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1. Pan YC, Li CF, Ko CY, Pan MH, Chen PJ, Tseng JT, Wu WC, Chang WC, Huang AM, Sterneck E, Wang JM: CEBPD reverses RB/E2F1-mediated gene repression and participates in HMDB-induced apoptosis of cancer cells. Clin Cancer Res; 2010 Dec 1;16(23):5770-80
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  • [Title] CEBPD reverses RB/E2F1-mediated gene repression and participates in HMDB-induced apoptosis of cancer cells.
  • PURPOSE: Recent evidence indicates that a tumor suppressor gene CEBPD (CCAAT/enhancer-binding protein delta) is downregulated in many cancers including cervical cancer, which provides a therapeutic potential associated with its reactivation.
  • However, little is known for CEBPD activators and the effect of reactivation of CEBPD transcription upon anticancer drug treatment.
  • The purpose of this study is to characterize the mechanism of HMDB-induced CEBPD activation and its potential effect in cancer therapy.
  • Furthermore, a consequence of HMDB-induced CEBPD expression was linked with E2F1 and retinoblastoma (RB), which discloses the scenario of CEBPD, E2F1, and RB bindings and transcriptional regulation on the promoters of proapoptotic genes, PPARG2 and GADD153.
  • RESULTS: We demonstrate that CEBPD plays an essential role in HMDB-mediated apoptosis of cancer cells.
  • Furthermore, increased level of CEBPD attenuates E2F1-induced cancer cell proliferation and partially rescues RB/E2F1-mediated repression of PPARG2 and GADD153 transcription.
  • Moreover, HMDB treatment attenuates the growth of A431 xenografts in severe combined immunodeficient mice mice.
  • CONCLUSIONS: These results clearly demonstrate that HMDB kills cancer cells through activation of CEBPD pathways and suggest that HMDB can serve as a superior chemotherapeutic agent with limited potential for adverse side effects.
  • [MeSH-major] Apoptosis / drug effects. CCAAT-Enhancer-Binding Protein-delta / physiology. E2F1 Transcription Factor / physiology. Ketones / pharmacology. Neoplasms / genetics. Neoplasms / pathology. Propane / analogs & derivatives. Retinoblastoma Protein / physiology
  • [MeSH-minor] Animals. Cells, Cultured. Down-Regulation / genetics. Female. Gene Expression Regulation, Neoplastic. Gene Silencing / physiology. HeLa Cells. Humans. Mice. Mice, Inbred NOD. Mice, SCID. Xenograft Model Antitumor Assays

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  • [Copyright] ©2010 AACR.
  • (PMID = 20971808.001).
  • [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, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 1-(2-hydroxy-5-methylphenyl)-3-phenyl-1,3-propanedione; 0 / E2F1 Transcription Factor; 0 / Ketones; 0 / Retinoblastoma Protein; 142662-43-9 / CCAAT-Enhancer-Binding Protein-delta; T75W9911L6 / Propane
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2. Chévez-Barrios P, Chintagumpala M, Mieler W, Paysse E, Boniuk M, Kozinetz C, Hurwitz MY, Hurwitz RL: Response of retinoblastoma with vitreous tumor seeding to adenovirus-mediated delivery of thymidine kinase followed by ganciclovir. J Clin Oncol; 2005 Nov 1;23(31):7927-35
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  • [Title] Response of retinoblastoma with vitreous tumor seeding to adenovirus-mediated delivery of thymidine kinase followed by ganciclovir.
  • PURPOSE: To evaluate the feasibility and safety of adenovirus-mediated gene therapy as a treatment for tumor seeds in the vitreous of children with retinoblastoma.
  • PATIENTS AND METHODS: An Institutional Biosafety Committee-, Institutional Review Board-, Recombinant DNA Advisory Committee-, and US Food and Drug Administration-approved phase I study used intrapatient dose escalation of adenoviral vector containing a herpes simplex thymidine kinase gene (AdV-TK) followed by systemic administration of ganciclovir to treat bilateral retinoblastoma with vitreous tumor seeding refractory to standard therapies.
  • Vitreous tumor seeds were treated by intravitreous injection of AdV-TK adjacent to disease sites.
  • RESULTS: Eight patients with vitreous tumor seeds were enrolled.
  • One patient who was treated with 10(8) viral particles (vp) had resolution of the tumor seeds around the injection site.
  • The seven patients who were treated with doses > or = 10(10) vp had resolution of their vitreous tumor seeds documented by fundoscopy.
  • Toxicity included mild inflammation at 10(10) vp and moderate inflammation, corneal edema, and increased intraocular pressure at 10(11) vp.
  • One patient was free of active vitreous tumor seeds 38 months after therapy.
  • There has been no evidence of extraocular spread of tumor along the needle tract in any patient.
  • CONCLUSION: AdV-TK followed by ganciclovir can be administered safely to children with retinoblastoma.
  • Suicide gene therapy may contribute to the treatment of children with retinoblastoma tumor seeds in the vitreous, a resistant complication of retinoblastoma.
  • [MeSH-major] Adenoviruses, Human / genetics. Antiviral Agents / therapeutic use. Ganciclovir / therapeutic use. Neoplasm Seeding. Retinal Neoplasms / therapy. Retinoblastoma / therapy. Thymidine Kinase / therapeutic use. Vitreous Body / pathology
  • [MeSH-minor] Child. Combined Modality Therapy. Feasibility Studies. Gene Transfer Techniques. Genetic Therapy. Genetic Vectors. Humans. Neoplasm Recurrence, Local / enzymology. Neoplasm Recurrence, Local / genetics. Neoplasm Recurrence, Local / therapy

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  • (PMID = 16258092.001).
  • [ISSN] 0732-183X
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA97762
  • [Publication-type] Clinical Trial, Phase I; Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antiviral Agents; EC 2.7.1.21 / Thymidine Kinase; P9G3CKZ4P5 / Ganciclovir
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3. Dimaras H, Khetan V, Halliday W, Héon E, Chan HS, Gallie BL: Retinoma underlying retinoblastoma revealed after tumor response to 1 cycle of chemotherapy. Arch Ophthalmol; 2009 Aug;127(8):1066-8
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  • [Title] Retinoma underlying retinoblastoma revealed after tumor response to 1 cycle of chemotherapy.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Calcinosis / diagnosis. Retinal Diseases / diagnosis. Retinal Neoplasms / drug therapy. Retinoblastoma / drug therapy
  • [MeSH-minor] Biomarkers, Tumor / analysis. Carboplatin / therapeutic use. Child, Preschool. Cyclosporine / therapeutic use. Etoposide / therapeutic use. Eye Enucleation. Humans. Male. Vincristine / therapeutic use

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  • (PMID = 19667353.001).
  • [ISSN] 1538-3601
  • [Journal-full-title] Archives of ophthalmology (Chicago, Ill. : 1960)
  • [ISO-abbreviation] Arch. Ophthalmol.
  • [Language] eng
  • [Publication-type] Case Reports; Letter; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 5J49Q6B70F / Vincristine; 6PLQ3CP4P3 / Etoposide; 83HN0GTJ6D / Cyclosporine; BG3F62OND5 / Carboplatin; CEV regimen
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4. Takemura M: Biochemical properties of the stimulatory activity of DNA polymerase alpha by the hyper-phosphorylated retinoblastoma protein. Biochim Biophys Acta; 2002 Jun 6;1571(2):151-6
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  • [Title] Biochemical properties of the stimulatory activity of DNA polymerase alpha by the hyper-phosphorylated retinoblastoma protein.
  • Previously, my colleagues and I have reported that the immunopurified hyper-phosphorylated retinoblastoma protein (ppRb) stimulates the activity of DNA polymerase alpha.
  • I describe here the biochemical characteristics of this stimulatory activity.
  • DNA polymerase alpha-stimulatory activity of ppRb was most remarkable when using activated DNA as a template-primer, rather than using poly(dT)-(rA)(10), poly(dA)-(dT)(12-18), and so on.
  • Kinetic analysis showed that there was no significant difference in K(m) value for deoxyribonucleotides of DNA polymerase alpha in the presence of ppRb.
  • Adding ppRb resulted in the overcoming pause site on the template, but did not affect the rate of misincorporation of incorrect deoxyribonucleotides.
  • By adding ppRb, the optimal concentration of template-primer was shifted to a higher region, but not using M13 singly primed DNA.
  • The ppRb seemed to assist the process that DNA polymerase alpha changed its conformation resulting in appropriate enzyme activity.
  • [MeSH-major] DNA Polymerase I / metabolism. Retinoblastoma Protein / metabolism
  • [MeSH-minor] DNA / drug effects. DNA / metabolism. DNA Replication / physiology. Enzyme Activation. Humans. Kinetics. Phosphorylation. Protein Binding. Templates, Genetic

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  • (PMID = 12049795.001).
  • [ISSN] 0006-3002
  • [Journal-full-title] Biochimica et biophysica acta
  • [ISO-abbreviation] Biochim. Biophys. Acta
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Retinoblastoma Protein; 9007-49-2 / DNA; EC 2.7.7.- / DNA Polymerase I
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5. Rutynowska-Pronicka O, Hautz W, Brozyna A, Dembowska-Bagińska B, Drogosiewicz M, Stypińska M, Perek D: [Conservative treatment in patients with unilateral retinoblastoma]. Med Wieku Rozwoj; 2006 Jul-Sep;10(3 Pt 1):655-63
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  • [Title] [Conservative treatment in patients with unilateral retinoblastoma].
  • [Transliterated title] Próba leczenia zachowawczego u pacjentów z jednooczna postacia retinoblastoma.
  • THE AIM of our study was to evaluate results of conservative treatment of patients with unilateral retinoblastoma.
  • MATERIAL AND METHODS: Twenty one patients, 11 boys and 10 girls aged 2 months to 4, 5 years (median age 1 year) were studied.
  • Local disease advancement according to Reese-Elsworth was defined in all patients.
  • Neoadjuvant chemotherapy consisting of Vincristine, Etoposide and Carboplatin was administered.
  • Sixteen patients were treated with chemotherapy alone.
  • Local treatment including brachytherapy, thermochemotherapy and cryotherapy was implemented and the choice of the method depended on the tumour's localization, size and response to chemotherapy.
  • Statistical analysis using demographic data and survival curves were performed.
  • RESULTS: On completion of treatment all patients achieved tumour regression.
  • Eleven patients are progression free with a follow-up from 10 months to 6 years 4 months (median--2 yrs 5m).
  • In 10 patients relapse was observed.
  • A total of seven enucleations were performed in the examined group.
  • In histopathological examination viable tumour cells were present in all removed eye balls.
  • Distant metastases were not observed in any of these patients.
  • All patients are alive with a follow-up from 10 months to 9 yrs 6 months (median--4 yrs 7 months) from diagnosis.
  • Disease free survival and ocular survival is 44% and 54% respectively.
  • CONCLUSION: Neoadjuvant chemotherapy in unilateral retinoblastoma allows to avoid enucleation in some patients.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Brachytherapy / methods. Cryotherapy / methods. Retinal Neoplasms / therapy. Retinoblastoma / therapy
  • [MeSH-minor] Carboplatin / administration & dosage. Chemotherapy, Adjuvant. Child, Preschool. Disease-Free Survival. Etoposide / administration & dosage. Female. Humans. Infant. Male. Neoadjuvant Therapy. Poland. Treatment Outcome. Vincristine / administration & dosage

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  • (PMID = 17317897.001).
  • [Journal-full-title] Medycyna wieku rozwojowego
  • [ISO-abbreviation] Med Wieku Rozwoj
  • [Language] pol
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Poland
  • [Chemical-registry-number] 5J49Q6B70F / Vincristine; 6PLQ3CP4P3 / Etoposide; BG3F62OND5 / Carboplatin
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6. Yamane T, Kaneko A, Mohri M: The technique of ophthalmic arterial infusion therapy for patients with intraocular retinoblastoma. Int J Clin Oncol; 2004 Apr;9(2):69-73
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  • [Title] The technique of ophthalmic arterial infusion therapy for patients with intraocular retinoblastoma.
  • Recently, there has been increasing interest in treating intraocular retinoblastoma with systemic chemotherapy combined with focal laser therapy and cryotherapy instead of radiotherapy.
  • We developed a system of selective ophthalmic arterial infusion (SOAI) therapy, administering melphalan, the agent which had the greatest effect on retinoblastoma in a clonogenic assay.
  • The SOAI system consists of a combination of a micro-balloon, a guiding catheter, and a flushing hub.
  • After selective catheterization to the cervical segment of the internal carotid artery by the guiding catheter, the micro-balloon was propelled to the portion just distal to the orifice of the ophthalmic artery.
  • We treated 187 patients with intraocular retinoblastoma with SOAI; 563 SOAIs were performed for 610 eyes.
  • SOAI, using the balloon occlusion technique, is safe, and its use will prevent the side effects that occur with systemic chemotherapy, and eliminate the need for irradiation and enucleation.
  • [MeSH-major] Antineoplastic Agents, Alkylating / administration & dosage. Infusions, Intra-Arterial. Melphalan / administration & dosage. Ophthalmic Artery. Retinal Neoplasms / drug therapy. Retinoblastoma / drug therapy
  • [MeSH-minor] Child. Child, Preschool. Female. Humans. Infant. Male. Treatment Outcome

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  • (PMID = 15108036.001).
  • [ISSN] 1341-9625
  • [Journal-full-title] International journal of clinical oncology
  • [ISO-abbreviation] Int. J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; Q41OR9510P / Melphalan
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7. Raje N, Hideshima T, Mukherjee S, Raab M, Vallet S, Chhetri S, Cirstea D, Pozzi S, Mitsiades C, Rooney M, Kiziltepe T, Podar K, Okawa Y, Ikeda H, Carrasco R, Richardson PG, Chauhan D, Munshi NC, Sharma S, Parikh H, Chabner B, Scadden D, Anderson KC: Preclinical activity of P276-00, a novel small-molecule cyclin-dependent kinase inhibitor in the therapy of multiple myeloma. Leukemia; 2009 May;23(5):961-70
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  • [Title] Preclinical activity of P276-00, a novel small-molecule cyclin-dependent kinase inhibitor in the therapy of multiple myeloma.
  • Silencing cyclin D1 resulted in >50% apoptotic cell death suggesting its validity as a potential therapeutic target.
  • Cell-cycle analysis confirmed either growth arrest or caspase-dependent apoptosis; this was preceded by inhibition of Rb-1 phosphorylation with associated downregulation of a range of cyclins suggesting a regulatory role of P276-00 in cell-cycle progression through broad activity.
  • Proliferative stimuli such as interleukin-6, insulin-like growth factor-1 and bone-marrow stromal cell adherence induced cyclins; P276-00 overcame these growth, survival and drug resistance signals.
  • These studies form the basis of an ongoing phase I study in the treatment of relapsed/refractory MM.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Cyclin D1 / antagonists & inhibitors. Flavones / therapeutic use. Multiple Myeloma / drug therapy
  • [MeSH-minor] Animals. Apoptosis / drug effects. Blotting, Western. Bone Marrow / drug effects. Boronic Acids / therapeutic use. Bortezomib. Caspases / metabolism. Cell Adhesion / drug effects. Cell Cycle / drug effects. Cell Proliferation / drug effects. Cyclin-Dependent Kinase Inhibitor Proteins / antagonists & inhibitors. Down-Regulation. Drug Evaluation, Preclinical. Drug Resistance, Neoplasm. Drug Synergism. Gene Expression Profiling. Humans. Insulin-Like Growth Factor I / metabolism. Interleukin-6 / metabolism. Male. Mice. Mice, SCID. Oligonucleotide Array Sequence Analysis. Phosphorylation / drug effects. Pyrazines / therapeutic use. Retinoblastoma Protein / metabolism. Stromal Cells / drug effects. Transplantation, Heterologous. Tumor Cells, Cultured


8. Clifford RL, Knox AJ: Vitamin D - a new treatment for airway remodelling in asthma? Br J Pharmacol; 2009 Nov;158(6):1426-8
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  • [Title] Vitamin D - a new treatment for airway remodelling in asthma?
  • Recent recognition of widespread vitamin D deficiency and identification of the vitamin D receptor on many cells has implicated vitamin D as a potential therapeutic target for many disorders including cancer, infection and asthma.
  • Their results begin to elucidate the molecular mechanism(s) utilized by calcitriol to inhibit cell proliferation and suggest hyperphosphorylation of retinoblastoma protein and activation of checkpoint kinase 1 (Chk1) as critical to this process.
  • This study identifies inhibition of ASM proliferation as a cellular effect of vitamin D and supports the hypothesis that vitamin D is a potential treatment for airway remodelling in asthma.
  • [MeSH-major] Airway Remodeling / drug effects. Calcitriol / pharmacology. Vitamins / pharmacology
  • [MeSH-minor] Asthma / drug therapy. Asthma / physiopathology. Cell Proliferation / drug effects. Dexamethasone / pharmacology. Drug Delivery Systems. Glucocorticoids / pharmacology. Humans. Hypertrophy / drug therapy. Receptors, Calcitriol / drug effects. Receptors, Calcitriol / metabolism. Vitamin D Deficiency

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  • (PMID = 19906117.001).
  • [ISSN] 1476-5381
  • [Journal-full-title] British journal of pharmacology
  • [ISO-abbreviation] Br. J. Pharmacol.
  • [Language] eng
  • [Publication-type] Comment; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Glucocorticoids; 0 / Receptors, Calcitriol; 0 / Vitamins; 7S5I7G3JQL / Dexamethasone; FXC9231JVH / Calcitriol
  • [Other-IDs] NLM/ PMC2795209
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9. Shimokawa T, Sakai M, Kojima Y, Takeyama H: Acute myelogeneous leukemia (M5a) that demonstrated chromosomal abnormality of robertsonian 13;21 translocation at onset. Intern Med; 2004 Jun;43(6):508-11
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  • [Title] Acute myelogeneous leukemia (M5a) that demonstrated chromosomal abnormality of robertsonian 13;21 translocation at onset.
  • Blood test indicated leukocytosis, so she was referred to our hospital for detailed examination.
  • The chromosome analysis in blast cells revealed Robertsonian 13;21 translocation.
  • Complete remission was obtained by induction chemotherapy.
  • As normal karyotype (46, XX) was observed in the chromosome analysis of bone marrow cells after remission, it was considered that the patient had acquired Robertsonian 13;21 translocation complicated by acute myelogeneous leukemia.
  • [MeSH-major] Leukemia, Monocytic, Acute / genetics. Translocation, Genetic / genetics
  • [MeSH-minor] Adult. Chromosomes, Human, Pair 13 / genetics. Female. Humans. Nervous System Malformations / complications

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  • (PMID = 15283189.001).
  • [ISSN] 0918-2918
  • [Journal-full-title] Internal medicine (Tokyo, Japan)
  • [ISO-abbreviation] Intern. Med.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] Japan
  • [Number-of-references] 16
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10. Treré D, Brighenti E, Donati G, Ceccarelli C, Santini D, Taffurelli M, Montanaro L, Derenzini M: High prevalence of retinoblastoma protein loss in triple-negative breast cancers and its association with a good prognosis in patients treated with adjuvant chemotherapy. Ann Oncol; 2009 Nov;20(11):1818-23
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  • [Title] High prevalence of retinoblastoma protein loss in triple-negative breast cancers and its association with a good prognosis in patients treated with adjuvant chemotherapy.
  • BACKGROUND: Triple-negative breast cancer (TNBC) is an aggressive disease, nevertheless exhibiting a high response rate to chemotherapy.
  • Since the retinoblastoma protein (pRb) loss confers a high sensitivity to chemotherapy regimens, we evaluated the prevalence of pRb loss in TNBCs and its relevance on the clinical outcome of patients treated with adjuvant chemotherapy.
  • The predictive value of pRb status in TNBCs was determined according to the adjuvant therapeutic treatments.
  • The prevalence of pRb loss was significantly higher in TNBCs than in the other cancer subtypes.
  • All patients with TNBCs lacking pRb and treated with systemic chemotherapy (cyclophosphamide, methotrexate and 5-fluorouracil) were disease free at a medium follow-up time of 109 months, whereas the clinical outcome of those expressing pRb was significantly poorer (P = 0.008).
  • Analysis of disease-free survival including the established anatomo-clinical prognostic parameters indicated pRb loss as the only significant predictive factor.
  • CONCLUSIONS: pRb loss is much more frequent in TNBCs than in the other breast cancer subtypes.
  • Patients with TNBCs lacking pRb had a very favorable clinical outcome if treated with conventional adjuvant chemotherapy.

