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1. Miettinen M: From morphological to molecular diagnosis of soft tissue tumors. Adv Exp Med Biol; 2006;587:99-113
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  • [Title] From morphological to molecular diagnosis of soft tissue tumors.
  • Many sarcomas are known to have such fusions, and the demonstration of the fusion transcripts in tumor tissue is of great value in specific diagnosis of synovial sarcoma (SYT-SSX), Ewing sarcoma (EWS-Fli1), clear cell sarcoma (EWS-ATF1), myxoid liposarcoma (FUS-CHOP), and other sarcomas.
  • Demonstration of SYT-SSX and EWS-ATF1 fusion assists in the diagnosis of synovial and clear cell sarcomas in unusual locations, such as the gastrointestinal tract, where these tumors occur with low frequency.
  • In two exceptional instances, the same translocation and gene fusion occurs in two unrelated diseases: ETV6-NTRK fusion in infantile fibrosarcoma and secretory carcinoma of the breast, and ALK-TPM3 fusion in inflammatory myofibroblastic tumor and large cell anaplastic lymphoma.
  • Mutation type influences therapy responsiveness, but fortunately very few GISTs carry primarily Imatinib-resistant mutations.
  • Secondary drug resistance acquired during Imatinib treatment based on new, Imatinib-resistant mutations is a major problem limiting treatment success.
  • Specific viral sequences of human herpesvirus 8 (HHV8) are diagnostic markers for Kaposi sarcoma (KS), and are absent in angiosarcoma.

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  • (PMID = 17163160.001).
  • [ISSN] 0065-2598
  • [Journal-full-title] Advances in experimental medicine and biology
  • [ISO-abbreviation] Adv. Exp. Med. Biol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 70
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2. Donnelly C, Olsen AM, Lewis LD, Eisenberg BL, Eastman A, Kinlaw WB: Conjugated linoleic acid (CLA) inhibits expression of the Spot 14 (THRSP) and fatty acid synthase genes and impairs the growth of human breast cancer and liposarcoma cells. Nutr Cancer; 2009;61(1):114-22
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  • [Title] Conjugated linoleic acid (CLA) inhibits expression of the Spot 14 (THRSP) and fatty acid synthase genes and impairs the growth of human breast cancer and liposarcoma cells.
  • We hypothesized that CLA inhibits S14 gene expression in human breast cancer and liposarcoma cells and that this will retard their growth.
  • Exposure of T47D breast cancer cells to a mixture of CLA isomers reduced the expression of the S14 and fatty acid synthase (FAS) genes.
  • Similar effects were observed in MDA-MB-231 breast cancer cells.
  • CLA likewise suppressed levels of S14 and FAS mRNAs in liposarcoma cells and caused growth inhibition that was prevented by palmitic acid.
  • We conclude that as in bovine mammary and mouse adipose cells, CLA suppresses S14 and FAS gene expression in human breast cancer and liposarcoma cells.

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  • (PMID = 19116881.001).
  • [ISSN] 1532-7914
  • [Journal-full-title] Nutrition and cancer
  • [ISO-abbreviation] Nutr Cancer
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P30 CA023108; United States / NCI NIH HHS / CA / R01 CA126618-05A2; United States / NCI NIH HHS / CA / R01 CA126618; United States / NCI NIH HHS / CA / CA126618-05A2; United States / NCI NIH HHS / CA / R01 CA23108
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Growth Inhibitors; 0 / Linoleic Acids, Conjugated; 0 / Nuclear Proteins; 0 / THRSP protein, human; 0 / Transcription Factors; EC 2.3.1.85 / Fatty Acid Synthases
  • [Other-IDs] NLM/ NIHMS95480; NLM/ PMC2872989
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3. Levine PH, Wei XJ, Gagner JP, Flax H, Mittal K, Blank SV: Pleomorphic liposarcoma of the uterus: case report and literature review. Int J Gynecol Pathol; 2003 Oct;22(4):407-11
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  • [Title] Pleomorphic liposarcoma of the uterus: case report and literature review.
  • A 62-year-old woman with a history of breast carcinoma being treated with tamoxifen presented with a rapidly enlarging pelvic mass.
  • Microscopic examination revealed a variety of patterns and cell types characteristic of liposarcoma that included myxoid/round cell, storiform/pleomorphic, epithelioid, and spindle cell areas.
  • Although a variety of uterine tumors have been associated with tamoxifen treatment, this appears to be the first example of tamoxifen-associated uterine liposarcoma.
  • [MeSH-major] Antineoplastic Agents, Hormonal / adverse effects. Liposarcoma / chemically induced. Liposarcoma / pathology. Tamoxifen / adverse effects. Uterine Neoplasms / chemically induced. Uterine Neoplasms / pathology
  • [MeSH-minor] Breast Neoplasms / drug therapy. Breast Neoplasms / prevention & control. Female. Humans. Middle Aged. Neoplasm Recurrence, Local / prevention & control

