PubMed:16288293 JSON TXT

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PubmedHPO

{"project":"PubmedHPO","denotations":[{"id":"T1","span":{"begin":43,"end":58},"obj":"HP_0012125"},{"id":"T2","span":{"begin":52,"end":58},"obj":"HP_0002664"},{"id":"T3","span":{"begin":84,"end":90},"obj":"HP_0002664"},{"id":"T4","span":{"begin":167,"end":177},"obj":"HP_0000718"},{"id":"T5","span":{"begin":187,"end":202},"obj":"HP_0012125"},{"id":"T6","span":{"begin":196,"end":202},"obj":"HP_0002664"},{"id":"T7","span":{"begin":333,"end":348},"obj":"HP_0012125"},{"id":"T8","span":{"begin":342,"end":348},"obj":"HP_0002664"}],"text":"Akt-regulated pathways in prostate cancer.\nProstate cancer remains a major cause of cancer-related mortality. Genetic clues to the molecular pathways driving the most aggressive forms of prostate cancer have been limited. Genetic inactivation of PTEN through either gene deletion or point mutation is reasonably common in metastatic prostate cancer and the resulting activation of phosphoinostide 3-kinase, AKT and mTOR provides a major therapeutic opportunity in this disease as mTOR inhibitors, HSP90 inhibitors and PI3K inhibitors begin to enter clinical development."}

DisGeNET5_gene_disease

DisGeNet-2017-sample

{"project":"DisGeNet-2017-sample","denotations":[{"id":"T1339","span":{"begin":246,"end":250},"obj":"gene:5728"},{"id":"T1340","span":{"begin":322,"end":348},"obj":"disease:C0936223"},{"id":"T1341","span":{"begin":407,"end":410},"obj":"gene:207"},{"id":"T1342","span":{"begin":497,"end":502},"obj":"gene:3320"},{"id":"T1343","span":{"begin":518,"end":522},"obj":"gene:5290"}],"relations":[{"id":"R1","pred":"associated_with","subj":"T1339","obj":"T1340"},{"id":"R2","pred":"associated_with","subj":"T1339","obj":"T1340"},{"id":"R3","pred":"associated_with","subj":"T1341","obj":"T1340"},{"id":"R4","pred":"associated_with","subj":"T1341","obj":"T1340"},{"id":"R5","pred":"associated_with","subj":"T1342","obj":"T1340"},{"id":"R6","pred":"associated_with","subj":"T1342","obj":"T1340"},{"id":"R7","pred":"associated_with","subj":"T1343","obj":"T1340"},{"id":"R8","pred":"associated_with","subj":"T1343","obj":"T1340"},{"id":"R9","pred":"associated_with","subj":"T1343","obj":"T1340"},{"id":"R10","pred":"associated_with","subj":"T1343","obj":"T1340"},{"id":"R11","pred":"associated_with","subj":"T1343","obj":"T1340"},{"id":"R12","pred":"associated_with","subj":"T1343","obj":"T1340"},{"id":"R13","pred":"associated_with","subj":"T1343","obj":"T1340"},{"id":"R14","pred":"associated_with","subj":"T1343","obj":"T1340"}],"namespaces":[{"prefix":"gene","uri":"http://www.ncbi.nlm.nih.gov/gene/"},{"prefix":"disease","uri":"http://purl.bioontology.org/ontology/MEDLINEPLUS/"}],"text":"Akt-regulated pathways in prostate cancer.\nProstate cancer remains a major cause of cancer-related mortality. Genetic clues to the molecular pathways driving the most aggressive forms of prostate cancer have been limited. Genetic inactivation of PTEN through either gene deletion or point mutation is reasonably common in metastatic prostate cancer and the resulting activation of phosphoinostide 3-kinase, AKT and mTOR provides a major therapeutic opportunity in this disease as mTOR inhibitors, HSP90 inhibitors and PI3K inhibitors begin to enter clinical development."}

sentences

{"project":"sentences","denotations":[{"id":"TextSentencer_T1","span":{"begin":0,"end":42},"obj":"Sentence"},{"id":"TextSentencer_T2","span":{"begin":43,"end":109},"obj":"Sentence"},{"id":"TextSentencer_T3","span":{"begin":110,"end":221},"obj":"Sentence"},{"id":"TextSentencer_T4","span":{"begin":222,"end":570},"obj":"Sentence"},{"id":"T1","span":{"begin":0,"end":42},"obj":"Sentence"},{"id":"T2","span":{"begin":43,"end":109},"obj":"Sentence"},{"id":"T3","span":{"begin":110,"end":221},"obj":"Sentence"},{"id":"T4","span":{"begin":222,"end":570},"obj":"Sentence"}],"namespaces":[{"prefix":"_base","uri":"http://pubannotation.org/ontology/tao.owl#"}],"text":"Akt-regulated pathways in prostate cancer.\nProstate cancer remains a major cause of cancer-related mortality. Genetic clues to the molecular pathways driving the most aggressive forms of prostate cancer have been limited. Genetic inactivation of PTEN through either gene deletion or point mutation is reasonably common in metastatic prostate cancer and the resulting activation of phosphoinostide 3-kinase, AKT and mTOR provides a major therapeutic opportunity in this disease as mTOR inhibitors, HSP90 inhibitors and PI3K inhibitors begin to enter clinical development."}

DisGeNET

{"project":"DisGeNET","denotations":[{"id":"T0","span":{"begin":246,"end":250},"obj":"gene:5728"},{"id":"T1","span":{"begin":322,"end":348},"obj":"disease:C0936223"},{"id":"T2","span":{"begin":518,"end":522},"obj":"gene:5294"},{"id":"T3","span":{"begin":322,"end":348},"obj":"disease:C0936223"},{"id":"T4","span":{"begin":518,"end":522},"obj":"gene:5293"},{"id":"T5","span":{"begin":322,"end":348},"obj":"disease:C0936223"},{"id":"T6","span":{"begin":518,"end":522},"obj":"gene:5290"},{"id":"T7","span":{"begin":322,"end":348},"obj":"disease:C0936223"},{"id":"T8","span":{"begin":518,"end":522},"obj":"gene:5291"},{"id":"T9","span":{"begin":322,"end":348},"obj":"disease:C0936223"}],"relations":[{"id":"R1","pred":"associated_with","subj":"T0","obj":"T1"},{"id":"R2","pred":"associated_with","subj":"T2","obj":"T3"},{"id":"R3","pred":"associated_with","subj":"T4","obj":"T5"},{"id":"R4","pred":"associated_with","subj":"T6","obj":"T7"},{"id":"R5","pred":"associated_with","subj":"T8","obj":"T9"}],"namespaces":[{"prefix":"gene","uri":"http://www.ncbi.nlm.nih.gov/gene/"},{"prefix":"disease","uri":"http://purl.bioontology.org/ontology/MEDLINEPLUS/"}],"text":"Akt-regulated pathways in prostate cancer.\nProstate cancer remains a major cause of cancer-related mortality. Genetic clues to the molecular pathways driving the most aggressive forms of prostate cancer have been limited. Genetic inactivation of PTEN through either gene deletion or point mutation is reasonably common in metastatic prostate cancer and the resulting activation of phosphoinostide 3-kinase, AKT and mTOR provides a major therapeutic opportunity in this disease as mTOR inhibitors, HSP90 inhibitors and PI3K inhibitors begin to enter clinical development."}