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1. Jee SH, Shen SC, Chiu HC, Tsai WL, Kuo ML: Overexpression of interleukin-6 in human basal cell carcinoma cell lines increases anti-apoptotic activity and tumorigenic potency. Oncogene; 2001 Jan 11;20(2):198-208
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Overexpression of interleukin-6 in human basal cell carcinoma cell lines increases anti-apoptotic activity and tumorigenic potency.
  • The aim of this study was to investigate the possible role of IL-6 in the tumorigenesis of basal cell carcinoma (BCC).
  • We also detected a greater abundance of IL-6-expressing cell colonies formed in soft agar than in the vector control cells.
  • Furthermore, BCC/IL-6 cells, but not vector control cells, were resistant to UV and photodynamic therapy (PDT)-induced apoptosis, as confirmed using DNA fragmentation and morphologic change analyses.
  • Transient transfection of IL-6 transfectants with antisense mcl-1 greatly enhanced their apoptosis frequency by UV treatment.
  • [MeSH-major] Apoptosis / physiology. Carcinoma, Basal Cell / pathology. Interleukin-6 / genetics. Proto-Oncogene Proteins c-bcl-2. Skin Neoplasms / pathology
  • [MeSH-minor] Aminolevulinic Acid / pharmacology. Animals. Carcinogenicity Tests. Cyclooxygenase 2. Endothelial Growth Factors / genetics. Humans. Isoenzymes / genetics. Lymphokines / genetics. Membrane Proteins. Mice. Mice, Nude. Myeloid Cell Leukemia Sequence 1 Protein. Neoplasm Proteins / genetics. Neoplasm Proteins / metabolism. Oligonucleotides, Antisense / pharmacology. Prostaglandin-Endoperoxide Synthases / genetics. Transfection. Tumor Cells, Cultured / drug effects. Tumor Cells, Cultured / radiation effects. Ultraviolet Rays. Vascular Endothelial Growth Factor A. Vascular Endothelial Growth Factors

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  • (PMID = 11313947.001).
  • [ISSN] 0950-9232
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Endothelial Growth Factors; 0 / Interleukin-6; 0 / Isoenzymes; 0 / Lymphokines; 0 / Mcl1 protein, mouse; 0 / Membrane Proteins; 0 / Myeloid Cell Leukemia Sequence 1 Protein; 0 / Neoplasm Proteins; 0 / Oligonucleotides, Antisense; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Vascular Endothelial Growth Factor A; 0 / Vascular Endothelial Growth Factors; 88755TAZ87 / Aminolevulinic Acid; EC 1.14.99.1 / Cyclooxygenase 2; EC 1.14.99.1 / PTGS2 protein, human; EC 1.14.99.1 / Prostaglandin-Endoperoxide Synthases
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2. Allen JD, Brinkhuis RF, van Deemter L, Wijnholds J, Schinkel AH: Extensive contribution of the multidrug transporters P-glycoprotein and Mrp1 to basal drug resistance. Cancer Res; 2000 Oct 15;60(20):5761-6
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  • [Title] Extensive contribution of the multidrug transporters P-glycoprotein and Mrp1 to basal drug resistance.
  • Despite accumulating evidence that multidrug resistance transporter proteins play a part in drug resistance in some clinical cancers, it remains unclear whether the relatively low levels of multidrug resistance transporter expression found in most untreated tumors could substantially affect their basal sensitivity to antineoplastic drugs.
  • To shed light on this problem, the drug sensitivities of wild-type mouse cell lines were compared with those of lines in which the Mdr1a and Mdr1b genes encoding P-glycoprotein (P-gp) were inactivated and lines in which the Mrp1 gene was inactivated in addition to Mdr1a and Mdr1b.
  • These models permit a clean dissection of the contribution of each transporter to drug resistance at expression levels similar to those in normal tissues and avoid complications that might arise from previous exposure of cell lines to drug selection.
  • For substrate drugs, we found that these contributions can indeed be very substantial.
  • Lines lacking both P-gp and Mrp1 were (compared with wild-type lines) hypersensitive to an even broader array of drugs, including epipodophyllotoxins (4-7-fold), anthracyclines (6-7-fold), camptothecins (3-fold), arsenite (4-fold) and Vinca alkaloids, especially vincristine (28-fold).
  • Thus, even very low levels of P-gp and Mrp1 expression that may be difficult to detect in tumors could significantly affect their innate sensitivity to a wide range of clinically important substrate drugs.
  • An implication is that the use of resistance reversal agents to sensitize drug-naive tumors may be appropriate in more cases than is presently appreciated.
  • [MeSH-major] ATP-Binding Cassette Transporters / physiology. ATP-Binding Cassette, Sub-Family B, Member 1 / physiology. Drug Resistance, Multiple / physiology. Drug Resistance, Neoplasm / physiology
  • [MeSH-minor] 3T3 Cells / drug effects. 3T3 Cells / metabolism. Animals. Antibiotics, Antineoplastic / pharmacology. Antineoplastic Agents, Phytogenic / pharmacology. Crosses, Genetic. Drug Screening Assays, Antitumor. Gene Silencing. Genotype. Mice. Mice, Knockout. Multidrug Resistance-Associated Proteins. Paclitaxel / pharmacology

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  • (PMID = 11059771.001).
  • [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 / ATP-Binding Cassette Transporters; 0 / ATP-Binding Cassette, Sub-Family B, Member 1; 0 / Antibiotics, Antineoplastic; 0 / Antineoplastic Agents, Phytogenic; 0 / Multidrug Resistance-Associated Proteins; P88XT4IS4D / Paclitaxel
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3. Ganapathy V, Ge R, Grazioli A, Xie W, Banach-Petrosky W, Kang Y, Lonning S, McPherson J, Yingling JM, Biswas S, Mundy GR, Reiss M: Targeting the Transforming Growth Factor-beta pathway inhibits human basal-like breast cancer metastasis. Mol Cancer; 2010 May 26;9:122
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  • [Title] Targeting the Transforming Growth Factor-beta pathway inhibits human basal-like breast cancer metastasis.
  • We set out to investigate the possible clinical utility of TGF-beta antagonists in a human metastatic basal-like breast cancer model.
  • We examined the effects of two types of the TGF-beta pathway antagonists (1D11, a mouse monoclonal pan-TGF-beta neutralizing antibody and LY2109761, a chemical inhibitor of TGF-beta type I and II receptor kinases) on sublines of basal cell-like MDA-MB-231 human breast carcinoma cells that preferentially metastasize to lungs (4175TR, 4173) or bones (SCP2TR, SCP25TR, 2860TR, 3847TR).
  • In addition, both antagonists significantly reduced the metastatic burden to either lungs or bones in vivo, seemingly independently of intrinsic differences between the individual tumor cell clones.
  • Besides inhibiting metastasis in a tumor cell autonomous manner, the TGF-beta antagonists inhibited angiogenesis associated with lung metastases and osteoclast number and activity associated with lytic bone metastases.
  • In aggregate, these studies support the notion that TGF-beta plays an important role in both bone-and lung metastases of basal-like breast cancer, and that inhibiting TGF-beta signaling results in a therapeutic effect independently of the tissue-tropism of the metastatic cells.
  • Targeting the TGF-beta pathway holds promise as a novel therapeutic approach for metastatic basal-like breast cancer.
  • CONCLUSIONS: In aggregate, these studies support the notion that TGF-beta plays an important role in both bone-and lung metastases of basal-like breast cancer, and that inhibiting TGF-beta signaling results in a therapeutic effect independently of the tissue-tropism of the metastatic cells.
  • Targeting the TGF-beta pathway holds promise as a novel therapeutic approach for metastatic basal-like breast cancer.

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  • (PMID = 20504320.001).
  • [ISSN] 1476-4598
  • [Journal-full-title] Molecular cancer
  • [ISO-abbreviation] Mol. Cancer
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA-120623; United States / NCI NIH HHS / CA / CA-72720
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antineoplastic Agents; 0 / LY2109761; 0 / Pyrazoles; 0 / Pyrroles; 0 / Transforming Growth Factor beta
  • [Other-IDs] NLM/ PMC2890606
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4. Marchini C, Montani M, Konstantinidou G, Orrù R, Mannucci S, Ramadori G, Gabrielli F, Baruzzi A, Berton G, Merigo F, Fin S, Iezzi M, Bisaro B, Sbarbati A, Zerani M, Galiè M, Amici A: Mesenchymal/stromal gene expression signature relates to basal-like breast cancers, identifies bone metastasis and predicts resistance to therapies. PLoS One; 2010;5(11):e14131
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  • [Title] Mesenchymal/stromal gene expression signature relates to basal-like breast cancers, identifies bone metastasis and predicts resistance to therapies.
  • BACKGROUND: Mounting clinical and experimental evidence suggests that the shift of carcinomas towards a mesenchymal phenotype is a common paradigm for both resistance to therapy and tumor recurrence.
  • METHODOLOGY/PRINCIPAL FINDINGS: By integrating in silico and in vitro studies with our epithelial and mesenchymal tumor models, we compare herein crucial molecular pathways of previously described carcinoma-derived mesenchymal tumor cells (A17) with that of both carcinomas and other mesenchymal phenotypes, such as mesenchymal stem cells (MSCs), breast stroma, and various types of sarcomas.
  • By using a recently developed computational approach with publicly available microarray data, we show that these signatures:.
  • 1) significantly relates to basal-like breast cancer subtypes;.
  • 3) are up-regulated after hormonal treatment;.
  • 4) predict resistance to neoadjuvant therapies.
  • CONCLUSIONS/SIGNIFICANCE: Our results demonstrate that mesenchymalization is an intrinsic property of the most aggressive tumors and it relates to therapy resistance as well as bone metastasis.
  • [MeSH-minor] Animals. Blotting, Western. Cell Line, Tumor. Cluster Analysis. Cyclooxygenase 2 / genetics. Cyclooxygenase 2 / metabolism. Drug Resistance, Neoplasm / genetics. Epithelial Cells / metabolism. Female. Humans. Mesenchymal Stromal Cells / metabolism. Mice. Neoadjuvant Therapy / methods. Oligonucleotide Array Sequence Analysis. Reverse Transcriptase Polymerase Chain Reaction. Signal Transduction

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  • (PMID = 21152434.001).
  • [ISSN] 1932-6203
  • [Journal-full-title] PloS one
  • [ISO-abbreviation] PLoS ONE
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] EC 1.14.99.- / Ptgs2 protein, mouse; EC 1.14.99.1 / Cyclooxygenase 2
  • [Other-IDs] NLM/ PMC2994727
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5. Shafee N, Smith CR, Wei S, Kim Y, Mills GB, Hortobagyi GN, Stanbridge EJ, Lee EY: Cancer stem cells contribute to cisplatin resistance in Brca1/p53-mediated mouse mammary tumors. Cancer Res; 2008 May 1;68(9):3243-50
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  • [Title] Cancer stem cells contribute to cisplatin resistance in Brca1/p53-mediated mouse mammary tumors.
  • The majority of BRCA1-associated breast cancers are basal cell-like, which is associated with a poor outcome.
  • Using a spontaneous mouse mammary tumor model, we show that platinum compounds, which generate DNA breaks during the repair process, are more effective than doxorubicin in Brca1/p53-mutated tumors.
  • At 0.5 mg/kg of daily cisplatin treatment, 80% primary tumors (n = 8) show complete pathologic response.
  • However, after 2 to 3 months of complete remission following platinum treatment, tumors relapse and become refractory to successive rounds of treatment.
  • Approximately 3.8% to 8.0% (mean, 5.9%) of tumor cells express the normal mammary stem cell markers, CD29(hi)24(med), and these cells are tumorigenic, whereas CD29(med)24(-/lo) and CD29(med)24(hi) cells have diminished tumorigenicity or are nontumorigenic, respectively.
  • Expression of a normal stem cell marker, Nanog, is decreased in the CD29(hi)24(med) populations in the secondary transplants.
  • Top2A expression is also down-regulated in secondary drug-resistant tumor populations and, in one case, was accompanied by genomic deletion of Top2A.
  • These studies identify distinct cancer cell populations for therapeutic targeting in breast cancer and implicate clonal evolution and expansion of cancer stem-like cells as a potential cause of chemoresistance.