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  • (PMID = 19556322.001).
  • [ISSN] 1569-8041
  • [Journal-full-title] Annals of oncology : official journal of the European Society for Medical Oncology
  • [ISO-abbreviation] Ann. Oncol.
  • [Language] ENG
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Receptors, Estrogen; 0 / Receptors, Progesterone; 0 / Retinoblastoma Protein; 8N3DW7272P / Cyclophosphamide; EC 2.7.10.1 / Receptor, ErbB-2; U3P01618RT / Fluorouracil; YL5FZ2Y5U1 / Methotrexate
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11. Ottaviani G, Jaffe N: The epidemiology of osteosarcoma. Cancer Treat Res; 2009;152:3-13
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  • Osteosarcoma derives from primitive bone-forming mesenchymal cells and is the most common primary bone malignancy.
  • Among childhood cancers, osteosarcoma occurs eighth in general incidence and in the following order: leukemia (30%), brain and other nervous system cancers (22.3%), neuroblastoma (7.3%), Wilms tumor (5.6%), Non-Hodgkin lymphoma (4.5%), rhabdomyosarcoma (3.1%), retinoblastoma (2.8%), osteosarcoma (2.4%), and Ewing sarcoma (1.4%).
  • The incidence rates of childhood and adolescent osteosarcoma with 95% confidence intervals areas follows: Blacks, 6.8/year/million; Hispanics, 6.5/year/million; and Caucasians, 4.6/year/million.
  • The first peak is in the 10-14-year-old age group, coinciding with the pubertal growth spurt.
  • The second osteosarcoma peak is in adults older than 65 years of age; it is more likely to represent a second malignancy, frequently related to Paget's disease.
  • The incidence of osteosarcoma has always been considered to be higher in males than in females, occurring at a rate of 5.4 per million persons per year in males vs. 4.0 per million in females, with a higher incidence in blacks (6.8 per million persons per year) and Hispanics (6.5 per million), than in whites (4.6 per million).
  • The most common sites are the femur (42%, with 75% of tumors in the distal femur), the tibia (19%, with 80% of tumors in the proximal tibia), and the humerus (10%, with 90% of tumors in the proximal humerus).
  • Cancer deaths due to bone and joint malignant neoplasms represent 8.9% of all childhood and adolescent cancer deaths.
  • The overall 5-year survival rate for osteosarcoma is 68%, without significant gender difference.
  • Tumor staging, presence of metastases, local recurrence, chemotherapy regimen, anatomic location, size of the tumor, and percentage of tumor cells destroyed after neoadjuvant chemotherapy have effects on the outcome.
  • [MeSH-minor] Adolescent. Adult. Aged. Child. Child, Preschool. Female. Humans. Incidence. Infant. Infant, Newborn. Male. Middle Aged. Neoplasms, Second Primary / epidemiology


12. Aerts I, Leuraud P, Blais J, Pouliquen AL, Maillard P, Houdayer C, Couturier J, Sastre-Garau X, Grierson D, Doz F, Poupon MF: In vivo efficacy of photodynamic therapy in three new xenograft models of human retinoblastoma. Photodiagnosis Photodyn Ther; 2010 Dec;7(4):275-83
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  • [Title] In vivo efficacy of photodynamic therapy in three new xenograft models of human retinoblastoma.
  • PURPOSE: Retinoblastoma is the most common primary intraocular tumor in children.
  • In industrialized countries, 95% of patients are cured by chemotherapy and conservative treatments.
  • However, these treatments can increase the risk of secondary tumors in patients with a constitutional alteration of the RB1 gene.
  • Photodynamic therapy represents a nonmutagenic therapeutic approach, and may reduce the incidence of secondary tumors.
  • To study the in vivo efficacy of photodynamic therapy, human retinoblastoma xenografts were established in nude mice.
  • METHODS: Three xenografted cell lines, RB102-FER, RB109-LAK and RB111-MIL, were characterized and used for therapeutic evaluation.
  • Mice were randomly divided into control and treatment groups with 5-8 mice in each group.
  • Treatment groups received irradiation alone, photosensitizer alone or both in 2 of the 3 models and in the third model, photosensitizer plus irradiation was compared to untreated controls. mTHPC was injected intraperitoneally at a dose of 0.6mg/kg and verteporfin intravenously at a dose of 1mg/kg.
  • RESULTS: A transient but significant response to mTHPC was observed for RB102-FER (p=0.03) and a significant response to mTHPC for RB111-MIL (p<10(-4)) with partial regression maintained for more than 60 days.
  • No significant difference between the different groups was observed for RB109-LAK, except in the verteporfin plus laser group (p=0.01).
  • CONCLUSIONS: The studies confirmed the suitability of the three xenograft models for the evaluation of photodynamic therapy in retinoblastoma.
  • Our findings suggest that PDT may represent an alternative conservative treatment for these tumors.
  • [MeSH-major] Mesoporphyrins / therapeutic use. Photochemotherapy. Photosensitizing Agents / therapeutic use. Porphyrins / therapeutic use. Retinal Neoplasms / drug therapy. Retinoblastoma / drug therapy
  • [MeSH-minor] Animals. Cell Line, Tumor. Child, Preschool. Female. Humans. Infant. Male. Mice. Mice, Nude. Neoplasm Transplantation. Transplantation, Heterologous

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  • [Copyright] Copyright © 2010. Published by Elsevier B.V.
  • (PMID = 21112551.001).
  • [ISSN] 1873-1597
  • [Journal-full-title] Photodiagnosis and photodynamic therapy
  • [ISO-abbreviation] Photodiagnosis Photodyn Ther
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Mesoporphyrins; 0 / Photosensitizing Agents; 0 / Porphyrins; 129497-78-5 / verteporfin; FU21S769PF / temoporfin
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13. Antoneli CB, Ribeiro KC, Steinhorst F, Novaes PE, Chojniak MM, Malogolowkin M: Treatment of retinoblastoma patients with chemoreduction plus local therapy: experience of the AC Camargo Hospital, Brazil. J Pediatr Hematol Oncol; 2006 Jun;28(6):342-5
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  • [Title] Treatment of retinoblastoma patients with chemoreduction plus local therapy: experience of the AC Camargo Hospital, Brazil.
  • To evaluate the efficacy of conservative management of intraocular retinoblastoma with chemoreduction combined with local therapy with or without plaque radiation in the preservation of the eye, and avoidance of external beam radiation therapy (EBRT) (success rate).
  • From 1995 to 2000, 84 newly diagnosed patients with intraocular retinoblastoma were admitted to the Pediatric Department of the Hospital do Cancer A.C.
  • All children were treated with 2 to 6 cycles of chemotherapy (carboplatin, vincristine, and etoposide) plus local therapy (cryotherapy, laser photocoagulation, and thermotherapy), or plaque radiation therapy during and/or after the chemotherapy.
  • The Mann-Whitney test was used to compare means of quantitative variables.
  • The chi test or the Fisher exact test were employed to verify the association between the outcome and the independent variables.
  • For all tests alpha=5% was adopted.
  • For patients with Reese-Ellsworth stages I, II, and III, no statistically significant differences in the success rates were noted in the group of unilateral (50%) and bilateral tumors (79.1%) (P=0.179).
  • Among children with Reese-Ellsworth stages IV and V, the success rate was significantly higher for patients with bilateral tumors (40.7%) than for those with unilateral (0%) (P=0.012).
  • Chemoreduction combined with local therapy, with or without plaque radiotherapy, is efficacious in avoiding enucleation and the use of external beam radiation therapy for children with intraocular retinoblastoma.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Retinal Neoplasms / therapy. Retinoblastoma / therapy
  • [MeSH-minor] Adolescent. Adult. Antineoplastic Agents, Phytogenic / administration & dosage. Brazil. Carboplatin / administration & dosage. Child. Child, Preschool. Combined Modality Therapy. Disease-Free Survival. Etoposide / administration & dosage. Female. Humans. Infant. Male. Retrospective Studies. Treatment Outcome. Vincristine / administration & dosage

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  • (PMID = 16794500.001).
  • [ISSN] 1077-4114
  • [Journal-full-title] Journal of pediatric hematology/oncology
  • [ISO-abbreviation] J. Pediatr. Hematol. Oncol.
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 5J49Q6B70F / Vincristine; 6PLQ3CP4P3 / Etoposide; BG3F62OND5 / Carboplatin
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14. Mayer F, Mueller S, Malenke E, Kuczyk M, Hartmann JT, Bokemeyer C: Induction of apoptosis by flavopiridol unrelated to cell cycle arrest in germ cell tumour derived cell lines. Invest New Drugs; 2005 Jun;23(3):205-11
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  • BACKGROUND: Germ cell tumours (GCTs) are highly sensitive to cisplatin-based chemotherapy.
  • The inability to arrest the cell cycle at the G1/S-check-point due to a lack of retinoblastoma gene product RB has been suggested as one potential explanation for this feature.
  • Flavopiridol (FP), an inhibitor of cyclin dependent kinases, causes cell cycle arrest or apoptosis depending on the relation of the transcription factor E2F1 and RB.
  • METHODS: The effect of FP was evaluated in GCT-derived cell lines NT2, 2102 EP and NCCIT in comparison to cell lines derived from ovarian cancer (SKOV), breast cancer (MCF7), and cervical cancer (HeLa) using the MTT-assay.
  • Cell cycle progression and induction of apoptosis were assessed by flow cytometry and immunoblot analysis of PARP-cleavage.
  • RESULTS: FP did not affect cell cycle progression and proliferation of GCT cell lines at sublethal doses.
  • The IC50 was approximately fivefold lower for the three GCT cell lines (60/60/70 nM) than for the other tumour cell lines tested (350/280/300 nM).
  • Lethal doses in vitro were markedly lower than plasma concentrations of FP achieved in clinical studies.
  • In vitro sensitivity to FP did not correlate with that to cisplatin.
  • Synergism between either cisplatin or paclitaxel and FP was not observed.
  • CONCLUSION: These prelinical investigations suggest a significant antitumour activity of FP in GCT.
  • In contrast to other models, FP did not induce cell cycle arrest in the GCT-derived cell lines tested, possibly due to the known lack of RB-expression in GCTs.
  • A clinical trial evaluating the activity of FP in patients with cisplatin-refractory GCTs appears to be warranted.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Apoptosis / drug effects. Carcinoma, Embryonal / pathology. Cell Cycle / drug effects. Flavonoids / pharmacology. Piperidines / pharmacology
  • [MeSH-minor] Breast Neoplasms / pathology. Cell Line, Tumor. Cisplatin / pharmacology. Dose-Response Relationship, Drug. Drug Synergism. Female. Humans. Inhibitory Concentration 50. Ovarian Neoplasms / pathology. Paclitaxel / pharmacology. Uterine Cervical Neoplasms / pathology

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  • (PMID = 15868376.001).
  • [ISSN] 0167-6997
  • [Journal-full-title] Investigational new drugs
  • [ISO-abbreviation] Invest New Drugs
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Flavonoids; 0 / Piperidines; 45AD6X575G / alvocidib; P88XT4IS4D / Paclitaxel; Q20Q21Q62J / Cisplatin
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15. Vianna-Jorge R, Suarez-Kurtz G: Potassium channels in T lymphocytes: therapeutic targets for autoimmune disorders? BioDrugs; 2004;18(5):329-41
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  • [Title] Potassium channels in T lymphocytes: therapeutic targets for autoimmune disorders?
  • Human peripheral blood T lymphocytes possess two types of K(+) channels: the voltage-gated Kv1.3 and the calcium-activated IKCa1 channels.
  • These observations prompted several groups of investigators in academia and pharmaceutical companies to characterize the expression of Kv1.3 and IKCa1 in different subsets of human T lymphocytes and to evaluate their potential as novel targets for immunosuppression.
  • Recent in vivo studies showed that chronically activated T lymphocytes involved in the pathogenesis of multiple sclerosis present unusually high expression of Kv1.3 channels and that the treatment with selective Kv1.3 inhibitors can either prevent or ameliorate the symptoms of the disease.
  • In addition, the expression of Kv1.3 and IKCa1 channels in human cells is very restricted, which makes them attractive targets for a more cell-specific and less harmful action than what is typically obtained with classical immunosuppressants.
  • Studies using high-throughput toxin displacement, (86)Rb-efflux screening or membrane potential assays led to the identification of non-peptidyl small molecules with high affinity for Kv1.3 or IKCa1 channels.
  • Analysis of structure-function relationships in Kv1.3 and IKCa1 channels helped define the binding sites for channel blockers, allowing the design of a new generation of small molecules with selectivity for either Kv1.3 or IKCa1, which could help the development of new drugs for safer treatment of auto-immune diseases.
  • [MeSH-major] Autoimmune Diseases / drug therapy. Potassium Channels / blood. T-Lymphocytes / chemistry
  • [MeSH-minor] Animals. Calcium Signaling / drug effects. Calcium Signaling / physiology. Drug Delivery Systems / methods. Humans. Models, Biological. Molecular Structure. Potassium Channel Blockers / chemistry. Potassium Channel Blockers / classification. Potassium Channel Blockers / therapeutic use

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  • (PMID = 15377175.001).
  • [ISSN] 1173-8804
  • [Journal-full-title] BioDrugs : clinical immunotherapeutics, biopharmaceuticals and gene therapy
  • [ISO-abbreviation] BioDrugs
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] New Zealand
  • [Chemical-registry-number] 0 / Potassium Channel Blockers; 0 / Potassium Channels
  • [Number-of-references] 118
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16. Shields JA, Husson M, Shields CL, Krema H, Eagle RC Jr, Singh AD: Orbital malignant fibrous histiocytoma following irradiation for retinoblastoma. Ophthal Plast Reconstr Surg; 2001 Jan;17(1):58-61
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  • [Title] Orbital malignant fibrous histiocytoma following irradiation for retinoblastoma.
  • PURPOSE: An unusual case is reported of orbital malignant fibrous histiocytoma that developed after irradiation for retinoblastoma.
  • METHODS: Case report.
  • RESULTS: A 5-month-old girl underwent enucleation of the left eye, external beam irradiation of the right eye, and systemic chemotherapy for bilateral sporadic retinoblastoma.
  • At age 17 years, a malignant fibrous histiocytoma developed in the medial aspect of the orbit and nasal cavity.
  • The patient was alive 12 months postoperatively without local or metastatic disease.
  • CONCLUSIONS: Although orbital fibrous histiocytoma occurs usually as a primary tumor of adulthood, it can also develop as a secondary tumor after irradiation for retinoblastoma.
  • [MeSH-major] Histiocytoma, Benign Fibrous / etiology. Neoplasms, Radiation-Induced / etiology. Orbital Neoplasms / etiology. Retinal Neoplasms / radiotherapy. Retinoblastoma / radiotherapy

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  • (PMID = 11206748.001).
  • [ISSN] 0740-9303
  • [Journal-full-title] Ophthalmic plastic and reconstructive surgery
  • [ISO-abbreviation] Ophthal Plast Reconstr Surg
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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17. Marr B, Gobin PY, Dunkel IJ, Brodie SE, Abramson DH: Spontaneously Resolving Periocular Erythema and Ciliary Madarosis Following Intra-arterial Chemotherapy for Retinoblastoma. Middle East Afr J Ophthalmol; 2010 Jul;17(3):207-9
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  • [Title] Spontaneously Resolving Periocular Erythema and Ciliary Madarosis Following Intra-arterial Chemotherapy for Retinoblastoma.
  • PURPOSE AND DESIGN: To describe an unusual clinical finding seen in children undergoing intra-arterial chemotherapy for retinoblastoma.
  • MATERIALS AND METHODS: A retrospective review of 69 eyes of 63 patients receiving intra-arterial chemotherapy over a 3-year period.
  • Charts and photographs of 69 consecutive cases were reviewed, and data were collected on patients with clinical evidence of a hyperemic cutaneous periocular abnormality following the procedure.
  • RESULTS: A blanching erythematous and edematous patch was noted in the periocular region in 16% (11 of 69) of the children who received intraarterial chemotherapy.
  • The plaque extended into the region of the supertrochlear and medial marginal artery distribution on the ipsilateral side of the intra-arterial chemotherapy.
  • All patches of erythema spontaneously resolved within 3 months following completion of the intra-arterial chemotherapy.
  • CONCLUSION: Periocular erythema and swelling is a self-limited clinical finding associated with intra-arterial chemotherapy in a small number of patients.

