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Biologic Targeting in RT

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arunmp's version from 2016-12-21 09:02

Biologic Targeting in RT

Features of Carcinogenesis- short note-what happesns to each
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Mutations with gain in function for(oncogenes)
Mutations with loss of function(tumor suppressor genes)
Mutations affectAffect molecular signaling pathways and causes
• (overexpression of ligands or receptors associated withself-sufficient growth factor signaling
• Loss of response to anti-proliferative signals
• Evasion ofcell death programs
• Increase inreplicative potential (telomeres)
• Promotion of tissue invasion and metastasis
• Sustained angiogenesis
• abnormalitiesDNA repair and genomic instability
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• Activation of cell cycle progression and survival pathways generally increasesradioresistance
• Activation of pro-apoptotic/cell cycle arrest pathways generallyradiosensitize
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Imatinib (Gleevec)Bcr-Abl, c-kit, PDGFR-a
Gefitinib (Iressa)EGFr
Erlotinib (Tarceva)EGFR
Bortezomib (Velcade)Proteasome
Sorafenib (Nexavar)c-Raf, BRA, Kit, EGFR
Sunitinib (Sutent)Multiple RTKs, VEGF, PDGF
Dasatinib (Sprycel)BCR-ABL, SRC family,
Bevacizumab (Avastin)VEGF
Alemtuzumab (Campath)CD52
Cetuximab (Erbitux)EGFR (HER-1)
Trastuzumab (Herceptin)HER2
Tositumomab (Bexxar)CD20
Rituximab (Rituxan )CD20
Ibritumomab tiuxetan (Zevalin)CD20
Gemtuzumab (Mylotarg)CD33
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Panitumumab(Vectibix) : EGFR
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Lapatiniboral tyrosine kinase inhibitor of ErbB1 and ErbB2 NEOALTO TRIAL
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Multiple target thera
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Dual kinase Inhibitor EGFR/VEGF Inhibitors Tyrosine Kinase Inhibitors- Vandatanib (ZD6474)
Dual kinase Inhibitor EGFR/HER 2 InhibitorsTyrosine Kinase Inhibitors- Lapatinib
Multi kinase InhibitorVEGFR, PDGFR, KIT and FLT3RTyrosine Kinase inhibitor- Sunitinib
Multi kinase InhibitorVEGFR2 and VEGFR3, FLT-3, PDGFR, c-KITTyrosine Kinase Inhibitor- Sorafenib
Sorafenib is an oral inhibitor of RAF
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Most molecular targeting agents are likely to be more cytostatic than cytotoxic, and are unlikely to be curative and adjuvant therapy with RT than radical
Imatinib (Gleevec) CML, GIST
Gefitinib (Iressa)NSLC-10% respond
Erlotinib (Tarceva)NSLC, mesothelioma
Bortezomib (Velcade)Multiple myeloma 1 year 23% of patients
Sorafenib (Nexavar)mRCc FLT-3, VEGFR, PDGFR-β
Sunitinib (Sutent)GIST and mRCC GIST: 25.5% MRCC: 36.5%
Dasatinib (Sprycel)CML and Ph+ ALL
Bevacizumab (Avastin)CRC,5 months prolonged survival,GBM, Her2/neu negative metastatic breast cancer,mrcc,metastatic adeno ca lung
Alemtuzumab (Campath)B-cell CLL ,9.5 months 30% patients
Cetuximab (Erbitux)CRC, pancreatic Ca increased response HNSCC, NSLC
Trastuzumab (Herceptin)HER2 Breast cancer 25 months for 26%
Tositumomab (Bexxar)NHL 57% to 71% respond
Rituximab (Rituxan )NHL, CLL,MM, HCL 3 months in 45% of patients
Ibritumomab tiuxetan (Zevalin)NHL 80% respond
Gemtuzumab (Mylotarg)AML 6 months 30% of patients
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Panitumumab(Vectibix) : Mcolorectalrc with kras+ PFS 96 days
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Non-selective COX I and 2 inhibitorsNSAIDs - aspirin, ibuprofen, indomethacin -
Selective COX2 inhibitorscelecoxib, rofecoxib, meloxicam, NS-398, etc
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Exploiting Low Tumor Oxygenation with Hypoxic CytotoxinsTripazapmine
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NF-kB is activated which transcribes anti-apoptotic factors inhibitors of apoptosis (IAPs) like survivin, Bcl-XL, etc