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1. Greenberger S, Adini I, Boscolo E, Mulliken JB, Bischoff J: Targeting NF-κB in infantile hemangioma-derived stem cells reduces VEGF-A expression. Angiogenesis; 2010 Dec;13(4):327-35
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  • [Title] Targeting NF-κB in infantile hemangioma-derived stem cells reduces VEGF-A expression.
  • BACKGROUND: infantile hemangioma (IH) is a most common tumor of infancy.
  • Using infantile hemangioma-derived stem cells (HemSCs), we recently demonstrated that corticosteroids suppress the expression of VEGF-A, monocyte chemoattractant protein-1 (MCP-1), urokinase plasminogen activator receptor (uPAR), and interleukin-6 (IL-6); each of these are known targets of the transcription factor nuclear factor κ-light-chain-enhancer of activated B cells (NF-κB).
  • MATERIALS AND METHODS: RNA extracted from IH tissue and hemangioma-derived stem cells (HemSCs) was used to analyze NF-κB target gene expression by reverse transcription-quantitative PCR (RT-qPCR).

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  • (PMID = 20872175.001).
  • [ISSN] 1573-7209
  • [Journal-full-title] Angiogenesis
  • [ISO-abbreviation] Angiogenesis
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / HL096384-03; United States / NHLBI NIH HHS / HL / R01 HL096384; United States / NHLBI NIH HHS / HL / R01 HL096384-03
  • [Publication-type] Evaluation Studies; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Boronic Acids; 0 / NF-kappa B; 0 / Pyrazines; 0 / VEGFA protein, human; 0 / Vascular Endothelial Growth Factor A; 69G8BD63PP / Bortezomib; 7S5I7G3JQL / Dexamethasone
  • [Other-IDs] NLM/ NIHMS268304; NLM/ PMC3034388
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2. Cosgrove D, Lassau N: [Assessment of tumour angiogenesis using contrast-enhanced ultrasound]. J Radiol; 2009 Jan;90(1 Pt 2):156-64
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  • [Transliterated title] Evaluation de l'angiogénèse tumorale à l'aide de l'échographie de contraste.
  • More sophisticated methods use quantitative approaches to measure the amount and the time course of bolus or reperfusion curves and have shown great promise in revealing effective tumour response to anti-angiogenic drugs in humans before tumour shrinkage occurs.
  • [MeSH-major] Angiogenesis Inhibitors / therapeutic use. Breast Neoplasms / ultrasonography. Carcinoma, Renal Cell / ultrasonography. Contrast Media. Focal Nodular Hyperplasia / ultrasonography. Hemangioma / ultrasonography. Kidney Neoplasms / ultrasonography. Liver Neoplasms / ultrasonography. Microbubbles. Neovascularization, Pathologic / ultrasonography. Phospholipids. Prostatic Neoplasms / ultrasonography. Sulfur Hexafluoride. Ultrasonography / methods
  • [MeSH-minor] Animals. Diagnosis, Differential. Disease Models, Animal. Female. Humans. Male. Treatment Outcome. Ultrasonography, Doppler / methods. Ultrasonography, Doppler, Color / methods


3. Kitayama T, Marubayashi S, Hayamizu K, Tashiro H, Ohdan H, Ikeda S, Okimoto T, Okajima M, Kataoka T, Sugino K, Asahara T, Fukuda Y, Dohi K: Allochronic overlapping malignancies after renal transplantation in a patient with p53 gene mutation: report of a case. Surg Today; 2004;34(5):473-6
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  • Left breast cancer was diagnosed 9 years after the renal transplantation, then colon cancers and meningeal epidermal meningioma were diagnosed, 10 years and 12 years post-transplant, respectively.
  • During the investigations for the breast and colon cancers, a p53 gene mutation was detected.
  • We suggest that the effects of the immunosuppressive drugs combined with the p53 gene abnormality accelerated tumor development in this patient.
  • [MeSH-major] Breast Neoplasms / etiology. Colonic Neoplasms / etiology. Genes, p53. Immunosuppressive Agents / administration & dosage. Kidney Transplantation / adverse effects. Mutation. Neoplasms, Multiple Primary
  • [MeSH-minor] Azathioprine / administration & dosage. Carcinoma, Ductal, Breast / etiology. Carcinoma, Ductal, Breast / genetics. Colonic Polyps / etiology. Colonic Polyps / surgery. Drug Therapy, Combination. Female. Graft Rejection. Hemangioma / pathology. Humans. Liver Neoplasms / secondary. Methylprednisolone / administration & dosage. Middle Aged. Postoperative Complications. Ribonucleosides / administration & dosage

