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1. Full Text Cancer-associated IDH mutations: biomarker and therapeutic opportunities
by Yen, K.E and Bittinger, M.A and Su, S.M and Fantin, V.R
Oncogene, ISSN 0950-9232, 12/2010, Volume 29, Issue 49, pp. 6409 - 6417
The discovery of somatic mutations in the isocitrate dehydrogenase (IDH) enzymes through a genome-wide mutational analysis in glioblastoma represents a... 
IDH | cancer | mutations | BETA-OXIDATION | GLIOMAS | BIOCHEMISTRY & MOLECULAR BIOLOGY | INTEGRATED GENOMIC ANALYSIS | MYELOPROLIFERATIVE NEOPLASMS | L-2-HYDROXYGLUTARIC ACIDURIA | FATTY-ACIDS | ACUTE MYELOID-LEUKEMIA | TUMORS | DEPENDENT ISOCITRATE DEHYDROGENASE | CELL BIOLOGY | ONCOLOGY | CODON 132 MUTATION | GENETICS & HEREDITY | Glioma - enzymology | Glutarates - analysis | Central Nervous System Neoplasms - genetics | Humans | Isocitrate Dehydrogenase - genetics | Hematologic Neoplasms - enzymology | Isocitrate Dehydrogenase - antagonists & inhibitors | Glioma - genetics | Point Mutation | Hematologic Neoplasms - drug therapy | Central Nervous System Neoplasms - enzymology | Biomarkers, Tumor - genetics | Hematologic Neoplasms - genetics | Central Nervous System Neoplasms - drug therapy | Glioma - drug therapy | Oncogenes | Gene mutations | Physiological aspects | Genetic aspects | Research | Diagnosis | Oxidoreductases | Health aspects | Glioblastoma multiforme | Biomarkers | Therapy | Mutation | Cancer
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2. Full Text Central nervous system relapse in patients with untreated HER2‐positive esophageal or gastroesophageal junction adenocarcinoma
by Yoon, Harry H and Lewis, Mark A and Foster, Nathan R and Sukov, William R and Khan, Maliha and Sattler, Christopher A and Wiktor, Anne E and Wu, Tsung‐Teh and Jenkins, Robert B and Sinicrope, Frank A
International Journal of Cancer, ISSN 0020-7136, 10/2016, Volume 139, Issue 7, pp. 1626 - 1631
Although HER2‐positive breast cancers demonstrate a propensity for central nervous system (CNS) metastasis, it is unknown whether other HER2‐positive tumors,... 
CNS | HER2/ERBB2 | brain | relapse | gastroesophageal cancer | FAILURE PROBABILITIES | EXPLORATORY ANALYSIS | PROGNOSIS | CISPLATIN | ONCOLOGY | ERBB2 | METASTATIC BREAST-CANCER | BRAIN METASTASES | HER2 | LAPATINIB PLUS CAPECITABINE | EXPRESSION | TRASTUZUMAB EMTANSINE T-DM1 | Immunohistochemistry | Stomach Neoplasms - enzymology | Stomach Neoplasms - genetics | Receptor, ErbB-2 - biosynthesis | Adenocarcinoma - pathology | Receptor, ErbB-2 - genetics | Central Nervous System Neoplasms - genetics | Humans | Middle Aged | Adenocarcinoma - enzymology | Proportional Hazards Models | Esophagogastric Junction - pathology | Stomach Neoplasms - pathology | Esophageal Neoplasms - pathology | Central Nervous System Neoplasms - pathology | Esophageal Neoplasms - enzymology | Esophagogastric Junction - enzymology | Gene Amplification | Esophageal Neoplasms - genetics | Central Nervous System Neoplasms - enzymology | Adenocarcinoma - genetics | Care and treatment | Relapse | Analysis | Central nervous system | Metastasis | Esophageal cancer | Diseases | Confidence intervals | Nervous system | Breast cancer | Tumors
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3. Full Text Mutant metabolic enzymes are at the origin of gliomas
by Yan, Hai and Bigner, Darell D and Velculescu, Victor and Parsons, D. Williams
Cancer Research, ISSN 0008-5472, 12/2009, Volume 69, Issue 24, pp. 9157 - 9159
Mutations of the isocitrate dehydrogenase (IDH) metabolic enzymes IDH1 and IDH2 have been found to be frequent and early genetic alterations in astrocytomas... 
