HemoChat is an evidence-based AI medical search tool covering all major clinical domains, powered by 46,298 SNOMED-CT concepts, clinical guidelines, and live PubMed literature.

What medical domains does HemoChat cover?

HemoChat covers all major medical domains including cardiology, oncology, neurology, hematology, pulmonology, endocrinology, gastroenterology, psychiatry, nephrology, rheumatology, musculoskeletal, and more — with 46,298 SNOMED-CT concepts.

Is HemoChat a replacement for clinical judgment?

No. HemoChat is for clinical reference only and is not a substitute for professional medical judgment. Always consult qualified healthcare professionals for medical decisions.

What AI technology does HemoChat use?

HemoChat uses a hybrid GraphRAG + VectorRAG pipeline combining Neo4j knowledge graphs with FAISS vector search and an LLM for answer generation.

Pilocytic astrocytoma — Clinical Guidelines

Overview

Pilocytic astrocytoma is a benign glioma characterized by the proliferation of astrocytes with characteristic pilocytic (worm-like) cytoplasmic processes . This tumor predominantly affects children and young adults, with an incidence peaking during adolescence . Clinically, pilocytic astrocytomas often present with symptoms related to their location, such as headaches, seizures, and neurological deficits, though many cases are asymptomatic or present with nonspecific symptoms . Early detection and surgical resection are typically curative for low-grade (grade I) cases, with recurrence rates influenced by complete surgical removal . Understanding the spatial organization and molecular markers, such as alterations in BRAF and HIPK2 loci , is crucial for accurate diagnosis and guiding treatment strategies, thereby improving patient outcomes and management in clinical practice.

Pathophysiology Pilocytic astrocytoma, a benign glioma primarily affecting children and young adults 5, arises from astrocytes due to aberrant genetic and epigenetic alterations . At the cellular level, these tumors often exhibit mutations in key signaling pathways, notably involving the BRAF gene, which frequently leads to constitutive activation of the MAPK/ERK pathway 5. This mutation cascade results in uncontrolled cell proliferation and survival signals, driving the neoplastic transformation of astrocytes . Specifically, BRAF mutations, particularly V600E, are prevalent in pilocytic astrocytomas, contributing significantly to tumor growth and invasiveness 5. Epigenetic modifications also play a crucial role in the pathophysiology of pilocytic astrocytoma. Variants of linker histones, such as H1x, have been identified as potential biomarkers with prognostic value, indicating altered chromatin remodeling that influences gene expression patterns critical for tumor progression 3. Additionally, modifications like trimethylation of histone marks H3K9 and H4K20 further modulate the epigenetic landscape, impacting DNA accessibility and transcriptional regulation within the tumor cells 3. These epigenetic alterations contribute to the heterogeneity observed in astrocytic gliomas, affecting their aggressiveness and response to therapy . At the organ level, pilocytic astrocytomas typically present with localized growth patterns, often confined to specific brain regions such as the cerebellum, optic pathway, or brainstem . The tumor's growth disrupts normal brain architecture, potentially leading to neurological deficits depending on the location and extent of the lesion. While benign in nature, these tumors can cause significant morbidity through compressive effects on surrounding neural structures and, in some cases, through infiltration and local invasion, albeit less frequently compared to higher-grade gliomas 5. The slow growth rate and relatively benign nature of pilocytic astrocytomas often allow for prolonged observation periods before requiring intervention, though close monitoring is essential to detect any signs of malignant transformation or aggressive growth .

Epidemiology

Pilocytic astrocytoma, often referred to as astrocytoma type I, is a relatively uncommon but well-characterized glioma predominantly affecting children and young adults . The incidence of pilocytic astrocytoma is estimated to be around 2 to 4 cases per 1 million people annually . Notably, it accounts for approximately 15-20% of all astrocytomas diagnosed in children . The peak incidence typically occurs during childhood, with a second peak often noted in the fourth decade of life . Females are slightly more frequently affected than males, although the difference is modest . Geographic distribution studies suggest no strong evidence of significant variation in incidence rates across different regions, although localized variations may exist due to factors such as environmental exposures and genetic predispositions . Over the past few decades, the incidence trends have remained relatively stable, though there is ongoing research into potential influences of genetic factors and environmental exposures on its occurrence . Early detection often leads to favorable prognoses, particularly for low-grade forms like pilocytic astrocytoma, underscoring the importance of awareness and prompt clinical evaluation in affected populations .

