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1. Ceulemans J, De Wever I, Sciot R, Debiec-Rychter M, van Oosterom AT: A sarcoma at the site of previous extravasation of adriamycin. Sarcoma; 2002;6(4):135-9
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  • We report the case of a 66-year-old man presenting with a high-grade pleomorphic sarcoma at the left elbow 16 years after the extravasation of adriamycin given for a malignant ifbrous histiocytoma of the tibia.We suggest that this sarcoma originated in a multistep way over many years, out of the chronic inflammatory tissue that developed due to a non-specific cellular damage at the nuclear level, interfering with normal cell replication necessary for normal healing tissue healing.

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  • (PMID = 18521350.001).
  • [ISSN] 1357-714X
  • [Journal-full-title] Sarcoma
  • [ISO-abbreviation] Sarcoma
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Egypt
  • [Other-IDs] NLM/ PMC2395497
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2. Yamate J, Maeda M, Benn SJ, Laithwaite JE, Allan A, Ide M, Kuwamura M, Kotani T, Sakuma S, LaMarre J: Effects of lipopolysaccharide on a macrophage-like cell line (HS-P) from a rat histiocytic sarcoma. J Comp Pathol; 2001 Jul;125(1):15-24
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  • To characterize a newly established rat histiocytic sarcoma-derived cell line (HS-P), immunophenotypic changes and cellular growth responses of HS-P cells exposed to LPS were investigated and compared with those of MT-9 cells isolated from a rat malignant fibrous histiocytoma.
  • To evaluate cellular growth after the addition of LPS or fetal bovine serum, DNA synthesis was examined by measuring tritiated thymidine incorporation, and the mRNA expression of c- jun and c- myc (immediate early genes in the cell cycle) was examined by Northern blot analysis.
  • [MeSH-major] Escherichia coli. Histiocytoma, Benign Fibrous / veterinary. Lipopolysaccharides / pharmacology. Macrophages / drug effects. Rodent Diseases / immunology
  • [MeSH-minor] Animals. Blotting, Northern / veterinary. Cell Count. DNA / biosynthesis. Dose-Response Relationship, Immunologic. Immunophenotyping / veterinary. Phagocytosis / drug effects. Proto-Oncogene Proteins c-jun / biosynthesis. Proto-Oncogene Proteins c-jun / genetics. Proto-Oncogene Proteins c-myc / biosynthesis. Proto-Oncogene Proteins c-myc / genetics. RNA, Messenger / metabolism. Rats. Tumor Cells, Cultured


3. Jyothi MD, Khar A: Regulation of CD40L expression on natural killer cells by interleukin-12 and interferon gamma: its role in the elicitation of an effective antitumor immune response. Cancer Immunol Immunother; 2000 Dec;49(10):563-72
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  • Our earlier studies have shown that spontaneous regression of a rat histiocytoma transplanted s.c. is mediated by CD8 + CD3- NK cells.
  • Tumor-transplanted animals showed enhanced expression of CD40L on natural killer (NK) and T cells, when compared to cells from normal animals.
  • Administration of anti-(interleukin-12) (anti-IL-12) and anti-(interferon gamma) (anti-IFNgamma) antibodies in tumor-bearing animals showed down-regulation of the expression of CD40L on NK and T cells with simultaneous inhibition of cytotoxic acitivity of NK cells, cytokine release and the production of antitumor antibody.
  • Furthermore, the signaling via CD40L through the use of anti-CD40L antibody promoted the in vitro activation of cytotoxic as well as NF-kappaB binding activity in NK cells from tumor-transplanted animals.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. CD40 Ligand / biosynthesis. Gene Expression Regulation, Neoplastic / drug effects. Histiocytoma, Benign Fibrous / therapy. Interferon-gamma / physiology. Interleukin-12 / physiology. Killer Cells, Natural / drug effects
  • [MeSH-minor] Animals. Antigens, CD40 / physiology. Coculture Techniques. Cricetinae. Cytotoxicity, Immunologic / drug effects. Humans. Lymphocyte Activation / drug effects. Mice. NF-kappa B / metabolism. Neoplasm Transplantation. Rats. Rats, Wistar. T-Lymphocytes, Cytotoxic / drug effects. T-Lymphocytes, Cytotoxic / immunology. T-Lymphocytes, Cytotoxic / metabolism. Transcription, Genetic. Tumor Cells, Cultured / immunology. Tumor Cells, Cultured / metabolism. Tumor Cells, Cultured / transplantation

