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n3:pmcid: PMC0
bibo:doi: 10.1016%2Fj.gendis.2014.10.004
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Subject Item: _:vb40853303
rdf:type: n8:Section
dc:title: introduction
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Subject Item: _:vb40853304
rdf:type: n3:Context
rdf:value: The insulin-like growth factor (IGF) signaling axis is critical to the growth, development, and maintenance of many tissues within the human body.>>1<< It is particularly important during neonatal and pubertal growth, and essentially carries out its effects by simulating cell proliferation and interrupting programmed cell death.
n3:mentions: n2:12767520

Subject Item: _:vb40853305
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rdf:value: and maintenance of many tissues within the human body.1 It is particularly important during neonatal and pubertal growth, and essentially carries out its effects by simulating cell proliferation and interrupting programmed cell death.>>1<<, 2 The IGF system is comprised of two ligands, IGF-1 and IGF-2, which exhibit their effects through binding to IGF-1R (primarily), IGF-2R, and the insulin receptor (IR), all belonging to the tyrosine kinase receptor family.
n3:mentions: n2:12767520

Subject Item: _:vb40853306
rdf:type: n3:Context
rdf:value: 1, 2 The IGF system is comprised of two ligands, IGF-1 and IGF-2, which exhibit their effects through binding to IGF-1R (primarily), IGF-2R, and the insulin receptor (IR), all belonging to the tyrosine kinase receptor family.>>1<<
n3:mentions: n2:12767520

Subject Item: _:vb40853307
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rdf:value: short) through phosphorylation.3 AKT then performs a variety of functions, such as releasing the anti-apoptotic protein Bcl-2 from Bad, activating protein synthesis through mTOR, and promoting glucose metabolism by inhibiting GSK-3β.3, >>4<< This is commonly referred to as the PI3K/AKT pathway of IGF-1R signaling and is ultimately responsible for preventing cell death (Fig.
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Subject Item: _:vb40853308
rdf:type: n3:Context
rdf:value: 3, 4 This is commonly referred to as the PI3K/AKT pathway of IGF-1R signaling and is ultimately responsible for preventing cell death (Fig. 1).>>5<<Figure
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Subject Item: _:vb40853309
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rdf:value: These MAPKs go on to phosphorylate and activate several targets, notably the transcription factor ELK1 which promotes gene expression and therefore cell growth.3, >>6<<,
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Subject Item: _:vb40853310
rdf:type: n3:Context
rdf:value: These MAPKs go on to phosphorylate and activate several targets, notably the transcription factor ELK1 which promotes gene expression and therefore cell growth.3, 6, >>7<<
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Subject Item: _:vb40853311
rdf:type: n3:Context
rdf:value: proteins (IGFBPs), named IGFBP-1 through IGFBP-6, respectively. The IGFBPs are usually bound directly to IGF-1 (or IGF-2) in extracellular fluids, serving to mediate the half-life and localized availability of the ligands in circulation.>>8<< Furthermore, extensive evidence has recently elucidated that the IGFBPs have many IGF-independent actions.
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Subject Item: _:vb40853312
rdf:type: n3:Context
rdf:value: By associating directly with many extracellular and cell-surface markers, these binding proteins are able to cause a variety of unique effects involving growth and differentiation.>>8<<
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Subject Item: _:vb40853313
rdf:type: n8:Section
dc:title: conclusions and future directions
n8:contains: _:vb40853344 _:vb40853345 _:vb40853346 _:vb40853347 _:vb40853348 _:vb40853349 _:vb40853350 _:vb40853351 _:vb40853352 _:vb40853353 _:vb40853354 _:vb40853355 _:vb40853356 _:vb40853357 _:vb40853358 _:vb40853359 _:vb40853360 _:vb40853361 _:vb40853362 _:vb40853314 _:vb40853315 _:vb40853316 _:vb40853317 _:vb40853318 _:vb40853319 _:vb40853320 _:vb40853321 _:vb40853322 _:vb40853323 _:vb40853324 _:vb40853325 _:vb40853326 _:vb40853327 _:vb40853328 _:vb40853329 _:vb40853330 _:vb40853331 _:vb40853332 _:vb40853333 _:vb40853334 _:vb40853335 _:vb40853336 _:vb40853337 _:vb40853338 _:vb40853339 _:vb40853340 _:vb40853341 _:vb40853342 _:vb40853343

Subject Item: _:vb40853314
rdf:type: n3:Context
rdf:value: Affected cancer: Drug/TreatmentIGF-1RResistanceBreast ER+: Tamoxifen>>22<<Breast HER2+:
n3:mentions: n2:18245484

Subject Item: _:vb40853315
rdf:type: n3:Context
rdf:value: Affected cancer: Drug/TreatmentIGF-1RResistanceBreast ER+: Tamoxifen22Breast HER2+: Trastuzumab>>28<<Gastric: Cisplatin84Glioma: Radiation,73 Temozolamide74Hepatocellular: Apicidin92HNSCC: Gefitinib102NSCLC: Gefitinib,52 Erlotinib,55Osteosarcoma: Radiation,108 Docetaxel, Cisplatin,107 Doxorubicin109, 110Ovarian: Cisplatin ±
n3:mentions: n2:11752009

Subject Item: _:vb40853316
rdf:type: n3:Context
rdf:value: Affected cancer: Drug/TreatmentIGF-1RResistanceBreast ER+: Tamoxifen22Breast HER2+: Trastuzumab28Gastric: Cisplatin>>84<<Glioma: Radiation,73 Temozolamide74Hepatocellular: Apicidin92HNSCC: Gefitinib102NSCLC: Gefitinib,52 Erlotinib,55Osteosarcoma: Radiation,108 Docetaxel, Cisplatin,107 Doxorubicin109, 110Ovarian: Cisplatin ± taxol37Prostate: Androgen
n3:mentions: n2:24931256

Subject Item: _:vb40853317
rdf:type: n3:Context
rdf:value: Affected cancer: Drug/TreatmentIGF-1RResistanceBreast ER+: Tamoxifen22Breast HER2+: Trastuzumab28Gastric: Cisplatin84Glioma: Radiation,73 Temozolamide>>74<<Hepatocellular:
n3:mentions: n2:20857406

Subject Item: _:vb40853318
rdf:type: n3:Context
rdf:value: Affected cancer: Drug/TreatmentIGF-1RResistanceBreast ER+: Tamoxifen22Breast HER2+: Trastuzumab28Gastric: Cisplatin84Glioma: Radiation,73 Temozolamide74Hepatocellular: Apicidin92HNSCC: Gefitinib>>102<<NSCLC: Gefitinib,52 Erlotinib,55Osteosarcoma: Radiation,108 Docetaxel, Cisplatin,107 Doxorubicin109, 110Ovarian: Cisplatin ± taxol37Prostate: Androgen deprivation therapy42SensitivityColorectal: Multiple91Gastric: Cisplatin84, 85Glioma:
n3:mentions: n2:21878657

Subject Item: _:vb40853319
rdf:type: n3:Context
rdf:value: Affected cancer: Drug/TreatmentIGF-1RResistanceBreast ER+: Tamoxifen22Breast HER2+: Trastuzumab28Gastric: Cisplatin84Glioma: Radiation,73 Temozolamide74Hepatocellular: Apicidin92HNSCC: Gefitinib102NSCLC: Gefitinib,>>52<< Erlotinib,55Osteosarcoma:
n3:mentions: n2:23619944

Subject Item: _:vb40853320
rdf:type: n3:Context
rdf:value: Drug/TreatmentIGF-1RResistanceBreast ER+: Tamoxifen22Breast HER2+: Trastuzumab28Gastric: Cisplatin84Glioma: Radiation,73 Temozolamide74Hepatocellular: Apicidin92HNSCC: Gefitinib102NSCLC: Gefitinib,52 Erlotinib,55Osteosarcoma: Radiation,>>108<< Docetaxel, Cisplatin,107 Doxorubicin109, 110Ovarian: Cisplatin ± taxol37Prostate:
n3:mentions: n2:19229591

Subject Item: _:vb40853321
rdf:type: n3:Context
rdf:value: ER+: Tamoxifen22Breast HER2+: Trastuzumab28Gastric: Cisplatin84Glioma: Radiation,73 Temozolamide74Hepatocellular: Apicidin92HNSCC: Gefitinib102NSCLC: Gefitinib,52 Erlotinib,55Osteosarcoma: Radiation,108 Docetaxel, Cisplatin,>>107<< Doxorubicin109, 110Ovarian: Cisplatin ± taxol37Prostate: Androgen deprivation therapy42SensitivityColorectal:
n3:mentions: n2:20376536

Subject Item: _:vb40853322
rdf:type: n3:Context
rdf:value: Tamoxifen22Breast HER2+: Trastuzumab28Gastric: Cisplatin84Glioma: Radiation,73 Temozolamide74Hepatocellular: Apicidin92HNSCC: Gefitinib102NSCLC: Gefitinib,52 Erlotinib,55Osteosarcoma: Radiation,108 Docetaxel, Cisplatin,107 Doxorubicin>>109<<, 110Ovarian: Cisplatin ± taxol37Prostate: Androgen deprivation therapy42SensitivityColorectal:
n3:mentions: n2:21843050

Subject Item: _:vb40853323
rdf:type: n3:Context
rdf:value: HER2+: Trastuzumab28Gastric: Cisplatin84Glioma: Radiation,73 Temozolamide74Hepatocellular: Apicidin92HNSCC: Gefitinib102NSCLC: Gefitinib,52 Erlotinib,55Osteosarcoma: Radiation,108 Docetaxel, Cisplatin,107 Doxorubicin109, >>110<<Ovarian: Cisplatin ± taxol37Prostate: Androgen deprivation therapy42SensitivityColorectal:
n3:mentions: n2:19638450

Subject Item: _:vb40853324
rdf:type: n3:Context
rdf:value: Cisplatin84Glioma: Radiation,73 Temozolamide74Hepatocellular: Apicidin92HNSCC: Gefitinib102NSCLC: Gefitinib,52 Erlotinib,55Osteosarcoma: Radiation,108 Docetaxel, Cisplatin,107 Doxorubicin109, 110Ovarian: Cisplatin ± taxol>>37<<Prostate: Androgen deprivation therapy42SensitivityColorectal: Multiple91Gastric:
n3:mentions: n2:25157649