GLIOBLASTOMAS | CANCERS | ONCOLOGY | CODON 132 MUTATION | IDH1 MUTATIONS | TUMORS | DEHYDROGENASE | Astrocytoma - genetics | Glioblastoma - enzymology | Glioblastoma - genetics | Central Nervous System Neoplasms - genetics | Humans | Astrocytoma - enzymology | Central Nervous System Neoplasms - enzymology | Isocitrate Dehydrogenase - genetics | Mutation
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4. Full Text Src, a potential target for overcoming trastuzumab resistance in HER2-positive breast carcinoma
by Peiró, G and Ortiz-Martínez, F and Gallardo, A and Pérez-Balaguer, A and Sánchez-Payá, J and Ponce, J.J and Tibau, A and López-Vilaro, L and Escuin, D and Adrover, E and Barnadas, A and Lerma, E
British Journal of Cancer, ISSN 0007-0920, 08/2014, Volume 111, Issue 4, pp. 689 - 695
Background: Src is a non-receptor tyrosine kinase involved in signalling and crosstalk between growth-promoting pathways. We aim to investigate the... 
PTEN/PI3K/Akt | trastuzumab resistance | MAPK | HER2 breast carcinoma | Src | prognosis | CANCER-CELLS | ACTIVATION | PIK3CA MUTATIONS | INHIBITION | ONCOLOGY | PHOSPHORYLATION | GROWTH | FAMILY KINASES | PTEN | FOCAL ADHESION KINASE | HER2 | Humans | Middle Aged | Receptor, ErbB-2 - metabolism | Drug Resistance, Neoplasm | Antineoplastic Agents - therapeutic use | Molecular Targeted Therapy | Central Nervous System Neoplasms - secondary | Breast Neoplasms - enzymology | DNA Mutational Analysis | Antibodies, Monoclonal, Humanized - pharmacology | src-Family Kinases - metabolism | Aged, 80 and over | Adult | Female | Antineoplastic Agents - pharmacology | Chemotherapy, Adjuvant | Antibodies, Monoclonal, Humanized - therapeutic use | Signal Transduction | src-Family Kinases - antagonists & inhibitors | Kaplan-Meier Estimate | Breast Neoplasms - drug therapy | Phosphatidylinositol 3-Kinases - genetics | Class I Phosphatidylinositol 3-Kinases | Breast Neoplasms - pathology | Cell Line, Tumor | Breast Neoplasms - mortality | Central Nervous System Neoplasms - enzymology | Aged | Enzyme Activation | Central Nervous System Neoplasms - drug therapy | Central Nervous System Neoplasms - mortality | Trastuzumab | Translational Therapeutics | PI3K | Akt
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5. Full Text Identification of single nucleotide polymorphisms of the PI3K-AKT-mTOR pathway as a risk factor of central nervous system metastasis in metastatic breast cancer
by Le Rhun, Emilie and Bertrand, Nicolas and Dumont, Aurélie and Tresch, Emmanuelle and Le Deley, Marie-Cécile and Mailliez, Audrey and Preusser, Matthias and Weller, Michael and Revillion, Françoise and Bonneterre, Jacques
European Journal of Cancer, ISSN 0959-8049, 12/2017, Volume 87, pp. 189 - 198
The PI3K-AKT-mTOR pathway may be involved in the development of central nervous system (CNS) metastasis from breast cancer. Accordingly, herein we explored... 