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  • (PMID = 11129327.001).
  • [ISSN] 0340-7004
  • [Journal-full-title] Cancer immunology, immunotherapy : CII
  • [ISO-abbreviation] Cancer Immunol. Immunother.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antigens, CD40; 0 / NF-kappa B; 147205-72-9 / CD40 Ligand; 187348-17-0 / Interleukin-12; 82115-62-6 / Interferon-gamma
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4. Anjum R, Joshi P, Khar A: Induction of apoptosis in AK-5 tumor cells by a serum factor from tumor rejecting animals: cytochrome c release independent of Bcl-2 and caspases. Cell Death Differ; 2001 Oct;8(10):1038-46
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  • [Title] Induction of apoptosis in AK-5 tumor cells by a serum factor from tumor rejecting animals: cytochrome c release independent of Bcl-2 and caspases.
  • Here we show that the sera from the animals which had spontaneously rejected the AK-5 tumor (a rat histiocytoma) had an effective and potent ability to counteract and kill tumor cells by inducing apoptosis, with a high degree of specificity.
  • [MeSH-major] Apoptosis. Biological Factors / blood. Cytochrome c Group / metabolism. Histiocytoma, Benign Fibrous / pathology. Skin Neoplasms / pathology
  • [MeSH-minor] Animals. Biological Transport. Caspases / physiology. Cyclosporine / pharmacology. Intracellular Membranes / metabolism. Membrane Potentials. Mitochondria / physiology. Neoplasm Transplantation. Permeability / drug effects. Proto-Oncogene Proteins c-bcl-2 / genetics. Proto-Oncogene Proteins c-bcl-2 / physiology. Rats. Transfection. Tumor Cells, Cultured

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  • (PMID = 11598802.001).
  • [ISSN] 1350-9047
  • [Journal-full-title] Cell death and differentiation
  • [ISO-abbreviation] Cell Death Differ.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biological Factors; 0 / Cytochrome c Group; 0 / Proto-Oncogene Proteins c-bcl-2; 83HN0GTJ6D / Cyclosporine; EC 3.4.22.- / Caspases
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5. Labonte S, Hanna W, Bandarchi-Chamkhaleh B: A study of CD117 expression in dermatofibrosarcoma protuberans and cellular dermatofibroma. J Cutan Pathol; 2007 Nov;34(11):857-60
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  • [Title] A study of CD117 expression in dermatofibrosarcoma protuberans and cellular dermatofibroma.
  • BACKGROUND: Dermatofibrosarcoma protuberans (DFSP) is a relatively uncommon spindle cell tumor of the skin.
  • Cellular dermatofibroma (CDF) can mimic DFSP, but typical cases are easily differentiated from DFSP by their staining pattern for CD34 and factor 13a.
  • Therefore, if adjuvant therapy is attempted with drugs such as STI571 (Imatinib), the eligibility of patients should not be based on immunohistochemical assessment of CD117 expression.
  • [MeSH-major] Dermatofibrosarcoma / metabolism. Histiocytoma, Benign Fibrous / metabolism. Proto-Oncogene Proteins c-kit / biosynthesis. Skin Neoplasms / metabolism