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  • (PMID = 18451150.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA04964; United States / NCI NIH HHS / CA / P30 CA016672; United States / NCI NIH HHS / CA / P50 CA098258; United States / NCI NIH HHS / CA / CA083639-100010; United States / NCI NIH HHS / CA / P50 CA083639; United States / NCI NIH HHS / CA / P50 CA083639-100010
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Antineoplastic Agents; 0 / DNA-Binding Proteins; EC 5.99.1.3 / DNA Topoisomerases, Type II; EC 5.99.1.3 / DNA topoisomerase II alpha; Q20Q21Q62J / Cisplatin
  • [Other-IDs] NLM/ NIHMS230363; NLM/ PMC2929908
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6. Gupta S, Adhami VM, Subbarayan M, MacLennan GT, Lewin JS, Hafeli UO, Fu P, Mukhtar H: Suppression of prostate carcinogenesis by dietary supplementation of celecoxib in transgenic adenocarcinoma of the mouse prostate model. Cancer Res; 2004 May 1;64(9):3334-43
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  • [Title] Suppression of prostate carcinogenesis by dietary supplementation of celecoxib in transgenic adenocarcinoma of the mouse prostate model.
  • Epidemiological studies and clinical observations suggest that nonsteroidal anti-inflammatory drugs and certain selective cyclooxygenase (COX)-2 inhibitors may reduce the relative risk of clinically evident prostate cancer.
  • This prompted us to investigate the chemopreventive potential of celecoxib, a selective COX-2 inhibitor, against prostate carcinogenesis in a transgenic adenocarcinoma of the mouse prostate (TRAMP) model.
  • The basal enzyme activity and protein expression of COX-2 is significantly higher (>4-fold) in the dorsolateral prostate of TRAMP mice up to 24 weeks of age compared with their nontransgenic littermates.
  • Eight-week-old TRAMP mice were randomly divided and fed either control diet (AIN 76A) or a custom prepared AIN 76A diet containing 1500-ppm celecoxib ad libitum for 24 weeks, a dosage that would compare with the normal recommended dose for the treatment of human disease.
  • [MeSH-minor] Animals. Biomarkers, Tumor / metabolism. Celecoxib. Cell Division / drug effects. Cyclooxygenase 2. Cyclooxygenase 2 Inhibitors. Dietary Supplements. Dinoprostone / blood. Female. Immunohistochemistry. Isoenzymes / biosynthesis. Isoenzymes / genetics. Isoenzymes / metabolism. Male. Mice. Mice, Inbred C57BL. Mice, Transgenic. Neoplasm Metastasis. Neovascularization, Pathologic / drug therapy. Neovascularization, Pathologic / metabolism. Proliferating Cell Nuclear Antigen / biosynthesis. Prostaglandin-Endoperoxide Synthases / biosynthesis. Prostaglandin-Endoperoxide Synthases / genetics. Prostaglandin-Endoperoxide Synthases / metabolism. Pyrazoles. RNA, Messenger / biosynthesis. RNA, Messenger / genetics

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  • (PMID = 15126378.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA 89739
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anticarcinogenic Agents; 0 / Biomarkers, Tumor; 0 / Cyclooxygenase 2 Inhibitors; 0 / Cyclooxygenase Inhibitors; 0 / Isoenzymes; 0 / Proliferating Cell Nuclear Antigen; 0 / Pyrazoles; 0 / RNA, Messenger; 0 / Sulfonamides; EC 1.14.99.1 / Cyclooxygenase 2; EC 1.14.99.1 / Prostaglandin-Endoperoxide Synthases; JCX84Q7J1L / Celecoxib; K7Q1JQR04M / Dinoprostone
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7. Ferrario A, von Tiehl KF, Rucker N, Schwarz MA, Gill PS, Gomer CJ: Antiangiogenic treatment enhances photodynamic therapy responsiveness in a mouse mammary carcinoma. Cancer Res; 2000 Aug 1;60(15):4066-9
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  • [Title] Antiangiogenic treatment enhances photodynamic therapy responsiveness in a mouse mammary carcinoma.
  • Photodynamic therapy (PDT) is a promising cancer treatment that induces localized tumor destruction via the photochemical generation of cytotoxic singlet oxygen.
  • PDT-mediated oxidative stress elicits direct tumor cell damage as well as microvascular injury within exposed tumors.
  • Reduction in vascular perfusion associated with PDT-mediated microvascular injury produces tumor tissue hypoxia.
  • Using a transplantable BA mouse mammary carcinoma, we show that Photofrin-mediated PDT induced expression of the hypoxia-inducible factor-1alpha (HIF-1alpha) subunit of the heterodimeric HIF-1 transcription factor and also increased protein levels of the HIF-1 target gene, vascular endothelial growth factor (VEGF), within treated tumors.
  • HIF-1alpha and VEGF expression were also observed following tumor clamping, which was used as a positive control for inducing tissue hypoxia.
  • PDT treatment of BA tumor cells grown in culture resulted in a small increase in VEGF expression above basal levels, indicating that PDT-mediated hypoxia and oxidative stress could both be involved in the overexpression of VEGF.
  • Tumor-bearing mice treated with combined antiangiogenic therapy (IM862 or EMAP-II) and PDT had improved tumoricidal responses compared with individual treatments.
  • We also demonstrated that PDT-induced VEGF expression in tumors decreased when either IM862 or EMAP-II was included in the PDT treatment protocol.
  • Our results indicate that combination procedures using antiangiogenic treatments can improve the therapeutic effectiveness of PDT.
  • [MeSH-major] Cytokines. Mammary Neoplasms, Experimental / blood supply. Mammary Neoplasms, Experimental / drug therapy. Neovascularization, Pathologic / drug therapy. Photochemotherapy / methods. Transcription Factors
  • [MeSH-minor] Angiogenesis Inhibitors / pharmacology. Animals. Cell Hypoxia. Combined Modality Therapy. DNA-Binding Proteins / biosynthesis. DNA-Binding Proteins / genetics. Dihematoporphyrin Ether / pharmacology. Dipeptides / pharmacology. Endothelial Growth Factors / biosynthesis. Endothelial Growth Factors / genetics. Female. Hypoxia-Inducible Factor 1. Hypoxia-Inducible Factor 1, alpha Subunit. Lymphokines / biosynthesis. Lymphokines / genetics. Mice. Mice, Inbred C3H. Neoplasm Proteins / pharmacology. Neoplasm Transplantation. Nuclear Proteins / biosynthesis. Nuclear Proteins / genetics. Photosensitizing Agents / pharmacology. RNA-Binding Proteins / pharmacology. Vascular Endothelial Growth Factor A. Vascular Endothelial Growth Factors

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  • (PMID = 10945611.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA-31230; United States / NHLBI NIH HHS / HL / HL-03981; United States / NHLBI NIH HHS / HL / HL-60061
  • [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.
  • [Publication-country] UNITED STATES
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Cytokines; 0 / DNA-Binding Proteins; 0 / Dipeptides; 0 / Endothelial Growth Factors; 0 / Hif1a protein, mouse; 0 / Hypoxia-Inducible Factor 1; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / Lymphokines; 0 / Neoplasm Proteins; 0 / Nuclear Proteins; 0 / Photosensitizing Agents; 0 / RNA-Binding Proteins; 0 / Transcription Factors; 0 / Vascular Endothelial Growth Factor A; 0 / Vascular Endothelial Growth Factors; 0 / small inducible cytokine subfamily E, member 1; 122933-59-9 / thymogen; 97067-70-4 / Dihematoporphyrin Ether
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8. Tanaka Y, Fujii T, Yamana H, Kato S, Morimatsu M, Shirouzu K: Experimental gene therapy using p21Waf1 gene for esophageal squamous cell carcinoma by gene gun technology. Int J Mol Med; 2004 Oct;14(4):545-51
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  • [Title] Experimental gene therapy using p21Waf1 gene for esophageal squamous cell carcinoma by gene gun technology.
  • In our previous study, the proliferation rate of esophageal squamous cell carcinoma cell lines, which poorly expressed p21Waf1, was found to be regulated by p21Waf1 gene transfection using adenovirus vector.
  • In the present study, in order to examine the effect of p21Waf1 gene therapy in esophageal cancer, we used gene gun technology, which proved to be a powerful method to introduce the p21Waf1 gene into esophageal cancer cells. p21Waf1 transfection to KE3 and YES2 cells (weakly expressed p21Waf1 protein cells) showed a high expression of p21Waf1 protein after applying this gene gun technique.
  • In in vivo transfection experiments, on day 14, the estimated volume of KE3 tumors subjected to p21Waf1 gene transfection was 95% in comparison with the pretreatment volume on day 0, while the volume of KE3 tumors subjected to LacZ gene therapy increased to 268%.
  • On day 14, the estimated volume of YES2 tumors subjected to either p21Waf1 or LacZ gene therapy increased to 474 and 686%, respectively.
  • In KE3 and YES2 cells, significant growth inhibition was observed after combination therapy using p21Waf1 transfection and anticancer drug 5-fluorouracil (5Fu) compared with 5Fu alone (KE3, p<0.0001; YES2, p<0.0001).
  • In conclusion, p21Waf1 gene therapy using the gene gun technique significantly inhibited the low basal p21Waf1 expressed esophageal cancer cell growth in vitro and in vivo.
  • Furthermore, p21Waf1 transfection strongly enhanced the effect of 5Fu suggesting that p21Waf1 may prove beneficial in chemotherapy combined with gene therapy using gene gun technology in patients with esophageal cancer who have a low level of p21Waf1 expressed tumor.
  • [MeSH-major] Biolistics / methods. Carcinoma, Squamous Cell / therapy. Cell Cycle Proteins / genetics. Cell Cycle Proteins / metabolism. Esophageal Neoplasms / genetics. Esophageal Neoplasms / therapy. Genetic Therapy / methods
  • [MeSH-minor] Animals. Cell Line, Tumor. Cell Proliferation / drug effects. Cyclin-Dependent Kinase Inhibitor p21. Fluorouracil / pharmacology. Humans. Male. Mice. Mice, Inbred BALB C. Neoplasm Transplantation. Transfection

