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Items 1 to 37 of about 37
1. Goto T, Tomizawa N, Kobayashi E, Fujimura A: A comparative pharmacology study between the intracolonic and oral routes of 5-FU administration in a colon cancer-bearing Yoshida sarcoma rat model. J Pharmacol Sci; 2004 Jun;95(2):163-73
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  • [Title] A comparative pharmacology study between the intracolonic and oral routes of 5-FU administration in a colon cancer-bearing Yoshida sarcoma rat model.
  • We prepared a colon cancer-bearing Yoshida sarcoma rat model to examine the dose-response relationship of antitumor activity of intracolonically or orally administered 5-fluorouracil (5-FU; 45, 30, 20, 13, and 8 mg/kg).
  • Regarding the time-course of body weight, even the 5-FU highest dose (45 mg/kg) intracolonic administration group showed no inhibited body weight increase compared to the control group.
  • [MeSH-major] Antimetabolites, Antineoplastic / administration & dosage. Antimetabolites, Antineoplastic / therapeutic use. Colonic Neoplasms / drug therapy. Fluorouracil / administration & dosage. Fluorouracil / therapeutic use. Sarcoma, Yoshida / drug therapy
  • [MeSH-minor] Administration, Oral. Animals. Blood Cell Count. Body Weight / drug effects. Catheterization. Colon. Dose-Response Relationship, Drug. Hemoglobins / metabolism. Male. Neoplasm Transplantation. Rats

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  • (PMID = 15215640.001).
  • [ISSN] 1347-8613
  • [Journal-full-title] Journal of pharmacological sciences
  • [ISO-abbreviation] J. Pharmacol. Sci.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0 / Hemoglobins; U3P01618RT / Fluorouracil
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2. Katoh R, Ooshiro M: Enhancement of antitumor effect of tegafur/uracil (UFT) plus leucovorin by combined treatment with protein-bound polysaccharide, PSK, in mouse models. Cell Mol Immunol; 2007 Aug;4(4):295-9
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  • [Title] Enhancement of antitumor effect of tegafur/uracil (UFT) plus leucovorin by combined treatment with protein-bound polysaccharide, PSK, in mouse models.
  • We evaluated the antitumor effect of combined therapy with tegafur/uracil (UFT) plus leucovorin (LV) (UFT/LV) and protein-bound polysaccharide, PSK, in three mouse models of transplantable tumors.
  • UFT/LV showed antitumor effect against Meth A sarcoma, and the antitumor effect was enhanced when PSK given concomitantly.
  • Colon 26 carcinoma was weakly responsive to UFT/LV, and no enhancement of antitumor effect was found even PSK was used in combination.
  • [MeSH-minor] Animals. Carcinoma, Lewis Lung / drug therapy. Colonic Neoplasms / drug therapy. Drug Therapy, Combination. Female. Male. Mice. Mice, Inbred BALB C. Mice, Inbred C57BL. Sarcoma / drug therapy. Xenograft Model Antitumor Assays

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  • (PMID = 17764620.001).
  • [ISSN] 1672-7681
  • [Journal-full-title] Cellular & molecular immunology
  • [ISO-abbreviation] Cell. Mol. Immunol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Proteoglycans; 1548R74NSZ / Tegafur; 56HH86ZVCT / Uracil; 66455-27-4 / krestin; Q573I9DVLP / Leucovorin
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3. Fang J, Sawa T, Akaike T, Akuta T, Sahoo SK, Khaled G, Hamada A, Maeda H: In vivo antitumor activity of pegylated zinc protoporphyrin: targeted inhibition of heme oxygenase in solid tumor. Cancer Res; 2003 Jul 1;63(13):3567-74
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  • Pharmacokinetic analysis revealed that PEG-ZnPP-administered i.v. had a circulation time in blood that was 40 times longer than that for nonpegylated ZnPP.
  • More important, PEG-ZnPP preferentially accumulated in solid tumor tissue in a murine model.
  • In vivo treatment with PEG-ZnPP (equivalent to 1.5 or 5 mg of ZnPP/kg, i.v., injected daily for 6 days) remarkably suppressed the growth of Sarcoma 180 tumors implanted in the dorsal skin of ddY mice without any apparent side effects.
  • In addition, this PEG-ZnPP treatment produced tumor-selective suppression of HO activity as well as induction of apoptosis.
  • The major reason for tumor-selective targeting of PEG-ZnPP is attributed to the enhanced permeability and retention effect that is observed commonly in solid tumors for biocompatible macromolecular drugs.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Colonic Neoplasms / drug therapy. Enzyme Inhibitors / therapeutic use. Heme Oxygenase (Decyclizing) / antagonists & inhibitors. Metalloporphyrins / therapeutic use. Polyethylene Glycols / therapeutic use
  • [MeSH-minor] Animals. Apoptosis / drug effects. Heme Oxygenase-1. Humans. In Situ Nick-End Labeling. Male. Membrane Proteins. Mice. Mice, Inbred Strains. Sarcoma, Experimental / drug therapy. Sarcoma, Experimental / pathology. Transplantation, Heterologous. Tumor Cells, Cultured

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  • (PMID = 12839943.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Enzyme Inhibitors; 0 / Membrane Proteins; 0 / Metalloporphyrins; 0 / pegylated zinc protoporphyrin; 30IQX730WE / Polyethylene Glycols; EC 1.14.99.3 / HMOX1 protein, human; EC 1.14.99.3 / Heme Oxygenase (Decyclizing); EC 1.14.99.3 / Heme Oxygenase-1; EC 1.14.99.3 / Hmox1 protein, mouse
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4. Lin CH, Wu KH, Lin WC, Tsai JD, Peng CT, Chen AC: Granulocytic sarcoma of the colon in a child with acute myeloid leukemia presenting as hematochezia. J Pediatr Hematol Oncol; 2008 Dec;30(12):981-3
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  • [Title] Granulocytic sarcoma of the colon in a child with acute myeloid leukemia presenting as hematochezia.
  • Granulocytic sarcoma (GS), an extramedullary myeloid tumor composed of immature cells of the granulocytic series, can occur in patients with acute myeloid leukemia (AML), myelodysplastic syndrome, or chronic myelogenous leukemia.
  • It can occur in any organ or tissue, but the most common involved areas are the skin, bone/spine, and lymph nodes.
  • However, its occurrence in the gastrointestinal tract is relatively rare, and is especially rare in the colon in adults.
  • No case of GS involving the colon in children has ever been reported.
  • We report here an extremely rare case of GS in the colon of a 10-year-old boy with AML presenting with hematochezia.
  • Colonic GS was diagnosed by colonofiberscopic biopsy.
  • His hematochezia responded rapidly to induction chemotherapy and the patient remained in complete remission after 3-month follow-up.
  • In conclusion, hematochezia may be due to colonic involvement of GS, which should be considered in the differentials in addition to thrombocytopenia, as it is usually encountered in AML patients.
  • [MeSH-major] Colonic Neoplasms / complications. Gastrointestinal Hemorrhage / complications. Gastrointestinal Hemorrhage / diagnosis. Leukemia, Myeloid, Acute / complications. Neoplasms, Multiple Primary / pathology. Sarcoma, Myeloid / complications


5. Sarti M, Sevignani C, Calin GA, Aqeilan R, Shimizu M, Pentimalli F, Picchio MC, Godwin A, Rosenberg A, Drusco A, Negrini M, Croce CM: Adenoviral transduction of TESTIN gene into breast and uterine cancer cell lines promotes apoptosis and tumor reduction in vivo. Clin Cancer Res; 2005 Jan 15;11(2 Pt 1):806-13
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  • EXPERIMENTAL DESIGN: We have analyzed the expression of TES gene in a panel of 25 breast tumors and 17 cell lines of breast, colon, and uterine cancers.
  • Furthermore, to evaluate the potential of TES gene therapy, we studied the effects of adenoviral TES transduction (Ad-TES) in cell lines with undetectable TES expression (T47D and MES-SA) as well as in MCF-7 cell line where TES expression is normal.
  • RESULTS: Twenty-five percent of primary breast tumor samples as well as the breast cancer cell line T47D and the uterine sarcoma cell line MES-SA were negative or displayed low levels of TES.
  • CONCLUSIONS: Ad-TES expression inhibit the growth of breast and uterine cancer cells lacking of TES expression through caspase-dependent and caspase-independent apoptosis, respectively, suggesting that Ad-TES infection should be explored as a therapeutic strategy.
  • [MeSH-major] Apoptosis / drug effects. Breast Neoplasms / therapy. Colonic Neoplasms / therapy. Homeodomain Proteins / therapeutic use. Transduction, Genetic. Tumor Suppressor Proteins / therapeutic use. Uterine Neoplasms / therapy
  • [MeSH-minor] Adenoviridae / genetics. Animals. Caspases / metabolism. Cytoskeletal Proteins. Female. Genetic Vectors. Green Fluorescent Proteins. Humans. LIM Domain Proteins. Mice. Mice, Nude. Sarcoma, Experimental / genetics. Sarcoma, Experimental / metabolism. Sarcoma, Experimental / therapy. Tumor Cells, Cultured. Xenograft Model Antitumor Assays

