5 – Growth Factors, Receptors, and Cancer – Flashcards
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mutations in the EGF receptor (EGF-R) that contribute to the development of cancer are MOST often due to:
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truncation of the ectodomain of the receptor
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provide FOUR different examples of a tyrosine kinase growth factor receptor that is often altered in cancer cells:
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1. ErbB2 2. Kit 3. FGF-R2 4. PDGF-Rβ
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provide an example of a tyrosine kinase growth factor receptor that is NOT often altered in cancer cells:
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VEGF
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in cells infected with simian sarcoma virus, the sis oncogene causes the cells to release increased amounts of Sis protein, which is recognized by PDGF-receptor molecules on the cells' surface - this type of signaling loop is an example of:
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AUTOCRINE signaling
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when a growth factor receptor is NOT bound to ligand, it is MOST likely in ___________________ configuration.
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MONOMERIC
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TGF-β receptors have:
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1. an extracellular ligand-binding 2. a transmembrane domain
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TGF-β receptors have kinase domains that...
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phosphorylate serine and threonine residues
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Type 1 and Type II TGF-β receptors form __________________.
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heterodimers
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the LIGANDS of nuclear receptors are ___________________.
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hydrophobic
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the LIGANDS of nuclear receptors may ACTIVATE ________________________.
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TRANSCRIPTION FACTORS
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the LIGANDS of nuclear receptors include:
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1. steroid sex hormones 2. retinoids 3. vitamin D
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INTEGRINS are ____________________ receptors
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cell surface
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cell surface receptors that are able to create mechanical stability by tethering cells to the extracellular matrix (ECM) are known as:
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INTEGRINS
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MUTATIONS often occur at codons ____, _____, or _____.
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12, 13, or 61
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ONCOGENIC mutations usually result in:
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HIGHER levels of GTP-bound Ras AND LOWER levels of GDP-bound Ras
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cells often have COMPROMISED activity of ________________________.
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GTPase-activating proteins (GAPs)
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the OVER-EXPRESSION of GROWTH RECEPTORS helps to promote cancer growth by:
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1. stimulating the dimerization and trans-phosphorylation of the receptors 2. promoting mitogenic signaling 3. turning ON DOWN-stream signaling
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ligand-INDEPENDENT signaling of receptor-tyrosine kinases can result from:
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1. mutations resulting in truncation of the receptor ectodomain 2. amino acid substitutions in the cytoplasmic domains of receptors
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