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1. Kunwar S, Mohapatra G, Bollen A, Lamborn KR, Prados M, Feuerstein BG: Genetic subgroups of anaplastic astrocytomas correlate with patient age and survival. Cancer Res; 2001 Oct 15;61(20):7683-8
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  • Astrocytomas are brain tumors with variable responses to radiation and chemotherapy.
  • Tumor grade and patient age are important prognostic factors but do not account for the variability in clinical outcome.
  • We hypothesized that genetic subgroups play a role in the outcome of grade III astrocytomas and studied 80 grade III astrocytomas by comparative genomic hybridization.
  • Some chromosomal aberrations (+7p/q, -9p, -10q, -13q, +19q) were related to aberrations that are frequent in grade IV astrocytoma, whereas others (+10p, -11q, +11p, -Xq) were more frequent in grade III astrocytoma.
  • Our results indicate that genetic events underlie the well-known effects of age on survival in grade III astrocytoma and demonstrate the importance of molecular classification in astrocytic tumors.
  • [MeSH-major] Astrocytoma / genetics. Brain Neoplasms / genetics
  • [MeSH-minor] Adolescent. Adult. Age Factors. Child. Child, Preschool. Chromosome Aberrations. Chromosome Disorders. Disease Progression. Female. Gene Dosage. Glioblastoma / genetics. Humans. Infant. Male. Middle Aged. Neoplasm Recurrence, Local / genetics. Nucleic Acid Hybridization. Prognosis. Survival Rate

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  • (PMID = 11606412.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA-13525; United States / NCI NIH HHS / CA / CA64877; United States / NCI NIH HHS / CA / CA64898
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
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2. Boon K, Edwards JB, Eberhart CG, Riggins GJ: Identification of astrocytoma associated genes including cell surface markers. BMC Cancer; 2004 Jul 21;4:39
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  • [Title] Identification of astrocytoma associated genes including cell surface markers.
  • BACKGROUND: Despite intense effort the treatment options for the invasive astrocytic tumors are still limited to surgery and radiation therapy, with chemotherapy showing little or no increase in survival.
  • The generation of Serial Analysis of Gene Expression (SAGE) profiles is expected to aid in the identification of astrocytoma-associated genes and highly expressed cell surface genes as molecular therapeutic targets.
  • METHODS: We generated and analyzed the SAGE transcription profiles of 25 primary grade II, III and IV astrocytomas 1.
  • These profiles were produced as part of the Cancer Genome Anatomy Project's SAGE Genie 2, and were used in an in silico search for candidate therapeutic targets by comparing astrocytoma to normal brain transcription.
  • Real-time PCR and immunohistochemistry were used for the validation of selected candidate target genes in 2 independent sets of primary tumors.
  • RESULTS: A restricted set of tumor-associated genes was identified for each grade that included genes not previously associated with astrocytomas (e.g.
  • CONCLUSIONS: This survey of transcription in malignant and normal brain tissues reveals a small subset of human genes that are activated in malignant astrocytomas.
  • In addition to providing insights into pathway biology, we have revealed and quantified expression for a significant portion of cell surface and extra-cellular astrocytoma genes.

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  • (PMID = 15265232.001).
  • [ISSN] 1471-2407
  • [Journal-full-title] BMC cancer
  • [ISO-abbreviation] BMC Cancer
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / U01 CA088128; United States / NCI NIH HHS / CA / U01 CA88128
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Membrane Proteins
  • [Other-IDs] NLM/ PMC497045
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3. Koukourakis MI, Koukouraki S, Fezoulidis I, Kelekis N, Kyrias G, Archimandritis S, Karkavitsas N: High intratumoural accumulation of stealth liposomal doxorubicin (Caelyx) in glioblastomas and in metastatic brain tumours. Br J Cancer; 2000 Nov;83(10):1281-6
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  • [Title] High intratumoural accumulation of stealth liposomal doxorubicin (Caelyx) in glioblastomas and in metastatic brain tumours.
  • The blood-brain barrier is a major obstacle for the chemotherapeutic drugs to effectively reach primary or secondary brain tumours.
  • Stealth liposomal drugs are highly accumulated in tumoural tissues.
  • In the present study we investigated the relative accumulation of(99m)Tc-DTPA radiolabelled stealth liposomal doxorubicin (Caelyx) in 10 patients with metastatic brain tumours and five patients with brain glioblastoma undergoing radiotherapy.
  • Patients with metastatic brain lesions were treated with 10 consecutive fractions of radiotherapy (whole brain, 3 Gy/fraction, day 1-12) followed by a booster dose of 9 Gy (3 Gy/fraction, day 21-23).
  • Radiolabelled Caelyx accumulation was 13-19 times higher in the glioblastomas and 7-13 times higher in the metastatic lesions, as compared to the normal brain.
  • The drug accumulation in the tumoural areas was 40-60% of the accumulation in the bone marrow of the skull bones.
  • The normal brain radioactivity was <4% of the bone marrow, confirming an important shielding effect of the blood-brain barrier in the normal but not in the tumoural tissue.
  • Four of 10 patients with metastatic lesions showed a complete response in CT-scan performed 2 months following therapy.
  • There was no severe toxicity related to radiotherapy or to chemotherapy noted.
  • It is concluded that stealth liposomal drugs selectively overcome the blood-brain barrier in the tumoural areas.
  • [MeSH-major] Antineoplastic Agents / administration & dosage. Antineoplastic Agents / pharmacokinetics. Brain Neoplasms / drug therapy. Doxorubicin / administration & dosage. Doxorubicin / pharmacokinetics. Glioblastoma / drug therapy
  • [MeSH-minor] Adult. Blood-Brain Barrier. Bone Marrow / chemistry. Humans. Liposomes. Radiopharmaceuticals. Skull / chemistry. Technetium Tc 99m Pentetate. Tissue Distribution