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  • (PMID = 15701871.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA 56336; United States / NCI NIH HHS / CA / CA 77738
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cytoskeletal Proteins; 0 / Homeodomain Proteins; 0 / LIM Domain Proteins; 0 / TES protein, human; 0 / Tumor Suppressor Proteins; 147336-22-9 / Green Fluorescent Proteins; EC 3.4.22.- / Caspases
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6. Morinaga Y, Suga Y, Ehara S, Harada K, Nihei Y, Suzuki M: Combination effect of AC-7700, a novel combretastatin A-4 derivative, and cisplatin against murine and human tumors in vivo. Cancer Sci; 2003 Feb;94(2):200-4
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  • The combination of AC-7700 and CDDP increased antitumor activity against murine colon 26 tumor in mice and cured the mice.
  • To study this combination effect, we measured the concentrations of CDDP in tumors, plasma and kidneys of the mice with colon 26 tumor.
  • These results suggest that AC-7700 may specifically augment the accumulation of CDDP in tumors, and thus has the potential to be useful in combination chemotherapy with CDDP.
  • [MeSH-major] Adenocarcinoma / drug therapy. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Colonic Neoplasms / drug therapy. Lung Neoplasms / drug therapy. Sarcoma 180 / drug therapy. Serine / analogs & derivatives
  • [MeSH-minor] Animals. Body Weight / drug effects. Cisplatin / administration & dosage. Cisplatin / pharmacokinetics. Drug Administration Schedule. Humans. Mice. Mice, Inbred ICR. Mice, Nude. Tumor Cells, Cultured / drug effects. Xenograft Model Antitumor Assays

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  • (PMID = 12708497.001).
  • [ISSN] 1347-9032
  • [Journal-full-title] Cancer science
  • [ISO-abbreviation] Cancer Sci.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / AC 7700; 452VLY9402 / Serine; Q20Q21Q62J / Cisplatin
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7. Tejeda M, Gaál D, Hullán L, Hegymegi-Barakonyi B, Kéri G: Evaluation of the antitumor efficacy of the somatostatin structural derivative TT-232 on different tumor models. Anticancer Res; 2006 Sep-Oct;26(5A):3477-83
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  • The effects of TT-232 by different routes of administration and treatment schedules were studied in various types of rodent and human xenograft tumor models.
  • In the rodent tumor models S-180 sarcoma and P-388 lymphoid leukemia tumor the infusion treatment resulted in 76%-100% tumor growth inhibition and in 20%-60% of the mice being long-term and tumor-free survivors.
  • In the aggressive C-26 colon carcinoma and MXT breast carcinoma, the TT-232 treatments resulted in 71%-75% tumor growth inhibition and an approximately 50% increased survival time.
  • In our study, the route of infusion was shown to increase drug efficacy relative to conventional delivery methods.
  • [MeSH-major] Colonic Neoplasms / drug therapy. Leukemia P388 / drug therapy. Mammary Neoplasms, Experimental / drug therapy. Peptides, Cyclic / therapeutic use. Sarcoma 180 / drug therapy
  • [MeSH-minor] Animals. Dose-Response Relationship, Drug. Drug Administration Schedule. Drug Screening Assays, Antitumor. HL-60 Cells. HT29 Cells. Humans. Male. Melanoma / drug therapy. Mice. Mice, Inbred Strains. Prostatic Neoplasms / drug therapy. Somatostatin / analogs & derivatives. Transplantation, Heterologous. Tumor Cells, Cultured

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  • (PMID = 17094470.001).
  • [ISSN] 0250-7005
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Peptides, Cyclic; 0 / TT2-32; 51110-01-1 / Somatostatin
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8. Bosincu L, Massarelli G, Cossu Rocca P, Isaac MA, Nogales FF: Rectal endometrial stromal sarcoma arising in endometriosis: report of a case. Dis Colon Rectum; 2001 Jun;44(6):890-2
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  • [Title] Rectal endometrial stromal sarcoma arising in endometriosis: report of a case.
  • PURPOSE: Endometriosis of the rectovaginal septum can harbor different types of secondary tumors that may involve the rectal wall and protrude into its lumen, thus making diagnosis difficult.
  • Extrauterine low-grade endometrial stromal sarcoma may rarely arise in endometriosis.
  • Laparotomy revealed a large pelvic mass involving the rectovaginal septum and the colonic wall and which protruded into the lumen forming endoluminal polypoid masses.
  • Histopathologically, primary endometriotic foci were found in close relationship with an endometrial stromal sarcoma which invaded the rectal wall.
  • The patient was treated by surgery and subsequent chemotherapy and was alive and well 20 months later.
  • [MeSH-major] Endometrial Neoplasms / etiology. Endometriosis / complications. Sarcoma / etiology

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  • (PMID = 11391154.001).
  • [ISSN] 0012-3706
  • [Journal-full-title] Diseases of the colon and rectum
  • [ISO-abbreviation] Dis. Colon Rectum
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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9. Svrcek M, Tiret E, Bennis M, Guyot P, Fléjou JF: KSHV/HHV8-associated intestinal Kaposi's sarcoma in patient with ulcerative colitis receiving immunosuppressive drugs: report of a case. Dis Colon Rectum; 2009 Jan;52(1):154-8
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  • [Title] KSHV/HHV8-associated intestinal Kaposi's sarcoma in patient with ulcerative colitis receiving immunosuppressive drugs: report of a case.
  • Kaposi sarcoma-associated herpesvirus (KSHV), also known as human herpesvirus 8 (HHV8), has been identified in all four forms of Kaposi's sarcoma (classic, endemic, HIV-associated and iatrogenic).
  • We report the rare case of an intestinal (small intestine and rectosigmoid) Kaposi's sarcoma in a 62-year-old HIV-negative man with ulcerative colitis.
  • This patient was receiving immunosuppressive therapy with steroids and azathioprine.
  • To date, the causative role of KSHV/HHV8 in the pathophysiology of Kaposi's sarcoma associated with ulcerative colitis has only been proven for cutaneous lesions but not for intestinal lesions of Kaposi's sarcoma.
  • We report for the first time, the expression of HHV8 (by using immunohistochemistry) in colonic Kaposi's sarcoma in a patient with an ulcerative colitis-related tumor.
  • At laparotomy, numerous Kaposi's sarcoma lesions were found in the small intestine, which were left in situ.
  • Forty months after surgery and following withdrawal of immunosuppressive therapy, the patient had no evidence of any disease and a normal abdominal and thoracic CT scan.
  • Cases of colorectal Kaposi's sarcoma complicating inflammatory bowel disease should be managed with a conservative approach and discontinuation of the immunosuppressive treatment.
  • However, discontinuation of the immunosuppression is not always possible and in those cases chemotherapy may be indicated.
  • [MeSH-major] Colitis, Ulcerative / drug therapy. Colorectal Neoplasms / complications. Herpesvirus 8, Human. Immunosuppressive Agents / therapeutic use. Sarcoma, Kaposi / complications. Sarcoma, Kaposi / virology

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  • (PMID = 19273971.001).
  • [ISSN] 1530-0358
  • [Journal-full-title] Diseases of the colon and rectum
  • [ISO-abbreviation] Dis. Colon Rectum
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Immunosuppressive Agents
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10. Hori T, Kondo T, Kanamori M, Tabuchi Y, Ogawa R, Zhao QL, Ahmed K, Yasuda T, Seki S, Suzuki K, Kimura T: Nutlin-3 enhances tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-induced apoptosis through up-regulation of death receptor 5 (DR5) in human sarcoma HOS cells and human colon cancer HCT116 cells. Cancer Lett; 2010 Jan 1;287(1):98-108
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  • [Title] Nutlin-3 enhances tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-induced apoptosis through up-regulation of death receptor 5 (DR5) in human sarcoma HOS cells and human colon cancer HCT116 cells.
  • Recently, nutlins, small-molecule antagonists of MDM2, have been developed to inhibit the p53-MDM2 interaction and activate p53 signaling.
  • In this study, the combined effects of nutlin-3 and TRAIL on apoptosis were investigated in HOS and HCT116 cells, which express wild-type p53.
  • These results indicate that the combination, treated with nutlin-3 and TRAIL, is useful for apoptosis induction in malignant cells expressing wild-type p53.
  • [MeSH-major] Apoptosis / drug effects. Colonic Neoplasms / drug therapy. Imidazoles / pharmacology. Piperazines / pharmacology. Receptors, TNF-Related Apoptosis-Inducing Ligand / genetics. TNF-Related Apoptosis-Inducing Ligand / pharmacology
  • [MeSH-minor] CASP8 and FADD-Like Apoptosis Regulating Protein / analysis. Caspase 3 / metabolism. Cell Survival / drug effects. Cyclin-Dependent Kinase Inhibitor p21 / analysis. Drug Synergism. HCT116 Cells. Humans. Metalloproteases / analysis. Promoter Regions, Genetic. Proto-Oncogene Proteins c-mdm2 / analysis. Tumor Suppressor Protein p53 / analysis. Up-Regulation