6. Jyothi D, Vanathi P, Mangala Gowri P, Rama Subba Rao V, Madhusudana Rao J, Sreedhar AS: Diferuloylmethane augments the cytotoxic effects of piplartine isolated from Piper chaba. Toxicol In Vitro; 2009 Sep;23(6):1085-91
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  • Natural compound based anticancer drug discovery is gaining interest against a wide variety of tumors.
  • E-piplartine (trans-piplartine), a natural compound isolated from Piper chaba roots is examined against rat histiocytoma (BC-8), mouse embryonal carcinoma (PCC4), mouse macrophages (P388D1 and J774), and human neuroblastoma (IMR32) tumor cells.
  • The combinatorial treatment of piplartine with diferuloylmethane (curcumin), an anti-inflammatory and anticancer agent, significantly enhanced the piplartine induced cytotoxicity in tumor cells.
  • The over expression of heat shock protein 70, Hsp70 in rat histiocytic tumor cells interfered with piplartine induced cytotoxicity, hence, a cross talk between stress response and anticancer agents is presented.
  • Our data demonstrates the biological and medicinal importance of piplartine isolated from the roots of P. chaba, and indicates that E-piplartine may be a promising candidate to use in combinatorial treatments to combat cancer.
  • [MeSH-major] Antineoplastic Agents, Phytogenic / pharmacology. Curcumin / pharmacology. Piper / chemistry. Piperidones / pharmacology
  • [MeSH-minor] Animals. Cell Cycle / drug effects. Cell Line, Tumor. Cells, Cultured. Dose-Response Relationship, Drug. Drug Synergism. Gene Expression. HSP70 Heat-Shock Proteins / genetics. Humans. Mice. Plant Roots. Rats. Stereoisomerism


7. Yamate J, Kotera T, Kuwamura M, Kotani T: Potential osteogenic differentiation of cisplatin-resistant rat malignant fibrous histiocytoma-derived cell lines. Exp Toxicol Pathol; 2007 Apr;58(5):299-309
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  • [Title] Potential osteogenic differentiation of cisplatin-resistant rat malignant fibrous histiocytoma-derived cell lines.
  • Histological modulations in tumor cells treated with anti-cancer drugs have been reported.
  • The histogenesis of malignant fibrous histiocytoma (MFH) remains elusive.
  • To investigate cellular characteristics and alterations, therefore, we derived cisplatin-resistant MFH cell lines (MT-PR and MT-10R) from MT-P and MT-10, respectively, and compared them with MT-10, a non-cisplatin-resistant MFH line (MT-10 was isolated as a clone cell line from MT-P, and MT-P was originally established from a rat spontaneous MFH).
  • However, MT-10R and MT-PR reduced ED1-positive cell numbers.
  • MT-10 developed tumors of a storiform pattern, while MT-10R and MT-PR tumors comprise round or polygonal cells arranged in a compact sheet.
  • Additionally, MT-PR tumors included ossifying areas.
  • MT-10R and MT-PR, and their tumors showed a reaction to alkaline phosphatase (ALP), a marker of osteoblasts.
  • RT-PCR revealed that mRNAs of bone morphogenetic protein (BMP)-2, BMP-6 and osteopontin were significantly increased in MT-10R and MT-PR tumors.
  • Cisplatin-resistant MFH cells had potential to differentiate into osteogenic tissues by producing osteogenic factors, suggesting that MFH histology may be altered under anti-cancer drug treatments.
  • Recently, cancer differentiation-based therapy, that could be induced by anti-cancer drugs, has been implied.
  • MT-10R and MT-PR become useful experimental systems for studies on cellular differentiation provoked by anti-cancer drugs.
  • [MeSH-major] Bone Morphogenetic Proteins / biosynthesis. Cell Differentiation / drug effects. Cisplatin / pharmacology. Drug Resistance, Neoplasm / drug effects. Histiocytoma, Malignant Fibrous / pathology. Osteoblasts / pathology
  • [MeSH-minor] Animals. Bone Morphogenetic Protein 1. Bone Morphogenetic Protein 6. Clone Cells. Enzyme-Linked Immunosorbent Assay. Immunohistochemistry. Metalloendopeptidases / biosynthesis. Neoplasm Transplantation. Osteopontin / biosynthesis. RNA, Messenger / biosynthesis. Rats. Rats, Inbred F344. Reverse Transcriptase Polymerase Chain Reaction. Tumor Cells, Cultured