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  • (PMID = 14501826.001).
  • [ISSN] 0277-1691
  • [Journal-full-title] International journal of gynecological pathology : official journal of the International Society of Gynecological Pathologists
  • [ISO-abbreviation] Int. J. Gynecol. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 094ZI81Y45 / Tamoxifen
  • [Number-of-references] 29
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4. Carboni JM, Wittman M, Yang Z, Lee F, Greer A, Hurlburt W, Hillerman S, Cao C, Cantor GH, Dell-John J, Chen C, Discenza L, Menard K, Li A, Trainor G, Vyas D, Kramer R, Attar RM, Gottardis MM: BMS-754807, a small molecule inhibitor of insulin-like growth factor-1R/IR. Mol Cancer Ther; 2009 Dec;8(12):3341-9
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  • BMS-754807 effectively inhibits the growth of a broad range of human tumor types in vitro, including mesenchymal (Ewing's, rhabdomyosarcoma, neuroblastoma, and liposarcoma), epithelial (breast, lung, pancreatic, colon, gastric), and hematopoietic (multiple myeloma and leukemia) tumor cell lines (IC50, 5-365 nmol/L); the compound caused apoptosis in a human rhabdomyosarcoma cell line, Rh41, as shown by an accumulation of the sub-G1 fraction, as well as by an increase in poly ADP ribose polymerase and Caspase 3 cleavage.
  • Combination studies with BMS-754807 have been done on multiple human tumor cell types and showed in vitro synergies (combination index, <1.0) when combined with cytotoxic, hormonal, and targeted agents.
  • The combination of cetuximab and BMS-754807 in vivo, at multiple dose levels, resulted in improved clinical outcome over single agent treatment.
  • These data show that BMS-754807 is an efficacious, orally active growth factor 1 receptor/insulin receptor family-targeted kinase inhibitor that may act in combination with a wide array of established anticancer agents.
  • [MeSH-major] Pyrazoles / pharmacology. Receptor, IGF Type 1 / antagonists & inhibitors. Receptor, Insulin / antagonists & inhibitors. Triazines / pharmacology
  • [MeSH-minor] Animals. Antibodies, Monoclonal / administration & dosage. Antibodies, Monoclonal, Humanized. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Blotting, Western. Caspase 3 / metabolism. Cell Cycle / drug effects. Cell Line, Tumor. Cell Proliferation / drug effects. Cetuximab. Dose-Response Relationship, Drug. Glucose Tolerance Test. Humans. Inhibitory Concentration 50. Mice. Mice, Nude. Molecular Structure. Neoplasms / drug therapy. Neoplasms / metabolism. Neoplasms / pathology. Poly(ADP-ribose) Polymerases / metabolism. Tumor Burden / drug effects. Xenograft Model Antitumor Assays