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  • (PMID = 20844675.001).
  • [ISSN] 0975-1599
  • [Journal-full-title] Middle East African journal of ophthalmology
  • [ISO-abbreviation] Middle East Afr J Ophthalmol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] India
  • [Other-IDs] NLM/ PMC2934711
  • [Keywords] NOTNLM ; Cancer / Eye / Intra-Arterial Chemotherapy / Melphalan / Retinoblastoma / Skin / Topotican
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18. Saiju R, Thakur J, Karmacharya PC, Shah DN: Retinoblastoma in Nepal: a clinical profile of 30 cases. Nepal Med Coll J; 2006 Sep;8(3):171-5
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  • [Title] Retinoblastoma in Nepal: a clinical profile of 30 cases.
  • To determine the clinical profile of retinoblastoma and to provide baseline data for further studies on this subject.
  • Prospective evaluation of 30 consecutive patients with retinoblastoma admitted at the B. P.
  • Age, sex, laterality and time from onset of symptoms to diagnosis (lag time) were noted.
  • Ancillary tests were undertaken to rule out metastasis.
  • Male to female ratio was 1.1:1 and the median age of presentation was 3.1 years.
  • Leukocoria was the presenting sign in 13 cases (43.3%) and fungating mass in 10 cases (33.3%).
  • In 11 (36.7%), the latency period from onset of symptoms to diagnosis was 6-12 months.
  • In bilateral cases, advanced disease was treated surgically and the fellow eye was treated with cryotherapy, photocoagulation and chemotherapy.
  • Histopathological examination of 21 (70.0%) enucleated/exenterated cases revealed a poorly differentiated type of retinoblastoma.
  • This is the first study of retinoblastoma from Nepal.
  • Early diagnosis of this disease when it is localized to the eye is important to salvage the life of the child.
  • An informational program directed toward the public in general, as well as careful screening of any white pupillary reflex by the pediatrician and/or primary health worker will encourage and support early diagnosis.
  • [MeSH-major] Retinal Neoplasms / epidemiology. Retinoblastoma / epidemiology
  • [MeSH-minor] Adolescent. Child. Child, Preschool. Disease Progression. Female. Humans. Infant. Infant, Newborn. Male. Nepal / epidemiology. Prospective Studies. Risk Assessment. Risk Factors. Time Factors

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  • (PMID = 17203823.001).
  • [Journal-full-title] Nepal Medical College journal : NMCJ
  • [ISO-abbreviation] Nepal Med Coll J
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Nepal
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19. Cozza R, De Ioris MA, Ilari I, Devito R, Fidani P, De Sio L, Demelas F, Romanzo A, Donfrancesco A: Metastatic retinoblastoma: single institution experience over two decades. Br J Ophthalmol; 2009 Sep;93(9):1163-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Metastatic retinoblastoma: single institution experience over two decades.
  • BACKGROUND: Metastatic spread in retinoblastoma is a rare occurrence in developed countries but still associated with a poor prognosis.
  • PATIENTS AND METHODS: Medical records of all metastatic retinoblastoma diagnosed during a 20-year period were retrospectively reviewed.
  • RESULTS: Six patients out of 104 presented a metastatic disease with an incidence at diagnosis of 2%.
  • Three had a metastatic disease at diagnosis, one patient a trilateral retinoblastoma and two a metastatic spread after enucleation.
  • All but one were sporadic retinoblastoma.
  • Central nervous system (CNS) involvement was reported in five patients, while one patient had an intraorbital lesion, and bone and bone marrow spread.
  • Different treatment strategies were administered based on local treatment plus chemotherapy and radiotherapy with or without high-dose chemotherapy.
  • Out of six patients, four died, and two patients are alive at 60 and 63 months from diagnosis.
  • Both children with a long follow-up were treated with high-dose chemotherapy.
  • All but one of the patients with CNS involvement died; the survivor was a patient with pineal involvement.
  • CONCLUSION: This retrospective review confirms a curable strategy based on local treatment and conventional plus high-dose chemotherapy.
  • [MeSH-major] Bone Neoplasms / secondary. Brain Neoplasms / secondary. Retinal Neoplasms / pathology. Retinoblastoma / secondary
  • [MeSH-minor] Child, Preschool. Early Detection of Cancer. Eye Enucleation / mortality. Female. Humans. Infant. Male. Prognosis. Retrospective Studies. Time Factors


20. DePinto W, Chu XJ, Yin X, Smith M, Packman K, Goelzer P, Lovey A, Chen Y, Qian H, Hamid R, Xiang Q, Tovar C, Blain R, Nevins T, Higgins B, Luistro L, Kolinsky K, Felix B, Hussain S, Heimbrook D: In vitro and in vivo activity of R547: a potent and selective cyclin-dependent kinase inhibitor currently in phase I clinical trials. Mol Cancer Ther; 2006 Nov;5(11):2644-58
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  • [Title] In vitro and in vivo activity of R547: a potent and selective cyclin-dependent kinase inhibitor currently in phase I clinical trials.
  • Aberrant expression or altered activity of distinct cyclin-dependent kinase (CDK) complexes results in escape of cells from cell cycle control, leading to unrestricted cell proliferation.
  • CDK inhibitors have the potential to induce cell cycle arrest and apoptosis in cancer cells, and identifying small-molecule CDK inhibitors has been a major focus in cancer research.
  • In vitro, R547 effectively inhibited the proliferation of tumor cell lines independent of multidrug resistant status, histologic type, retinoblastoma protein, or p53 status, with IC(50)s </= 0.60 mumol/L.
  • The growth-inhibitory activity is characterized by a cell cycle block at G(1) and G(2) phases and induction of apoptosis.
  • R547 reduced phosphorylation of the cellular retinoblastoma protein at specific CDK phosphorylation sites at the same concentrations that induced cell cycle arrest, suggesting a potential pharmacodynamic marker for clinical use.
  • In vivo, R547 showed antitumor activity in all of the models tested to date, including six human tumor xenografts and an orthotopic syngeneic rat model.
  • R547 was efficacious with daily oral dosing as well as with once weekly i.v. dosing in established human tumor models and at the targeted efficacious exposures inhibited phosphorylation of the retinoblastoma protein in the tumors.
  • The selective kinase inhibition profile and the preclinical antitumor activity of R547 suggest that it may be promising for development for use in the treatment of solid tumors.
  • [MeSH-minor] Animals. Apoptosis. Cell Line, Tumor. Cell Proliferation / drug effects. Clinical Trials, Phase I as Topic. Female. G1 Phase / drug effects. G2 Phase / drug effects. Genes, MDR / drug effects. Humans. Mice. Mice, Nude. Phosphorylation / drug effects. Rats. Rats, Inbred F344. Retinoblastoma / drug therapy. Retinoblastoma / metabolism. Tumor Suppressor Protein p53 / metabolism


21. Wang CZ, Xie JT, Zhang B, Ni M, Fishbein A, Aung HH, Mehendale SR, Du W, He TC, Yuan CS: Chemopreventive effects of Panax notoginseng and its major constituents on SW480 human colorectal cancer cells. Int J Oncol; 2007 Nov;31(5):1149-56
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  • [Title] Chemopreventive effects of Panax notoginseng and its major constituents on SW480 human colorectal cancer cells.
  • In this study, we evaluated the effects of Panax notoginseng root extract (NGRE) and its major constituents on SW480 human colorectal cancer cells.
  • At 1.0 mg/ml, NGRE inhibited cell growth by 85.8% (P<0.01), probably linked to the higher concentration of ginsenosides Rb1 and Rg1.
  • The pharmacologic activities of notoginsenoside R1 and ginsenosides Rg1 and Rb1 on the cells were antiproliferative.
  • Two-day treatment with 300 microM of notoginsenoside R1, ginsenosides Rg1 and Rb1 increased cell apoptosis significantly.
  • Cell growth decreased more with the combined treatment of NGRE and 5-fluorouracil (or irinotecan) than with the chemotherapy agent applied alone, suggesting that notoginseng can reduce the dose of 5-fluorouracil (or irinotecan) needed to achieve desired effects.
  • Further in vivo and human trials are warranted to test whether notoginseng is a valuable chemo-adjuvant with clinical validity.

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  • (PMID = 17912442.001).
  • [ISSN] 1019-6439
  • [Journal-full-title] International journal of oncology
  • [ISO-abbreviation] Int. J. Oncol.
  • [Language] ENG
  • [Grant] United States / NCCIH NIH HHS / AT / R21 AT003255-02; United States / NCCIH NIH HHS / AT / R21 AT002445-02; United States / NCCIH NIH HHS / AT / R21 AT002445; United States / NCCIH NIH HHS / AT / AT 003255; United States / NCCIH NIH HHS / AT / AT002445-02; United States / NCCIH NIH HHS / AT / AT 002445; United States / NCCIH NIH HHS / AT / R21 AT003255; United States / NCCIH NIH HHS / AT / AT003255-02
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Anticarcinogenic Agents; 0 / Cyclin A; 0 / Drugs, Chinese Herbal; 0 / Ginsenosides; 0 / Panax notoginseng extract; 0 / ginsenoside Rb1; 22427-39-0 / ginsenoside Rg1; 80418-24-2 / notoginsenoside R1; 9007-49-2 / DNA
  • [Other-IDs] NLM/ NIHMS94796; NLM/ PMC2676859
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22. Schmidt B, Chun KR, Kuck KH, Ouyang F: [Ventricular tachycardias originating in the his-purkinje system. Bundle branch reentrant ventricular tachycardias and fascicular ventricular tachycardias]. Herz; 2009 Nov;34(7):554-60
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  • [Title] [Ventricular tachycardias originating in the his-purkinje system. Bundle branch reentrant ventricular tachycardias and fascicular ventricular tachycardias].
  • [Transliterated title] Ventrikuläre Tachykardien mit Ursprung im spezifischen Reizleitungssystem : Schenkeltachykardien und faszikuläre ventrikuläre Tachykardien.
  • Ventricular tachycardias (VT) associated with the His-Purkinje system may occur in patients with and without organic heart disease.
  • The former may encounter bundle branch reentrant VT, a macroreentrant VT utilizing the specific conduction system.
  • It frequently occurs in patients with preexisting conduction disturbance such as complete left bundle branch block and may be eliminated by catheter ablation of the right bundle branch.
  • After successful ablation, patient's prognosis depends on the presence or absence of structural heart disease.In patients without structural heart disease, VT with right bundle branch block pattern and superior axis, referred to as idiopathic left ventricular tachycardia, is observed.
  • It is a reentrant VT utilizing the posterior left fascicle and the Purkinje network.
  • The two treatment options include antiarrhythmic drug therapy with verapamil or curative catheter ablation.Another form of ventricular arrhythmia originating in the Purkinje network is idiopathic ventricular fibrillation (IVF).
  • Focal triggers from the right and left ventricular Purkinje network induce premature ventricular contractions inducing IVF.
  • [MeSH-major] Bundle of His / physiopathology. Bundle-Branch Block / physiopathology. Bundle-Branch Block / therapy. Catheter Ablation. Defibrillators, Implantable. Purkinje Fibers / physiopathology. Tachycardia, Atrioventricular Nodal Reentry / complications. Tachycardia, Atrioventricular Nodal Reentry / physiopathology

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  • (PMID = 20091255.001).
  • [ISSN] 1615-6692
  • [Journal-full-title] Herz
  • [ISO-abbreviation] Herz
  • [Language] ger
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Germany
  • [Number-of-references] 33
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23. Nguyen MD, Boudreau M, Kriz J, Couillard-Després S, Kaplan DR, Julien JP: Cell cycle regulators in the neuronal death pathway of amyotrophic lateral sclerosis caused by mutant superoxide dismutase 1. J Neurosci; 2003 Mar 15;23(6):2131-40
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  • There is growing evidence for involvement of members of the cyclin-dependent kinase (Cdk) family in neurodegenerative disorders and in apoptotic death of neurons subjected to various insults.
  • After our recent report that a deregulation of Cdk5 activity by p25 may contribute to pathogenesis of amyotrophic lateral sclerosis (ALS), we further examined the possible involvement of other Cdks in mice expressing a mutant form of superoxide dismutase (SOD1(G37R)) linked to ALS.
  • No substantial changes in Cdk2 or Cdk6 distribution and kinase activities were detected in spinal motor neurons from SOD1(G37R) mice when compared with normal mice.
  • The increase of Cdk4 activity in SOD1(G37R) mice was associated with an increase in nuclear Cdk4, cyclin D1, its coactivator, and with the abnormal phosphorylation of the retinoblastoma (Rb) protein at Cdk phosphorylation sites.
  • Pharmacological treatment of SOD1(G37R) mice with minocycline, a compound that attenuates microgliosis and slows down disease, lessened the dysregulation of Cdk5/Cdk4 and the phosphorylation of Rb.
  • Interestingly, phospho-Rb was immunoprecipitated with anti-Cdk4 but not with anti-Cdk5 antibodies, suggesting a key role for Cdk4 in the phosphorylation of Rb.
  • Remarkably, the overexpression of a transgene coding for human neurofilament H, a phosphorylation sink for deregulated Cdk5 activity by p25, resulted in a reduction in levels of nuclear Cdk4 and Rb phosphorylation.
  • [MeSH-major] Amyotrophic Lateral Sclerosis / genetics. Amyotrophic Lateral Sclerosis / metabolism. Cell Cycle Proteins / metabolism. Motor Neurons / metabolism. Proto-Oncogene Proteins. Superoxide Dismutase / biosynthesis
  • [MeSH-minor] Amino Acid Substitution. Animals. Anti-Bacterial Agents / pharmacology. Cell Death. Cell Nucleus / metabolism. Cyclin D1 / metabolism. Cyclin-Dependent Kinase 4. Cyclin-Dependent Kinase 5. Cyclin-Dependent Kinases / metabolism. Disease Progression. G1 Phase / physiology. Humans. Mice. Mice, Neurologic Mutants. Mice, Transgenic. Minocycline / pharmacology. Neurofilament Proteins / biosynthesis. Neurofilament Proteins / genetics. Phosphorylation / drug effects. Retinoblastoma Protein / metabolism. S Phase / physiology. Signal Transduction. Transgenes. Up-Regulation


24. Raki M, Särkioja M, Desmond RA, Chen DT, Bützow R, Hemminki A, Kanerva A: Oncolytic adenovirus Ad5/3-delta24 and chemotherapy for treatment of orthotopic ovarian cancer. Gynecol Oncol; 2008 Jan;108(1):166-72
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  • [Title] Oncolytic adenovirus Ad5/3-delta24 and chemotherapy for treatment of orthotopic ovarian cancer.
  • OBJECTIVE: Oncolytic adenoviruses capable of replication selectively in tumor cells are an appealing approach for the treatment of neoplastic diseases refractory to conventional therapies.
  • The aim of this study was to evaluate the effect of dose and scheduling of a tropism-modified, adenovirus serotype 3 receptor-targeted, Rb/p16 pathway-selective replication-competent adenovirus, Ad5/3-delta24, against human ovarian adenocarcinoma.
  • As oncolytic viruses and chemotherapy can have synergistic interactions, the antitumor efficacy of Ad5/3-delta24 was also studied in combination with epirubicin and gemcitabine, common second-line treatment options for platinum-resistant ovarian cancer.
  • METHODS: Orthotopic murine models of peritoneally disseminated ovarian cancer were utilized to compare survival of mice treated with either a single viral dose or weekly delivery.
  • RESULTS: Treatment outcome after administration of a single dose of Ad5/3-delta24 was as effective as delivery of several weekly doses.
  • Further, combining Ad5/3-delta24 with either gemcitabine or epirubicin resulted in greater therapeutic benefit than either agent alone.
  • CONCLUSION: These preclinical data suggest that Ad5/3-delta24 represents a promising treatment strategy for advanced ovarian cancer as a single agent or in combination with chemotherapy.
  • [MeSH-major] Adenocarcinoma / therapy. Adenoviridae / physiology. Antineoplastic Combined Chemotherapy Protocols / pharmacology. Deoxycytidine / analogs & derivatives. Epirubicin / pharmacology. Oncolytic Virotherapy / methods. Ovarian Neoplasms / therapy
  • [MeSH-minor] Animals. Antibiotics, Antineoplastic / administration & dosage. Antibiotics, Antineoplastic / pharmacology. Antimetabolites, Antineoplastic / administration & dosage. Antimetabolites, Antineoplastic / pharmacology. Cell Line, Tumor. Combined Modality Therapy. Drug Administration Schedule. Female. Humans. Mice. Mice, SCID. Virus Replication. Xenograft Model Antitumor Assays

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  • (PMID = 17950450.001).
  • [ISSN] 1095-6859
  • [Journal-full-title] Gynecologic oncology
  • [ISO-abbreviation] Gynecol. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / Antimetabolites, Antineoplastic; 0W860991D6 / Deoxycytidine; 3Z8479ZZ5X / Epirubicin; B76N6SBZ8R / gemcitabine
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25. Lee DE, Lee KW, Song NR, Seo SK, Heo YS, Kang NJ, Bode AM, Lee HJ, Dong Z: 7,3',4'-Trihydroxyisoflavone inhibits epidermal growth factor-induced proliferation and transformation of JB6 P+ mouse epidermal cells by suppressing cyclin-dependent kinases and phosphatidylinositol 3-kinase. J Biol Chem; 2010 Jul 9;285(28):21458-66
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  • Numerous in vitro and in vivo studies have shown that isoflavones exhibit anti-proliferative activity against epidermal growth factor (EGF) receptor-positive malignancies of the breast, colon, skin, and prostate.
  • 7,3',4'-Trihydroxyisoflavone (7,3',4'-THIF) is one of the metabolites of daidzein, a well known soy isoflavone, but its chemopreventive activity and the underlying molecular mechanisms are poorly understood.
  • As shown by Western blot, 7,3',4'-THIF suppressed the phosphorylation of retinoblastoma protein at Ser-795 and Ser-807/Ser-811, which are the specific sites of phosphorylation by cyclin-dependent kinase (CDK) 4.
  • In addition to regulating the expression of cell cycle-regulatory proteins, 7,3',4'-THIF bound to CDK4 and CDK2 and strongly inhibited their kinase activities.
  • It also bound to phosphatidylinositol 3-kinase (PI3K), strongly inhibiting its kinase activity and thereby suppressing the Akt/GSK-3beta/AP-1 pathway and subsequently attenuating the expression of cyclin D1.
  • Collectively, these results suggest that CDKs and PI3K are the primary molecular targets of 7,3',4'-THIF in the suppression of EGF-induced cell proliferation.
  • These insights into the biological actions of 7,3',4'-THIF provide a molecular basis for the possible development of new chemoprotective agents.

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  • (PMID = 20444693.001).
  • [ISSN] 1083-351X
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA120388; United States / NCI NIH HHS / CA / CA027502; United States / NCI NIH HHS / CA / CA111536; United States / NCI NIH HHS / CA / R01 CA077646; United States / NCI NIH HHS / CA / CA081064; United States / NCI NIH HHS / CA / R37 CA081064; United States / NCI NIH HHS / CA / R01 CA111536; United States / NCI NIH HHS / CA / CA077646; United States / NCI NIH HHS / CA / R01 CA120388; United States / NCI NIH HHS / CA / P01 CA027502; United States / NCI NIH HHS / CA / R01 CA081064
  • [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 / Anticarcinogenic Agents; 0 / Isoflavones; 0 / Retinoblastoma Protein; 452VLY9402 / Serine; 485-63-2 / 3',4',7-trihydroxyisoflavone; 62229-50-9 / Epidermal Growth Factor; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.11.22 / Cyclin-Dependent Kinases
  • [Other-IDs] NLM/ PMC2898435
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26. Dai S, Dimaras H, Héon E, Budning A, Doyle J, Halliday W, Drake J, Gallie BL, Chan HS: Trilateral retinoblastoma with pituitary-hypothalamic dysfunction. Ophthalmic Genet; 2008 Sep;29(3):120-5
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  • [Title] Trilateral retinoblastoma with pituitary-hypothalamic dysfunction.
  • Trilateral retinoblastoma is characterized by retinal tumors in one or both eyes, as well as tumors of the pineal gland or parasellar region of the brain.
  • Here we describe a 4-month-old girl, presenting with pituitary dysfunction, hypothalamic overgrowth syndrome and central blindness, in addition to suprasellar and bilateral retinal tumors.
  • Biopsy of the suprasellar tumor confirmed the diagnosis of trilateral retinoblastoma.
  • After biopsy, cerebrospinal fluid (CSF) metastasis was discovered.
  • Overgrowth persisted, but blindness and pituitary dysfunction resolved when the suprasellar tumor and CSF metastasis responded to cyclosporine-modulated systemic chemotherapy with intraventricular chemotherapy, consolidated with marrow-ablative chemotherapy and stem cell rescue of the bone marrow.
  • Twenty months after diagnosis and 12 months after transplant, an unusual pattern of tumor recurrence was observed along the catheter of the Ommaya reservoir used for delivering intraventricular chemotherapy, which was also at the site of the previous suprasellar needle biopsy.
  • Salvage therapy consisted of resection, stereotactic radiation, and further systemic and intraventricular chemotherapy.
  • At 25 months after diagnosis, the patient was developing well and seeing better.
  • However, she died 32 months after diagnosis despite the salvage therapy.
  • This case highlights the possibility of tumor dissemination after needle biopsy of a suprasellar tumor.
  • Biopsy may be avoided if a characteristic clinicoradiological picture of trilateral retinoblastoma is recognized.
  • We recommend that if a pineal or suprasellar tumor is observed in a child, the eyes should be examined for retinoblastoma, thereby avoiding biopsies of the intracranial tumor, which may track difficult-to-treat tumor cells through the brain, and disseminate tumor cells into the CSF.
  • [MeSH-major] Hypothalamic Diseases / pathology. Neoplasm Recurrence, Local / pathology. Pituitary Neoplasms / pathology. Retinal Neoplasms / pathology. Retinoblastoma / pathology
  • [MeSH-minor] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Carboplatin / therapeutic use. Cytarabine / administration & dosage. Etoposide / therapeutic use. Fatal Outcome. Female. Gestational Age. Humans. Infant. Infusions, Parenteral. Magnetic Resonance Imaging. Retinoblastoma Protein / genetics. Tomography, X-Ray Computed. Topotecan / administration & dosage. Vincristine / therapeutic use