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  • (PMID = 15108094.001).
  • [ISSN] 0941-1291
  • [Journal-full-title] Surgery today
  • [ISO-abbreviation] Surg. Today
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Immunosuppressive Agents; 0 / Ribonucleosides; 50924-49-7 / bredinin; MRK240IY2L / Azathioprine; X4W7ZR7023 / Methylprednisolone
  • [Number-of-references] 17
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4. Finlay GA, Malhowski AJ, Polizzi K, Malinowska-Kolodziej I, Kwiatkowski DJ: Renal and liver tumors in Tsc2(+/-) mice, a model of tuberous sclerosis complex, do not respond to treatment with atorvastatin, a 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor. Mol Cancer Ther; 2009 Jul;8(7):1799-807
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  • We tested atorvastatin as a therapy for (a) ethylnitrosourea (ENU)-enhanced renal cystadenoma and (b) spontaneous liver hemangioma in 129Sv/Jae Tsc2(+/-) mice.
  • Pathologic analyses revealed a predominance of renal cystadenoma in ENU-treated and liver hemangioma in non-ENU-treated 129Sv/Jae Tsc2(+/-) mice.
  • Following atorvastatin treatment, no significant reduction in tumor size, morphology, or phosphorylated S6 levels was observed for either ENU-associated renal cystadenoma or spontaneous liver hemangioma as compared with the untreated groups.
  • In conclusion, although the marked reduction in cholesterol levels indicates that atorvastatin was effective as an 3-hydroxy-3-methylglutaryl CoA reductase inhibitor, it did not inhibit the growth of tumors that develop in these Tsc2(+/-) models, suggesting that it is unlikely to have benefit as a single-agent therapy for TSC-associated tumors.

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  • (PMID = 19584242.001).
  • [ISSN] 1538-8514
  • [Journal-full-title] Molecular cancer therapeutics
  • [ISO-abbreviation] Mol. Cancer Ther.
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / K08 HL074113; United States / NHLBI NIH HHS / HL / K08 HL074113-03; United States / NCI NIH HHS / CA / P01 CA120964; United States / NHLBI NIH HHS / HL / K08 HL074113-05; United States / NHLBI NIH HHS / HL / HL074113-05
  • [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 / Heptanoic Acids; 0 / Hydroxymethylglutaryl-CoA Reductase Inhibitors; 0 / Pyrroles; 0 / Tumor Suppressor Proteins; 48A5M73Z4Q / Atorvastatin Calcium; 4JG2LF96VF / tuberous sclerosis complex 2 protein; 97C5T2UQ7J / Cholesterol
  • [Other-IDs] NLM/ NIHMS119618; NLM/ PMC2712945
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5. Arbiser JL, Bonner MY, Berrios RL: Hemangiomas, angiosarcomas, and vascular malformations represent the signaling abnormalities of pathogenic angiogenesis. Curr Mol Med; 2009 Nov;9(8):929-34
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  • [Title] Hemangiomas, angiosarcomas, and vascular malformations represent the signaling abnormalities of pathogenic angiogenesis.
  • Hemangiomas, benign tumors of endothelial cells, represent the most common tumor of childhood.
  • In our previous studies, we have found that tumor vasculature in human solid tumors expresses similarities in signaling to that of hemangiomas, making the knowledge of signaling in hemangiomas widely applicable.
  • The incidence of these tumors is expected to rise due to environmental insults, such as radiation and lumpectomy for breast cancer, dietary and industrial carcinogens (hepatic angiosarcoma), and chronic ultraviolet exposure and potential Agent Orange exposure.
  • I hypothesize that hemangiomas, angiosarcomas, and vascular malformations represent the extremes of signaling abnormalities seen in pathogenic angiogenesis.
  • [MeSH-major] Hemangioma / blood supply. Hemangiosarcoma / blood supply. Neovascularization, Pathologic / pathology. Signal Transduction. Vascular Malformations / physiopathology
  • [MeSH-minor] Animals. Humans






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