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  • [Copyright] Copyright 2009 Elsevier Ireland Ltd. All rights reserved.
  • (PMID = 19577358.001).
  • [ISSN] 1872-7980
  • [Journal-full-title] Cancer letters
  • [ISO-abbreviation] Cancer Lett.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / CASP8 and FADD-Like Apoptosis Regulating Protein; 0 / CDKN1A protein, human; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / Imidazoles; 0 / Piperazines; 0 / Receptors, TNF-Related Apoptosis-Inducing Ligand; 0 / TNF-Related Apoptosis-Inducing Ligand; 0 / Tumor Suppressor Protein p53; 0 / nutlin 3; EC 3.4.- / Metalloproteases; EC 3.4.22.- / Caspase 3; EC 6.3.2.19 / MDM2 protein, human; EC 6.3.2.19 / Proto-Oncogene Proteins c-mdm2
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11. Jung KO, Park SY, Park KY: Longer aging time increases the anticancer and antimetastatic properties of doenjang. Nutrition; 2006 May;22(5):539-45
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  • [Title] Longer aging time increases the anticancer and antimetastatic properties of doenjang.
  • This study investigated the effects of fermentation time of doenjang on its inhibitory activity against solid tumor formation and lung metastasis.
  • METHODS: Effects of methanol extracts from doenjang prepared with long-term fermentation on tumor formation, natural killer cell activity in spleen, and glutathione S-transferase activity in liver were investigated in sarcoma-180 cell-transplanted mice.
  • Inhibitory effects of these samples on lung metastasis of colon 26-M3.1 cells were also evaluated in Balb/c mice.
  • RESULTS: Doenjang fermented for 24 mo exhibited a two- to three-fold increase in antitumor effects on sarcoma-180-injected mice and antimetastatic effects in colon 26-M 3.1 cells in mice compared with the 3- or 6-mo fermented doenjang.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Colonic Neoplasms / secondary. Food Handling / methods. Lung Neoplasms / drug therapy. Neoplasm Metastasis / prevention & control. Soy Foods
  • [MeSH-minor] Animals. Cell Transplantation. Female. Fermentation. Glutathione Transferase / metabolism. Korea. Liver / enzymology. Male. Mice. Mice, Inbred BALB C. Sarcoma 180. Time Factors. Tumor Cells, Cultured

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  • (PMID = 16504476.001).
  • [ISSN] 0899-9007
  • [Journal-full-title] Nutrition (Burbank, Los Angeles County, Calif.)
  • [ISO-abbreviation] Nutrition
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; EC 2.5.1.18 / Glutathione Transferase
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12. Yamakawa S, Asai T, Uchida T, Matsukawa M, Akizawa T, Oku N: (-)-Epigallocatechin gallate inhibits membrane-type 1 matrix metalloproteinase, MT1-MMP, and tumor angiogenesis. Cancer Lett; 2004 Jul 8;210(1):47-55
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  • [Title] (-)-Epigallocatechin gallate inhibits membrane-type 1 matrix metalloproteinase, MT1-MMP, and tumor angiogenesis.
  • Membrane-type 1 matrix metalloproteinase (MT1-MMP), which hydrolyzes type I collagen and activates MMP-2, are deeply involved in angiogenesis as well as in tumor cell invasion and metastasis.
  • Finally, we observed that both colon 26 NL17 carcinoma and Meth A sarcoma growth was suppressed in these tumor-bearing mice by EGCG administration, at least partly though the inhibition of angiogenesis.
  • [MeSH-major] Antineoplastic Agents, Phytogenic / therapeutic use. Catechin / analogs & derivatives. Catechin / therapeutic use. Colonic Neoplasms / blood supply. Metalloendopeptidases / antagonists & inhibitors. Neovascularization, Pathologic / drug therapy. Sarcoma, Experimental / blood supply
  • [MeSH-minor] Angiogenesis Inhibitors / pharmacology. Animals. Cell Division / drug effects. Cell Movement / drug effects. Endothelium, Vascular / drug effects. Endothelium, Vascular / enzymology. Endothelium, Vascular / ultrastructure. Humans. Matrix Metalloproteinase 14. Matrix Metalloproteinases, Membrane-Associated. Methylcholanthrene. Mice. Tumor Cells, Cultured. Umbilical Veins. Urokinase-Type Plasminogen Activator / antagonists & inhibitors

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  • [Copyright] Copyright 2004 Elsevier Ireland Ltd.
  • (PMID = 15172120.001).
  • [ISSN] 0304-3835
  • [Journal-full-title] Cancer letters
  • [ISO-abbreviation] Cancer Lett.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Antineoplastic Agents, Phytogenic; 0 / Mmp14 protein, mouse; 56-49-5 / Methylcholanthrene; 8R1V1STN48 / Catechin; BQM438CTEL / epigallocatechin gallate; EC 3.4.21.73 / Urokinase-Type Plasminogen Activator; EC 3.4.24.- / Matrix Metalloproteinases, Membrane-Associated; EC 3.4.24.- / Metalloendopeptidases; EC 3.4.24.80 / Matrix Metalloproteinase 14
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13. Reynolds JT, Reinke D, Weiler S: Irradiated haploidetical donor lymphocytes: A different approach to the immunotherapy of advanced solid tumors. J Clin Oncol; 2004 Jul 15;22(14_suppl):2573

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  • The basic concept of this treatment is to grow cytotoxic T-cells and helper T-cells against the tumor in the patients themselves rather than in the laboratory.
  • Standard chemotherapy is used to generate the tumor antigen, as the tumor cells undergo apoptosis.
  • The treatment is based on a murine leukemia model.
  • METHODS: All patients had painful bulky heavily pre-treated cancer, rapidly progressive despite salvage therapy.
  • Treatment consisted of intravenous VP-16 100 mg/m<sup>2</sup>/d plus cyclosporine 1 mg/kg/d for three days followed by GM-CSF 500 μgr/d s.q. for 5 days.
  • IL-2 is also given s.q. three times a week at a starting dose of 10x10<sup>6</sup> IU/m<sup>2</sup>.
  • RESULTS: Patients with clear cell sarcoma, colon and small lung cancer have been enrolled.
  • A large delayed type hypersensitivity (DTH) reaction occurs at the site of IL-2 injection.
  • The patient with lung cancer is again in clinical remission with further weekly IL-2 and chemotherapy and an even larger DTH reaction.

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  • (PMID = 28015302.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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14. Correale P, Del Vecchio MT, La Placa M, Montagnani F, Di Genova G, Savellini GG, Terrosi C, Mannucci S, Giorgi G, Francini G, Cusi MG: Chemotherapeutic drugs may be used to enhance the killing efficacy of human tumor antigen peptide-specific CTLs. J Immunother; 2008 Feb-Mar;31(2):132-47
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  • [Title] Chemotherapeutic drugs may be used to enhance the killing efficacy of human tumor antigen peptide-specific CTLs.
  • The effects of anticancer chemotherapy on antigen-specific cytotoxic T lymphocytes (CTLs) are mostly unknown.
  • We tested the effects of cytotoxic drugs such as 5-fluorouracil, gemcitabine, and oxaliplatin on the functional activity of antigen-specific CTL cultures derived from the peripheral blood mononuclear cells of human donors.
  • We found that a biweekly drug-exposure of human HLA-A(*)02.01+ CTLs derived from bulk cultures led to completely different effects if occurring early (day second) or late (day thirteenth) after the in vitro stimulations with the cognate peptides.
  • Results of immunocytofluorimetric studies and CTL/natural killer inhibition assays suggested that the latter effect could be related to a more selective drug-mediated inhibition of cohabitant T regulatory (reg) cells.
  • These results were translated in an in vivo therapeutic mouse model where humanized HLA-A(*)02.01 transgenic mice inoculated with EL-4/humanized HLA-A(*)02.01 transgenic mice showed a prolonged survival and the greatest rate of cure when receiving a combined treatment with a thymidylate synthase-specific peptide vaccine and a multidrug chemotherapy regimen administered late after immunization.
  • Tumor samples derived from this group of mice showed a reduced expression of the target thymidylate synthase antigen, a marked reduction of T(reg)s, and a noteworthy infiltration of C8+ T cells.
  • These results may have clinical implications for the design of new translational anticancer regimens aimed at combining chemotherapy and immunotherapy.
  • [MeSH-major] Antigens, Neoplasm / immunology. Antineoplastic Agents / pharmacology. Cytotoxicity, Immunologic / drug effects. T-Lymphocytes, Cytotoxic / immunology
  • [MeSH-minor] Animals. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cancer Vaccines / immunology. Cancer Vaccines / therapeutic use. Carcinoembryonic Antigen / immunology. Cell Line. Cell Line, Tumor. Colonic Neoplasms / immunology. Colonic Neoplasms / pathology. Deoxycytidine / therapeutic use. Dose-Response Relationship, Drug. Fluorouracil / therapeutic use. HLA-A Antigens / genetics. HLA-A Antigens / immunology. HLA-A2 Antigen. Humans. Interleukin-2 Receptor alpha Subunit / analysis. Leucovorin / therapeutic use. Lymphoma, T-Cell / immunology. Lymphoma, T-Cell / pathology. Lymphoma, T-Cell / therapy. Mice. Mice, Inbred Strains. Mice, Transgenic. Organoplatinum Compounds / therapeutic use. Peptides / immunology. Peptides / pharmacology. Peptides / therapeutic use. Rous sarcoma virus / immunology. Sandfly fever Naples virus / immunology. Survival Analysis. T-Lymphocytes, Regulatory / chemistry. T-Lymphocytes, Regulatory / drug effects. T-Lymphocytes, Regulatory / immunology. Thymidylate Synthase / metabolism