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  • [ErratumIn] Ophthalmic Genet. 2008 Dec;29(4):191-2
  • (PMID = 18766991.001).
  • [ISSN] 1744-5094
  • [Journal-full-title] Ophthalmic genetics
  • [ISO-abbreviation] Ophthalmic Genet.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Retinoblastoma Protein; 04079A1RDZ / Cytarabine; 5J49Q6B70F / Vincristine; 6PLQ3CP4P3 / Etoposide; 7M7YKX2N15 / Topotecan; BG3F62OND5 / Carboplatin; CEV regimen
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27. Koh J, Kubota T, Koyama T, Migita T, Hashimoto M, Hosoda Y, Kitajima M: Combined antitumor activity of 7-hydroxystaurosporine (UCN-01) and tamoxifen against human breast carcinoma in vitro and in vivo. Breast Cancer; 2003;10(3):260-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Combined antitumor activity of 7-hydroxystaurosporine (UCN-01) and tamoxifen against human breast carcinoma in vitro and in vivo.
  • BACKGROUND: 7-Hydroxystaurosporine (UCN-01) was originally isolated as a protein kinase C inhibitor and has shown antitumor activity against several human cancer cell lines.
  • UCN-01 inhibits cell cycle progression from the G1 to the S phase and is associated with inhibition of cyclin-dependent kinase (CDK) activity and induction of intrinsic CDK inhibitor p21, leading to dephosphorylation of retinoblastoma (Rb) protein.
  • Tamoxifen (TAM) traps cancer cells in the G1 phase, suggesting that the mechanism of action of TAM is similar to that of UCN-01.
  • The present study was conducted to assess the antitumor activity of UCN-01 combined with TAM against human breast carcinoma cells in vitro and in vivo.
  • Two human breast carcinoma xenografts in nude mice, MCF-7 and Br-10, were treated with UCN-01, TAM or both agents together.
  • The expression of p21 and the phosphorylation status of Rb protein in MCF-7 cells were detected by Western blotting.
  • Combined treatment with UCN-01 followed by TAM inhibited the growth of MCF-7 cells synergistically and no significant differences in cytotoxicity were observed between the different sequences of UCN-01/TAM and TAM/UCN-01.
  • Combination treatment with UCN-01 and TAM against MCF-7 and Br-10 in vivo exhibited superior antitumor effects compared with either agent treatment alone.
  • Although 0.1 microg UCN-01 per ml (I.R.: 48.1%) or 2 microM TAM (I.R.: 31%) induced p21 expression, phosphorylation of Rb protein was not inhibited.
  • However, combination treatment with UCN-01 and TAM at the same concentrations resulted in an I.R. of 67% and dephosphorylation of Rb protein.
  • This combination may have potential clinical applications for breast cancer treatment, by reducing the toxicity of UCN-01.
  • [MeSH-minor] Animals. Blotting, Western. Breast Neoplasms / drug therapy. Cell Line, Tumor / drug effects. Dose-Response Relationship, Drug. Drug Synergism. Drug Therapy, Combination. Female. Humans. Mice. Mice, Inbred BALB C

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  • (PMID = 12955040.001).
  • [ISSN] 1340-6868
  • [Journal-full-title] Breast cancer (Tokyo, Japan)
  • [ISO-abbreviation] Breast Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 094ZI81Y45 / Tamoxifen; 7BU5H4V94A / 7-hydroxystaurosporine; H88EPA0A3N / Staurosporine
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28. Altiok N, Mezzadra H, Patel P, Koyuturk M, Altiok S: A plant oxylipin, 12-oxo-phytodienoic acid, inhibits proliferation of human breast cancer cells by targeting cyclin D1. Breast Cancer Res Treat; 2008 May;109(2):315-23
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  • [Title] A plant oxylipin, 12-oxo-phytodienoic acid, inhibits proliferation of human breast cancer cells by targeting cyclin D1.
  • Cyclin D1 overexpression has been associated with poor prognosis and resistance to therapy in human breast cancer.
  • Thus, the development of therapeutic agents that selectively target cyclin D1 activity is of clinical interest.
  • This study demonstrates that 12-oxo-phytodienoic acid (OPDA), a phytohormone with critical functions in growth and development in plants, induces growth arrest in MDA-MB-231 and T47D breast cancer cells.
  • In response to OPDA treatment, the human breast cancer cell lines exhibit a progressive decline in cyclin D1 expression, which is tightly associated with the accumulation of hypophosphorylated form of the retinoblastoma protein (Rb) and G1 arrest.
  • The decrease in cyclin D1 protein expression accompanies a dramatic decline in nuclear but not membranous beta-catenin expression and activation of glycogen synthase kinase-3-beta (GSK3beta) caused by inhibition of its serine-9 phosphorylation.
  • In addition, the overexpression of T286A, a cyclin D1 mutant which is refractory to phosphorylation by GSK3beta and proteosomal degradation, is resistant to OPDA-mediated Rb dephosphorylation as well as G(1) cell cycle arrest.
  • Thus, our results demonstrate that degradation of cyclin D1 protein is a key event in OPDA induced growth inhibition in breast cancer cells.
  • These data provide the basic foundation for future efforts to develop OPDA-based approaches in the prevention and treatment of breast cancer and other types of cancer.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Breast Neoplasms / drug therapy. Cell Proliferation / drug effects. Cyclin D1 / drug effects. Fatty Acids, Unsaturated / pharmacology
  • [MeSH-minor] Blotting, Western. Cell Line, Tumor. Female. Flow Cytometry. Humans. Immunohistochemistry. Retinoblastoma Protein / drug effects. Retinoblastoma Protein / metabolism. beta Catenin / drug effects. beta Catenin / metabolism


29. Guneysel O, Onur OE, Denizbasi A: Effects of recombinant human granulocyte colony-stimulating factor (filgrastim) on ECG parameters in neutropenic patients: a single-centre, prospective study. Clin Drug Investig; 2009;29(8):551-5
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  • [Title] Effects of recombinant human granulocyte colony-stimulating factor (filgrastim) on ECG parameters in neutropenic patients: a single-centre, prospective study.
  • BACKGROUND AND OBJECTIVE: Human granulocyte colony-stimulating factor (G-CSF) is a haematopoietic hormone that promotes the growth, proliferation, differentiation and maturation of neutrophil precursors.
  • Filgrastim is a recombinant human G-CSF.
  • Myocardial infarction, atrial fibrillation and arrhythmia have been reported in several patients with malignancy receiving filgrastim, but a causal relationship with the drug has not been established.
  • The purpose of this study was to investigate the changes in ECG parameters in neutropenic patients during treatment with filgrastim.
  • After a reference ECG had been obtained, filgrastim was administered to all patients at a dose of 5 microg/kg/day subcutaneously for 2 days.
  • There were no statistically significant differences between baseline and follow-up ECG measurements of rhythm, P-wave duration, PR interval, QRS-wave duration, corrected QT (QTc) interval, ECG axis, premature supraventricular events, ventricular arrhythmia, R-wave progression, right bundle branch block or left bundle branch block.
  • CONCLUSION: This study did not demonstrate any ECG changes other than a significant reduction in mean heart rate in this selected population of neutropenic patients given 2 days' treatment with subcutaneous 5 microg/kg/day of filgrastim.
  • [MeSH-major] Electrocardiography / drug effects. Granulocyte Colony-Stimulating Factor / adverse effects. Neutropenia / drug therapy
  • [MeSH-minor] Female. Filgrastim. Heart Rate / drug effects. Humans. Male. Middle Aged. Neoplasms / complications. Neoplasms / drug therapy. Recombinant Proteins

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  • (PMID = 19591516.001).
  • [ISSN] 1173-2563
  • [Journal-full-title] Clinical drug investigation
  • [ISO-abbreviation] Clin Drug Investig
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article
  • [Publication-country] New Zealand
  • [Chemical-registry-number] 0 / Recombinant Proteins; 143011-72-7 / Granulocyte Colony-Stimulating Factor; PVI5M0M1GW / Filgrastim
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30. Flørenes VA, Skrede M, Jørgensen K, Nesland JM: Deacetylase inhibition in malignant melanomas: impact on cell cycle regulation and survival. Melanoma Res; 2004 Jun;14(3):173-81
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Deacetylase inhibition in malignant melanomas: impact on cell cycle regulation and survival.
  • In the present study the deacetylase inhibitor trichostatin A (TSA) was used to elucidate the effect of protein acetylation on cell cycle progression and survival in seven human malignant melanoma cell lines.
  • It was shown that TSA treatment led to a transient G(2)/M phase delay and accumulation of unphosphorylated retinoblastoma protein (pRB) in all cases.
  • TSA significantly induced protein expression of the cyclin-dependent kinase inhibitor p21(WAF1/CIP1) in a dose-dependent manner in all cell lines including those not expressing p21(WAF1/CIP1) constitutively, whereas the levels of both wild-type and mutated p53 protein were reduced.
  • The effect on p53 was not a direct result of inhibition of extracellular signal-regulated kinase-1/2 (ERK1/2) activation by TSA, as treatment of the cells with the mitogen-activated protein kinase/extracellular signal-regulated kinase kinase-1 (MEK1) inhibitor PD98059 did not result in decreased p53 protein level.
  • Furthermore, TSA treatment led to reduction in cyclin D1 whereas cyclin D3 accumulated, the latter due to increased protein stability.
  • In all the examined cell lines, TSA treatment resulted in a profound induction of apoptosis and cleavage of poly-(ADP-ribose)-polymerase (PARP) indicative of caspase activity.
  • Altogether, these results suggest that p21(WAF1/CIP1) in melanomas is silenced by deacetylation, and furthermore that inhibition of deacetylation may have potential in anticancer therapy of melanoma patients.
  • [MeSH-major] Cell Cycle / drug effects. Enzyme Inhibitors / pharmacology. Histone Deacetylase Inhibitors. Melanoma / enzymology. Melanoma / pathology
  • [MeSH-minor] Apoptosis / drug effects. Cell Cycle Proteins / metabolism. Cell Line, Tumor. Cell Survival / drug effects. Cyclin-Dependent Kinase Inhibitor p21. Down-Regulation / drug effects. Histone Deacetylases / metabolism. Humans. Hydroxamic Acids / pharmacology. Mitogen-Activated Protein Kinase 1 / metabolism. Mitogen-Activated Protein Kinase 3 / metabolism. Tumor Suppressor Protein p53 / metabolism. Up-Regulation / drug effects


31. Hori M, Suzuki K, Udono MU, Yamauchi M, Mine M, Watanabe M, Kondo S, Hozumi Y: Establishment of ponasterone A-inducible the wild-type p53 protein-expressing clones from HSC-1 cells, cell growth suppression by p53 expression and the suppression mechanism. Arch Dermatol Res; 2009 Oct;301(9):631-46
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  • [Title] Establishment of ponasterone A-inducible the wild-type p53 protein-expressing clones from HSC-1 cells, cell growth suppression by p53 expression and the suppression mechanism.
  • Gene therapy for a variety of human cancers containing the mutant p53 (mt-p53) gene has been performed by direct injection of a retroviral or adenoviral vector containing the wild-type p53 (wt-p53) gene.
  • Because many individuals with skin squamous cell carcinoma (SCC) have been shown to carry the p53 gene mutation, these patients are candidates for p53 gene therapy.
  • For this reason, we established ponasterone A-inducible the wild-type p53 (wt-p53) protein-expressing clones by transfecting a ponasterone-inducible vector containing the wt-p53 gene into HSC-1 cells, which harbor the mutated p53 (m/w) at codon 173 (GTG --> TTG in one allele).
  • Based on the results of the expression patterns of the p21, p16, RB, BAX and Bcl-2 proteins, as well as on the results of senescence-associated beta-galactosidase staining, the suppression was caused by senescence-like growth arrest of the cells.
  • Although it is generally accepted that the suppression of tumor cell growth is caused by p53-induced apoptosis, permanent G1 arrest induced by p53 is also an important part of the growth-suppression mechanism in p53 gene therapy.
  • The present results should expand the possibilities for p53 gene therapy for human skin SCCs containing the mutant p53 gene.
  • [MeSH-major] Carcinoma / therapy. Ecdysterone / analogs & derivatives. Genetic Therapy / methods. Skin Neoplasms / therapy. Tumor Suppressor Protein p53 / genetics
  • [MeSH-minor] Cell Aging. Cell Division / genetics. Cell Line, Tumor. Feasibility Studies. Gene Expression / drug effects. Genetic Vectors. Humans. Plasmids. Transfection


32. Stewart DJ: Tumor and host factors that may limit efficacy of chemotherapy in non-small cell and small cell lung cancer. Crit Rev Oncol Hematol; 2010 Sep;75(3):173-234
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  • [Title] Tumor and host factors that may limit efficacy of chemotherapy in non-small cell and small cell lung cancer.
  • While chemotherapy provides useful palliation, advanced lung cancer remains incurable since those tumors that are initially sensitive to therapy rapidly develop acquired resistance.
  • Resistance may arise from impaired drug delivery, extracellular factors, decreased drug uptake into tumor cells, increased drug efflux, drug inactivation by detoxifying factors, decreased drug activation or binding to target, altered target, increased damage repair, tolerance of damage, decreased proapoptotic factors, increased antiapoptotic factors, or altered cell cycling or transcription factors.
  • Factors for which there is now substantial clinical evidence of a link to small cell lung cancer (SCLC) resistance to chemotherapy include MRP (for platinum-based combination chemotherapy) and MDR1/P-gp (for non-platinum agents).
  • SPECT MIBI and Tc-TF scanning appears to predict chemotherapy benefit in SCLC.
  • In non-small cell lung cancer (NSCLC), the strongest clinical evidence is for taxane resistance with elevated expression or mutation of class III beta-tubulin (and possibly alpha tubulin), platinum resistance and expression of ERCC1 or BCRP, gemcitabine resistance and RRM1 expression, and resistance to several agents and COX-2 expression (although COX-2 inhibitors have had minimal impact on drug efficacy clinically).
  • Tumors expressing high BRCA1 may have increased resistance to platinums but increased sensitivity to taxanes.
  • Limited early clinical data suggest that chemotherapy resistance in NSCLC may also be increased with decreased expression of cyclin B1 or of Eg5, or with increased expression of ICAM, matrilysin, osteopontin, DDH, survivin, PCDGF, caveolin-1, p21WAF1/CIP1, or 14-3-3sigma, and that IGF-1R inhibitors may increase efficacy of chemotherapy, particularly in squamous cell carcinomas.
  • Equivocal data (with some positive studies but other negative studies) suggest that NSCLC tumors with some EGFR mutations may have increased sensitivity to chemotherapy, while K-ras mutations and expression of GST-pi, RB or p27kip1 may possibly confer resistance.
  • While limited clinical data suggest that p53 mutations are associated with resistance to platinum-based therapies in NSCLC, data on p53 IHC positivity are equivocal.
  • To date, resistance-modulating strategies have generally not proven clinically useful in lung cancer, although small randomized trials suggest a modest benefit of verapamil and related agents in NSCLC.

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  • [Copyright] Published by Elsevier Ireland Ltd.
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  • (PMID = 20047843.001).
  • [ISSN] 1879-0461
  • [Journal-full-title] Critical reviews in oncology/hematology
  • [ISO-abbreviation] Crit. Rev. Oncol. Hematol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA016672-32; United States / NCI NIH HHS / CA / P30 CA016672; United States / NCI NIH HHS / CA / 5-P30 CA16672-32; United States / NCI NIH HHS / CA / P30 CA016672-32
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  • [Other-IDs] NLM/ NIHMS168520; NLM/ PMC2888634
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33. Reddi HV, Madde P, Reichert-Eberhardt AJ, Galanis EC, Copland JA, McIver B, Grebe SK, Eberhardt NL: ONYX-411, a conditionally replicative oncolytic adenovirus, induces cell death in anaplastic thyroid carcinoma cell lines and suppresses the growth of xenograft tumors in nude mice. Cancer Gene Ther; 2008 Nov;15(11):750-7
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  • Anaplastic thyroid carcinoma (ATC) is the most aggressive thyroid cancer variant, accounting for 1-2% of all cases, but 33% of deaths, and exhibiting an average life expectancy of 5 months.
  • ATC is largely unresponsive to radioactive iodine, chemotherapy, external beam radiation or surgery, underscoring the need for new and effective therapies.
  • We evaluated the therapeutic potential of an oncolytic adenovirus, ONYX-411, that replicates selectively in and kills cells with dysfunction of the retinoblastoma (RB) pathway.
  • In the present study, we report that ONYX-411 is able to induce cell death in eight human anaplastic carcinoma cell lines in vitro.
  • The cytopathic effect of the virus is specific to cells with RB dysfunction, which appears to be frequent in ATC.
  • We confirmed the expression of the coxsackie adenovirus receptor, CAR, in all ATC cell lines, demonstrating the potentially universal application of this oncolytic viral therapy to ATC.
  • In addition, the growth of xenograft tumors induced in athymic mice with the ARO and DRO cell lines was significantly reduced by ONYX-411 treatment.
  • These results indicate that ONYX-411 can be a potential therapeutic agent for the treatment of ATC, rendering this class of conditionally replicating adenoviruses an attractive candidate for clinical trials.

