text:
Summary: Gap junction alpha-8 protein (Cx50)
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This is the Wikipedia entry entitled "GJA8". More...
GJA8 Edit Wikipedia article
Gap junction protein, alpha 8, 50kDa | |||||||||||||
Identifiers | |||||||||||||
Symbols | GJA8; CAE; CAE1; CX50; CZP1; MP70 | ||||||||||||
External IDs | OMIM: 600897 MGI: 99953 HomoloGene: 3857 IUPHAR: Cx50 GeneCards: GJA8 Gene | ||||||||||||
RNA expression pattern | |||||||||||||
More reference expression data | |||||||||||||
Orthologs | |||||||||||||
Species | Human | Mouse | |||||||||||
Entrez | 2703 | 14616 | |||||||||||
Ensembl | ENSG00000121634 | ENSMUSG00000049908 | |||||||||||
UniProt | P48165 | P28236 | |||||||||||
RefSeq (mRNA) | NM_005267.4 | NM_008123.2 | |||||||||||
RefSeq (protein) | NP_005258.2 | NP_032149.1 | |||||||||||
Location (UCSC) | Chr 1: 147.37 147.38 Mb |
Chr 3: 96.92 96.93 Mb |
PubMed search | [1] | [2] | |||||||||||
Identifiers | |||||||||
Symbol | Connexin50 | ||||||||
Pfam | PF03509 | ||||||||
InterPro | IPR002266 | ||||||||
Gap junction alpha-8 protein is a protein that in humans is encoded by the GJA8 gene.[1][2][3] It is also known as connexin 50.
Contents |
[edit] Related gene problems
- 1q21.1 deletion syndrome[4]
- 1q21.1 duplication syndrome[4]
- microphthalmia[5] and other vision pathologies
[edit] Interactions
GJA8 has been shown to interact with Tight junction protein 1.[6]
[edit] References
- ^ Shiels A, Mackay D, Ionides A, Berry V, Moore A, Bhattacharya S (Apr 1998). "A missense mutation in the human connexin50 gene (GJA8) underlies autosomal dominant "zonular pulverulent" cataract, on chromosome 1q". Am J Hum Genet 62 (3): 52632. doi:10.1086/301762. PMC 1376956. PMID 9497259. //www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=1376956.
- ^ Church RL, Wang JH, Steele E (Aug 1995). "The human lens intrinsic membrane protein MP70 (Cx50) gene: clonal analysis and chromosome mapping". Curr Eye Res 14 (3): 21521. doi:10.3109/02713689509033517. PMID 7796604.
- ^ "Entrez Gene: GJA8 gap junction protein, alpha 8, 50kDa". http://www.ncbi.nlm.nih.gov/sites/entrez?Db=gene&Cmd=ShowDetailView&TermToSearch=2703.
- ^ a b Mefford HC, Sharp AJ, Baker C, Itsara A, Jiang Z, Buysse K, Huang S, Maloney VK, Crolla JA, Baralle D, et al. (October 2008). "Recurrent rearrangements of chromosome 1q21.1 and variable pediatric phenotypes". N. Engl. J. Med. 359 (16): 168599. doi:10.1056/NEJMoa0805384. PMC 2703742. PMID 18784092. //www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2703742.
- ^ Rong P, Wang X, Niesman I, Wu Y, Benedetti LE, Dunia I, Levy E, Gong X (January 2002). "Disruption of Gja8 (alpha8 connexin) in mice leads to microphthalmia associated with retardation of lens growth and lens fiber maturation". Development 129 (1): 16774. PMID 11782410. http://dev.biologists.org/content/129/1/167.long.
- ^ Nielsen PA, Baruch A, Shestopalov VI, Giepmans BN, Dunia I, Benedetti EL, Kumar NM (June 2003). "Lens connexins alpha3Cx46 and alpha8Cx50 interact with zonula occludens protein-1 (ZO-1)". Mol. Biol. Cell 14 (6): 247081. doi:10.1091/mbc.E02-10-0637. PMC 194895. PMID 12808044. //www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=194895.
[edit] Further reading
- Andrew L Harris and Darren Locke (2009). Connexins, A Guide. New York: Springer. pp. 574. ISBN 978-1-934115-46-6. http://www.springer.com/978-1-934115-46-6.
- Cook PJ, Hamerton JL (1980). "Report of the committee on the genetic constitution of chromosome 1.". Cytogenet. Cell Genet. 25 (1-4): 920. doi:10.1159/000131394. PMID 396131.
- Jarvis LJ, Louis CF (1993). "The permeability of reconstituted liposomes containing the purified lens fiber cell integral membrane proteins MP20, MP26 and MP70.". J. Membr. Biol. 130 (3): 25163. PMID 1491428.
- Church RL, Wang JH, Steele E (1996). "The human lens intrinsic membrane protein MP70 (Cx50) gene: clonal analysis and chromosome mapping.". Curr. Eye Res. 14 (10): 97981. doi:10.3109/02713689508995138. PMID 8549164.
- Geyer DD, Church RL, Steele EC, et al. (1998). "Regional mapping of the human MP70 (Cx50; connexin 50) gene by fluorescence in situ hybridization to 1q21.1.". Mol. Vis. 3: 13. PMID 9479004.
- Dunia I, Recouvreur M, Nicolas P, et al. (1998). "Assembly of connexins and MP26 in lens fiber plasma membranes studied by SDS-fracture immunolabeling.". J. Cell. Sci. 111 (15): 210920. PMID 9664032.
- Hopperstad MG, Srinivas M, Spray DC (2000). "Properties of gap junction channels formed by Cx46 alone and in combination with Cx50.". Biophys. J. 79 (4): 195466. doi:10.1016/S0006-3495(00)76444-7. PMC 1301086. PMID 11023900. //www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=1301086.
- Xu X, Berthoud VM, Beyer EC, Ebihara L (2002). "Functional role of the carboxyl terminal domain of human connexin 50 in gap junctional channels.". J. Membr. Biol. 186 (2): 10112. doi:10.1007/s00232-001-0139-5. PMC 2744361. PMID 11944087. //www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2744361.
- Nielsen PA, Baruch A, Shestopalov VI, et al. (2004). "Lens connexins alpha3Cx46 and alpha8Cx50 interact with zonula occludens protein-1 (ZO-1).". Mol. Biol. Cell 14 (6): 247081. doi:10.1091/mbc.E02-10-0637. PMC 194895. PMID 12808044. //www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=194895.
- Arora A, Minogue PJ, Liu X, et al. (2006). "A novel GJA8 mutation is associated with autosomal dominant lamellar pulverulent cataract: further evidence for gap junction dysfunction in human cataract.". J. Med. Genet. 43 (1): e2. doi:10.1136/jmg.2005.034108. PMC 2564510. PMID 16397066. //www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2564510.
- Devi RR, Vijayalakshmi P (2006). "Novel mutations in GJA8 associated with autosomal dominant congenital cataract and microcornea.". Mol. Vis. 12: 1905. PMID 16604058.
- Zhang X, Zou T, Liu Y, Qi Y (2006). "The gating effect of calmodulin and calcium on the connexin50 hemichannel.". Biol. Chem. 387 (5): 595601. doi:10.1515/BC.2006.076. PMID 16740131.
- Ni X, Valente J, Azevedo MH, et al. (2007). "Connexin 50 gene on human chromosome 1q21 is associated with schizophrenia in matched case control and family-based studies.". J. Med. Genet. 44 (8): 5326. doi:10.1136/jmg.2006.047944. PMC 2597930. PMID 17412882. //www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2597930.
- Kotsias BA, Salim M, Peracchia LL, Peracchia C (2007). "Interplay between cystic fibrosis transmembrane regulator and gap junction channels made of connexins 45, 40, 32 and 50 expressed in oocytes.". J. Membr. Biol. 214 (1): 18. doi:10.1007/s00232-006-0064-8. PMID 17546509.
- Hansen L, Yao W, Eiberg H, et al. (2007). "Genetic heterogeneity in microcornea-cataract: five novel mutations in CRYAA, CRYGD, and GJA8.". Invest. Ophthalmol. Vis. Sci. 48 (9): 393744. doi:10.1167/iovs.07-0013. PMID 17724170.
This article on a gene on chromosome 1 is a stub. You can help Wikipedia by expanding it. |
This page is based on a Wikipedia article. The text is available under the Creative Commons Attribution/Share-Alike License.
This tab holds the annotation information that is stored in the Pfam database. As we move to using Wikipedia as our main source of annotation, the contents of this tab will be gradually replaced by the Wikipedia tab.
Gap junction alpha-8 protein (Cx50) Provide feedback
No Pfam abstract.
External database links
Pseudofam: | PF03509 |
SYSTERS: | Connexin50 |
This tab holds annotation information from the InterPro database.