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  • (PMID = 18481383.001).
  • [ISSN] 1524-9557
  • [Journal-full-title] Journal of immunotherapy (Hagerstown, Md. : 1997)
  • [ISO-abbreviation] J. Immunother.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Antineoplastic Agents; 0 / Cancer Vaccines; 0 / Carcinoembryonic Antigen; 0 / HLA-A Antigens; 0 / HLA-A*02:01 antigen; 0 / HLA-A2 Antigen; 0 / Interleukin-2 Receptor alpha Subunit; 0 / Organoplatinum Compounds; 0 / Peptides; 0W860991D6 / Deoxycytidine; EC 2.1.1.45 / Thymidylate Synthase; Q573I9DVLP / Leucovorin; U3P01618RT / Fluorouracil; GOLF protocol
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15. Fabbrini M, Trachsel E, Soldani P, Bindi S, Alessi P, Bracci L, Kosmehl H, Zardi L, Neri D, Neri P: Selective occlusion of tumor blood vessels by targeted delivery of an antibody-photosensitizer conjugate. Int J Cancer; 2006 Apr 1;118(7):1805-13
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  • As a consequence, the doses of chemotherapy necessary to achieve complete tumor eradication are associated with unacceptably high toxicities.
  • By contrast, a photosensitizer conjugate obtained with an antibody of identical pharmacokinetic properties but irrelevant specificity did not exhibit a significant therapeutic effect.
  • These results confirm that vascular targeting strategies, aimed at the selective occlusion/disruption of tumor blood vessels, have a significant anticancer therapeutic potential and encourage the use of antibody-photosensitizer conjugates for the therapy of superficial tumors and possibly other angiogenesis-related pathologies.
  • [MeSH-minor] Adenocarcinoma / blood supply. Adenocarcinoma / drug therapy. Animals. Antibodies. Colonic Neoplasms / blood supply. Colonic Neoplasms / drug therapy. Immunoglobulin Variable Region. Mice. Rats. Regional Blood Flow. Sarcoma / blood supply. Sarcoma / drug therapy. Teratocarcinoma / blood supply. Teratocarcinoma / drug therapy. Transplantation, Heterologous

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  • (PMID = 16217760.001).
  • [ISSN] 0020-7136
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies; 0 / Immunoglobulin Variable Region; 0 / Photosensitizing Agents
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16. Berg K, Dietze A, Kaalhus O, Høgset A: Site-specific drug delivery by photochemical internalization enhances the antitumor effect of bleomycin. Clin Cancer Res; 2005 Dec 1;11(23):8476-85
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  • [Title] Site-specific drug delivery by photochemical internalization enhances the antitumor effect of bleomycin.
  • PURPOSE: Photochemical internalization is under development for improving macromolecular therapy by inducing photochemical damage to endocytic vesicles.
  • This damage leads to the release of therapeutic macromolecules entrapped in endocytic vesicles into the cytosol.
  • The macromolecules may in this way be able to interact with therapeutic targets instead of being degraded by lysosomal hydrolases.
  • Bleomycin is used in several standard cancer chemotherapy regimens.
  • The purpose of this study was to evaluate the therapeutic potential of aluminum phthalocyanine disulfonate (AlPcS2a)-based photochemical delivery of bleomycin.
  • The tumor volume was measured frequently after treatment and the time for the tumor volume to reach 800 to 1,000 mm3 was selected as the end point.
  • RESULTS: The photochemical delivery of bleomycin induced a delayed tumor regrowth, and in two out of three tumor models, lead to 60% complete response, whereas no complete responses were seen after treatment with bleomycin alone.
  • Combination of the photochemical treatment and bleomycin was found to induce a synergistic delay in tumor growth.
  • This treatment combination should be further considered for clinical utilization.
  • [MeSH-major] Antibiotics, Antineoplastic / therapeutic use. Bleomycin / therapeutic use. Colonic Neoplasms / drug therapy. Indoles / therapeutic use. Organometallic Compounds / therapeutic use. Photochemotherapy. Photosensitizing Agents / therapeutic use. Sarcoma, Experimental / drug therapy
  • [MeSH-minor] Aluminum. Animals. Cells, Cultured. Cricetinae. Drug Delivery Systems. Endosomes. Female. Fibroblasts / cytology. Fibroblasts / drug effects. Fibroblasts / metabolism. Humans. Lung / drug effects. Lung / metabolism. Lung / pathology. Mice. Mice, Inbred BALB C. Mice, Nude. Survival Rate. Xenograft Model Antitumor Assays

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  • (PMID = 16322311.001).
  • [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 / Antibiotics, Antineoplastic; 0 / Indoles; 0 / Organometallic Compounds; 0 / Photosensitizing Agents; 11056-06-7 / Bleomycin; 68637-19-4 / aluminum phthalocyanine disulfonate; CPD4NFA903 / Aluminum
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17. Mitsiades N, Yu WH, Poulaki V, Tsokos M, Stamenkovic I: Matrix metalloproteinase-7-mediated cleavage of Fas ligand protects tumor cells from chemotherapeutic drug cytotoxicity. Cancer Res; 2001 Jan 15;61(2):577-81
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  • [Title] Matrix metalloproteinase-7-mediated cleavage of Fas ligand protects tumor cells from chemotherapeutic drug cytotoxicity.
  • Recent evidence suggests that one mechanism whereby cytotoxic drugs, such as doxorubicin, kill tumors is the induction or up-regulation of Fas ligand (FasL) expression on the tumor cell surface.
  • However, despite cytotoxic drug-induced FasL expression, Fas-sensitive tumors frequently resist chemotherapy, suggesting that they may possess a mechanism that prevents or inactivates Fas-FasL interactions.
  • [MeSH-minor] Antigens, CD95 / metabolism. Apoptosis / drug effects. Colonic Neoplasms / metabolism. Colonic Neoplasms / pathology. Colonic Neoplasms / prevention & control. Drug Resistance, Neoplasm. Fas Ligand Protein. Humans. Hydrolysis. Immunoblotting. Sarcoma, Ewing / metabolism. Sarcoma, Ewing / pathology. Sarcoma, Ewing / prevention & control. Signal Transduction / drug effects. Tumor Cells, Cultured / cytology. Tumor Cells, Cultured / drug effects. Tumor Cells, Cultured / metabolism

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  • (PMID = 11212252.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD95; 0 / Antineoplastic Agents; 0 / FASLG protein, human; 0 / Fas Ligand Protein; 0 / Membrane Glycoproteins; 80168379AG / Doxorubicin; EC 3.4.24.23 / Matrix Metalloproteinase 7
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18. Misset JL, Gamelin E, Campone M, Delaloge S, Latz JE, Bozec L, Fumoleau P: Phase I and pharmacokinetic study of the multitargeted antifolate pemetrexed in combination with oxaliplatin in patients with advanced solid tumors. Ann Oncol; 2004 Jul;15(7):1123-9
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  • Up to two previous chemotherapy regimens were allowed.
  • CONCLUSIONS: This pemetrexed-oxaliplatin combination (without vitamin supplementation) every 21 days can be administered using full therapeutic doses of each agent with acceptable tolerability and no overlapping toxicity.