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  • (PMID = 15375580.001).
  • [ISSN] 1107-3756
  • [Journal-full-title] International journal of molecular medicine
  • [ISO-abbreviation] Int. J. Mol. Med.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / CDKN1A protein, human; 0 / Cdkn1a protein, mouse; 0 / Cell Cycle Proteins; 0 / Cyclin-Dependent Kinase Inhibitor p21; U3P01618RT / Fluorouracil
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9. Wick W, Platten M, Weller M: Glioma cell invasion: regulation of metalloproteinase activity by TGF-beta. J Neurooncol; 2001 Jun;53(2):177-85
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  • [Title] Glioma cell invasion: regulation of metalloproteinase activity by TGF-beta.
  • MMPs are implicated in tumor cell invasion because they mediate the breakdown of the basal membrane.
  • In addition, they seem to be important for the creation and maintenance of a microenvironment that facilitates tumor cell survival.
  • Furthermore, we have defined a novel pathway for hepatocyte growth factor (HGF)-induced glioma cell migration and invasion which requires the induction of TGF-beta2 expression.
  • Here, we demonstrate that TGF-beta2 induces MMP-2 expression and suppresses tissue inhibitor of metalloproteinases (TIMP)-2 expression and that concentration-dependently promotes the invasion of U87MG and LN-229 glioma cells in a matrigel invasion assay.
  • TGF-beta continues to be one of the most promising targets for the experimental therapy of human malignant glioma.
  • [MeSH-major] Brain Neoplasms / pathology. Glioma / pathology. Matrix Metalloproteinase 2 / biosynthesis. Neoplasm Invasiveness / physiopathology. Neoplasm Proteins / biosynthesis. Transforming Growth Factor beta / pharmacology
  • [MeSH-minor] 3T3 Cells. Animals. Cell Movement. Collagen. Cytoskeletal Proteins. Drug Combinations. Enzyme Induction / drug effects. Extracellular Matrix / metabolism. Humans. Laminin. Mice. Phosphoproteins / genetics. Phosphoproteins / physiology. Proteoglycans. Proto-Oncogene Proteins c-bcl-2 / biosynthesis. Proto-Oncogene Proteins c-bcl-2 / genetics. Receptors, Vitronectin / biosynthesis. Receptors, Vitronectin / genetics. Recombinant Proteins / pharmacology. Tissue Inhibitor of Metalloproteinase-2 / biosynthesis. Tissue Inhibitor of Metalloproteinase-2 / genetics. Transfection. Transforming Growth Factor beta1. Transforming Growth Factor beta2. Tumor Cells, Cultured / drug effects. Tumor Cells, Cultured / enzymology. Tumor Cells, Cultured / pathology. bcl-X Protein

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  • (PMID = 11716069.001).
  • [ISSN] 0167-594X
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / BCL2L1 protein, human; 0 / Bcl2l1 protein, mouse; 0 / Cytoskeletal Proteins; 0 / Drug Combinations; 0 / Laminin; 0 / Neoplasm Proteins; 0 / Phosphoproteins; 0 / Proteoglycans; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Receptors, Vitronectin; 0 / Recombinant Proteins; 0 / TGFB1 protein, human; 0 / TGFB2 protein, human; 0 / Tgfb1 protein, mouse; 0 / Transforming Growth Factor beta; 0 / Transforming Growth Factor beta1; 0 / Transforming Growth Factor beta2; 0 / bcl-X Protein; 0 / ezrin; 119978-18-6 / matrigel; 127497-59-0 / Tissue Inhibitor of Metalloproteinase-2; 9007-34-5 / Collagen; EC 3.4.24.24 / Matrix Metalloproteinase 2
  • [Number-of-references] 60
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10. Cory AH, Cory JG: Lactacystin, a proteasome inhibitor, potentiates the apoptotic effect of parthenolide, an inhibitor of NFkappaB activation, on drug-resistant mouse leukemia L1210 cells. Anticancer Res; 2002 Nov-Dec;22(6C):3805-9
The Lens. Cited by Patents in .

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  • [Title] Lactacystin, a proteasome inhibitor, potentiates the apoptotic effect of parthenolide, an inhibitor of NFkappaB activation, on drug-resistant mouse leukemia L1210 cells.
  • An L1210 cell line (Y8) selected for resistance to deoxyadenosine does not express p53 mRNA or protein but expresses WAF1/p21 even under basal conditions.
  • The Y8 cell line had been previously shown to have an increased apoptotic response to a variety of agents that included DNA damaging agents, kinase inhibitors and drugs directed at NFkappa B activation.
  • The combination of drugs had no effects on the parental wild-type L1210 cells.
  • Cell-free extracts prepared from the LC plus PA combination-treated cells had activated caspase activities in the caspase cascade: caspase-3 >> caspase-8 > caspase-6 and caspase-10.
  • These results suggest that there are interacting pathways involving aspects of NFkappa B activation and proteasome activity that could be exploited in therapy directed at p53-deficient tumor cells that would lead to caspase-3 activation and apoptosis bypassing the p53-dependent chemotherapy insensitivity.
  • [MeSH-major] Acetylcysteine / analogs & derivatives. Acetylcysteine / pharmacology. Antineoplastic Combined Chemotherapy Protocols / pharmacology. Apoptosis / drug effects. Cysteine Proteinase Inhibitors / pharmacology. Leukemia L1210 / drug therapy. Sesquiterpenes / pharmacology
  • [MeSH-minor] Animals. Caspase 3. Caspase Inhibitors. Caspases / metabolism. Cyclin-Dependent Kinase Inhibitor p21. Cyclins / biosynthesis. Cysteine Endopeptidases. Drug Resistance, Neoplasm. Drug Synergism. Enzyme Activation / drug effects. Mice. Multienzyme Complexes / antagonists & inhibitors. NF-kappa B / antagonists & inhibitors. Proteasome Endopeptidase Complex. Tumor Suppressor Protein p53 / biosynthesis

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  • (PMID = 12552998.001).
  • [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 / Caspase Inhibitors; 0 / Cdkn1a protein, mouse; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / Cyclins; 0 / Cysteine Proteinase Inhibitors; 0 / Multienzyme Complexes; 0 / NF-kappa B; 0 / Sesquiterpenes; 0 / Tumor Suppressor Protein p53; 133343-34-7 / lactacystin; 2RDB26I5ZB / parthenolide; EC 3.4.22.- / Casp3 protein, mouse; EC 3.4.22.- / Caspase 3; EC 3.4.22.- / Caspases; EC 3.4.22.- / Cysteine Endopeptidases; EC 3.4.25.1 / Proteasome Endopeptidase Complex; WYQ7N0BPYC / Acetylcysteine
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11. Zander SA, Kersbergen A, van der Burg E, de Water N, van Tellingen O, Gunnarsdottir S, Jaspers JE, Pajic M, Nygren AO, Jonkers J, Borst P, Rottenberg S: Sensitivity and acquired resistance of BRCA1;p53-deficient mouse mammary tumors to the topoisomerase I inhibitor topotecan. Cancer Res; 2010 Feb 15;70(4):1700-10
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  • [Title] Sensitivity and acquired resistance of BRCA1;p53-deficient mouse mammary tumors to the topoisomerase I inhibitor topotecan.
  • There is no tailored therapy yet for human basal-like mammary carcinomas.
  • We have evaluated this putative synthetic lethality in a genetically engineered mouse model for BRCA1-associated breast cancer, using the topoisomerase I (Top1) poison topotecan as monotherapy and in combination with poly(ADP-ribose) polymerase inhibition by olaparib.
  • Although topotecan increased mouse survival, all tumors eventually acquired resistance.
  • As mechanisms of in vivo resistance, we identified overexpression of Abcg2/Bcrp and markedly reduced protein levels of the drug target Top1 (without altered mRNA levels).
  • Despite the lack of ABCG2, a putative tumor-initiating cell marker, none of the 11 Abcg2(-/-);Brca1(-/-);p53(-/-) tumors were eradicated, not even by the combination topotecan-olaparib.
  • [MeSH-major] Carcinoma / drug therapy. Drug Resistance, Neoplasm / genetics. Genes, BRCA1 / physiology. Genes, p53 / physiology. Mammary Neoplasms, Animal / drug therapy. Topotecan / therapeutic use
  • [MeSH-minor] ATP Binding Cassette Transporter, Sub-Family B. ATP Binding Cassette Transporter, Sub-Family G, Member 2. ATP-Binding Cassette Transporters / genetics. ATP-Binding Cassette, Sub-Family B, Member 1. Animals. Antineoplastic Agents / administration & dosage. Antineoplastic Agents / therapeutic use. Doxorubicin / therapeutic use. Drug Evaluation, Preclinical. Enzyme Inhibitors / administration & dosage. Enzyme Inhibitors / therapeutic use. Female. Gene Expression Regulation, Neoplastic / drug effects. Maximum Tolerated Dose. Mice. Mice, Knockout. Phthalazines / pharmacology. Phthalazines / therapeutic use. Piperazines / pharmacology. Piperazines / therapeutic use. Topoisomerase I Inhibitors