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  • [Copyright] Copyright 2000 Cancer Research Campaign.
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  • (PMID = 11044350.001).
  • [ISSN] 0007-0920
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] SCOTLAND
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Liposomes; 0 / Radiopharmaceuticals; 80168379AG / Doxorubicin; VW78417PU1 / Technetium Tc 99m Pentetate
  • [Other-IDs] NLM/ PMC2408790
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4. Lefranc F, Rynkowski M, DeWitte O, Kiss R: Present and potential future adjuvant issues in high-grade astrocytic glioma treatment. Adv Tech Stand Neurosurg; 2009;34:3-35
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  • [Title] Present and potential future adjuvant issues in high-grade astrocytic glioma treatment.
  • Despite major advances in the management of malignant gliomas of which glioblastomas represent the ultimate grade of malignancy, they remain characterized by dismal prognoses.
  • Glioblastoma patients have a median survival expectancy of only 14 months on the current standard treatment of surgical resection to the extent feasible, followed by adjuvant radiotherapy plus temozolomide, given concomitantly with and after radiotherapy.
  • Malignant gliomas are associated with such dismal prognoses because glioma cells can actively migrate through the narrow extra-cellular spaces in the brain, often travelling relatively long distances, making them elusive targets for effective surgical management.
  • Clinical and experimental data have demonstrated that invasive malignant glioma cells show a decrease in their proliferation rates and a relative resistance to apoptosis (type I programmed cell death) as compared to the highly cellular centre of the tumor, and this may contribute to their resistance to conventional pro-apoptotic chemotherapy and radiotherapy.
  • Monoclonal antibodies and low molecular-weight kinase inhibitors of these pathways are the most common classes of agents in targeted cancer treatment.
  • Despite resistance to apoptosis being closely linked to tumorigenesis, tumor cells can still be induced to die by non-apoptotic mechanisms such as necrosis, senescence, autophagy (type II programmed cell death) and mitotic catastrophe.
  • Temozolomide brings significant therapeutic benefits in glioblastoma treatment.
  • Autophagy, type II programmed cell death, represents an alternative mechanism to overcome, at least partly, the dramatic resistance of many cancers to pro-apoptotic-related therapies.
  • Another way to potentially overcome apoptosis resistance is to decrease the migration of malignant glioma cells in the brain, which then should restore a level of sensitivity to pro-apoptotic drugs.
  • The present chapter focuses on (i) the major signaling pathways making glioblastomas resistant to apoptosis, (ii) the signaling pathways distinctly activated by pro-autophagic drugs as compared to pro-apoptotic ones, (iii) autophagic cell death as an alternative to combat malignant gliomas, (iv) the major scientific data already obtained by researchers to prove that temozolomide is actually a pro-autophagic and pro-apoptotic drug, (v) the molecular and cellular therapies and local drug delivery which could be used to complement conventional treatments, and a review of some of the currently ongoing clinical trials, (vi) the fact that reducing the levels of malignant glioma cell motility can restore pro-apoptotic drug sensitivity, (vii) the observation that inhibiting the sodium pump activity reduces both glioma cell proliferation and migration, (viii) the brain tumor stem cells as a target to complement conventional treatment.
  • [MeSH-major] Astrocytoma / pathology. Astrocytoma / therapy. Brain Neoplasms / pathology. Brain Neoplasms / therapy
  • [MeSH-minor] Antineoplastic Agents / therapeutic use. Autophagy. Biological Therapy. Combined Modality Therapy. Humans. Immunity, Innate. Neurosurgical Procedures


5. Hofer S, Herrmann R: Chemotherapy for malignant brain tumors of astrocytic and oligodendroglial lineage. J Cancer Res Clin Oncol; 2001 Feb;127(2):91-5
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  • [Title] Chemotherapy for malignant brain tumors of astrocytic and oligodendroglial lineage.
  • To date, surgery and irradiation remain the standard therapies for anaplastic astrocytoma (AA, WHO grade III) and glioblastoma multiforme (GBM, WHO grade IV).
  • Due to infiltrative tumor growth a complete surgical resection is never achieved and more than 90% of the tumors will recur within 2 cm of the primary tumor location.
  • Postoperative radiotherapy prolongs survival but is not curative and prognosis remains poor with only a few patients being alive 2 years after diagnosis.
  • Over the past decades multiple trials dealt with the question of whether chemotherapy (CT) may influence the outcome of malignant brain tumor patients.
  • Drugs showing some activity in malignant brain tumors and therapeutic concepts will be discussed.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Astrocytoma / drug therapy. Brain Neoplasms / drug therapy. Oligodendroglioma / drug therapy
  • [MeSH-minor] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Humans. Prognosis

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  • (PMID = 11216919.001).
  • [ISSN] 0171-5216
  • [Journal-full-title] Journal of cancer research and clinical oncology
  • [ISO-abbreviation] J. Cancer Res. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  • [Number-of-references] 29
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6. Stukel JM, Caplan MR: Targeted drug delivery for treatment and imaging of glioblastoma multiforme. Expert Opin Drug Deliv; 2009 Jul;6(7):705-18
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  • [Title] Targeted drug delivery for treatment and imaging of glioblastoma multiforme.
  • Glioblastoma multiforme is a grade IV astrocytic tumor with a very high mortality rate.
  • Although current treatment often includes surgical resection, this rarely removes all primary tumor cells, so is usually followed by radiation and/or chemotherapy.
  • Remaining migratory tumor cells invade surrounding healthy tissue and contribute to secondary and tertiary tumor recurrence; therefore, despite significant research into glioma removal and treatment, prognosis remains poor.
  • A variety of treatment modalities have been investigated to deliver drug to these cells, including systemic, diffusive and convection-enhanced delivery (CED).
  • As systemic delivery is limited by molecules larger than approximately 500 Da being unable to cross the blood-brain barrier (BBB), therapeutic concentrations are difficult to attain; thus, localized delivery options relying on diffusion and CED have been used to circumvent the BBB.
  • Although CED enables delivery to a greater volume of tissue than diffusive delivery alone, limitations still exist, requiring that these delivery strategies be improved.
  • [MeSH-major] Antineoplastic Agents / administration & dosage. Drug Delivery Systems. Glioblastoma / drug therapy
  • [MeSH-minor] Animals. Blood-Brain Barrier / metabolism. Combined Modality Therapy. Humans. Models, Theoretical. Tissue Distribution