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  • (PMID = 15205208.001).
  • [ISSN] 0923-7534
  • [Journal-full-title] Annals of oncology : official journal of the European Society for Medical Oncology
  • [ISO-abbreviation] Ann. Oncol.
  • [Language] ENG
  • [Publication-type] Clinical Trial; Clinical Trial, Phase I; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Glutamates; 0 / Organoplatinum Compounds; 04Q9AIZ7NO / Pemetrexed; 04ZR38536J / oxaliplatin; 5Z93L87A1R / Guanine
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19. Garin AM, Gorbunova VA, Gershanovich ML, Manziuk LV, Borodkina AG, Breder VV, Karmanovskaia OB, Zubrikhina GN, Madzhuga AV, Zimakova NI, Trapeznikov NN: [Results of a phase I clinical trial of "theraphthal + ascorbic acid" catalytic system]. Vopr Onkol; 2001;47(6):676-9
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  • No side-effects characteristic of antitumor cytostatic drugs were registered.
  • The gravest side-effect ever recorded was a collapse which could not be linked to teraphtal dosage and was probably caused by hypersensitivity to the drug.
  • The drug was recommended for phase II trials.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Indoles / therapeutic use
  • [MeSH-minor] Adrenal Gland Neoplasms / drug therapy. Breast Neoplasms / drug therapy. Colonic Neoplasms / drug therapy. Female. Humans. Kidney Neoplasms / drug therapy. Male. Melanoma / drug therapy. Middle Aged. Sarcoma / drug therapy. Skin Neoplasms / drug therapy. Soft Tissue Neoplasms / drug therapy

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  • (PMID = 11826487.001).
  • [ISSN] 0507-3758
  • [Journal-full-title] Voprosy onkologii
  • [ISO-abbreviation] Vopr Onkol
  • [Language] rus
  • [Publication-type] Clinical Trial; Clinical Trial, Phase I; Comparative Study; English Abstract; Journal Article
  • [Publication-country] Russia
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Indoles; 0 / theraphthal
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20. Manuelli M, De Luca L, Iaria G, Tatangelo P, Sforza D, Perrone L, Bellini MI, Angelico R, Anselmo A, Tisone G: Conversion to rapamycin immunosuppression for malignancy after kidney transplantation. Transplant Proc; 2010 May;42(4):1314-6
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  • INTRODUCTION: Malignancies are a well-known complication of immunosuppressive therapy among renal transplant recipients, representing an important cause of long-term morbidity and mortality.
  • METHODS: Fifteen patients developed the following malignancies at a mean of 90.3 months (range = 10-252) after kidney transplantation: metastatic gastric cancer (n = 1), metastatic colon cancer (n = 1), bilateral nephrourothelioma (n = 1), skin cancer (n = 2), Kaposi's sarcoma (n = 2), posttransplant lymphoproliferative disorder (PTLD; n = 4), renal cell carcinoma T1 (n = 1), MALT lymphoma (n = 1), intramucous colon carcinoma (n = 1), liposarcoma of the spermatic cord (n = 1).
  • RESULTS: Both patients with metastatic cancer underwent chemotherapy but succumbed after 6 and 13 months.
  • Two patients with PTLD who underwent chemotherapy died after 12 and 36 months.
  • Nevertheless, it is difficult to assess whether tumor regression was due to rapamycin treatment or to the reduced immunosuppression.
  • [MeSH-major] Kidney Transplantation / immunology. Neoplasms / immunology. Sirolimus / therapeutic use
  • [MeSH-minor] Cell Division / drug effects. Cell Line, Tumor. Colonic Neoplasms / immunology. Colonic Neoplasms / pathology. Genital Neoplasms, Male / immunology. Genital Neoplasms, Male / pathology. Humans. Immunosuppression / methods. Immunosuppressive Agents / therapeutic use. Liposarcoma / immunology. Liposarcoma / pathology. Male. Neoplasm Metastasis. Skin Neoplasms / immunology. Skin Neoplasms / pathology. Stomach Neoplasms / immunology. Stomach Neoplasms / pathology

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  • [Copyright] Copyright (c) 2010. Published by Elsevier Inc.
  • (PMID = 20534289.001).
  • [ISSN] 1873-2623
  • [Journal-full-title] Transplantation proceedings
  • [ISO-abbreviation] Transplant. Proc.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Immunosuppressive Agents; W36ZG6FT64 / Sirolimus
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21. Mrad K, Morice P, Fabre A, Pautier P, Lhommé C, Duvillard P, Sabourin JC: Krukenberg tumor: a clinico-pathological study of 15 cases. Ann Pathol; 2000 May;20(3):202-6
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  • Two main histological types were found in our series : the classic form with sarcoma-like storiform tumoral stroma and an alternative cellular-acellular pattern.
  • Nor surgery, neither chemotherapy is efficient but bilateral oophorectomy should be proposed in post-menopausal women with gastric linitis removed surgically.
  • [MeSH-major] Breast Neoplasms / diagnosis. Colonic Neoplasms / diagnosis. Krukenberg Tumor / secondary. Ovarian Neoplasms / secondary. Stomach Neoplasms / diagnosis

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  • (PMID = 10891713.001).
  • [ISSN] 0242-6498
  • [Journal-full-title] Annales de pathologie
  • [ISO-abbreviation] Ann Pathol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] FRANCE
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22. Zhang JS, Imai T, Suenaga A, Otagiri M: Molecular-weight-dependent pharmacokinetics and cytotoxic properties of cisplatin complexes prepared with chondroitin sulfate A and C. Int J Pharm; 2002 Jun 20;240(1-2):23-31
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  • The obtained plasma concentration-time curves during the 3 h period studied for all complexes are biphasic.
  • CDDP-CSA-2 and CDDP-CSC-2, with similar urinary excretion as CDDP, gave rise to approximately five and four-fold increase in AUC(0-3 h) values, respectively, than that was achieved with native CDDP treatment.
  • Both complexes effectively suppressed the extensive distribution of CDDP into most tissues, especially kidney.
  • In addition, a significantly higher accumulation in tumor tissue was found with the administration of CDDP-CSA-2 than CDDP.
  • Moreover, CSA complexes displayed an IC(50) of 6 microM Pt-equivalents against SW4800 human colon cancer cells, similar to that of CDDP, whereas CSC complexes were less active than CDDP.
  • These studies indicate that the complex prepared with CSA, which is greater than 20 kDa of molecular size, is superior to that of CSC, exhibiting improved pharmacokinetics and similar pharmacological activity to the native drug.
  • [MeSH-minor] Animals. Cell Survival / drug effects. Colonic Neoplasms. Drug Carriers / chemistry. Humans. Inhibitory Concentration 50. Male. Mice. Mice, Inbred Strains. Molecular Weight. Neoplasm Transplantation. Rats. Rats, Wistar. Sarcoma 180 / drug therapy. Sarcoma 180 / metabolism. Tissue Distribution. Tumor Cells, Cultured

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  • (PMID = 12062498.001).
  • [ISSN] 0378-5173
  • [Journal-full-title] International journal of pharmaceutics
  • [ISO-abbreviation] Int J Pharm
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Drug Carriers; 9007-28-7 / Chondroitin Sulfates; Q20Q21Q62J / Cisplatin
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23. Wasowska M, Wietrzyk J, Opolski A, Oszczapowicz J, Oszczapowicz I: Effect of structural modifications of anthracyclines on the ability to overcome drug resistance of cancer cells. Anticancer Res; 2006 May-Jun;26(3A):2009-12
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  • [Title] Effect of structural modifications of anthracyclines on the ability to overcome drug resistance of cancer cells.
  • In the search for new derivatives of anthracycline antibiotics with the ability to overcome the drug resistance barrier, a series of new analogs of these antibiotics, containing the amidino group at C-3' position of the daunosamine moiety, have been synthesized.
  • The majority of these derivatives appeared to be able, completely or partially, to overcome the drug resistance barrier of cancer cells.
  • The obtained results indicated that introduction of the amidino group into the daunosamine moiety of anthracycline molecules appears to overcome the drug resistance of cancer cells.
  • [MeSH-minor] Cell Line, Tumor. Colonic Neoplasms / drug therapy. Daunorubicin / pharmacology. Doxorubicin / pharmacology. Drug Resistance, Multiple. Drug Resistance, Neoplasm. Drug Screening Assays, Antitumor. Epirubicin / pharmacology. Female. HL-60 Cells. Humans. Sarcoma / drug therapy. Structure-Activity Relationship. Uterine Neoplasms / drug therapy

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  • (PMID = 16827137.001).
  • [ISSN] 0250-7005
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Anthracyclines; 0 / Antibiotics, Antineoplastic; 3Z8479ZZ5X / Epirubicin; 66322-65-4 / 3'-epidaunorubicin; 80168379AG / Doxorubicin; ZS7284E0ZP / Daunorubicin
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24. Erickson-Miller CL, Chadderton A, Gibbard A, Kirchner J, Pillarisetti K, Baker K, Pandite L, El-Hariry I, Mostafa Kamel Y, Liu Y, Martin AM, Messam C: Thrombopoietin receptor levels in tumor cell lines and primary tumors. J Oncol; 2010;2010:135354
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  • Thrombopoietin (TPO) receptor agonists represent a new approach for the treatment of thrombocytopenia, which may develop as a consequence of immune thrombocytopenia, chemotherapy treatment, chronic hepatitis C infection, or myelodysplastic syndromes.
  • There are concerns that use of certain growth factors can hasten disease progression in some types of hematologic malignancies and solid tumors.
  • In this study, expression of MPL (TPO-R) mRNA was examined in tumor cell lines, patient tumor samples (renal cell carcinoma, prostatic carcinoma, soft tissue and bony/cartilage sarcoma, colon cancer, and lymphoma), and normal tissues using microarray analysis and qRT-PCR.