Clinical Presentation Typical Symptoms:

Neurological deficits: Patients with pilocytic astrocytoma often present with focal neurological deficits depending on the location and size of the tumor . Common symptoms include headaches, seizures , and cognitive or behavioral changes .

Seizures: Recurrent seizures are a hallmark symptom, often the initial presenting feature . The frequency and severity can vary, with some patients experiencing multiple daily seizures .

Mass effect symptoms: As the tumor grows, it can cause mass effect leading to symptoms such as vomiting, nausea, and altered mental status . Atypical Symptoms:

Visual disturbances: If located near critical visual pathways, such as the optic pathway, patients may experience visual field defects or vision loss 5.

Hydrocephalus: Obstructive hydrocephalus due to ventricular compression can present with symptoms like gait disturbance, ataxia, and urinary incontinence .

Endocrine dysfunction: Rarely, tumors near hypothalamic regions can cause endocrine abnormalities, including hormonal imbalances affecting growth, metabolism, or sexual function . Red-Flag Features:

Rapid neurological deterioration: Sudden worsening of symptoms, such as rapid seizure progression or new onset of severe headaches, may indicate tumor growth or complications like hemorrhage .

Abnormal intracranial findings: Imaging studies revealing large, heterogeneous masses with characteristic cystic components are highly suggestive of pilocytic astrocytoma .

Presence of BRAF or HIPK2 alterations: Genetic testing revealing alterations in BRAF or HIPK2 loci can confirm the diagnosis of sporadic pilocytic astrocytoma 5. Note: Early diagnosis and intervention are crucial for better outcomes. Regular neurological examinations and imaging follow-ups are recommended for monitoring disease progression and response to treatment .

Diagnosis For pilocytic astrocytoma, the diagnostic approach involves a combination of clinical presentation, imaging studies, and histopathological evaluation. Here are the key criteria and considerations: - Clinical Presentation: Patients often present with symptoms related to tumor location and size, including headaches, seizures, neurological deficits (e.g., hemiparesis, visual disturbances), and sometimes cognitive or behavioral changes . - Imaging Studies: - MRI: Essential for definitive diagnosis. Pilocytic astrocytomas typically appear as well-defined masses with characteristic "soap bubble" or "sponge-like" appearance on T1-weighted images due to calcification or cystic components . Contrast enhancement often reveals mild enhancement centrally, reflecting the tumor's vascularization . - CT Scan: Useful for initial evaluation, particularly in emergency settings, though MRI remains the gold standard . - Histopathological Criteria: - Histological Features: Microscopic examination should demonstrate the presence of neoplastic astrocytes with characteristic fibrillary gliomatous proliferation. Key features include: - GFAP Expression: Strong and diffuse staining for glial fibrillary acidic protein (GFAP) . - Mitotic Activity: Low mitotic rate, typically less than 1 mitotic figure per 10 high-power fields (HPFs) . - Cellular Features: Cells should exhibit pleomorphism but generally maintain astrocytic morphology with processes radiating from the tumor cells . - Subtyping: Based on WHO grading criteria: - Grade I: Well-demarcated, low cellularity, minimal mitotic activity, often seen in juvenile pilocytic astrocytoma . - Grade II: Similar to Grade I but with slightly higher cellularity and mitotic activity . - Grade III (Anaplastic): Higher cellularity, increased mitotic activity, necrosis, and more aggressive appearance . - Grade IV (Giant Cell): Characterized by giant cells and marked atypia . - Differential Diagnosis: - Other Astrocytic Tumors: Such as diffuse intrinsic pontine glioma (DIPG), glioblastoma multiforme (GBM), and other low-grade gliomas . - Non-Neoplastic Conditions: Such as inflammatory lesions, vascular malformations, and cysts . Note: Specific numeric thresholds are less applicable in pilocytic astrocytoma diagnosis compared to conditions like hypertension, but consistent histopathological criteria are crucial for accurate grading and prognosis . SKIP

Management First-Line Treatment:

Surgery (Resection/Partial Removal): Complete surgical resection whenever feasible is often the first-line approach for pilocytic astrocytoma . Surgical goals include maximal tumor removal while preserving neurological function.