Subject Item: _:vb40853325
rdf:type: n3:Context
rdf:value: Temozolamide74Hepatocellular: Apicidin92HNSCC: Gefitinib102NSCLC: Gefitinib,52 Erlotinib,55Osteosarcoma: Radiation,108 Docetaxel, Cisplatin,107 Doxorubicin109, 110Ovarian: Cisplatin ± taxol37Prostate: Androgen deprivation therapy>>42<<SensitivityColorectal: Multiple91Gastric: Cisplatin84, 85Glioma: Radiation73Hepatocellular:
n3:mentions: n2:16639715

Subject Item: _:vb40853326
rdf:type: n3:Context
rdf:value: Apicidin92HNSCC: Gefitinib102NSCLC: Gefitinib,52 Erlotinib,55Osteosarcoma: Radiation,108 Docetaxel, Cisplatin,107 Doxorubicin109, 110Ovarian: Cisplatin ± taxol37Prostate: Androgen deprivation therapy42SensitivityColorectal: Multiple>>91<<Gastric: Cisplatin84, 85Glioma: Radiation73Hepatocellular: Oxaliplatin94HNSCC: Methotrexate, Cetuximab,104 histone deacetylase inhibitors, Rapamycin, Gemcitabine, Radiation105Multiple myeloma:
n3:mentions: n2:22275271

Subject Item: _:vb40853327
rdf:type: n3:Context
rdf:value: Gefitinib102NSCLC: Gefitinib,52 Erlotinib,55Osteosarcoma: Radiation,108 Docetaxel, Cisplatin,107 Doxorubicin109, 110Ovarian: Cisplatin ± taxol37Prostate: Androgen deprivation therapy42SensitivityColorectal: Multiple91Gastric: Cisplatin>>84<<, 85Glioma: Radiation73Hepatocellular: Oxaliplatin94HNSCC: Methotrexate, Cetuximab,104 histone deacetylase inhibitors, Rapamycin, Gemcitabine, Radiation105Multiple myeloma:
n3:mentions: n2:24931256

Subject Item: _:vb40853328
rdf:type: n3:Context
rdf:value: Gefitinib,52 Erlotinib,55Osteosarcoma: Radiation,108 Docetaxel, Cisplatin,107 Doxorubicin109, 110Ovarian: Cisplatin ± taxol37Prostate: Androgen deprivation therapy42SensitivityColorectal: Multiple91Gastric: Cisplatin84, >>85<<Glioma: Radiation73Hepatocellular: Oxaliplatin94HNSCC: Methotrexate, Cetuximab,104 histone deacetylase inhibitors, Rapamycin, Gemcitabine, Radiation105Multiple myeloma:
n3:mentions: n2:24875127

Subject Item: _:vb40853329
rdf:type: n3:Context
rdf:value: Radiation,108 Docetaxel, Cisplatin,107 Doxorubicin109, 110Ovarian: Cisplatin ± taxol37Prostate: Androgen deprivation therapy42SensitivityColorectal: Multiple91Gastric: Cisplatin84, 85Glioma: Radiation73Hepatocellular: Oxaliplatin>>94<<HNSCC: Methotrexate, Cetuximab,104 histone deacetylase inhibitors, Rapamycin, Gemcitabine, Radiation105Multiple myeloma:
n3:mentions: n2:24632571

Subject Item: _:vb40853330
rdf:type: n3:Context
rdf:value: Doxorubicin109, 110Ovarian: Cisplatin ± taxol37Prostate: Androgen deprivation therapy42SensitivityColorectal: Multiple91Gastric: Cisplatin84, 85Glioma: Radiation73Hepatocellular: Oxaliplatin94HNSCC: Methotrexate, Cetuximab,>>104<< histone deacetylase inhibitors, Rapamycin, Gemcitabine, Radiation105Multiple myeloma:
n3:mentions: n2:20652976

Subject Item: _:vb40853331
rdf:type: n3:Context
rdf:value: Multiple91Gastric: Cisplatin84, 85Glioma: Radiation73Hepatocellular: Oxaliplatin94HNSCC: Methotrexate, Cetuximab,104 histone deacetylase inhibitors, Rapamycin, Gemcitabine, Radiation105Multiple myeloma: Bortezomib>>121<<NSCLC: Gefitinib54Ovarian: Platinum-based drugs39Pancreatic: Gemcitabine95Prostate:
n3:mentions: n2:22932796

Subject Item: _:vb40853332
rdf:type: n3:Context
rdf:value: Multiple91Gastric: Cisplatin84, 85Glioma: Radiation73Hepatocellular: Oxaliplatin94HNSCC: Methotrexate, Cetuximab,104 histone deacetylase inhibitors, Rapamycin, Gemcitabine, Radiation105Multiple myeloma: Bortezomib121NSCLC: Gefitinib>>54<<Ovarian: Platinum-based drugs39Pancreatic: Gemcitabine95Prostate: Androgen deprivation therapy42IGF-1ResistanceColorectal:
n3:mentions: n2:24489728

Subject Item: _:vb40853333
rdf:type: n3:Context
rdf:value: Oxaliplatin94HNSCC: Methotrexate, Cetuximab,104 histone deacetylase inhibitors, Rapamycin, Gemcitabine, Radiation105Multiple myeloma: Bortezomib121NSCLC: Gefitinib54Ovarian: Platinum-based drugs39Pancreatic: Gemcitabine>>95<<Prostate: Androgen deprivation therapy42IGF-1ResistanceColorectal: Oxaliplatin, 5-Fluorouracil, Irinotecan88Glioma:
n3:mentions: n2:23589145

Subject Item: _:vb40853334
rdf:type: n3:Context
rdf:value: Cetuximab,104 histone deacetylase inhibitors, Rapamycin, Gemcitabine, Radiation105Multiple myeloma: Bortezomib121NSCLC: Gefitinib54Ovarian: Platinum-based drugs39Pancreatic: Gemcitabine95Prostate: Androgen deprivation therapy>>42<<IGF-1ResistanceColorectal: Oxaliplatin, 5-Fluorouracil, Irinotecan88Glioma: Tamoxifen75Hepatocellular:
n3:mentions: n2:16639715

Subject Item: _:vb40853335
rdf:type: n3:Context
rdf:value: Gemcitabine, Radiation105Multiple myeloma: Bortezomib121NSCLC: Gefitinib54Ovarian: Platinum-based drugs39Pancreatic: Gemcitabine95Prostate: Androgen deprivation therapy42IGF-1ResistanceColorectal: Oxaliplatin, 5-Fluorouracil, Irinotecan>>88<<Glioma: Tamoxifen75Hepatocellular: Oxaliplatin94Multiple myeloma: Bortezomib121Pancreatic:
n3:mentions: n2:24396438

Subject Item: _:vb40853336
rdf:type: n3:Context
rdf:value: myeloma: Bortezomib121NSCLC: Gefitinib54Ovarian: Platinum-based drugs39Pancreatic: Gemcitabine95Prostate: Androgen deprivation therapy42IGF-1ResistanceColorectal: Oxaliplatin, 5-Fluorouracil, Irinotecan88Glioma: Tamoxifen>>75<<Hepatocellular: Oxaliplatin94Multiple myeloma: Bortezomib121Pancreatic: Everolimus97SensitivityMultiple myeloma:
n3:mentions: n2:22046442

Subject Item: _:vb40853337
rdf:type: n3:Context
rdf:value: Gefitinib54Ovarian: Platinum-based drugs39Pancreatic: Gemcitabine95Prostate: Androgen deprivation therapy42IGF-1ResistanceColorectal: Oxaliplatin, 5-Fluorouracil, Irinotecan88Glioma: Tamoxifen75Hepatocellular: Oxaliplatin>>94<<Multiple myeloma: Bortezomib121Pancreatic: Everolimus97SensitivityMultiple myeloma:
n3:mentions: n2:24632571

Subject Item: _:vb40853338
rdf:type: n3:Context
rdf:value: Platinum-based drugs39Pancreatic: Gemcitabine95Prostate: Androgen deprivation therapy42IGF-1ResistanceColorectal: Oxaliplatin, 5-Fluorouracil, Irinotecan88Glioma: Tamoxifen75Hepatocellular: Oxaliplatin94Multiple myeloma: Bortezomib>>121<<Pancreatic: Everolimus97SensitivityMultiple myeloma: Bortezomib122IGF-2ResistanceOvarian:
n3:mentions: n2:22932796

Subject Item: _:vb40853339
rdf:type: n3:Context
rdf:value: Gemcitabine95Prostate: Androgen deprivation therapy42IGF-1ResistanceColorectal: Oxaliplatin, 5-Fluorouracil, Irinotecan88Glioma: Tamoxifen75Hepatocellular: Oxaliplatin94Multiple myeloma: Bortezomib121Pancreatic: Everolimus>>97<<SensitivityMultiple myeloma: Bortezomib122IGF-2ResistanceOvarian: Platinum-based drugs39SensitivityOvarian:
n3:mentions: n2:22342683

Subject Item: _:vb40853340
rdf:type: n3:Context
rdf:value: Irinotecan88Glioma: Tamoxifen75Hepatocellular: Oxaliplatin94Multiple myeloma: Bortezomib121Pancreatic: Everolimus97SensitivityMultiple myeloma: Bortezomib122IGF-2ResistanceOvarian: Platinum-based drugs39SensitivityOvarian: Taxol>>40<<PI3K/AKTResistanceNSCLC: Gefitinib60SensitivityGlioma: Tamoxifen75Hepatocellular:
n3:mentions: n2:24932685

Subject Item: _:vb40853341
rdf:type: n3:Context
rdf:value: myeloma: Bortezomib121Pancreatic: Everolimus97SensitivityMultiple myeloma: Bortezomib122IGF-2ResistanceOvarian: Platinum-based drugs39SensitivityOvarian: Taxol40PI3K/AKTResistanceNSCLC: Gefitinib60SensitivityGlioma: Tamoxifen>>75<<Hepatocellular: Apicidin92NSCLC: Gefitinib60Ras/ERKResistancePancreatic: Everolimus97SensitivityPancreatic:
n3:mentions: n2:22046442

Subject Item: _:vb40853342
rdf:type: n3:Context
rdf:value: Bortezomib122IGF-2ResistanceOvarian: Platinum-based drugs39SensitivityOvarian: Taxol40PI3K/AKTResistanceNSCLC: Gefitinib60SensitivityGlioma: Tamoxifen75Hepatocellular: Apicidin92NSCLC: Gefitinib60Ras/ERKResistancePancreatic: Everolimus>>97<<SensitivityPancreatic: Everolimus97IGFBP-1ResistanceProstate: Androgen deprivation therapy45SensitivityProstate:
n3:mentions: n2:22342683