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  • (PMID = 21318160.001).
  • [ISSN] 1687-8469
  • [Journal-full-title] Journal of oncology
  • [ISO-abbreviation] J Oncol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Egypt
  • [Other-IDs] NLM/ PMC3026977
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25. Kelter G, Schierholz JM, Fischer IU, Fiebig HH: Cytotoxic activity and absence of tumor growth stimulation of standardized mistletoe extracts in human tumor models in vitro. Anticancer Res; 2007 Jan-Feb;27(1A):223-33
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  • Mistletoe extracts are widely used in complementary and alternative cancer therapy in Europe.
  • None of the human tumor cell lines in the panel showed growth stimulation (T/C (Test/Control) > 125%) by the mistletoe extracts or ML-1, apart from two exceptions in the colon carcinoma cell line HCC-2998, in which Helixor M and ML-1 showed a marginal stimulation (TIC 128% and 131%, respectively) at one concentration only.
  • [MeSH-major] Mistletoe / chemistry. Neoplasms / drug therapy. Plant Extracts / pharmacology
  • [MeSH-minor] Cell Growth Processes / drug effects. Cell Line, Tumor. Colonic Neoplasms / drug therapy. Colonic Neoplasms / pathology. Doxorubicin / pharmacology. Humans. Interleukin-6 / pharmacology. Melanoma / drug therapy. Melanoma / pathology. Plant Preparations / pharmacology. Plant Proteins / pharmacology. Ribosome Inactivating Proteins, Type 2. Sarcoma / drug therapy. Sarcoma / pathology. Toxins, Biological / pharmacology

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  • (PMID = 17352237.001).
  • [ISSN] 0250-7005
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Interleukin-6; 0 / Plant Extracts; 0 / Plant Preparations; 0 / Plant Proteins; 0 / Ribosome Inactivating Proteins, Type 2; 0 / Toxins, Biological; 0 / mistletoe lectin I; 75882-01-8 / Helixor; 80168379AG / Doxorubicin
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26. Rose WC, Fairchild C, Lee FY: Preclinical antitumor activity of two novel taxanes. Cancer Chemother Pharmacol; 2001;47(2):97-105
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  • BMS-184476 was found to be clearly superior to paclitaxel in three human xenograft tumor models: A2780 ovarian carcinoma; HCT/pk, a moderately paclitaxel-resistant colon carcinoma; and L2987 lung carcinoma.
  • BMS-184476 and paclitaxel were inactive in two murine model systems, M5076 sarcoma and the paclitaxel-resistant M109/txlr lung carcinoma.
  • Like paclitaxel and BMS-184476, BMS-188797 was inactive versus M5076 sarcoma.
  • [MeSH-major] Antineoplastic Agents, Phytogenic / therapeutic use. Paclitaxel / analogs & derivatives. Paclitaxel / therapeutic use
  • [MeSH-minor] Animals. Colonic Neoplasms / drug therapy. Female. Humans. Lung Neoplasms / drug therapy. Mice. Mice, Inbred Strains. Ovarian Neoplasms / drug therapy. Rats. Tumor Cells, Cultured

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  • (PMID = 11269747.001).
  • [ISSN] 0344-5704
  • [Journal-full-title] Cancer chemotherapy and pharmacology
  • [ISO-abbreviation] Cancer Chemother. Pharmacol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; P88XT4IS4D / Paclitaxel
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27. Busch TM, Hahn SM, Wileyto EP, Koch CJ, Fraker DL, Zhang P, Putt M, Gleason K, Shin DB, Emanuele MJ, Jenkins K, Glatstein E, Evans SM: Hypoxia and Photofrin uptake in the intraperitoneal carcinomatosis and sarcomatosis of photodynamic therapy patients. Clin Cancer Res; 2004 Jul 15;10(14):4630-8
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  • [Title] Hypoxia and Photofrin uptake in the intraperitoneal carcinomatosis and sarcomatosis of photodynamic therapy patients.
  • PURPOSE: Response to photodynamic therapy depends on adequate tumor oxygenation as well as sufficient accumulation of photosensitizer in the tumor.
  • In separate tumor nodules from 10 patients, Photofrin uptake was measured by fluorescence after tissue solubilization.
  • Three patients with severely hypoxic tumor nodules exhibited moderate levels of Photofrin uptake of 3.9 +/- 0.4 to 3.9 +/- 0.5 ng/mg (mean +/- SE).
  • The four patients with tumors of physiological oxygenation did not consistently exhibit high tumor concentrations of Photofrin: mean +/- SE drug uptake among these patients ranged from 0.6 +/- 0.8 to 5.8 +/- 0.5 ng/mg.
  • These data emphasize the need for reconsideration of the generally accepted paradigm of small tumor size, good oxygenation, and good drug delivery because this may vary on an individual tumor basis.
  • [MeSH-major] Dihematoporphyrin Ether / pharmacokinetics. Etanidazole / analogs & derivatives. Gastrointestinal Neoplasms / metabolism. Ovarian Neoplasms / metabolism. Sarcoma / metabolism
  • [MeSH-minor] Appendiceal Neoplasms / metabolism. Appendiceal Neoplasms / pathology. Appendiceal Neoplasms / therapy. Benzimidazoles / chemistry. Binding, Competitive / drug effects. Carbocyanines / chemistry. Colonic Neoplasms / metabolism. Colonic Neoplasms / pathology. Colonic Neoplasms / therapy. Female. Gastrointestinal Stromal Tumors / metabolism. Gastrointestinal Stromal Tumors / pathology. Gastrointestinal Stromal Tumors / therapy. Humans. Hydrocarbons, Fluorinated / chemistry. Hydrocarbons, Fluorinated / metabolism. In Vitro Techniques. Intestine, Small / metabolism. Intestine, Small / pathology. Male. Microscopy, Fluorescence. Oxygen / pharmacology. Photochemotherapy

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  • (PMID = 15269134.001).
  • [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 / CA75285; United States / NCI NIH HHS / CA / CA85831; United States / NCI NIH HHS / CA / CA87971; United States / NCRR NIH HHS / RR / M01-RR0040
  • [Publication-type] Comparative Study; Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 2-(2-nitro-1H-imidazol-1-yl)-N-(2,2,3,3,3-pentafluoropropyl)acetamide; 0 / Benzimidazoles; 0 / Carbocyanines; 0 / Hydrocarbons, Fluorinated; 0 / cyanine dye 3; 23491-52-3 / HOE 33342; 30DKA3Q1HL / Etanidazole; 97067-70-4 / Dihematoporphyrin Ether; S88TT14065 / Oxygen
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28. Beganovic S: Clinical significance of the KRAS mutation. Bosn J Basic Med Sci; 2009 Oct;9 Suppl 1:17-20
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  • Physicians now have the opportunity to use specific biomarkers to personalize therapeutic options in various settings.
  • Recent research has demonstrated that presence of Kirsten rat sarcoma viral oncogene homolog (KRAS) mutation may directly influence medical decisions in patients with colon and lung cancer.
  • Use of KRAS oncogene as a selection marker for specific treatment is a good example of individualized medicine approach to cancer treatment.