12. Marinov M, Ziogas A, Pardo OE, Tan LT, Dhillon T, Mauri FA, Lane HA, Lemoine NR, Zangemeister-Wittke U, Seckl MJ, Arcaro A: AKT/mTOR pathway activation and BCL-2 family proteins modulate the sensitivity of human small cell lung cancer cells to RAD001. Clin Cancer Res; 2009 Feb 15;15(4):1277-87
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  • [Title] AKT/mTOR pathway activation and BCL-2 family proteins modulate the sensitivity of human small cell lung cancer cells to RAD001.
  • PURPOSE: The Akt/mammalian target of rapamycin (mTOR) pathway is frequently activated in human cancers and plays an important role in small cell lung cancer (SCLC) biology.
  • EXPERIMENTAL DESIGN: The expression of mTOR in patient specimens and in a panel of SCLC cell lines was analyzed.
  • The effects on SCLC cell survival and downstream signaling were determined following mTOR inhibition by the rapamycin derivative RAD001 (Everolimus) or down-regulation by small interfering RNA.
  • RESULTS: We found elevated expression of mTOR in patient specimens and SCLC cell lines, compared with normal lung tissue and normal lung epithelial cells.
  • RAD001 treatment impaired basal and growth factor-stimulated cell growth in a panel of SCLC cell lines.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Carcinoma, Small Cell / drug therapy. Lung Neoplasms / drug therapy. Protein Kinases / physiology. Proto-Oncogene Proteins c-akt / physiology. Proto-Oncogene Proteins c-bcl-2 / physiology. Sirolimus / analogs & derivatives
  • [MeSH-minor] Animals. Cell Line, Tumor. Cyclin-Dependent Kinase Inhibitor p21 / metabolism. Drug Resistance, Neoplasm. Etoposide / pharmacology. Everolimus. Humans. Mice. Signal Transduction / physiology. Stem Cell Factor / pharmacology. TOR Serine-Threonine Kinases

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  • (PMID = 19228731.001).
  • [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 Kingdom / Cancer Research UK / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / CDKN1A protein, human; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Stem Cell Factor; 624KN6GM2T / temsirolimus; 6PLQ3CP4P3 / Etoposide; 9HW64Q8G6G / Everolimus; EC 2.7.- / Protein Kinases; EC 2.7.1.1 / MTOR protein, human; EC 2.7.1.1 / TOR Serine-Threonine Kinases; EC 2.7.1.1 / mTOR protein, mouse; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; W36ZG6FT64 / Sirolimus
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13. Welsh SJ, Titley J, Brunton L, Valenti M, Monaghan P, Jackman AL, Aherne GW: Comparison of thymidylate synthase (TS) protein up-regulation after exposure to TS inhibitors in normal and tumor cell lines and tissues. Clin Cancer Res; 2000 Jun;6(6):2538-46
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  • [Title] Comparison of thymidylate synthase (TS) protein up-regulation after exposure to TS inhibitors in normal and tumor cell lines and tissues.
  • Thymidylate synthase (TS) is an important target for cancer chemotherapy.
  • This study has investigated TS protein up-regulation using a range of TS inhibitors in both tumor and nonmalignant cell lines in vitro and in vivo.
  • Up-regulation of TS protein showed a time-, dose-, and cell-type-specific response to treatment with ZD9331.
  • Elevation of TS protein only persisted up to 12 h after removal of drug.
  • The extent of induction does not depend on basal TS levels.
  • In vivo experiments using the L5178Y thymidine kinase -/- mouse lymphoma implanted into DBA2 mice also showed greater up-regulation of TS protein in normal intestinal epithelial cells compared with tumor cells.
  • These results confirm that TS up-regulation is a common feature of TS inhibition in tumor cells and that it may occur to a greater extent in normal tissues, although the clinical implications of these findings remain to be determined.
  • [MeSH-minor] Analysis of Variance. Animals. Antimetabolites, Antineoplastic / pharmacology. Antineoplastic Agents / pharmacology. Blotting, Western. Dose-Response Relationship, Drug. Enzyme-Linked Immunosorbent Assay. Female. Fibroblasts / metabolism. Flow Cytometry. Fluorouracil / pharmacology. Glutamates / pharmacology. Humans. Indoles / pharmacology. Inhibitory Concentration 50. Isoindoles. Mice. Mice, Inbred DBA. Microscopy, Confocal. Neoplasm Transplantation. Pemetrexed. Quinazolines / pharmacology. Thiophenes / pharmacology. Time Factors. Tumor Cells, Cultured

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  • (PMID = 10873110.001).
  • [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 / Antimetabolites, Antineoplastic; 0 / Antineoplastic Agents; 0 / Glutamates; 0 / Indoles; 0 / Isoindoles; 0 / Quinazolines; 0 / Thiophenes; 0 / ZD 9331; 04Q9AIZ7NO / Pemetrexed; 139987-54-5 / 1843U89; 5Z93L87A1R / Guanine; EC 2.1.1.45 / Thymidylate Synthase; FCB9EGG971 / raltitrexed; K75ZUN743Q / nolatrexed; U3P01618RT / Fluorouracil
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14. Takahashi H, Itoh Y, Nakajima S, Sakata I, Iizuka H: A novel ATX-S10(Na) photodynamic therapy for human skin tumors and benign hyperproliferative skin. Photodermatol Photoimmunol Photomed; 2004 Oct;20(5):257-65
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  • [Title] A novel ATX-S10(Na) photodynamic therapy for human skin tumors and benign hyperproliferative skin.
  • BACKGROUND/PURPOSE: Photodynamic therapy (PDT) is a promising treatment for various skin tumors and other skin diseases.
  • We investigated the potential therapeutic effects of PDT using ATX-S10(Na) ointment and a diode laser in mouse skin models of experimental skin tumors as well as transplanted human samples of superficial skin tumors and lesional psoriatic skin.
  • METHODS: ATX-S10(Na) ointment (1% w/v) was introduced into tape-stripped mouse skin, transplanted squamous cell carcinoma (SCC) samples and human skin diseases after topical application, then PDT was performed.
  • RESULTS: ATX-S10(Na) ointment (1% w/v) was introduced effectively into tape-stripped mouse skin and transplanted SCC samples after topical application, but was not detected after 48 h, as assessed by fluorescence microscopy.
  • PDT, using 1% ATX-S10(Na) ointment and diode laser (50 J/cm(2)), was found to decrease epidermal thickness in 12-0-tetradecanoylphorbol-13-acetate (TPA)-treated mouse skin by 6 days.
  • PDT against Bowen disease, basal-cell carcinoma, and psoriasis xenografts onto SCID mice also showed marked suppression of tumor growth and cell proliferation, respectively.
  • CONCLUSION: Our results indicate that ATX-S10(Na)-PDT is an effective treatment for various skin tumors and psoriasis in experimental mouse models.
  • [MeSH-major] Photochemotherapy. Porphyrins / therapeutic use. Radiation-Sensitizing Agents / therapeutic use. Skin Diseases / drug therapy. Skin Neoplasms / drug therapy
  • [MeSH-minor] Animals. Bowen's Disease / drug therapy. Carcinogens / adverse effects. Carcinoma, Basal Cell / drug therapy. Carcinoma, Squamous Cell / drug therapy. Disease Models, Animal. Female. Humans. Laser Therapy. Mice. Mice, Hairless. Mice, Inbred BALB C. Mice, SCID. Neoplasm Transplantation. Ointments. Psoriasis / drug therapy. Skin / drug effects. Tetradecanoylphorbol Acetate / adverse effects. Transplantation, Heterologous

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  • (PMID = 15379877.001).
  • [ISSN] 0905-4383
  • [Journal-full-title] Photodermatology, photoimmunology & photomedicine
  • [ISO-abbreviation] Photodermatol Photoimmunol Photomed
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / ATX-S10; 0 / Carcinogens; 0 / Ointments; 0 / Porphyrins; 0 / Radiation-Sensitizing Agents; NI40JAQ945 / Tetradecanoylphorbol Acetate
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15. Marangoni E, Lecomte N, Durand L, de Pinieux G, Decaudin D, Chomienne C, Smadja-Joffe F, Poupon MF: CD44 targeting reduces tumour growth and prevents post-chemotherapy relapse of human breast cancers xenografts. Br J Cancer; 2009 Mar 24;100(6):918-22
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  • [Title] CD44 targeting reduces tumour growth and prevents post-chemotherapy relapse of human breast cancers xenografts.
  • Moreover, treatment with this antibody prevents tumour relapse after chemotherapy-induced remission in a basal-like HBCx.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Antigens, CD44 / physiology. Mammary Neoplasms, Experimental / drug therapy. Neoplasm Recurrence, Local / prevention & control

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  • (PMID = 19240712.001).
  • [ISSN] 1532-1827
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antigens, CD44; 0 / Cd44 protein, mouse
  • [Other-IDs] NLM/ PMC2661796
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16. Wan X, Helman LJ: Effect of insulin-like growth factor II on protecting myoblast cells against cisplatin-induced apoptosis through p70 S6 kinase pathway. Neoplasia; 2002 Sep-Oct;4(5):400-8
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  • Cisplatin treatment of C2C12 mouse myoblasts led to cell death associated with an inhibition of p70 S6K activity.
  • This protection was associated in both cases with an increase in p70 S6K basal activity as well as resistance to cisplatin-induced decreased activity.
  • Furthermore, treatment of IGF-II-overexpressing Rh30 and CTR rhabdomyosarcoma cells with rapamycin restored sensitivity to cisplatin-induced apoptosis.
  • Thus, inhibition of the p70 S6 pathway may enhance chemotherapy-induced apoptosis in the treatment of IGF-II-overexpressing tumors.
  • [MeSH-major] Antineoplastic Agents / toxicity. Apoptosis / drug effects. Cisplatin / toxicity. Insulin-Like Growth Factor II / pharmacology. Myoblasts / drug effects. Ribosomal Protein S6 Kinases, 70-kDa / metabolism. Signal Transduction
  • [MeSH-minor] Adaptor Proteins, Signal Transducing. Animals. Antibiotics, Antineoplastic / pharmacology. Blotting, Western. Carrier Proteins / antagonists & inhibitors. Cell Division. Cell Line. Cytoprotection. Drug Resistance, Neoplasm. Flow Cytometry. Humans. Mice. Phosphoproteins / antagonists & inhibitors. Phosphorylation. Rhabdomyosarcoma / drug therapy. Sirolimus / pharmacology. Transfection. Up-Regulation