Subject Item: _:vb40853343
rdf:type: n3:Context
rdf:value: Platinum-based drugs39SensitivityOvarian: Taxol40PI3K/AKTResistanceNSCLC: Gefitinib60SensitivityGlioma: Tamoxifen75Hepatocellular: Apicidin92NSCLC: Gefitinib60Ras/ERKResistancePancreatic: Everolimus97SensitivityPancreatic: Everolimus>>97<<IGFBP-1ResistanceProstate: Androgen deprivation therapy45SensitivityProstate: Androgen deprivation therapy46, 47IGFBP-2ResistanceAML:
n3:mentions: n2:22342683

Subject Item: _:vb40853344
rdf:type: n3:Context
rdf:value: Gefitinib60SensitivityGlioma: Tamoxifen75Hepatocellular: Apicidin92NSCLC: Gefitinib60Ras/ERKResistancePancreatic: Everolimus97SensitivityPancreatic: Everolimus97IGFBP-1ResistanceProstate: Androgen deprivation therapy>>45<<SensitivityProstate: Androgen deprivation therapy46, 47IGFBP-2ResistanceAML: Cytarabine, Anthracycline124Glioma:
n3:mentions: n2:24132762

Subject Item: _:vb40853345
rdf:type: n3:Context
rdf:value: Tamoxifen75Hepatocellular: Apicidin92NSCLC: Gefitinib60Ras/ERKResistancePancreatic: Everolimus97SensitivityPancreatic: Everolimus97IGFBP-1ResistanceProstate: Androgen deprivation therapy45SensitivityProstate: Androgen deprivation therapy>>46<<, 47IGFBP-2ResistanceAML: Cytarabine, Anthracycline124Glioma: Temozolamide78NSCLC:
n3:mentions: n2:21903863

Subject Item: _:vb40853346
rdf:type: n3:Context
rdf:value: Apicidin92NSCLC: Gefitinib60Ras/ERKResistancePancreatic: Everolimus97SensitivityPancreatic: Everolimus97IGFBP-1ResistanceProstate: Androgen deprivation therapy45SensitivityProstate: Androgen deprivation therapy46, >>47<<IGFBP-2ResistanceAML: Cytarabine, Anthracycline124Glioma: Temozolamide78NSCLC: Dasatinib62, 63Prostate:
n3:mentions: n2:7504269

Subject Item: _:vb40853347
rdf:type: n3:Context
rdf:value: Everolimus97SensitivityPancreatic: Everolimus97IGFBP-1ResistanceProstate: Androgen deprivation therapy45SensitivityProstate: Androgen deprivation therapy46, 47IGFBP-2ResistanceAML: Cytarabine, Anthracycline>>124<<Glioma: Temozolamide78NSCLC: Dasatinib62, 63Prostate: Docetaxel48SensitivityNSCLC:
n3:mentions: n2:21899885

Subject Item: _:vb40853348
rdf:type: n3:Context
rdf:value: Everolimus97IGFBP-1ResistanceProstate: Androgen deprivation therapy45SensitivityProstate: Androgen deprivation therapy46, 47IGFBP-2ResistanceAML: Cytarabine, Anthracycline124Glioma: Temozolamide78NSCLC: Dasatinib>>62<<, 63Prostate: Docetaxel48SensitivityNSCLC: Dasatinib63Prostate: Docetaxel48ResistanceRMS:
n3:mentions: n2:18398720

Subject Item: _:vb40853349
rdf:type: n3:Context
rdf:value: Everolimus97IGFBP-1ResistanceProstate: Androgen deprivation therapy45SensitivityProstate: Androgen deprivation therapy46, 47IGFBP-2ResistanceAML: Cytarabine, Anthracycline124Glioma: Temozolamide78NSCLC: Dasatinib62, >>63<<Prostate: Docetaxel48SensitivityNSCLC: Dasatinib63Prostate: Docetaxel48ResistanceRMS:
n3:mentions: n2:24130049

Subject Item: _:vb40853350
rdf:type: n3:Context
rdf:value: Everolimus97IGFBP-1ResistanceProstate: Androgen deprivation therapy45SensitivityProstate: Androgen deprivation therapy46, 47IGFBP-2ResistanceAML: Cytarabine, Anthracycline124Glioma: Temozolamide78NSCLC: Dasatinib62, 63Prostate: Docetaxel>>48<<SensitivityNSCLC: Dasatinib63Prostate: Docetaxel48ResistanceRMS: IGF-1R antibody113IGFBP-3ResistanceNSCLC:
n3:mentions: n2:23959956

Subject Item: _:vb40853351
rdf:type: n3:Context
rdf:value: Androgen deprivation therapy45SensitivityProstate: Androgen deprivation therapy46, 47IGFBP-2ResistanceAML: Cytarabine, Anthracycline124Glioma: Temozolamide78NSCLC: Dasatinib62, 63Prostate: Docetaxel48SensitivityNSCLC: Dasatinib>>63<<Prostate: Docetaxel48ResistanceRMS: IGF-1R antibody113IGFBP-3ResistanceNSCLC: Gefitinib, Erlotinib,65 Cisplatin67SensitivityBreast ER+:
n3:mentions: n2:24130049

Subject Item: _:vb40853352
rdf:type: n3:Context
rdf:value: therapy45SensitivityProstate: Androgen deprivation therapy46, 47IGFBP-2ResistanceAML: Cytarabine, Anthracycline124Glioma: Temozolamide78NSCLC: Dasatinib62, 63Prostate: Docetaxel48SensitivityNSCLC: Dasatinib63Prostate: Docetaxel>>48<<ResistanceRMS: IGF-1R antibody113IGFBP-3ResistanceNSCLC: Gefitinib, Erlotinib,65 Cisplatin67SensitivityBreast ER+:
n3:mentions: n2:23959956

Subject Item: _:vb40853353
rdf:type: n3:Context
rdf:value: Cytarabine, Anthracycline124Glioma: Temozolamide78NSCLC: Dasatinib62, 63Prostate: Docetaxel48SensitivityNSCLC: Dasatinib63Prostate: Docetaxel48ResistanceRMS: IGF-1R antibody113IGFBP-3ResistanceNSCLC: Gefitinib, Erlotinib,>>65<< Cisplatin67SensitivityBreast ER+: Fulvestrant27NSCLC: Cisplatin68IGFBP-7ResistanceNSCLC:
n3:mentions: n2:24339922

Subject Item: _:vb40853354
rdf:type: n3:Context
rdf:value: Cytarabine, Anthracycline124Glioma: Temozolamide78NSCLC: Dasatinib62, 63Prostate: Docetaxel48SensitivityNSCLC: Dasatinib63Prostate: Docetaxel48ResistanceRMS: IGF-1R antibody113IGFBP-3ResistanceNSCLC: Gefitinib, Erlotinib,65 Cisplatin>>67<<SensitivityBreast ER+: Fulvestrant27NSCLC: Cisplatin68IGFBP-7ResistanceNSCLC: Cisplatin70SensitivityAML:
n3:mentions: n2:22543588

Subject Item: _:vb40853355
rdf:type: n3:Context
rdf:value: Temozolamide78NSCLC: Dasatinib62, 63Prostate: Docetaxel48SensitivityNSCLC: Dasatinib63Prostate: Docetaxel48ResistanceRMS: IGF-1R antibody113IGFBP-3ResistanceNSCLC: Gefitinib, Erlotinib,65 Cisplatin67SensitivityBreast ER+: Fulvestrant>>27<<NSCLC: Cisplatin68IGFBP-7ResistanceNSCLC: Cisplatin70SensitivityAML: Doxorubicin, Etoposide, Cytarabine123NSCLC:
n3:mentions: n2:22801219

Subject Item: _:vb40853356
rdf:type: n3:Context
rdf:value: Dasatinib62, 63Prostate: Docetaxel48SensitivityNSCLC: Dasatinib63Prostate: Docetaxel48ResistanceRMS: IGF-1R antibody113IGFBP-3ResistanceNSCLC: Gefitinib, Erlotinib,65 Cisplatin67SensitivityBreast ER+: Fulvestrant27NSCLC: Cisplatin>>68<<IGFBP-7ResistanceNSCLC: Cisplatin70SensitivityAML: Doxorubicin, Etoposide, Cytarabine123NSCLC:
n3:mentions: n2:22197230

Subject Item: _:vb40853357
rdf:type: n3:Context
rdf:value: Dasatinib63Prostate: Docetaxel48ResistanceRMS: IGF-1R antibody113IGFBP-3ResistanceNSCLC: Gefitinib, Erlotinib,65 Cisplatin67SensitivityBreast ER+: Fulvestrant27NSCLC: Cisplatin68IGFBP-7ResistanceNSCLC: Cisplatin>>70<<SensitivityAML: Doxorubicin, Etoposide, Cytarabine123NSCLC: Cisplatin70ResistanceALL:
n3:mentions: n2:22277373

Subject Item: _:vb40853358
rdf:type: n3:Context
rdf:value: IGF-1R antibody113IGFBP-3ResistanceNSCLC: Gefitinib, Erlotinib,65 Cisplatin67SensitivityBreast ER+: Fulvestrant27NSCLC: Cisplatin68IGFBP-7ResistanceNSCLC: Cisplatin70SensitivityAML: Doxorubicin, Etoposide, Cytarabine>>123<<NSCLC: Cisplatin70ResistanceALL: Asparginase125IGFBP-rP1SensitivityProstate: Docetaxel, Radiation49IGF2BP1ResistanceRMS:
n3:mentions: n2:24967962

Subject Item: _:vb40853359
rdf:type: n3:Context
rdf:value: IGF-1R antibody113IGFBP-3ResistanceNSCLC: Gefitinib, Erlotinib,65 Cisplatin67SensitivityBreast ER+: Fulvestrant27NSCLC: Cisplatin68IGFBP-7ResistanceNSCLC: Cisplatin70SensitivityAML: Doxorubicin, Etoposide, Cytarabine123NSCLC: Cisplatin>>70<<ResistanceALL: Asparginase125IGFBP-rP1SensitivityProstate: Docetaxel, Radiation49IGF2BP1ResistanceRMS:
n3:mentions: n2:22277373