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  • (PMID = 19912113.001).
  • [ISSN] 1512-8601
  • [Journal-full-title] Bosnian journal of basic medical sciences
  • [ISO-abbreviation] Bosn J Basic Med Sci
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] Bosnia and Herzegovina
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / KRAS protein, human; 0 / Proto-Oncogene Proteins; 0 / Quinazolines; 2S9ZZM9Q9V / Bevacizumab; DA87705X9K / Erlotinib Hydrochloride; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 3.6.5.2 / ras Proteins
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29. Daftarian P, Song GY, Ali S, Faynsod M, Longmate J, Diamond DJ, Ellenhorn JD: Two distinct pathways of immuno-modulation improve potency of p53 immunization in rejecting established tumors. Cancer Res; 2004 Aug 1;64(15):5407-14
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  • CpG ODN with MVAp53 resulted in tumor rejection in BALB/c mice bearing poorly immunogenic 11A-1 murine mammary carcinomas or Meth A sarcomas and C57Bl/6 mice bearing MC-38 colon carcinomas.
  • [MeSH-major] CD8-Positive T-Lymphocytes / immunology. Colonic Neoplasms / therapy. Mammary Neoplasms, Animal / therapy. Sarcoma, Experimental / therapy. Signal Transduction. Tumor Suppressor Protein p53 / pharmacology
  • [MeSH-minor] Adjuvants, Immunologic / pharmacology. Adjuvants, Immunologic / therapeutic use. Animals. Antibodies, Monoclonal / metabolism. Antigens, CD. Antigens, Differentiation / chemistry. CTLA-4 Antigen. Cells, Cultured. Combined Modality Therapy. Cricetinae. Cytotoxicity Tests, Immunologic. DNA-Binding Proteins / genetics. DNA-Binding Proteins / physiology. Drug Synergism. Female. Homozygote. Humans. Immunization. Interleukin-6 / genetics. Interleukin-6 / physiology. Killer Cells, Natural / immunology. Killer Cells, Natural / metabolism. Mice. Mice, Inbred BALB C. Mice, Inbred C57BL. Mice, Knockout. Oligodeoxyribonucleotides / pharmacology. Receptors, Cell Surface / genetics. Receptors, Cell Surface / physiology. Toll-Like Receptor 9

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  • (PMID = 15289349.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA 33572; United States / NCI NIH HHS / CA / P01 CA 30206; United States / NCI NIH HHS / CA / R01 CA 77544; United States / NCI NIH HHS / CA / R29 CA 70819
  • [Publication-type] Comparative Study; 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 / Adjuvants, Immunologic; 0 / Antibodies, Monoclonal; 0 / Antigens, CD; 0 / Antigens, Differentiation; 0 / CPG-oligonucleotide; 0 / CTLA-4 Antigen; 0 / CTLA4 protein, human; 0 / Ctla4 protein, mouse; 0 / DNA-Binding Proteins; 0 / Interleukin-6; 0 / Oligodeoxyribonucleotides; 0 / Receptors, Cell Surface; 0 / TLR9 protein, human; 0 / Tlr9 protein, mouse; 0 / Toll-Like Receptor 9; 0 / Tumor Suppressor Protein p53
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30. Lee FY, Borzilleri R, Fairchild CR, Kim SH, Long BH, Reventos-Suarez C, Vite GD, Rose WC, Kramer RA: BMS-247550: a novel epothilone analog with a mode of action similar to paclitaxel but possessing superior antitumor efficacy. Clin Cancer Res; 2001 May;7(5):1429-37
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  • BMS-247550, a novel epothilone derivative, is being developed by Bristol-Myers Squibb Company (BMS) as an anticancer agent for the treatment of patients with malignant tumors.
  • Importantly, BMS-247550 retains its antineoplastic activity against human cancers that are naturally insensitive to paclitaxel or that have developed resistance to paclitaxel, both in vitro and in vivo.
  • (b) paclitaxel-insensitive: Pat-26 human pancreatic carcinoma (clinical isolate) and M5076 murine fibrosarcoma; and (c) paclitaxel sensitive: A2780 ovarian, LS174T, and HCT116 human colon carcinoma.
  • These efficacy data demonstrate that BMS-247550 has the potential to surpass Taxol in both clinical efficacy and ease of use (i.e., less frequent treatment schedule and/or oral administration).
  • [MeSH-minor] Administration, Oral. Animals. Breast Neoplasms / drug therapy. Cell Cycle / drug effects. Cell Survival / drug effects. Colonic Neoplasms / drug therapy. Disease Models, Animal. Drug Resistance, Neoplasm. Female. Humans. Infusions, Parenteral. Mice. Mice, Inbred BALB C. Mice, Inbred C57BL. Mice, Inbred DBA. Neoplasm Transplantation. Ovarian Neoplasms / drug therapy. Pancreatic Neoplasms / drug therapy. Sarcoma / drug therapy. Tubulin / genetics. Tubulin / metabolism. Tumor Cells, Cultured. Tumor Stem Cell Assay. Xenograft Model Antitumor Assays

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  • (PMID = 11350914.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Epothilones; 0 / Epoxy Compounds; 0 / Thiazoles; 0 / Tubulin; K27005NP0A / ixabepilone; P88XT4IS4D / Paclitaxel; UEC0H0URSE / epothilone B
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31. Tejeda M, Gaál D, Csuka O, Ullrich A, Schwab R, Pap A, Horváth A, Kéri G: The antitumour effect of the somatostatin analogue TT-232 depends on the treatment regimen. Cancer Detect Prev; 2003;27(2):155-62
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The antitumour effect of the somatostatin analogue TT-232 depends on the treatment regimen.
  • We studied the effect of TT-232 in different routes of administration and treatment schedules on various types of mouse tumour models.
  • The infusion treatment with inserted Alzet osmotic minipumps proved to be superior to both twice daily subcutaneous (s.c.) or intravenous (i.v.) injections in a 2 weeks period.
  • In the case of S-180 tumour the infusion treatment resulted in 77-100% tumour growth inhibition and in 40-60% of mice long-term and tumour-free survivors.
  • In the very aggressive Colon-26 (C-26) and MXT, the TT-232 treatment resulted in 71-75% tumour growth inhibition and increased survival time by about 50%.
  • [MeSH-major] Antineoplastic Agents / administration & dosage. Neoplasms, Experimental / drug therapy. Peptides, Cyclic / administration & dosage
  • [MeSH-minor] Animals. Colonic Neoplasms / drug therapy. Colonic Neoplasms / pathology. Dose-Response Relationship, Drug. Female. Growth Hormone / metabolism. Injections, Intravenous. Injections, Subcutaneous. Leukemia P388 / drug therapy. Leukemia P388 / pathology. Mammary Neoplasms, Experimental / drug therapy. Mammary Neoplasms, Experimental / pathology. Mice. Mice, Inbred BALB C. Sarcoma 180 / drug therapy. Sarcoma 180 / pathology. Somatostatin / analogs & derivatives. Survival Rate. Tumor Cells, Cultured / transplantation

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  • (PMID = 12670528.001).
  • [ISSN] 0361-090X
  • [Journal-full-title] Cancer detection and prevention
  • [ISO-abbreviation] Cancer Detect. Prev.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Peptides, Cyclic; 0 / TT2-32; 51110-01-1 / Somatostatin; 9002-72-6 / Growth Hormone
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32. Rader C, Sinha SC, Popkov M, Lerner RA, Barbas CF 3rd: Chemically programmed monoclonal antibodies for cancer therapy: adaptor immunotherapy based on a covalent antibody catalyst. Proc Natl Acad Sci U S A; 2003 Apr 29;100(9):5396-400
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Chemically programmed monoclonal antibodies for cancer therapy: adaptor immunotherapy based on a covalent antibody catalyst.
  • Proposing that a blend of the chemical diversity of small synthetic molecules with the immunological characteristics of the antibody molecule will lead to therapeutic agents with superior properties, we here present a device that equips small synthetic molecules with both effector function and long serum half-life of a generic antibody molecule.
  • As a prototype, we developed a targeting device that is based on the formation of a covalent bond of defined stoichiometry between a 1,3-diketone derivative of an integrin alpha(v)beta(3) and alpha(v)beta(5) targeting Arg-Gly-Asp peptidomimetic and the reactive lysine of aldolase antibody 38C2.
  • The resulting complex was shown to (i) spontaneously assemble in vitro and in vivo, (ii) selectively retarget antibody 38C2 to the surface of cells expressing integrins alpha(v)beta(3) and alpha(v)beta(5), (iii) dramatically increase the circulatory half-life of the Arg-Gly-Asp peptidomimetic, and (iv) effectively reduce tumor growth in animal models of human Kaposi's sarcoma and colon cancer.
  • Further, by use of a generic antibody molecule that forms a covalent bond with a 1,3-diketone functionality, essentially any compound can be turned into an immunotherapeutic agent thereby not only increasing the diversity space that can be accessed but also multiplying the therapeutic effect.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Immunotherapy. Neoplasms / therapy