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  • (PMID = 19996272.001).
  • [ISSN] 1538-8514
  • [Journal-full-title] Molecular cancer therapeutics
  • [ISO-abbreviation] Mol. Cancer Ther.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / BMS 754807; 0 / Pyrazoles; 0 / Triazines; EC 2.4.2.30 / Poly(ADP-ribose) Polymerases; EC 2.7.10.1 / Receptor, IGF Type 1; EC 2.7.10.1 / Receptor, Insulin; EC 3.4.22.- / Caspase 3; PQX0D8J21J / Cetuximab
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5. Campistol JM, Eris J, Oberbauer R, Friend P, Hutchison B, Morales JM, Claesson K, Stallone G, Russ G, Rostaing L, Kreis H, Burke JT, Brault Y, Scarola JA, Neylan JF: Sirolimus therapy after early cyclosporine withdrawal reduces the risk for cancer in adult renal transplantation. J Am Soc Nephrol; 2006 Feb;17(2):581-9
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  • Nonskin cancers included those of the lung, larynx, oropharynx, kidney, gastrointestinal tract, prostate, breast, thyroid, and cervix as well as glioma, liposarcoma, astrocytoma, leukemia, lymphoma, and Kaposi's sarcoma.
  • [MeSH-major] Cyclosporine / administration & dosage. Immunosuppressive Agents / administration & dosage. Kidney Transplantation. Neoplasms / epidemiology. Sirolimus / administration & dosage
  • [MeSH-minor] Adult. Disease-Free Survival. Dose-Response Relationship, Drug. Drug Administration Schedule. Drug Therapy, Combination. Follow-Up Studies. Humans. Incidence. Risk Assessment


6. Skubitz KM, Pambuccian S, Manivel JC, Skubitz AP: Identification of heterogeneity among soft tissue sarcomas by gene expression profiles from different tumors. J Transl Med; 2008 May 06;6:23
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  • Morphologic features are generally good predictors of biologic behavior, however, metastatic propensity, tumor growth, and response to chemotherapy may be determined by gene expression patterns that do not correlate well with morphology.
  • In this study, gene expression in 53 samples of STS and AF [including 16 malignant fibrous histiocytoma (MFH), 9 leiomyosarcoma, 12 liposarcoma, 4 synovial sarcoma, and 12 samples of AF] was determined at Gene Logic Inc. (Gaithersburg, MD) using Affymetrix GeneChip U_133 arrays containing approximately 40,000 genes/ESTs.
  • These results suggest that these subgroups may have biological significance, and that these gene sets may be useful for sub-classification of STS.
  • In addition, several genes that are targets of some anti-tumor drugs were found to be differentially expressed in particular subsets of STS.

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  • (PMID = 18460215.001).
  • [ISSN] 1479-5876
  • [Journal-full-title] Journal of translational medicine
  • [ISO-abbreviation] J Transl Med
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA106878-03; United States / NCI NIH HHS / CA / R01 CA106878; United States / NCI NIH HHS / CA / R01 CA106878-03; United States / NCI NIH HHS / CA / R01CA106878
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / RNA, Neoplasm
  • [Other-IDs] NLM/ PMC2412854
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7. Olsen AM, Eisenberg BL, Kuemmerle NB, Flanagan AJ, Morganelli PM, Lombardo PS, Swinnen JV, Kinlaw WB: Fatty acid synthesis is a therapeutic target in human liposarcoma. Int J Oncol; 2010 May;36(5):1309-14
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  • [Title] Fatty acid synthesis is a therapeutic target in human liposarcoma.
  • This study demonstrates the dependence of LS on de novo long-chain fatty acid synthesis for growth.
  • Importantly, the anti-proliferative effect of each agent was prevented by the co-administration of palmitate, the major product of cellular long-chain fatty acid synthesis.
  • Four biochemically distinct agents that target critical points in the fatty acid synthetic pathway exert anti-proliferative effects on LS cells, and rescue of cell growth by palmitic acid suggests that reduced tumor cell lipogenesis mediates the growth inhibition.
  • These findings warrant further studies aimed at the clinical exploitation of the dependence of LS cell growth on fatty acids.