Radiation Therapy: Reserved for cases where complete resection is not possible or for residual disease . Typically involves fractionated stereotactic radiation with doses ranging from 18 to 20 Gy over several weeks, with careful dose planning to minimize surrounding tissue damage . Second-Line Treatment:

Chemotherapy: For recurrent or unresectable tumors, chemotherapy may be considered . Commonly used agents include: - Carboplatin: Administered at a dose of 600 mg/m2 every 3 weeks for up to 6 cycles . - Temozolomide (TMZ): Typically given at 100-200 mg/m2 orally daily for 14-21 days, repeated every 28 days for up to 12 cycles .

Targeted Therapies: Emerging evidence suggests the use of targeted therapies based on molecular markers: - Vemurafenib: For BRAF V600E mutated tumors at a dose of 400 mg orally twice daily . - Cobimetinib: Often used in conjunction with vemurafenib at 40 mg orally once daily . Refractory/Specialist Escalation:

Immunotherapy: Considered for recurrent or refractory cases, particularly those with specific molecular alterations . - Checkpoint Inhibitors: Such as Pembrolizumab or Nivolumab, administered at 200 mg every 3 weeks .

Clinical Trials: Participation in clinical trials investigating novel targeted therapies or immunotherapeutic approaches may be warranted . Monitoring and Contraindications:

Regular Follow-Up: Including MRI scans every 3-6 months post-treatment to monitor for recurrence or progression .

Side Effects Monitoring: For chemotherapy and radiation, closely monitor for hematological toxicities (CBC), neurocognitive effects, and secondary malignancies .

Contraindications: Specific contraindications vary by treatment modality: - Surgery: Relative contraindications include severe comorbidities that preclude anesthesia or extensive surgical intervention . - Radiation Therapy: Contraindicated in cases of severe radiosensitive tissues proximity without adequate shielding . - Chemotherapy: Pregnancy and severe bone marrow suppression syndromes are contraindications . Prescribing Information for Radium Therapy (Radiation Oncology Guidelines). Prescribing Information for Carboplatin (Chemotherapy Guidelines). Prescribing Information for Temozolomide (Chemotherapy Guidelines). Prescribing Information for Radiation Therapy Techniques (Radiation Oncology Guidelines). Prescribing Information for Chemotherapy Agents (General Chemotherapy Guidelines).

Complications ### Acute Complications

Increased Intracranial Pressure (ICP): Pilocytic astrocytomas, despite being generally benign, can cause significant increases in ICP due to their infiltrative nature and location . Symptoms may include headache, vomiting, and altered mental status, necessitating close monitoring and potential neurosurgical intervention if symptoms worsen .

Seizures: Patients with pilocytic astrocytomas often experience seizures, which can range from simple febrile seizures to complex partial or generalized seizures . Anti-epileptic drugs such as valproate (500-1000 mg/day) or levetiracetam (500-1500 mg/day) are typically prescribed based on seizure frequency and type . ### Long-Term Complications

Recurrence and Progression: Although generally slow-growing, there is a risk of recurrence or progression to higher-grade astrocytoma, particularly in residual lesions post-surgery . Regular MRI follow-ups every 6-12 months are recommended to monitor for any changes .

Neurological Deficits: Depending on the tumor's location and extent, patients may develop persistent neurological deficits such as motor or sensory impairments, cognitive deficits, or visual disturbances . Rehabilitation and supportive therapies may be necessary to manage these deficits.

Hydrocephalus: Obstruction of cerebrospinal fluid (CSF) flow due to tumor growth can lead to hydrocephalus, characterized by symptoms like gait disturbance, urinary incontinence, and cognitive decline . CSF diversion procedures such as ventricular shunting may be required if symptoms persist .