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  • (PMID = 19538036.001).
  • [ISSN] 1744-7593
  • [Journal-full-title] Expert opinion on drug delivery
  • [ISO-abbreviation] Expert Opin Drug Deliv
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  • [Number-of-references] 118
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7. Chen YL, Jian MH, Lin CC, Kang JC, Chen SP, Lin PC, Hung PJ, Chen JR, Chang WL, Lin SZ, Harn HJ: The induction of orphan nuclear receptor Nur77 expression by n-butylenephthalide as pharmaceuticals on hepatocellular carcinoma cell therapy. Mol Pharmacol; 2008 Oct;74(4):1046-58
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  • [Title] The induction of orphan nuclear receptor Nur77 expression by n-butylenephthalide as pharmaceuticals on hepatocellular carcinoma cell therapy.
  • N-butylidenephthalide (BP), isolated from the chloroform extract of Angelica sinensis, has been examined for its antitumor effects on glioblastoma multiforme brain tumors; however, little is known about its antitumor effects on hepatocellular carcinoma cells.
  • N-butylidenephthalide-related tumor apoptosis was associated with phosphatidylinositol 3-kinase/protein kinase B (AKT)/glycogen synthase kinase-3beta rather than the mitogen-activated protein kinase or protein kinase C pathway.
  • Besides, the increasing apoptosis by BP via transfection wild-type cAMP-response element-binding protein (CREB) into tumor cell was suppressed by dominant phosphorylation site mutation of CREB.
  • This finding suggested CREB pathway was also partly involved in tumor apoptosis caused by BP.
  • [MeSH-major] Angelica sinensis / chemistry. Carcinoma, Hepatocellular / drug therapy. DNA-Binding Proteins / metabolism. Drugs, Chinese Herbal / pharmacology. Liver Neoplasms / drug therapy. Phthalic Anhydrides / pharmacology. Receptors, Steroid / metabolism
  • [MeSH-minor] Apoptosis / drug effects. Cell Line, Tumor. Cell Survival / drug effects. Humans. Nuclear Receptor Subfamily 4, Group A, Member 1

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  • (PMID = 18577687.001).
  • [ISSN] 1521-0111
  • [Journal-full-title] Molecular pharmacology
  • [ISO-abbreviation] Mol. Pharmacol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / Drugs, Chinese Herbal; 0 / NR4A1 protein, human; 0 / Nuclear Receptor Subfamily 4, Group A, Member 1; 0 / Phthalic Anhydrides; 0 / Receptors, Steroid; 0 / angelicae sinensis extract; S9178G4B3F / butylidenephthalide
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8. Łata S, Molczyk A: [Side effects of temozolomide treatment in patient with glioblastoma multiforme--case study]. Przegl Lek; 2010;67(5):445-6
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  • [Title] [Side effects of temozolomide treatment in patient with glioblastoma multiforme--case study].
  • In case study, we presented patient with glioblastoma multiforme-brain tumor-grade IV-WHO.
  • Patient after surgery, followed by radiotherapy and chemotherapy, after cycles of chemotherapy with temozolomid.
  • During therapy with temozolomid, it is recommended to check morphology on the 22nd day of cycle.
  • [MeSH-major] Antineoplastic Agents, Alkylating / adverse effects. Brain Neoplasms / drug therapy. Dacarbazine / analogs & derivatives. Glioblastoma / drug therapy. Nervous System Diseases / chemically induced. Pancytopenia / chemically induced
  • [MeSH-minor] Chemotherapy, Adjuvant. Female. Humans. Middle Aged. Radiotherapy, Adjuvant

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  • (PMID = 20684359.001).
  • [ISSN] 0033-2240
  • [Journal-full-title] Przegla̧d lekarski
  • [ISO-abbreviation] Prz. Lek.
  • [Language] pol
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 7GR28W0FJI / Dacarbazine; 85622-93-1 / temozolomide
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9. Hagemann C, Gloger J, Anacker J, Said HM, Gerngras S, Kühnel S, Meyer C, Rapp UR, Kämmerer U, Vordermark D, Flentje M, Roosen K, Vince GH: RAF expression in human astrocytic tumors. Int J Mol Med; 2009 Jan;23(1):17-31
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  • [Title] RAF expression in human astrocytic tumors.
  • Malignant gliomas are the most prevalent primary brain tumors of adults.
  • They are highly invasive and very difficult to treat, despite of surgery, gamma-irradiation and chemotherapy.
  • Although a role of the mitogenic Ras-RAF-MEK-ERK signalling cascade in brain tumor development is well established, there are only few reports available addressing alterations in RAF sequence or protein expression and function in human gliomas.
  • Then we checked for RAF gene amplification by dot blot hybridization and examined RAF mRNA and protein expression patterns in human astrocytic gliomas of WHO grade II (LGA) and IV (GBM) by semiquantitative RT-PCR and Western blotting, respectively.
  • We showed that RAF mutations are a rare event in glioblastoma multiforme.
  • Our data indicate that RAF proteins might be valuable targets for small molecule therapies.
  • [MeSH-major] Astrocytoma / genetics. Glioblastoma / genetics. Proto-Oncogene Proteins A-raf / genetics. Proto-Oncogene Proteins B-raf / genetics. Proto-Oncogene Proteins c-raf / genetics
  • [MeSH-minor] Cell Line, Tumor. Cell Movement. Cell Proliferation. Gene Expression Regulation. Humans. Mutant Proteins / genetics. Prognosis. RNA, Messenger / genetics. Sequence Analysis, DNA