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  • (PMID = 20372807.001).
  • [ISSN] 1791-2423
  • [Journal-full-title] International journal of oncology
  • [ISO-abbreviation] Int. J. Oncol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01CA126618; United States / NIDDK NIH HHS / DK / DK07508; United States / Howard Hughes Medical Institute / / ; United States / NCI NIH HHS / CA / R01 CA126618; United States / NIDDK NIH HHS / DK / T32 DK007508
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Fatty Acids; 0 / Lactones; 0 / Lipids; 95M8R751W8 / orlistat; EC 2.3.1.85 / Fatty Acid Synthases; EC 6.4.1.2 / Acetyl-CoA Carboxylase
  • [Other-IDs] NLM/ NIHMS496463; NLM/ PMC3754849
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8. Hatton JL, Yee LD: Clinical Use of PPARgamma Ligands in Cancer. PPAR Res; 2008;2008:159415
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  • Given the antiproliferative and differentiating effects of PPARgamma ligands on liposarcoma cells, investigation of PPARgamma expression and ligand activation in other solid tumors such as breast, colon, and prostate cancers ensued.
  • The anticancer effects of PPARgamma ligands in cell culture and rodent models of a multitude of tumor types suggest broad applicability of these agents to cancer therapy.

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  • (PMID = 19125177.001).
  • [ISSN] 1687-4757
  • [Journal-full-title] PPAR research
  • [ISO-abbreviation] PPAR Res
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / K07 CA086020; United States / NCRR NIH HHS / RR / M01 RR000034
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC2605846
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9. Mancini A, Borrelli A, Masucci MT, Schiattarella A, Filice S, Rashan J, Maggino T: A conditioned medium from a human liposarcoma-derived cell line induces p53-dependent apoptosis in several tumor cell lines. Oncol Rep; 2000 May-Jun;7(3):629-37
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  • [Title] A conditioned medium from a human liposarcoma-derived cell line induces p53-dependent apoptosis in several tumor cell lines.
  • A novel cell line, named LSA, has been obtained, stabilized, and characterized from a human liposarcoma.
  • LSA-CM had cytostatic and cytotoxic effects (apoptosis and necrosis) associated with down-regulation of c-myc and upregulation of p53 in several human cell lines (breast, lung, glioblastoma, etc. ).
  • In contrast, in the untreated animals the tumor masses were 4 times larger than initial lesions, and numerous metastases were found in the lungs.
  • [MeSH-major] Apoptosis. Culture Media, Conditioned / pharmacology. Liposarcoma. Mammary Neoplasms, Experimental / pathology. Tumor Suppressor Protein p53 / metabolism
  • [MeSH-minor] Animals. Breast Neoplasms. Cell Division / drug effects. Cisplatin / toxicity. Female. Glioblastoma. Guinea Pigs. Humans. Lung Neoplasms. Mice. Mice, Inbred C3H. Mutagenicity Tests. Necrosis. Neoplasm Metastasis / prevention & control. Salmonella typhimurium / drug effects. Skin / drug effects. Skin / pathology. Tumor Cells, Cultured

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  • (PMID = 10767381.001).
  • [ISSN] 1021-335X
  • [Journal-full-title] Oncology reports
  • [ISO-abbreviation] Oncol. Rep.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] GREECE
  • [Chemical-registry-number] 0 / Culture Media, Conditioned; 0 / Tumor Suppressor Protein p53; Q20Q21Q62J / Cisplatin
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10. Li WW, Takahashi N, Jhanwar S, Cordon-Cardo C, Elisseyeff Y, Jimeno J, Faircloth G, Bertino JR: Sensitivity of soft tissue sarcoma cell lines to chemotherapeutic agents: identification of ecteinascidin-743 as a potent cytotoxic agent. Clin Cancer Res; 2001 Sep;7(9):2908-11
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  • [Title] Sensitivity of soft tissue sarcoma cell lines to chemotherapeutic agents: identification of ecteinascidin-743 as a potent cytotoxic agent.
  • The cytotoxic effects of ecteinascidin-743(ET-743), a novel marine natural product, were evaluated and compared with that of clinically used anticancer agents methotrexate, doxorubicin, etoposide, and paclitaxel in eight human soft tissue sarcoma (STS) cell lines.
  • Other cell lines (IC50s) varied considerably and were more resistant to these agents.
  • ET-743 was more potent than any of these agents, with IC50s in the pM range in all of the cell lines.
  • Three colon adenocarcinoma cell lines, HCT-8, HT-29, and HCT-116, and one breast cancer cell line, MCF-7, were 1-2 logs less sensitive to ET-743 than the STS cell lines.
  • Cell lines were also characterized as to expression of oncogenes and tumor suppressor genes to attempt to correlate sensitivity of these cell lines to ET-743 and other chemotherapeutic agents.
  • Only HS-18, a liposarcoma cell line, lacked expression of the retinoblastoma protein.
  • None of the cell lines had detectable expression of P-glycoprotein as measured by immunohistochemistry.
  • ET-743 is an extremely potent cytotoxic agent against human STS cell lines and is being evaluated as an antitumor agent in this disease.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Dioxoles / pharmacology. Isoquinolines / pharmacology. Sarcoma / drug therapy
  • [MeSH-minor] Blotting, Western. Cell Cycle / drug effects. Cell Survival / drug effects. Dose-Response Relationship, Drug. Doxorubicin / pharmacology. Etoposide / pharmacology. Humans. Inhibitory Concentration 50. Methotrexate / pharmacology. P-Glycoprotein / drug effects. P-Glycoprotein / metabolism. Proto-Oncogene Proteins c-bcl-2 / drug effects. Proto-Oncogene Proteins c-bcl-2 / metabolism. Retinoblastoma Protein / drug effects. Retinoblastoma Protein / metabolism. Sensitivity and Specificity. Tetrahydroisoquinolines. Tumor Cells, Cultured. Tumor Suppressor Protein p53 / drug effects. Tumor Suppressor Protein p53 / metabolism

