Database : MEDLINE
Search on : Hypothalamic and Neoplasms [Words]
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[PMID]: 29339528
[Au] Autor:Engels M; Gehrmann K; Falhammar H; Webb EA; Nordenström A; Sweep FC; Span PN; van Herwaarden AE; Rohayem J; Richter-Unruh A; Bouvattier C; Köhler B; Kortmann BB; Arlt W; Roeleveld N; Reisch N; Stikkelbroeck NMML; Claahsen-van der Grinten HL; dsd-LIFE group
[Ad] Address:Department of PediatricsAmalia Children's Hospital, Radboud University Medical Center, Nijmegen, the Netherlands.
[Ti] Title:Gonadal function in adult male patients with congenital adrenal hyperplasia.
[So] Source:Eur J Endocrinol;178(3):285-294, 2018 Mar.
[Is] ISSN:1479-683X
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:CONTEXT: Current knowledge on gonadal function in congenital adrenal hyperplasia (CAH) is mostly limited to single-center/country studies enrolling small patient numbers. Overall data indicate that gonadal function can be compromised in men with CAH. OBJECTIVE: To determine gonadal function in men with CAH within the European 'dsd-LIFE' cohort. DESIGN: Cross-sectional clinical outcome study, including retrospective data from medical records. METHODS: Fourteen academic hospitals included 121 men with CAH aged 16-68 years. Main outcome measures were serum hormone concentrations, semen parameters and imaging data of the testes. RESULTS: At the time of assessment, 14/69 patients had a serum testosterone concentration below the reference range; 7 of those were hypogonadotropic, 6 normogonadotropic and 1 hypergonadotropic. In contrast, among the patients with normal serum testosterone (55/69), 4 were hypogonadotropic, 44 normogonadotropic and 7 hypergonadotropic. The association of decreased testosterone with reduced gonadotropin concentrations (odds ratio (OR) = 12.8 (2.9-57.3)) was weaker than the association between serum androstenedione/testosterone ratio ≥1 and reduced gonadotropin concentrations (OR = 39.3 (2.1-732.4)). Evaluation of sperm quality revealed decreased sperm concentrations (15/39), motility (13/37) and abnormal morphology (4/28). Testicular adrenal rest tumor (TART)s were present in 39/80 patients, with a higher prevalence in patients with the most severe genotype (14/18) and in patients with increased current 17-hydroxyprogesterone 20/35) or androstenedione (12/18) serum concentrations. Forty-three children were fathered by 26/113 patients. CONCLUSIONS: Men with CAH have a high risk of developing hypothalamic-pituitary-gonadal disturbances and spermatogenic abnormalities. Regular assessment of endocrine gonadal function and imaging for TART development are recommended, in addition to measures for fertility protection.
[Mh] MeSH terms primary: Adrenal Hyperplasia, Congenital/blood
Androstenedione/blood
Gonadotropins/blood
Hypogonadism/blood
Testosterone/blood
[Mh] MeSH terms secundary: Adolescent
Adrenal Hyperplasia, Congenital/complications
Adrenal Hyperplasia, Congenital/epidemiology
Adrenal Rest Tumor/blood
Adrenal Rest Tumor/epidemiology
Adult
Aged
Cross-Sectional Studies
Europe/epidemiology
Humans
Hydroxyprogesterones/blood
Hypogonadism/complications
Male
Middle Aged
Odds Ratio
Oligospermia/complications
Prevalence
Semen Analysis
Sperm Count
Sperm Motility
Testicular Neoplasms/blood
Testicular Neoplasms/epidemiology
Young Adult
[Pt] Publication type:JOURNAL ARTICLE
[Nm] Name of substance:0 (Gonadotropins); 0 (Hydroxyprogesterones); 3XMK78S47O (Testosterone); 409J2J96VR (Androstenedione)
[Em] Entry month:1802
[Cu] Class update date: 180220
[Lr] Last revision date:180220
[Js] Journal subset:IM
[Da] Date of entry for processing:180118
[St] Status:MEDLINE
[do] DOI:10.1530/EJE-17-0862

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[PMID]: 29280458
[Au] Autor:Tsang DS; Murphy ES; Merchant TE
[Ad] Address:Department of Radiation Oncology, St. Jude Children's Research Hospital, Memphis, Tennessee.
[Ti] Title:Radiation Therapy for Optic Pathway and Hypothalamic Low-Grade Gliomas in Children.
[So] Source:Int J Radiat Oncol Biol Phys;99(3):642-651, 2017 Nov 01.
