Ch 23 Cancer Genetics Flashcards
(40 cards)
what is cancer?
a heterogenous group of disorders characterized by the presence of cells that do not respond to normal cell division
what is a tumor?
a distinct mass of abnormal cells
what is meant when cancer is benign?
tumor cells remain localized
what is meant when cancer is malignant?
tumor cells invade other tissues
what is meant when cancer is metastatic?
tumor cells travel to other sites where they can establish secondary tumors
how can cancer be nongenetic?
- 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
what does Knudsen’s proposal suggest about cancer?
cancer is a multistep process that requires several mutations
explain the clonal evolution of tumors
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
normal cellular gene responsible for normal cell gunction
proto-oncogene
gene that stimulates cell division, leading to tumors forming and cancer
oncogene
are oncogenes dominant or recessive acting? why?
dominant-acting; the amount of gene product produced by one allele is enough to have a stimulatory effect
genes that normally inhibit cell division
tumor-suppressor genes
are tumor-suppressor genes dominant or recessive acting? why?
both copies of the allele must be mutated to remove inhibition
inactivation of remaining wild-type allele of a heterozygote
loss of heterozygosity
appearance of mutant phenotype in individual that is heterozygous for the trait
haploinsuffiency
explain how mutations in (proto)oncogenes can contribute to cancer?
a mutation in a proto-oncogene results in an oncogene that stimulates cell division without normal controls, leading to cell proliferation
explain how mutations in tumor-suppressor genes can contribute to cancer?
a mutation in a tumor-suppressor gene prevents the gene from inhibiting cell division, leading to excessive cell proliferation
what are the roles of CDKs? how are they functional?
CDKs add phosphate groups to other proteins, either activating or inactivating the protein
they are functional only when they are associated with cyclin
what are the roles of cyclin and how do they contribute to the cell cycle?
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
describe the G1-S transition
(what checkpoint? what proteins are involved? how does the cell transition into the next stage?)
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
what is the role of the retinoblastoma (RB) protein in the G1-S transition?
RB prevents the cell from passing the G1/S checkpoint by binding E2F and inactivating it
what would happen if there was a mutation in the RB protein?
the RB protein won’t be able to bind and inactivate E2F, therefore cell division is always occurring without normal controls
describe the G2-M transition
inactive MPF (cyclin-B + CDK) is dephosphorylated, and critical levels of active MPF allow cell to enter mitosis and divide
what is the mitosis-promoting factor (MPF) composed of?
cyclin-B and CDK