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  • (PMID = 11555609.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P01-CA-47179
  • [Publication-type] Comparative Study; Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Dioxoles; 0 / Isoquinolines; 0 / P-Glycoprotein; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Retinoblastoma Protein; 0 / Tetrahydroisoquinolines; 0 / Tumor Suppressor Protein p53; 114899-77-3 / trabectedin; 6PLQ3CP4P3 / Etoposide; 80168379AG / Doxorubicin; YL5FZ2Y5U1 / Methotrexate
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11. Chandler DS, Singh RK, Caldwell LC, Bitler JL, Lozano G: Genotoxic stress induces coordinately regulated alternative splicing of the p53 modulators MDM2 and MDM4. Cancer Res; 2006 Oct 1;66(19):9502-8
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  • Altered transcripts of the human homologue of mdm2, MDM2, have been identified in human tumors, such as invasive carcinoma of the breast, lung carcinoma, and liposarcoma.
  • MDM2 alternate forms act to negatively regulate the normal MDM2 gene product, thus activating p53.
  • [MeSH-major] Alternative Splicing / radiation effects. Genes, p53. Nuclear Proteins / physiology. Proto-Oncogene Proteins / physiology. Proto-Oncogene Proteins c-mdm2 / physiology. Ubiquitin-Protein Ligases / physiology
  • [MeSH-minor] Animals. Ataxia Telangiectasia Mutated Proteins. Caffeine / pharmacology. Cell Cycle Proteins / antagonists & inhibitors. Cell Line, Tumor / drug effects. Cell Line, Tumor / metabolism. Cell Line, Tumor / radiation effects. Cisplatin / toxicity. DNA Damage. DNA Modification Methylases / genetics. DNA Repair Enzymes / genetics. DNA, Neoplasm / drug effects. DNA, Neoplasm / radiation effects. DNA-Binding Proteins / antagonists & inhibitors. Humans. Mice. Protein Isoforms / genetics. Protein Isoforms / physiology. Protein-Serine-Threonine Kinases / antagonists & inhibitors. Recombinant Fusion Proteins / physiology. Tumor Suppressor Proteins / antagonists & inhibitors. Tumor Suppressor Proteins / genetics. Ultraviolet Rays