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  • (PMID = 19082503.001).
  • [ISSN] 1107-3756
  • [Journal-full-title] International journal of molecular medicine
  • [ISO-abbreviation] Int. J. Mol. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Mutant Proteins; 0 / RNA, Messenger; EC 2.7.11.1 / Proto-Oncogene Proteins A-raf; EC 2.7.11.1 / Proto-Oncogene Proteins B-raf; EC 2.7.11.1 / Proto-Oncogene Proteins c-raf
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10. Lin CC, Chen JT, Yang JS, Lu HF, Hsu SC, Tan TW, Lin YT, Ma YS, Ip SW, Wu JJ, Li YC, Chung JG: Danthron inhibits the migration and invasion of human brain glioblastoma multiforme cells through the inhibition of mRNA expression of focal adhesion kinase, Rho kinases-1 and metalloproteinase-9. Oncol Rep; 2009 Nov;22(5):1033-7
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  • [Title] Danthron inhibits the migration and invasion of human brain glioblastoma multiforme cells through the inhibition of mRNA expression of focal adhesion kinase, Rho kinases-1 and metalloproteinase-9.
  • In this study, we investigated the effect of danthron on the cell migration and invasion of human brain glioblastoma multiforme GBM 8401 cells in vitro.
  • The changes of migration and invasion of GBM 8401 cells after treatment with danthron were detected by cell migration assay and cell invasion assay.
  • The levels of mRNA gene expression associated with cell migration and invasion were detected by real-time PCR.
  • Results indicated that human brain glioblastoma multiforme GBM 8401 cells treated with danthron in vitro migrated and invaded less than cells treated with phosphate-buffered saline (PBS) (control).
  • Real-time PCR assay also showed that danthron inhibited the mRNA expression of matrix metalloproteinase-9 (MMP-9), FAK and ROCK-1 of GBM 8401 cells.
  • Thus, danthron may be considered a therapeutic agent that can inhibit primary tumor growth and prevent metastasis.
  • [MeSH-major] Anthraquinones / pharmacology. Cell Movement / drug effects. Focal Adhesion Kinase 1 / genetics. Gene Expression Regulation, Neoplastic / drug effects. Glioblastoma / drug therapy. Matrix Metalloproteinase 9 / genetics. rho-Associated Kinases / genetics
  • [MeSH-minor] Blotting, Western. Brain Neoplasms / drug therapy. Brain Neoplasms / genetics. Brain Neoplasms / pathology. Cell Adhesion / drug effects. Humans. Mutagens / pharmacology. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Tumor Cells, Cultured

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  • (PMID = 19787217.001).
  • [ISSN] 1021-335X
  • [Journal-full-title] Oncology reports
  • [ISO-abbreviation] Oncol. Rep.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Anthraquinones; 0 / Mutagens; 0 / RNA, Messenger; EC 2.7.10.2 / Focal Adhesion Kinase 1; EC 2.7.10.2 / PTK2 protein, human; EC 2.7.11.1 / rho-Associated Kinases; EC 3.4.24.35 / Matrix Metalloproteinase 9; Z4XE6IBF3V / danthron
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11. Peca C, Pacelli R, Elefante A, Del Basso De Caro ML, Vergara P, Mariniello G, Giamundo A, Maiuri F: Early clinical and neuroradiological worsening after radiotherapy and concomitant temozolomide in patients with glioblastoma: tumour progression or radionecrosis? Clin Neurol Neurosurg; 2009 May;111(4):331-4
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  • [Title] Early clinical and neuroradiological worsening after radiotherapy and concomitant temozolomide in patients with glioblastoma: tumour progression or radionecrosis?
  • OBJECTIVES: This study investigates the diagnosis and management of patients with resected brain glioblastomas who presented early clinical and neuroradiological worsening after the completion of the Stupp protocol.
  • METHODS: Fifty patients with brain glioblastoma treated by surgical resection and Stupp protocol were reviewed; 15 among them (30%) had early clinical and neuroradiological worsening at the 6-month follow-up.
  • A correct diagnosis is necessary to avoid useless reoperations and incorrect withdrawal of temozolomide.
  • [MeSH-major] Antineoplastic Agents, Alkylating / therapeutic use. Brain Neoplasms / drug therapy. Brain Neoplasms / radiotherapy. Dacarbazine / analogs & derivatives. Glioblastoma / drug therapy. Glioblastoma / radiotherapy. Neoplasm Recurrence, Local / diagnosis. Radiation Injuries / diagnosis. Radiation Tolerance / drug effects
  • [MeSH-minor] Adult. Aged. Ataxia / etiology. Chemotherapy, Adjuvant. Confusion / etiology. Diagnosis, Differential. Female. Follow-Up Studies. Humans. Magnetic Resonance Spectroscopy. Male. Middle Aged. Necrosis. Radiotherapy, Adjuvant. Reoperation. Treatment Outcome