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  • (PMID = 12192598.001).
  • [ISSN] 1522-8002
  • [Journal-full-title] Neoplasia (New York, N.Y.)
  • [ISO-abbreviation] Neoplasia
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / Antibiotics, Antineoplastic; 0 / Antineoplastic Agents; 0 / Carrier Proteins; 0 / EIF4EBP1 protein, human; 0 / Eif4ebp1 protein, mouse; 0 / Phosphoproteins; 67763-97-7 / Insulin-Like Growth Factor II; EC 2.7.11.1 / Ribosomal Protein S6 Kinases, 70-kDa; Q20Q21Q62J / Cisplatin; W36ZG6FT64 / Sirolimus
  • [Other-IDs] NLM/ PMC1564119
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17. Hassouna I, Sperling S, Kim E, Schulz-Schaeffer W, Rave-Fränk M, Hasselblatt M, Jelkmann W, Giese A, Ehrenreich H: Erythropoietin augments survival of glioma cells after radiation and temozolomide. Int J Radiat Oncol Biol Phys; 2008 Nov 1;72(3):927-34
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  • PURPOSE: Despite beneficial effects of irradiation/chemotherapy on survival of glioblastoma (GBM) patients, collateral damage to intact neural tissue leads to "radiochemobrain" and reduced quality of life in survivors.
  • METHODS AND MATERIALS: Human GBM-derived cell lines U87, G44, G112, and the gliosarcoma-derived line G28 were treated with EPO, with and without combinations of irradiation or temozolomide (TMZ).
  • Responsiveness of glioma cells to EPO was measured by cell migration from spheroids, cell proliferation, and clonogenic survival.
  • Implantation of U87 cells into brains of nude mice, followed 5 days later by EPO treatment (5,000 U/kg intraperitoneal every other day for 2 weeks) should reveal effects of EPO on tumor growth in vivo.
  • Reverse transcriptase-polymerase chain reaction was performed for EPOR, HIF-1alpha, and epidermal growth factor receptor (EGFR)vIII in cell lines and 22 human GBM specimens.
  • RESULTS: EPO did not modulate basal glioma cell migration and stimulated proliferation in only one of four cell lines.
  • Importantly, EPO did not enhance tumor growth in mouse brains.
  • Preincubation of glioma cells with EPO for 3 h, followed by irradiation and TMZ for another 24 h, resulted in protection against chemoradiation-induced cytotoxicity in three cell lines.
  • CONCLUSIONS: EPO is unlikely to appreciably influence basal glioma growth.
  • However, concomitant use of EPO with irradiation/chemotherapy in GBM patients is not advisable.
  • [MeSH-major] Antineoplastic Agents, Alkylating / therapeutic use. Cell Division / drug effects. Cell Survival / drug effects. Dacarbazine / analogs & derivatives. Erythropoietin / pharmacology. Glioma / drug therapy. Glioma / pathology. Glioma / radiotherapy
  • [MeSH-minor] Animals. Brain Neoplasms / drug therapy. Brain Neoplasms / pathology. Brain Neoplasms / radiotherapy. Cell Line, Tumor. Cell Movement / drug effects. Combined Modality Therapy. Gliosarcoma / drug therapy. Gliosarcoma / pathology. Gliosarcoma / radiotherapy. Humans. Mice. Mice, Nude. Neoplasm Transplantation. Transplantation, Heterologous

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  • (PMID = 19014782.001).
  • [ISSN] 1879-355X
  • [Journal-full-title] International journal of radiation oncology, biology, physics
  • [ISO-abbreviation] Int. J. Radiat. Oncol. Biol. Phys.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 11096-26-7 / Erythropoietin; 7GR28W0FJI / Dacarbazine; 85622-93-1 / temozolomide
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18. Unruh A, Ressel A, Mohamed HG, Johnson RS, Nadrowitz R, Richter E, Katschinski DM, Wenger RH: The hypoxia-inducible factor-1 alpha is a negative factor for tumor therapy. Oncogene; 2003 May 22;22(21):3213-20
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  • [Title] The hypoxia-inducible factor-1 alpha is a negative factor for tumor therapy.
  • Tumor hypoxia negatively regulates cell growth and causes a more malignant phenotype by increasing the expression of genes encoding angiogenic, metabolic and metastatic factors.
  • Of clinical importance, insufficient tumor oxygenation affects the efficiency of chemotherapy and radiotherapy by poorly understood mechanisms.
  • The hypoxia-inducible factor (HIF)-1 is a master transcriptional activator of oxygen-regulated genes and HIF-1 is constitutively upregulated in several tumor types.
  • HIF-1 might thus be implicated in tumor therapy resistance.
  • We found that transformed mouse embryonic fibroblasts deficient for HIF-1alpha are more susceptible to the treatment with carboplatin, etoposide and ionizing radiation than wild-type cells.
  • Increased cell death in HIF-1alpha-deficient cells was because of apoptosis and did not involve p53 induction.
  • Tumor chemotherapy of experimental fibrosarcoma in immunocompromised mice with carboplatin and etoposide confirmed the enhanced susceptibility of HIF-1alpha-deficient cells.
  • Agents that did not cause DNA double-strand breaks, such as DNA-synthesis inhibitors or a DNA single-strand break-causing agent equally impaired cell growth, independent of the HIF-1alpha genotype.
  • Thus, hypoxia-independent basal HIF-1alpha expression in tumor cells, as known from untransformed embryonic stem cells, is sufficient to induce target gene expression, probably including DNA double-strand break repair enzymes.
  • [MeSH-major] Neoplasms, Experimental / drug therapy. Transcription Factors / physiology
  • [MeSH-minor] Animals. Antineoplastic Agents / therapeutic use. Antineoplastic Agents / toxicity. Apoptosis. Carboplatin / therapeutic use. Carboplatin / toxicity. Cell Line, Transformed. DNA Repair. Drug Resistance, Neoplasm. Enzyme Inhibitors / toxicity. Etoposide / therapeutic use. Etoposide / toxicity. Gene Deletion. Hypoxia-Inducible Factor 1, alpha Subunit. Iron Chelating Agents / toxicity. Male. Mice. Mice, Nude. Topoisomerase I Inhibitors. Tumor Suppressor Protein p53 / physiology

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  • (PMID = 12761491.001).
  • [ISSN] 0950-9232
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Enzyme Inhibitors; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / Iron Chelating Agents; 0 / Topoisomerase I Inhibitors; 0 / Transcription Factors; 0 / Tumor Suppressor Protein p53; 6PLQ3CP4P3 / Etoposide; BG3F62OND5 / Carboplatin
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19. Wang J, Kuiatse I, Lee AV, Pan J, Giuliano A, Cui X: Sustained c-Jun-NH2-kinase activity promotes epithelial-mesenchymal transition, invasion, and survival of breast cancer cells by regulating extracellular signal-regulated kinase activation. Mol Cancer Res; 2010 Feb;8(2):266-77
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  • The c-Jun NH(2)-terminus kinase (JNK) mediates stress-induced apoptosis and the cytotoxic effect of anticancer therapies.
  • Here, we show that overexpression of a constitutively active JNK in human breast cancer cells did not cause apoptosis, but actually induced cell migration and invasion, a morphologic change associated with epithelial-mesenchymal transition (EMT), expression of mesenchymal-specific markers vimentin and fibronectin, and activity of activator protein transcription factors.
  • Supporting this observation, mouse mammary tumor cells that have undergone EMT showed upregulated JNK activity, and the EMT was reversed by JNK inhibition.
  • In addition, hyperactive JNK attenuated the apoptosis of breast cancer cells treated by the chemotherapy drug paclitaxel, which is in contrast to the requirement for inducible JNK activity in response to cytotoxic chemotherapy.
  • Blockade of extracellular signal-regulated kinase activity diminished hyperactive JNK-induced cell invasion and survival.
  • Our data suggest that the role of JNK changes when its activity is elevated persistently above the basal levels associated with cell apoptosis, and that JNK activation may serve as a marker of breast cancer progression and resistance to cytotoxic drugs.

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  • (PMID = 20145041.001).
  • [ISSN] 1557-3125
  • [Journal-full-title] Molecular cancer research : MCR
  • [ISO-abbreviation] Mol. Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P50CA58183; United States / NCI NIH HHS / CA / P50 CA058183; United States / NCI NIH HHS / CA / R01 CA094118; United States / NCI NIH HHS / CA / R01CA94118; United States / NCI NIH HHS / CA / R01 CA094118-01
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Insulin Receptor Substrate Proteins; 0 / Irs2 protein, mouse; 0 / Proto-Oncogene Proteins c-fos; 0 / Transcription Factor AP-1; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases; EC 2.7.11.24 / JNK Mitogen-Activated Protein Kinases; P88XT4IS4D / Paclitaxel
  • [Other-IDs] NLM/ NIHMS167062; NLM/ PMC2824784
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20. Gil-ad I, Shtaif B, Shiloh R, Weizman A: Evaluation of the neurotoxic activity of typical and atypical neuroleptics: relevance to iatrogenic extrapyramidal symptoms. Cell Mol Neurobiol; 2001 Dec;21(6):705-16
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  • Typical neuroleptic therapy often results in extrapyramidal symptoms (EPS) and tardive dyskinesia (TD).
  • Perphenazine, haloperidol, clozapine, sulpiride, and risperidone (10-100 microM) were administered, either alone or combined with dopamine, to primary mouse neuronal or intact brain culture and to a human neuroblastoma (NB) cell line (SK-N-SH).
  • Cell viability (measured by neutral red and alamar blue), DNA fragmentation (flow cytometry-NB) were determined.
  • Lower concentrations increased the G1 phase and decreased S phase in the cell cycle.
  • Dopamine (0.5 mM) did not modify the effect of the drugs in the primary cultures.
  • Neuroleptics possess differential neurotoxic activity with higher sensitivity of neoplasm tissue (NB compared to primary cultures).
  • Neurotoxicity is independent of dopamine and is associated with cell cycle arrest and apoptosis.
  • [MeSH-major] Antipsychotic Agents / toxicity. Brain / drug effects. Dyskinesia, Drug-Induced / metabolism. Neurons / drug effects. Neurotoxins / toxicity
  • [MeSH-minor] Animals. Basal Ganglia Diseases / chemically induced. Basal Ganglia Diseases / metabolism. Basal Ganglia Diseases / physiopathology. Cell Cycle / drug effects. Cell Survival / drug effects. Cell Survival / physiology. Clozapine / toxicity. DNA Fragmentation / drug effects. Dopamine / metabolism. Dopamine / toxicity. Dose-Response Relationship, Drug. Female. Haloperidol / toxicity. Humans. Iatrogenic Disease / prevention & control. Mice. Mice, Inbred ICR. Perphenazine / toxicity. Pregnancy. Risperidone / toxicity. Tumor Cells, Cultured