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  • (PMID = 17018606.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA16672; United States / NCI NIH HHS / CA / CA47296; United States / NCI NIH HHS / CA / CA90036
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cell Cycle Proteins; 0 / DNA, Neoplasm; 0 / DNA-Binding Proteins; 0 / MDM4 protein, human; 0 / Mdm4 protein, mouse; 0 / Nuclear Proteins; 0 / Protein Isoforms; 0 / Proto-Oncogene Proteins; 0 / Recombinant Fusion Proteins; 0 / Tumor Suppressor Proteins; 3G6A5W338E / Caffeine; EC 2.1.1.- / DNA Modification Methylases; EC 2.1.1.63 / MGMT protein, human; EC 2.7.11.1 / ATM protein, human; EC 2.7.11.1 / ATR protein, human; EC 2.7.11.1 / Ataxia Telangiectasia Mutated Proteins; EC 2.7.11.1 / Atm protein, mouse; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 6.3.2.19 / MDM2 protein, human; EC 6.3.2.19 / Mdm2 protein, mouse; EC 6.3.2.19 / Proto-Oncogene Proteins c-mdm2; EC 6.3.2.19 / Ubiquitin-Protein Ligases; EC 6.5.1.- / DNA Repair Enzymes; Q20Q21Q62J / Cisplatin
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12. Takashima T, Fujiwara Y, Higuchi K, Arakawa T, Yano Y, Hasuma T, Otani S: PPAR-gamma ligands inhibit growth of human esophageal adenocarcinoma cells through induction of apoptosis, cell cycle arrest and reduction of ornithine decarboxylase activity. Int J Oncol; 2001 Sep;19(3):465-71
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  • Peroxisome proliferator-activated receptor gamma (PPAR-gamma), a member of the nuclear hormone receptor superfamily, is involved in suppression of growth of several types of tumors such as liposarcoma, breast cancer, prostate cancer, and colon cancer, possibly through induction of cell cycle arrest and/or apoptosis.
  • [MeSH-major] Adenocarcinoma / metabolism. Apoptosis / drug effects. Cell Cycle / drug effects. Esophageal Neoplasms / metabolism. Ornithine Decarboxylase / metabolism. Prostaglandin D2 / pharmacology. Receptors, Cytoplasmic and Nuclear / genetics. Thiazolidinediones. Transcription Factors / genetics
  • [MeSH-minor] Antineoplastic Agents / pharmacology. Blotting, Western. Carcinoma, Squamous Cell / metabolism. Carcinoma, Squamous Cell / pathology. Cell Division / drug effects. Chromans / pharmacology. DNA Primers / chemistry. Flow Cytometry. Humans. Immunologic Factors / pharmacology. Ligands. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Tetrazolium Salts. Thiazoles / pharmacology. Thymidine / chemistry. Tumor Cells, Cultured / drug effects. Tumor Cells, Cultured / physiology