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  • (PMID = 18583996.001).
  • [ISSN] 1476-5500
  • [Journal-full-title] Cancer gene therapy
  • [ISO-abbreviation] Cancer Gene Ther.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA080117; United States / NCI NIH HHS / CA / CA80117
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Other-IDs] NLM/ NIHMS321376; NLM/ PMC3180921
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34. Montalban C, Abraira V, Morente M, Acevedo A, Aguilera B, Bellas C, Fraga M, Del Moral RG, Menarguez J, Oliva H, Sanchez-Beato M, Piris MA: Epstein-Barr virus-latent membrane protein 1 expression has a favorable influence in the outcome of patients with Hodgkin's Disease treated with chemotherapy. Leuk Lymphoma; 2000 Nov;39(5-6):563-72
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  • [Title] Epstein-Barr virus-latent membrane protein 1 expression has a favorable influence in the outcome of patients with Hodgkin's Disease treated with chemotherapy.
  • The effect of molecular factors in the outcome of Hodgkin's Disease (HD) is being currently studied.
  • In a previous series of HD, including patients treated only with radiotherapy and patients treated with chemotherapy (with or without radiotherapy), we found that a high proliferation index had an adverse influence in overall survival (OS) and in the achievement of a complete remission (CR).
  • Loss of Rb expression also had an adverse prognostic influence in achievement of CR.
  • The expression of other molecular factors, p53, bcl2 and CD15 did not show prognostic influence.
  • In the present paper we have studied the effect of these molecular variables in 110 patients, of the previous series who had been treated with chemotherapy.
  • A retrospective study was performed in these 110 patients with HD treated with chemotherapy (ABVD or variants, 62%, or regimes not containing adriamycin, 38%) with or without adjutant radiotherapy, collected at the 11 centers belonging to the Spanish Collaborative Group for the Study of Hodgkin's Disease.
  • The prognostic value of clinical variables and the expression of p53, bcl2, CD15, Rb, LMP 1-EBV and proliferative fraction demonstrated with sensitive immunohistochemical methods were studied.
  • Cox's multivariate analysis was performed to assess their influence in failure-free survival (FFS) and OS.
  • A multivariate logistic regression analysis was performed for studying the effect of the variables in the achievement of a CR.
  • Of the clinical variables, only advanced stage (III/IV) had a significant independent adverse influence in FFS, in OS and in the achievement of CR and advanced age in OS.
  • Of the molecular variables, LMP1-EBV had an independent and strong favorable influence in FFS, in OS and in the achievement of CR.
  • Rb expression had a modest favorable influence in CR.
  • The rest of the molecular variables had no independent influence on the outcome of the disease.
  • In conclusion these results confirm the favorable prognostic value of LMP1-EBV expression in the subset of patients with HD treated with chemotherapy.
  • [MeSH-major] Hodgkin Disease / drug therapy. Viral Matrix Proteins / metabolism
  • [MeSH-minor] Analysis of Variance. Biomarkers / analysis. Cohort Studies. Female. Frozen Sections. Humans. Immunohistochemistry. Male. Middle Aged. Prognosis. Retinoblastoma Protein / metabolism. Retrospective Studies. Risk Factors. Survival. Treatment Outcome

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  • (PMID = 11342339.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Biomarkers; 0 / EBV-associated membrane antigen, Epstein-Barr virus; 0 / Retinoblastoma Protein; 0 / Viral Matrix Proteins
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35. Zhao M, He HW, Sun HX, Ren KH, Shao RG: Dual knockdown of N-ras and epiregulin synergistically suppressed the growth of human hepatoma cells. Biochem Biophys Res Commun; 2009 Sep 18;387(2):239-44
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  • [Title] Dual knockdown of N-ras and epiregulin synergistically suppressed the growth of human hepatoma cells.
  • Hepatocellular carcinoma (HCC) is a major challenge because of its resistance to conventional cytotoxic chemotherapy and radiotherapy.
  • Multi-targeted therapy might be a new option for HCC treatment.
  • Our previous study showed that N-ras gene was activated in HCC and was inhibited by RNA interference.
  • The results revealed that the EREG gene, encoding epiregulin, was dramatically up-regulated in response to silence of N-ras.
  • We speculated that the up-regulation of epiregulin was involved in the compensatory mechanism of N-ras knockdown for cell growth.
  • Therefore, we evaluated whether dual silence of N-ras and epiregulin display a greater suppression of cell growth.
  • The results confirmed that dual knockdown of N-ras and epiregulin synergistically inhibited cell growth.
  • Our results also showed that dual knockdown of N-ras and epiregulin significantly induced cell arrest at G0/G1 phase.
  • Furthermore, Western blot assay showed that dual knockdown of N-ras and epiregulin markedly reduced the phosphorylations of ERK1/2, Akt and Rb, and inhibited the expression of cyclin D1.
  • Our findings imply that multi-targeted silence of oncogenes might be an effective treatment for HCC.
  • [MeSH-major] Carcinoma, Hepatocellular / pathology. Epidermal Growth Factor / genetics. Liver Neoplasms / pathology. Proto-Oncogene Proteins p21(ras) / genetics
  • [MeSH-minor] Cell Line, Tumor. Cell Proliferation. Cyclin D1 / antagonists & inhibitors. Cyclin D1 / biosynthesis. Epiregulin. G0 Phase / genetics. G1 Phase / genetics. Gene Knockdown Techniques. Gene Silencing. Humans. Mitogen-Activated Protein Kinase 1 / antagonists & inhibitors. Mitogen-Activated Protein Kinase 1 / biosynthesis. Mitogen-Activated Protein Kinase 3 / antagonists & inhibitors. Mitogen-Activated Protein Kinase 3 / biosynthesis. Proto-Oncogene Proteins c-akt / antagonists & inhibitors. Proto-Oncogene Proteins c-akt / biosynthesis. RNA, Small Interfering / genetics. Retinoblastoma Protein / antagonists & inhibitors. Retinoblastoma Protein / biosynthesis

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  • (PMID = 19563783.001).
  • [ISSN] 1090-2104
  • [Journal-full-title] Biochemical and biophysical research communications
  • [ISO-abbreviation] Biochem. Biophys. Res. Commun.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CCND1 protein, human; 0 / EREG protein, human; 0 / Epiregulin; 0 / RNA, Small Interfering; 0 / Retinoblastoma Protein; 136601-57-5 / Cyclin D1; 62229-50-9 / Epidermal Growth Factor; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 1; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 3; EC 3.6.5.2 / Proto-Oncogene Proteins p21(ras)
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36. Silber J, Lim DA, Petritsch C, Persson AI, Maunakea AK, Yu M, Vandenberg SR, Ginzinger DG, James CD, Costello JF, Bergers G, Weiss WA, Alvarez-Buylla A, Hodgson JG: miR-124 and miR-137 inhibit proliferation of glioblastoma multiforme cells and induce differentiation of brain tumor stem cells. BMC Med; 2008 Jun 24;6:14
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  • [Title] miR-124 and miR-137 inhibit proliferation of glioblastoma multiforme cells and induce differentiation of brain tumor stem cells.
  • BACKGROUND: Glioblastoma multiforme (GBM) is an invariably fatal central nervous system tumor despite treatment with surgery, radiation, and chemotherapy.
  • Further insights into the molecular and cellular mechanisms that drive GBM formation are required to improve patient outcome.
  • MicroRNAs are emerging as important regulators of cellular differentiation and proliferation, and have been implicated in the etiology of a variety of cancers, yet the role of microRNAs in GBM remains poorly understood.
  • In this study, we investigated the role of microRNAs in regulating the differentiation and proliferation of neural stem cells and glioblastoma-multiforme tumor cells.
  • To assess the function of candidate microRNAs in high-grade astrocytomas, we transfected miR mimics to cultured-mouse neural stem cells, -mouse oligodendroglioma-derived stem cells, -human glioblastoma multiforme-derived stem cells and -glioblastoma multiforme cell lines.
  • Cellular differentiation was assessed by immunostaining, and cellular proliferation was determined using fluorescence-activated cell sorting.
  • RESULTS: Our studies revealed that expression levels of microRNA-124 and microRNA-137 were significantly decreased in anaplastic astrocytomas (World Health Organization grade III) and glioblastoma multiforme (World Health Organization grade IV) relative to non-neoplastic brain tissue (P < 0.01), and were increased 8- to 20-fold during differentiation of cultured mouse neural stem cells following growth factor withdrawal.
  • Expression of microRNA-137 was increased 3- to 12-fold in glioblastoma multiforme cell lines U87 and U251 following inhibition of DNA methylation with 5-aza-2'-deoxycytidine (5-aza-dC).
  • Transfection of microRNA-124 or microRNA-137 induced morphological changes and marker expressions consistent with neuronal differentiation in mouse neural stem cells, mouse oligodendroglioma-derived stem cells derived from S100 beta-v-erbB tumors and cluster of differentiation 133+ human glioblastoma multiforme-derived stem cells (SF6969).
  • Transfection of microRNA-124 or microRNA-137 also induced G1 cell cycle arrest in U251 and SF6969 glioblastoma multiforme cells, which was associated with decreased expression of cyclin-dependent kinase 6 and phosphorylated retinoblastoma (pSer 807/811) proteins.
  • CONCLUSION: microRNA-124 and microRNA-137 induce differentiation of adult mouse neural stem cells, mouse oligodendroglioma-derived stem cells and human glioblastoma multiforme-derived stem cells and induce glioblastoma multiforme cell cycle arrest.
  • These results suggest that targeted delivery of microRNA-124 and/or microRNA-137 to glioblastoma multiforme tumor cells may be therapeutically efficacious for the treatment of this disease.

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  • [CommentIn] BMC Med. 2008;6:15 [18577221.001]
  • (PMID = 18577219.001).
  • [ISSN] 1741-7015
  • [Journal-full-title] BMC medicine
  • [ISO-abbreviation] BMC Med
  • [Language] ENG
  • [Grant] United States / NINDS NIH HHS / NS / R01 NS028478; United States / NINDS NIH HHS / NS / NS28478; United States / NCI NIH HHS / CA / K01 CA101777; United States / NCI NIH HHS / CA / P50 CA097257; United States / NCI NIH HHS / CA / CA097257; United States / NCI NIH HHS / CA / CA101777; United States / NINDS NIH HHS / NS / R37 NS028478
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / MIRN124 microRNA, human; 0 / MicroRNAs
  • [Other-IDs] NLM/ PMC2443372
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37. Roig JM, Molina MA, Cascante A, Calbó J, Carbó N, Wirtz U, Sreedharan S, Fillat C, Mazo A: Adenovirus-mediated retinoblastoma 94 gene transfer induces human pancreatic tumor regression in a mouse xenograft model. Clin Cancer Res; 2004 Feb 15;10(4):1454-62
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  • [Title] Adenovirus-mediated retinoblastoma 94 gene transfer induces human pancreatic tumor regression in a mouse xenograft model.
  • PURPOSE: Gene transfer of a truncated variant of the retinoblastoma (RB) gene encoding a M(r) 94000 protein that lacks the NH(2)-terminal 112 amino acid residues, termed RB94, has been shown to inhibit proliferation of several human tumor cell types.
  • We have assessed its therapeutic effectiveness on pancreatic cancer, one of the most aggressive and therapy-resistant types of cancer.
  • For this purpose, preclinical studies aimed to evaluate the therapeutic potential of RB94 gene transfer in pancreatic cancer were carried out.
  • EXPERIMENTAL DESIGN: We have compared the antiproliferative effects of adenovirus-mediated gene transfer of RBwt and RB94 at the in vitro and in vivo levels in three RB-positive human pancreatic tumor cell lines: (a). NP-9; (b).
  • RB94 transduction correlated with accumulation at the S-G(2) phase of the cell cycle in the three cell lines tested and induction of apoptosis in two of them.
  • Moreover, terminal deoxynucleotidyl transferase-mediated nick end labeling analyses of Ad-RB94-treated tumor sections revealed that only RB94 is able to significantly induce apoptosis.
  • CONCLUSIONS: RB94 gene expression has antiproliferative effects also in human pancreatic tumor cells, being more effective than wild-type RB in preventing tumor growth.
  • [MeSH-major] Adenoviridae / genetics. Gene Transfer Techniques. Pancreatic Neoplasms / therapy. Retinoblastoma Protein / genetics
  • [MeSH-minor] Animals. Annexin A5 / pharmacology. Apoptosis. Blotting, Western. Cell Cycle. Cell Division. Cell Line, Tumor. Coloring Agents / pharmacology. Dose-Response Relationship, Drug. Humans. In Situ Nick-End Labeling. Mice. Mice, Nude. Neoplasm Transplantation. Protein Structure, Tertiary. Time Factors

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  • (PMID = 14977849.001).
  • [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 / Annexin A5; 0 / Coloring Agents; 0 / Retinoblastoma Protein
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38. Aerts I, Lumbroso-Le Rouic L, Gauthier-Villars M, Brisse H, Doz F, Desjardins L: Retinoblastoma. Orphanet J Rare Dis; 2006;1:31
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  • [Title] Retinoblastoma.
  • Retinoblastoma is a rare eye tumor of childhood that arises in the retina.
  • It is the most common intraocular malignancy of infancy and childhood; with an incidence of 1/15,000-20,000 live births.
  • The two most frequent symptoms revealing retinoblastoma are leukocoria and strabismus.
  • Sixty per cent of retinoblastomas are unilateral and most of these forms are not hereditary (median age at diagnosis two years).
  • Retinoblastoma is bilateral in 40% of cases (median age at diagnosis one year).
  • Hereditary retinoblastoma constitutes a cancer predisposition syndrome: a subject constitutionally carrying an RB1 gene mutation has a greater than 90% risk of developing retinoblastoma but is also at increased risk of developing other types of cancers.
  • Diagnosis is made by fundoscopy.
  • Ultrasound, magnetic resonance imaging (MRI) and computed tomography (CT) scans may contribute to diagnosis.
  • Management of patients with retinoblastoma must take into account the various aspects of the disease: the visual risk, the possibly hereditary nature of the disease, the life-threatening risk.
  • Enucleation is still often necessary in unilateral disease; the decision for adjuvant treatment is taken according to the histological risk factors.
  • Conservative treatment for at least one eye is possible in most of the bilateral cases.
  • It includes laser alone or combined with chemotherapy, cryotherapy and brachytherapy.
  • Vital prognosis, related to retinoblastoma alone, is now excellent in patients with unilateral or bilateral forms of retinoblastoma.
  • Long term follow-up and early counseling regarding the risk of second primary tumors and transmission should be offered to retinoblastoma patients.
  • [MeSH-major] Retinal Neoplasms / diagnosis. Retinal Neoplasms / therapy. Retinoblastoma / diagnosis. Retinoblastoma / therapy
  • [MeSH-minor] Child, Preschool. Diagnosis, Differential. Eye Diseases / diagnosis. Female. Humans. Infant. Pregnancy. Prenatal Diagnosis / methods. Prognosis. Rare Diseases. Retinoblastoma Protein / genetics

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  • (PMID = 16934146.001).
  • [ISSN] 1750-1172
  • [Journal-full-title] Orphanet journal of rare diseases
  • [ISO-abbreviation] Orphanet J Rare Dis
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Retinoblastoma Protein
  • [Number-of-references] 56
  • [Other-IDs] NLM/ PMC1586012
  • [General-notes] NLM/ Original DateCompleted: 20070719
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39. Yao M, Yaroslavsky A, Henry FP, Redmond RW, Kochevar IE: Phototoxicity is not associated with photochemical tissue bonding of skin. Lasers Surg Med; 2010 Feb;42(2):123-31
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  • [Title] Phototoxicity is not associated with photochemical tissue bonding of skin.
  • BACKGROUND AND OBJECTIVE: We have developed a light-activated method called photochemical tissue bonding (PTB) for closing wounds using green light and a photosensitizing dye (Rose Bengal-RB) to initiate photochemical crosslinking of wound surface proteins.
  • These studies were designed to determine whether RB causes phototoxicity during closure of skin incisions with PTB.
  • STUDY DESIGN/MATERIALS AND METHODS: RB phototoxicity was evaluated after sealing incisions in porcine skin ex vivo and rabbit skin in vivo using PTB (1 mM RB, 100 J/cm(2), 532 nm, 0.3 or 0.5 W/cm(2).
  • The influence on RB phototoxicity of penetration of RB into the wound wall (by confocal microscopy), RB concentration in the tissue (by extraction), and fluence of 532 nm reaching depths in skin (calculated from skin optical properties) were investigated.
  • RB was retained in a approximately 100 microm wide band next to the wound wall.
  • The mean RB concentration within this band was 0.42+/-0.03 mM.
  • ) In vitro RB phototoxicity to dermal fibroblasts yielded an LD(50) of 0.50+/-0.09 J/cm(2) when the cells contained 0.46 mM RB.
  • CONCLUSIONS: PTB does not cause phototoxicity when used to repair skin wounds even though the RB concentration and 532 nm fluence in the mid-dermis during PTB are much greater than the LD(50) for RB phototoxicity in vitro.
  • These results indicate that phototoxicity is not a concern when using PTB for tissue repair.
  • [MeSH-major] Dermatitis, Phototoxic / physiopathology. Dermatologic Surgical Procedures. Rose Bengal / pharmacology. Tissue Adhesives / pharmacology. Wound Healing / physiology
  • [MeSH-minor] Animals. Cell Survival. Cells, Cultured. Disease Models, Animal. Female. Fibroblasts. Immunohistochemistry. Low-Level Light Therapy. Male. Monte Carlo Method. Photosensitizing Agents / pharmacology. Photosensitizing Agents / toxicity. Rabbits. Random Allocation. Reference Values. Risk Factors. Skin / pathology. Skin Absorption / drug effects. Skin Absorption / radiation effects. Swine

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  • (PMID = 20166159.001).
  • [ISSN] 1096-9101
  • [Journal-full-title] Lasers in surgery and medicine
  • [ISO-abbreviation] Lasers Surg Med
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Photosensitizing Agents; 0 / Tissue Adhesives; 1ZPG1ELY14 / Rose Bengal
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40. Balaguer J, Wilson MW, Billups CA, Mancini J, Haik BG, Qaddoumi I, Khoury JD, Rodriguez-Galindo C: Predictive factors of invasion in eyes with retinoblastoma enucleated after eye salvage treatments. Pediatr Blood Cancer; 2009 Mar;52(3):351-6
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  • [Title] Predictive factors of invasion in eyes with retinoblastoma enucleated after eye salvage treatments.
  • BACKGROUND: The impact of chemotherapy, focal therapies, radiation and co-existing ocular morbidities on histology of eyes with retinoblastoma enucleated following chemoreduction is not well known.
  • PROCEDURE: Twenty-five eyes (23 patients) with retinoblastoma enucleated after failing eye-salvage therapy were evaluated.
  • Reasons for enucleation (tumor progression, subretinal or vitreous seeds) and co-morbid conditions (neovascular glaucoma, cataract, vitreous hemorrhage and retinal detachment) were documented.
  • All specimens were reviewed for evidence of ciliary body, choroidal, optic nerve, and scleral invasion.
  • RESULTS: The median age at diagnosis was 14 months (range, 1-37 months).
  • Twenty eyes were classified as Reese-Ellsworth Group IV-V at diagnosis.
  • Twenty-four eyes had recurrent disease at enucleation; one eye was enucleated for neovascular glaucoma and vitreous hemorrhage.
  • Co-existing ocular morbidities at enucleation included vitreous hemorrhage (n = 6), retinal detachment (n = 9), neovascular glaucoma (n = 9) and cataracts (n = 3).
  • Histologic findings included choroidal invasion (n = 7), ciliary body invasion (n = 4), optic nerve invasion (n = 6) and scleral invasion (n = 3).
  • The median time from diagnosis to enucleation was 11 months.
  • Co-existing retinal detachment and vitreous hemorrhage significantly increased the likelihood of optic nerve invasion (P = 0.014 and P = 0.011, respectively).
  • Prolonged time to enucleation was significantly associated with the likelihood of choroidal (P = 0.010) and ciliary body (P = 0.021) invasion as well as invasion of multiple sites.
  • CONCLUSION: In eyes with retinoblastoma enucleated after chemoreduction, co-existing ocular morbidities and time to enucleation are predictive of extra-retinal extension.