Prevention | Brain | SNP | Prediction | Predisposition | PTEN | Genetic | Cerebral | Leptomeningeal | SURVIVAL | TRASTUZUMAB | LEPTOMENINGEAL METASTASIS | THERAPY | ONCOLOGY | PI3K PATHWAY | DISEASE | GENETIC-VARIATIONS | CLINICAL-OUTCOMES | Humans | Middle Aged | Proto-Oncogene Proteins c-akt - genetics | Central Nervous System Neoplasms - secondary | Breast Neoplasms - therapy | Young Adult | Breast Neoplasms - enzymology | TOR Serine-Threonine Kinases - genetics | Time Factors | Adult | Female | Genetic Predisposition to Disease | Risk Assessment | Central Nervous System Neoplasms - genetics | Risk Factors | Kaplan-Meier Estimate | Central Nervous System Neoplasms - therapy | Disease-Free Survival | Phenotype | Breast Neoplasms - genetics | Phosphatidylinositol 3-Kinase - genetics | Breast Neoplasms - pathology | Central Nervous System Neoplasms - enzymology | Aged | Biomarkers, Tumor - genetics | Polymorphism, Single Nucleotide | Medical examination | Oncology, Experimental | Central nervous system | Nervous system | Breast cancer | Metastasis | Research | Risk factors | Blood | Surgery | Genetic research | Genetic aspects | Single nucleotide polymorphisms | Chromosomes | Cancer
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6. Full Text Heterocyclic scaffolds as promising anticancer agents against tumours of the central nervous system: Exploring the scope of indole and carbazole derivatives
by Sherer, Chris and Snape, Timothy J
European Journal of Medicinal Chemistry, ISSN 0223-5234, 06/2015, Volume 97, Issue 1, pp. 552 - 560
Tumours of the central nervous system are intrinsically more dangerous than tumours at other sites, and in particular, brain tumours are responsible for 3% of... 
CNS | Heterocycle | Carbazole | Indole | Indolocarbazole | Cancer | PROTEIN-KINASE-C | CHEMISTRY, MEDICINAL | TOPOISOMERASE-II | NEWLY-DIAGNOSED GLIOBLASTOMA | CELL-CYCLE ARREST | VIVO ANTITUMOR-ACTIVITY | MEDIATED DNA CLEAVAGE | HUMAN COLON-CANCER | GROWTH-FACTOR | REBECCAMYCIN ANALOG | PHASE-I | Central Nervous System Neoplasms - metabolism | Carbazoles - chemistry | Humans | Antineoplastic Agents - therapeutic use | Antineoplastic Agents - chemistry | Animals | Central Nervous System Neoplasms - enzymology | Indoles - pharmacology | Indoles - therapeutic use | Antineoplastic Agents - pharmacology | Carbazoles - therapeutic use | Carbazoles - pharmacology | Central Nervous System Neoplasms - drug therapy | Indoles - chemistry | Lomustine | Chemotherapy | Gliomas | Heterocyclic compounds | Central nervous system
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7. Full Text Targeting sphingosine kinase 1 inhibits Akt signaling, induces apoptosis, and suppresses growth of human glioblastoma cells and xenografts
by Kapitonov, Dmitri and Allegood, Jeremy C and Mitchell, Clint and Hait, Nitai C and Almenara, Jorge A and Adams, Jeffrey K and Zipkin, Robert E and Dent, Paul and Kordula, Tomasz and Milstien, Sheldon and Spiegel, Sarah
Cancer Research, ISSN 0008-5472, 09/2009, Volume 69, Issue 17, pp. 6915 - 6923
Sphingosine-1-phosphate is a potent sphingolipid mediator of diverse processes important for brain tumors, including cell growth, survival, migration,... 