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  • (PMID = 11494023.001).
  • [ISSN] 1019-6439
  • [Journal-full-title] International journal of oncology
  • [ISO-abbreviation] Int. J. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / 15-deoxy-delta(12,14)-prostaglandin J2; 0 / Antineoplastic Agents; 0 / Chromans; 0 / DNA Primers; 0 / Immunologic Factors; 0 / Ligands; 0 / RNA, Messenger; 0 / Receptors, Cytoplasmic and Nuclear; 0 / Tetrazolium Salts; 0 / Thiazoles; 0 / Thiazolidinediones; 0 / Transcription Factors; 298-93-1 / thiazolyl blue; EC 4.1.1.17 / Ornithine Decarboxylase; I66ZZ0ZN0E / troglitazone; RXY07S6CZ2 / Prostaglandin D2; VC2W18DGKR / Thymidine
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13. Dass CR, Galloway SJ, Choong PF: Dz13, a c-jun DNAzyme, is a potent inducer of caspase-2 activation. Oligonucleotides; 2010 Jun;20(3):137-46
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  • Dz13-mediated cell death occurred even in the absence of known caspase-2 molecular partners in p53-induced protein with a death domain, RIP-associated Ich-1/CED homologous protein with death domain, or DNA-dependent protein kinase catalytic subunit, or other caspases in cell lines of breast cancer, prostate cancer, osteosarcoma, and liposarcoma. z-VDVAD-fmk, caspase-2(-/-) mouse embryonic fibroblasts and siRNA silencing of caspase-2 in tumor cells abrogated Dz13-mediated cell death.
  • These findings provide hope that Dz13, and other agents that evoke activation of caspase-2, may be therapeutic clinically.
  • [MeSH-minor] Animals. Base Sequence. Catalytic Domain. Cell Line, Tumor. DNA Primers. Enzyme Activation. Female. Humans. Immunohistochemistry. In Situ Nick-End Labeling. Mice. Mice, Inbred BALB C. Mice, Nude. Neoplasms / enzymology. Neoplasms / pathology. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 20180631.001).
  • [ISSN] 1557-8526
  • [Journal-full-title] Oligonucleotides
  • [ISO-abbreviation] Oligonucleotides
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA Primers; 0 / DNA, Catalytic; 0 / Dz13 DNAzyme; EC 3.4.22.- / Caspase 2
  • [Number-of-references] 34
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14. Hughes DT, Martel PM, Kinlaw WB, Eisenberg BL: The synthetic triterpenoid CDDO-Im inhibits fatty acid synthase expression and has antiproliferative and proapoptotic effects in human liposarcoma cells. Cancer Invest; 2008 Mar;26(2):118-27
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  • [Title] The synthetic triterpenoid CDDO-Im inhibits fatty acid synthase expression and has antiproliferative and proapoptotic effects in human liposarcoma cells.
  • This study characterizes a novel human liposarcoma cell line (LiSa-2) and defines the mechanism of its response to a synthetic triterpenoid.
  • Fatty acid synthase (FAS) is a key enzyme of de-novo fatty acid synthesis and is highly expressed in both human liposarcoma tissue specimens and LiSa-2 cells.
  • Thus, CDDO-Im and Cerulenin act at different loci to inhibit long chain fatty acid synthesis in liposarcoma cells.
  • The observed dependence of liposarcomas on lipogenesis to support their growth and survival provides a novel approach to the treatment of liposarcomas with agents that target fatty acid production.
  • [MeSH-major] Apoptosis / drug effects. Cell Proliferation / drug effects. Fatty Acid Synthases / antagonists & inhibitors. Imidazoles / pharmacology. Liposarcoma / drug therapy. Oleanolic Acid / analogs & derivatives
  • [MeSH-minor] Adipocytes / cytology. Adipocytes / drug effects. Adipocytes / metabolism. Antigens, CD95 / genetics. Antigens, CD95 / metabolism. Blotting, Western. Cerulenin / pharmacology. Drug Synergism. Drug Therapy, Combination. Fatty Acid Synthesis Inhibitors / pharmacology. Glycerolphosphate Dehydrogenase / metabolism. Humans. Palmitic Acid / metabolism. Tumor Cells, Cultured / drug effects

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  • (PMID = 18259941.001).
  • [ISSN] 1532-4192
  • [Journal-full-title] Cancer investigation
  • [ISO-abbreviation] Cancer Invest.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA126618
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 1-(2-cyano-3,12-dioxooleana-1,9-dien-28-oyl) imidazole; 0 / Antigens, CD95; 0 / FAS protein, human; 0 / Fatty Acid Synthesis Inhibitors; 0 / Imidazoles; 17397-89-6 / Cerulenin; 2V16EO95H1 / Palmitic Acid; 6SMK8R7TGJ / Oleanolic Acid; EC 1.1.- / Glycerolphosphate Dehydrogenase; EC 2.3.1.85 / Fatty Acid Synthases
  • [Other-IDs] NLM/ NIHMS503932; NLM/ PMC3768287
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15. Sporn MB, Suh N, Mangelsdorf DJ: Prospects for prevention and treatment of cancer with selective PPARgamma modulators (SPARMs). Trends Mol Med; 2001 Sep;7(9):395-400
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  • Peroxisome proliferator-activated receptor gamma (PPARgamma), a nuclear receptor and transcription factor that regulates the expression of many genes relevant to carcinogenesis, is now an important target for development of new drugs for the prevention and treatment of cancer.
  • Ligands for PPARgamma suppress breast carcinogenesis in experimental models and induce differentiation of human liposarcoma cells.
  • [MeSH-major] Neoplasms / drug therapy. Neoplasms / prevention & control. Receptors, Cytoplasmic and Nuclear / metabolism. Transcription Factors / metabolism
  • [MeSH-minor] Animals. Antineoplastic Agents / therapeutic use. Disease Susceptibility. Humans. Ligands. Models, Molecular. Neoplasm Invasiveness. Protein Conformation. Selective Estrogen Receptor Modulators / therapeutic use