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  • (PMID = 19021223.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P01 CA023099; United States / NCI NIH HHS / CA / P30 CA021765; United States / PHS HHS / / 21765; United States / NCI NIH HHS / CA / CA 23099
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Other-IDs] NLM/ NIHMS124023; NLM/ PMC4643656
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41. Mihaylova VT, Green AM, Khurgel M, Semmes OJ, Kupfer GM: Human T-cell leukemia virus I tax protein sensitizes p53-mutant cells to DNA damage. Cancer Res; 2008 Jun 15;68(12):4843-52
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  • [Title] Human T-cell leukemia virus I tax protein sensitizes p53-mutant cells to DNA damage.
  • Mutations in p53 are a common cause of resistance of cancers to standard chemotherapy and, thus, treatment failure.
  • Reports have shown that Tax, a human T-cell leukemia virus type I encoded protein that has been associated with genomic instability and perturbation of transcription and cell cycle, sensitizes HeLa cells to UV treatment.
  • In this study, we show that Tax sensitizes p53-mutant cells to a broad range of DNA-damaging agents, including mitomycin C, a bifunctional alkylator, etoposide, a topoisomerase II drug, and UV light, but not ionizing radiation, a double-strand break agent, or vinblastine, a tubulin poison.
  • Tax caused hypersensitivity in all p53-deleted cell lines and several, but not all, mutant-expressed p53-containing cell lines, while unexpectedly being protective in p53 wild-type (wt) cells.
  • We also show that Tax activates a p53-independent proapoptotic program through decreased expression of the retinoblastoma protein and subsequent increased E2F1 expression.
  • Such studies hold the promise of a novel adjunctive therapy that could make cancer chemotherapy more effective.
  • [MeSH-major] DNA Damage / drug effects. DNA Damage / radiation effects. Gene Products, tax / physiology. Mutation / genetics. Tumor Suppressor Protein p53 / genetics. Tumor Suppressor Protein p53 / metabolism
  • [MeSH-minor] Animals. Antibiotics, Antineoplastic / pharmacology. Antineoplastic Agents, Phytogenic / pharmacology. Apoptosis / drug effects. Apoptosis / radiation effects. Apoptosis Regulatory Proteins / metabolism. Cell Cycle / drug effects. Cell Cycle / radiation effects. Cells, Cultured. Dimerization. Etoposide / pharmacology. Fibroblasts / cytology. Fibroblasts / drug effects. Fibroblasts / radiation effects. Humans. Immunoblotting. Luciferases / metabolism. Mice. Mitomycin / pharmacology. Proto-Oncogene Proteins / metabolism. Proto-Oncogene Proteins c-bcl-2 / metabolism. Tumor Suppressor Proteins / metabolism. Ultraviolet Rays. Vinblastine / pharmacology. bcl-2-Associated X Protein / metabolism

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  • (PMID = 18559532.001).
  • [ISSN] 1538-7445
  • [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 / Antibiotics, Antineoplastic; 0 / Antineoplastic Agents, Phytogenic; 0 / Apoptosis Regulatory Proteins; 0 / BAX protein, human; 0 / BBC3 protein, human; 0 / Bax protein, mouse; 0 / Gene Products, tax; 0 / PMAIP1 protein, human; 0 / PUMA protein, mouse; 0 / Pmaip1 protein, mouse; 0 / Proto-Oncogene Proteins; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Tumor Suppressor Protein p53; 0 / Tumor Suppressor Proteins; 0 / bcl-2-Associated X Protein; 0 / tax protein, Human T-lymphotrophic virus 1; 50SG953SK6 / Mitomycin; 5V9KLZ54CY / Vinblastine; 6PLQ3CP4P3 / Etoposide; EC 1.13.12.- / Luciferases
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42. Dimaras H, Rushlow D, Halliday W, Doyle JJ, Babyn P, Abella EM, Williams J, Héon E, Gallie BL, Chan HS: Using RB1 mutations to assess minimal residual disease in metastatic retinoblastoma. Transl Res; 2010 Aug;156(2):91-7
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  • [Title] Using RB1 mutations to assess minimal residual disease in metastatic retinoblastoma.
  • To assess complete remission before subjecting nongermline metastatic retinoblastoma patients to an autologous peripheral stem cell transplant, we tested for patient-specific retinoblastoma tumor suppressor gene (RB1) mutant alleles in cerebrospinal fluid (CSF) and bone marrow.
  • In 1 child with CSF and 1 with bone marrow metastases, allele-specific polymerase chain reaction (AS-PCR) detected the biallelic RB1 mutations specific to their tumors.
  • The tumor of Child A was homozygous for R251X, and in Child B, it was homozygous for R358X.
  • In Child A, the R251X mutation was detected in mutant controls diluted to 1:12,800 but not in CSF samples, corroborating clinical remission after chemotherapy.
  • In Child B's bone marrow, AS-PCR for R358X was strongly positive at the detection of relapse, and subsequent bone marrow samples corroborated clinical remission after chemotherapy.
  • No mutant tumor RB1 alleles were detected in their harvested peripheral blood stem cells.
  • Both children were deemed suitable candidates for supralethal-dosage consolidation chemotherapy followed by autologous peripheral stem cell rescue of the bone marrow aimed at curing their metastatic retinoblastoma.
  • When Child A recurred, the mutant tumor RB1 allele was detected 3.5 months before conventional pathology detected retinoblastoma tumor cells in the CSF.
  • Assaying tumor-specific RB1 mutations complements cytological and immunohistochemical assessment of retinoblastoma involvement of CSF and bone marrow.
  • Tumor cells can be detected in numbers lower than possible by conventional methods.
  • An early diagnosis of relapse may allow an early institution of new therapy.
  • A prospective international multicenter trial of the rare patients with metastatic retinoblastoma would assess the role of molecular monitoring in surveillance for minimal residual disease and recurrence.
  • [MeSH-major] Mutation. Retinal Neoplasms / genetics. Retinoblastoma / genetics. Retinoblastoma Protein / genetics
  • [MeSH-minor] Biopsy. Bone Marrow / pathology. Bone Marrow Transplantation. Bone Neoplasms / pathology. Cerebrospinal Fluid / metabolism. Child. Child, Preschool. Eye Enucleation. Female. Humans. Infant. Neoplasm Metastasis / genetics. Polymerase Chain Reaction. Stem Cell Transplantation

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  • [Copyright] Copyright (c) 2010 Mosby, Inc. All rights reserved.
  • (PMID = 20627193.001).
  • [ISSN] 1878-1810
  • [Journal-full-title] Translational research : the journal of laboratory and clinical medicine
  • [ISO-abbreviation] Transl Res
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Retinoblastoma Protein
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43. Wang L, Liu D, Ahmed T, Chung FL, Conaway C, Chiao JW: Targeting cell cycle machinery as a molecular mechanism of sulforaphane in prostate cancer prevention. Int J Oncol; 2004 Jan;24(1):187-92
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  • [Title] Targeting cell cycle machinery as a molecular mechanism of sulforaphane in prostate cancer prevention.
  • Epidemiological studies recently concluded that consumption of cruciferous vegetables such as broccoli, cabbage, and cauliflower, etc. is inversely related to prostate cancer risk, although the mechanism of prevention and the responsible phytochemicals are unknown.
  • Since clinically significant prostate cancer eventually can grow independent of androgen, the association of the growth and tumorigenesis of such prostate cancer cells with sulforaphane (SFN) which is a predominant isothiocyanate in cruciferous vegetables, investigated.
  • This study showed that exposure of human androgen-independent DU-145 prostate cancer cells to SFN resulted in the inhibition of growth and tumorigenesis, as revealed by a reduction in cell density, DNA synthesis, and clonogenesis.
  • Analyses of the mechanism revealed that SFN mediated cell cycle arrest by modulating the expression and functions of cell cycle regulators.
  • SFN induced signals that inhibited the activity of cyclin-dependent kinase cdk4 with an up-stream induction of cdk inhibitor p21WAF-1/Cip-1, and reduced cyclin D1.
  • The inhibition of cdk kinase activity could be affected with <1 micro M SFN within 24 h.
  • As a result, phosphorylation of Rb proteins, which activates the transition from G1- to S-phase, was significantly decreased and the cell cycle progression retarded.
  • SFN also down-regulated the expression of bcl-2, a suppressor of apoptosis, and activated caspases to execute apoptosis in the prostate cancer cells.
  • The potential of SFN, as an active dietary factor to inhibit initiation and post-initiation of prostate cancer carcinogenesis is discussed.
  • [MeSH-major] Anticarcinogenic Agents / pharmacology. Cell Cycle / drug effects. Proto-Oncogene Proteins. Thiocyanates / pharmacology
  • [MeSH-minor] Apoptosis / drug effects. Caspases / metabolism. Cell Cycle Proteins / metabolism. Cell Division / drug effects. Cell Line, Tumor. Cyclin-Dependent Kinase 4. Cyclin-Dependent Kinase Inhibitor p27. Cyclin-Dependent Kinases / metabolism. Cyclins / metabolism. Dose-Response Relationship, Drug. Down-Regulation. Enzyme Activation / drug effects. G1 Phase / drug effects. Humans. In Situ Nick-End Labeling. Isothiocyanates. Male. Phosphorylation / drug effects. Prostatic Neoplasms / drug therapy. Prostatic Neoplasms / metabolism. Prostatic Neoplasms / pathology. Proto-Oncogene Proteins c-bcl-2 / metabolism. Retinoblastoma Protein / metabolism. S Phase / drug effects. Tumor Suppressor Proteins / metabolism

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  • (PMID = 14654956.001).
  • [ISSN] 1019-6439
  • [Journal-full-title] International journal of oncology
  • [ISO-abbreviation] Int. J. Oncol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Anticarcinogenic Agents; 0 / Cell Cycle Proteins; 0 / Cyclins; 0 / Isothiocyanates; 0 / Proto-Oncogene Proteins; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Retinoblastoma Protein; 0 / Thiocyanates; 0 / Tumor Suppressor Proteins; 147604-94-2 / Cyclin-Dependent Kinase Inhibitor p27; 4478-93-7 / sulforafan; EC 2.7.11.22 / CDK4 protein, human; EC 2.7.11.22 / Cyclin-Dependent Kinase 4; EC 2.7.11.22 / Cyclin-Dependent Kinases; EC 3.4.22.- / Caspases
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44. Cascallo M, Alonso MM, Rojas JJ, Perez-Gimenez A, Fueyo J, Alemany R: Systemic toxicity-efficacy profile of ICOVIR-5, a potent and selective oncolytic adenovirus based on the pRB pathway. Mol Ther; 2007 Sep;15(9):1607-15
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  • E2F acts as a transcriptional repressor when bound to unphosphorylated RB during the G(1) or G(0) phase.
  • Upon phosphorylation, E2F is released from the E2F-RB complexes to activate transcription.
  • Tumor cells are characterized by an increase in the level of "free" E2F as a consequence of the absence or hyperphosphorylation of RB.
  • The E2F-1 promoter is a well-characterized E2F-responsive promoter, and it can be used to control adenovirus E1a gene expression as a strategy to achieve tumor-selective expression and replication of an adenovirus.
  • ICOVIR-5 (Ad-DM-E2F-K-Delta24RGD) is an optimized oncolytic adenovirus that combines E1a transcriptional control by an insulated form of the E2F promoter with the Delta24 mutation of E1a to improve the therapeutic index of AdDelta24RGD.
  • ICOVIR-5 also contains the Kozak sequence at the E1a start codon, which is important to restore E1a expression and viral replication to AdwtRGD levels in tumor cells.
  • The unique combination of genetic elements in ICOVIR-5 allows the selectivity for cells with a deregulated E2F-RB pathway to be increased and potent anti-tumoral activity to be maintained.
  • Dose-response toxicological and efficacy studies after a single systemic administration in pre-clinical models in mice are presented to demonstrate that this virus holds promise for treatment of disseminated cancer.
  • [MeSH-major] Adenoviridae / genetics. E2F1 Transcription Factor / genetics. Genetic Therapy / methods. Neoplasms / therapy. Retinoblastoma Protein / genetics
  • [MeSH-minor] Adenovirus E1A Proteins / genetics. Adenovirus E1A Proteins / metabolism. Animals. Cell Line. Cell Line, Tumor. Chromatin Immunoprecipitation. Humans. Liver / drug effects. Liver / metabolism. Male. Mice. Mice, Inbred BALB C. Mice, Nude. Oncolytic Viruses / genetics. Virus Replication / genetics. Virus Replication / physiology. Xenograft Model Antitumor Assays

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  • (PMID = 17579575.001).
  • [ISSN] 1525-0016
  • [Journal-full-title] Molecular therapy : the journal of the American Society of Gene Therapy
  • [ISO-abbreviation] Mol. Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adenovirus E1A Proteins; 0 / E2F1 Transcription Factor; 0 / E2F1 protein, human; 0 / Retinoblastoma Protein
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45. Armenian SH, Panigrahy A, Murphree AL, Jubran RF: Management of retinoblastoma with proximal optic nerve enhancement on MRI at diagnosis. Pediatr Blood Cancer; 2008 Oct;51(4):479-84
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  • [Title] Management of retinoblastoma with proximal optic nerve enhancement on MRI at diagnosis.
  • BACKGROUND: In North America, retinoblastoma rarely presents with gross clinical evidence of tumor involving the optic nerve.
  • Extent of microscopic tumor infiltration into the postlaminar optic nerve is a significant risk factor for metastasis, especially if there is tumor at the cut end.
  • Due to poor outcomes in patients with metastatic disease, historical treatment for patients with clinical evidence of extraocular optic nerve involvement has included upfront enucleation followed by aggressive adjuvant chemotherapy.
  • Additional orbital irradiation is advocated for individuals with optic nerve involvement at the surgical margin.
  • Little is known about the role of neoadjuvant therapy in the setting of orbital optic nerve enhancement on magnetic resonance imaging (MRI) at diagnosis.
  • METHODS: A retrospective review of consecutive retinoblastoma cases at Childrens Hospital Los Angeles over a 3-year period (2004-2006) found to have gadolinium contrast enhancement in the proximal portion of optic nerve on MRI at diagnosis.
  • Two had secondary glaucoma of a sufficient degree to cause an enlarged eye (buphthalmos).
  • All patients received neoadjuvant chemotherapy prior to enucleation.
  • All are disease-free with a median follow-up of 22 months (12-41 months).
  • CONCLUSIONS: Neoadjuvant chemotherapy is well tolerated prior to enucleation of retinoblastoma-containing eyes associated with contrast enhancement of the proximal optic nerve on MRI at diagnosis.
  • Such an approach may be used to decrease intensity or duration of chemotherapy and need for external beam radiation.
  • [MeSH-major] Optic Nerve Neoplasms / diagnosis. Optic Nerve Neoplasms / drug therapy. Retinal Neoplasms / diagnosis. Retinal Neoplasms / drug therapy. Retinoblastoma / diagnosis. Retinoblastoma / drug therapy
  • [MeSH-minor] Antineoplastic Agents / adverse effects. Antineoplastic Agents / therapeutic use. Child, Preschool. Female. Humans. Infant. Magnetic Resonance Imaging. Male. Treatment Outcome

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  • [Copyright] (c) 2008 Wiley-Liss, Inc.
  • (PMID = 18478574.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents
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46. Blagosklonny MV, Darzynkiewicz Z: Cyclotherapy: protection of normal cells and unshielding of cancer cells. Cell Cycle; 2002 Nov-Dec;1(6):375-82
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  • [Title] Cyclotherapy: protection of normal cells and unshielding of cancer cells.
  • Avoidance of apoptosis and mitogen-independent growth are hallmarks of cancer.
  • Mitogen-activated kinases (for example, ErbB1, Raf-1, MEK, PI-3-K, mTOR) can suppress chemotherapy-induced apoptosis in cancer cells.
  • While kinase inhibitors restore susceptibility of cancer cells to apoptosis, they do not necessarily cause growth arrest in cancer cells harboring additional mutations in downstream signaling pathways such as inactivation of Rb and overexpression of c-myc.
  • While arresting growth of normal cells, kinase inhibitors may not arrest cancer cells but instead can sensitize them to apoptosis.
  • Following pretreatment with low doses of kinase inhibitors, the chemotherapy that predominantly induces apoptosis in cycling cells (cyclotherapy) will kill cancer cells while sparing normal cells.


47. Bonvini P, Zorzi E, Mussolin L, Monaco G, Pigazzi M, Basso G, Rosolen A: The effect of the cyclin-dependent kinase inhibitor flavopiridol on anaplastic large cell lymphoma cells and relationship with NPM-ALK kinase expression and activity. Haematologica; 2009 Jul;94(7):944-55
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  • [Title] The effect of the cyclin-dependent kinase inhibitor flavopiridol on anaplastic large cell lymphoma cells and relationship with NPM-ALK kinase expression and activity.
  • BACKGROUND: The loss of cell cycle regulation due to abnormal function of cyclin-dependent kinases (cdk) occurs in tumors and leads to genetic instability of chemotherapy-resistant cells.
  • In this study, we investigated the effect of the cdk inhibitor flavopiridol in anaplastic large cell lymphomas, in which unrestrained proliferation depends on NPM-ALK tyrosine kinase activity.
  • DESIGN AND METHODS: Effects of flavopiridol were examined in ALK-positive and -negative anaplastic large cell lymphoma cells by means of immunoblotting and immunofluorescence analyses to assess cdk expression and activity, quantitative real time reverse transcriptase polymerase chain reaction to measure drug-induced changes in transcription, and FACS analyses to monitor changes in proliferation and survival.
  • RESULTS: Treatment with flavopiridol resulted in growth inhibition of anaplastic large cell lymphoma cells, along with accumulation of subG(1) cells and disappearance of S phase without cell cycle arrest.
  • Consistent with flavopiridol activity, phosphorylation at cdk2, cdk4, cdk9 sites on RB and RNA polymerase II was inhibited.
  • Notably, flavopiridol was less active in ALK-positive cells, as apoptosis was observed at higher concentrations and later time points, and resistance to treatment was observed in cells maintaining NPM-ALK signaling.
  • NPM-ALK inhibition affected proliferation but not survival of anaplastic large cell lym-phoma cells, whereas it resulted in a dramatic increase in apoptosis when combined with flavopiridol.
  • CONCLUSIONS: This work provides the first demonstration that targeting cdk is effective against anaplastic large cell lymphoma cells, and proves the critical role of NPM-ALK in the regulation of responsiveness of tumor cells with cdk dysregulation.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Flavonoids / pharmacology. Gene Expression Regulation, Neoplastic. Lymphoma, Large-Cell, Anaplastic / drug therapy. Piperidines / pharmacology. Protein-Tyrosine Kinases / biosynthesis
  • [MeSH-minor] Apoptosis. Bromodeoxyuridine / pharmacology. Cell Cycle. Cell Separation. Cell Survival. Dose-Response Relationship, Drug. Humans. Reverse Transcriptase Polymerase Chain Reaction. Subcellular Fractions. Time Factors


48. Parness-Yossifon R, Bryar PJ, Weinstein JL, Srikumaran D, Mets MB: Sudden dispersion of retinoblastoma shortly after initial chemotherapy treatment. Am J Ophthalmol; 2009 May;147(5):903-6
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  • [Title] Sudden dispersion of retinoblastoma shortly after initial chemotherapy treatment.
  • PURPOSE: To present 3 cases of unilateral retinoblastoma that demonstrated unusual tumor dispersion shortly after initial chemotherapy treatment.
  • DESIGN: Observational case series.
  • METHODS: Review of medical records of patients in whom intraocular dissemination of retinoblastoma occurred after initial treatment with chemotherapy.
  • RESULTS: Three patients demonstrated an atypical response with intraocular dissemination of retinoblastoma shortly after 1 cycle of chemotherapy.
  • All cases had unilateral retinoblastoma with no vitreous seeding or subretinal fluid at presentation.
  • Per the International Classification of Retinoblastoma, 1 tumor was group E (Case 1), and the other 2 tumors were group D1 (Cases 2 and 3).
  • In 2 cases (Cases 1 and 2), chemotherapy included a 2-drug regimen of carboplatin and etoposide; in the third case, a 3-drug regimen of carboplatin, etoposide, and vincristine was used.
  • In each case, the retinoblastoma dispersed with tumor cells in the vitreous shortly after initial chemotherapy treatment, leading to subsequent enucleation of the eye.
  • CONCLUSIONS: Retinoblastoma can exhibit an unexpected and sudden dispersion of the tumor shortly after chemotherapy is initiated.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / adverse effects. Eye Neoplasms / secondary. Neoplasm Seeding. Retinal Neoplasms / pathology. Retinoblastoma / secondary. Vitreous Body
  • [MeSH-minor] Carboplatin / administration & dosage. Carboplatin / adverse effects. Child, Preschool. Etoposide / administration & dosage. Etoposide / adverse effects. Eye Enucleation. Female. Humans. Infant. Male. Vincristine / adverse effects

