pancreatic tumor model. Cancer Res; 2009 Jul 15;69(14):5843-50
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  • The cell surface receptor alpha(v)beta(6) is epithelial specific, and its expression is tightly regulated; it is low or undetectable in adult tissues but has been shown to be increased in many different cancers, including pancreatic, cervical, lung, and colon cancers.
  • We have recently shown the feasibility of imaging alpha(v)beta(6) in vivo by positron emission tomography (PET) using the peptide [(18)F]FBA-A20FMDV2.
  • Here, we describe improved alpha(v)beta(6) imaging agents and test their efficacy in a mouse model with endogenous alpha(v)beta(6) expression.
  • In vivo studies using either a melanoma cell line (transduced alpha(v)beta(6) expression) or the BxPC-3 human pancreatic carcinoma cell line (endogenous alpha(v)beta(6) expression) revealed that the modified compounds showed significantly improved tumor retention.
  • Pancreatic ductal adenocarcinoma is highly metastatic and current preoperative evaluation of resectability using noninvasive imaging has limited success, with most patients having metastases at time of surgery.
  • The fact that these tumors express alpha(v)beta(6) suggests that this probe has significant potential for the in vivo detection of this malignancy, thus having important implications for patient care and therapy.

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  • (PMID = 19549907.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA107792-02; United States / NCI NIH HHS / CA / R21 CA107792; United States / NCI NIH HHS / CA / R21 CA107792-02
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Benzoates; 0 / Fluorine Radioisotopes; 0 / Integrins; 0 / Radiopharmaceuticals; 0 / Viral Proteins; 0 / integrin alphavbeta6; V5ROO2HOU4 / 4-fluorobenzoic acid
  • [Other-IDs] NLM/ NIHMS117292; NLM/ PMC2711989
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30. Jain RK, Lahdenranta J, Fukumura D: Targeting PDGF signaling in carcinoma-associated fibroblasts controls cervical cancer in mouse model. PLoS Med; 2008 Jan 29;5(1):e24
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  • [Title] Targeting PDGF signaling in carcinoma-associated fibroblasts controls cervical cancer in mouse model.

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  • [CommentOn] PLoS Med. 2008 Jan 29;5(1):e19 [18232728.001]
  • (PMID = 18232729.001).
  • [ISSN] 1549-1676
  • [Journal-full-title] PLoS medicine
  • [ISO-abbreviation] PLoS Med.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P01 CA080124; United States / NCI NIH HHS / CA / R01 CA096915; United States / NCI NIH HHS / CA / CA80124; United States / NCI NIH HHS / CA / CA96915
  • [Publication-type] Comment; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Neoplasm Proteins; 0 / Piperazines; 0 / Platelet-Derived Growth Factor; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Receptors, Platelet-Derived Growth Factor
  • [Other-IDs] NLM/ PMC2214795
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