Cell Bio Cancer

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HER2

undergoes V to Q substitution to generate Neu oncogene

EGF receptor

gene deletion to generate ErbB oncogene

Herceptin

blocks EGF binding to HER2, increases HER2 endocytosis

SOS

GEF for Ras, exchanges GDP for GTP to activate

NF1

GAP for Ras, increases GTPase activity of Ras to deactivate

RasD

activates Raf, can be mutated to be constitutively active oncogene by altering G12 or Q61 to X

B-Raf

activated by Ras through dimerization, mutated oncogene works as monomer

vemurafenib

inhibits mutant B-Raf, but truncated variant of mutant B-Raf has evolved resistance to vemurafenib

Bcr-Abl

fusion oncokinase created by translocation of Abl gene from 9 to 22 chromosome, causes CML

Imatinib(Gleevec)

binds to active site of Bcr-Abl to prevent substrate binding.1st drug targeting a tumor-specific kinase

Tarceva

Binds to EGF receptor; however binds to many other kinases since they are similar in structure.

MYC

produces transcription factor Myc, which regulates genes involved in cell growth. can be activated by mutagenesis, retroviral insertion, or translocations of chromosomes.

Retrovirus

can integrate next to c-myc gene and elevate transcription. Requires chronic viral infection

Cyclin D

Ultimate target of RTK signaling. activates CDK4. Phosphorylates Rb which dissociates from E2F

p16

binds to CycD/CDK4 complex to inhibit it. can be swamped by excess CycD

Rb

Tumor surpressor gene that inhibits E2F, dissociates when phosphorylated

E2F

activator of transcription of proteins needed for DNA synthesis.

HPV E7

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.

Direct acting carcinogen

mutates DNA without metabolic activation by liver enzymes

Indirect acting carcinogen(procarcinogen)

mutate DNA after converted metabolically to ultimate carcinogens

Benzeo(a)pyrene

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

PhIP

indirect carcinogen in hotdogs, oxidation by P-450 in liver turns it into a mutagen.

Aflatoxin B

indirect carcinogen on mold in peanuts.

ATR

intra-S phase checkpoint. inhibits cdc25C preventing cyclin-CDK to begin mitosis

Mad2

APC target: spindle-assembly checkpoint. inhibit cdc20 preventing activation of separase and anaphase.

Tem-1

APC target: spindle-position checkpoint. prevents cdc14 activation and degradation of mitotic cyclins

ATM, ATR

DNA-damage checkpoint. inhibits cdc25A preventing entry to S phase.

p53

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.

ATM

Kinase that stabilizes p53 and inactivates Mdm2 through phosphorylation

Chk2

phosphorylated by ATM, phosphorylates Cdc25A to deactivate it

Mdm2

ubiquitin ligase that degrades p53, is deactivated by ATM resulting in an increase of p53 protein. also deactivated by pArf14

Apoptosis

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

Necrosis

cell murder, caused by absence of nutrients, changes in temperature, external stress. DNA is randomly cleaved

DFF40

cleaves DNA into 200 bp fragments which are degraded

Apaf-1

Part of the apoptosis pathway, activated by Cytochrome C and p53. Activates Caspase-9

Caspase-9

Part of the apoptosis pathway, activated by Apaf-1 and p53. Activates Caspase 3,7

Cytochrome C w/dATP

starts the caspase cascade when it is released from the mitochondria, activates Apaf-1

Caspase-3,7

Part of the apoptosis pathway, targets cellular signals that cause apoptosis, activated by Caspase-9

Bcl-2

inhibits the release of Cytochrome C and dATP conversion. Is inhibited by p53.

IAPs

inhibits activation of Caspase 3,7 and of its targets

p53 mutations

eliminate DNA binding and destabilize the protein. Only requires one p53 subunit to eliminate function in a p53 tetramer. mostly missense spots.

HPV E6

viral protein that targets p53, acting as a ubiquitin ligase

Loss-of-heterozygosity

becoming homozygous for the recessive loss-of-function gene in tumor surpressors. occurs by mis-segregation of alleles in mitosis or mitotic recombination

Senescence

When cell goes into Go indefinitely, associated with aging. Occurs after about 50 cell cycle generations because of telomere loss

Clonal expansion

expansion of cancer stem cells that occurs with an oncogenic mutation. each successive expansion occurs when another mutation occurs.

Hallmarks (phenotypes)

specific physical properties of cancer cells that are caused by various oncogenic genetic mutations.

progesterone

stimulates oocytes arrested in G2 to begin meiosis. example of an MPF

CDKs (Cyclin Dependent Kinases)

drive the cell cycle, regulated by synthesis and degradation of cyclin subunit, and phosphorylation of catalytic CDK unit

cdc mutant

arrests cell at a certain point in cell cycle when mutated, generates string like cells

MPF(maturation/mitosis promoting factor)

Drives oocytes from G2 arrest to M, aka cyclin/CDK complex

Cyclin D/E

G1/S cyclins that work with CDK to drive the cell cycle

Cyclin A/B

G2/M cyclins that complex with CDK to drive the cell cycle to M (A is also an S cyclin)

APC(Anaphase promoting complex)

ubiquitinates cyclins, is phosphorylated/activated by cyclin/CDK

PP2-B55

indirectly inhibited by MPF. when MPF is degraded, PP2-B55 dephosphorylates MPF. Always opposite to MPF in concentration

wee mutant

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

Lamin B

forms mesh like tetramers and filaments to form nuclear membrane. phosphorylated by MPF to be depolymerized

Condensins

phosphorylated by MPF and packs chromatin into chromosomes

Histone H1

phosphorylated by MPF and packs nucleosomes

Pericentrin Gene

loss of function mutations in this gene cause Dwarfism

XMAP215

+ end stabilizing protein that is inactivated by MPF phosphorylation

Centromere

non-coding DNA sequence with a structural function, not informational

Securin

inhibits separase, degraded by APC in order to allow sister chromatid to separate

Separase

cleaves Kleisin to release cohesins that hold the sister chromatids together

Mitotic Spindle Checkpoint (MSC)

prevents activation of APC, MAD1/MAD2 inhibit activation of APC until all kinetochores are captured

Aurora B Kinase

activates the spindle checkpoint, opposite to protein phosphatase 1

Phosphatase 1

turns off spindle checkpoint

Anaphase A

Kinetochore MTs depolymerize at both ends separating the chromosomes

Anaphase B

Poles move further apart by dyneins pulling the astral MTs apart and kinesins pushing the polar MTs apart.

Taxol

inhibits depolymerization of MTs, therefore inhibiting Anaphase A

Colchicine

inhibits polar MT polymerization, therefore inhibiting Anaphase B

Midbody Remnants

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

Cytokinesis

requires actin/myosin. Karyomeres fuse to form nucleus, contractile ring forms and contracts to split cells

Free HER1

HEGF receptor not bound to any EGF. endocytosed much slower from cell than the active dimer form.

GRB2

protein binds to active phosphorylated HER1, SH3 subunit then binds SOS that activates Ras

14-3-3

inhibitor of Raf, binds and inactivates it when Raf is phosphorylated by MAPK

MEK

dual specificity kinase activated by Raf, activates MAPK

MAPK

T,Y kinase activated MEK after phosphorylation. Activates p90rsk and TCF

p90rsk

phosphorylates SRF that binds to SRE which codes transcription for c-fos, jun, c-myc which activate Cyclin D expression

TCF

activated by MAPK and also binds to SRE which codes transcription for c-fos, jun, c-myc which activate Cyclin D expression

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