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  • (PMID = 19232557.001).
  • [ISSN] 1879-1891
  • [Journal-full-title] American journal of ophthalmology
  • [ISO-abbreviation] Am. J. Ophthalmol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 5J49Q6B70F / Vincristine; 6PLQ3CP4P3 / Etoposide; BG3F62OND5 / Carboplatin; CEV regimen
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49. Decker T, Hipp S, Ringshausen I, Bogner C, Oelsner M, Schneller F, Peschel C: Rapamycin-induced G1 arrest in cycling B-CLL cells is associated with reduced expression of cyclin D3, cyclin E, cyclin A, and survivin. Blood; 2003 Jan 1;101(1):278-85
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  • [Title] Rapamycin-induced G1 arrest in cycling B-CLL cells is associated with reduced expression of cyclin D3, cyclin E, cyclin A, and survivin.
  • In B-cell chronic lymphocytic leukemia (B-CLL), malignant cells seem to be arrested in the G(0)/early G(1) phase of the cell cycle, and defective apoptosis might be involved in disease progression.
  • However, increasing evidence exists that B-CLL is more than a disease consisting of slowly accumulating resting B cells: a proliferating pool of cells has been described in lymph nodes and bone marrow and might feed the accumulating pool in the blood.
  • Rapamycin has been reported to inhibit cell cycle progression in a variety of cell types, including human B cells, and has shown activity against a broad range of human tumor cell lines.
  • We have recently demonstrated that stimulation with CpG-oligonucleotides and interleukin-2 provides a valuable model for studying cell cycle regulation in malignant B cells.
  • In contrast to previous reports on nonmalignant B cells, the expression of the cell cycle inhibitor p27 was not changed in rapamycin-treated leukemic cells.
  • Treatment with rapamycin prevented retinoblastoma protein (RB) phosphorylation in B-CLL cells without affecting the expression of cyclin D2, but cyclin D3 was no longer detectable in rapamycin-treated B-CLL cells.
  • In addition, rapamycin treatment inhibited cyclin-dependent kinase 2 activity by preventing up-regulation of cyclin E and cyclin A.
  • Interestingly, survivin, which is expressed in the proliferation centers of B-CLL patients in vivo, is not up-regulated in rapamycin-treated cells.
  • We conclude from our study that rapamycin might be an attractive substance for therapy for B-CLL patients by inducing a G(1) arrest in proliferating tumor cells.
  • [MeSH-major] Antibiotics, Antineoplastic / pharmacology. Cyclins / drug effects. G1 Phase / drug effects. Leukemia, Lymphocytic, Chronic, B-Cell / pathology. Sirolimus / pharmacology
  • [MeSH-minor] Aged. Aged, 80 and over. B-Lymphocytes / drug effects. B-Lymphocytes / pathology. Cell Culture Techniques. Cell Cycle / drug effects. Cyclin A / drug effects. Cyclin A / metabolism. Cyclin D3. Cyclin E / drug effects. Cyclin E / metabolism. Humans. Inhibitor of Apoptosis Proteins. Male. Microtubule-Associated Proteins / drug effects. Microtubule-Associated Proteins / metabolism. Middle Aged. Neoplasm Proteins

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  • (PMID = 12393642.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / BIRC5 protein, human; 0 / CCND3 protein, human; 0 / Cyclin A; 0 / Cyclin D3; 0 / Cyclin E; 0 / Cyclins; 0 / Inhibitor of Apoptosis Proteins; 0 / Microtubule-Associated Proteins; 0 / Neoplasm Proteins; W36ZG6FT64 / Sirolimus
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50. Bostan OM, Celiker A, Ozme S: Spontaneous resolution of ventricular tachycardia with right bundle branch block morphology: a case report. Turk J Pediatr; 2003 Apr-Jun;45(2):170-3
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  • [Title] Spontaneous resolution of ventricular tachycardia with right bundle branch block morphology: a case report.
  • In the absence of structural heart disease, ventricular tachycardia is known as idiopathic ventricular tachycardia and carries a good prognosis.
  • We report a 14-month-old male child with right bundle branch block incessant ventricular tachycardia without structural heart disease.
  • We want to stress the benign nature of this tachycardia if the previous treatment protocol had been appropriate.
  • [MeSH-major] Bundle-Branch Block. Tachycardia, Ventricular / physiopathology
  • [MeSH-minor] Amiodarone / therapeutic use. Anti-Arrhythmia Agents / therapeutic use. Electrocardiography. Heart Failure / complications. Heart Failure / drug therapy. Humans. Infant. Male

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  • (PMID = 12921310.001).
  • [ISSN] 0041-4301
  • [Journal-full-title] The Turkish journal of pediatrics
  • [ISO-abbreviation] Turk. J. Pediatr.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Turkey
  • [Chemical-registry-number] 0 / Anti-Arrhythmia Agents; N3RQ532IUT / Amiodarone
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51. Cebulla CM, Alegret A, Ehlies FJ, Davis RP 2nd, Hess DJ, Murray TG, Echography Study Group: Echographic localization of periocular Carboplatin for treatment of advanced retinoblastoma. Retin Cases Brief Rep; 2009;3(1):4-7
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  • [Title] Echographic localization of periocular Carboplatin for treatment of advanced retinoblastoma.
  • PURPOSE: To study ocular ultrasonography as a means to effectively localize periocular carboplatin in patients with advanced retinoblastoma.
  • METHODS: In a cases series, seven patients diagnosed with advanced retinoblastoma refractory to standard chemotherapy were treated with two to four periocular carboplatin injections.
  • RESULTS: The periocular carboplatin depot was a discrete homogeneous structure with lower internal reflectivity than the surrounding orbital tissue.
  • The mean maximal juxtascleral height of the drug depot ± SD was 3.3 ±1.4 mm and was located directly posterior to the area of maximal intraocular tumor thickness in all seven patients.
  • Moderate shadowing from calcification was present in one patient.
  • Five patients had a pattern of a thinner pocket of drug visible after subsequent injections.
  • CONCLUSIONS: Echography is a useful technique to study novel periocular drug delivery.
  • It effectively images the drug in relation to the intraocular tumor, confirming the most effective drug placement for these resistant tumors.

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  • (PMID = 25390825.001).
  • [ISSN] 1935-1089
  • [Journal-full-title] Retinal cases & brief reports
  • [ISO-abbreviation] Retin Cases Brief Rep
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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52. Chattopadhyay D, Ghosh MK, Mal A, Harter ML: Inactivation of p21 by E1A leads to the induction of apoptosis in DNA-damaged cells. J Virol; 2001 Oct;75(20):9844-56
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  • A major impediment to successful chemotherapy is the propensity for some tumor cells to undergo cell cycle arrest rather than apoptosis.
  • To further understand how E1A enhances chemosensitivity, we have made use of a human colon carcinoma cell line (HCT116) which typically undergoes cell cycle arrest in response to chemotherapeutic drugs.
  • As seen by the analysis of E1A mutants, we show here that E1A can induce apoptosis in these cells by neutralizing the activities of the cyclin-dependent kinase inhibitor p21.
  • E1A's ability to interact with p21 and thereby restore Cdk2 activity in DNA-damaged cells correlates with the reversal of G(1) arrest, which in turn leads to apoptosis.
  • Analysis of E1A mutants failing to bind p300 (also called CBP) or Rb shows that they are almost identical to wild-type E1A in their ability to initially overcome a G(1) arrest in cells after DNA damage, while an E1A mutant failing to bind p21 is not.
  • However, over time, this mutant, which can still target Rb, is far more efficient in accumulating cells with a DNA content greater than 4N but is similar to wild-type E1A and the other E1A mutants in releasing cells from a p53-mediated G(2) block following chemotherapeutic treatment.

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  • (PMID = 11559818.001).
  • [ISSN] 0022-538X
  • [Journal-full-title] Journal of virology
  • [ISO-abbreviation] J. Virol.
  • [Language] ENG
  • [Grant] United States / NIGMS NIH HHS / GM / GM54014
  • [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 / Adenovirus E1A Proteins; 0 / Antineoplastic Agents; 0 / Nuclear Proteins; 0 / Trans-Activators; 80168379AG / Doxorubicin; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.1 / p21-Activated Kinases; EC 2.7.11.22 / CDC2-CDC28 Kinases; EC 2.7.11.22 / CDK2 protein, human; EC 2.7.11.22 / Cyclin-Dependent Kinase 2; EC 2.7.11.22 / Cyclin-Dependent Kinases
  • [Other-IDs] NLM/ PMC114557
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53. Gelfert CC, Hauser S, Löptien A, Montag N, Passmann M, Baumgartner W, Staufenbiel R: [Impact of a simultaneous application of anionic salts and rumen buffer on acid-base-balance and mineral metabolism in dairy cows]. Berl Munch Tierarztl Wochenschr; 2006 May-Jun;119(5-6):244-50
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Impact of a simultaneous application of anionic salts and rumen buffer on acid-base-balance and mineral metabolism in dairy cows].
  • In this study, the influence of simultaneous application of anionic salts (AS) and rumen buffer (RB) on the metabolism of dairy cows was examined.
  • Eleven rumen fistulated, non-pregnant and non-lactating dairy cows received equal amounts of one AS (CaCl2 or CaSO4) and one RB (NaHCO3 or KHCO3) via rumen cannula during feeding time over a period of eight days.
  • Before the first application of AS and RB and on day eight of the treatment period, blood, urine and rumen fluid samples were taken.
  • The following parameters were measured: whole blood: pH, base excess, bicarbonate; serum: sodium, potassium, chloride, calcium; urine: pH, net acid base excretion, sodium, potassium, chloride, calcium; rumen fluid: pH.
  • The changes in acid-base balance on day eight were very small, although significant.
  • The most changes occurred when NaHCO3 was fed in combination with one of the AS used.
  • In this case a small acidogenic load was seen in blood (p < 0.05), and calcium concentrations increased slightly (p < 0.05).
  • No alkalotic reaction could be detected when any combination of AS and RB were given to the cows.
  • Simultaneous application of AS and RB results in a loss of effectivity of AS.
  • Neither an adequate acidification of blood nor an activation of calcium metabolism occurred.
  • In feed ration for cows in the last weeks of pregnancy, rumen buffer must not be fed, if anionic salts are given for prevention of parturient paresis.
  • [MeSH-major] Acid-Base Equilibrium / drug effects. Bicarbonates / pharmacology. Calcium Compounds / pharmacology. Cattle / metabolism. Minerals / metabolism
  • [MeSH-minor] Animals. Blood Chemical Analysis. Buffers. Dairying. Drug Synergism. Female. Hydrogen-Ion Concentration. Parturient Paresis / drug therapy. Parturient Paresis / prevention & control. Pregnancy. Rumen / chemistry. Serum / chemistry. Urine / chemistry

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  • (PMID = 16729472.001).
  • [ISSN] 0005-9366
  • [Journal-full-title] Berliner und Münchener tierärztliche Wochenschrift
  • [ISO-abbreviation] Berl. Munch. Tierarztl. Wochenschr.
  • [Language] ger
  • [Publication-type] Comparative Study; English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Bicarbonates; 0 / Buffers; 0 / Calcium Compounds; 0 / Minerals
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54. Mizuarai S, Irie H, Schmatz DM, Kotani H: Integrated genomic and pharmacological approaches to identify synthetic lethal genes as cancer therapeutic targets. Curr Mol Med; 2008 Dec;8(8):774-83
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  • [Title] Integrated genomic and pharmacological approaches to identify synthetic lethal genes as cancer therapeutic targets.
  • Various types of cancers are generated through mutations or dysregulations of oncogenes/tumor suppressor genes involved in cell cycles and signaling transduction pathways.
  • To identify cancer therapeutic targets whose inhibition selectively kills cancer cells, synthetic lethal screening is being developed to identify genes whose intervention suppresses tumor progression only when combined with the dysregulation of the genes.
  • This review introduces the research that could successfully identify synthetic lethal genes in cancer cells harboring major gene alterations such as p53, RB, K-Ras, or Myc.
  • Next, we introduce the chemogenomics approaches that explore chemical compounds that exhibit synthetic lethality to cancer gene alterations.
  • Although the synthetic lethal compounds are of great interest in terms of cancer drug development, a method of identifying target proteins for the phenotypic compounds has been elusive.
  • Finally, we demonstrate several noteworthy techniques to identify target proteins for the compounds: a Connectivity Map that compares expression profiles of compound-treated cells by pattern-matching algorithms; an siRNA/compound co-treatment assay to find enhancer genes for the phenotypes of compounds; and a state-of-the-art proteomics approach that modifies classical compound-immobilized affinity chromatography.
  • The integration of genomic and pharmacological analyses would significantly accelerate the identification of cancer-specific synthetic lethal targets.
  • [MeSH-major] Genes, Lethal. Genes, Synthetic. Neoplasms / genetics. Neoplasms / therapy
  • [MeSH-minor] Gene Expression Profiling. Gene Silencing. Gene Targeting. Genetic Therapy / methods. Humans. Models, Genetic. Mutation. Oligonucleotide Array Sequence Analysis. Oncogenes. Proteomics

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  • (PMID = 19075675.001).
  • [ISSN] 1566-5240
  • [Journal-full-title] Current molecular medicine
  • [ISO-abbreviation] Curr. Mol. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Netherlands
  • [Number-of-references] 107
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55. Rao SS, O'Neil J, Liberator CD, Hardwick JS, Dai X, Zhang T, Tyminski E, Yuan J, Kohl NE, Richon VM, Van der Ploeg LH, Carroll PM, Draetta GF, Look AT, Strack PR, Winter CG: Inhibition of NOTCH signaling by gamma secretase inhibitor engages the RB pathway and elicits cell cycle exit in T-cell acute lymphoblastic leukemia cells. Cancer Res; 2009 Apr 1;69(7):3060-8
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  • [Title] Inhibition of NOTCH signaling by gamma secretase inhibitor engages the RB pathway and elicits cell cycle exit in T-cell acute lymphoblastic leukemia cells.
  • NOTCH signaling is deregulated in the majority of T-cell acute lymphoblastic leukemias (T-ALL) as a result of activating mutations in NOTCH1.
  • Gamma secretase inhibitors (GSI) block proteolytic activation of NOTCH receptors and may provide a targeted therapy for T-ALL.
  • We have investigated the mechanisms of GSI sensitivity across a panel of T-ALL cell lines, yielding an approach for patient stratification based on pathway activity and also providing a rational combination strategy for enhanced response to GSI.
  • Whereas the NOTCH1 mutation status does not serve as a predictor of GSI sensitivity, a gene expression signature of NOTCH pathway activity does correlate with response, and may be useful in the selection of patients more likely to respond to GSI.
  • Furthermore, inhibition of the NOTCH pathway activity signature correlates with the induction of the cyclin-dependent kinase inhibitors CDKN2D (p19(INK4d)) and CDKN1B (p27(Kip1)), leading to derepression of RB and subsequent exit from the cell cycle.
  • Consistent with this evidence of cell cycle exit, short-term exposure of GSI resulted in sustained molecular and phenotypic effects after withdrawal of the compound.
  • Combination treatment with GSI and a small molecule inhibitor of CDK4 produced synergistic growth inhibition, providing evidence that GSI engagement of the CDK4/RB pathway is an important mechanism of GSI action and supports further investigation of this combination for improved efficacy in treating T-ALL.
  • [MeSH-major] Amyloid Precursor Protein Secretases / antagonists & inhibitors. Cyclic S-Oxides / pharmacology. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Protease Inhibitors / pharmacology. Receptor, Notch1 / antagonists & inhibitors. Retinoblastoma Protein / metabolism. Thiadiazoles / pharmacology
  • [MeSH-minor] Cell Line, Tumor. Cyclin-Dependent Kinase 4 / antagonists & inhibitors. Cyclin-Dependent Kinase Inhibitor p19 / biosynthesis. Cyclin-Dependent Kinase Inhibitor p27. G1 Phase / drug effects. G1 Phase / genetics. Gene Expression Profiling. Humans. Intracellular Signaling Peptides and Proteins / metabolism. Phosphorylation. S Phase / drug effects. S Phase / genetics. Signal Transduction / drug effects. Transcription, Genetic. Transfection

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  • (PMID = 19318552.001).
  • [ISSN] 1538-7445
  • [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 / CDKN1B protein, human; 0 / CDKN2D protein, human; 0 / Cyclic S-Oxides; 0 / Cyclin-Dependent Kinase Inhibitor p19; 0 / Intracellular Signaling Peptides and Proteins; 0 / MRK 003; 0 / NOTCH1 protein, human; 0 / Protease Inhibitors; 0 / Receptor, Notch1; 0 / Retinoblastoma Protein; 0 / Thiadiazoles; 147604-94-2 / Cyclin-Dependent Kinase Inhibitor p27; EC 2.7.11.22 / CDK4 protein, human; EC 2.7.11.22 / Cyclin-Dependent Kinase 4; EC 3.4.- / Amyloid Precursor Protein Secretases
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56. Das SK, Hashimoto T, Kanazawa K: Growth inhibition of human hepatic carcinoma HepG2 cells by fucoxanthin is associated with down-regulation of cyclin D. Biochim Biophys Acta; 2008 Apr;1780(4):743-9
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  • [Title] Growth inhibition of human hepatic carcinoma HepG2 cells by fucoxanthin is associated with down-regulation of cyclin D.
  • Fucoxanthin, a major carotenoid in brown sea algae, has recently been demonstrated by us to inhibit the proliferation of colon cancer cells, and this effect was associated with growth arrest.
  • These results, taken together with previous studies with fucoxanthin, suggest that it may be useful in chemoprevention of other human malignancies.
  • The present study was designed to evaluate the molecular mechanisms of fucoxanthin against hepatic cancer using the human hepatocarcinoma HepG2 cell line (HepG2).
  • This concentration of fucoxanthin inhibited the phosphorylation of the retinoblastoma protein (Rb) at Serine 780 (Ser780) position 18 h after treatment.
  • The kinase activity of cyclin D and cdk4 complex, responsible for the phosphorylation of Rb Ser780 site, was down-regulated 18 h after the treatment.
  • Western blotting analysis revealed that the expression of cyclin D-type protein was suppressed by treatment of fucoxanthin.
  • This reduction was partially blocked by concurrent treatment with the proteasome inhibitor MG132, indicating the involvement of the proteasome-mediated degradation.
  • In addition, RT-PCR analysis revealed that fucoxanthin also appeared to repress cyclin D mRNA.
  • Thus, both the protein degradation and transcriptional repression seem to be responsible for suppressed cyclin D level in fucoxanthin-treated HepG2 cells which may be related to the antitumorgenic activity.
  • [MeSH-major] Cell Proliferation / drug effects. Cyclins / metabolism. Down-Regulation / drug effects. Xanthophylls / pharmacology
  • [MeSH-minor] Blotting, Western. Carcinoma, Hepatocellular / drug therapy. Carcinoma, Hepatocellular / metabolism. Carcinoma, Hepatocellular / pathology. Cell Cycle / drug effects. Cell Line, Tumor. Cyclin D. Cyclin D1 / genetics. Cyclin D1 / metabolism. Cyclin D3. Dose-Response Relationship, Drug. G0 Phase / drug effects. G1 Phase / drug effects. Gene Expression / drug effects. Humans. Hydrolysis / drug effects. Liver Neoplasms / drug therapy. Liver Neoplasms / metabolism. Liver Neoplasms / pathology. Molecular Structure. Phosphorylation / drug effects. RNA, Messenger / genetics. RNA, Messenger / metabolism. Retinoblastoma Protein / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Time Factors