[Is] ISSN:1879-355X
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:PURPOSE: The long-term survival of pediatric patients with optic pathway or hypothalamic low-grade glioma (LGG) who receive radiation therapy (RT) has not been previously assessed. METHODS AND MATERIALS: A retrospective study was performed of all patients with optic-hypothalamic pediatric LGG treated with RT at a single institution. Eligible patients were aged ≤21 years at the time of RT and had localized LGG diagnosed by neuroimaging or histology. The median RT dose was 54 Gy, delivered in 30 fractions. Event-free survival (EFS) was defined as survival without progression or secondary high-grade glioma. Days were counted from the first day of RT. RESULTS: Eighty-nine patients were included in the study, with a median follow-up period of 12.5 years. Of the patients, 14 had neurofibromatosis type 1 (NF-1). The 10-year EFS rate was 61.9% (95% confidence interval [CI], 31.2%-82.1%) for patients with NF-1 and 67.5% (95% CI, 54.8%-77.3%) for those without NF-1. The 10-year overall survival rate was 92.3% (95% CI, 56.6%-98.9%) for patients with NF-1 and 98.4% (95% CI, 89.1%-99.8%) for those without NF-1. Pre-RT chemotherapy (which was more commonly given to younger patients) was associated with reduced EFS, whereas younger age was associated with reduced overall survival. Possible RT-induced neoplasms developed in 8 patients, including 4 with NF-1. The 10-year cumulative incidence of clinically significant vasculopathy was 7.1% (95% CI, 2.9%-13.9%); vasculopathy did not develop in any child aged >10 years at the commencement of RT. CONCLUSIONS: RT is an effective treatment for optic-hypothalamic LGG. Older children without NF-1 have a low risk of late toxicity. RT can be considered for selected younger patients or individuals with NF-1 as a salvage treatment after progression.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1712
[Cu] Class update date: 171227
[Lr] Last revision date:171227
[St] Status:In-Data-Review

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[PMID]: 28708330
[Au] Autor:Upadhyaya SA; Ghazwani Y; Wu S; Broniscer A; Boop FA; Gajjar A; Qaddoumi I
[Ad] Address:Division of Neuro-Oncology, Department of Oncology, St. Jude Children's Research Hospital, Memphis, Tennessee.
[Ti] Title:Mortality in children with low-grade glioma or glioneuronal tumors: A single-institution study.
[So] Source:Pediatr Blood Cancer;65(1), 2018 Jan.
[Is] ISSN:1545-5017
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:BACKGROUND: While pediatric low-grade glioma/glioneuronal tumors (LGG/LGGNTs) are considered slow-growing, indolent tumors with excellent long-term prognosis, mortality due to the disease is not unknown. Few studies have addressed the cause of death in this population. METHODS: Retrospective review of clinicopathologic and radiologic data for children 21 years or younger with LGG/LGGNT who died at St. Jude Children's Research Hospital between April 1985 and June 2015. Our primary objective was to determine the causes and timing of mortality in affected children. RESULTS: For the 87 eligible patients, median age at diagnosis was 7.7 years (range, 0.21-21 years), median age at death was 14.26 years (range, 0.58-32 years), and median time to death from diagnosis was 4.02 years (range, 0.21-24 years). Midbrain/thalamus was the most common tumor location (n = 34), followed by suprasellar/hypothalamic (n = 18) and cerebrocortical (n = 13). Astrocytoma not otherwise specified (n = 24), pilocytic astrocytoma (n = 23), and fibrillary astrocytoma (n = 11) were the predominant histologic diagnoses. Causes of death included progressive primary disease (PD) (n = 43), progression of PD with histological features of a high-grade glioma at progression or at autopsy (PD-HGG) (n = 15), second cancer (n = 3), suicide (n = 4), and vehicular accident (n = 3). Among the 15 patients with PD-HGG, 12 received radiation therapy before histologic confirmation of progression. CONCLUSIONS: PD and PD-HGG contributed to 66% of the mortality in our patient cohort. Early psychological intervention should be included as part of the multidisciplinary management approach of children with LGG/LGGNT to reduce the risk of suicide in vulnerable subjects.