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  • (PMID = 12043843.001).
  • [ISSN] 0272-4340
  • [Journal-full-title] Cellular and molecular neurobiology
  • [ISO-abbreviation] Cell. Mol. Neurobiol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antipsychotic Agents; 0 / Neurotoxins; FTA7XXY4EZ / Perphenazine; J60AR2IKIC / Clozapine; J6292F8L3D / Haloperidol; L6UH7ZF8HC / Risperidone; VTD58H1Z2X / Dopamine
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21. Puppe J, Drost R, Liu X, Joosse SA, Evers B, Cornelissen-Steijger P, Nederlof P, Yu Q, Jonkers J, van Lohuizen M, Pietersen AM: BRCA1-deficient mammary tumor cells are dependent on EZH2 expression and sensitive to Polycomb Repressive Complex 2-inhibitor 3-deazaneplanocin A. Breast Cancer Res; 2009;11(4):R63
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  • INTRODUCTION: Treatment of breast cancer is becoming more individualized with the recognition of tumor subgroups that respond differently to available therapies.
  • Breast cancer 1 gene (BRCA1)-deficient tumors are usually of the basal subtype and associated with poor survival rates, highlighting the need for more effective therapy.
  • METHODS: We investigated a mouse model that closely mimics breast cancer arising in BRCA1-mutation carriers to better understand the molecular mechanism of tumor progression and tested whether targeting of the Polycomb-group protein EZH2 would be a putative therapy for BRCA1-deficient tumors.
  • RESULTS: Gene expression analysis demonstrated that EZH2 is overexpressed in BRCA1-deficient mouse mammary tumors.
  • The overexpression of EZH2 in all basal-like breast cancers warrants further investigation of the potential for targeting the genetic make-up of this particular breast cancer type.
  • [MeSH-minor] Animals. Cell Line, Tumor / drug effects. Cell Line, Tumor / metabolism. DNA Repair / genetics. Drug Delivery Systems. Female. Gene Knockdown Techniques. Humans. Mice. Mutation. Polycomb Repressive Complex 2. RNA, Messenger / biosynthesis. RNA, Neoplasm / biosynthesis. RNA, Small Interfering / pharmacology. Recombinant Fusion Proteins / physiology

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  • (PMID = 19709408.001).
  • [ISSN] 1465-542X
  • [Journal-full-title] Breast cancer research : BCR
  • [ISO-abbreviation] Breast Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / BRCA1 Protein; 0 / BRCA1 protein, human; 0 / RNA, Messenger; 0 / RNA, Neoplasm; 0 / RNA, Small Interfering; 0 / Recombinant Fusion Proteins; 102052-95-9 / 3-deazaneplanocin; EC 2.1.1.43 / Ezh2 protein, mouse; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase; EC 2.1.1.43 / Polycomb Repressive Complex 2; K72T3FS567 / Adenosine
  • [Other-IDs] NLM/ PMC2750125
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22. Huss WJ, Gray DR, Greenberg NM, Mohler JL, Smith GJ: Breast cancer resistance protein-mediated efflux of androgen in putative benign and malignant prostate stem cells. Cancer Res; 2005 Aug 01;65(15):6640-50
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  • Malignantly transformed stem cells represent a potential common nidus for the primary cancer and the recurrent cancer that arises after treatment failure.
  • Putative prostate stem cells and prostate tumor stem cells in benign and malignant human prostate tissue, in primary human prostate xenografts, and in the transgenic adenocarcinoma of the mouse prostate (TRAMP) mouse model of prostate cancer, are defined by expression of breast cancer resistance protein (BCRP), a marker of pluripotent hematopoietic, muscle, and neural stem cells, and by an absence of androgen receptor (AR) protein.
  • Inhibition of BCRP-mediated efflux of dihydrotestosterone by novobiocin or fumitremorgin C in a rat prostate progenitor cell line that expresses BCRP and AR mRNAs, but minimal AR protein, results in stabilization and nuclear translocation of AR protein, providing a mechanism for lack of AR protein in BCRP-expressing stem cells.
  • In both benign and malignant human prostate tissue, the rare epithelial cells that express BCRP and lack AR protein are localized in the basal cell compartment, survive androgen deprivation, and maintain proliferative potential in the hypoxic, androgen-deprived prostate.
  • Therefore, BCRP expression isolates prostate stem/tumor stem cells from the prostate tissue microenvironment through constitutive efflux of androgen, protecting the putative tumor stem cells from androgen deprivation, hypoxia, or adjuvant chemotherapy, and providing the nidus for recurrent prostate cancer.
  • [MeSH-major] ATP-Binding Cassette Transporters / biosynthesis. Androgens / metabolism. Neoplasm Proteins / biosynthesis. Neoplastic Stem Cells / metabolism. Prostatic Neoplasms / metabolism
  • [MeSH-minor] ATP Binding Cassette Transporter, Sub-Family G, Member 2. Animals. Cell Line. Cell Nucleus / metabolism. Humans. Indoles / pharmacology. Male. Mice. Mice, Inbred C57BL. Mice, Transgenic. Novobiocin / pharmacology. Prostate / metabolism. Protein Processing, Post-Translational. RNA, Messenger / biosynthesis. RNA, Messenger / genetics. Rats. Receptors, Androgen / biosynthesis. Receptors, Androgen / deficiency. Receptors, Androgen / genetics. Receptors, Androgen / metabolism. Transplantation, Heterologous

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  • (PMID = 16061644.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA84296; United States / NCI NIH HHS / CA / P01 CA077739; United States / NCI NIH HHS / CA / CA77739; United States / NCI NIH HHS / CA / CA64851; United States / NIEHS NIH HHS / ES / ES07017; United States / NCI NIH HHS / CA / CA64865
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / ABCG2 protein, human; 0 / ATP Binding Cassette Transporter, Sub-Family G, Member 2; 0 / ATP-Binding Cassette Transporters; 0 / Androgens; 0 / Indoles; 0 / Neoplasm Proteins; 0 / RNA, Messenger; 0 / Receptors, Androgen; 17EC19951N / Novobiocin; CW5S8OP3VO / tryptoquivaline
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23. Spinella F, Rosanò L, Di Castro V, Decandia S, Albini A, Nicotra MR, Natali PG, Bagnato A: Green tea polyphenol epigallocatechin-3-gallate inhibits the endothelin axis and downstream signaling pathways in ovarian carcinoma. Mol Cancer Ther; 2006 Jun;5(6):1483-92
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  • The endothelin A receptor (ET(A)R)/endothelin-1 (ET-1) axis is overexpressed in ovarian carcinoma representing a novel therapeutic target.
  • In this study, we examined the green tea and EGCG effects on two ovarian carcinoma cell lines, HEY and OVCA 433.
  • EGCG inhibited ovarian cancer cell growth and induced apoptosis that was associated with a decrease in Bcl-X(L) expression and activation of caspase-3.
  • Treatment with green tea or EGCG inhibited ET(A)R and ET-1 expression and reduced the basal and ET-1-induced cell proliferation and invasion.
  • Remarkably, EGCG treatment resulted in a lowering of basal and ET-1-induced angiogenesis and invasiveness mediators, such as vascular endothelial growth factor and tumor proteinase activation.
  • [MeSH-major] Anticarcinogenic Agents / pharmacology. Catechin / analogs & derivatives. Endothelin-1 / antagonists & inhibitors. Ovarian Neoplasms / drug therapy. Signal Transduction / drug effects. Tea
  • [MeSH-minor] Animals. Apoptosis / drug effects. Caspase 3. Caspases / metabolism. Cell Proliferation / drug effects. Enzyme Activation / drug effects. Female. Humans. Mice. Mice, Nude. Mitogen-Activated Protein Kinases / metabolism. Neoplasm Invasiveness. Phosphatidylinositol 3-Kinases / metabolism. Receptor, Endothelin A / metabolism. Transplantation, Heterologous. Urokinase-Type Plasminogen Activator / antagonists & inhibitors. Vascular Endothelial Growth Factor A / metabolism. bcl-X Protein / metabolism

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  • (PMID = 16818507.001).
  • [ISSN] 1535-7163
  • [Journal-full-title] Molecular cancer therapeutics
  • [ISO-abbreviation] Mol. Cancer Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anticarcinogenic Agents; 0 / Endothelin-1; 0 / Receptor, Endothelin A; 0 / Tea; 0 / VEGFA protein, human; 0 / Vascular Endothelial Growth Factor A; 0 / bcl-X Protein; 8R1V1STN48 / Catechin; BQM438CTEL / epigallocatechin gallate; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.11.24 / Mitogen-Activated Protein Kinases; EC 3.4.21.73 / Urokinase-Type Plasminogen Activator; EC 3.4.22.- / CASP3 protein, human; EC 3.4.22.- / Casp3 protein, mouse; EC 3.4.22.- / Caspase 3; EC 3.4.22.- / Caspases
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24. Shen SC, Lee WR, Fang YP, Hu CH, Fang JY: In vitro percutaneous absorption and in vivo protoporphyrin IX accumulation in skin and tumors after topical 5-aminolevulinic acid application with enhancement using an erbium:YAG laser. J Pharm Sci; 2006 Apr;95(4):929-38
Hazardous Substances Data Bank. YTTRIUM, ELEMENTAL .

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  • 5-aminolevulinic acid (ALA) is used as a precursor of protoporphyrin IX (PpIX) for photodynamic therapy (PDT) of superficial skin cancers and subcutaneous metastases of internal malignancies.
  • The permeability of ALA across intact skin is always low, making it difficult to achieve the desired therapeutic benefits.
  • The aim of this study was to determine the in vivo kinetics of PpIX generation in mouse tissues after topical ALA application enhanced by an erbium (Er):yttrium-aluminum-garnet (YAG) laser.
  • The efficacy of the improved drug delivery was determined as a function of various laser fluences and cancer models.
  • The enhancement ratios (ER) of laser-treated skin ranged from 1.7 to 4.9 times as compared to the control depending to the fluences used.
  • [MeSH-major] Aminolevulinic Acid / therapeutic use. Carcinoma, Basal Cell / drug therapy. Lasers. Photochemotherapy. Photosensitizing Agents / therapeutic use. Protoporphyrins / metabolism. Protoporphyrins / therapeutic use. Skin Absorption. Skin Neoplasms / drug therapy
  • [MeSH-minor] Administration, Cutaneous. Aluminum. Animals. Cell Line, Tumor. Erbium. Female. In Vitro Techniques. Mice. Mice, Inbred BALB C. Neoplasm Transplantation. Water Loss, Insensible. Yttrium

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  • (PMID = 16493590.001).
  • [ISSN] 0022-3549
  • [Journal-full-title] Journal of pharmaceutical sciences
  • [ISO-abbreviation] J Pharm Sci
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Photosensitizing Agents; 0 / Protoporphyrins; 0 / yttrium-aluminum-garnet; 553-12-8 / protoporphyrin IX; 58784XQC3Y / Yttrium; 77B218D3YE / Erbium; 88755TAZ87 / Aminolevulinic Acid; CPD4NFA903 / Aluminum
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25. Kyriazi M, Alexandratou E, Yova D, Rallis M, Trebst T: Topical photodynamic therapy of murine non-melanoma skin carcinomas with aluminum phthalocyanine chloride and a diode laser: pharmacokinetics, tumor response and cosmetic outcomes. Photodermatol Photoimmunol Photomed; 2008 Apr;24(2):87-94
MedlinePlus Health Information. consumer health - Skin Cancer.