InterPro entry IPR002266
The connexins are a family of integral membrane proteins that oligomerise to form intercellular channels that are clustered at gap junctions. These channels are specialised sites of cell-cell contact that allow the passage of ions, intracellular metabolites and messenger molecules (with molecular weight less than 1-2kDa) from the cytoplasm of one cell to its opposing neighbours. They are found in almost all vertebrate cell types, and somewhat similar proteins have been cloned from plant species. Invertebrates utilise a different family of molecules, innexins, that share a similar predicted secondary structure to the vertebrate connexins, but have no sequence identity to them [PUBMED:9769729].
Vertebrate gap junction channels are thought to participate in diverse biological functions. For instance, in the heart they permit the rapid cell-cell transfer of action potentials, ensuring coordinated contraction of the cardiomyocytes. They are also responsible for neurotransmission at specialised 'electrical' synapses. In non-excitable tissues, such as the liver, they may allow metabolic cooperation between cells. In the brain, glial cells are extensively-coupled by gap junctions; this allows waves of intracellular Ca2+ to propagate through nervous tissue, and may contribute to their ability to spatially-buffer local changes in extracellular K+ concentration [PUBMED:7685944].
The connexin protein family is encoded by at least 13 genes in rodents, with many homologues cloned from other species. They show overlapping tissue expression patterns, most tissues expressing more than one connexin type. Their conductances, permeability to different molecules, phosphorylation and voltage-dependence of their gating, have been found to vary. Possible communication diversity is increased further by the fact that gap junctions may be formed by the association of different connexin isoforms from apposing cells. However, in vitro studies have shown that not all possible combinations of connexins produce active channels [PUBMED:8811187, PUBMED:8608591].
Hydropathy analysis predicts that all cloned connexins share a common transmembrane (TM) topology. Each connexin is thought to contain 4 TM domains, with two extracellular and three cytoplasmic regions. This model has been validated for several of the family members by in vitro biochemical analysis. Both N- and C-termini are thought to face the cytoplasm, and the third TM domain has an amphipathic character, suggesting that it contributes to the lining of the formed-channel. Amino acid sequence identity between the isoforms is ~50-80%, with the TM domains being well conserved. Both extracellular loops contain characteristically conserved cysteine residues, which likely form intramolecular disulphide bonds. By contrast, the single putative intracellular loop (between TM domains 2 and 3) and the cytoplasmic C terminus are highly variable among the family members. Six connexins are thought to associate to form a hemi-channel, or connexon. Two connexons then interact (likely via the extracellular loops of their connexins) to form the complete gap junction channel.
NH2-*** *** *************-COOH ** ** ** ** ** ** ** ** Cytoplasmic ---**----**-----**----**---------------- ** ** ** ** Membrane ** ** ** ** ---**----**-----**----**---------------- ** ** ** ** Extracellular ** ** ** ** ** **
Two sets of nomenclature have been used to identify the connexins. The first, and most commonly used, classifies the connexin molecules according to molecular weight, such as connexin43 (abbreviated to Cx43), indicating a connexin of molecular weight close to 43kDa. However, studies have revealed cases where clear functional homologues exist across species that have quite different molecular masses; therefore, an alternative nomenclature was proposed based on evolutionary considerations, which divides the family into two major subclasses, alpha and beta, each with a number of members [PUBMED:1320430]. Due to their ubiquity and overlapping tissue distributions, it has proved difficult to elucidate the functions of individual connexin isoforms. To circumvent this problem, particular connexin-encoding genes have been subjected to targeted-disruption in mice, and the phenotype of the resulting animals investigated. Around half the connexin isoforms have been investigated in this manner [PUBMED:9861669]. Further insight into the functional roles of connexins has come from the discovery that a number of human diseases are caused by mutations in connexin genes. For instance, mutations in Cx32 give rise to a form of inherited peripheral neuropathy called X-linked dominant Charcot-Marie-Tooth disease [PUBMED:7570999]. Similarly, mutations in Cx26 are responsible for both autosomal recessive and dominant forms of nonsyndromic deafness, a disorder characterised by hearing loss, with no apparent effects on other organ systems.
Gap junction alpha-8 protein (also called connexin50, Cx50, or lens fibre protein MP70) is a connexin of ~431 amino acid residues. The chicken isoform is shorter (399 residues) and is hence known as Cx45.6. Cx50 and Cx46 are the two gap junction proteins normally found in lens fibre cells of the eye. Evidence from both genetically-engineered mice, and from the identification of mutations in the human Cx50-encoding gene, highlight the importance of this connexin in maintaining lens transparency. Deletion of mice Cx50 produces a viable phenotype, but these animals start to develop cataracts (of the zonular pulverant type) at about one week old. They also have abnormally small eyes and lenses. Similarly, mutations in the human gene encoding Cx50 have been associated with the occurrence of congenital cataracts. Affected individuals develop cataracts (with zonular pulverent opacities), and analysis shows they have a single point mutation in the Cx50 coding region, resulting in a non-conservative substitution in the second putative TM domain of a serine residue for a proline.
Gene Ontology
The mapping between Pfam and Gene Ontology is provided by InterPro. If you use this data please cite InterPro.
Cellular component | connexon complex (GO:0005922) |
Biological process | cell communication (GO:0007154) |
Domain organisation
Below is a listing of the unique domain organisations or architectures in which this domain is found. More...
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We store a range of different sequence alignments for families. As well as the seed alignment from which the family is built, we provide the full alignment, generated by searching the sequence database using the family HMM. We also generate alignments using four representative proteomes (RP) sets, the NCBI sequence database, and our metagenomics sequence database. More...
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We make a range of alignments for each Pfam-A family. You can see a description of each above. You can view these alignments in various ways but please note that some types of alignment are never generated while others may not be available for all families, most commonly because the alignments are too large to handle.
Seed (4) |
Full (47) |
Representative proteomes | NCBI (40) |
Meta (0) |
Jalview | ||||||||
PP/heatmap | 1 | |||||||
Pfam viewer |
1Cannot generate PP/Heatmap alignments for seeds; no PP data available
Key: available, not generated, — not available.
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We make all of our alignments available in Stockholm format. You can download them here as raw, plain text files or as gzip-compressed files.
Seed (4) |
Full (47) |
Representative proteomes | NCBI (40) |
Meta (0) |
Raw Stockholm | ||||||||
Gzipped |
You can also download a FASTA format file containing the full-length sequences for all sequences in the full alignment.
External links
MyHits provides a collection of tools to handle multiple sequence alignments. For example, one can refine a seed alignment (sequence addition or removal, re-alignment or manual edition) and then search databases for remote homologs using HMMER3.
HMM logo
HMM logos is one way of visualising profile HMMs. Logos provide a quick overview of the properties of an HMM in a graphical form. You can see a more detailed description of HMM logos and find out how you can interpret them here. More...
This page displays the phylogenetic tree for this family's seed alignment. We use FastTree to calculate neighbour join trees with a local bootstrap based on 100 resamples (shown next to the tree nodes). FastTree calculates approximately-maximum-likelihood phylogenetic trees from our seed alignment.
Note: You can also download the data file for the tree.
Curation and family details
This section shows the detailed information about the Pfam family. You can see the definitions of many of the terms in this section in the glossary and a fuller explanation of the scoring system that we use in the scores section of the help pages.
Seed source: | PRINTS |
Previous IDs: | none |
Type: | Family |
Author: | Griffiths-Jones SR |
Number in seed: | 4 |
Number in full: | 47 |
Average length of the domain: | 66.60 aa |
Average identity of full alignment: | 70 % |
Average coverage of the sequence by the domain: | 15.69 % |
HMM information
HMM build commands: |
build method: hmmbuild -o /dev/null HMM SEED
search method: hmmsearch -Z 23193494 -E 1000 --cpu 4 HMM pfamseq
Model details: |
Model length: | 66 | ||||||||||||
Family (HMM) version: | 9 | ||||||||||||
Download: | download the raw HMM for this family |
Species distribution
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Tag Results
129 posts tagged pop pilates
129 posts tagged pop pilates
I want you to click play and do this inner thigh challenge with me right now. If you want toned legs for summer and also love Clarity by Zedd…this workout is kinda for you. And by kinda, I mean really.
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- inner thighs
- obliques
What more cold you ask for!? Get down on the floor. Let's do this.
<3 Cassey
I'm headed to NYC tomorrow! Do any East Coast POPsters wanna meet up? I'm leading a free POP Pilates class in Manhattan!
Will you please come? I'd love to meet you!
Here are the deets:
DATE: Sunday April 14th, 2013
TIME: Doors open at 10:15am and class starts promptly at 10:30am. (The POP Pilates class will run for 1 hr and then we will have time to take pics and talk over free snacks!!)