[Mh] MeSH terms primary: Brain Neoplasms/mortality
Glioma/mortality
[Mh] MeSH terms secundary: Adolescent
Adult
Age Factors
Brain Neoplasms/pathology
Child
Child, Preschool
Female
Glioma/pathology
Humans
Infant
Male
Retrospective Studies
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1712
[Cu] Class update date: 171201
[Lr] Last revision date:171201
[Js] Journal subset:IM
[Da] Date of entry for processing:170715
[St] Status:MEDLINE
[do] DOI:10.1002/pbc.26717

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[PMID]: 29020588
[Au] Autor:Curran MA; Madhavan VL; Caruso PA; Ebb DH; Williams EA
[Ad] Address:From the Departments of Pediatrics (M.A.C., V.L.M., D.H.E.), Radiology (P.A.C.), and Pathology (E.A.W.), Massachusetts General Hospital, and the Departments of Pediatrics (M.A.C., V.L.M., D.H.E.), Radiology (P.A.C.), and Pathology (E.A.W.), Harvard Medical School - both in Boston.
[Ti] Title:Case 31-2017. A 19-Month-Old Girl with Failure to Thrive.
[So] Source:N Engl J Med;377(15):1468-1477, 2017 10 12.
[Is] ISSN:1533-4406
[Cp] Country of publication:United States
[La] Language:eng
[Mh] MeSH terms primary: Astrocytoma/diagnostic imaging
Failure to Thrive/etiology
Hypothalamic Neoplasms/diagnostic imaging
[Mh] MeSH terms secundary: Astrocytoma/complications
Astrocytoma/pathology
Blood Chemical Analysis
Cachexia/etiology
Diagnosis, Differential
Energy Intake
Female
Humans
Hypothalamic Diseases/diagnosis
Hypothalamic Neoplasms/complications
Hypothalamic Neoplasms/pathology
Infant
Magnetic Resonance Imaging
[Pt] Publication type:CASE REPORTS; CLINICAL CONFERENCE; JOURNAL ARTICLE
[Em] Entry month:1710
[Cu] Class update date: 171019
[Lr] Last revision date:171019
[Js] Journal subset:AIM; IM
[Da] Date of entry for processing:171012
[St] Status:MEDLINE
[do] DOI:10.1056/NEJMcpc1706106

  5 / 4738 MEDLINE  
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[PMID]: 28980149
[Au] Autor:Prasad GL; Nandeesh BN; Menon GR
[Ad] Address:Department of Neurosurgery, Kasturba Medical College, Manipal University, Manipal, 576104, India. lakshmi.prasad@manipal.edu.
[Ti] Title:Hemorrhagic presentation of intracranial pilocytic astrocytomas: literature review.
[So] Source:Neurosurg Rev;, 2017 Oct 04.
[Is] ISSN:1437-2320
[Cp] Country of publication:Germany
[La] Language:eng
[Ab] Abstract:Pilocytic astrocytomas (PAs) are seemingly innocuous and benign tumors. However, in recent times, many case series have documented high rates of hemorrhage in these neoplasms. We hereby provide a detailed analysis on hemorrhagic pilocytic astrocytomas (HPA) in adults and report one such case managed at our institute. In addition, salient differences between adult and pediatric hemorrhagic PA have been briefed. Hospital records were retrieved for our case. Literature review was conducted by searching online databases for the following keywords-pilocytic astrocytoma, hemorrhage, cranial, pediatric, and adults. A 22-year-old male with neurofibromatosis-1 presented with sudden onset headache and vomiting of 3-day duration. Imaging revealed a lobulated suprasellar lesion with obstructive hydrocephalus. Pterional transsylvian approach and subtotal resection were performed. Histopathology showed features of PA with bleed. Including current report, a total of 26 cases have been reported. Mean age was 37 years (21-75 years) and they are mostly found in the third decade. The male:female ratio was 2.1:1. Sudden headache with vomiting was the most common symptoms. Tumors were mostly located in cerebral hemispheres (n = 9/34.6%), hypothalamus/suprasellar region (n = 7/27%), and cerebellum (n = 6/23%). Two-thirds underwent gross total excision. There were two deaths and except one case, no recurrences were reported in those with available follow-ups. Hemorrhagic presentation of a PA is rare, although more commonly seen in adults and most commonly located in cerebral hemispheres. Maximal safe resection is the standard treatment and recurrences are rare.
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Em] Entry month:1710
[Cu] Class update date: 171104
[Lr] Last revision date:171104
[St] Status:Publisher
[do] DOI:10.1007/s10143-017-0915-z

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[PMID]: 28886081
[Au] Autor:Wan X; Liu Y; Zhao Y; Sun X; Fan D; Guo L
[Ad] Address:Department of Medical Oncology, First Affiliated Hospital, China Medical University, Shenyang, Liaoning, P.R. China.