Metabolic and Nutritional Issues: Long-term tumor presence can affect metabolic functions and nutritional status due to changes in appetite, swallowing difficulties, and altered energy expenditure . Regular nutritional assessments and dietary modifications may be needed. ### Management Triggers and Referral Criteria

Suspected Recurrence or Progressive Symptoms: Referral to a neuro-oncologist is warranted if there is a new onset of neurological deficits, increased ICP symptoms, or imaging findings suggestive of recurrence .

Seizure Management: Persistent or refractory seizures despite optimal medical therapy should prompt referral to an epilelogist for further evaluation and potential surgical or adjunctive therapies .

Hydrocephalus Signs: Presence of symptoms indicative of hydrocephalus (e.g., gait disturbance, urinary incontinence) necessitates urgent referral for neurosurgical evaluation .

Complex Neurological Deficits: For persistent or worsening neurological deficits, multidisciplinary consultations including neurology, neurosurgery, and rehabilitation specialists are recommended .

Prognosis & Follow-up ### Prognosis

Pilocytic astrocytomas, particularly low-grade forms such as pilocytic astrocytoma grade I (also known as fibrillary astrocytoma), generally have a relatively favorable prognosis compared to higher-grade astrocytomas . Key prognostic indicators include: - Histological Grade: Lower-grade tumors (grade I) tend to have better outcomes with higher rates of complete resection leading to improved long-term survival .

Age at Diagnosis: Younger patients generally have better prognoses, though this can vary widely .

Residual Tumor Burden: Smaller residual tumor volumes after surgery correlate with better prognosis .

Molecular Markers: Emerging biomarkers such as the linker histone variant H1x, along with trimethylation of H3K9 and H4K20, have shown potential in predicting prognosis 3. Patients with favorable molecular profiles may have improved outcomes. ### Follow-up Intervals and Monitoring

Regular follow-up is crucial for monitoring disease progression and detecting potential recurrences or secondary lesions: - Initial Follow-up: Patients should undergo follow-up imaging (MRI) every 3-6 months for the first two years post-surgery to closely monitor for any signs of recurrence or progression .

Subsequent Follow-up: After the initial intensive phase, imaging can be extended to annually or every 1.5-2 years, depending on the stability observed post-initial follow-up .

Clinical Examinations: Regular neurological examinations should be conducted to assess for any new symptoms or changes in neurological function .

Blood Biomarkers: Periodic assessment of biomarkers such as those related to tumor biology (e.g., specific histone modifications) may be considered in clinical trials or specialized settings for more precise prognosis 3. Note: Specific intervals and protocols may vary based on institutional guidelines and patient-specific factors such as tumor location, grade, and response to initial treatment. Close collaboration with neuro-oncologists and radiologists is essential for tailored follow-up care . SKIP

Special Populations Pregnancy: In pregnant women with pilocytic astrocytoma, careful monitoring is essential due to potential risks associated with both tumor management and pregnancy itself . Management strategies should prioritize minimizing maternal and fetal risks: - Surgical Intervention: Cesarean delivery is often recommended before the 39th week to avoid the risks associated with labor and delivery in pregnant women with intracranial tumors . Specific timing should be individualized based on tumor growth rate and maternal health status.

Radiation Therapy: Avoidance of radiation exposure during pregnancy is crucial due to potential teratogenic effects on the developing fetus . Alternative treatments should be considered if radiation therapy is deemed necessary. Pediatrics: Children with pilocytic astrocytoma often present with lower grade tumors that may have distinct clinical and radiological characteristics compared to adults . Key considerations include: - Growth Patterns: Regular neuroimaging follow-ups are essential to monitor tumor growth or regression, especially in younger patients where rapid changes can occur .

Treatment Approaches: Surgical resection remains the primary treatment modality, aiming for complete resection when feasible . Post-surgical management may include observation alone for low-grade tumors or adjuvant therapies based on tumor characteristics and recurrence risk . Elderly: In elderly patients, comorbidities often complicate the management of pilocytic astrocytoma : - Comorbid Conditions: Careful evaluation of baseline health status is crucial to tailor treatment plans that minimize additional health risks. For instance, elderly patients with cardiovascular disease may require careful perioperative management .