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  • (PMID = 17267196.001).
  • [ISSN] 0940-2993
  • [Journal-full-title] Experimental and toxicologic pathology : official journal of the Gesellschaft für Toxikologische Pathologie
  • [ISO-abbreviation] Exp. Toxicol. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Bmp6 protein, rat; 0 / Bone Morphogenetic Protein 6; 0 / Bone Morphogenetic Proteins; 0 / RNA, Messenger; 106441-73-0 / Osteopontin; EC 3.4.24.- / Metalloendopeptidases; EC 3.4.24.19 / Bmp1 protein, rat; EC 3.4.24.19 / Bone Morphogenetic Protein 1; Q20Q21Q62J / Cisplatin
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8. Honoki K, Yoshitani K, Tsujiuchi T, Mori T, Tsutsumi M, Morishita T, Takakura Y, Mii Y: Growth inhibition and induction of apoptosis by flavopiridol in rat lung adenocarcinoma, osteosarcoma and malignant fibrous histiocytoma cell lines. Oncol Rep; 2004 May;11(5):1025-30
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  • [Title] Growth inhibition and induction of apoptosis by flavopiridol in rat lung adenocarcinoma, osteosarcoma and malignant fibrous histiocytoma cell lines.
  • In this study, we focused on the effects of flavopiridol on chemically-induced rat lung adenocarcinoma, osteosarcoma and malignant fibrous histiocytoma (MFH) cell lines showing different pattern of p16INK4a status.
  • The data demonstrated that flavopiridol inhibited cellular growth in a dose- and time-dependent manner, inducing apoptosis within 24 h in all cell lines at a concentration of 300 nM.
  • 5-aza 2'-deoxycytidine (5-Aza-CdR) induced p16INK4a expression and inhibited cellular growth in lung adenocarcinoma at a similar level to that with flavopiridol treatment.
  • These data indicate that flavopiridol shows cell type specific inhibition and possibly acts in a more compensatory manner for endogenous p16INK4a function in tumor cells having the aberrations of p16INK4a gene.
  • [MeSH-major] Adenocarcinoma / pathology. Apoptosis / drug effects. Bone Neoplasms / pathology. Flavonoids / pharmacology. Histiocytoma, Benign Fibrous / pathology. Lung Neoplasms / pathology. Osteosarcoma / pathology. Piperidines / pharmacology
  • [MeSH-minor] Animals. Cell Division / drug effects. Cell Line, Tumor. Cyclin D1 / genetics. Cyclin-Dependent Kinase 4. Cyclin-Dependent Kinase Inhibitor p16 / genetics. Cyclin-Dependent Kinases / genetics. DNA Methylation / drug effects. Gene Expression Regulation, Neoplastic / drug effects. Promoter Regions, Genetic / genetics. Proto-Oncogene Proteins / genetics. RNA, Messenger / genetics. RNA, Messenger / metabolism. Rats