[Ti] Title:Orexin A affects HepG2 human hepatocellular carcinoma cells glucose metabolism via HIF-1α-dependent and -independent mechanism.
[So] Source:PLoS One;12(9):e0184213, 2017.
[Is] ISSN:1932-6203
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Orexins are hypothalamic neuropeptides that regulate feeding, reward, wakefulness and energy homeostasis. The present study sought to characterize the involvement of orexin A in glucose metabolism in HepG2 human hepatocellular carcinoma cells, and investigated the role of hypoxia-inducible factor-1α (HIF-1α) in the response. HepG2 cells were exposed to different concentrations of orexin A (10-9 to 10-7 M) in vitro, without or with the orexin receptor 1 (OX1R) inhibitor (SB334867), HIF-1α inhibitor (YC-1) or a combination of both inhibitors. Subsequently, OX1R, HIF-1α expression and localization, glucose uptake, glucose transporter 1 (GLUT1) expression and ATP content were measured. We further investigated the intracellular fate of glucose by measuring the gene expression of pyruvate dehydrogenase kinase 1 (PDK1), lactate dehydrogenase (LDHA) and pyruvate dehydrogenase B (PDHB), as well as metabolite levels including lactate generation and mitochondrial pyruvate dehydrogenase (PDH) activity. The activity of phosphoinositide 3-kinase (PI3K)/Akt/mammalian target of rapamycin (mTOR) pathway was also assessed. Our results showed that the expression of OX1R was predominantly located in the nucleus in HepG2 cells. Orexin A oxygen-independently promoted the mRNA and protein expression of HIF-1α as well as its nuclear accumulation in HepG2 cells and the elevated HIF-1α protein was associated, at least partly, with the activation of the PI3K/Akt/mTOR pathway. Orexin A stimulated GLUT1 expression, glucose uptake as well as ATP generation in HepG2 cells via OX1R acting through the HIF-1α pathway. Moreover, orexin A inhibited LDHA, PDK1 expression and lactate production, stimulated PDHB expression and PDH enzyme activity independent of HIF-1α. Our results indicated that orexin signaling facilitated the glucose flux into mitochondrial oxidative metabolism rather than glycolysis in HepG2 cells. These findings provide new insight into the regulation of glucose metabolism by orexin A in hepatocellular carcinoma cells.
[Mh] MeSH terms primary: Carcinoma, Hepatocellular/metabolism
Glucose/metabolism
Hypoxia-Inducible Factor 1, alpha Subunit/metabolism
Liver Neoplasms/metabolism
Metabolic Networks and Pathways/drug effects
Orexins/pharmacology
[Mh] MeSH terms secundary: Adenosine Triphosphate/metabolism
Carcinoma, Hepatocellular/genetics
Citric Acid Cycle/drug effects
Gene Expression
Gene Expression Regulation/drug effects
Glucose Transporter Type 1/genetics
Glucose Transporter Type 1/metabolism
Glycolysis
Hep G2 Cells
Humans
Lactic Acid/metabolism
Liver Neoplasms/genetics
Orexin Receptors/genetics
Orexin Receptors/metabolism
Phosphatidylinositol 3-Kinases/metabolism
Protein Transport
Proto-Oncogene Proteins c-akt/metabolism
Pyruvate Dehydrogenase Complex/metabolism
Signal Transduction/drug effects
TOR Serine-Threonine Kinases/metabolism
[Pt] Publication type:JOURNAL ARTICLE
[Nm] Name of substance:0 (Glucose Transporter Type 1); 0 (Hypoxia-Inducible Factor 1, alpha Subunit); 0 (Orexin Receptors); 0 (Orexins); 0 (Pyruvate Dehydrogenase Complex); 33X04XA5AT (Lactic Acid); 8L70Q75FXE (Adenosine Triphosphate); EC 2.7.1.- (Phosphatidylinositol 3-Kinases); EC 2.7.1.1 (TOR Serine-Threonine Kinases); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt); IY9XDZ35W2 (Glucose)
[Em] Entry month:1710
[Cu] Class update date: 171018
[Lr] Last revision date:171018
[Js] Journal subset:IM
[Da] Date of entry for processing:170909
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0184213

  7 / 4738 MEDLINE  
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[PMID]: 28780517
[Au] Autor:Reimondo G; Puglisi S; Zaggia B; Basile V; Saba L; Perotti P; De Francia S; Volante M; Zatelli MC; Cannavò S; Terzolo M
[Ad] Address:Internal Medicine 1Department of Clinical and Biological Sciences, University of Turin, Orbassano, Italy.