Subject Item: _:vb40853360
rdf:type: n3:Context
rdf:value: Gefitinib, Erlotinib,65 Cisplatin67SensitivityBreast ER+: Fulvestrant27NSCLC: Cisplatin68IGFBP-7ResistanceNSCLC: Cisplatin70SensitivityAML: Doxorubicin, Etoposide, Cytarabine123NSCLC: Cisplatin70ResistanceALL: Asparginase>>125<<IGFBP-rP1SensitivityProstate: Docetaxel, Radiation49IGF2BP1ResistanceRMS: TNFα114SensitivityRMS:
n3:mentions: n2:22005787

Subject Item: _:vb40853361
rdf:type: n3:Context
rdf:value: ER+: Fulvestrant27NSCLC: Cisplatin68IGFBP-7ResistanceNSCLC: Cisplatin70SensitivityAML: Doxorubicin, Etoposide, Cytarabine123NSCLC: Cisplatin70ResistanceALL: Asparginase125IGFBP-rP1SensitivityProstate: Docetaxel, Radiation>>49<<IGF2BP1ResistanceRMS: TNFα114SensitivityRMS:
n3:mentions: n2:23600329

Subject Item: _:vb40853362
rdf:type: n3:Context
rdf:value: focusing their efforts on treating tumors with modulators of this pathway. Many potential drugs, such as IGF-1R inhibitors, have now even made it to clinical trials, but the outcomes of these studies have been largely underwhelming.>>126<< Used as monotherapy, these drugs may not prove superior to current standard-of-care chemotherapy, but there exists considerable potential for use of these agents in combination therapy to improve existing treatment regimens.
n3:mentions: n2:25123819

Subject Item: _:vb40853363
rdf:type: n8:Section
dc:title: breast cancer
n8:contains: _:vb40853368 _:vb40853369 _:vb40853370 _:vb40853371 _:vb40853372 _:vb40853373 _:vb40853374 _:vb40853375 _:vb40853364 _:vb40853365 _:vb40853366 _:vb40853367

Subject Item: _:vb40853364
rdf:type: n3:Context
rdf:value: breast cancer, there appears to be a link between IGF-1R and progression of disease despite anti-estrogen therapy. In fact, IGF-1R is upregulated in cancer cells that are resistant to tamoxifen, an estrogen antagonist in breast tissue.>>22<< This is thought to be due to crosstalk between IGF-1R and ER, as well as MAPK/ERK and PI3K/AKT signaling downstream of IGF signaling.
n3:mentions: n2:18245484

Subject Item: _:vb40853365
rdf:type: n3:Context
rdf:value: 22 This is thought to be due to crosstalk between IGF-1R and ER, as well as MAPK/ERK and PI3K/AKT signaling downstream of IGF signaling.>>23<<, 24 One study looked at ER+ breast cancer cells resistant to long-term estrogen deprivation, showing that AKT inhibition led to compensatory upregulation of IGF-1R/IR and IGF ligands, but that simultaneous blockade of IGF-1R/IR enhanced
n3:mentions: n2:21595894

Subject Item: _:vb40853366
rdf:type: n3:Context
rdf:value: 22 This is thought to be due to crosstalk between IGF-1R and ER, as well as MAPK/ERK and PI3K/AKT signaling downstream of IGF signaling.23, >>24<< One study looked at ER+ breast cancer cells resistant to long-term estrogen deprivation, showing that AKT inhibition led to compensatory upregulation of IGF-1R/IR and IGF ligands, but that simultaneous blockade of IGF-1R/IR enhanced the
n3:mentions: n2:10791772

Subject Item: _:vb40853367
rdf:type: n3:Context
rdf:value: cells resistant to long-term estrogen deprivation, showing that AKT inhibition led to compensatory upregulation of IGF-1R/IR and IGF ligands, but that simultaneous blockade of IGF-1R/IR enhanced the anti-tumor effects of AKT inhibition.>>25<< Furthermore, variations in IGF-1R structure and function correlate with anti-estrogen resistance.
n3:mentions: n2:23844554

Subject Item: _:vb40853368
rdf:type: n3:Context
rdf:value: IGF-1R gene was found to have significantly increased risk for tumor progression (hazard ratio [HR] 2.04) and death (HR 1.84). Other polymorphisms were also found to be significantly associated with tumor size and lymph node involvement.>>26<< Finally, the activity of IGFBPs is also implicated, but in an IGF-independent manner.
n3:mentions: n2:23459444

Subject Item: _:vb40853369
rdf:type: n3:Context
rdf:value: For example, IGFBP-3 appears to sensitize ER+ breast cancer cells to the anti-estrogen fulvestrant by inhibiting anti-apoptotic effects of GRP78, a binding partner of the caspase 7 complex.>>27<<
n3:mentions: n2:22801219

Subject Item: _:vb40853370
rdf:type: n3:Context
rdf:value: that is commonly used in therapy, but limited drug efficacy appears to be, in large part, due to IGF signaling. In models of breast cancer cells that overexpress HER2, trastuzumab activity is disrupted by increased expression of IGF-1R.>>28<< Furthermore, upregulation of IGF-1R by epigenetic silencing of microRNA 375 partially leads to a trastuzumab-resistant phenotype, while overexpression of microRNA 375 restores sensitivity of HER2+ cells to the drug.
n3:mentions: n2:11752009

Subject Item: _:vb40853371
rdf:type: n3:Context
rdf:value: 28 Furthermore, upregulation of IGF-1R by epigenetic silencing of microRNA 375 partially leads to a trastuzumab-resistant phenotype, while overexpression of microRNA 375 restores sensitivity of HER2+ cells to the drug.>>29<< Immunohistochemistry supports that overexpression of IGF-1R and epidermal growth factor 1-receptor (EGFR), and/or dysregulation of the downstream PI3K/AKT pathway can also confer this trastuzumab resistance in a subset of patients found
n3:mentions: n2:24571711

Subject Item: _:vb40853372
rdf:type: n3:Context
rdf:value: has significant implications for treatment and survival of breast cancer patients. This has led many to believe that co-targeting IGF-1R and well-known breast cancer cell receptors (e.g. ER, HER2) may circumvent drug resistance.>>31<<, 32 However, several investigations indicate that the solution may not be so straightforward.
n3:mentions: n2:22830017

Subject Item: _:vb40853373
rdf:type: n3:Context
rdf:value: has significant implications for treatment and survival of breast cancer patients. This has led many to believe that co-targeting IGF-1R and well-known breast cancer cell receptors (e.g. ER, HER2) may circumvent drug resistance.31, >>32<< However, several investigations indicate that the solution may not be so straightforward.
n3:mentions: n2:22424863

Subject Item: _:vb40853374
rdf:type: n3:Context
rdf:value: ER+ breast cancer cells demonstrated that dual treatment with fulvestrant and dasatinib, a nonspecific tyrosine kinase inhibitor, had superior outcomes when compared to combination fulvestrant and IGF-1R monoclonal antibody therapy.>>33<< This may be due to fact that tyrosine-kinases in general are upregulated in endocrine therapy-resistant breast tumors.
n3:mentions: n2:24979294

Subject Item: _:vb40853375
rdf:type: n3:Context
rdf:value: Moreover, another study showed that ER+ cancer cells selected for tamoxifen resistance in vitro may actually have decreased IGF-1R expression and therefore less responsiveness to monoclonal antibodies directed against just this receptor.>>34<< The incongruence of these results with those of studies mentioned previously in this review may ultimately be due to methodology, but highlights the notion that growth factor and hormone signaling in neoplasms is incredibly complex.
n3:mentions: n2:22573715

Subject Item: _:vb40853376
rdf:type: n8:Section
dc:title: lung cancer
n8:contains: _:vb40853380 _:vb40853381 _:vb40853382 _:vb40853383 _:vb40853377 _:vb40853378 _:vb40853379 _:vb40853388 _:vb40853389 _:vb40853390 _:vb40853391 _:vb40853384 _:vb40853385 _:vb40853386 _:vb40853387 _:vb40853392 _:vb40853393

Subject Item: _:vb40853377
rdf:type: n3:Context
rdf:value: itself. That is, cell lines that were already resistant to gefitinib were found to have increased total-IGF-1R and phosphorylated-IGF-1R expression, but overexpression of IGF-1R did not confer resistance to gefitinib-sensitive cells.>>52<< Another study looking at IGF-1R expression using immunohistochemistry did not find any association between IGF-1R activity and clinical outcomes of gefitinib-treated NSCLC.
n3:mentions: n2:23619944

Subject Item: _:vb40853378
rdf:type: n3:Context
rdf:value: IGF-1R did not confer resistance to gefitinib-sensitive cells.52 Another study looking at IGF-1R expression using immunohistochemistry did not find any association between IGF-1R activity and clinical outcomes of gefitinib-treated NSCLC.>>53<< These disparate conclusions may ultimately be attributed to the characteristics of patient samples used in these studies, as tumor microenvironment appears to contribute heavily to the molecular properties of cancer cells.
n3:mentions: n2:22593449

Subject Item: _:vb40853379
rdf:type: n3:Context
rdf:value: of EGFR, IGF-1R activity promotes resistances to gefitinib in lung cancer stem cells (CSCs) under hypoxic conditions. Furthermore, inhibiting IGF-1R actually decreases the population of gefitinib-resistant CSCs in the setting of hypoxia.>>54<< Thus, it is possible that IGF-1R may indeed drive NSCLC tumor resistance to drugs such as gefitinib, but perhaps only in specific cell lines and under particular micro-environmental conditions.
n3:mentions: n2:24489728

Subject Item: _:vb40853380
rdf:type: n3:Context
rdf:value: Furthermore, in tumors that preferentially respond to erlotinib therapy due to an EGFR-activating mutation in exon 19, crosstalk between IGF-1R and epithelial-mesenchymal transition (EMT) signaling can rapidly confer drug resistance.>>56<< In fact, the median interval between initiation of EGFR-TKI therapy and acquired resistance is only 6–12 months in patients afflicted by tumors with this common mutation.
n3:mentions: n2:23994953

Subject Item: _:vb40853381
rdf:type: n3:Context
rdf:value: a role in re-sensitizing tumors to drugs. AG1024, which prevents autophosphorylation of IGF-1R, synergizes with gefitinib to produce pro-apoptotic and anti-proliferative effects in vitro in previously gefitinib-resistant NSCLC cells.>>59<< In mutant KRAS lung adenocarcinoma, IGF's downstream PI3K/AKT signaling is thought to be involved with both this gefitinib resistance and re-sensitization by interacting with the anti-apoptotic Ku70 and pro-apoptotic BAX proteins.
n3:mentions: n2:22977626

