Chapter 19 Practice Problems Flashcards
signals a cell to leave G0 and enter G1
mitogenic growth factor
mutations in these genes are recessive at the cellular level for cancer formation
tumor-suppressor genes
cell cycle enzymes that phosphorylate proteins
cyclin dependent protein kinases
programmed cell death
apoptosis
mutation in these genes are dominant for cancer formation
oncogenes
protein that binds a hormone
growth factor receptor
series of steps by which a message is transmitted
signal transduction
control progress in the cell cycle in response to DNA damage
checkpoints
proteins that are active cyclically during the cell cycle
cyclins
some germ line mutations predispose individuals to cancer, yet often environmental factors (chemicals, exposure to radiation) are considered major risks for developing cancer. Do these views of the cause of cancer conflict, or can they be reconciled?
some of the environmental agents that are implicated in increased cancer risk cause increased level of mutations, so this fact is consistent with the idea that mutations in genes are necessary to cause cancer. The inherited mutations that lead to predisposition to cancer inactivate one allele of a gene (often a tumor-suppressor gene) that inhibits cell growth.
a carcinogenic compound is placed on the skin of inbred laboratory mice. In many of these mice, skin tumors develop at the site of exposure, but only months after the chemical is no longer detectable. Why don’t all the mice develop tumors, and why don’t the tumors appear much sooner?
The development of tumors depends upon random mutational events that must “hit” several oncogenes and tumor-suppressor genes within a cell lineage. and it takes time for these mutations to accumulate through random, rare events
which one of the following events is unlikely to be associated with cancer?
a. a mutation of a cellular proto-oncogene in a normal diploid cell
b. a chromosomal translocation with a breakpoint near a cellular proto-oncogene
c. deletion of a cellular proton-oncogene
d. mitotic nondisjunction in a cell carrying a deletion of a tumor suppressor gene
e. incorporation of a cellular oncogene into a retrovirus chromoosome
c will not be associated with cancer
why don’t all loss of function mutations that are recessive at the cellular level behave as dominants at the organism level? is this property restricted to tumor-suppressor gene mutations?
In cells that undergo many divisions during the human lifespan, a few cells heterozygous for any mutation are likely to become homozygous. In many cases, the homozygous mutant cell will die; in other cases, no obvious mutant phenotype will result In essence, homozygosity for most loss-of-function mutations will not result in a phenotype visible in the whole organism, while homozygosity for loss-of-function of tumor suppressor genes leads to a large clone of cells with a cancerous phenotype that can be seen in the whole organism.
Chromothripisis is a rare phenomenon, first discovered in cancer cells where a single chromosome “shatters” into many fragments and is reassembled in a rearranged form by the DNA repair machinery. (the underlying mechanism for causing the shattering is not under stood.) Approximately 2% of cancers contain cells with a shattered chromosome. Explain how chromothripsis could contribute to cancer
Chromosomal rearrangements due to chromothripsis could generate oncogenes by bringing regulatory regions and coding regions of different genes together, or by fusing genes within their coding regions so that they generate fusion proteins. Loss-of-function mutations in tumor suppressors could also be generated at rearrangement breakpoints or by deletions. In essence, chromothripsis creates a situation that leads to a high frequency of mutagenic events along the “shattered” chromosome, and we have seen that mutations are intimately associated with cancer.
a female patient 19 years old, whose symptoms are anemia and internal bleeding due to a massive build up of leukemic white blood cells, is diagnosed with chronic myelogenous leukemia (CML). Karyotype analysis shows that the leukemic cells of this patient are heterozygous for a reciprocal translocation involving chromosomes 9 and 22. However, none of the normal, nonleukemic cells of this patient contain the translocation. Which of the following statements is true and which is false?
a. the translocation results in the inactivation (loss of function) of tumor suppressor gene
b. the translocation results in the inactivation of an oncogene
c. there is a 50% chance that any child of this patient will have CML
d. this patient is a somatic mosaic in terms of the karyotype
e. DNA extracted from leukemic cells of this patient, if taken up by normal mouse tissue culture cells, could potentially transform the mouse cells into cells capable of causing tumors
f. the normal function of the affected tumor suppressor gene or proto-oncogene at the translocation breakpoint could potentially block the function for the cyclin proteins that drive the cell cycle forward
g. two rare events must have occurred to disrupt both copies of the tumor suppressor gene or proto-oncogene at the translocation breakpoint in the leukemic cells
h. a possible treatment of the leukemia would involve a drug that would turn on the expression of the tumor suppressor gene or oncogene at the translocation breakpoint in the leukemic cells
a. false
b. false
c. false
d. true
e. true
f. false
g. false
h. false