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  • [Title] Topical photodynamic therapy of murine non-melanoma skin carcinomas with aluminum phthalocyanine chloride and a diode laser: pharmacokinetics, tumor response and cosmetic outcomes.
  • BACKGROUND/PURPOSE: Topical photodynamic therapy (PDT) is potentially useful for the treatment of non-melanoma skin cancer and other skin diseases.
  • We investigated the therapeutic effects of PDT using topical application of aluminum phthalocyanine chloride (AlClPc) and a diode laser emitting at 670 nm in murine non-melanoma skin carcinomas.
  • The penetration depth and the optimum drug-light interval were assessed using pharmacokinetic studies.
  • Then, PDT was performed on a murine model of non-melanoma skin cancer using seven different combinations of therapeutic parameters (fluence rate and energy dose).
  • RESULTS: Pharmacokinetic studies revealed that AlClPc was absorbed 40 times more and penetrated 19 times deeper in tumors than normal skin.
  • CONCLUSIONS: The results indicate that AlClPc-PDT is an effective treatment for non-melanoma skin carcinomas in experimental mouse models.
  • [MeSH-major] Carcinoma, Basal Cell / drug therapy. Indoles / administration & dosage. Neoplasm Recurrence, Local / drug therapy. Organometallic Compounds / administration & dosage. Photochemotherapy. Photosensitizing Agents / administration & dosage. Skin Neoplasms / drug therapy
  • [MeSH-minor] Administration, Cutaneous. Animals. Female. Male. Mice. Mice, Inbred Strains. Neoplasm Transplantation

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  • (PMID = 18353089.001).
  • [ISSN] 1600-0781
  • [Journal-full-title] Photodermatology, photoimmunology & photomedicine
  • [ISO-abbreviation] Photodermatol Photoimmunol Photomed
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Indoles; 0 / Organometallic Compounds; 0 / Photosensitizing Agents; 14154-42-8 / chloroaluminum phthalocyanine
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26. Holland ML, Lau DT, Allen JD, Arnold JC: The multidrug transporter ABCG2 (BCRP) is inhibited by plant-derived cannabinoids. Br J Pharmacol; 2007 Nov;152(5):815-24
Hazardous Substances Data Bank. NOVANTRONE .

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  • BACKGROUND AND PURPOSE: Cannabinoids are used therapeutically for the palliation of the adverse side effects associated with cancer chemotherapy.
  • The cytotoxicity and chemosensitization by cannabinoids was determined with cell viability assays.
  • KEY RESULTS: CBN, CBD and THC increased the intracellular accumulation of the Abcg2/ABCG2 substrate, mitoxantrone, in an over-expressing cell line.
  • The plant cannabinoids inhibited both basal and substrate stimulated ATPase activity of human ABCG2.
  • Cannabinoid cytotoxicity occurred in the absence of known cannabinoid cell surface receptors, and only at concentrations higher than those required for Abcg2/ABCG2 inhibition.
  • Sub-toxic concentrations of the cannabinoids resensitized the overexpressing cell line to the cytotoxic effect of Abcg2/ABCG2 substrates, mitoxantrone and topotecan.
  • [MeSH-major] ATP-Binding Cassette Transporters / antagonists & inhibitors. Cannabinoids / pharmacology. Neoplasm Proteins / antagonists & inhibitors. Plant Extracts / pharmacology
  • [MeSH-minor] ATP Binding Cassette Transporter, Sub-Family G, Member 2. Adenosine Triphosphatases / metabolism. Animals. Cell Line. Cell Line, Tumor. Cell Survival / drug effects. Dose-Response Relationship, Drug. Dronabinol / analogs & derivatives. Dronabinol / pharmacology. Flow Cytometry. Humans. Immunoblotting. Inhibitory Concentration 50. Mice. Mitoxantrone / pharmacology. Receptor, Cannabinoid, CB1 / genetics. Receptor, Cannabinoid, CB1 / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Sulfasalazine / pharmacology. TRPV Cation Channels / genetics. TRPV Cation Channels / metabolism. Topotecan / pharmacology

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  • (PMID = 17906686.001).
  • [ISSN] 0007-1188
  • [Journal-full-title] British journal of pharmacology
  • [ISO-abbreviation] Br. J. Pharmacol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / ABCG2 protein, human; 0 / ATP Binding Cassette Transporter, Sub-Family G, Member 2; 0 / ATP-Binding Cassette Transporters; 0 / Cannabinoids; 0 / Neoplasm Proteins; 0 / Plant Extracts; 0 / Receptor, Cannabinoid, CB1; 0 / TRPV Cation Channels; 0 / TRPV1 protein, mouse; 3XC8GUZ6CB / Sulfasalazine; 4TPC9E4A32 / 11-nor-delta(9)-tetrahydrocannabinol-9-carboxylic acid; 7J8897W37S / Dronabinol; 7M7YKX2N15 / Topotecan; BZ114NVM5P / Mitoxantrone; EC 3.6.1.- / Adenosine Triphosphatases
  • [Other-IDs] NLM/ PMC2190019
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27. Fernando MA, Heaney AP: Alpha1-adrenergic receptor antagonists: novel therapy for pituitary adenomas. Mol Endocrinol; 2005 Dec;19(12):3085-96
Hazardous Substances Data Bank. Corticotropin .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Alpha1-adrenergic receptor antagonists: novel therapy for pituitary adenomas.
  • Doxazosin (dox), a selective alpha(1)-adrenergic receptor antagonist, used to treat hypertension, also inhibits prostate cancer cell proliferation.
  • We examined the effects of dox on murine and human pituitary tumor cell proliferation in vitro and in vivo. dox treatment inhibited proliferation of murine pituitary tumor cells, induced G(0)-G(1) cell cycle arrest, and reduced phosphorylated retinoblastoma levels.
  • In addition, increased annexin-fluorescein isothiocyanate immunoreactivity and cleaved caspase-3 levels, in keeping with dox-mediated apoptosis, were observed in the human and murine pituitary tumor cells, and dox administration to mice, harboring corticotroph tumors, decreased tumor growth and reduced plasma ACTH levels. dox-mediated antiproliferative and proapoptotic actions were not confined to alpha-adrenergic receptor-expressing pituitary tumor cells and were unaffected by cotreatment with the alpha-adrenergic receptor blocker, phenoxybenzamine. dox treatment led to reduced phosphorylated inhibitory kappaB (IkappaB)-alpha expression, and nuclear factor-kappaB transcription and decreased basal and TNFalpha-induced proopiomelanocortin transcriptional activation.
  • These results demonstrate that the selective alpha(1)-adrenergic receptor antagonist dox inhibits pituitary tumor cell growth in vitro and in vivo by mechanisms that are in part independent of its alpha-adrenergic receptor-blocking actions and involve down-regulation of nuclear factor-kappaB signaling. dox is proposed as a possible novel medical therapy for pituitary tumors.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / drug therapy. Adenoma / drug therapy. Adrenergic alpha-1 Receptor Antagonists. Adrenergic alpha-Antagonists / therapeutic use. Antineoplastic Agents / therapeutic use. Doxazosin / therapeutic use
  • [MeSH-minor] Adrenocorticotropic Hormone / blood. Animals. Apoptosis. Caspase 3. Caspases / metabolism. Cell Cycle / drug effects. Cell Proliferation / drug effects. Humans. I-kappa B Proteins / metabolism. Mice. Mice, Nude. NF-kappa B / metabolism. Neoplasm Transplantation. Pro-Opiomelanocortin / genetics. Receptors, Adrenergic, alpha-1 / genetics. Receptors, Adrenergic, alpha-1 / metabolism. Transcriptional Activation. Tumor Cells, Cultured. Tumor Necrosis Factor-alpha / metabolism

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  • (PMID = 16020484.001).
  • [ISSN] 0888-8809
  • [Journal-full-title] Molecular endocrinology (Baltimore, Md.)
  • [ISO-abbreviation] Mol. Endocrinol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adrenergic alpha-1 Receptor Antagonists; 0 / Adrenergic alpha-Antagonists; 0 / Antineoplastic Agents; 0 / I-kappa B Proteins; 0 / NF-kappa B; 0 / Receptors, Adrenergic, alpha-1; 0 / Tumor Necrosis Factor-alpha; 139874-52-5 / NF-kappaB inhibitor alpha; 66796-54-1 / Pro-Opiomelanocortin; 9002-60-2 / Adrenocorticotropic Hormone; EC 3.4.22.- / CASP3 protein, human; EC 3.4.22.- / Casp3 protein, mouse; EC 3.4.22.- / Caspase 3; EC 3.4.22.- / Caspases; NW1291F1W8 / Doxazosin
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28. Kuljaca S, Liu T, Tee AE, Haber M, Norris MD, Dwarte T, Marshall GM: Enhancing the anti-angiogenic action of histone deacetylase inhibitors. Mol Cancer; 2007;6:68
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

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  • BACKGROUND: Histone deacetylase inhibitors (HDACIs) have many effects on cancer cells, such as growth inhibition, induction of cell death, differentiation, and anti-angiogenesis, all with a wide therapeutic index.
  • RESULTS: Trichostatin A (TSA) and alpha-interferon (IFNalpha) were the most effective combination across a range of different cancer cell lines, while normal non-malignant cells did not respond in the same manner to the combination therapy.
  • There was a close correlation between absence of basal p21WAF1 expression and response to TSA and IFNalpha treatment.
  • Moreover, inhibition of p21WAF1 expression in a p21WAF1-expressing breast cancer cell line by a specific siRNA increased the cytotoxic effects of TSA and IFNalpha.
  • In vitro assays of endothelial cell function showed that TSA and IFNalpha decreased endothelial cell migration, invasion, and capillary tubule formation, without affecting endothelial cell viability.
  • Combination TSA and IFNalpha therapy markedly reduced tumour angiogenesis in neuroblastoma-bearing transgenic mice.
  • CONCLUSION: Our results indicate that combination TSA and IFNalpha therapy has potent co-operative cytotoxic and anti-angiogenic activity.
  • High basal p21WAF1 expression appears to be acting as a resistance factor to the combination therapy.
  • [MeSH-minor] Animals. Anoxia. Cell Movement. Cyclin-Dependent Kinase Inhibitor p21 / metabolism. Drug Synergism. Humans. Hydroxamic Acids / pharmacology. Interferon-alpha / metabolism. Mice. Models, Biological. Neoplasm Invasiveness. Neoplasm Transplantation

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  • (PMID = 17958916.001).
  • [ISSN] 1476-4598
  • [Journal-full-title] Molecular cancer
  • [ISO-abbreviation] Mol. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / CDKN1A protein, human; 0 / Cdkn1a protein, mouse; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / Enzyme Inhibitors; 0 / Histone Deacetylase Inhibitors; 0 / Hydroxamic Acids; 0 / Interferon-alpha; 3X2S926L3Z / trichostatin A
  • [Other-IDs] NLM/ PMC2173905
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29. Darash-Yahana M, Pikarsky E, Abramovitch R, Zeira E, Pal B, Karplus R, Beider K, Avniel S, Kasem S, Galun E, Peled A: Role of high expression levels of CXCR4 in tumor growth, vascularization, and metastasis. FASEB J; 2004 Aug;18(11):1240-2
The Lens. Cited by Patents in .