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  • (PMID = 19117668.001).
  • [ISSN] 1872-6968
  • [Journal-full-title] Clinical neurology and neurosurgery
  • [ISO-abbreviation] Clin Neurol Neurosurg
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 7GR28W0FJI / Dacarbazine; 85622-93-1 / temozolomide
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12. Varveris H, Petinelli E, Stratakis J, Mazonakis M: Phase I study of weekly topotecan combined to concurrent external cranial irradiation in adults with glioblastoma multiforme of the brain. Oncol Rep; 2008 Feb;19(2):447-55
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  • [Title] Phase I study of weekly topotecan combined to concurrent external cranial irradiation in adults with glioblastoma multiforme of the brain.
  • Although the standard of care for patients with glioblastoma multiforme (GM) remains postoperative radiotherapy (RT) in combination with chemotherapy (CT), the optimal regimen awaits verification.
  • A phase I study was performed to determine the dose limiting toxicity (DLT) and the maximum tolerated dose (MTD) of topotecan (Hycamptin), given concurrently with RT, in patients with previously untreated glioblastoma multiforme (GM) of the brain.
  • After surgery or stereotactic biopsy, patients received conventional external cranial RT (59.4 Gy/33 fractions in 6.6 weeks).
  • No grade 4 toxicities were seen.
  • Grade 2/3 hematologic toxicity was observed in 4 patients.
  • Of the 11 patients included at level 2 (topotecan dose 1.25 mg/m(2)/day twice a week), 3 presented with grade 3 leucopenia and 2 with grade 3 thrombocytopenia.
  • Of the 15 patients accrued to level 3 (topotecan dose 1.5 mg/m(2), twice a week), six had episodes of grade 4 leucopenia and two developed grade 4 thrombocytopenia.
  • No other serious, early non-hematologic or late toxicities were seen at 21 months median follow-up time (range 6-36 months).
  • From the cases included at level 2 and 3, five patients experienced episodes of grade 2/3 asthenia (13.8%), headache 9 (25%), confusion 5 (13.8%), seizure 4 (11%), and cutaneous erythema 3 (8.3%).
  • [MeSH-major] Antineoplastic Agents / administration & dosage. Brain Neoplasms / therapy. Cranial Irradiation. Glioblastoma / therapy. Topotecan / administration & dosage
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Combined Modality Therapy. Drug Administration Schedule. Female. Humans. Male. Middle Aged. Treatment Outcome

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  • (PMID = 18202794.001).
  • [ISSN] 1021-335X
  • [Journal-full-title] Oncology reports
  • [ISO-abbreviation] Oncol. Rep.
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase I; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 7M7YKX2N15 / Topotecan
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13. Samaras V, Piperi C, Korkolopoulou P, Zisakis A, Levidou G, Themistocleous MS, Boviatsis EI, Sakas DE, Lea RW, Kalofoutis A, Patsouris E: Application of the ELISPOT method for comparative analysis of interleukin (IL)-6 and IL-10 secretion in peripheral blood of patients with astroglial tumors. Mol Cell Biochem; 2007 Oct;304(1-2):343-51
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  • Glioblastoma, (grade IV astrocytoma), is characterized by rapid growth and resistance to treatment.
  • Identification of markers of aggressiveness in this tumor could represent new therapeutic targets.
  • Interleukins (IL)-6 and IL-10 may be considered as possible candidates, regulating cell growth, resistance to chemotherapy and angiogenesis.
  • IL-6 and IL-10 secretion levels were determined using ELISPOT methodology in peripheral blood mononuclear cells of 18 patients with astrocytic neoplasms (3 grade II and 15 grade IV), in parallel with 18 healthy controls.
  • Additionally, immunohistochemical expression of these two cytokines was performed in paraffin-embedded neoplastic tissue in 12 of these patients.
  • In addition, IL-10 secretion from peripheral mononuclear and tumor cells of glioma patients was also higher as compared to healthy controls (P = 0.0002).
  • Based on immunohistochemical staining, IL-6 expression was localized in tumor cells and macrophages as well as in areas of large ischemic necrosis, while the major source of IL-10 expression in glioblastomas was the microglia/macrophage cells.
  • This study demonstrates for the first time the usefulness of ELISPOT in estimating the secretion of IL-6 and IL-10 from peripheral blood and the correlation of their expression in neoplastic cells.
  • [MeSH-major] Astrocytoma / blood. Brain Neoplasms / blood. Enzyme-Linked Immunosorbent Assay / methods. Interleukin-10 / blood. Interleukin-10 / secretion. Interleukin-6 / blood. Interleukin-6 / secretion
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Case-Control Studies. Female. Glioblastoma / blood. Humans. Leukocytes / secretion. Male. Middle Aged

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  • (PMID = 17551671.001).
  • [ISSN] 0300-8177
  • [Journal-full-title] Molecular and cellular biochemistry
  • [ISO-abbreviation] Mol. Cell. Biochem.
  • [Language] eng
  • [Publication-type] Comparative Study; Evaluation Studies; Journal Article
  • [Publication-country] Netherlands
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14. Oh S, Ohlfest JR, Todhunter DA, Vallera VD, Hall WA, Chen H, Vallera DA: Intracranial elimination of human glioblastoma brain tumors in nude rats using the bispecific ligand-directed toxin, DTEGF13 and convection enhanced delivery. J Neurooncol; 2009 Dec;95(3):331-342
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  • [Title] Intracranial elimination of human glioblastoma brain tumors in nude rats using the bispecific ligand-directed toxin, DTEGF13 and convection enhanced delivery.
  • A bispecific ligand-directed toxin (BLT) consisting of human interleukin-13, epithelial growth factor, and the first 389 amino acids of diphtheria toxin was assembled in order to target human glioblastoma.
  • In vitro, DTEGF13 selectively killed the human glioblastoma cell line U87-luc as well as other human glioblastomas.
  • Aggressive brain tumors established intracranially (IC) in nude rats with U87 glioma genetically marked with a firefly luciferase reporter gene were treated with two injections of DTEGF13 using convection enhanced delivery resulting in tumor eradication in 50% of the rats which survived with tumor free status at least 110 days post tumor inoculation.
  • Combination of monospecific DTEGF and DTIL13 did not inhibit tumor growth.
  • ELISA assay indicated that anti-DT antibodies were not generated in normal immunocompetent rats given identical intracranial DTEGF13 therapy.
  • Thus, DTEGF13 is safe and efficacious as an alternative drug for glioblastoma therapy and warrants further study.
  • [MeSH-major] Brain Neoplasms / drug therapy. Drug Delivery Systems / methods. Glioblastoma / drug therapy. Recombinant Fusion Proteins / pharmacokinetics. Recombinant Fusion Proteins / toxicity
  • [MeSH-minor] Animals. Antibody Specificity. Cell Division / drug effects. Cell Line, Tumor. Enzyme-Linked Immunosorbent Assay. Genes, Reporter. Humans. Immunoglobulin G / blood. Ligands. Liver / drug effects. Luciferases / genetics. Neoplasm Transplantation. Rats. Rats, Nude. Xenograft Model Antitumor Assays