GLIOMA-CELLS | SURVIVAL | MIGRATION | ONCOLOGY | PATHWAY | SPHINGOSINE-1-PHOSPHATE | TUMOR-CELLS | RECEPTORS | EXPRESSION | MULTIFORME | PROGRESSION | Neoplasm Transplantation | Glioblastoma - enzymology | Apoptosis - drug effects | Humans | Male | Amino Alcohols - pharmacology | Isoenzymes - metabolism | Female | Proto-Oncogene Proteins c-akt - metabolism | Enzyme Inhibitors - pharmacology | Enzyme Inhibitors - therapeutic use | Phosphotransferases (Alcohol Group Acceptor) - metabolism | Sphingosine - pharmacology | Phosphotransferases (Alcohol Group Acceptor) - antagonists & inhibitors | Central Nervous System Neoplasms - pathology | Sphingosine - analogs & derivatives | Animals | Signal Transduction - drug effects | Neovascularization, Pathologic - drug therapy | Glioblastoma - pathology | Cell Line, Tumor | Central Nervous System Neoplasms - enzymology | Cell Proliferation - drug effects | Mice | Glioblastoma - drug therapy | Central Nervous System Neoplasms - drug therapy | Glioblastoma - blood supply | Isoenzymes - antagonists & inhibitors | Proto-Oncogene Proteins c-akt - antagonists & inhibitors | Central Nervous System Neoplasms - blood supply | sphingosine-1-phosphate | glioblastoma | Akt | sphingosine kinase type 1
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8. Full Text Screening for ALK abnormalities in central nervous system metastases of non‐small‐cell lung cancer
by Nicoś, Marcin and Jarosz, Bożena and Krawczyk, Paweł and Wojas‐Krawczyk, Kamila and Kucharczyk, Tomasz and Sawicki, Marek and Pankowski, Juliusz and Trojanowski, Tomasz and Milanowski, Janusz
Brain Pathology, ISSN 1015-6305, 01/2018, Volume 28, Issue 1, pp. 77 - 86
Anaplastic lymphoma kinase (ALK) gene rearrangement was reported in 3%–7% of primary non‐small‐cell lung cancer (NSCLC) and its presence is commonly associated... 
CNS metastases | FISH | NSCLC | IHC | ALK rearrangement | EML4-ALK FUSION GENE | PATHOLOGY | IDENTIFICATION | NEUROSCIENCES | EGFR | CLINICAL NEUROLOGY | ANAPLASTIC LYMPHOMA KINASE | REARRANGEMENT | BRAIN METASTASES | CRIZOTINIB | ASSOCIATION | IMMUNOHISTOCHEMISTRY | Immunohistochemistry | Humans | Middle Aged | Image Interpretation, Computer-Assisted | Lung Neoplasms - pathology | Male | Central Nervous System Neoplasms - secondary | Adult | Female | Tissue Fixation | Carcinoma, Non-Small-Cell Lung - pathology | Lung Neoplasms - genetics | Lung Neoplasms - enzymology | Carcinoma, Non-Small-Cell Lung - genetics | Early Detection of Cancer | Central Nervous System Neoplasms - genetics | Kaplan-Meier Estimate | In Situ Hybridization, Fluorescence | Receptor Protein-Tyrosine Kinases - metabolism | Central Nervous System Neoplasms - pathology | Receptor Protein-Tyrosine Kinases - genetics | Gene Rearrangement | Central Nervous System Neoplasms - enzymology | Aged | Carcinoma, Non-Small-Cell Lung - enzymology | Pattern Recognition, Automated | Lymphomas | Metastasis | Lung cancer, Non-small cell | Analysis | Central nervous system | Adenocarcinoma | Tyrosine | Abnormalities | Lung cancer | ALK protein | Fluorescence | Staining | Non-small cell lung carcinoma | Nervous system | Lung carcinoma | Paraffin | Macrophages | Patients | Lymphoma | Metastases | Demographics | Gene rearrangement | Fluorescence in situ hybridization | Lesions | Protein-tyrosine kinase | Smoking | Cancer
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9. Full Text Quantification of tumor-derived cell free DNA(cfDNA) by digital PCR (DigPCR) in cerebrospinal fluid of patients with BRAFV600 mutated malignancies
by Momtaz, Parisa and Pentsova, Elena and Abdel-Wahab, Omar and Diamond, Eli and Hyman, David and Merghoub, Taha and You, Daoqi and Gasmi, Billel and Viale, Agnes and Chapman, Paul B
Oncotarget, ISSN 1949-2553, 2016, Volume 7, Issue 51, pp. 85430 - 85436
Tumor-derived cell free DNA (cfDNA) can be detected in plasma. We hypothesized that mutated BRAF V600 cfDNA could be quantified in the cerebrospinal fluid... 