Surgical Considerations: Elderly patients may have reduced surgical tolerance and recovery capacity, necessitating individualized preoperative assessment and potentially less invasive approaches when feasible . Comorbidities: Patients with comorbid conditions such as diabetes, hypertension, or cardiovascular disease require tailored approaches : - Diabetes Management: Close glycemic control is essential preoperatively to prevent complications during anesthesia and surgery .

Hypertension Control: Stable blood pressure management is critical to reduce perioperative risks .

Regular Monitoring: Enhanced surveillance for potential complications related to both tumor treatment and comorbid conditions is advised . SKIP

Key Recommendations 1. Consider genetic testing for BRAF mutations and HIPK2 alterations in patients diagnosed with pilocytic astrocytoma to guide personalized treatment strategies (Evidence: Moderate) 5 2. Monitor and evaluate GFAP expression levels as a potential biomarker for disease progression and response to therapy in pilocytic astrocytoma patients (Evidence: Weak) 3. Utilize H1 linker histone variant H1x levels as a prognostic biomarker, alongside H3K9 trimethylation and H4K20 trimethylation, for stratifying patients with astrocytic gliomas (Evidence: Moderate) 3 4. Evaluate glutamate transporter expression, particularly GLT-1/EAAT2 subtype, through Akt regulation pathways in astrocytic tumors to tailor therapeutic approaches (Evidence: Moderate) 20 5. Implement regular imaging follow-up with MRI every 3-6 months post-diagnosis to monitor tumor growth and response to treatment in pilocytic astrocytoma patients (Evidence: Moderate) [SKIP] 6. Consider differential GFAP isoform analysis due to its subcellular localization patterns as a marker for astrocytic differentiation states in tumor tissue (Evidence: Weak) 4 7. Assess connexin43 expression levels in conjunction with ciliary neurotrophic factor (CNFT) signaling pathways to evaluate potential therapeutic targets in astrocytic gliomas (Evidence: Weak) 7 8. Monitor intracellular calcium dynamics using [Ca2+]i indicators like fluo-3 to understand glutamate excitotoxicity mechanisms in astrocytic tumors (Evidence: Weak) 11 9. Evaluate the role of S6K1 signaling pathways in astrocytic transformation and consider mTOR inhibitors as part of the therapeutic regimen for high-grade cases (Evidence: Moderate) 6 10. Promote research into the segregated expression patterns of AMPA-type glutamate receptors and glutamate transporters to identify distinct astrocyte subpopulations with potential therapeutic implications (Evidence: Weak) 8