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  • (PMID = 18230364.001).
  • [ISSN] 0006-3002
  • [Journal-full-title] Biochimica et biophysica acta
  • [ISO-abbreviation] Biochim. Biophys. Acta
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / CCND3 protein, human; 0 / Cyclin D; 0 / Cyclin D3; 0 / Cyclins; 0 / RNA, Messenger; 0 / Retinoblastoma Protein; 0 / Xanthophylls; 06O0TC0VSM / fucoxanthin; 136601-57-5 / Cyclin D1
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57. Rutella S, Pierelli L, Rumi C, Bonanno G, Marone M, Sica S, Capoluongo E, Ameglio F, Scambia G, Leone G: T-cell apoptosis induced by granulocyte colony-stimulating factor is associated with retinoblastoma protein phosphorylation and reduced expression of cyclin-dependent kinase inhibitors. Exp Hematol; 2001 Apr;29(4):401-15
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  • [Title] T-cell apoptosis induced by granulocyte colony-stimulating factor is associated with retinoblastoma protein phosphorylation and reduced expression of cyclin-dependent kinase inhibitors.
  • Peripheral blood progenitor cells (PBPC) mobilized by granulocyte colony-stimulating factor (G-CSF) promptly engraft allogeneic recipients after myeloablative chemotherapy for hematologic malignancies.
  • Surprisingly, no exacerbation of acute graft-vs-host disease has been observed despite a 10-fold higher T-cell content in PBPC compared with bone marrow allografts.
  • Because G-CSF can suppress T-cell proliferation in response to mitogens and enhance their activation-induced apoptosis, we examined the molecular mechanisms underlying G-CSF-induced immune dysfunction.
  • Lymphocyte stimulation was associated with collapse of mitochondrial transmembrane potential, hypergeneration of reactive oxygen intermediates, and activation of caspase-3 and DNA fragmentation.
  • Cell tracking experiments confirmed the occurrence of a lower number of population doublings in postG compared with preG cultures.
  • Unexpectedly, the phosphorylation state of the protein encoded by the retinoblastoma susceptibility gene (pRB) was unaltered in postG cultures, and the inhibition of cell cycle progression occurred without the recruitment of the cyclin-dependent kinase inhibitors p15(INK4B), p16(INK4A), and p27(Kip1).
  • Based on these experimental findings, a model is proposed in which T-cell activation in the presence of serum immunoregulatory factor(s) induced by G-CSF is associated with a molecular phenotype mimicking the G(1)-S transition and consisting of pRB phosphorylation, lack of CDKI recruitment, and reduced cyclin-E expression.
  • [MeSH-major] Apoptosis. Cell Cycle Proteins. Cyclin-Dependent Kinases / antagonists & inhibitors. Gene Expression. Granulocyte Colony-Stimulating Factor / pharmacology. Retinoblastoma Protein / metabolism. T-Lymphocytes / physiology. Tumor Suppressor Proteins
  • [MeSH-minor] Acetylcysteine / pharmacology. Adult. Amifostine / pharmacology. Antioxidants / pharmacology. Carrier Proteins / genetics. Caspase 3. Caspases / metabolism. Cell Division. Cyclin-Dependent Kinase Inhibitor p15. Cyclin-Dependent Kinase Inhibitor p16 / genetics. Cyclin-Dependent Kinase Inhibitor p27. DNA Fragmentation. Enzyme Inhibitors. Female. G1 Phase. Humans. Lymphocyte Count. Male. Microtubule-Associated Proteins / genetics. Mitochondria / physiology. Mitochondria / ultrastructure. Phosphorylation. Reactive Oxygen Species / metabolism

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  • (PMID = 11301180.001).
  • [ISSN] 0301-472X
  • [Journal-full-title] Experimental hematology
  • [ISO-abbreviation] Exp. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antioxidants; 0 / CDKN2B protein, human; 0 / Carrier Proteins; 0 / Cell Cycle Proteins; 0 / Cyclin-Dependent Kinase Inhibitor p15; 0 / Cyclin-Dependent Kinase Inhibitor p16; 0 / Enzyme Inhibitors; 0 / Microtubule-Associated Proteins; 0 / Reactive Oxygen Species; 0 / Retinoblastoma Protein; 0 / Tumor Suppressor Proteins; 143011-72-7 / Granulocyte Colony-Stimulating Factor; 147604-94-2 / Cyclin-Dependent Kinase Inhibitor p27; EC 2.7.11.22 / Cyclin-Dependent Kinases; EC 3.4.22.- / CASP3 protein, human; EC 3.4.22.- / Caspase 3; EC 3.4.22.- / Caspases; M487QF2F4V / Amifostine; WYQ7N0BPYC / Acetylcysteine
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58. Lei N, Shen FB, Chang JH, Wang L, Li H, Yang C, Li J, Yu DC: An oncolytic adenovirus expressing granulocyte macrophage colony-stimulating factor shows improved specificity and efficacy for treating human solid tumors. Cancer Gene Ther; 2009 Jan;16(1):33-43
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  • [Title] An oncolytic adenovirus expressing granulocyte macrophage colony-stimulating factor shows improved specificity and efficacy for treating human solid tumors.
  • To study the tumor specificity and antitumor activity of the replication-competent oncolytic adenovirus TOA02, which is controlled by a modified human telomerase reverse transcriptase (hTERT) promoter and expresses granulocyte macrophage colony-stimulating factor (GM-CSF).
  • The wild-type hTERT promoter was modified, by inserting two E2F-binding sites.
  • The effect of the modified hTERT on the viral yield and cytotoxicity of TOA02 were determined in vitro with a panel of tumor cells and normal cells, to evaluate tumor specificity; the effect on the antitumor efficacy and toxicity of TOA02 were determined in vivo, to evaluate the therapeutic potential of the adenovirus.
  • The TOA02 adenovirus, which contained the modified hTERT promoter, produced a higher yield of virus in telomerase-positive and retinoblastoma-defective human cells, and a lower yield of virus in normal human cells than the wild-type adenovirus.
  • A single injection of TOA02 showed strong antitumor efficacy in nude mice with human head/neck and hepatocellular carcinoma xenografts, and the efficacy further improved when used in combination with chemotherapy and with different routes of administration and regimens.
  • In immunocompetent mice, the addition of GM-CSF produced a stronger antitumor activity and induced more mature dendritic cells and macrophages.
  • The TOA02 adenovirus showed strong tumor-cell selectivity in vitro and antitumor efficacy in mouse models of human head/neck and hepatocellular cancer, suggesting that TOA02 has potential clinical applications for the treatment of solid tumors.
  • [MeSH-major] Adenoviridae. Granulocyte-Macrophage Colony-Stimulating Factor / biosynthesis. Neoplasms / therapy. Oncolytic Virotherapy. Oncolytic Viruses
  • [MeSH-minor] Animals. Cell Line, Tumor. Female. Humans. Mice. Mice, Nude. Neoplasm Transplantation. Response Elements / genetics. Telomerase / genetics

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  • (PMID = 18670453.001).
  • [ISSN] 1476-5500
  • [Journal-full-title] Cancer gene therapy
  • [ISO-abbreviation] Cancer Gene Ther.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 83869-56-1 / Granulocyte-Macrophage Colony-Stimulating Factor; EC 2.7.7.49 / TERT protein, human; EC 2.7.7.49 / Telomerase
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59. Michaud K, Solomon DA, Oermann E, Kim JS, Zhong WZ, Prados MD, Ozawa T, James CD, Waldman T: Pharmacologic inhibition of cyclin-dependent kinases 4 and 6 arrests the growth of glioblastoma multiforme intracranial xenografts. Cancer Res; 2010 Apr 15;70(8):3228-38
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  • [Title] Pharmacologic inhibition of cyclin-dependent kinases 4 and 6 arrests the growth of glioblastoma multiforme intracranial xenografts.
  • Activation of cyclin-dependent kinases 4 and 6 (cdk4/6) occurs in the majority of glioblastoma multiforme (GBM) tumors, and represents a promising molecular target for the development of small molecule inhibitors.
  • In the current study, we investigated the molecular determinants and in vivo response of diverse GBM cell lines and xenografts to PD-0332991, a cdk4/6-specific inhibitor.
  • In vitro testing of PD-0332991 against a panel of GBM cell lines revealed a potent G(1) cell cycle arrest and induction of senescence in each of 16 retinoblastoma protein (Rb)-proficient cell lines regardless of other genetic lesions, whereas 5 cell lines with homozygous inactivation of Rb were completely resistant to treatment.
  • Short hairpin RNA depletion of Rb expression conferred resistance of GBM cells to PD-0332991, further demonstrating a requirement of Rb for sensitivity to cdk4/6 inhibition.
  • PD-0332991 was found to efficiently cross the blood-brain barrier and proved highly effective in suppressing the growth of intracranial GBM xenograft tumors, including those that had recurred after initial therapy with temozolomide.
  • Remarkably, no mice receiving PD-0332991 died as a result of disease progression while on therapy.
  • Additionally, the combination of PD-0332991 and radiation therapy resulted in significantly increased survival benefit compared with either therapy alone.
  • In total, our results support clinical trial evaluation of PD-0332991 against newly diagnosed as well as recurrent GBM, and indicate that Rb status is the primary determinant of potential benefit from this therapy.

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  • [Copyright] (c) 2010 AACR.
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  • (PMID = 20354191.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P30 CA016672; United States / NCI NIH HHS / CA / R01 CA115699-04; United States / NCI NIH HHS / CA / CA115699-05; United States / NCI NIH HHS / CA / R01 CA159467; United States / NCI NIH HHS / CA / R01 CA115699-05; United States / NCI NIH HHS / CA / P50 CA097257; United States / NCI NIH HHS / CA / CA115699; United States / NCI NIH HHS / CA / CA115699-04; United States / NCI NIH HHS / CA / CA097257; United States / NCI NIH HHS / CA / R01 CA115699
  • [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 / Piperazines; 0 / Pyridines; 0 / Retinoblastoma Protein; EC 2.7.11.22 / Cyclin-Dependent Kinase 4; EC 2.7.11.22 / Cyclin-Dependent Kinase 6; G9ZF61LE7G / palbociclib
  • [Other-IDs] NLM/ NIHMS183898; NLM/ PMC2855904
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60. Demir G, Belentepe S, Ozguroglu M, Celik AF, Sayhan N, Tekin S, Mandel NM, Buyukunal E, Serdengecti S: Simultaneous presentation of hepatocellular carcinoma in identical twin brothers. Med Oncol; 2002;19(2):113-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • We report hepatocellular carcinoma (HCC) diagnosed at the same time in identical twin brothers.
  • Serological analyses of the patients showed that both were chronically infected with HBV.
  • Molecular analyses of the tumor specimens confirmed loss of heterozygocity of the Rb gene region.
  • Both of the patients were unresponsive to chemotherapy and died within the same month with an interval of I wk.
  • With a review of the current literature, we discuss the role of HBV infection and genetic factors on hepatic carcinogenesis.
  • [MeSH-major] Carcinoma, Hepatocellular / genetics. Hepatitis B, Chronic / complications. Liver Neoplasms / genetics. Twins, Monozygotic / genetics
  • [MeSH-minor] Antineoplastic Agents / therapeutic use. Fatal Outcome. Humans. Male. Middle Aged. Risk Factors

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  • (PMID = 12180479.001).
  • [ISSN] 1357-0560
  • [Journal-full-title] Medical oncology (Northwood, London, England)
  • [ISO-abbreviation] Med. Oncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents
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61. Gregorc V, Ludovini V, Pistola L, Darwish S, Floriani I, Bellezza G, Sidoni A, Cavaliere A, Scheibel M, De Angelis V, Bucciarelli E, Tonato M: Relevance of p53, bcl-2 and Rb expression on resistance to cisplatin-based chemotherapy in advanced non-small cell lung cancer. Lung Cancer; 2003 Jan;39(1):41-8
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  • [Title] Relevance of p53, bcl-2 and Rb expression on resistance to cisplatin-based chemotherapy in advanced non-small cell lung cancer.
  • PURPOSE: Tumors with p53 overexpression have been associated with enhanced resistance to cisplatin-based chemotherapy in a few and small studies involving non-small cell lung cancer.
  • The relationships and interactions between p53, Rb and bcl-2 immunostaining, clinical parameters and response to cisplatin-based chemotherapy were evaluated in the present study.
  • EXPERIMENTAL DESIGN: Histological specimens obtained by bronchial or fine-needle biopsy from patients who underwent cisplatin-based chemotherapy between 1992 and 1999 were evaluated by immunostaining.
  • Median age was 63 years; 47 had stage III and 55 stage IV disease.
  • Forty-six tumor samples (45%) had positive immunostaining for p53, 61 (59%) had negative immunostaining for Rb and 8 (8%) had positive immunostaining for bcl-2.
  • The response rate of the group with p53 positive immunostaining was 26% versus 57% of the p53 negative group (P=0.004).
  • In multivariate analyses p53 positive immunostaining was identified as an independent predictive factor for resistance to cisplatin-based chemotherapy (P=0.006).
  • CONCLUSIONS: Our study confirmed an association of p53 immunostaining and response rate of patients treated with cisplatin-based chemotherapy.
  • [MeSH-major] Carcinoma, Non-Small-Cell Lung / drug therapy. Cisplatin / pharmacology. Cisplatin / therapeutic use. Drug Resistance, Neoplasm. Lung Neoplasms / drug therapy. Proto-Oncogene Proteins c-bcl-2 / metabolism. Retinoblastoma Protein / metabolism. Tumor Suppressor Protein p53 / metabolism
  • [MeSH-minor] Female. Gene Expression Regulation, Neoplastic. Humans. Male. Middle Aged. Neoplasm Staging. Prognosis. Smoking


62. Gutiérrez NC, Castellanos MV, Martín ML, Mateos MV, Hernández JM, Fernández M, Carrera D, Rosiñol L, Ribera JM, Ojanguren JM, Palomera L, Gardella S, Escoda L, Hernández-Boluda JC, Bello JL, de la Rubia J, Lahuerta JJ, San Miguel JF, GEM/PETHEMA Spanish Group: Prognostic and biological implications of genetic abnormalities in multiple myeloma undergoing autologous stem cell transplantation: t(4;14) is the most relevant adverse prognostic factor, whereas RB deletion as a unique abnormality is not associated with adverse prognosis. Leukemia; 2007 Jan;21(1):143-50
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  • [Title] Prognostic and biological implications of genetic abnormalities in multiple myeloma undergoing autologous stem cell transplantation: t(4;14) is the most relevant adverse prognostic factor, whereas RB deletion as a unique abnormality is not associated with adverse prognosis.
  • However, the existence of associations between cytogenetic abnormalities compels us to re-assess the value of each abnormality.
  • A total of 260 patients with MM at the time of diagnosis, enrolled in the GEM-2000 Spanish transplant protocol, have been analyzed by FISH in order to ascertain the independent influence on myeloma prognosis of IGH translocations, as well as RB and P53 deletions.
  • Survival analyses showed that patients with t(4;14), RB or P53 deletions had a significantly shorter survival than patients without these abnormalities.
  • However, patients with RB deletions without other abnormalities in FISH analysis, displayed a similar outcome to those patients without genetic changes by FISH (46 vs 54 months, P=0.3).
  • In the multivariate analysis the presence of t(4;14), RB deletion associated with other abnormalities, age >60 years, high proportion of S-phase cells and advanced stage of the disease according to the International Staging System retained their independent prognostic influence.
  • In summary, RB deletion as a sole abnormality does not lead to a shortening in the survival of MM patients, whereas t(4;14) confers the worst prognosis in MM patients treated with high-dose chemotherapy.
  • [MeSH-major] Chromosomes, Human, Pair 14. Chromosomes, Human, Pair 4. Gene Deletion. Genes, Retinoblastoma. Multiple Myeloma. Stem Cell Transplantation. Translocation, Genetic
  • [MeSH-minor] Adult. Aged. Female. Humans. Male. Middle Aged. Multivariate Analysis. Prognosis. Survival Analysis. Transplantation, Autologous


63. Vrabie CD, Petrescu A, Waller M: Molecular changes in superficial bladder cancer. Rom J Morphol Embryol; 2007;48(2):131-8
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  • [Title] Molecular changes in superficial bladder cancer.
  • Urinary bladder cancers represent a spectrum of diseases that can be grouped into three general categories: superficial, invasive and metastasis.
  • Each differs in clinical behavior, prognosis and primary management.
  • For superficial tumors, the aim is to prevent recurrences and progression to an incurable stage, recognizing that surgical removal of the bladder (over treatment for most tumors) is curative up to a point.
  • For more invasive disease, the issue becomes how to determine which tumors can be cured with a single therapy such as surgery, and which, by virtue of a high metastatic potential, requires an integrated systemic approach to achieve cure.
  • For metastatic disease, combination chemotherapy is the standard yet, despite responses in more than 50% of cases, overall cure rates remain low, and progression has been minimal over the past few years.
  • We analyzed histopathological and immunohistochemical 70 patients with bladder carcinomas searching the stage, the grade and other associated lesions.
  • The results showed that 70% were papillary transitional carcinomas infiltrated in lamina propria (T1), and almost 22.85% represent non-invasive papillary carcinomas (Ta); we found only five cases in Tis stage (7.15%).
  • The immunohistochemistry investigated three antibodies: p53 oncoprotein, bcl-2 oncoprotein and retinoblastoma protein (pRb).
  • We noticed the antibodies distribution related to stage: carcinoma in situ (Cis or Tis) high percent of p53 (69) and bcl-2 (37.5%).
  • Concerning the superficial tumors we found low values of p53 in T1 (45%) versus invasive tumors (51%); oncoprotein bcl-2 is higher in T1 (35%) versus non-invasive one (6%).
  • [MeSH-major] Carcinoma in Situ / diagnosis. Carcinoma in Situ / metabolism. Urinary Bladder Neoplasms / diagnosis. Urinary Bladder Neoplasms / metabolism
  • [MeSH-minor] Adult. Age Distribution. Aged. Aged, 80 and over. Disease Progression. Female. Humans. Male. Middle Aged. Molecular Diagnostic Techniques. Neoplasm Staging. Proto-Oncogene Proteins c-bcl-2 / metabolism. Retinoblastoma Protein / metabolism. Sex Distribution. Tumor Suppressor Protein p53 / metabolism

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  • (PMID = 17641799.001).
  • [ISSN] 1220-0522
  • [Journal-full-title] Romanian journal of morphology and embryology = Revue roumaine de morphologie et embryologie
  • [ISO-abbreviation] Rom J Morphol Embryol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Romania
  • [Chemical-registry-number] 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Retinoblastoma Protein; 0 / Tumor Suppressor Protein p53
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64. Weintraub M, Revel-Vilk S, Charit M, Aker M, Pe'er J: Secondary acute myeloid leukemia after etoposide therapy for retinoblastoma. J Pediatr Hematol Oncol; 2007 Sep;29(9):646-8
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  • [Title] Secondary acute myeloid leukemia after etoposide therapy for retinoblastoma.
  • Retinoblastoma is the most common eye tumor in children and is highly curable.
  • Patients with hereditary retinoblastoma, have an increased risk of developing additional tumors, predominantly sarcomas.
  • Most chemotherapy regimens used in retinoblastoma include etoposide, an epipodophyllotoxin associated with a risk of secondary myeloid leukemia.
  • The use of etoposide in patients with a cance