PLACE: "Dance Manhattan" at 39 W. 19th St. (5th Floor) New York, NY 10001
RSVP here: http://www.bit.ly/blogilatesNYC
And I am having a huge fitness party at UCLA when I come back! You're so invited!
LA 80's STYLE FITNESS PARTY!
Come to the Blogilates 80's themed fitness party at UCLA, Wilson Plaza on April 20th 10-12pm! Also free. RSVP here: http://www.bit.ly/blogilatesUCLA
See you at one of these hopefully! Love you :)
<3 Cassey
I designed a full stretch routine for you to do to really open up your back and your hip muscles. It really feels SOOOOO GOOD. Please try to do this before and/or after your workout.
Very relaxing…and yes, Little Things piano is playing in the background :)
<3 Cassey
Fun new total body workout! This one is animal themed and Jackelyn is back. So you know it's gonna be crazy but hard. Have fun!! Lemme know how you like it!
<3 Cassey
Happy Valentine's Day!
I have some TOUGH LOVE for you…it's the TOUGH LOVE HANDLES Workout.
Have fun and ask your Valentine to do this with you :0
xo <3 Cassey
HIITilates: Beautiful Burn
Here's the video if you wanna do it with me :)
The official prom dress workout!
<3 Cassey
Try this awesome HIITilates routine! (HIIT + Pilates)
If you don't know what the moves are, watch this video!


text:
SUPPORT SERVICES ABOUT HOW TO HELP ABOUT ThyCa To view files, you need Adobe Acrobat Reader. |
Stimulating Hormone (TSH) Suppression
Patients treated for differentiated thyroid cancer take a daily thyroid hormone replacement pill called levothyroxine (also known as T4). They take it both to avoid hypothyroidism (underactive thyroid condition) and to prevent growth or recurrence of their thyroid cancer. Usually they receive a T4 dose large enough to suppress their blood level of thyroid stimulating hormone (TSH) below the normal TSH range. This is called TSH suppression. The ATA and ETA guidelines suggest TSH suppression when a patient has active tumor or has a very aggressive tumor that has been treated with surgery and radioactive iodine (I 131). However, about 85% of patients can be shown to be free of disease after initial tumor treatment by testing the patient' serum thyroglobulin levels and performing neck ultrasonography. When the patient is felt to be free of tumor on this basis, the ATA and ETA guidelines suggest maintaining the blood TSH in the low normal level, which is particularly important in children. Patients whose thyroid glands have been removed will need to be on levothyroxine medication for the rest of their lives. The medication, which is necessary for maintaining a person's full health, must be taken on an empty stomach. Generally, it should not be taken with other drugs, since a large number of drugs interfere with thyroid hormone getting into the blood stream. Drugs as common as vitamins with iron can do this. It is necessary to check with the pharmacist and physician when new drugs are being prescribed There are several brands of levothyroxine. Thyroid cancer specialist physicians recommend that patients stay on the same brand and not change unless a re-test of their blood is done 6 weeks later, because the brands may not result in the same TSH level, even at the same dose. More information about levothyroxine is in the web site section titled "Know Your Pills." The American Thyroid Association Guidelines (2009) have more information and recommendations. They are linked from the web site in the sections titled Newly Diagnosed and Thyroid Cancer Types. TSH in Initial Management and Long-Term Management The American Thyroid Association's Guidelines (2009) make several recommendations regarding TSH. For initial TSH suppression, for high-risk and intermediate-risk patients, the guidelines recommend initial TSH below 0.1 mU/L, and, for low-risk patients TSH at or slightly below the lower limit of normal (0.1–0.5 mU/L). (Recommendation 40). For long-term management, the guidelines recommend (Recommendation 49):
About 85% of postoperative patients are low-risk, according to the guidelines. The Guidelines, plus other information linked in the Newly Diagnosed section explain low, intermediate, and high risk of persistent or recurrent disease. |


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Notes and Splinters is a chapbook-length set of poems that I wrote, with a few exceptions, between 1996 and 2000. The title is an amalgamation of the last and first pieces — Note to Self and splinters strewn across the hard wood floor, respectively — but it's more than just a mildly clever manipulation of labels. Thematically, the poems in this volume may be categorized as either notes or splinters.
The splinters are painful pieces. They are the irritations that niggle, still, ten to fifteen years later. They are monuments to mistakes and missed opportunities. They are the slightly darker shade of the tooth you had to cap because you fell off your bike when you were twelve and hit your face on a rock, and now whenever you brush your teeth, you see that tooth and remember the fall, the fright, the pain, the bloody walk home as you balance your bike and cry mostly because you're pissed at yourself for falling but also a little because you got hurt.
The notes are ruminations. They are the meanderings of a wanderlustful mind. They are the things I want to remember, in the way I want to remember them. They evoke the sight, smell, sound, taste, thoughts, emotions, sensations, colorings of tidbits of my life. Some of them are significant, some of them are not, but I'm not sure I'd be able to tell which are which.
The notes and the splinters are together because, in many cases, they are both.
The three that were written more recently are Your lover, my love, Excuses for the Dogs and Epiphany. I included them here because they just seemed to fit. There are reasons why they fit, thematically and stylistically, but I think they also fit because I have returned to a frame of mind that I had during the period when the bulk of these poems were written. I've been so far, but in some ways I've not gone anywhere. These three notes and splinters prove that.


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Mary Johnson, 92
Mary A. "Marie" Johnson, age 92, died on Tuesday, Dec. 4, at Deerfield Gables in New Richmond, Wis.
Mary A. "Marie" Johnson, age 92, died on Tuesday, Dec. 4, at Deerfield Gables in New Richmond, Wis.
She was born to Joseph and Celestina (Pechacek) Brooks on May 13, 1920, in Cherma, Wis. Mary attended Forestville and Donegal Schools. She married Marshall Johnson on Sept. 12, 1939. She worked for Lang Wear and River Falls Medical Clinic.
Mary enjoyed spending time with her family, sewing and cooking. She made many crafts and quilts.
She is survived by her sons, Gary and Ron (Karen); daughters, Phyllis (Don) Foley and Deb Iverson; brother Joe (Margaret) Brooks; 14 grandchildren, 22 great-grandchildren; two great-great grandchildren; and many other relatives and friends.
Mary was preceded in death by her parents; husband, Marshall; grandson Cory; brother Milton; son-in-law Jim Iverson.
Mass of Christian Burial for Mary will be held at 10:30 a.m. Friday, Dec. 7, at St. Bridget Catholic Church in River Falls. Visitation will be 1 hour prior to the service at the church. Burial will be at St. Bridget Cemetery.
In lieu of flowers, memorials are preferred to the family.
To send an online condolence, please visit www.hillfuneralhome.com. Cashman-Hill Funeral Home and Cremation Services is assisting the family.
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Tammy P.
Stone Lake, WI 12/14/2012 9:27 AM
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This information is produced and provided by the National Cancer Institute (NCI). The information in this topic may have changed since it was written. For the most current information, contact the National Cancer Institute via the Internet web site at http://cancer.gov or call 1-800-4-CANCER.
The National Cancer Institute provides the PDQ pediatric cancer treatment information summaries as a public service to increase the availability of evidence-based cancer information to health professionals, patients, and the public. The PDQ childhood brain tumor treatment summaries are organized primarily according to the 2000 World Health Organization classification of nervous system tumors.[1]
Dramatic improvements in survival have been achieved for children and adolescents with cancer. Between 1975 and 2002, childhood cancer mortality has decreased by more than 50%.[2] Childhood and adolescent cancer survivors require close follow-up because cancer therapy side effects may persist or develop months or years after treatment. Refer to the PDQ summary on Late Effects of Treatment for Childhood Cancer for specific information about the incidence, type, and monitoring of late effects in childhood and adolescent cancer survivors.
Primary brain tumors are a diverse group of diseases that together constitute the most common solid tumor of childhood. Brain tumors are classified according to histology, but tumor location and extent of spread are important factors that affect treatment and prognosis. Immunohistochemical analysis, cytogenetic and molecular genetic findings, and measures of mitotic activity are increasingly used in tumor diagnosis and classification. Refer to the PDQ summary on Childhood Brain and Spinal Cord Tumors for information about the general classification of childhood brain and spinal cord tumors.
Diagnostic Evaluation
Every patient with newly diagnosed medulloblastoma should be evaluated with diagnostic imaging of the entire neuraxis and, when possible and safe, lumbar cerebrospinal fluid analysis.
