inhibits mutant B-Raf, but truncated variant of mutant B-Raf has evolved resistance to vemurafenib
binds to active site of Bcr-Abl to prevent substrate binding.1st drug targeting a tumor-specific kinase
Binds to EGF receptor; however binds to many other kinases since they are similar in structure.
produces transcription factor Myc, which regulates genes involved in cell growth. can be activated by mutagenesis, retroviral insertion, or translocations of chromosomes.
can integrate next to c-myc gene and elevate transcription. Requires chronic viral infection
Ultimate target of RTK signaling. activates CDK4. Phosphorylates Rb which dissociates from E2F
Oncoprotein that binds Rb and prevents it from binding to E2F, resulting in E2F passing freely through R point.
The Ames Test
Demonstrated carcinogens are mutagens by selective for a rare mutation unable to grow without histidine. Observe for mutation that allows them to grow without histidine.
Indirect acting carcinogen(procarcinogen)
mutate DNA after converted metabolically to ultimate carcinogens
an indirect carcinogen that modifies G to pair with A instead of C. If left unrepaired, converts G to T, causing loss of function in p53
APC target: spindle-assembly checkpoint. inhibit cdc20 preventing activation of separase and anaphase.
APC target: spindle-position checkpoint. prevents cdc14 activation and degradation of mitotic cyclins
tumor surpressor gene that activates checkpoints at various points in cell cycle. At low concentration, targets growth arrest genes. At medium concentration, targets DNA repair genes. At high concentration, targets Apoptosis regulating genes.
ubiquitin ligase that degrades p53, is deactivated by ATM resulting in an increase of p53 protein. also deactivated by pArf14
individual cell programmed suicide. results in bodies consumed by neighboring cells. can be caused by genome damage or other unfixable problems in cell. DNA is cleaved at specific sites
cell murder, caused by absence of nutrients, changes in temperature, external stress. DNA is randomly cleaved
Cytochrome C w/dATP
starts the caspase cascade when it is released from the mitochondria, activates Apaf-1
Part of the apoptosis pathway, targets cellular signals that cause apoptosis, activated by Caspase-9
eliminate DNA binding and destabilize the protein. Only requires one p53 subunit to eliminate function in a p53 tetramer. mostly missense spots.
becoming homozygous for the recessive loss-of-function gene in tumor surpressors. occurs by mis-segregation of alleles in mitosis or mitotic recombination
When cell goes into Go indefinitely, associated with aging. Occurs after about 50 cell cycle generations because of telomere loss
expansion of cancer stem cells that occurs with an oncogenic mutation. each successive expansion occurs when another mutation occurs.
specific physical properties of cancer cells that are caused by various oncogenic genetic mutations.
CDKs (Cyclin Dependent Kinases)
drive the cell cycle, regulated by synthesis and degradation of cyclin subunit, and phosphorylation of catalytic CDK unit
indirectly inhibited by MPF. when MPF is degraded, PP2-B55 dephosphorylates MPF. Always opposite to MPF in concentration
causes a small cell phenotype representing decreased G2 time. the Normal wee1 inhibits Cyclin/CDK(MPF) to delay entry to M.
CAK (cdc-activating Kinase)
phosphorylates MPF, is activated when ribosomes have doubled in number, aka cell has doubled in mass
forms mesh like tetramers and filaments to form nuclear membrane. phosphorylated by MPF to be depolymerized
Mitotic Spindle Checkpoint (MSC)
prevents activation of APC, MAD1/MAD2 inhibit activation of APC until all kinetochores are captured
Poles move further apart by dyneins pulling the astral MTs apart and kinesins pushing the polar MTs apart.
Left over remnants after cytokinesis from the mid region of the two cells. If left in cell, it remains pluripotent (stem cell). If absent from cell, differentiation occurs
requires actin/myosin. Karyomeres fuse to form nucleus, contractile ring forms and contracts to split cells
HEGF receptor not bound to any EGF. endocytosed much slower from cell than the active dimer form.
phosphorylates SRF that binds to SRE which codes transcription for c-fos, jun, c-myc which activate Cyclin D expression