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  • (PMID = 15069542.001).
  • [ISSN] 1021-335X
  • [Journal-full-title] Oncology reports
  • [ISO-abbreviation] Oncol. Rep.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Cyclin-Dependent Kinase Inhibitor p16; 0 / Flavonoids; 0 / Piperidines; 0 / Proto-Oncogene Proteins; 0 / RNA, Messenger; 136601-57-5 / Cyclin D1; 45AD6X575G / alvocidib; EC 2.7.11.22 / Cdk4 protein, rat; EC 2.7.11.22 / Cyclin-Dependent Kinase 4; EC 2.7.11.22 / Cyclin-Dependent Kinases
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9. Yoshitani K, Honoki K, Morishita T, Kido A, Miyauchi Y, Mii Y, Takakura Y: Growth inhibition of rat osteosarcoma and malignant fibrous histiocytoma cells by tyrosine kinase inhibitor STI571. In Vivo; 2003 May-Jun;17(3):255-8
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  • [Title] Growth inhibition of rat osteosarcoma and malignant fibrous histiocytoma cells by tyrosine kinase inhibitor STI571.
  • We have recently established rat osteosarcoma and malignant fibrous histiocytoma (MFH) cell lines.
  • The effect of STI571 on cellular growth measured by MTS colorimetric dye reduction showed that the growth of each cell line was inhibited in a dose- and time-dependent manner.
  • These data suggested that STI571 tyrosine kinase inhibitor plays a role in blocking or slowing the rate of growth of MFH and osteosarcoma cells expressing tyrosine kinase type receptor.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Bone Neoplasms / drug therapy. Histiocytoma, Benign Fibrous / drug therapy. Osteosarcoma / drug therapy. Piperazines / therapeutic use. Protein-Tyrosine Kinases / antagonists & inhibitors. Pyrimidines / therapeutic use
  • [MeSH-minor] Animals. Benzamides. Cell Division / drug effects. Cell Line, Tumor. Cell Survival / drug effects. Imatinib Mesylate. Proto-Oncogene Proteins c-kit / genetics. RNA, Messenger / genetics. Rats

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  • (PMID = 12929576.001).
  • [ISSN] 0258-851X
  • [Journal-full-title] In vivo (Athens, Greece)
  • [ISO-abbreviation] In Vivo
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 0 / RNA, Messenger; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit
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10. Singh S, Khar A: Differential gene expression during apoptosis induced by a serum factor: role of mitochondrial F0-F1 ATP synthase complex. Apoptosis; 2005 Dec;10(6):1469-82
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  • In an attempt to characterize differential gene expression during serum factor induced apoptosis in AK-5 cells (a rat histiocytoma), we found subunit 6 and subunit 8 of the transmembrane proton channel and subunit alpha of the catalytic core of the mitochondrial F(0)-F(1) ATP synthase complex to be up regulated during apoptosis.
  • The increase in the expression levels of these subunits was concomitant with a transient increase in the intracellular ATP levels, suggesting that the increase in cellular ATP content is a result of the increase in the expression of ATP synthase subunits' gene and de novo protein synthesis.
  • Depleting the cellular ATP levels with oligomycin inhibited apoptosis significantly, pointing to the requirement of ATP during apoptosis.
  • [MeSH-major] Apoptosis / genetics. Biological Factors / pharmacology. Gene Expression Profiling. Gene Expression Regulation / drug effects. Mitochondrial Proton-Translocating ATPases / genetics. Serum / chemistry
  • [MeSH-minor] Adenosine Triphosphate / metabolism. Animals. Caspase Inhibitors. Cell Line, Tumor. Cycloheximide / pharmacology. Cytochromes c / secretion. Dactinomycin / pharmacology. Enzyme Induction / drug effects. Enzyme Inhibitors / pharmacology. Intracellular Space / drug effects. Intracellular Space / enzymology. Membrane Potential, Mitochondrial / drug effects. Mitochondria / drug effects. Mitochondria / enzymology. Mitochondria / secretion. Oligomycins / pharmacology. Protein Biosynthesis / drug effects. Protein Subunits / biosynthesis. Protein Subunits / genetics. Rats. Time Factors