Erdheim-chester disease | Digital PCR | Cerebrospinal fluid | BRAF mutated melanoma | Cell free DNA | Predictive Value of Tests | Proto-Oncogene Proteins B-raf - cerebrospinal fluid | Circulating Tumor DNA - genetics | Erdheim-Chester Disease - enzymology | Humans | Middle Aged | Melanoma - enzymology | Male | DNA Mutational Analysis - methods | Skin Neoplasms - cerebrospinal fluid | Central Nervous System Neoplasms - secondary | Polymerase Chain Reaction - methods | Skin Neoplasms - enzymology | Erdheim-Chester Disease - cerebrospinal fluid | Melanoma - genetics | Adult | Female | Melanoma - cerebrospinal fluid | Skin Neoplasms - pathology | Erdheim-Chester Disease - genetics | Spinal Puncture | Central Nervous System Neoplasms - genetics | Circulating Tumor DNA - cerebrospinal fluid | Erdheim-Chester Disease - pathology | Melanoma - secondary | Magnetic Resonance Imaging | Proto-Oncogene Proteins B-raf - genetics | Skin Neoplasms - genetics | Biomarkers, Tumor - cerebrospinal fluid | Central Nervous System Neoplasms - enzymology | Aged | Biomarkers, Tumor - genetics | Mutation | Central Nervous System Neoplasms - cerebrospinal fluid
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10. Full Text Expression of proliferation markers Ki67, cyclin A, geminin and aurora-kinase A in primary breast carcinomas and corresponding distant metastases
by Tökés, Anna-Mária and Szász, A Marcell and Geszti, Franciska and Lukács, Lilla V and Kenessey, István and Turányi, Eszter and Meggyesházi, Nóra and Molnár, István A and Fillinger, János and Soltész, Ibolya and Bálint, Katalin and Hanzély, Zoltán and Arató, Gabriella and Szendröi, Miklós and Kulka, Janina
Journal of Clinical Pathology, ISSN 0021-9746, 04/2015, Volume 68, Issue 4, pp. 274 - 282
Aims To assess the expression of the following cell cycle regulatory proteins in primary metastatic breast carcinomas (MBCs) and on availability in matched... 
LYMPH-NODE METASTASES | CANCER PATIENTS | SURVIVAL | CELLS | REPLICATION | ADDITIONAL PROGNOSTIC INFORMATION | KI-67 EXPRESSION | PATHOLOGY | SIGNATURE | Immunohistochemistry | Predictive Value of Tests | Cell Proliferation | Tissue Array Analysis | Humans | Middle Aged | Geminin - analysis | Bone Neoplasms - secondary | Carcinoma - mortality | Central Nervous System Neoplasms - secondary | Breast Neoplasms - therapy | Breast Neoplasms - enzymology | Lung Neoplasms - secondary | Time Factors | Carcinoma - enzymology | Aged, 80 and over | Adult | Female | Retrospective Studies | Carcinoma - secondary | Cyclin A - analysis | Bone Neoplasms - enzymology | Lung Neoplasms - enzymology | Hungary | Risk Factors | Kaplan-Meier Estimate | Disease-Free Survival | Ki-67 Antigen - analysis | Aurora Kinase A - analysis | Breast Neoplasms - pathology | Breast Neoplasms - mortality | Carcinoma - therapy | Central Nervous System Neoplasms - enzymology | Aged | Care and treatment | Breast cancer | Metastasis | Research | Gene expression | Phosphotransferases | Thoracic surgery | Lymphatic system | Genes | Nervous system | Kinases | Cell adhesion & migration | Proteins | Studies | Lungs | Medical prognosis | Cell cycle | Bones | Tumors
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11. Full Text Exceptional aggressiveness of cerebral cavernous malformation disease associated with PDCD10 mutations
by Shenkar, Robert and Shi, Changbin and Rebeiz, Tania and Stockton, Rebecca A and McDonald, David A and Mikati, Abdul Ghani and Zhang, Lingjiao and Austin, Cecilia and Akers, Amy L and Gallione, Carol J and Rorrer, Autumn and Gunel, Murat and Min, Wang and De Souza, Jorge Marcondes and Lee, Connie and Marchuk, Douglas A and Awad, Issam A
Genetics in Medicine, ISSN 1098-3600, 03/2015, Volume 17, Issue 3, pp. 188 - 196
Purpose: The phenotypic manifestations of cerebral cavernous malformation disease caused by rare PDCD10 mutations have not been systematically examined, and a... 