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  • (PMID = 19517064.001).
  • [ISSN] 1573-7373
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01-CA108637; United States / NINDS NIH HHS / NS / R21-NS055738
  • [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 / DTEGF13 cytotoxin; 0 / Immunoglobulin G; 0 / Ligands; 0 / Recombinant Fusion Proteins; EC 1.13.12.- / Luciferases
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15. Dresemann G: Imatinib and hydroxyurea in pretreated progressive glioblastoma multiforme: a patient series. Ann Oncol; 2005 Oct;16(10):1702-8
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  • [Title] Imatinib and hydroxyurea in pretreated progressive glioblastoma multiforme: a patient series.
  • BACKGROUND: Grade IV malignancies of the brain, such as glioblastoma multiforme (GBM), are associated with a dismal prognosis.
  • Autocrine and paracrine loops of platelet-derived growth factor (PDGF) signaling, as well as other signal transduction pathways, have been postulated to play a role in glioblastoma transformation, and molecules involved in these pathways can potentially serve as targets for therapeutic inhibitory agents.
  • Imatinib, an inhibitor of PDGF receptors alpha and beta, as well as other selected tyrosine kinases, is indicated for treatment of chronic myelogenous leukemia (CML) and gastrointestinal stromal tumor (GIST).
  • PATIENTS AND METHODS: We tested the combination of hydroxyurea and imatinib in 30 grade IV progressive GBM patients refractory to chemo- and radiotherapy.
  • All 30 patients were evaluable after a median 19 weeks observation time.
  • RESULTS: Combination therapy with imatinib and hydroxyurea resulted in a 20% response rate, including complete and partial responses.
  • Median time to progression was 10 weeks and median overall survival was 19 weeks.
  • Three patients continue to survive on combination therapy, with the shortest duration being 106 weeks.
  • CONCLUSION: The efficacy results, combined with findings that imatinib and hydroxyurea were well tolerated, suggest that this combination shows promise as therapy for GBM.

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  • (PMID = 16033874.001).
  • [ISSN] 0923-7534
  • [Journal-full-title] Annals of oncology : official journal of the European Society for Medical Oncology
  • [ISO-abbreviation] Ann. Oncol.
  • [Language] ENG
  • [Publication-type] Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate; X6Q56QN5QC / Hydroxyurea
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16. Lopez-Gonzalez MA, Sotelo J: Brain tumors in Mexico: characteristics and prognosis of glioblastoma. Surg Neurol; 2000 Feb;53(2):157-62
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  • [Title] Brain tumors in Mexico: characteristics and prognosis of glioblastoma.
  • BACKGROUND: Frequency and clinical characteristics of brain tumors have been studied in several populations from different genetic backgrounds; their peculiarities in the Mexican mestizo population shed light on the descriptive and comparative epidemiologic analysis of the genetic participation in brain tumors.
  • Glioblastoma cases were followed to investigate survival and prognostic factors.
  • RESULTS: In a seven-year period 1,776 patients with brain tumors were treated; 419 (24%) had pituitary adenoma; 586 (33%) had glioma.
  • Of the latter, 165 had glioblastoma multiforme, representing 28% of all gliomas and 9% of all neoplasms.
  • Mean survival for glioblastoma was 16 months and the longest mean survival was obtained in patients with radical neurosurgical resection plus radiotherapy and chemotherapy.
  • Factors that showed prognostic significance were age, therapeutic approach, tumor size, and pre- and postoperative clinical status (p < 0.05).
  • CONCLUSIONS: This study comprises the largest series on the frequency of brain tumors in a Latin American population.
  • When compared with other studies, the proportion of glioma and glioblastoma among brain neoplasms was low whereas pituitary adenoma was high.
  • Mean survival for glioblastoma was similar to other reports; in these patients, the overall therapeutic response is still far from satisfactory.
  • [MeSH-major] Brain Neoplasms / diagnosis. Brain Neoplasms / therapy. Glioma / diagnosis. Glioma / therapy
  • [MeSH-minor] Adenoma / diagnosis. Female. Glioblastoma / diagnosis. Humans. Karnofsky Performance Status. Male. Meningeal Neoplasms / diagnosis. Meningioma / diagnosis. Mexico / epidemiology. Middle Aged. Pituitary Neoplasms / diagnosis. Predictive Value of Tests. Prognosis. Retrospective Studies. Risk Factors. Sarcoma / diagnosis. Survival Analysis. Treatment Outcome

