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Terms in this set (48)
increase in cell size signal
Dominant somatic mutation
-creates oncogenes that promote development of cancer by conferring a survival or rapid-proliferation phenotype
Recessive somatic mutation
-deletes or inactivates tumor-suppressor genes
-can be inherited
tumor suppressor gene
p53 tumor suppressor gene
If tumor cell lacks this, the cell cycle will not be arrested upon DNA damage leading to continued mutation, cancer, or death
-stage of colorectal cancer
-polyp present in colon
-result of metastasis of primary tumor
-90% of cancer patients that die, die from these
-change of one base to another of the same nucleic acid family; purine -> purine; pyrimidine -> pyrimidine
Deamination of cytosine to form uracil in DNA
mutation that converts C:G base pairing to A:T base pairing
mutation that forms abasic site in DNA
Deamination of deoxy-5-methyl-cytosine to form deoxythymidine glycol
mutation that converts cytosine to thymine
mutation resulting from reactive oxygen species (ROS) like the superoxide ion leaking into cytoplasm from oxidative processes in the mitochondria and into the nucleus
change in one base to another; purine -> pyrimidine; pyrimidine -> purine
Thymine/Cytosine dimers and (6-4) photoproducts
What does UV radiation cause?
Formation of abasic sites
Breakage of phosphodiester backbone (ss breaks & ds breaks)
What does ionizing radiation cause?
Double strand breaks (DSBs)
What is the most sever form of damage and the most difficult to repair?
induction of p53 causing cell cycle arrest -> leads to repair of DNA damage or apoptosis
What is the cell's response to cellular DNA damage?
Oxidation of guanosine, making it large and bulky in DNA backbone, results in basepairing with adensosine (transversion mutation)
-mutation resulting from superoxide ion oxidative damage
-Formation of 8-oxo-deoxyguanosine
Formation of covalent DNA adducts by carcinogens being oxidatively processed in cell that attack guanine and are converted to thymine upon DNA replication
-mutation causing G to T transversion by carcinogenic oxidative processing
Polcyclic Aromatic Hydrocarbons from incomplete combustion of cigarette smoke
-carcinogen resulting from incomplete combustion - cigarette smoke (give example)
Mixed-function oxidases (MFOs)
Ex: cytochrome P450
-enzymes that oxidize (add -OHs) hydrophobic molecules such as xenobiotics and drugs for excretion from the body
carcinogen that causes liver cancer at very low exposure levels; from black mold (used to be common on peanuts)
What enzyme oxidizes the above compound?
Receptor Tyrosine Kinase
-largest class of enzyme-linked receptors
-Epidermal Growth Factor (EGF) causes cross-phosphorylation of its kinase domains (activated form)
1. effectors (enzymes that are activated by docking) or adaptors (link receptor to other effectors) dock to the tyrosine-phosphorylated sites on the activated receptor
2. termination of signal by dephosphoylation by protein tyrosine phosphatases
How is a signal transduced by receptor tyrosine kinase (RTK)?
Cell division, differentiation, death, shape and motility
What do kinase-coupled receptors regulate?
Main adaptor protein + Ras-activating protein that transduces signal from receptor tyrosine kinase to Ras (intermediate adaptor)
What is Grb-2-Sos?
-key element in the major pathway for signaling from receptor tyrosine kinases
-activated by Grb-2-Sos (Sos is a GEF protein)
-causes mitogen-activated protein kinase (MAP kinase) pathway
What is Ras?
-stimulates the mitogen-activated protein kinase (MAP kinase) pathway
-MAP kinase kinase kinase (Raf) -> MAP kinase kinase (Mek) -> MAP kinase (Erk) -> phosphorylates proteins to increase proliferation
Ras -> Raf -> Mek -> Erk -> phosphorylation of gene expression proteins
What does activated Ras do?
affects cell proliferation, gene expression, and protein synthesis
What do ERK/MAPK pathways affect?
control survival, growth, and proliferaiton
What to PI3 kinase/Akt/PKB pathways control?
regulates cytoskeleton dynamics, movement, and motility
What do Ral-GEF pathways regulate?
-inserted into cells by viruses or produced by mutation of proto-oncogenes
-contribute to loss of cellular growth control and thus are capable of transforming cells
-same function as proto-oncogenes except cannot be regulated i.e. out of control
What are oncogenes?
-normal version of oncogene, controlled and functional
-key cellular regulators of growth and development (growth factor receptors, tyrosine kinases, transcription factors, signaling molecules)
What are proto-oncogenes?
-gene that produces constitutively active protein tyrosine kinase
-inserted into genome by avian leukemia virus that uses reverse transcriptase to insert gene as provirus
-mutation in viral dna replication led to src oncogene included in viral genome, giving rise to RSV (Rous sarcoma virus)
What is the src oncogene and where does it come from?
How are proto-oncogenes converted/activated to oncogenes?
-mutations make Ras insensitive to GAP (unable to hydrolyze bound GTP to GDP) making it constitutively active
-30% of all human cancers bear Ras mutations
How is Ras an oncogene?
-encodes a truncated form of epidermal growth factor (EGF) receptor for receptor tyrosine kinase
-creates unrestrained tyrosine kinase activity = constitutively active tryosine kinase
-comes from erythroblastis virus
What does the erbB oncogene do?
-proto-oncogenes encoding transcription factors c-Fos and cMyc that are normally activated early in cell cycle
-mutations in these lead to unregulated expression and increased proliferation
What are the FOS and MYC genes?
-oncogene that is the result of chromosomal rearrangement forming a Bcr-Abl fusion protein
-this protein is a tyrosine kinase=becomes constitutively active
-occurs in myeloblastic precursor stem cells -> chronic myelogenous leukemia (CML)
What is the Philadelphia chromosome?
drug that is inhibitor of the Abl kinase protein which is produced by the Philadelphia chromosome (result of chromosomal rearrangement of chromosome 9 & 22)
What is Gleevec?
-gene in neural precursor cells of retina
-encodes inhibitor of E2F protein which activates/promotes cell division
What is the Rb gene?
mitogen binds to receptor tyrosine kinase -> activates Ras -> activates MAP kinase cascade -> activates Fos & Myc -> activated G1-Cdk (cell cycle dependent kinases) -> phosphorylates Rb protein inactivating it -> unbinds E2F protein -> activates gene program (cyclins & Cdks) to promote cell division
What is the pathway of the cell cycle clock?
-result of mutation in Rb gene that encodes protein inhibiting cell division
-at cellular level, is inherited recessively (one functional gene is good enough)
-at organisimal level, inherited dominantly (loss of heterozygosity common)
What is Retinoblastoma and how does it originate?
-nondisjunction, chromosome loss, mitotic recombination, gene conversion, deletion, point mutation
How does loss of heterozygosity of retinoblastoma happen?
-transcription factor protein
-activation/expression by cell DNA damage causes arrest in cell growth or induces apoptosis
What is p53?
DNA damage detected by kinases -> phosphorylate p53 -> stabilized from Ub-mediated degradation -> increase in p53 concentration -> binds/activates to p21 gene -> p21 binds Cdk's arresting cell growth
What is the pathway of p53 activation?
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