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  • (PMID = 12702756.001).
  • [ISSN] 0027-8424
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal
  • [Other-IDs] NLM/ PMC154356
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33. Rizell M, Lindner P: Inhibition of mTOR suppresses experimental liver tumours. Anticancer Res; 2005 Mar-Apr;25(2A):789-93
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  • After one week of daily sirolimus treatment, initiated on the day of tumour-cell inoculation, a dose-response relationship was shown at doses between 0.01 mg/kg/day and 1 mg/kg/day, decreasing tumour weight from 0.5+/-0.1 g in control rats (n=9) to 0.09+/-0.04 g for sirolimus 1 mg/kg (n=9).
  • Trough concentration in blood was 6.4+/-0.2 ng/ml after five days of daily treatment with 1 mg/kg sirolimus intraperitoneally.
  • The three tumours studied, an nitrosoguanidin-induced adenocarcinoma, a Leydig cell sarcoma and a hepatoma, all responded, establishing sirolimus as a promising anticancer drug.
  • [MeSH-major] Antibiotics, Antineoplastic / pharmacology. Liver Neoplasms, Experimental / drug therapy. Liver Neoplasms, Experimental / enzymology. Protein Kinase Inhibitors / pharmacology. Protein Kinases / metabolism. Sirolimus / pharmacology
  • [MeSH-minor] Adenocarcinoma / drug therapy. Adenocarcinoma / enzymology. Animals. Colonic Neoplasms / drug therapy. Colonic Neoplasms / enzymology. Dose-Response Relationship, Drug. Eating / drug effects. Leydig Cell Tumor / drug therapy. Leydig Cell Tumor / enzymology. Liver / anatomy & histology. Liver / metabolism. Organ Size / drug effects. Rats. Rats, Inbred WF. Spleen / anatomy & histology. TOR Serine-Threonine Kinases

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  • (PMID = 15868910.001).
  • [ISSN] 0250-7005
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / Protein Kinase Inhibitors; EC 2.7.- / Protein Kinases; EC 2.7.1.1 / TOR Serine-Threonine Kinases; EC 2.7.1.1 / mTOR protein, rat; W36ZG6FT64 / Sirolimus
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34. Van Putte BP, Hendriks JM, Romijn S, Guetens G, De Boeck G, De Bruijn EA, Van Schil PE: Single-pass isolated lung perfusion versus recirculating isolated lung perfusion with melphalan in a rat model. Ann Thorac Surg; 2002 Sep;74(3):893-8; discussion 898
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  • BACKGROUND: Isolated lung perfusion (ILuP) with melphalan (MN) is superior to intravenous infusion for the treatment of pulmonary carcinoma and sarcoma metastases.
  • In a third experiment, tumor levels were compared between SP, RP, or intravenous therapy with a dose of 0.5 mg.
  • For induction of pulmonary metastases, 0.5 x 10(6) single adenocarcinoma cells were injected intravenously and therapy was given on day 30.
  • For comparison of drug concentrations, unpaired Student's t test was applied.
  • Tumor levels were significantly higher after ILuP compared with intravenous therapy.
  • CONCLUSIONS: Both ILuP techniques resulted in significantly higher MN lung levels than after intravenous therapy.
  • [MeSH-major] Adenocarcinoma / secondary. Chemotherapy, Cancer, Regional Perfusion / instrumentation. Colonic Neoplasms / pathology. Infusions, Intra-Arterial / instrumentation. Lung Neoplasms / secondary. Melphalan / pharmacology
  • [MeSH-minor] Animals. Biological Availability. Infusions, Intravenous. Lung / drug effects. Lung / pathology. Male. Neoplasm Transplantation. Rats. Rats, Inbred Strains. Tumor Cells, Cultured

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  • (PMID = 12238857.001).
  • [ISSN] 0003-4975
  • [Journal-full-title] The Annals of thoracic surgery
  • [ISO-abbreviation] Ann. Thorac. Surg.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] Q41OR9510P / Melphalan
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35. Nefedova Y, Nagaraj S, Rosenbauer A, Muro-Cacho C, Sebti SM, Gabrilovich DI: Regulation of dendritic cell differentiation and antitumor immune response in cancer by pharmacologic-selective inhibition of the janus-activated kinase 2/signal transducers and activators of transcription 3 pathway. Cancer Res; 2005 Oct 15;65(20):9525-35
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Regulation of dendritic cell differentiation and antitumor immune response in cancer by pharmacologic-selective inhibition of the janus-activated kinase 2/signal transducers and activators of transcription 3 pathway.
  • Here, using a novel selective inhibitor of JAK2/STAT3 JSI-124, we investigated the possibility of pharmacologic regulation of dendritic cell differentiation in cancer.
  • This indicates that pharmacologic inhibition of the JAK2/STAT3 pathway can be an important new therapeutic strategy to enhance antitumor activity of cancer immunotherapy.

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  • (PMID = 16230418.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA 100062; United States / NCI NIH HHS / CA / P01 CA078038; United States / NCI NIH HHS / CA / R01 CA084488; United States / NCI NIH HHS / CA / CA 84488; United States / NCI NIH HHS / CA / F32 CA103393; United States / NCI NIH HHS / CA / 5P01 CA 78038; United States / NCI NIH HHS / CA / R01 CA100062
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Epitopes, T-Lymphocyte; 0 / Proto-Oncogene Proteins; 0 / STAT3 Transcription Factor; 0 / Stat3 protein, mouse; 0 / Triterpenes; 2222-07-3 / cucurbitacin I; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / Jak2 protein, mouse; EC 2.7.10.2 / Janus Kinase 2
  • [Other-IDs] NLM/ NIHMS5099; NLM/ PMC1351362
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36. Rajendra T, Ann Lee K, Thomas J, Hong A, Chan C: Results of surgical treatment for cerebral metastases. J Clin Neurosci; 2003 Mar;10(2):190-4
MedlinePlus Health Information. consumer health - Brain Tumors.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Results of surgical treatment for cerebral metastases.
  • Medical and radiation therapy confer median survival ranging from 3 to 6 months only.
  • The primary cancer was breast in nine cases, eight were lung cancers, six colonic cancers, two unknown primaries and one was a soft tissue sarcoma.
  • Two patients underwent a radiosurgical boost and six patients underwent adjuvant chemotherapy.
  • Surgical treatment appears beneficial, with subgroups such as breast cancer possibly doing better.
  • [MeSH-minor] Adult. Aged. Cerebellum / pathology. Cerebellum / radiography. Female. Humans. Male. Middle Aged. Neoplasm Metastasis. Retrospective Studies. Survival Rate. Treatment Outcome

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  • (PMID = 12637047.001).
  • [ISSN] 0967-5868
  • [Journal-full-title] Journal of clinical neuroscience : official journal of the Neurosurgical Society of Australasia
  • [ISO-abbreviation] J Clin Neurosci
  • [Language] eng
  • [Publication-type] Clinical Trial; Comparative Study; Journal Article
  • [Publication-country] Scotland
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37. Skobeleva N, Menon S, Weber L, Golemis EA, Khazak V: In vitro and in vivo synergy of MCP compounds with mitogen-activated protein kinase pathway- and microtubule-targeting inhibitors. Mol Cancer Ther; 2007 Mar;6(3):898-906
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • An important clinical task is to coherently integrate the use of protein-targeted drugs into preexisting therapeutic regimens, with the goal of improving treatment efficacy.
  • Constitutive activation of Ras-dependent signaling is important in many tumors, and agents that inhibit this pathway might be useful in numerous therapeutic combinations.
  • In this study, we investigate the ability of the MCP110 compound to synergistically enhance the activity of other therapeutic agents.
  • The synergistic activity of MCP110 and paclitaxel was further established by experiments showing that in Kaposi's sarcoma oncogenically transformed cell lines, cellular models for tumors treated with taxanes in the clinic and in which Raf-dependent signaling plays an important role, MCP110 synergizes with paclitaxel and limit growth.
  • Finally, in vivo testing indicate that MCP110 is bioavailable, inhibits the growth of LXFA 629 lung and SW620 colon carcinoma cells in xenograft models, and again strongly synergizes with paclitaxel.

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  • (PMID = 17363484.001).
  • [ISSN] 1535-7163
  • [Journal-full-title] Molecular cancer therapeutics
  • [ISO-abbreviation] Mol. Cancer Ther.
  • [Language] ENG
  • [Grant] None / None / / P30 CA006927-46; United States / NCI NIH HHS / CA / CA 06927; United States / NCI NIH HHS / CA / R01 CA063366; United States / NCI NIH HHS / CA / R01 CA 63366; United States / NCI NIH HHS / CA / CA063366-07; United States / NCI NIH HHS / CA / P30 CA006927-46; United States / NCI NIH HHS / CA / P30 CA006927; United States / NCI NIH HHS / CA / R01 CA063366-07
  • [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 / Enzyme Inhibitors; 0 / Taxoids; 15H5577CQD / docetaxel; 5J49Q6B70F / Vincristine; EC 2.7.11.1 / Proto-Oncogene Proteins c-raf; EC 2.7.11.24 / Mitogen-Activated Protein Kinases; EC 3.6.5.2 / Proto-Oncogene Proteins p21(ras); P88XT4IS4D / Paclitaxel
  • [Other-IDs] NLM/ NIHMS101208; NLM/ PMC2670615
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