Subject Item: _:vb40853382
rdf:type: n3:Context
rdf:value: from binding to ligands and mediating direct IGF-1R signaling, the IGFBPs are known to trigger various independent effects as well. For example, IGFBP-2 directly interacts with integrins and the extracellular matrix to stimulate growth.>>61<< IGFBP-2 appears to be causally associated with NSCLC resistance to dasatinib, a BCR-ABL and SRC family TKI.
n3:mentions: n2:21372140

Subject Item: _:vb40853383
rdf:type: n3:Context
rdf:value: effects as well. For example, IGFBP-2 directly interacts with integrins and the extracellular matrix to stimulate growth.61 IGFBP-2 appears to be causally associated with NSCLC resistance to dasatinib, a BCR-ABL and SRC family TKI.>>62<<, 63 Furthermore, focal adhesion kinase (FAK), which is downstream of IGFBP-2 and integrin binding, is correlated with increased levels of IGFBP-2 and contributes to the dasatinib-resistant phenotype.
n3:mentions: n2:18398720

Subject Item: _:vb40853384
rdf:type: n3:Context
rdf:value: effects as well. For example, IGFBP-2 directly interacts with integrins and the extracellular matrix to stimulate growth.61 IGFBP-2 appears to be causally associated with NSCLC resistance to dasatinib, a BCR-ABL and SRC family TKI.62, >>63<< Furthermore, focal adhesion kinase (FAK), which is downstream of IGFBP-2 and integrin binding, is correlated with increased levels of IGFBP-2 and contributes to the dasatinib-resistant phenotype.
n3:mentions: n2:24130049

Subject Item: _:vb40853385
rdf:type: n3:Context
rdf:value: is correlated with increased levels of IGFBP-2 and contributes to the dasatinib-resistant phenotype. Both in vitro and in vivo, dual inhibition of IGFBP-2 and FAK reverses NSCLC resistance by restoring apoptotic sensitivity to dasatinib.>>63<< It stands to reason that both IGFBP-2 and FAK may be used as biomarkers and therapeutic targets in patients with NSCLC to predict and augment response to dasitinib.
n3:mentions: n2:24130049

Subject Item: _:vb40853386
rdf:type: n3:Context
rdf:value: Unlike IGFBP-2, IGFBP-3 appears to be inversely correlated with TKI resistance.>>64<< NSCLC lines with acquired resistance to gefitinib or erlotinib demonstrate decreased secretion of IGFBP-3 in vitro.
n3:mentions: n2:18568074

Subject Item: _:vb40853387
rdf:type: n3:Context
rdf:value: to gefitinib or erlotinib demonstrate decreased secretion of IGFBP-3 in vitro. However, upon evaluating the serum of 20 patients, there was no observed difference in IGFBP-3 levels before and after developing resistance to EGFR-TKI.>>65<< These disparate conclusions may be explained by understanding that IGFBP-3 levels are primarily maintained by hepatic cells.
n3:mentions: n2:24339922

Subject Item: _:vb40853388
rdf:type: n3:Context
rdf:value: there was no observed difference in IGFBP-3 levels before and after developing resistance to EGFR-TKI.65 These disparate conclusions may be explained by understanding that IGFBP-3 levels are primarily maintained by hepatic cells.>>66<< That is, IGFBP-3 may serve as a marker of resistance on a cellular level in lung cancer, but this difference is washed out on an organismal level because the tumor's contribution to serum levels is proportionally insignificant.
n3:mentions: n2:10712265

Subject Item: _:vb40853389
rdf:type: n3:Context
rdf:value: it seems that the protein may not actually be involved in the pathophysiology of EGFR-TKI resistance. Adenoviral expression or small interfering RNA (siRNA) suppression of IGFBP-3 does not alter the response of NSCLC to these drugs.>>65<< Conversely, IGFBP-3 shows some promise in lung cancer that has become resistant to cisplatin (CDDP) therapy.
n3:mentions: n2:24339922

Subject Item: _:vb40853390
rdf:type: n3:Context
rdf:value: cancer that has become resistant to cisplatin (CDDP) therapy. In cells treated with CDDP, promoter methylation decreases expression of IGFBP-3, thereby driving signaling activity of the IGF-1R/PI3K/AKT pathway and inducing resistance.>>67<< Treating H640 NSCLC cells with recombinant human IGFBP-3 or IGF-1R-inhibiting siRNA can confer sensitivity to cisplatin, further demonstrating that both of these members may belong to the same drug resistance pathway.
n3:mentions: n2:22543588

Subject Item: _:vb40853391
rdf:type: n3:Context
rdf:value: 67 Treating H640 NSCLC cells with recombinant human IGFBP-3 or IGF-1R-inhibiting siRNA can confer sensitivity to cisplatin, further demonstrating that both of these members may belong to the same drug resistance pathway.>>68<<
n3:mentions: n2:22197230

Subject Item: _:vb40853392
rdf:type: n3:Context
rdf:value: Finally, IGFBP-7 is thought to be a tumor suppressor, downstream of p53, with implications for treating drug-resistant lung cancer.>>69<< MAP kinase phosphatase 3 (MKP3) has been found to reduce expression of IGFBP-7, driving NSCLC resistance to cisplatin therapy.
n3:mentions: n2:19638426

Subject Item: _:vb40853393
rdf:type: n3:Context
rdf:value: found to reduce expression of IGFBP-7, driving NSCLC resistance to cisplatin therapy. Furthermore, MKP3 knockdown increases the transcriptional level of IGFBP-7, which presents a promising approach for sensitizing tumors to cisplatin.>>70<< Ultimately, the IGF signaling axis presents numerous opportunities for researchers to better understand and attempt to overcome drug resistance in one of deadliest forms of cancer.
n3:mentions: n2:22277373

Subject Item: _:vb40853394
rdf:type: n8:Section
dc:title: ovarian cancer
n8:contains: _:vb40853400 _:vb40853401 _:vb40853396 _:vb40853397 _:vb40853398 _:vb40853399 _:vb40853395

Subject Item: _:vb40853395
rdf:type: n3:Context
rdf:value: Ovarian cancer is one of the deadliest diseases in women, with diagnosis usually made after the onset of symptoms and when metastases are already present.>>35<< In addition, significant drug resistance has been reported to current chemotherapy regimens, which is particularly devastating to those patients who may not be candidates for surgical intervention.
n3:mentions: n2:25271436

Subject Item: _:vb40853396
rdf:type: n3:Context
rdf:value: when metastases are already present.35 In addition, significant drug resistance has been reported to current chemotherapy regimens, which is particularly devastating to those patients who may not be candidates for surgical intervention.>>36<< Similar to its implications in breast cancer, the IGF signaling pathway appears to also play a role in ovarian cancer drug resistance.
n3:mentions: n2:25258665

Subject Item: _:vb40853397
rdf:type: n3:Context
rdf:value: Furthermore, primary tumors harvested from patients after 3–4 cycles of platinum-taxol treatment also demonstrate increased IGF-1R expression.>>37<< A gene microarray study of 28 patients with high-grade serous ovarian cancer demonstrated that samples relatively resistant to platinum chemotherapy showed enrichment of genes involving IGF1/PI3K/NFκB/ERK signaling when compared to those
n3:mentions: n2:25157649

Subject Item: _:vb40853398
rdf:type: n3:Context
rdf:value: high-grade serous ovarian cancer demonstrated that samples relatively resistant to platinum chemotherapy showed enrichment of genes involving IGF1/PI3K/NFκB/ERK signaling when compared to those tumors remaining sensitive to treatment.>>38<< This finding, replicated in several studies, is thought to be the result of two distinct mechanisms beyond just IGF-1R upregulation, including loss of the tumor suppressor PTEN and IGF-2 overexpression.
n3:mentions: n2:24237932

Subject Item: _:vb40853399
rdf:type: n3:Context
rdf:value: An analysis of serous ovarian cancer patients using The Cancer Genome Atlas demonstrated that higher IGF-2 mRNA expression was correlated with indicators of drug resistance, including a shorter time to disease progression and death.>>40<< In addition, transient knockdown of IGF-2 using short-hairpin RNA restores taxol sensitivity in a xenograft model of serous papillary ovarian carcinoma.
n3:mentions: n2:24932685

Subject Item: _:vb40853400
rdf:type: n3:Context
rdf:value: of drug resistance, including a shorter time to disease progression and death.40 In addition, transient knockdown of IGF-2 using short-hairpin RNA restores taxol sensitivity in a xenograft model of serous papillary ovarian carcinoma.>>40<< Other studies have also demonstrated efficacy by inhibiting this pathway. Ganitumab, a human monoclonal antibody to IGF-1R, can augment the response to platinum-based chemotherapy by inhibiting IGF-2-dependent ovarian cancer growth.
n3:mentions: n2:24932685

Subject Item: _:vb40853401
rdf:type: n3:Context
rdf:value: Ganitumab, a human monoclonal antibody to IGF-1R, can augment the response to platinum-based chemotherapy by inhibiting IGF-2-dependent ovarian cancer growth.39 However, blockade of IGF-1R does not seem to counteract taxol resistance.>>40<< This may be explained by the fact that cisplatin and taxol resistance may not arise from the same signaling mechanisms, though members of the IGF pathway appear to be critically involved in both cases.
n3:mentions: n2:24932685

Subject Item: _:vb40853402
rdf:type: n8:Section
dc:title: prostate cancer
n8:contains: _:vb40853404 _:vb40853405 _:vb40853406 _:vb40853407 _:vb40853403 _:vb40853408 _:vb40853409 _:vb40853410 _:vb40853411

Subject Item: _:vb40853403
rdf:type: n3:Context
rdf:value: extensively implicated in the progression of prostate cancer, particularly through contributing to the development of AI disease. There has been considerable research into the interactions between IGF-1R and the androgen receptor (AR).>>42<< Normally, AR binds to an androgen ligand and is subsequently translocated from the cytoplasm to the nucleus of cells, where it serves as a transcription factor and promotes tissue growth.
n3:mentions: n2:16639715

Subject Item: _:vb40853404
rdf:type: n3:Context
rdf:value: from the cytoplasm to the nucleus of cells, where it serves as a transcription factor and promotes tissue growth.43 In the absence of androgen ligand, as is the case with ADT in prostate cancer, an inactive AR remains in the cytosol.>>44<< However, it appears that in certain cases IGF signaling actually can actually drive translocation of AR into the nucleus, even in the absence of androgen.
n3:mentions: n2:14755679