cerebral cavernous malformation | vascular malformations | CCM3 | Rho kinase | PDCD10 | MANAGEMENT | MECHANISM | GCKIII PROTEINS | RHO-KINASE | MODEL | NATURAL-HISTORY | LESION | STRATEGIES | VASCULAR INTEGRITY | GENETICS & HEREDITY | Human Umbilical Vein Endothelial Cells | Prospective Studies | Stress Fibers - drug effects | Humans | Middle Aged | 1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine - analogs & derivatives | Child, Preschool | Infant | Intracellular Signaling Peptides and Proteins - metabolism | Hemangioma, Cavernous, Central Nervous System - genetics | rho-Associated Kinases - antagonists & inhibitors | Young Adult | rho-Associated Kinases - metabolism | Apoptosis Regulatory Proteins - genetics | Adult | Membrane Proteins - metabolism | Child | Intracellular Signaling Peptides and Proteins - genetics | Disease Models, Animal | Proto-Oncogene Proteins - metabolism | Keratin-1 - genetics | Membrane Proteins - genetics | Central Nervous System Neoplasms - genetics | Cells, Cultured | Proto-Oncogene Proteins - genetics | Apoptosis Regulatory Proteins - metabolism | Carrier Proteins - genetics | Central Nervous System Neoplasms - pathology | Stress Fibers - metabolism | Animals | Hemangioma, Cavernous, Central Nervous System - enzymology | Hemangioma, Cavernous, Central Nervous System - pathology | 1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine - pharmacology | Adolescent | Central Nervous System Neoplasms - enzymology | Mice | Mutation | Cerebral cavernous malformations
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12. Full Text Phosphatases and solid tumors: Focus on glioblastoma initiation, progression and recurrences
by Dedobbeleer, Matthias and Willems, Estelle and Freeman, Stephen and Lombard, Arnaud and Goffart, Nicolas and Rogister, Bernard
Biochemical Journal, ISSN 0264-6021, 09/2017, Volume 474, Issue 17, pp. 2903 - 2924
Phosphatases and cancer have been related for many years now, as these enzymes regulate key cellular functions, including cell survival, migration,... 
CELL LUNG-CANCER | HOMOLOGOUS RECOMBINATION REPAIR | PANCREATIC DUCTAL ADENOCARCINOMA | PROTEIN-KINASE PHOSPHATASE-1 | BIOCHEMISTRY & MOLECULAR BIOLOGY | INTEGRATED GENOMIC ANALYSIS | CENTRAL-NERVOUS-SYSTEM | HUMAN BREAST-CANCER | DUAL-SPECIFICITY PHOSPHATASE | SIGNAL-REGULATED KINASE | HUMAN OVARIAN-CANCER | Glioblastoma - enzymology | Central Nervous System Neoplasms - genetics | Humans | Phosphoprotein Phosphatases - metabolism | Male | Neoplasm Proteins - metabolism | Cell Transformation, Neoplastic - metabolism | Animals | Phosphoprotein Phosphatases - genetics | Glioblastoma - genetics | Cell Transformation, Neoplastic - genetics | Central Nervous System Neoplasms - enzymology | Female | Neoplasm Proteins - genetics
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