Predictors of Outcome
Patients with disseminated disease at diagnosis are clearly at highest risk for disease relapse.[3,4,5] Other factors that portend an unfavorable outcome include younger age at diagnosis (in the absence of extensive nodularity) and possibly, a subtotal resection; however, the amount of residual disease after surgery has not been found to be a robust predictor of outcome, especially when chemotherapy was added to radiation therapy as part of postoperative treatment.[6,7] Similarly, the presence of brain stem involvement at diagnosis has not been shown to be predictive of outcome.[7,8]
In addition, histopathologic features such as large cell variant, anaplasia, and desmoplasia have been shown in retrospective analyses to correlate with outcome.[9,10] These molecular genetic immunohistochemical and histopathologic findings have not been shown to be predictive of outcome in prospective studies and with the exception of anaplasia/large cell variant, are not yet incorporated into stratification schema. However, it is likely that one or more of these biologic findings may yet be utilized, possibly in combination with factors such as extent of dissemination at the time of diagnosis, age of the patient, and amount of residual disease after surgery to better categorize patients with medulloblastoma into risk subgroups.[11,12,13,14,15,16]
A host of biologic parameters that may be predictive of outcome have been identified. These parameters include the following:
Among these genetic alterations, the most robust predictors of outcome appear to be the following:
1. | Amplification ofMYCfamily oncogenes (approximately 5%–10% of cases) andTP53mutations, which confers the worst prognosis. |
2. | Loss of chromosome 6q associated with activated Wnt pathway in conjunction with mutations of beta-catenin in tumors typically found in older children, which confers the best prognosis. |
Integrated genomics identifies multiple medulloblastoma subtypes with distinct genetic profiles, pathway signatures, and clinicopathological features. Interestingly, in a recent study of adult medulloblastomas, MYC oncogene amplifications were rarely observed and tumors with 6q deletion and nuclear beta-catenin activation did not share the excellent prognosis seen with pediatric medulloblastomas.[11,12,13,14,30,32,34,37,38,39]
Furthermore, DNA sequencing studies have demonstrated fewer mutations in medulloblastoma than in adult carcinomas and a positive correlation between patient age and the number of mutations found. The relatively low numbers of mutations suggest that fewer driver mutations are required for medulloblastoma tumorigenesis. In addition, genome-wide association studies have identified mutated genes previously not implicated in medulloblastoma pathogenesis, such as the tumor suppressors MLL2 and MLL3, from the family of genes affecting histone methylation.[40] These findings add an additional layer of complexity to the biologic understanding of medulloblastoma.
The classification of a childhood brain tumor is based on both the histopathologic characteristics of the tumor and its location in the brain.[1,2,3] The histopathological classification of childhood central nervous system (CNS) embryonal tumors remains somewhat controversial. These tumors all develop on the background of an undifferentiated round cell tumor but show a variety of divergent patterns of differentiation. Although it has been proposed that these tumors be merged under the term primitive neuroectodermal tumor, histologically similar tumors in different locations in the CNS demonstrate different genetic alterations.[4,5,6,7] In the 2007 World Health Organization (WHO) classification, embryonal tumors include the following:[2,8]
Pineoblastoma, a tumor histologically similar to CNS embryonal tumors, is reviewed in this summary, although pineoblastoma is grouped with tumors of the pineal region in the WHO classification.
By definition, medulloblastomas must arise in the posterior fossa.[1,2,3] Five different subtypes of medulloblastoma are recognized by the WHO classification and includes the following:
Significant attention has been focused on medulloblastomas that display anaplastic features, including increased nuclear size, marked cytological pleomorphism, numerous mitoses, and apoptotic bodies.[9,10] Classification is a complicated matter because most medulloblastomas have some degree of anaplasia, foci of anaplasia may appear in tumors with histologic features of both classic and large cell medulloblastomas, and there is significant overlap between the anaplastic and large cell variant.[9,10,11,12] The incidence of medulloblastoma with desmoplastic variant is higher in infants, is less common in children, and increases again in adolescents and adults. The desmoplastic variant subtype is different from medulloblastoma with extensive nodularity; the nodular variant having an expanded lobular architecture. The nodular subtype occurs almost exclusively in infants and carries an excellent prognosis.[12]
CNS PNETs generally arise in the cerebrum or suprasellar region. According to the 2007 WHO classification, tumors demonstrating areas of distinct neuronal differentiation are termed cerebral neuroblastomas and, if ganglion cells are also present, ganglioneuroblastomas. The pineoblastoma is histologically similar to the medulloblastoma; however, according to the WHO, its histogenesis is linked to a pineal cell, the pineocyte. Histologically different from the pineocyte, a pineal parenchymal tumor of intermediate differentiation showing elements of pineoblastoma and pineocytoma is recognized, although its natural history is variable and poorly characterized.[1,2]
Both medulloepithelioma and ependymoblastoma are identified as histologically discrete tumors within the WHO classification system.[8,13] Medulloepithelioma and ependymoblastoma tumors are rare and tend to arise most commonly in infants and young children. Medulloepitheliomas, which histologically recapitulate the embryonal neural tube, tend to arise supratentorially, primarily intraventricularly, but may arise infratentorially, in the cauda, and even extraneural, along nerve roots.[8,13]
The existence of ependymoblastomas as a discrete entity has been questioned, although it remains in the most recent WHO classification. Ependymoblastoma is characterized by the presence of true multilayered (or ependymoblastic) rosettes.[14,15] The tumor has a supratentorial predilection, but like medulloepithelioma, it may occur in the spine, especially in the sacrococcygeal region. Histologically, the tumor shares features with other embryonal tumors and with a rare tumor type, the "embyronal tumor with abundant neuropil and true rosettes" (ETANTR).[14,15,16,17] The latter entity is characterized by young age at diagnosis (median age approximately 2 years), primarily supratentorial presentation, poor prognosis, and tumors showing true multilayered/ependymoblastic rosettes within a background of abundant neuropil-like areas.[15,17,18] In addition to sharing clinical characteristics (i.e., age, primary site, and prognosis), ependymoblastoma and ETANTR show common genomic alterations, including chromosome 2 gain and focal amplification at chromosome band 19q13.42. The latter chromosome region contains a cluster of microRNA coding genes,[19] and its amplification appears to be present in virtually all pediatric embryonal tumors with true multilayered rosettes (i.e., ependymoblastoma and ETANTR).[18,19,20] By contrast, 19q13.42 amplification has not been detected in more than 300 other pediatric brain tumors, suggesting that it may be a useful diagnostic marker for ependymoblastoma and ETANTR.[18]
The pathologic classification of pediatric brain tumors is a specialized area that is evolving. Immunohistochemical staining is now a routine component of evaluation.[9,10] Molecular genetic profiles are also being incorporated into evaluation and may radically alter classification in the future.[21,22,23,24] For example, gene expression profiling divides medulloblastoma into distinctive biological subtypes that differ in their clinical presentation, their underlying genomic abnormalities, and their immunohistochemical staining pattern.[23,24]
Possible subgroups include the following:
Staging of Medulloblastoma
Evidence suggests that medulloblastomas originate from two different germinal zones within the cerebellum. The ventricular zone gives rise to the more common classic midline medulloblastomas, whereas granule neuron precursor cells of the external granule layer are believed to give rise to the lateral cerebellar hemispheric desmoplastic medulloblastomas. The tumors may spread contiguously to the cerebellar peduncle, along the floor of the fourth ventricle, into the cervical spine, or above the tentorium. At the time of diagnosis there is spread via the cerebrospinal fluid (CSF) to other intracranial sites, the spinal cord, or both in 10% to 30% of patients.[1,2,3]
Magnetic resonance imaging (MRI) is the method of choice to evaluate for intracranial or spinal cord subarachnoid metastases. To avoid postoperative artifacts, such imaging is best performed preoperatively, but postoperative evaluation is also useful when obtained at least 10 days following the operative procedure. The entire spine must be imaged in at least two planes, with contiguous magnetic resonance slices performed before and after gadolinium enhancement. The significance of positive CSF cytology in samples obtained within the first 7 to 10 days of diagnosis is unclear, as is the significance of tumor cells in cisternal fluid obtained at the time of surgery. However, CSF tumor cells found 2 to 3 weeks after diagnosis portends a poorer prognosis.[1,2,3] Extracranial spread of medulloblastoma at the time of diagnosis is less than 1%. Although bone scans and bone marrows have been routinely obtained in some older prospective studies, their yield was low and they are primarily recommended for infants or those with widespread intracranial disease, intraspinal disease, or those with symptoms and signs consistent with possible dissemination.[2,3] CSF shunts placed at the time of surgery have not been shown to increase the risk of leptomeningeal relapse.[2]
Historically, staging has been primarily based on an intraoperative evaluation of both the size and extent of the tumor, coupled with postoperative neuroimaging of the brain and spine and cytological evaluation of CSF. MRI of the brain and spine (often done preoperatively), postoperative MRI of the brain to determine the amount of residual disease, and lumbar CSF analysis are now used to determine staging.[1,2,3] Surgical impressions, including direct observation of dissemination at the time of diagnosis, extent of residual disease following surgery, and involvement of the brain stem, are still incorporated into staging systems.