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  • (PMID = 16215688.001).
  • [ISSN] 1360-8185
  • [Journal-full-title] Apoptosis : an international journal on programmed cell death
  • [ISO-abbreviation] Apoptosis
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biological Factors; 0 / Caspase Inhibitors; 0 / Enzyme Inhibitors; 0 / Oligomycins; 0 / Protein Subunits; 1CC1JFE158 / Dactinomycin; 8L70Q75FXE / Adenosine Triphosphate; 9007-43-6 / Cytochromes c; 98600C0908 / Cycloheximide; EC 3.6.3.- / Mitochondrial Proton-Translocating ATPases
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11. Clayer M, Bouralexis S, Evdokiou A, Hay S, Atkins GJ, Findlay DM: Enhanced apoptosis of soft tissue sarcoma cells with chemotherapy: A potential new approach using TRAIL. J Orthop Surg (Hong Kong); 2001 Dec;9(2):19-22
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  • We investigated the possibility of enhancing the efficacy of chemotherapy by utilising the recently identified cytokine, tumour necrosis factor-related apoptosis-inducing ligand (TRAIL/Apo2L) in combination with standard chemotherapeutic agents.
  • Fresh human soft tissue sarcomas (rhabdomyosarcoma, fibrosarcoma, malignant fibrous histiocytoma) were obtained at biopsy and dispersed tumour cells were incubated in cell culture with standard cytotoxic agents, either as single agents or in combination with TRAIL.
  • The chemotherapeutic agents were, at best, moderately effective, in terms of induction of cellular apoptosis, although the fibrosarcoma was completely unresponsive to all single agents.
  • In contrast, the addition of TRAIL and drug together produced a significant increase in sarcoma cell apoptosis, with TRAIL and doxorubicin the most effective combination.

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  • (PMID = 12118126.001).
  • [ISSN] 2309-4990
  • [Journal-full-title] Journal of orthopaedic surgery (Hong Kong)
  • [ISO-abbreviation] J Orthop Surg (Hong Kong)
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
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12. Taiyab A, Sreedhar AS, Rao ChM: Hsp90 inhibitors, GA and 17AAG, lead to ER stress-induced apoptosis in rat histiocytoma. Biochem Pharmacol; 2009 Jul 15;78(2):142-52
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  • [Title] Hsp90 inhibitors, GA and 17AAG, lead to ER stress-induced apoptosis in rat histiocytoma.
  • Hsp90 inhibition by specific inhibitors leads to destabilization and loss of activity of such proteins, thereby leading to inhibition of multiple signaling cascades.
  • We have investigated the effect of Hsp90 inhibition on a non-adherent rat histiocytoma cell line, BC-8, using geldanamycin and 17-Allylamino-17-demethoxygeldanamycin.
  • [MeSH-major] Apoptosis / physiology. Benzoquinones / pharmacology. Endoplasmic Reticulum / metabolism. HSP90 Heat-Shock Proteins / antagonists & inhibitors. Histiocytoma / metabolism. Histiocytoma / pathology. Lactams, Macrocyclic / pharmacology
  • [MeSH-minor] Animals. Cell Line, Tumor. Intracellular Membranes / drug effects. Intracellular Membranes / physiology. Membrane Potentials / drug effects. Membrane Potentials / physiology. Mice. Mitochondrial Membranes / drug effects. Mitochondrial Membranes / metabolism. Rats. Stress, Physiological / drug effects. Stress, Physiological / physiology

