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Self-sufficiency in growth signals
Produces more growth factors or more receptors to stimulate own division.
Insensitivity to anti-growth signals
Loses the ability to respond to growth inhibitors that stop division.
Evading apoptosis
Loses the ability to undergo programmed cell death.
Limitless replicative potential
Ability to restore chromosomal ends (telomeres) after cell division.
Sustained angiogenesis
Ability to induce the formation of new blood vessels for nutrient supply.
Tissue invasion and metastasis
Spreads from the primary site to other parts of the body.
G0 Phase
DNA Content: n
G1 Phase
DNA Content: n
S Phase
Between n and 2n
G2 Phase
2n
M Phase
2n (before cytokinesis)
Cells in this phase remain non-dividing for long periods of time, possibly indefinitely.
G0 Phase
Cells in this phase synthesize proteins, produce organelles, and grow in size. There is no synthesis of DNA.
G1 Phase
Cells in this phase synthesize DNA.
S Phase
During this phase, the nucleus divides to form two nuclei (karyokinesis). The division of cell (cytokinesis) usually occurs after karyokinesis.
M Phase
A phase in between S phase and M phase, which ensures that the cell is ready for nuclear division.
G2 Phase
Which mutations lead to cancer?
Mutations in genes that control the cell cycle and Mutations in genes that repairs DNA
AGY75 transformed with pMSH2, then plated on SD/-His, -Trp, -Leu, -Thr, +FOA media
No growth
AGY75 transformed with pMSH2' (assume that the mutant MSH2 is nonfunctional), then plated on SD/-His, -Trp, -Leu, -Thr, +FOA media
Growth
AGY75 transformed with pRS413, then plated on SD/-His, -Trp, -Leu, -Thr, +FOA media
Growth
AGY75 transformed with pMSH2, then plated on SD/-His, -Trp, -Leu, -Thr, -Ura, +FOA media
No growth
AGY75 transformed with pMSH2' (assume that the mutant MSH2 is nonfunctional), then plated on SD/-His, -Trp, -Leu, -Thr, -Ura, +FOA media
No growth
AGY75 transformed with pRS413, then plated on SD/-His, -Trp, -Leu, -Thr, -Ura, +FOA media
No growth
AGY75 plated on SD/-His media
No growth
AGY75 plated on SD/-Ura media
No growth
AGY75 plated on SD/-Trp media
Growth
AGY75 transformed with pMSH2, then plated on SD/-His media
Growth
AGY75 transformed with pMSH2, then plated on SD/-Ura media
Growth
AGY75 transformed with pMSH2, then plated on SD/-Trp media
Growth
What is NOT a Cancer treatment?
Inhibiting MMR (Inhibiting repair actually causes more mutations/cancer)