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  • Positive staining for CXCL12, the ligand for CXCR4, was mainly present in the tumor-associated blood vessels and basal cell hyperplasia.
  • Moreover, blood vessel density, functionality, invasiveness of tumors into the surrounding tissues, and metastasis to the lymph node and lung were significantly increased in these tumors.
  • Thus high levels of the chemokine receptor CXCR4 induce a more aggressive phenotype in prostate cancer cells and identify CXCR4 as a potential therapeutic target in advanced cases of metastatic prostate cancer.
  • [MeSH-major] Adenocarcinoma / metabolism. Neoplasm Metastasis / genetics. Neoplasm Proteins / physiology. Neovascularization, Pathologic / genetics. Prostatic Neoplasms / metabolism. Receptors, CXCR4 / physiology
  • [MeSH-minor] Animals. Bone Marrow / pathology. Bone Neoplasms / secondary. Breast Neoplasms / pathology. Cell Adhesion / drug effects. Cell Line, Tumor / drug effects. Cell Line, Tumor / metabolism. Cell Line, Tumor / pathology. Cell Movement / drug effects. Chemokine CXCL12. Chemokines, CXC / analysis. Chemokines, CXC / pharmacology. Female. Humans. Hyperplasia. Lung Neoplasms / secondary. Lymphatic Metastasis. Magnetic Resonance Imaging. Male. Mice. Mice, Inbred NOD. Mice, SCID. Organ Specificity. Ovarian Neoplasms / pathology. Phenotype. Recombinant Fusion Proteins / physiology. Transplantation, Heterologous. Vascular Endothelial Growth Factor A / secretion

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  • (PMID = 15180966.001).
  • [ISSN] 1530-6860
  • [Journal-full-title] FASEB journal : official publication of the Federation of American Societies for Experimental Biology
  • [ISO-abbreviation] FASEB J.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CXCL12 protein, human; 0 / Chemokine CXCL12; 0 / Chemokines, CXC; 0 / Cxcl12 protein, mouse; 0 / Neoplasm Proteins; 0 / Receptors, CXCR4; 0 / Recombinant Fusion Proteins; 0 / Vascular Endothelial Growth Factor A
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30. Bennett JA, DeFreest L, Anaka I, Saadati H, Balulad S, Jacobson HI, Andersen TT: AFPep: an anti-breast cancer peptide that is orally active. Breast Cancer Res Treat; 2006 Jul;98(2):133-41
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  • BACKGROUND: We have synthesized a cyclic nonapeptide (AFPep) that is effective, after being administered by parenteral routes, for the treatment or the prevention of breast cancer.
  • METHODS: Using a human breast cancer xenograft model in mice for therapeutic activity, a carcinogen-induced breast cancer model in rats for prevention efficacy, and a mouse uterus growth inhibition model of anti-estrogenic activity, AFPep was administered by oral gavage (p.o.) and its effects compared to those following intraperitoneal (i.p.) and subcutaneous (s.c.) administration.
  • Preliminary mechanistic studies were carried out in T47D human breast cancer cells growing in culture and evaluated the effect of AFPep on estrogen-stimulated cell growth, phosphorylation of the estrogen receptor (ER), and on level of ER-related kinases.
  • RESULTS: Orally administered AFPep stopped the growth of human tumor xenografts in mice, decreased the incidence and multiplicity of breast cancers in carcinogen-exposed rats, and inhibited the estrogen-stimulated growth of mouse uteri.
  • In culture, AFPep inhibited the estrogen-stimulated growth, but not the basal growth, of T47D cells, and it inhibited the estrogen-stimulated phosphorylation of Serine 118 in the ER of these cells, which was not explainable by early changes in ER-related kinases.
  • CONCLUSIONS: Chronic oral administration of AFPep appears to be safe and effective for the treatment or prevention of breast cancer in animal models.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Breast Neoplasms / drug therapy. Peptides, Cyclic / therapeutic use. alpha-Fetoproteins
  • [MeSH-minor] Administration, Oral. Animals. Cell Line, Tumor. Humans. Male. Mice. Mice, SCID. Neoplasm Transplantation. Transplantation, Heterologous

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  • (PMID = 16538538.001).
  • [ISSN] 0167-6806
  • [Journal-full-title] Breast cancer research and treatment
  • [ISO-abbreviation] Breast Cancer Res. Treat.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA102540
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Peptides, Cyclic; 0 / alpha-Fetoproteins
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31. Dasgupta S, Jana M, Zhou Y, Fung YK, Ghosh S, Pahan K: Antineuroinflammatory effect of NF-kappaB essential modifier-binding domain peptides in the adoptive transfer model of experimental allergic encephalomyelitis. J Immunol; 2004 Jul 15;173(2):1344-54
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  • It has been shown that peptides corresponding to the NF-kappaB essential modifier-binding domain (NBD) of IkappaB kinase alpha or IkappaB kinase beta specifically inhibit the induction of NF-kappaB activation without inhibiting the basal NF-kappaB activity.
  • Clinical symptoms of EAE were much lower in mice receiving wild-type (wt)NBD peptides compared with those receiving mutated (m)NBD peptides.
  • Histological and immunocytochemical analysis showed that wtNBD peptides inhibited EAE-induced spinal cord mononuclear cell invasion and normalized p65 (the RelA subunit of NF-kappaB) expression within the spinal cord.
  • Taken together, our results support the conclusion that NBD peptides are antineuroinflammatory, and that NBD peptides may have therapeutic effect in neuroinflammatory disorders such as multiple sclerosis.

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  • (PMID = 15240729.001).
  • [ISSN] 0022-1767
  • [Journal-full-title] Journal of immunology (Baltimore, Md. : 1950)
  • [ISO-abbreviation] J. Immunol.
  • [Language] ENG
  • [Grant] United States / NINDS NIH HHS / NS / NS039940-04; United States / NINDS NIH HHS / NS / NS39940; United States / NINDS NIH HHS / NS / R01 NS039940-04
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents; 0 / Carrier Proteins; 0 / NBD peptide, mouse; 0 / NF-kappa B; 0 / Neoplasm Proteins; 0 / Peptides; 0 / Rela protein, mouse; 0 / Transcription Factor RelA
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32. Zhang J, Dai J, Qi Y, Lin DL, Smith P, Strayhorn C, Mizokami A, Fu Z, Westman J, Keller ET: Osteoprotegerin inhibits prostate cancer-induced osteoclastogenesis and prevents prostate tumor growth in the bone. J Clin Invest; 2001 May;107(10):1235-44
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  • Furthermore, OPG had no effect on CaP cell viability, proliferation, or basal apoptotic rate in vitro.

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  • (PMID = 11375413.001).
  • [ISSN] 0021-9738
  • [Journal-full-title] The Journal of clinical investigation
  • [ISO-abbreviation] J. Clin. Invest.
  • [Language] ENG
  • [Grant] United States / NCRR NIH HHS / RR / T32 RR007008; United States / NIA NIH HHS / AG / R01 AG-15904; United States / NCI NIH HHS / CA / P50 CA069568; United States / NCI NIH HHS / CA / P50 CA-69568; United States / NCRR NIH HHS / RR / T32 RR-07008
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Carrier Proteins; 0 / Glycoproteins; 0 / Membrane Glycoproteins; 0 / Osteoprotegerin; 0 / RANK Ligand; 0 / Receptor Activator of Nuclear Factor-kappa B; 0 / Receptors, Cytoplasmic and Nuclear; 0 / Receptors, Tumor Necrosis Factor; 0 / TNFRSF11A protein, human; 0 / TNFRSF11B protein, human; 0 / TNFSF11 protein, human; 0 / Tnfrsf11a protein, mouse; 0 / Tnfrsf11b protein, mouse; 0 / Tnfsf11 protein, mouse
  • [Other-IDs] NLM/ PMC209296
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33. Jaspers JE, Rottenberg S, Jonkers J: Therapeutic options for triple-negative breast cancers with defective homologous recombination. Biochim Biophys Acta; 2009 Dec;1796(2):266-80
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  • [Title] Therapeutic options for triple-negative breast cancers with defective homologous recombination.
  • Breast cancer is the most common malignancy among women in developed countries, affecting more than a million women per year worldwide.
  • Over the last decades, our increasing understanding of breast cancer biology has led to the development of endocrine agents against hormone receptor-positive tumors and targeted therapeutics against HER2-expressing tumors.
  • However, no targeted therapy is available for patients with triple-negative breast cancer, lacking expression of hormone receptors and HER2.
  • Overlap between BRCA1-mutated breast cancers and triple-negative tumors suggests that an important part of the triple-negative tumors may respond to therapeutics targeting BRCA1-deficient cells.
  • Here, we review the features shared between triple-negative, basal-like and BRCA1-related breast cancers.
  • We also discuss the development of novel therapeutic strategies to target BRCA1-mutated tumors and triple-negative tumors with BRCA1-like features.
  • Finally, we highlight the utility of mouse models for BRCA1-mutated breast cancer to optimize (combination) therapy and to understand drug resistance.
  • [MeSH-major] Breast Neoplasms / chemistry. Breast Neoplasms / drug therapy. Receptor, ErbB-2 / analysis. Receptors, Estrogen / analysis. Receptors, Progesterone / analysis. Recombination, Genetic
  • [MeSH-minor] Animals. Cell Cycle. DNA Repair. Disease Models, Animal. Drug Resistance, Neoplasm. Female. Genes, BRCA1. Humans. Mice. Mutation. Poly(ADP-ribose) Polymerase Inhibitors. Protein Kinase Inhibitors / therapeutic use

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  • (PMID = 19616605.001).
  • [ISSN] 0006-3002
  • [Journal-full-title] Biochimica et biophysica acta
  • [ISO-abbreviation] Biochim. Biophys. Acta
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Poly(ADP-ribose) Polymerase Inhibitors; 0 / Protein Kinase Inhibitors; 0 / Receptors, Estrogen; 0 / Receptors, Progesterone; EC 2.7.10.1 / ERBB2 protein, human; EC 2.7.10.1 / Receptor, ErbB-2
  • [Number-of-references] 241
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