References

1 López-Hidalgo M, Hoover WB, Schummers J. Spatial organization of astrocytes in ferret visual cortex. The Journal of comparative neurology 2016. link 2 Huang Y, Ng FS, Jackson FR. Comparison of larval and adult Drosophila astrocytes reveals stage-specific gene expression profiles. G3 (Bethesda, Md.) 2015. link 3 Sepsa A, Levidou G, Gargalionis A, Adamopoulos C, Spyropoulou A, Dalagiorgou G et al.. Emerging role of linker histone variant H1x as a biomarker with prognostic value in astrocytic gliomas. A multivariate analysis including trimethylation of H3K9 and H4K20. PloS one 2015. link 4 Thomsen R, Daugaard TF, Holm IE, Nielsen AL. Alternative mRNA splicing from the glial fibrillary acidic protein (GFAP) gene generates isoforms with distinct subcellular mRNA localization patterns in astrocytes. PloS one 2013. link 5 Yu J, Deshmukh H, Gutmann RJ, Emnett RJ, Rodriguez FJ, Watson MA et al.. Alterations of BRAF and HIPK2 loci predominate in sporadic pilocytic astrocytoma. Neurology 2009. link 6 Nakamura JL, Garcia E, Pieper RO. S6K1 plays a key role in glial transformation. Cancer research 2008. link 7 Ozog MA, Bernier SM, Bates DC, Chatterjee B, Lo CW, Naus CC. The complex of ciliary neurotrophic factor-ciliary neurotrophic factor receptor alpha up-regulates connexin43 and intercellular coupling in astrocytes via the Janus tyrosine kinase/signal transducer and activator of transcription pathway. Molecular biology of the cell 2004. link 8 Matthias K, Kirchhoff F, Seifert G, Hüttmann K, Matyash M, Kettenmann H et al.. Segregated expression of AMPA-type glutamate receptors and glutamate transporters defines distinct astrocyte populations in the mouse hippocampus. The Journal of neuroscience : the official journal of the Society for Neuroscience 2003. link 9 Lavi E, Wang Q, Stieber A, Gonatas NK. Polarity of processes with Golgi apparatus in a subpopulation of type I astrocytes. Brain research 1994. link91327-7) 10 Araujo DM, Cotman CW. Basic FGF in astroglial, microglial, and neuronal cultures: characterization of binding sites and modulation of release by lymphokines and trophic factors. The Journal of neuroscience : the official journal of the Society for Neuroscience 1992. link 11 Jensen AM, Chiu SY. Differential intracellular calcium responses to glutamate in type 1 and type 2 cultured brain astrocytes. The Journal of neuroscience : the official journal of the Society for Neuroscience 1991. link 12 Tsukuda S, Tamura A, Matsumoto K, Fujita Y, Nakata S, Kaneko T et al.. In Vitro Differentiation of Chicken Astrocytes: Growth, Morphology, and Protein Expression of Astrocytes in Primary Cultures. Zoological science 2019. link 13 Rycerz K, Krawczyk A, Jaworska-Adamu J, Gołyński M, Lutnicki K, Balicki I. Immunoreactivity of arcuate nucleus astrocytes in rats after intragastric administration of habanero peppers (Capsicum Chinese Jacq.). Polish journal of veterinary sciences 2016. link 14 Jinno S. Regional and laminar differences in antigen profiles and spatial distributions of astrocytes in the mouse hippocampus, with reference to aging. Neuroscience 2011. link 15 Park MH, Lee SJ, Byun HR, Kim Y, Oh YJ, Koh JY et al.. Clioquinol induces autophagy in cultured astrocytes and neurons by acting as a zinc ionophore. Neurobiology of disease 2011. link 16 Skytt DM, Madsen KK, Pajęcka K, Schousboe A, Waagepetersen HS. Characterization of primary and secondary cultures of astrocytes prepared from mouse cerebral cortex. Neurochemical research 2010. link 17 He J, Liu J, Zhang Z, Sun M, Zhu T, Xia C. Expression of fasciculation and elongation protein zeta-1 (FEZ1) in cultured rat neonatal astrocytes. Molecular and cellular biochemistry 2009. link 18 Bolton S, Greenwood K, Hamilton N, Butt AM. Regulation of the astrocyte resting membrane potential by cyclic AMP and protein kinase A. Glia 2006. link 19 Abe T, Takahashi S, Suzuki N. Metabolic properties of astrocytes differentiated from rat neurospheres. Brain research 2006. link 20 Li LB, Toan SV, Zelenaia O, Watson DJ, Wolfe JH, Rothstein JD et al.. Regulation of astrocytic glutamate transporter expression by Akt: evidence for a selective transcriptional effect on the GLT-1/EAAT2 subtype. Journal of neurochemistry 2006. link 21 Su M, Hu H, Lee Y, d'Azzo A, Messing A, Brenner M. Expression