[Ti] Title:Effects of mitotane on the hypothalamic-pituitary-adrenal axis in patients with adrenocortical carcinoma.
[So] Source:Eur J Endocrinol;177(4):361-367, 2017 Oct.
[Is] ISSN:1479-683X
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:OBJECTIVE: Mitotane, a drug used to treat adrenocortical cancer (ACC), inhibits multiple enzymatic steps of adrenocortical steroid biosynthesis, potentially causing adrenal insufficiency. Recent studies have also documented a direct inhibitory effect of mitotane at the pituitary level. The present study was aimed to assess the hypothalamic-pituitary-adrenal axis in patients with ACC receiving mitotane. DESIGN AND METHODS: We prospectively enrolled 16 patients on adjuvant treatment with mitotane after radical surgical resection of ACC, who underwent standard hormone evaluation and h-CRH stimulation. A group of 10 patients with primary adrenal insufficiency (PAI) served as controls for the CRH test. RESULTS: We demonstrated a close correlation between cortisol-binding globulin (CBG) and plasma mitotane levels, and a non-significant trend between mitotane dose and either serum or salivary cortisol in ACC patients. We did not find any correlation between the dose of cortisone acetate and either ACTH or cortisol levels. ACTH levels were significantly higher in patients with PAI than that in patients with ACC, both in baseline conditions (88.99 (11.04-275.00) vs 24.53 (6.16-121.88) pmol/L, = 0.031) and following CRH (158.40 (34.32-275.00) vs 67.43 (8.8-179.52) pmol/L = 0.016). CONCLUSIONS: The observation of lower ACTH levels in patients with ACC than that in patients with PAI, both in basal conditions and after CRH stimulation, suggests that mitotane may play an inhibitory effect on ACTH secretion at the pituitary levels. In conclusion, the present study shows that mitotane affects the HPA axis at multiple levels and no single biomarker may be used for the assessment of adrenal insufficiency.
[Mh] MeSH terms primary: Adrenal Cortex Neoplasms/drug therapy
Adrenocortical Carcinoma/drug therapy
Antineoplastic Agents, Hormonal/therapeutic use
Hypothalamo-Hypophyseal System/drug effects
Mitotane/therapeutic use
Pituitary-Adrenal System/drug effects
[Mh] MeSH terms secundary: Adrenal Cortex Neoplasms/blood
Adrenocortical Carcinoma/blood
Adrenocorticotropic Hormone/blood
Adult
Aged
Antineoplastic Agents, Hormonal/blood
Antineoplastic Agents, Hormonal/pharmacology
Female
Humans
Hypothalamo-Hypophyseal System/metabolism
Male
Middle Aged
Mitotane/blood
Mitotane/pharmacology
Pituitary-Adrenal System/metabolism
Prospective Studies
Treatment Outcome
[Pt] Publication type:JOURNAL ARTICLE
[Nm] Name of substance:0 (Antineoplastic Agents, Hormonal); 78E4J5IB5J (Mitotane); 9002-60-2 (Adrenocorticotropic Hormone)
[Em] Entry month:1710
[Cu] Class update date: 171003
[Lr] Last revision date:171003
[Js] Journal subset:IM
[Da] Date of entry for processing:170807
[St] Status:MEDLINE
[do] DOI:10.1530/EJE-17-0452

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[PMID]: 28739680
[Au] Autor:Radin DP; Patel P
[Ad] Address:Department of Pharmacology, Stony Brook University School of Medicine, Stony Brook, NY, U.S.A. danradin1@gmail.com.
[Ti] Title:BDNF: An Oncogene or Tumor Suppressor?
[So] Source:Anticancer Res;37(8):3983-3990, 2017 08.