Staging of Pineoblastoma
Staging for children with pineoblastomas is the same as that performed for children with medulloblastoma.[4] Dissemination at the time of diagnosis occurs in 10% to 30% of patients.[4] Because of the location of the tumor, total resections are uncommon, and most patients have only a biopsy or a subtotal resection before postsurgical treatment.[4,5] Similar to other central nervous system (CNS) primitive neuroectodermal tumors (PNETs), all pineoblastomas are treated as high-risk embryonal tumors. Prognosis is worse for patients with disseminated disease at the time of diagnosis.[4,5]
Staging of CNS PNETs
Patients with CNS PNETs are staged in a fashion similar to that used for children with medulloblastoma. CNS PNETs may be disseminated at the time of diagnosis, although the incidence of dissemination may be somewhat less than that of medulloblastomas or pineoblastomas, with dissemination at diagnosis being documented in approximately 10% to 20% of patients.[6,7] CNS PNETs are often amenable to resection; in series, 50% to 60% of patients were totally or near-totally resected.[6,7]
Staging of Other CNS Embryonal Tumors
Dissemination of both medulloepitheliomas and ependymoblastomas may occur, and the tumors are staged in the same way as medulloblastoma.
Note: Some citations in the text of this section are followed by a level of evidence. The PDQ editorial boards use a formal ranking system to help the reader judge the strength of evidence linked to the reported results of a therapeutic strategy. (Refer to the PDQ summary on Levels of Evidence for more information.)
Risk Stratification for Medulloblastoma
On the basis of neuroradiographic evaluation for disseminated disease, cerebrospinal fluid (CSF) cytological examination, postoperative neuroimaging evaluation for the amount of residual disease, age of the patient, and impression of the surgeon at the time of surgery, patients with medulloblastoma have been historically stratified into the following two risk groups:
The 1.5 cm standard was arbitrarily chosen for evaluation in prospective studies. Metastatic disease includes neuroradiographic evidence of disseminated disease, positive cytology in lumbar or ventricular CSF obtained more than 7 days postsurgery, or extraneural disease.[2]
An intense area of study is the use of molecular and immunohistochemical analysis for disease stratification. In a large, multi-institution, retrospective biologic study, 397 medulloblastoma specimens were analyzed by transcriptional profiling (103 specimens) and immunohistochemical analysis.[3] Four unique clusters of medulloblastomas were identified. The following two subgroups clearly stood out:
Patients from both of these subgroups had excellent prognoses; 80% or greater 5-year progression-free survival (PFS) and overall survival (OS). The remainder of medulloblastomas, which comprise the majority of the study cohort, were separable into two other subgroups, which had greater overlap and shared a poorer prognosis, including a 30% to 45% chance of dissemination. The latter two subsets (termed Group C and Group D) differed in the following ways:
PFS for patients with Group C and D tumors ranged between 32% and 63%.[3] Other studies have confirmed the excellent prognosis of children with WNT tumors and poor prognosis of those with tumors with MYC amplification.[4,5] If this type of molecular and immunohistochemical separation can be confirmed in a homogeneously treated population of patients, preferably studied prospectively, it will dramatically alter disease stratification and likely therapy offered.[6]
Surgery is usually the initial treatment for children with medulloblastoma, both to confirm diagnosis and to remove as much tumor as is safely possible. Evidence suggests that more extensive surgical resections are related to an improved rate of survival, primarily in children with nondisseminated disease at the time of diagnosis.[7,8] One study in high-risk patients utilized presurgical chemotherapy (after tumor biopsy) to reduce tumor bulk and make subsequent resection of the tumor easier.[9] This small study did not demonstrate a high rate of survival, and postchemotherapy surgery did not seem easier and was not related to a reduced incidence of postoperative complications.
Postoperatively, children may have significant neurologic deficits caused by preoperative tumor-related brain injury, hydrocephalus, or surgery-related brain injury.[10][Level of evidence: 3iC] In addition, a significant number of patients with medulloblastoma will develop delayed onset of mutism, suprabulbar palsies, ataxia, hypotonia, and emotional lability. This constellation of findings has been termed the cerebellar mutism syndrome, and its etiology remains unclear, although cerebellar vermian damage has been postulated as a possible cause for the mutism.[11,12]; [13][Level of evidence: 3iC] In two Children's Cancer Group studies evaluating children with both average-risk and poor-risk medulloblastoma, the syndrome has been identified in nearly 25% of patients.[12,13]; [14][Level of evidence: 3iiiC] Many patients with this syndrome may manifest neurologic and neurocognitive sequelae posttreatment.[13,14]
Radiation Therapy
Radiation therapy is usually initiated after surgery with or without concomitant chemotherapy.[15,16,17] To date, the best survival results for children with medulloblastoma have been obtained when radiation therapy is begun within 4 to 6 weeks postsurgery.[15,16,17,18]; [19][Level of evidence: 1iA]
Prospective randomized trials and single-arm trials suggest that adjuvant chemotherapy given during and after radiation therapy improves overall survival for children with both average-risk and poor-risk medulloblastoma.[14,15,16,17,18,19] Although medulloblastoma is often sensitive to chemotherapy, preradiation chemotherapy has not been shown to improve survival compared with treatment with radiation therapy and subsequent chemotherapy. In some prospective studies, preradiation chemotherapy has been related to a poorer rate of survival.[16,17,18,19]
Children of all ages are susceptible to the adverse effects of radiation on brain development. Debilitating effects on growth and neurologic/cognitive development have been frequently observed, especially in younger children.[20,21,22,23] For this reason, the role of chemotherapy in allowing a delay in the administration of radiation therapy has been and is being studied. Results suggest that chemotherapy can be used to delay and sometimes obviate the need for radiation therapy in 20% to 40% of children younger than 3 years with nondisseminated medulloblastoma.[24,25]; [26][Level of evidence: 3iiiC] Children are also at risk for long-term endocrine dysfunction.[26]
Surveillance Testing
Surveillance testing is a part of all ongoing medulloblastoma studies.[27,28,29] Although most treatment failures in patients newly diagnosed with medulloblastoma will occur within the first 18 months postdiagnosis, relapses many years after diagnosis have been noted.[30] In addition, secondary tumors have been increasingly diagnosed in long-term survivors.[29,30]; [31][Level of evidence: 2A] As with initial management, long-term management is complex and requires a multidisciplinary approach.
Note: Some citations in the text of this section are followed by a level of evidence. The PDQ editorial boards use a formal ranking system to help the reader judge the strength of evidence linked to the reported results of a therapeutic strategy. (Refer to the PDQ summary on Levels of Evidence for more information.)
Children with medulloblastoma are stratified into average-risk and poor-risk subsets. Owing to concerns about the long-term neurocognitive sequelae of whole-brain radiation therapy on the developing brain, radiation therapy for younger children has often been delayed or eliminated. Children younger than 3 years and sometimes as old as 5 years have not received the same treatment as older patients.
In all subgroups of patients, surgery is the initial means of therapy, and maximal tumor resection is the goal of treatment. Postsurgical treatment has diverged, to some degree, on the basis of risk stratification and age of the patient.
Average Risk
Standard treatment options
The traditional postsurgical treatment for patients with average-risk medulloblastoma has been 54 Gy to 55 Gy of radiation therapy to the posterior fossa and 36 Gy to the entire neuraxis (i.e., the whole brain and spine).[1,2,3,4] With radiation therapy alone, 5-year event-free survival (EFS) ranges between 50% and 65% in those with nondisseminated disease.[2,3] While the standard boost in medulloblastoma is the entire posterior fossa, patterns of failure data suggest that radiation therapy to the tumor bed instead of the entire posterior fossa would be equally effective and possibly associated with reduced toxicity.[5,6] The minimal dose of craniospinal radiation needed for disease control is unknown. Attempts to lower the dose of craniospinal radiation therapy to 23.4 Gy without chemotherapy have resulted in an increased incidence of isolated leptomeningeal relapse.[4]
Chemotherapy is now a standard component of the treatment of children with average-risk medulloblastoma; a variety of chemotherapeutic regimens have been successfully used, including the combination of cisplatin, lomustine, and vincristine or the combination of cisplatin, cyclophosphamide, and vincristine.[1,2,7] Radiation therapy and chemotherapy given during and after radiation therapy has demonstrated 5-year EFS rates of 70% to 85%.[1,2,3]; [8][Level of evidence: 2A] A lower radiation dose of 23.4 Gy to the neuraxis when coupled with chemotherapy has been shown to result in disease control in up to 85% of patients and may decrease the severity of long-term neurocognitive sequelae.[7,9,10,11]
Long-term survivors who were prepubertal at the time of diagnosis are at high risk for growth failure due to radiation-related hypothalamic failure as well as effects of radiation on spinal growth. Lower doses of craniospinal radiation therapy may decrease the incidence of hypothalamic dysfunction, but this has not yet been proven. Growth hormone replacement therapy has not been shown to increase the likelihood of disease relapse.[12]
Treatment options under clinical evaluation
The following is an example of a national and/or institutional clinical trial that is currently being conducted. Information about ongoing clinical trials is available from the NCI Web site.