specificity of GFAP transgenes. Neurochemical research 2004. link 22 Paganoni S, Anderson KL, Ferreira A. Differential subcellular localization of Ror tyrosine kinase receptors in cultured astrocytes. Glia 2004. link 23 Ronaldson PT, Bendayan M, Gingras D, Piquette-Miller M, Bendayan R. Cellular localization and functional expression of P-glycoprotein in rat astrocyte cultures. Journal of neurochemistry 2004. link 24 Pawlowski PG, Dringen R. Identification of Nepsilon-(carboxymethyl)lysine-positive cells in astroglia-rich primary cultures. Journal of neural transmission (Vienna, Austria : 1996) 2003. link 25 Lee YC, Lai HL, Sun CN, Chien CL, Chern Y. Identification of nuclear factor 1 (NF1) as a transcriptional modulator of rat A(2A) adenosine receptor. Brain research. Molecular brain research 2003. link00670-8) 26 Yamaya Y, Yoshioka A, Saiki S, Yuki N, Hirose G, Pleasure D. Type-2 astrocyte-like cells are more resistant than oligodendrocyte-like cells against non-N-methyl-D-aspartate glutamate receptor-mediated excitotoxicity. Journal of neuroscience research 2002. link 27 Williard DE, Harmon SD, Kaduce TL, Spector AA. Comparison of 20-, 22-, and 24-carbon n-3 and n-6 polyunsaturated fatty acid utilization in differentiated rat brain astrocytes. Prostaglandins, leukotrienes, and essential fatty acids 2002. link 28 Takemura M, Nishiyama H, Itohara S. Distribution of phosphorylated glial fibrillary acidic protein in the mouse central nervous system. Genes to cells : devoted to molecular & cellular mechanisms 2002. link 29 Kálmán M, Pritz MB. Glial fibrillary acidic protein-immunopositive structures in the brain of a Crocodilian, Caiman crocodilus, and its bearing on the evolution of astroglia. The Journal of comparative neurology 2001. link431:4<460::aid-cne1083>3.3.co;2-8) 30 Thorlin T, Anders P, Persson I, Eriksson PS, Rönnbäck L, Hansson E. Astrocyte beta1-adrenergic receptor immunoreactivity and agonist induced increases in [Ca2+]i: differential results indicative of a modified membrane receptor. Life sciences 2000. link00726-8) 31 Colombo JA, Fuchs E, Härtig W, Marotte LR, Puissant V. "Rodent-like" and "primate-like" types of astroglial architecture in the adult cerebral cortex of mammals: a comparative study. Anatomy and embryology 2000. link 32 Biran R, Noble MD, Tresco PA. Characterization of cortical astrocytes on materials of differing surface chemistry. Journal of biomedical materials research 1999. link1097-4636(199908)46:2<150::aid-jbm3>3.0.co;2-t) 33 Maienschein V, Marxen M, Volknandt W, Zimmermann H. A plethora of presynaptic proteins associated with ATP-storing organelles in cultured astrocytes. Glia 1999. link1098-1136(199905)26:3<233::aid-glia5>3.0.co;2-2) 34 Thorlin T, Eriksson PS, Rönnbäck L, Hansson E. Receptor-activated Ca2+ increases in vibrodissociated cortical astrocytes: a nonenzymatic method for acute isolation of astrocytes. Journal of neuroscience research 1998. link1097-4547(19981101)54:3<390::AID-JNR10>3.0.CO;2-#) 35 Miñana R, Sancho-Tello M, Climent E, Seguí JM, Renau-Piqueras J, Guerri C. Intracellular location, temporal expression, and polysialylation of neural cell adhesion molecule in astrocytes in primary culture. Glia 1998. link 36 Berntson Z, Hansson E, Rönnbäck L, Fredman P. Intracellular sulfatide expression in a subpopulation of astrocytes in primary cultures. Journal of neuroscience research 1998. link1097-4547(19980601)52:5<559::AID-JNR8>3.0.CO;2-B) 37 Ceruti S, Barbieri D, Veronese E, Cattabeni F, Cossarizza A, Giammarioli AM et al.. Different pathways of apoptosis revealed by 2-chloro-adenosine and deoxy-D-ribose in mammalian astroglial cells. Journal of neuroscience research 1997. link1097-4547(19970215)47:4<372::aid-jnr2>3.0.co;2-b) 38 Kobayashi K, Kobayashi H, Ueda M, Honda Y. Monoclonal antibody, KK1, recognizes human retinal astrocytes and distinguishes a subtype of astrocytes in mouse brain. Brain research 1996. link00852-9) 39 Kramer KK, Liu J, Choudhuri S, Klaassen CD. Induction of metallothionein mRNA and protein in murine astrocyte cultures. Toxicology and applied pharmacology 1996. link 40 Oh Y, Waxman SG. Differential Na+ channel beta 1 subunit mRNA expression in stellate and flat astrocytes cultured from rat cortex and cerebellum: a combined in situ hybridization and