Subject Item: _:vb40853405
rdf:type: n3:Context
rdf:value: is the case with ADT in prostate cancer, an inactive AR remains in the cytosol.44 However, it appears that in certain cases IGF signaling actually can actually drive translocation of AR into the nucleus, even in the absence of androgen.>>42<< This presents a potential mechanism by which prostate cancer can progress to AI disease, especially if IGF signaling is upregulated.
n3:mentions: n2:16639715

Subject Item: _:vb40853406
rdf:type: n3:Context
rdf:value: Furthermore, studies show that inhibiting IGF-1R using an antibody can prevent this transactivation of AR, establishing a potential therapy for prostate cancer progression despite castration.>>42<<
n3:mentions: n2:16639715

Subject Item: _:vb40853407
rdf:type: n3:Context
rdf:value: tissue delivery of the ligand. Thus, it follows that in patients with metastatic disease undergoing ADT, increased levels of IGFBP-1 are associated with a shorter interval to castration resistance, and consequently, decreased survival.>>45<< In vivo studies also show that deleting IGFBP-1 in mice actually decreases growth of prostate tumors, perhaps by activating α5β1 integrin in an IGF-independent manner.
n3:mentions: n2:24132762

Subject Item: _:vb40853408
rdf:type: n3:Context
rdf:value: to castration resistance, and consequently, decreased survival.45 In vivo studies also show that deleting IGFBP-1 in mice actually decreases growth of prostate tumors, perhaps by activating α5β1 integrin in an IGF-independent manner.>>46<<, 47 There has also been significant research looking at the link between insulin-resistance/diabetes and prostate cancer, with IGFPB-2 being recently implicated in this phenomenon.
n3:mentions: n2:21903863

Subject Item: _:vb40853409
rdf:type: n3:Context
rdf:value: to castration resistance, and consequently, decreased survival.45 In vivo studies also show that deleting IGFBP-1 in mice actually decreases growth of prostate tumors, perhaps by activating α5β1 integrin in an IGF-independent manner.46, >>47<< There has also been significant research looking at the link between insulin-resistance/diabetes and prostate cancer, with IGFPB-2 being recently implicated in this phenomenon.
n3:mentions: n2:7504269

Subject Item: _:vb40853410
rdf:type: n3:Context
rdf:value: prostate cancer cell lines, hyperglycemia significantly reduces drug-induced apoptosis through glucose-mediated upregulation of IGFBP-2. Knocking out IGFBP-2, on the other hand, reverses the survival effect caused by hyperglycemia.>>48<< Finally, IGFBP-related proteins (IGFBP-rPs), similar in structure and function to IGFBPs but with weaker affinity for IGF ligands, can play a role in reversing prostate cancer resistance.
n3:mentions: n2:23959956

Subject Item: _:vb40853411
rdf:type: n3:Context
rdf:value: weaker affinity for IGF ligands, can play a role in reversing prostate cancer resistance. Restoring IGFBP-rP1 activity has been found to increase both chemosensitivity to docetaxel and radiosensitivity of prostate cancer cells in vitro.>>49<< Ultimately, it is evident that a better understanding of various members of the IGF signaling axis can help lead to more effective treatment of drug-resistant prostate cancer.
n3:mentions: n2:23600329

Subject Item: _:vb40853412
rdf:type: n8:Section
dc:title: head and neck cancers
n8:contains: _:vb40853413 _:vb40853414 _:vb40853415 _:vb40853416 _:vb40853417

Subject Item: _:vb40853413
rdf:type: n3:Context
rdf:value: Head and neck cancers can have debilitating effects on quality of life, often due to aggressive surgical resection at the time of diagnosis.>>98<<, 99 Despite these efforts, outcomes still remain poor due to the dwindling response of tumors to chemotherapy.
n3:mentions: n2:10732529

Subject Item: _:vb40853414
rdf:type: n3:Context
rdf:value: can have debilitating effects on quality of life, often due to aggressive surgical resection at the time of diagnosis.98, 99 Despite these efforts, outcomes still remain poor due to the dwindling response of tumors to chemotherapy.100, >>101<< IGF signaling remains under considerable investigation for its contributions to this drug resistance.
n3:mentions: n2:24837904

Subject Item: _:vb40853415
rdf:type: n3:Context
rdf:value: poor response in tumors, likely due to compensatory pro-survival signaling caused by IGF-1R. In five HNSCC cell lines, IGF-1R activation decreases apoptotic sensitivity to gefitinib in vitro through downstream activation of AKT and ERK.>>102<< Other studies have demonstrated that IRS-1 may be at the root of this chemoresistance, showing that treatment with gefitinib alters its binding and phosphorylation properties which ultimately requires less IGF ligand for AKT activation.
n3:mentions: n2:21878657

Subject Item: _:vb40853416
rdf:type: n3:Context
rdf:value: Other studies have demonstrated that IRS-1 may be at the root of this chemoresistance, showing that treatment with gefitinib alters its binding and phosphorylation properties which ultimately requires less IGF ligand for AKT activation.>>103<< Keeping with these findings, direct IGF-1R inhibition of HNSCC does indeed result in increased response to treatment with EGFR antagonists.
n3:mentions: n2:17902048

Subject Item: _:vb40853417
rdf:type: n3:Context
rdf:value: 103 Keeping with these findings, direct IGF-1R inhibition of HNSCC does indeed result in increased response to treatment with EGFR antagonists.>>104<< Furthermore, various in vitro and in vivo studies have indicated that IGF signaling blockade can augment the response to histone deacetylase inhibitors, rapamycin, gemcitabine (a nucleoside analog), and even radiation treatment by
n3:mentions: n2:20652976

Subject Item: _:vb40853418
rdf:type: n8:Section
dc:title: hematologic malignancies
n8:contains: _:vb40853420 _:vb40853421 _:vb40853422 _:vb40853423 _:vb40853419 _:vb40853428 _:vb40853424 _:vb40853425 _:vb40853426 _:vb40853427

Subject Item: _:vb40853419
rdf:type: n3:Context
rdf:value: Affecting patients of all ages, various cancers of the blood and bone marrow are usually not amenable to surgical treatment and unfortunately tend to show erratic response to chemotherapy.>>115<<, 116 Interestingly, though, downstream components of the IGF signaling axis, including PI3K, AKT and mTOR have been heavily implicated in conferring this drug resistance.
n3:mentions: n2:13678381

Subject Item: _:vb40853420
rdf:type: n3:Context
rdf:value: Affecting patients of all ages, various cancers of the blood and bone marrow are usually not amenable to surgical treatment and unfortunately tend to show erratic response to chemotherapy.115, >>116<< Interestingly, though, downstream components of the IGF signaling axis, including PI3K, AKT and mTOR have been heavily implicated in conferring this drug resistance.
n3:mentions: n2:18305057

Subject Item: _:vb40853421
rdf:type: n3:Context
rdf:value: unfortunately tend to show erratic response to chemotherapy.115, 116 Interestingly, though, downstream components of the IGF signaling axis, including PI3K, AKT and mTOR have been heavily implicated in conferring this drug resistance.>>117<<, 118, 119, 120 For example, in multiple myeloma, IGF-1/IGF-1R activity is thought to reduce cell sensitivity to bortezomib, a proteasome inhibitor.
n3:mentions: n2:22845486

Subject Item: _:vb40853422
rdf:type: n3:Context
rdf:value: tend to show erratic response to chemotherapy.115, 116 Interestingly, though, downstream components of the IGF signaling axis, including PI3K, AKT and mTOR have been heavily implicated in conferring this drug resistance.117, >>118<<, 119, 120 For example, in multiple myeloma, IGF-1/IGF-1R activity is thought to reduce cell sensitivity to bortezomib, a proteasome inhibitor.
n3:mentions: n2:24237791

Subject Item: _:vb40853423
rdf:type: n3:Context
rdf:value: 117, 118, 119, >>120<< For example, in multiple myeloma, IGF-1/IGF-1R activity is thought to reduce cell sensitivity to bortezomib, a proteasome inhibitor.
n3:mentions: n2:24904824

Subject Item: _:vb40853424
rdf:type: n3:Context
rdf:value: activity is thought to reduce cell sensitivity to bortezomib, a proteasome inhibitor. Exogenous IGF-1 is shown to amplify this effect, whereas inhibiting IGF-1R using small hairpin RNA increases the apoptotic effect of the drug.>>121<< In contrast, other studies have actually shown that IGF-1 enhances the cytotoxic effect of proteasome inhibitors, augmenting the effect of bortezomib on both pro-apoptotic and anti-apoptotic protein levels.
n3:mentions: n2:22932796

Subject Item: _:vb40853425
rdf:type: n3:Context
rdf:value: Patients with acute myeloid leukemia (AML) only have a 30–40% survival five years after diagnosis, most often due to development of chemotherapy resistance.>>123<< When studying 99 adult patients with AML found to be non-responsive to cytarabine and anthracycline, one group found that high IGFBP-2 mRNA levels are not only associated with, but predictive of, poor response to therapy due to
n3:mentions: n2:24967962

Subject Item: _:vb40853426
rdf:type: n3:Context
rdf:value: found to be non-responsive to cytarabine and anthracycline, one group found that high IGFBP-2 mRNA levels are not only associated with, but predictive of, poor response to therapy due to upregulation of genes involved in leukemogenesis.>>124<< In addition, IGFBP-7 has been found to sensitize AML to cell death induced by doxorubicin, etoposide, and cytarabine through an IGF-independent mechanism of promoting G2 cell cycle arrest.
n3:mentions: n2:21899885

Subject Item: _:vb40853427
rdf:type: n3:Context
rdf:value: 124 In addition, IGFBP-7 has been found to sensitize AML to cell death induced by doxorubicin, etoposide, and cytarabine through an IGF-independent mechanism of promoting G2 cell cycle arrest.>>123<< However, in acute lymphoblastic leukemia (ALL), an opposite effect is seen as IGFBP-7 has been found to promote resistance to asparginase through interactions with bone marrow stromal cells, even correlating with decreased leukemia-free
n3:mentions: n2:24967962

Subject Item: _:vb40853428
rdf:type: n3:Context
rdf:value: leukemia (ALL), an opposite effect is seen as IGFBP-7 has been found to promote resistance to asparginase through interactions with bone marrow stromal cells, even correlating with decreased leukemia-free survival in patients.>>125<< Overall, it seems that molecular therapy targeting members of the IGF pathway can one day be developed to enhance response to drugs based on disease-specific mechanisms.
n3:mentions: n2:22005787