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  • (PMID = 10713194.001).
  • [ISSN] 0090-3019
  • [Journal-full-title] Surgical neurology
  • [ISO-abbreviation] Surg Neurol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] UNITED STATES
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17. Capper D, Mittelbronn M, Meyermann R, Schittenhelm J: Pitfalls in the assessment of MGMT expression and in its correlation with survival in diffuse astrocytomas: proposal of a feasible immunohistochemical approach. Acta Neuropathol; 2008 Feb;115(2):249-59
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  • Implementation of this data in routine clinical diagnostics is limited due to often inappropriate study designs, e.g. pooling of tumor entities, WHO grades or primary and secondary glioblastomas, disregard concerning the infiltration zone or various epidemiological factors.
  • For this, 162 astrocytic tumors WHO II-IV (36 diffuse astrocytomas WHO II, 51 anaplastic astrocytomas, 75 primary glioblastomas) as well as 25 glioblastoma infiltration zones and 19 glioblastoma relapses were analyzed for immunohistochemical MGMT protein expression using tissue microarray technique.
  • Expression of MGMT significantly decreased from WHO grade II (25.6%) to glioblastoma (16.8%, p = 0.01) with lowest levels in grade III tumors (10.2%, II/III p < 0.0001).
  • Significant negative associations of MGMT and survival were detected for WHO grade II and IV (p = 0.003 and 0.013).
  • We conclude that immunohistochemical MGMT assessment has potential as a powerful diagnostic tool but analysis should only be performed in a grade dependent manner, before radio-/chemotherapy and with special attention to the infiltration zone of diffuse astrocytomas.
  • [MeSH-major] Astrocytoma / metabolism. Astrocytoma / mortality. Biomarkers, Tumor / analysis. Brain Neoplasms / metabolism. Brain Neoplasms / mortality. DNA Modification Methylases / biosynthesis. DNA Repair Enzymes / biosynthesis. Tumor Suppressor Proteins / biosynthesis
  • [MeSH-minor] Adult. Antineoplastic Agents / therapeutic use. Female. Humans. Immunohistochemistry. Kaplan-Meier Estimate. Male. Middle Aged. Neurosurgical Procedures. Prognosis. Radiotherapy. Tissue Array Analysis

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  • (PMID = 17965865.001).
  • [ISSN] 0001-6322
  • [Journal-full-title] Acta neuropathologica
  • [ISO-abbreviation] Acta Neuropathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Biomarkers, Tumor; 0 / Tumor Suppressor Proteins; EC 2.1.1.- / DNA Modification Methylases; EC 2.1.1.63 / MGMT protein, human; EC 6.5.1.- / DNA Repair Enzymes
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18. Caroli E, Salvati M, Ferrante L: Spinal glioblastoma with brain relapse in a child: clinical considerations. Spinal Cord; 2005 Sep;43(9):565-7
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  • [Title] Spinal glioblastoma with brain relapse in a child: clinical considerations.
  • OBJECTIVES: To describe a child with intramedullary glioblastoma at T9-T10-T11, and to discuss the clinical features of this rare pathology.
  • CASE REPORT: Spinal cord glioblastoma in children has only rarely been reported.
  • This report describes one case of thoracic glioblastoma multiforme in a 6-year-old child and reviews other cases reported in the literature.
  • Postoperative radiotherapy and chemotherapy were given, but 4 months later the patient presented with a brain relapse of the tumour.
  • At 9 months after diagnosis the patient died from cerebral tumour regrowth.
  • The prognosis after multimodality therapy (surgery, radiotherapy, chemotherapy) remains poor.
  • [MeSH-major] Brain Neoplasms / diagnosis. Brain Neoplasms / surgery. Glioblastoma / diagnosis. Glioblastoma / surgery. Neoplasm Recurrence, Local / diagnosis. Spinal Cord Neoplasms / diagnosis. Spinal Cord Neoplasms / surgery
  • [MeSH-minor] Child. Humans. Magnetic Resonance Imaging. Male. Treatment Outcome