High Risk
Standard treatment options
In high-risk patients, numerous studies have demonstrated that multimodality therapy improves the duration of disease control and overall disease-free survival (DFS).[13,14] In contrast to standard-risk treatment, the craniospinal radiation dose is generally 36 Gy. Studies show that approximately 50% to 60% of patients with high-risk disease will experience long-term disease control.[1,13,14,15,16] The drugs that have been found to be useful in children with average-risk disease are the same drugs that have been used extensively in children with poor-risk disease, including cisplatin, lomustine, cyclophosphamide, etoposide, and vincristine.
Treatment options under clinical evaluation
The following is an example of a national and/or institutional clinical trial that is currently being conducted. Information about ongoing clinical trials is available from the NCI Web site.
Children Aged 3 Years and Younger
Standard treatment options
The treatment of children younger than 3 years with newly diagnosed medulloblastoma continues to evolve. Due to concerns over the likely deleterious effects of craniospinal radiation on the immature nervous system, therapeutic approaches have attempted to delay and, in some cases, avoid the use of craniospinal radiation therapy. Results have been variable, and comparison across studies has been difficult because of differences in drug regimens used and the utilization of craniospinal and local boost radiotherapy at the end of chemotherapy or when children reached age 3 years in some studies. Five-year, DFS rates have ranged between 30% and 70% with the majority of long-term survivors successfully treated with chemotherapy alone, having nondisseminated, totally resected tumors.[17,18,19] The histologic finding of desmoplasia has been found to connote a better prognosis, and preliminary results also suggest that specific molecular findings, such as elevated TrkC expression and low MYC expression may also identify subsets of patients who are more likely to be successfully treated with chemotherapy alone.[20,21,22,23]; [24][Level of evidence: 2A]
Therapies have included the use of multiagent chemotherapeutic approaches, including drugs such as cyclophosphamide, etoposide, cisplatin, and vincristine, with or without concomitant high-dose intravenous methotrexate and/or intrathecal methotrexate or mafosfamide.[17,18,19,25,26,27]; [28][Level of evidence: 2A] Another approach that utilized multiagent chemotherapy followed by radiation therapy to the primary tumor site also resulted in disease control in nearly 70% of patients with nondisseminated disease; again disease control was better in those patients with desmoplastic histology.(ISPNO abstract INF 12)[29] Those patients with desmoplastic tumors with extensive nodularity should be carefully evaluated for stigmata of Gorlin syndrome. Gorlin syndrome is an autosomal dominant disorder, also known as the nevoid basal cell carcinoma syndrome, in which those affected are predisposed to the development of basal cell carcinomas later in life, especially in the radiation portal after radiation therapy. The syndrome can be diagnosed early in life by characteristic dermatological and skeletal features including keratocysts of the jaw, bifid or fused ribs, macrocephaly, and calcifications of the falx.[29] Results of trials utilizing higher-dose, marrow ablative, chemotherapeutic regimens supported by autologous stem cell rescue or peripheral stem cell rescue have also demonstrated that a subgroup of patients with medulloblastoma who are younger than 3 years at the time of diagnosis can be treated with chemotherapy alone.[30]; [31][Level of evidence: 2A]
In contrast to children with standard-risk disease, children with disseminated disease at presentation fare poorly with less than 30% of infants and young children surviving despite the use of higher-dose therapy supplemented with methotrexate, either intravenously or intrathecally, and higher-dose chemotherapeutic regimens supported with stem cell rescue. In patients with disseminated disease, there is no consensus on when and how much radiotherapy should be given and at what age radiotherapy should be instituted.[17,18,19]
Treatment options under clinical evaluation
The following are examples of national and/or institutional clinical trials that are currently being conducted. Information about ongoing clinical trials is available from the NCI Web site.
Current Clinical Trials
Check for U.S. clinical trials from NCI's list of cancer clinical trials that are now accepting patients with childhood medulloblastoma. The list of clinical trials can be further narrowed by location, drug, intervention, and other criteria.
General information about clinical trials is also available from the NCI Web site.
Note: Some citations in the text of this section are followed by a level of evidence. The PDQ editorial boards use a formal ranking system to help the reader judge the strength of evidence linked to the reported results of a therapeutic strategy. (Refer to the PDQ summary on Levels of Evidence for more information.)
Children Older Than 3 Years
Standard treatment options
The usual postsurgical treatment for pineoblastomas begins with radiation therapy, although some trials have utilized preradiation chemotherapy. The total dose of radiation therapy to the tumor site is 54 Gy to 55.8 Gy using conventional fractionation.[1,2] Craniospinal irradiation with doses ranging between 23.4 Gy and 36 Gy are also recommended because of the propensity of this tumor to disseminate throughout the subarachnoid space.[1,2] Chemotherapy is usually utilized in the same way as outlined for poor-risk medulloblastomas in children with nondisseminated disease at the time of diagnosis. Five-year disease-free survival is approximately 50%.[1,2,3] For patients with disseminated disease at the time of diagnosis, survival is considerably poorer.[1,2] Similar treatment is given for pineal parenchymal tumors of intermediate differentiation; however, there are no data on response to therapy or outcome.
Treatment options under clinical evaluation
For patients with pineoblastoma, a variety of different treatment approaches are under evaluation, including the use of higher doses of chemotherapy following radiation supported by peripheral stem cell rescue and the use of chemotherapy during radiation.
The following is an example of a national and/or institutional clinical trial that is currently being conducted. Information about ongoing clinical trials is available from the NCI Web site.
Children Aged 3 Years and Younger
Children 3 years and younger with pineoblastoma are usually treated initially with chemotherapy in the hope of delaying, if not obviating, the need for radiation therapy.[4] High-dose, marrow ablative, chemotherapy with autologous bone marrow rescue or peripheral stem cell rescue has been used with some success in young children.[5][Level of evidence: 2Di] The timing and amount of radiation therapy required following chemotherapy in children responding to chemotherapy is unclear.
Current Clinical Trials
Check for U.S. clinical trials from NCI's list of cancer clinical trials that are now accepting patients with untreated childhood pineoblastoma and childhood pineal parenchymal tumor. The list of clinical trials can be further narrowed by location, drug, intervention, and other criteria.
General information about clinical trials is also available from the NCI Web site.
Note: Some citations in the text of this section are followed by a level of evidence. The PDQ editorial boards use a formal ranking system to help the reader judge the strength of evidence linked to the reported results of a therapeutic strategy. (Refer to the PDQ summary on Levels of Evidence for more information.)
Children Older Than 3 Years
Standard treatment options
Attempting aggressive surgical resection is the first step in the management of newly diagnosed central nervous system primitive neuroectodermal tumors (CNS PNETs), although studies have yet to demonstrate that the extent of resection is predictive of outcome.[1,2,3] After surgery, children with CNS PNETs usually receive treatment similar to that received by children with poor-risk medulloblastoma. Best results have been obtained after radiation to the entire neuraxis with local boost radiation therapy, as given for medulloblastoma.[3] However, the local boost radiation therapy may be problematic because of the size of the tumor and its location in the cerebral cortex. The chemotherapeutic approaches during and after radiation therapy are similar to those used for children with poor-risk medulloblastoma. Three- to 5-year overall survival (OS) rates of 40% to 50% have been noted.[1,2,3]; [4][Level of evidence: 2A]; [5][Level of evidence: 3iiiB] Patients with disseminated disease at the time of diagnosis have poorer OS, with reported survival rates at 5 years ranging from 20% to 30%.[1,2,3]
Children Aged 3 Years and Younger
Standard treatment options
Treatment of children aged younger than 3 years with CNS PNETs is similar to that outlined for children with medulloblastoma. With the use of chemotherapy alone, outcome has been variable, with survival rates at 5 years ranging between 0% and 50%.[6,7,8]; [9][Level of evidence: 2Di]
Treatment options under clinical evaluation
The following is an example of a national and/or institutional clinical trial that is currently being conducted. Information about ongoing clinical trials is available from the NCI Web site.