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  • (PMID = 11530334.001).
  • [ISSN] 1471-4914
  • [Journal-full-title] Trends in molecular medicine
  • [ISO-abbreviation] Trends Mol Med
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA78814
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Ligands; 0 / Receptors, Cytoplasmic and Nuclear; 0 / Selective Estrogen Receptor Modulators; 0 / Transcription Factors
  • [Number-of-references] 75
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16. Taamma A, Misset JL, Riofrio M, Guzman C, Brain E, Lopez Lazaro L, Rosing H, Jimeno JM, Cvitkovic E: Phase I and pharmacokinetic study of ecteinascidin-743, a new marine compound, administered as a 24-hour continuous infusion in patients with solid tumors. J Clin Oncol; 2001 Mar 01;19(5):1256-65
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  • Antitumor activity was observed at the three highest DLs, including three partial responses (breast cancer, osteosarcoma, and liposarcoma), and four patients (all with progressing soft tissue sarcomas) had stable disease lasting > or = 3 months.
  • [MeSH-major] Antineoplastic Agents, Alkylating / administration & dosage. Dioxoles / administration & dosage. Isoquinolines / administration & dosage. Neoplasms / drug therapy
  • [MeSH-minor] Adult. Aged. Area Under Curve. Dose-Response Relationship, Drug. Female. Humans. Infusions, Intravenous. Male. Middle Aged. Neutropenia / chemically induced. Tetrahydroisoquinolines. Thrombocytopenia / chemically induced

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  • (PMID = 11230466.001).
  • [ISSN] 0732-183X
  • [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] Clinical Trial; Clinical Trial, Phase I; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 0 / Dioxoles; 0 / Isoquinolines; 0 / Tetrahydroisoquinolines; ID0YZQ2TCP / trabectedin
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17. Krzystyniak KL: Current strategies for anticancer chemoprevention and chemoprotection. Acta Pol Pharm; 2002 Nov-Dec;59(6):473-8
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  • Relatively new targets in drug design projects in cancer pharmacology include cytostatic agents, immune system modulators, and angiogenesis inhibitors.
  • Preventive oncology applies pharmacological agents to reverse, retard, or halt progression of neoplastic cells to invasive malignancy.
  • Ligands for the peroxisome proliferator-activated receptor gamma (PPAR-gamma) suppress breast carcinogenesis in experimental models and induce differentiation of human liposarcoma cells.
  • Enzymatic approach in endocrine-related tumors involve inhibition of aromatase to prevent breast cancer and inhibition of 5-alpha-reductase to prevent prostate cancer.
  • [MeSH-major] Anticarcinogenic Agents / pharmacology. Neoplasms / prevention & control
  • [MeSH-minor] 5-alpha Reductase Inhibitors. Alkyl and Aryl Transferases / antagonists & inhibitors. Animals. Apoptosis / drug effects. Aromatase Inhibitors. Farnesyltranstransferase. Humans. Inflammation / pathology. Prostaglandins / physiology. Receptors, Cytoplasmic and Nuclear / antagonists & inhibitors. Receptors, Retinoic Acid / antagonists & inhibitors. Retinoid X Receptors. Selective Estrogen Receptor Modulators. Transcription Factors / antagonists & inhibitors

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  • (PMID = 12669776.001).
  • [ISSN] 0001-6837
  • [Journal-full-title] Acta poloniae pharmaceutica
  • [ISO-abbreviation] Acta Pol Pharm
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / 5-alpha Reductase Inhibitors; 0 / Anticarcinogenic Agents; 0 / Aromatase Inhibitors; 0 / Prostaglandins; 0 / Receptors, Cytoplasmic and Nuclear; 0 / Receptors, Retinoic Acid; 0 / Retinoid X Receptors; 0 / Selective Estrogen Receptor Modulators; 0 / Transcription Factors; EC 2.5.- / Alkyl and Aryl Transferases; EC 2.5.1.29 / Farnesyltranstransferase
  • [Number-of-references] 32
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