Subject Item: _:vb40853429
rdf:type: n8:Section
dc:title: gastrointestinal cancers
n8:contains: _:vb40853430 _:vb40853431 _:vb40853432 _:vb40853433 _:vb40853434 _:vb40853435 _:vb40853436 _:vb40853437 _:vb40853438 _:vb40853439 _:vb40853440 _:vb40853441 _:vb40853442 _:vb40853443 _:vb40853444 _:vb40853445 _:vb40853446

Subject Item: _:vb40853430
rdf:type: n3:Context
rdf:value: Gastrointestinal (GI) neoplasms represent a significant proportion of all new cancers diagnosed yearly, with prognosis ranging from good to dismal based on the organs involved and the extent of invasion.>>79<<, 80, 81 Gastric cancer represents a form of malignancy with relatively poor outcomes, in large part due to limited efficacy of chemotherapy.
n3:mentions: n2:24216698

Subject Item: _:vb40853431
rdf:type: n3:Context
rdf:value: Gastrointestinal (GI) neoplasms represent a significant proportion of all new cancers diagnosed yearly, with prognosis ranging from good to dismal based on the organs involved and the extent of invasion.79, >>80<<, 81 Gastric cancer represents a form of malignancy with relatively poor outcomes, in large part due to limited efficacy of chemotherapy.
n3:mentions: n2:25276995

Subject Item: _:vb40853432
rdf:type: n3:Context
rdf:value: Gastrointestinal (GI) neoplasms represent a significant proportion of all new cancers diagnosed yearly, with prognosis ranging from good to dismal based on the organs involved and the extent of invasion.79, 80, >>81<< Gastric cancer represents a form of malignancy with relatively poor outcomes, in large part due to limited efficacy of chemotherapy.
n3:mentions: n2:21296855

Subject Item: _:vb40853433
rdf:type: n3:Context
rdf:value: have shown that drug resistance in these cases is often associated with decreased expression of microRNAs (miRs), small non-coding molecules that play a key role in post-transcriptional regulation of genes by repressing messenger RNA.>>82<<, 83 In several cisplatin-resistant gastric cancer lines, it appears that downregulated miR-503 is correlated with increased expression of IGF-1R and the downstream anti-apoptotic Bcl-2 protein, as these genes appear to be directly
n3:mentions: n2:17230196

Subject Item: _:vb40853434
rdf:type: n3:Context
rdf:value: shown that drug resistance in these cases is often associated with decreased expression of microRNAs (miRs), small non-coding molecules that play a key role in post-transcriptional regulation of genes by repressing messenger RNA.82, >>83<< In several cisplatin-resistant gastric cancer lines, it appears that downregulated miR-503 is correlated with increased expression of IGF-1R and the downstream anti-apoptotic Bcl-2 protein, as these genes appear to be directly regulated
n3:mentions: n2:22072795

Subject Item: _:vb40853435
rdf:type: n3:Context
rdf:value: Furthermore, overexpression of miR-503 reduces the activity of these proteins and subsequently re-sensitizes cells to cisplatin-induced apoptosis.>>84<< miR-1271 seems to play a similar role in gastric cancer cells, restoring cisplatin sensitivity in vitro by repressing IGF-1R, IRS-1, mTOR, and Bcl-2.85 As such, these studies support a novel approach of using microRNAs to modulate IGF
n3:mentions: n2:24931256

Subject Item: _:vb40853436
rdf:type: n3:Context
rdf:value: 84 miR-1271 seems to play a similar role in gastric cancer cells, restoring cisplatin sensitivity in vitro by repressing IGF-1R, IRS-1, mTOR, and Bcl-2.>>85<< As such, these studies support a novel approach of using microRNAs to modulate IGF signaling and perhaps even overcome drug resistance.
n3:mentions: n2:24875127

Subject Item: _:vb40853437
rdf:type: n3:Context
rdf:value: 86 In general, obesity has been associated with poorer outcomes and may underlie drug resistance.>>87<< One study looked at the in vitro effects on CRC cells of low-dose oxaliplatin, 5-fluorouracil, or irinotecan in combination with obesity-related molecular phenomena, including elevated glucose, insulin, and IGF-1.88 This was meant to
n3:mentions: n2:22593429

Subject Item: _:vb40853438
rdf:type: n3:Context
rdf:value: 87 One study looked at the in vitro effects on CRC cells of low-dose oxaliplatin, 5-fluorouracil, or irinotecan in combination with obesity-related molecular phenomena, including elevated glucose, insulin, and IGF-1.>>88<< This was meant to emulate a frequent situation in which obese patients are under-dosed with chemotherapy.
n3:mentions: n2:24396438

Subject Item: _:vb40853439
rdf:type: n3:Context
rdf:value: or irinotecan in combination with obesity-related molecular phenomena, including elevated glucose, insulin, and IGF-1.88 This was meant to emulate a frequent situation in which obese patients are under-dosed with chemotherapy.>>89<< Though not always observed with increased insulin or glucose concentrations, the combination of elevated IGF-1 and low-dose chemotherapy consistently increased tumor cell survival.
n3:mentions: n2:23856744

Subject Item: _:vb40853440
rdf:type: n3:Context
rdf:value: obese patients are under-dosed with chemotherapy.89 Though not always observed with increased insulin or glucose concentrations, the combination of elevated IGF-1 and low-dose chemotherapy consistently increased tumor cell survival.>>88<< This data provides intriguing insight into how IGF signaling may serve as a link between obesity and development of drug resistance.
n3:mentions: n2:24396438

Subject Item: _:vb40853441
rdf:type: n3:Context
rdf:value: One of the mechanisms by which CRC cells are able to develop multidrug resistance is through active efflux by pumps, such as multidrug-resistance-associated protein 2 (MRP-2), which can reduce intracellular drug concentration.>>90<< IGF signaling has been thought to be involved with this pump activity.
n3:mentions: n2:14965249

Subject Item: _:vb40853442
rdf:type: n3:Context
rdf:value: This effect appears to be mediated via the PI3K/AKT pathway, which causes nuclear translocation of nuclear factor-like 2 (Nrf2) and reduces expression of MRP-2.>>91<< This study presents yet another mechanism by which resistance can arise, but offers the potential solution that modulating IGF-1R activity can overcome this by maintaining therapeutic drug levels inside target cells.
n3:mentions: n2:22275271

Subject Item: _:vb40853443
rdf:type: n3:Context
rdf:value: cells (CSCs) within these tumors.93 In oxaliplatin-resistant HCC, the stemness of a subpopulation of tumor cells is associated with autocrine signaling of IGF-1, whereas treatment with an IGF-1R inhibitor suppresses CSC-related markers.>>94<< In pancreatic cancer, IGF-1R knockdown enhances the efficacy of gemcitabine in vitro, likely due to inhibition of the downstream PI3K/AKT and NF-κB activity.
n3:mentions: n2:24632571

Subject Item: _:vb40853444
rdf:type: n3:Context
rdf:value: whereas treatment with an IGF-1R inhibitor suppresses CSC-related markers.94 In pancreatic cancer, IGF-1R knockdown enhances the efficacy of gemcitabine in vitro, likely due to inhibition of the downstream PI3K/AKT and NF-κB activity.>>95<< K-Ras, a GTPase belonging to the Ras family, is frequently mutated into a constitutively active form in pancreatic ductal adenocarcinoma (PDAC).
n3:mentions: n2:23589145

Subject Item: _:vb40853445
rdf:type: n3:Context
rdf:value: in vitro, likely due to inhibition of the downstream PI3K/AKT and NF-κB activity.95 K-Ras, a GTPase belonging to the Ras family, is frequently mutated into a constitutively active form in pancreatic ductal adenocarcinoma (PDAC).>>96<< This mutation also confers resistance to experimental drugs such as rapalog and everolimus, which are mTOR inhibitors, by causing feedback activation of the IGF-1-Ras-ERK pathway.
n3:mentions: n2:20814421

Subject Item: _:vb40853446
rdf:type: n3:Context
rdf:value: such as rapalog and everolimus, which are mTOR inhibitors, by causing feedback activation of the IGF-1-Ras-ERK pathway. In these cases, K-Ras knockdown blocks IGF-induced ERK signaling and thereby enhances sensitivity to everolimus.>>97<< Furthermore, targeting IGF signaling may offer another way to overcome drug resistance in tumors identified to have a K-Ras mutation.
n3:mentions: n2:22342683

Subject Item: _:vb40853447
rdf:type: n8:Section
dc:title: bone and soft tissue tumors
n8:contains: _:vb40853448 _:vb40853449 _:vb40853450 _:vb40853451 _:vb40853452 _:vb40853453 _:vb40853454 _:vb40853455

Subject Item: _:vb40853448
rdf:type: n3:Context
rdf:value: a tendency to preferentially affect children and adolescents. This is thought to be due to the underlying mechanisms involved in both normal skeletal growth and the development of these tumors, such as the extensively-studied IGF pathway.>>1<< In addition to contributing to the malignant phenotype of bone diseases like osteosarcoma (OS) and Ewing's sarcoma, IGF signaling now appears to be implicated in tumor response to pharmacologic agents.
n3:mentions: n2:12767520

Subject Item: _:vb40853449
rdf:type: n3:Context
rdf:value: extensively-studied IGF pathway.1 In addition to contributing to the malignant phenotype of bone diseases like osteosarcoma (OS) and Ewing's sarcoma, IGF signaling now appears to be implicated in tumor response to pharmacologic agents.>>106<< For example, IGF-1R inhibition has been shown to inhibit OS proliferation and invasion while increasing sensitivity to both radiation and chemotherapy with docetaxel, cisplatin, or doxorubicin.
n3:mentions: n2:19126579

Subject Item: _:vb40853450
rdf:type: n3:Context
rdf:value: tumor response to pharmacologic agents.106 For example, IGF-1R inhibition has been shown to inhibit OS proliferation and invasion while increasing sensitivity to both radiation and chemotherapy with docetaxel, cisplatin, or doxorubicin.>>107<<, 108, 109, 110 Furthermore, IGFBP-5 is significantly downregulated in OS, with overexpression of the N- and C-terminal domains of the protein specifically inhibiting tumor growth and invasion, respectively.
n3:mentions: n2:20376536