Current Clinical Trials
Check for U.S. clinical trials from NCI's list of cancer clinical trials that are now accepting patients with childhood supratentorial primitive neuroectodermal tumor. The list of clinical trials can be further narrowed by location, drug, intervention, and other criteria.
General information about clinical trials is also available from the NCI Web site.
There are few data on which to base treatment of medulloepithelioma and ependymoblastoma tumors. Treatment considerations are usually the same as those for children with poor-risk medulloblastoma and for children 3 years and younger at diagnosis with other embryonal tumors. Prognosis is poor, with 5-year survival rates ranging between 0% and 30%.[1,2]
Current Clinical Trials
Check for U.S. clinical trials from NCI's list of cancer clinical trials that are now accepting patients with childhood ependymoblastoma and childhood medulloepithelioma. The list of clinical trials can be further narrowed by location, drug, intervention, and other criteria.
General information about clinical trials is also available from the NCI Web site.
Note: Some citations in the text of this section are followed by a level of evidence. The PDQ editorial boards use a formal ranking system to help the reader judge the strength of evidence linked to the reported results of a therapeutic strategy. (Refer to the PDQ summary on Levels of Evidence for more information.)
Recurrence of all forms of central nervous system embryonal tumors is not uncommon, usually occurring within 18 months of treatment; however, recurrent tumors may develop many years after initial treatment.[1,2] Disease may recur at the primary site or may be disseminated at the time of relapse. Sites of noncontiguous relapse may include the spinal leptomeninges, intracranial sites, and cerebrospinal fluid, in isolation or in any combination, and is variably associated with primary tumor relapse.[1,2,3] One series has found that, independent of the dose of radiation therapy employed or the type of chemotherapy utilized, approximately one-third of patients will relapse at the primary tumor site alone, one-third will relapse at the primary tumor site plus distant sites, and one-third will relapse at distant sites without relapse at the primary site.[1,2,3] At the time of relapse, a complete evaluation for extent of recurrence is indicated for all embryonal tumors. Biopsy or surgical resection may be necessary for confirmation of relapse because other entities such as secondary tumors and treatment-related brain necrosis may be clinically indistinguishable from tumor recurrence. The need for surgical intervention must be individualized on the basis of the initial tumor type, the length of time between initial treatment and the reappearance of the lesion, and clinical symptomatology. Extraneural disease relapse may occur but is rare and is seen primarily in patients treated with radiation therapy alone.[4][Level of evidence: 3iiiA]
Patients with recurrent embryonal tumors who have already received radiation therapy and chemotherapy may be candidates for salvage chemotherapy and/or stereotactic radiation therapy.[5] These tumors can be responsive to chemotherapeutic agents used singularly or in combination, including cyclophosphamide, cisplatin, carboplatin, lomustine, etoposide, and topotecan.[6,7,8,9,10,11,12,13,14]; [15][Level of evidence: 2A] Approximately 30% to 50% of these patients will have objective responses to conventional chemotherapy, but long-term disease control is rare. For select patients with recurrent medulloblastoma, primarily infants and young children who were treated at the time of diagnosis with chemotherapy alone and developed local recurrence, long-term disease control may be obtained after further treatment with chemotherapy plus local radiation therapy.[16][Level of evidence: 2A] For patients who have previously received radiation therapy, higher-dose chemotherapeutic regimens, supported with autologous bone marrow rescue or peripheral stem cell support, have been used with variable results.[17,18,19,20][Level of evidence: 2A]; [21][Level of evidence: 3iiB]; [22,23][Level of evidence: 3iiiA] With such regimens, objective response is frequent, occurring in 50% to 75% of patients; however, long-term disease control is obtained in fewer than 30% of patients and is primarily seen in patients in first relapse and in those with only localized disease at the time of relapse.[19]; [21][Level of evidence: 3iiB] Long-term disease control for patients with disseminated disease is infrequent.[24][Level of evidence: 3iA]
Treatment Options Under Clinical Evaluation
Early phase therapeutic trials may be available for selected patients. These trials may be available via Children's Oncology Group phase I institutions, the Pediatric Brain Tumor Consortium, or other entities.
Current Clinical Trials
Check for U.S. clinical trials from NCI's list of cancer clinical trials that are now accepting patients with childhood pineal parenchymal tumor, recurrent childhood pineoblastoma, childhood ependymoblastoma, recurrent childhood medulloblastoma and recurrent childhood supratentorial primitive neuroectodermal tumor. The list of clinical trials can be further narrowed by location, drug, intervention, and other criteria.
General information about clinical trials is also available from the NCI Web site.
The PDQ cancer information summaries are reviewed regularly and updated as new information becomes available. This section describes the latest changes made to this summary as of the date above.
Treatment Option Overview
Added text to state that other studies have confirmed the excellent prognosis of children with WNT tumors and poor prognosis of those with tumors with MYC amplification (cited Ellison et al. [Acta Neuropathologica 2011], Cho et al., and Ellison et al. [Journal of Clinical Oncology 2011] as references 4, 5, and 6, respectively).
Purpose of This Summary
This PDQ cancer information summary for health professionals provides comprehensive, peer-reviewed, evidence-based information about the treatment of childhood central nervous system embryonal tumors. It is intended as a resource to inform and assist clinicians who care for cancer patients. It does not provide formal guidelines or recommendations for making health care decisions.
Reviewers and Updates
This summary is reviewed regularly and updated as necessary by the PDQ Pediatric Treatment Editorial Board, which is editorially independent of the National Cancer Institute (NCI). The summary reflects an independent review of the literature and does not represent a policy statement of NCI or the National Institutes of Health (NIH).
Board members review recently published articles each month to determine whether an article should:
Changes to the summaries are made through a consensus process in which Board members evaluate the strength of the evidence in the published articles and determine how the article should be included in the summary.
The lead reviewers for Childhood Central Nervous System Embryonal Tumors Treatment are:
Any comments or questions about the summary content should be submitted to Cancer.gov through the Web site's Contact Form. Do not contact the individual Board Members with questions or comments about the summaries. Board members will not respond to individual inquiries.
Levels of Evidence
Some of the reference citations in this summary are accompanied by a level-of-evidence designation. These designations are intended to help readers assess the strength of the evidence supporting the use of specific interventions or approaches. The PDQ Pediatric Treatment Editorial Board uses a formal evidence ranking system in developing its level-of-evidence designations.
Permission to Use This Summary
PDQ is a registered trademark. Although the content of PDQ documents can be used freely as text, it cannot be identified as an NCI PDQ cancer information summary unless it is presented in its entirety and is regularly updated. However, an author would be permitted to write a sentence such as "NCI's PDQ cancer information summary about breast cancer prevention states the risks succinctly: [include excerpt from the summary]."
The preferred citation for this PDQ summary is:
National Cancer Institute: PDQ® Childhood Central Nervous System Embryonal Tumors Treatment. Bethesda, MD: National Cancer Institute. Date last modified <MM/DD/YYYY>. Available at: http://www.cancer.gov/cancertopics/pdq/treatment/childCNSembryonal/healthprofessional. Accessed <MM/DD/YYYY>.
Images in this summary are used with permission of the author(s), artist, and/or publisher for use within the PDQ summaries only. Permission to use images outside the context of PDQ information must be obtained from the owner(s) and cannot be granted by the National Cancer Institute. Information about using the illustrations in this summary, along with many other cancer-related images, is available in Visuals Online, a collection of over 2,000 scientific images.
Based on the strength of the available evidence, treatment options may be described as either "standard" or "under clinical evaluation." These classifications should not be used as a basis for insurance reimbursement determinations. More information on insurance coverage is available on Cancer.gov on the Coping with Cancer: Financial, Insurance, and Legal Information page.
Contact Us
More information about contacting us or receiving help with the Cancer.gov Web site can be found on our Contact Us for Help page. Questions can also be submitted to Cancer.gov through the Web site's Contact Form.
Call 1-800-4-CANCER
For more information, U.S. residents may call the National Cancer Institute's (NCI's) Cancer Information Service toll-free at 1-800-4-CANCER (1-800-422-6237) Monday through Friday from 8:00 a.m. to 8:00 p.m., Eastern Time. A trained Cancer Information Specialist is available to answer your questions.
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The NCI's LiveHelp® online chat service provides Internet users with the ability to chat online with an Information Specialist. The service is available from 8:00 a.m. to 11:00 p.m. Eastern time, Monday through Friday. Information Specialists can help Internet users find information on NCI Web sites and answer questions about cancer.
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Search the NCI Web site
The NCI Web site provides online access to information on cancer, clinical trials, and other Web sites and organizations that offer support and resources for cancer patients and their families. For a quick search, use the search box in the upper right corner of each Web page. The results for a wide range of search terms will include a list of "Best Bets," editorially chosen Web pages that are most closely related to the search term entered.
