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ON6 Targeted Therapies

Deleted user 9 questions

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  1. 1Targeted cancer therapies are products of [blank_start]rational[blank_end] drug design, act on [blank_start]specific[blank_end] molecular targets, and are generally [blank_start]cytostatic[blank_end]. They interfere with specific molecules involved in cancer cell [blank_start]growth and survival[blank_end]. Can be:
    1. [blank_start]Small molecule[blank_end] drugs, easily enter tumour cell
    or
    2. [blank_start]Moncolonal antibodies[blank_end], bind to specific targets on cell surface
    1. Arational
    2. Bspecific
    3. Ccytostatic
    4. Dgrowth and survival
    5. ESmall molecule
    6. FMoncolonal antibodies
  2. 2Tumour associated antigens (TIAs) are optimal blocking targets.
    1. ATrue
    2. BFalse
  3. 3
    Products of activated oncogenes include cell surface receptors that [blank_start]activate[blank_end] tyrosine kinases. Tyrosine kinase [blank_start]autophosphorylates[blank_end] the receptors in the cell to make: [blank_start]vascular endothelium[blank_end] derived growth factor receptors, human [blank_start]epidermal[blank_end] growth factor, and [blank_start]platelet[blank_end]-derived growth factor receptors. These stimulate [blank_start]proliferation[blank_end] and block [blank_start]apoptosis[blank_end].

    Chromosomal abnormalities are in cancer cells but not normal cells. [blank_start]Thee[blank_end] fusion gene which causes the abnormality makes fusion proteins that[blank_start]. drive[blank_end] cancer development. We can identify cancerous proteins and [blank_start]block[blank_end] their production. Example: Chronic [blank_start]myeloid leukaemia[blank_end] often have the Philadelphia chromosome, which creates a [blank_start]BCR-ABL[blank_end] fusion protein. In cancer it causes constitutively active [blank_start]tyrosine kinase[blank_end] activity.
    1. Aactivate
    2. Bautophosphorylates
    3. Cvascular endothelium
    4. Depidermal
    5. Eplatelet
    6. Fproliferation
    7. Gapoptosis
    8. HThe
    9. Idrive
    10. Jblock
    11. Kmyeloid leukaemia
    12. LBCR-ABL
    13. Mtyrosine kinase
  4. 4Imatinib: First NIB approved by FDA. The suffix "nib" indicates a small-molecule [blank_start]inhibitor[blank_end] ("nib" is verbal shorthand for "inhibit") of kinase enzymes.
    - A small molecule [blank_start]intracellular[blank_end] inhibitor of tyrosine kinase
    - Treats chronic myeloid leukaemia; as it is selective for [blank_start]BCR-ABL[blank_end] TK fusion protein and competes with [blank_start]ATP[blank_end] for binding siten inhibiting phosphorylation (and [blank_start]proliferation[blank_end]).

    Other NIBs in clinical use: gefitinib, erlotinib, sorafenib, sunitinib, and dasatinib.
    - Share [blank_start]same[blank_end] mechanism of action (competitive ATP inhibition at catalytic binding site of TK) BUT difference is the [blank_start]spectrum[blank_end] of targeted kinases
    e.g. [blank_start]sunitinib[blank_end] inhibits signals from several Rs including VEGF and PDGRF families.

    NIBs are well tolerated but frequently cause [blank_start]myelosupression, rash, GI upset, fatigue[blank_end], arthralgia, & myalgia. Rarely
    cumulative cardiotoxicity: [blank_start]monitoring[blank_end] needed.
    1. Ainhibitor
    2. Bintracellular
    3. CBCR-ABL
    4. Dproliferation
    5. EATP
    6. Fsame
    7. Gspectrum
    8. Hsunitinib
    9. Imyelosupression, rash, GI upset, fatigue
    10. Jmonitoring
  5. 5Targeted therapy with monoclonal antibodies:
    Target is angiogenesis, specifically the key targets [blank_start]VEGF-A and VEGFR2[blank_end].