[Is] ISSN:1791-7530
[Cp] Country of publication:Greece
[La] Language:eng
[Ab] Abstract:Neurotrophins are a family of growth factors that are vital to the proper development of the central nervous system. Their effects on cells are governed by the expression and activation of the tyrosine kinase receptors TrkA, TrkB and TrkC. TrkB has been immensely implicated in mediating neuronal migration, development and differentiation. It has also been shown to protect several neuronal cell types from an array of cytotoxic stressors after activation by its conjugate ligand brain-derived neurotrophic factor (BDNF). Over the past two decades, it has been shown that TrkB and BDNF are up-regulated in many types of cancers, conferring aggressive phenotypes underpinned by their resistance to several standard chemotherapeutic agents. This resistance to chemotherapy is modulated by the downstream targets of the TrkB receptor which include the well-characterized PI3K /Akt growth pathway, a hallmark of uncontrolled cancer cell growth and proliferation. Pre-clinical efforts to develop inhibitors of this receptor are promising, and such inhibitors also seem to sensitize cancer cells to standard chemotherapies. However, new evidence suggests that BDNF overexpression in the hypothalamus has immunoaugmenting properties, eliciting an increased anti-tumor immune response and reducing the activity of several proteins that would normally confer resistance to chemotherapeutic agents. In the current work, we provide a global analysis of the physiological consequences of TrkB receptor activation in vitro and discuss the dynamic consequences of TrkB activation in vivo. Finally, we propose a clinically-feasible option for increasing BDNF expression in the hypothalamus to more readily utilize the oncolytic effects of BDNF.
[Mh] MeSH terms primary: Brain-Derived Neurotrophic Factor/genetics
Membrane Glycoproteins/genetics
Neoplasms/drug therapy
Neoplasms/genetics
Protein-Tyrosine Kinases/genetics
[Mh] MeSH terms secundary: Brain-Derived Neurotrophic Factor/biosynthesis
Drug Resistance, Neoplasm/genetics
Gene Expression Regulation, Neoplastic
Genes, Tumor Suppressor
Humans
Hypothalamus/metabolism
Membrane Glycoproteins/biosynthesis
Neoplasms/pathology
Oncogenes/genetics
Protein-Tyrosine Kinases/biosynthesis
Receptor, trkA/biosynthesis
Receptor, trkA/genetics
Receptor, trkB
Receptor, trkC/biosynthesis
Receptor, trkC/genetics
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Nm] Name of substance:0 (Brain-Derived Neurotrophic Factor); 0 (Membrane Glycoproteins); 0 (TRKA protein, human); 0 (brain-derived neurotrophic factor, human); EC 2.7.10.1 (Protein-Tyrosine Kinases); EC 2.7.10.1 (Receptor, trkA); EC 2.7.10.1 (Receptor, trkB); EC 2.7.10.1 (Receptor, trkC); EC 2.7.10.1 (tropomyosin-related kinase-B, human)
[Em] Entry month:1708
[Cu] Class update date: 171116
[Lr] Last revision date:171116
[Js] Journal subset:IM
[Da] Date of entry for processing:170726
[St] Status:MEDLINE

  9 / 4738 MEDLINE  
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[PMID]: 28732411
[Au] Autor:Yano S; Hide T; Shinojima N
[Ad] Address:Faculty of Life Sciences Research, Kumamoto University Graduate School, Neurosurgery, Kumamoto, Japan. Electronic address: yanoshige7@gmail.com.
[Ti] Title:In Reply to "Craniopharyngioma: Surgical Outcome as Related to the Degree of Hypothalamic Involvement".
[So] Source:World Neurosurg;104:1011-1013, 2017 08.
[Is] ISSN:1878-8769
[Cp] Country of publication:United States
[La] Language:eng
[Mh] MeSH terms primary: Craniopharyngioma/surgery
Hypothalamus/surgery
[Mh] MeSH terms secundary: Humans
Pituitary Neoplasms/surgery
[Pt] Publication type:LETTER; COMMENT
[Em] Entry month:1709
[Cu] Class update date: 170904
[Lr] Last revision date:170904
[Js] Journal subset:IM
[Da] Date of entry for processing:170723
[St] Status:MEDLINE

  10 / 4738 MEDLINE  
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[PMID]: 28732410
[Au] Autor:Prieto R; Pascual JM; Castro-Dufourny I; Carrasco R; Barrios L
[Ad] Address:Department of Neurosurgery, Puerta de Hierro University Hospital, Madrid, Spain. Electronic address: rprieto29@hotmail.com.
[Ti] Title:Craniopharyngioma: Surgical Outcome as Related to the Degree of Hypothalamic Involvement.
[So] Source:World Neurosurg;104:1006-1010, 2017 08.
[Is] ISSN:1878-8769
[Cp] Country of publication:United States
[La] Language:eng
[Mh] MeSH terms primary: Craniopharyngioma/surgery
Hypothalamus/surgery
[Mh] MeSH terms secundary: Humans
Pituitary Neoplasms/surgery
[Pt] Publication type:LETTER; COMMENT
[Em] Entry month:1709
[Cu] Class update date: 170904
[Lr] Last revision date:170904
[Js] Journal subset:IM
[Da] Date of entry for processing:170723
[St] Status:MEDLINE


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