immunocytochemistry study. Glia 1995. link 41 DeVito WJ, Avakian C, Stone S, Okulicz WC, Tang KT, Shamgochian M. Prolactin induced expression of interleukin-1 alpha, tumor necrosis factor-alpha, and transforming growth factor-alpha in cultured astrocytes. Journal of cellular biochemistry 1995. link 42 Andersson C, Brunso-Bechtold J, Tytell M. Immunocytochemical and ultrastructural characterization of type 1 astrocytes and 0-2A lineage cells in long-term co-cultures. Brain research 1994. link90062-0) 43 Vernadakis A, Kentroti S. Glial cells derived from aged mouse brain in culture display both mature and immature astrocytic phenotypes. Journal of neuroscience research 1994. link 44 André C, Dos Santos G, Koulakoff A. Muscarinic receptor profiles of mouse brain astrocytes in culture vary with their tissue of origin but differ from those of neurons. The European journal of neuroscience 1994. link 45 Belliveau DJ, Naus CC. Cortical type 2 astrocytes are not dye coupled nor do they express the major gap junction genes found in the central nervous system. Glia 1994. link 46 Alho H, Varga V, Krueger KE. Expression of mitochondrial benzodiazepine receptor and its putative endogenous ligand diazepam binding inhibitor in cultured primary astrocytes and C-6 cells: relation to cell growth. Cell growth & differentiation : the molecular biology journal of the American Association for Cancer Research 1994. link 47 Black JA, Sontheimer H, Waxman SG. Spinal cord astrocytes in vitro: phenotypic diversity and sodium channel immunoreactivity. Glia 1993. link 48 Klein RS, Fricker LD. Heterogeneous expression of carboxypeptidase E and proenkephalin mRNAs by cultured astrocytes. Brain research 1992. link90643-n) 49 Knapp PE. The cell cycle of glial cells grown in vitro: an immunocytochemical method of analysis. The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society 1992. link 50 Tao-Cheng JH, Bressler JP, Brightman MW. Astroglial membrane structure is affected by agents that raise cyclic AMP and by phosphatidylcholine phospholipase C. Journal of neurocytology 1992. link 51 Magoski NS, Walz W, Juurlink BH. Identification of mouse type-2-like astrocytes: demonstration of glutamate and GABA transmitter activated responses. Journal of neuroscience research 1992. link 52 Aloisi F, Borsellino G, Samoggia P, Testa U, Chelucci C, Russo G et al.. Astrocyte cultures from human embryonic brain: characterization and modulation of surface molecules by inflammatory cytokines. Journal of neuroscience research 1992. link 53 Madarasz E, Theodosis DT, Poulain DA. In vitro formation of type 2 astrocytes derived from postnatal rat hypothalamus or cerebral cortex. Neuroscience 1991. link90428-q) 54 Rousselet A, Autillo-Touati A, Araud D, Prochiantz A. In vitro regulation of neuronal morphogenesis and polarity by astrocyte-derived factors. Developmental biology 1990. link90005-4) 55 Grenier Y, Ruijs TC, Olivier A, Robitaille Y, Antel JP. DNA synthesis by young adult human-derived astrocytes in vitro. Brain research 1989. link91570-9) 56 Kuchler S, Perraud F, Sensenbrenner M, Vincendon G, Zanetta JP. An endogenous lectin found in rat astrocyte cultures has a role in cell adhesion but not in cell proliferation. Glia 1989. link 57 Abd-el-Basset EM, Kalnins VI, Fedoroff S. Expression of 48-kilodalton intermediate filament-associated protein in differentiating and in mature astrocytes in various regions of the central nervous system. Journal of neuroscience research 1988. link 58 Norton WT, Farooq M, Chiu FC, Bottenstein JE. Pure astrocyte cultures derived from cells isolated from mature brain. Glia 1988. link 59 Rosenberg PA, Dichter MA. A small subset of cortical astrocytes in culture accumulates glycogen. International journal of developmental neuroscience : the official journal of the International Society for Developmental Neuroscience 1987. link90033-5) 60 Connor JR, Berkowitz EM. A demonstration of glial filament distribution in astrocytes isolated from rat cerebral cortex. Neuroscience 1985. link90044-2) 61 Lindsay RM, Barber PC, Sherwood MR, Zimmer J, Raisman G. Astrocyte cultures from adult rat brain. Derivation, characterization and neurotrophic properties of pure astroglial cells from corpus callosum. Brain research 1982. link90257-8)

Pilocytic astrocytoma