There are also many other places to get materials and information about cancer treatment and services. Hospitals in your area may have information about local and regional agencies that have information on finances, getting to and from treatment, receiving care at home, and dealing with problems related to cancer treatment.
Find Publications
The NCI has booklets and other materials for patients, health professionals, and the public. These publications discuss types of cancer, methods of cancer treatment, coping with cancer, and clinical trials. Some publications provide information on tests for cancer, cancer causes and prevention, cancer statistics, and NCI research activities. NCI materials on these and other topics may be ordered online or printed directly from the NCI Publications Locator. These materials can also be ordered by telephone from the Cancer Information Service toll-free at 1-800-4-CANCER (1-800-422-6237).
Last Revised: 2011-12-14
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Multimedia | PracticeSharp (Practice#) 1.6.3
Date: 03/17/2013 01:12 PM Size: 692 KB License: Freeware Requires: Win7/Vista/XP Downloads: 1118 times TIP: Click here to Update all your PC's Drivers! |
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Use it daily and it will turn your playing skills sharper!
Practice# can be used for:
Practice# was designed as a practical tool, therefore it is minimalistic and doesn't have features that would bloat it. There are minimal menus, two dialog windows (one of them is the About dialog), and in general all possible actions are shown on the main screen in an intuitive and direct way. Keyboard shortcuts allow even easier and immediate control, than using a mouse.
- MP3, WAV, WMA, AIFF, Ogg Vorbis and FLAC


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The Adolescence Education Program provides individuals who have a baccalaureate degree in a content subject the opportunity to become initially certified to teach that subject in grades 7-12 in New York. The program provides courses and experiences in pedagogy, assessment, curriculum, and other topics that prepare individuals to be effective teachers.
Field experiences include a 30 hour tutoring program, an intensive field experience in the semester(s) prior to student teaching, and a semester-long full-time student teaching experience. Candidates in this program can pursue certification in English, math, social studies, French, Spanish, biology, chemistry, physics and earth science.
Those preparing to teach math, languages or a science subject may be eligible to benefit from the new federal TEACH Grant program and/or the New York State Math & Science Teaching Incentive. See the Money Matters page for more information.
Contact InformationIf you wish to apply to this program, please contact the Graduate Admissions Office at St. Bonaventure University at (716) 375-2021 or email@example.com for graduate admission materials.For more information regarding the degree in adolescence education, please contactDr. Paula Kenneson, DirectorPlassmann Hall B38, St. Bonaventure UniversitySt. Bonaventure, NY 14778(716) 375-2177


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The Zis Music Library - Inspired Vol. 2
52 Royalty Free Music Tracks on 1 CD
ZiS Music – Inspired Vol 2 is all about music for motivation, inspiration and achievement. These beautifully produced royalty free music themes share a sense of 'forward motion'. Very uplifting, the emotions range from introspection to determination, but all will inspire dreams and goals through a wide variety of styles including Rock, Pop, Hip-Hop, Orchestral, New Age, Techno and more. All music tracks for corporate video are very editable and are approx. 2:30 with 30 & 60 second edits as well as 2 alternate intros and outros for even more editing options. There are 52 tracks in total on ZiS Music – Inspired Vol 2.
List of Content
Download the The Zis Music Library - Inspired Vol. 2 File Listing to see the complete contents of this package.
Musical Compositions by:
Music Published by:
The Zis Music Library - Inspired Vol. 2
- Unified Theory
- Stay On Track
- Extensive Research
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- Innertech
- Bold Strategies
- Tomorrow's Endeavors
- Form And Function
Once a track is playing, you may move forwards and backwards
in the track by clicking anywhere within the progress bar.
Distributed by Sound Ideas


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Head of School Search News and Announcements
Friday, September 23, 2011 We are pleased to announce Gould's next head of school, Matthew Ruby. Please read the announcement below from Board of Trustees Chair, Richard Packard '66. Dear Gould Community, On behalf of the board of trustees and the Head of…More »


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Read Labor & Employment Law updates, alerts, news, and legal analysis from leading lawyers and law firms:
Failed Unpaid Intern Class Action Hints at Impact of Comcast v. Behrend
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Social Media At Work - What's Allowed and What Isn't? PODCAST - Inside Law
Yahoo's New Parental Leave Policy Raises Some Interesting FMLA Questions
Ann Curry's Departure from the Today Show Presents a Number of Lessons for Employers
Businessweek Reporter: BigLaw Is "Crash Landing"
[Legal Perspective] When Is It NOT Okay to Delete Your Social Media Account?
D.C. Court Wreaks Havoc on NLRB Pro-Worker Cases
Can You Be Fired for a Tattoo?
President Obama Appoints Three Members to NLRB, but Will They Be Confirmed?
Social Media Law Report - Who Owns Your LinkedIn Account, FTC Guidance on Social Ads, More...
Your Employer Doesn't Own Your LinkedIn Account, and They Shouldn't Try To
What You Need to Know About New Secretary of Labor Thomas Perez
Study Reveals Alarming Statistics On Theft and Employee Misuse of Company Data
As Expected, Noel Canning v. NLRB Headed to the Supreme Court
Marijuana in the Workplace
5 Risks of Telecommuting (And How Employers Should Handle Them)
Two Key Elements Every Social Media Policy Should Include
Corporate Law Report: Global HR, Textual Harassment, Working Interviews, and Other Workplace Issues
As Supreme Court Defines "Clothes," Biggest Impact Will Be on Judiciary's Deference to DOL
The Great Recession has altered the consumer landscape, forcing such familiar retailers as Borders, Circuit City and The Sharper Image into bankruptcy. And anyone who's tried to buy a Twinkie in the last few weeks knows that...more
This article briefly discusses the prohibition of indebtedness of shareholders, partners, Board Members, Managers and their relatives in Joint Stock Companies and Limited Liability Partnerships, under the Turkish Commercial...more
On September 4, 2012, Judge Sean H. Lane granted American's renewed motion to reject its CBA with the Allied Pilots Association. As discussed HERE, on August 15, the court denied American's original motion to reject the CBA...more
In the midst of bankruptcy proceedings, American Airlines has asked a judge to allow it to stop paying retiree health insurance and life insurance benefits. - Airline hopes to save over $1.3 billion annually in benefits...more
May 31 (Bloomberg Law) -- Kent Zimmermann, consultant at the Zeughauser Group, and Bill Rochelle from Bloomberg News talk with Bloomberg Law's Lee Pacchia about law firm Dewey & LeBoeuf's bankruptcy filing in the Southern...more
In a recent decision in the VeraSun bankruptcy cases, the U.S. Bankruptcy Court for the District of Delaware held that "change in control" agreements between former executives and the debtors are "employment contracts" under...more
In the midst of conflicting reports about the nation's economic recovery, questions abound among the tri-state's business leaders and entrepreneurs. Are lenders ready to make loans again? When will we see unemployment numbers...more
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Welcome to GRE dictionary, a free online GRE test preparation and vocabulary building tool, including:
We are still in beta version, and will be rolling out features that are still being tested in the coming days. The features you can look forward include:
You will need a Google Account in order to make use of these features. Google accounts are free and the registration only takes a minute. If you have a Gmail email address, you already have a Google account!


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9:00 am
Fri November 30, 2012
McCullough Sentencing Postponed
UPDATE: Friday, November 30, 2012 11:10 am
McCullough's sentencing has been rescheduled for Monday, December 10th, at 10:00 am.
Sentencing for convicted killer Jack McCullough has been postponed. The former Sycamore resident was to be sentenced Friday morning at 11:00 for the 1957 kidnapping and murder of seven-year-old Maria Ridulph.
Chicago Tribune: Sentencing delayed in 1957 Sycamore murder case
But DeKalb County Circuit Clerk Maureen Josh's office confirms Thursday afternoon that sentencing has been postponed. Friday's court appearance has now been changed to a status hearing, where a new sentencing date will be set.
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Citizen JY0064-00L Mens Watch Skyhawk AT Blue Angels Multi-Band Atomic Eco-Drive Flight Chronograph
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For my matcha of the day, I went with one of my favorites. I have a few Matcha that I've not yet tried, still sealed in their shiny gold pouches, but I have quite a few reviews on queue back at the SororiTea Sisters blog that before I add more to the list I think I should drink a bit of what I have opened. Once upon a time I did make a "deal" with myself that I wouldn't open any others until I finished off at least one … and I went bad on that deal but I still want to polish off some of these.
There is a reason why this Matcha has obtained the top spot on the Teas page, it's awesome. Sweet, delicious and caramel-y. So good. It's amazing how well the caramel goes with the vegetative Matcha. It's a bit like a melted candy in a tea bowl… only better.