    Bevacizumab (brand name Avastin): [blank_start]recombinant humanized[blank_end] monoclonal v VEGF-A, given by [blank_start]intravenous[blank_end] infusion, first line for [blank_start]colorectal, lung, renal[blank_end] cancer.
    Mode of action:
    Prevents VEGF-A [blank_start]binding[blank_end] and so prevents tumour vascularisation and growth. Serious unwanted effects:, [blank_start]Hyper[blank_end]tension
    • Infections (from [blank_start]neutropaenia[blank_end]), impaired [blank_start]would[blank_end] healing, bleeding, GI perforation, haemorrhage. [blank_start]DVT, PE[blank_end] in the elderly.
    1. AVEGF-A and VEGFR2
    2. Brecombinant humanized
    3. Cintravenous
    4. Dcolorectal, lung, & renal
    5. Ebinding
    6. FHyper
    7. Gneutropaenia
    8. Hwound
    9. IDVT, PE
  6. 6Target: Human epidermal growth factor 2 (HER-2)
    Receptor coupled [blank_start]enzyme[blank_end], binds to EGF.
    • Normally promotes growth and [blank_start]differentiation[blank_end]
    • Integral [blank_start]tyrosine kinase[blank_end] activity inhibits p27 (cyclin dependent cell cycle [blank_start]regulator[blank_end])
    • Stimulates [blank_start]proliferation[blank_end]
    • HER2 is found in 20-30% of breast tumours.
    1. Aenzyme
    2. Bdifferentiation
    3. Ctyrosine kinase
    4. Dregulator
    5. Eproliferation
  7. 7Trastuzumab (Herceptin):
    [blank_start]Humanised mouse[blank_end] monoclonal of HER2, for [blank_start]metastatic[blank_end] breast cancer.
    Mode of action: G1 [blank_start]arrest[blank_end] - less proliferation(no change in HER2 expression). Downregulates [blank_start]kinase[blank_end] activation, causing less [blank_start]PI3K, Akt[blank_end], which activates [blank_start]p27[blank_end] and halts cell cycle.

    Pertuzumab:
    inhibits HER2 [blank_start]dimerisation[blank_end].
    1. AHumanised mouse
    2. Bmetastatic
    3. Carrest
    4. Dkinase
    5. EPI3K, Akt
    6. Fp27
    7. Gdimerisation
  8. 8Unwanted effects of monoclonal ABs:
    Mechanism dependent.
    Common:
    • [blank_start]Infusion[blank_end] related SEs ([blank_start]cytokine[blank_end] release syndrome), 1st infusion
    • [blank_start]Fever, chills,[blank_end] nausea and vomiting, hypersensitivity
    More Serious
    • [blank_start]Tumour Lysis Syndrome[blank_end] - release of cellular contents: high K+, P, uric acid, N, low Ca2+ = kidney [blank_start]failure[blank_end], seizures, [blank_start]cardiac[blank_end] arrhythmias, death.
    • Increased [blank_start]infection[blank_end] risk (HepB/reactivation)
    • Caution: autoimmune disease, HIV
    1. AInfusion
    2. Bcytokine
    3. CFever, chills,
    4. DTumour Lysis Syndrome
    5. Efailure
    6. Fcardiac
    7. Ginfection
  9. 9Target: Cell surface glycoproteins.
    [blank_start]CD20[blank_end] antigen found on the surface of normal and malignant B lymphocytes, function unknown. Can activate [blank_start]B[blank_end] cells.

    Drug: Rituxumab.
    Mediates B cell [blank_start]lysis[blank_end].
    - [blank_start]Complement[blank_end] dependent cytotoxicity (CDCC)
    - [blank_start]Antibody[blank_end] dependent cell-mediated cytotoxicity (ADCC)
    - Apotosis
    • [blank_start]Increases[blank_end] NK cell success from 40-80%
    Unwanted effects, most serious:
    • Cardiomyopathy
    • [blank_start]Infusion[blank_end] related SEs
    • Hypersensitivity ([blank_start]first[blank_end] infusion)
    • Myelosupression
    1. ACD20
    2. BB
    3. Clysis
    4. DComplement
    5. EAntibody
    6. FIncreases
    7. GInfusion
    8. Hfirst

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User has deleted their subject information Quiz on ON6 Targeted Therapies, created by Deleted user on 09/10/2019.
Author
Deleted user
Language
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