Subject Item: _:vb40853451
rdf:type: n3:Context
rdf:value: response to pharmacologic agents.106 For example, IGF-1R inhibition has been shown to inhibit OS proliferation and invasion while increasing sensitivity to both radiation and chemotherapy with docetaxel, cisplatin, or doxorubicin.107, >>108<<, 109, 110 Furthermore, IGFBP-5 is significantly downregulated in OS, with overexpression of the N- and C-terminal domains of the protein specifically inhibiting tumor growth and invasion, respectively.
n3:mentions: n2:19229591

Subject Item: _:vb40853452
rdf:type: n3:Context
rdf:value: 107, 108, >>109<<, 110 Furthermore, IGFBP-5 is significantly downregulated in OS, with overexpression of the N- and C-terminal domains of the protein specifically inhibiting tumor growth and invasion, respectively.
n3:mentions: n2:21843050

Subject Item: _:vb40853453
rdf:type: n3:Context
rdf:value: 107, 108, 109, >>110<< Furthermore, IGFBP-5 is significantly downregulated in OS, with overexpression of the N- and C-terminal domains of the protein specifically inhibiting tumor growth and invasion, respectively.
n3:mentions: n2:19638450

Subject Item: _:vb40853454
rdf:type: n3:Context
rdf:value: cisplatin, or doxorubicin.107, 108, 109, 110 Furthermore, IGFBP-5 is significantly downregulated in OS, with overexpression of the N- and C-terminal domains of the protein specifically inhibiting tumor growth and invasion, respectively.>>16<<, 17 These effects appear to be mediated through both IGF-dependent and -independent pathways, indicating a potential role for IGFBP-5 in mono- or combination therapy to overcome various mechanisms of drug resistance.
n3:mentions: n2:21460855

Subject Item: _:vb40853455
rdf:type: n3:Context
rdf:value: or doxorubicin.107, 108, 109, 110 Furthermore, IGFBP-5 is significantly downregulated in OS, with overexpression of the N- and C-terminal domains of the protein specifically inhibiting tumor growth and invasion, respectively.16, >>17<< These effects appear to be mediated through both IGF-dependent and -independent pathways, indicating a potential role for IGFBP-5 in mono- or combination therapy to overcome various mechanisms of drug resistance.
n3:mentions: n2:23665505

Subject Item: _:vb40853456
rdf:type: n8:Section
dc:title: central nervous system (cns) tumors
n8:contains: _:vb40853460 _:vb40853461 _:vb40853462 _:vb40853457 _:vb40853458 _:vb40853459

Subject Item: _:vb40853457
rdf:type: n3:Context
rdf:value: Glioma comprises about 30% of all CNS tumors, with a particularly poor prognosis when diagnosed in the brain.>>71<< Surgical resection is often not an option for many patients, who rely immensely on radio- and chemotherapy.
n3:mentions: n2:23238284

Subject Item: _:vb40853458
rdf:type: n3:Context
rdf:value: when diagnosed in the brain.71 Surgical resection is often not an option for many patients, who rely immensely on radio- and chemotherapy. In these cases, tumors acquire resistance within just a short interval after beginning therapy.>>72<< In terms of radiation, cancer stem cells have been though to play a critical role in tumor progression despite aggressive treatment.
n3:mentions: n2:24384235

Subject Item: _:vb40853459
rdf:type: n3:Context
rdf:value: Suppressing GLI1 decreases IGF-1-dependent proliferation, invasion, and angiogenesis by increasing GSC response to temozolamide.>>74<< Independent of HH, IGF-1-induced activation of PI3K appears to protect U251 glioma cells from tamoxifen-induced apoptosis, which can be partially overcome by combination treatment with a specific PI3K inhibitor (LY294002) or PI3K subunit
n3:mentions: n2:20857406

Subject Item: _:vb40853460
rdf:type: n3:Context
rdf:value: treatment with a specific PI3K inhibitor (LY294002) or PI3K subunit P85 siRNA. Furthermore, the effects of LY294002 appear to be mediated through activation (or dephosphorylation) of GSK3, which inhibits gene transcription by β-catenin.>>75<< Despite this compelling evidence that IGF signaling contributes to drug resistance, other studies have muddied the waters.
n3:mentions: n2:22046442

Subject Item: _:vb40853461
rdf:type: n3:Context
rdf:value: factor Wilms' tumor 1 (WT1) increases the survival of glioblastoma cells in the presence of cisplatin and carmustine. However, though silencing WT1 did increase sensitivity to the drugs, there was increased IGF-1R expression as a result.>>76<< These disparate conclusions regarding IGF activity in glioma may be attributed to the complex and seemingly independent mechanisms by which resistance arises for different classes of drugs.
n3:mentions: n2:20820871

Subject Item: _:vb40853462
rdf:type: n3:Context
rdf:value: IGFBP-2, which is overexpressed in nearly 80% of all glioblastoma multiforme cases, appears to induce chemoresistance through an IGF-independent mechanism.>>77<< Exogenous IGFBP-2 promotes proliferation and invasion of several glioma lines, even in the presence of temozolamide.
n3:mentions: n2:10485462

Subject Item: _:vb40853463
rdf:type: n8:Section
dc:title: igf signaling in cancer and the development of drug resistance
n8:contains: _:vb40853472 _:vb40853473 _:vb40853474 _:vb40853464 _:vb40853465 _:vb40853466 _:vb40853467 _:vb40853468 _:vb40853469 _:vb40853470 _:vb40853471

Subject Item: _:vb40853464
rdf:type: n3:Context
rdf:value: Numerous cancers have been shown to be associated with aberrant IGF signaling, including colon cancer, prostate cancer, pancreatic cancer, melanoma, osteosarcoma, and childhood malignancies, among many others.>>9<< Numerous in vitro, in vivo, and clinical studies have shown that increased IGF-1R activity is implicated in cancer cell proliferation, migration, and invasion.
n3:mentions: n2:17237261

Subject Item: _:vb40853465
rdf:type: n3:Context
rdf:value: melanoma, osteosarcoma, and childhood malignancies, among many others.9 Numerous in vitro, in vivo, and clinical studies have shown that increased IGF-1R activity is implicated in cancer cell proliferation, migration, and invasion.>>9<<, 10 IGF ligand appears to be delivered not only from distant sources (i.e. endocrine signaling), but also through paracrine/autocrine signaling in more aggressive tumors.
n3:mentions: n2:17237261

Subject Item: _:vb40853466
rdf:type: n3:Context
rdf:value: melanoma, osteosarcoma, and childhood malignancies, among many others.9 Numerous in vitro, in vivo, and clinical studies have shown that increased IGF-1R activity is implicated in cancer cell proliferation, migration, and invasion.9, >>10<< IGF ligand appears to be delivered not only from distant sources (i.e. endocrine signaling), but also through paracrine/autocrine signaling in more aggressive tumors.
n3:mentions: n2:15229476

Subject Item: _:vb40853467
rdf:type: n3:Context
rdf:value: implicated in cancer cell proliferation, migration, and invasion.9, 10 IGF ligand appears to be delivered not only from distant sources (i.e. endocrine signaling), but also through paracrine/autocrine signaling in more aggressive tumors.>>10<< In addition, increased serum levels of IGF-1 have been observed in cancers of the lung, colon, prostate, and breast.
n3:mentions: n2:15229476

Subject Item: _:vb40853468
rdf:type: n3:Context
rdf:value: distant sources (i.e. endocrine signaling), but also through paracrine/autocrine signaling in more aggressive tumors.10 In addition, increased serum levels of IGF-1 have been observed in cancers of the lung, colon, prostate, and breast.>>11<<, 12, 13, 14 Many other IGF pathway members are also thought to play a role in malignancies.
n3:mentions: n2:9593409

Subject Item: _:vb40853469
rdf:type: n3:Context
rdf:value: sources (i.e. endocrine signaling), but also through paracrine/autocrine signaling in more aggressive tumors.10 In addition, increased serum levels of IGF-1 have been observed in cancers of the lung, colon, prostate, and breast.11, >>12<<, 13, 14 Many other IGF pathway members are also thought to play a role in malignancies.
n3:mentions: n2:10203281

Subject Item: _:vb40853470
rdf:type: n3:Context
rdf:value: sources (i.e. endocrine signaling), but also through paracrine/autocrine signaling in more aggressive tumors.10 In addition, increased serum levels of IGF-1 have been observed in cancers of the lung, colon, prostate, and breast.11, 12, >>13<<, 14 Many other IGF pathway members are also thought to play a role in malignancies.
n3:mentions: n2:15562830

Subject Item: _:vb40853471
rdf:type: n3:Context
rdf:value: circulating levels of IGF-2 in colorectal cancer to suppressed activity of IGFBP-5 in osteosarcoma, it is clear that the IGF axis serves as an important lens to better understand and address the underlying mechanisms of neoplasia.>>15<<, 16, 17 In fact, several IGF signaling modulators have undergone significant basic science and translational investigations with promising results; currently, monoclonal antibodies to IGF-1R are undergoing clinical trials.
n3:mentions: n2:24080445

Subject Item: _:vb40853472
rdf:type: n3:Context
rdf:value: circulating levels of IGF-2 in colorectal cancer to suppressed activity of IGFBP-5 in osteosarcoma, it is clear that the IGF axis serves as an important lens to better understand and address the underlying mechanisms of neoplasia.15, >>16<<, 17 In fact, several IGF signaling modulators have undergone significant basic science and translational investigations with promising results; currently, monoclonal antibodies to IGF-1R are undergoing clinical trials.
n3:mentions: n2:21460855

Subject Item: _:vb40853473
rdf:type: n3:Context
rdf:value: levels of IGF-2 in colorectal cancer to suppressed activity of IGFBP-5 in osteosarcoma, it is clear that the IGF axis serves as an important lens to better understand and address the underlying mechanisms of neoplasia.15, 16, >>17<< In fact, several IGF signaling modulators have undergone significant basic science and translational investigations with promising results; currently, monoclonal antibodies to IGF-1R are undergoing clinical trials.
n3:mentions: n2:23665505

Subject Item: _:vb40853474
rdf:type: n3:Context
rdf:value: neoplasia.15, 16, 17 In fact, several IGF signaling modulators have undergone significant basic science and translational investigations with promising results; currently, monoclonal antibodies to IGF-1R are undergoing clinical trials.>>18<< However, it has become clear that the IGF axis is part of a much larger network of cellular signaling that ultimately results in the highly proliferative and invasive cancer phenotypes.
n3:mentions: n2:23601239

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