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  • (PMID = 15838531.001).
  • [ISSN] 1362-4393
  • [Journal-full-title] Spinal cord
  • [ISO-abbreviation] Spinal Cord
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
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19. Avramis IA, Christodoulopoulos G, Suzuki A, Laug WE, Gonzalez-Gomez I, McNamara G, Sausville EA, Avramis VI: In vitro and in vivo evaluations of the tyrosine kinase inhibitor NSC 680410 against human leukemia and glioblastoma cell lines. Cancer Chemother Pharmacol; 2002 Dec;50(6):479-89
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] In vitro and in vivo evaluations of the tyrosine kinase inhibitor NSC 680410 against human leukemia and glioblastoma cell lines.
  • PURPOSE: NSC 680410, the novel adamantyl ester of AG957, an inhibitor of the p210bcr/abl tyrosine kinase (CML, Ph(+)) and possibly other kinases, was tested for antitumor activity in ten human leukemia and human glioblastoma cell lines.
  • METHODS: CEM/0, seven ara-C- and/or ASNase-resistant clones, Jurkat/0, the myelomonocytic line U937 and U87 MG glioblastoma cell lines were used for these studies.
  • The drug-resistant leukemic clones lack p53, express bcl-2 and VEGF-R1, and thus are refractory to apoptosis.
  • Since tyrosine kinases drive many proliferative pathways and these activities are increased in many leukemic cells, we hypothesized that NSC 680410 may induce cytotoxicity in drug-resistant leukemia clones, independently of p210bcr/abl expression.
  • RESULTS: NSC 680410 exhibited significant antileukemic activity in CEM/0, Jurkat E6-1, and in the drug-resistant leukemic cell lines.
  • Western blot analyses after NSC 680410 treatment demonstrated caspase-3 cleavage and ELISAs showed a fivefold upregulation of its activity in cellular extracts.
  • In addition, U87 MG human glioblastoma cells, which express VEGF-R1, were treated with the Flt-1/Fc chimera, a specific inhibitor of VEGF, and showed 30-43% cell kill in the MTT assay.
  • Treatment with NSC 680410 alone produced no weight changes and increased the median survival to 133%, whereas treatment with NSC680410 plus Flt-1/Fc chimera increased survival to 142% over control.
  • The combination treatment resulted in small residual tumors around the needle track, indicating significant inhibition of tumor growth.
  • CONCLUSIONS: These studies demonstrate that the tyrosine kinase inhibitor NSC 680410 has significant antileukemic activity in p53-null, drug-resistant human leukemia cell lines, as well as significant antitumor activity in combination with Flt-1/Fc chimera against U87 MG glioblastoma brain tumors implanted in situ in athymic mice.
  • [MeSH-major] Adamantane / analogs & derivatives. Adamantane / therapeutic use. Brain Neoplasms / drug therapy. Enzyme Inhibitors / therapeutic use. Glioblastoma / drug therapy. Hydroquinones / therapeutic use. Leukemia, T-Cell / drug therapy. Protein-Tyrosine Kinases / antagonists & inhibitors
  • [MeSH-minor] Animals. Blotting, Western. Caspase 3. Caspases / metabolism. DNA, Neoplasm / metabolism. Drug Resistance, Neoplasm. Endothelial Growth Factors / metabolism. Enzyme-Linked Immunosorbent Assay. Extracellular Matrix Proteins / pharmacology. Female. Fusion Proteins, bcr-abl / antagonists & inhibitors. Fusion Proteins, bcr-abl / metabolism. Humans. In Vitro Techniques. Intercellular Signaling Peptides and Proteins / metabolism. Lymphokines / metabolism. Mice. Mice, Nude. Myosin Heavy Chains. Neoplasm Transplantation. Nonmuscle Myosin Type IIB. Proto-Oncogene Proteins c-bcl-2 / metabolism. Tumor Cells, Cultured / drug effects. Tumor Cells, Cultured / metabolism. Vascular Endothelial Growth Factor A. Vascular Endothelial Growth Factor Receptor-1 / metabolism. Vascular Endothelial Growth Factors

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  • (PMID = 12451475.001).
  • [ISSN] 0344-5704
  • [Journal-full-title] Cancer chemotherapy and pharmacology
  • [ISO-abbreviation] Cancer Chemother. Pharmacol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / DNA, Neoplasm; 0 / Endothelial Growth Factors; 0 / Enzyme Inhibitors; 0 / Extracellular Matrix Proteins; 0 / Hydroquinones; 0 / Intercellular Signaling Peptides and Proteins; 0 / Lymphokines; 0 / NSC 680410; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Vascular Endothelial Growth Factor A; 0 / Vascular Endothelial Growth Factors; EC 2.7.10.1 / FLT1 protein, human; EC 2.7.10.1 / Flt1 protein, mouse; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-1; EC 2.7.10.2 / Fusion Proteins, bcr-abl; EC 3.4.22.- / CASP3 protein, human; EC 3.4.22.- / Casp3 protein, mouse; EC 3.4.22.- / Caspase 3; EC 3.4.22.- / Caspases; EC 3.6.1.- / Nonmuscle Myosin Type IIB; EC 3.6.1.- / nonmuscle myosin type IIB heavy chain; EC 3.6.4.1 / Myosin Heavy Chains; PJY633525U / Adamantane
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20. Armitage PA, Schwindack C, Bastin ME, Whittle IR: Quantitative assessment of intracranial tumor response to dexamethasone using diffusion, perfusion and permeability magnetic resonance imaging. Magn Reson Imaging; 2007 Apr;25(3):303-10
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Quantitative assessment of intracranial tumor response to dexamethasone using diffusion, perfusion and permeability magnetic resonance imaging.
  • There is increasing interest in obtaining quantitative imaging parameters to aid in the assessment of tumor responses to treatment.
  • Eight patients with glioblastoma, five with meningioma and three with metastatic carcinoma underwent MRI prior to and 48-72 h following dexamethasone administration.
  • The MRI protocol enabled quantification of the volume transfer constant (K(trans)), extracellular space volume fraction (nu(e)), plasma volume fraction (nu(p)), regional cerebral blood flow (rCBF), regional cerebral blood volume (rCBV), longitudinal relaxation time (T(1)) and mean diffusivity (D(av)).
  • Significant reductions were observed after the treatment for K(trans), nu(e) and nu(p) in enhancing tumor as well as for T(1) and D(av) in the edematous brain in glioblastoma; on the other hand, for meningioma, significant differences were seen only in edematous brain T(1) and D(av).
  • In addition, no significant difference was observed for enhancing tumor rCBF and rCBV in any of the tumor types, although the general trend was for rCBV to be reduced and for rCBF to be more variable.
  • The yielded parameters provide a wealth of physiologic information and contribute to the understanding of dexamethasone actions on different types of intracranial tumors.
  • [MeSH-major] Brain / drug effects. Brain / pathology. Brain Neoplasms / diagnosis. Brain Neoplasms / drug therapy. Dexamethasone / administration & dosage. Diffusion Magnetic Resonance Imaging / methods. Image Interpretation, Computer-Assisted / methods
  • [MeSH-minor] Aged. Antineoplastic Agents, Hormonal / administration & dosage. Contrast Media. Female. Humans. Male. Middle Aged. Perfusion / methods. Permeability. Prognosis. Reproducibility of Results. Sensitivity and Specificity. Treatment Outcome

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  • (PMID = 17371718.001).
  • [ISSN] 0730-725X
  • [Journal-full-title] Magnetic resonance imaging
  • [ISO-abbreviation] Magn Reson Imaging
  • [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, Hormonal; 0 / Contrast Media; 7S5I7G3JQL / Dexamethasone
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