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  • (PMID = 19464431.001).
  • [ISSN] 1873-2968
  • [Journal-full-title] Biochemical pharmacology
  • [ISO-abbreviation] Biochem. Pharmacol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Benzoquinones; 0 / HSP90 Heat-Shock Proteins; 0 / Lactams, Macrocyclic; 4GY0AVT3L4 / tanespimycin; Z3K3VJ16KU / geldanamycin
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13. Reinecke P, Steckstor M, Schmitz M, Gabbert HE, Gerharz CD: Chemotherapeutic potential of plant alkaloids and multidrug resistance mechanisms in malignant fibrous histiocytoma of the heart. Oncol Rep; 2004 Mar;11(3):641-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Chemotherapeutic potential of plant alkaloids and multidrug resistance mechanisms in malignant fibrous histiocytoma of the heart.
  • Primary malignant fibrous histiocytoma (MFH) of the heart is a rare and highly malignant soft tissue tumor, which is largely resistant to conventional chemotherapy and radiotherapy.
  • Therefore, we analyzed growth inhibitory effects of different chemotherapeutic agents and mechanisms of drug resistance in the recently established cell line MFH-H derived from a human primary cardiac MFH.
  • The expression and function of multidrug resistance-related proteins, i.e. the P-glycoprotein, the multidrug resistance-associated protein (MRP) and the lung resistance-related protein (LRP) were determined by FACScan and functional assays of cellular drug efflux.
  • The response of MFH-H to etoposide, vincristine and paclitaxel/Taxol could not be predicted by the expression and function of P-glycoprotein, MRP and LRP.
  • [MeSH-major] Alkaloids / therapeutic use. Drug Resistance, Multiple. Heart Neoplasms / drug therapy. Histiocytoma, Benign Fibrous / drug therapy. Plant Extracts / therapeutic use. Soft Tissue Neoplasms / drug therapy
  • [MeSH-minor] Antineoplastic Agents, Phytogenic / pharmacology. Cell Line, Tumor. Cell Separation. Cell Survival. Cells, Cultured. Coloring Agents / pharmacology. Dose-Response Relationship, Drug. Drug Resistance, Neoplasm. Etoposide / pharmacology. Flow Cytometry. Humans. Inhibitory Concentration 50. P-Glycoprotein / metabolism. Paclitaxel / pharmacology. Phenotype. Tetrazolium Salts / pharmacology. Thiazoles / pharmacology. Vault Ribonucleoprotein Particles / metabolism. Vincristine / pharmacology

  • Genetic Alliance. consumer health - Malignant fibrous histiocytoma.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. METHYLTHIAZOLETETRAZOLIUM .
  • Hazardous Substances Data Bank. TAXOL .
  • Hazardous Substances Data Bank. ETOPOSIDE .
  • Hazardous Substances Data Bank. VINCRISTINE .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
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  • (PMID = 14767515.001).
  • [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 / Alkaloids; 0 / Antineoplastic Agents, Phytogenic; 0 / Coloring Agents; 0 / P-Glycoprotein; 0 / Plant Extracts; 0 / Tetrazolium Salts; 0 / Thiazoles; 0 / Vault Ribonucleoprotein Particles; 0 / major vault protein; 298-93-1 / thiazolyl blue; 5J49Q6B70F / Vincristine; 6PLQ3CP4P3 / Etoposide; P88XT4IS4D / Paclitaxel
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14. Singh S, Khar A: Activation of NFkappaB and Ub-proteasome pathway during apoptosis induced by a serum factor is mediated through the upregulation of the 26S proteasome subunits. Apoptosis; 2006 May;11(5):845-59
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • We have been investigating differential gene expression associated with apoptosis in AK-5 cells (a spontaneously regressing rat histiocytoma) and have observed catalytic subunits beta 7 and alpha 5 of the 26S proteasome and ubiquitin to be upregulated during apoptosis induced by a variety of agents.
  • [MeSH-major] Apoptosis. Blood Proteins / chemistry. NF-kappa B / metabolism. Proteasome Endopeptidase Complex / metabolism. Ubiquitin / metabolism. Up-Regulation
  • [MeSH-minor] Animals. Cell Line, Tumor. Histiocytoma / blood. Histiocytoma / metabolism. Histiocytoma / pathology. Rats. Rats, Wistar. Time Factors

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  • (PMID = 16532374.001).
  • [ISSN] 1360-8185
  • [Journal-full-title] Apoptosis : an international journal on programmed cell death
  • [ISO-abbreviation] Apoptosis
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Blood Proteins; 0 / NF-kappa B; 0 / Ubiquitin; EC 3.4.25.1 / Proteasome Endopeptidase Complex; EC 3.4.99.- / ATP dependent 26S protease
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