Ch 23 Cancer Genetics Flashcards

(40 cards)

1
Q

what is cancer?

A

a heterogenous group of disorders characterized by the presence of cells that do not respond to normal cell division

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2
Q

what is a tumor?

A

a distinct mass of abnormal cells

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3
Q

what is meant when cancer is benign?

A

tumor cells remain localized

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4
Q

what is meant when cancer is malignant?

A

tumor cells invade other tissues

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5
Q

what is meant when cancer is metastatic?

A

tumor cells travel to other sites where they can establish secondary tumors

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6
Q

how can cancer be nongenetic?

A
  • if cancer is inherited, every cell should have cancer, caused by the cancer causing gene
  • tumors appear only in some tissues
  • tumors often appear when a certain age is reached
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7
Q

what does Knudsen’s proposal suggest about cancer?

A

cancer is a multistep process that requires several mutations

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8
Q

explain the clonal evolution of tumors

A

mutations enhance cells’ ability to proliferate and become the most common cells in a clone, allowing the clone to become increasingly rapid in growth and aggressive in proliferation properties

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9
Q

normal cellular gene responsible for normal cell gunction

A

proto-oncogene

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10
Q

gene that stimulates cell division, leading to tumors forming and cancer

A

oncogene

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11
Q

are oncogenes dominant or recessive acting? why?

A

dominant-acting; the amount of gene product produced by one allele is enough to have a stimulatory effect

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12
Q

genes that normally inhibit cell division

A

tumor-suppressor genes

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13
Q

are tumor-suppressor genes dominant or recessive acting? why?

A

both copies of the allele must be mutated to remove inhibition

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14
Q

inactivation of remaining wild-type allele of a heterozygote

A

loss of heterozygosity

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15
Q

appearance of mutant phenotype in individual that is heterozygous for the trait

A

haploinsuffiency

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16
Q

explain how mutations in (proto)oncogenes can contribute to cancer?

A

a mutation in a proto-oncogene results in an oncogene that stimulates cell division without normal controls, leading to cell proliferation

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17
Q

explain how mutations in tumor-suppressor genes can contribute to cancer?

A

a mutation in a tumor-suppressor gene prevents the gene from inhibiting cell division, leading to excessive cell proliferation

18
Q

what are the roles of CDKs? how are they functional?

A

CDKs add phosphate groups to other proteins, either activating or inactivating the protein
they are functional only when they are associated with cyclin

19
Q

what are the roles of cyclin and how do they contribute to the cell cycle?

A

cyclins associate with CDKs, activating them and making them function. cyclins levels oscillate during the cell cycle, allowing the cell to pass through certain stages

20
Q

describe the G1-S transition
(what checkpoint? what proteins are involved? how does the cell transition into the next stage?)

A

retinoblastoma (RB) protein binds to E2F, inactivating it
as cyclins D & E increase in G1, they associate with CDKs and phosphorylate RB, inactivating it, which releases E2F
E2F goes to transcribe products necessary for DNA replication –> S phase

21
Q

what is the role of the retinoblastoma (RB) protein in the G1-S transition?

A

RB prevents the cell from passing the G1/S checkpoint by binding E2F and inactivating it

22
Q

what would happen if there was a mutation in the RB protein?

A

the RB protein won’t be able to bind and inactivate E2F, therefore cell division is always occurring without normal controls

23
Q

describe the G2-M transition

A

inactive MPF (cyclin-B + CDK) is dephosphorylated, and critical levels of active MPF allow cell to enter mitosis and divide

24
Q

what is the mitosis-promoting factor (MPF) composed of?

A

cyclin-B and CDK

25
what occurs when cyclin-B levels increase in G2
increasing cyclin-B concentrations combine with CDKs to form active MPFs, which phosphorylates other proteins that bring about events of mitosis
26
what happens in metaphase, regard cyclin levels?
cyclin-B is rapidly degraded in metaphase, which lowers the amount of active MPF, bringing about events that end mitosis
27
what is p53 and what is it regulate?
p53 is a tumor-suppressor gene; regulate an inhibitor of CDK
28
what would happen if there was a mutation in the p53 gene?
CDK activity would stay constant, causing cell proliferation
29
programmed cell death
apoptosis
30
how does apoptosis relate to cancer?
cancer cells usually have defects in cellular components that stimulate apoptosis, and cells that need to die proliferate
31
how does autophagy relate to cancer?
autophagy allows cancer cells to s
32
explain how the Ras signal transduction pathway is important in the cell cycle
external growth factors bind to receptors that allow adapter molecules to bind, which link to an inactive Ras protein. Ras binds GTP, activating, and activates a series of steps, resulting in the activation of transcription factors that transcribe genes of the cell cycle
33
how do mutations in Ras genes contribute to cancer?
mutations in Ras genes produce mutant Ras proteins that are always active and continuously stimulate cell division
34
how are DNA-repair genes and mechanisms associated with cancer?
defects in DNA-repair genes prevent DNA-repair mechanisms fixing defects in genes that may contribute to cancer
35
explain how mutations in telomerase expression contribute to cancer?
mutations in telomerase lead to telomerase being constantly expressed in somatic cells, which allows for unlimited cell division
36
growth of new blood vessels
angiogenesis
37
how do mutations in genes that promote vascularization contribute to cancer?
tumors need oxygen and nutrients to survive. mutations in genes that promote the growth of new blood vessels allows these tumors to stay and grow
38
why would a reduction in miRNAs contribute to cancer?
miRNAs are responsible for degrading or inhibiting the translation of mRNA reduction in miRNAs may allow oncogenes that are normally suppressed to be highly expressed
39
explain how hypomethylation is associated with cancer
lowered DNA methylation leads to transcription of oncogenes that allow for cancer
40
explain how hypermethylation is associated with cancer
higher DNA methylation leads to tumor-suppressant genes being inhibited