Chat with AIExam 10: Cancer Genetics and Genomics
Fill in the blanks below with single words.
_____1_____ is an important natural process that is devoted to eliminating diseased or potentially harmful deviant cells. There are two classes of pathways. In one of these neighboring cells deliver signals that are received by ____2____ on the surface of those cells selected to undergo ____1____. Other pathways, such as the mitochondrial ____1____ pathway, respond to certain types of ____ 3____damage (such as that caused by harmful ____4_____ ____5_____ species or exposure to dangerous levels of _____6_____ radiation). In most cases the _____1______ pathway ends by inducing the cell to produce a class of proteolytic enzymes known as _____7_____. ____7_____ are the cell's executioners: they inactivate all kinds of important proteins in the cell, and they release an _____8______ that cleaves DNA into small fragments. Because each of our cells has the potential to commit suicide, the pathways of _____1_____ need to be tightly regulated.
(38) 
Verified1. apoptosis.
2. receptors.
3. oxidative 4. reactive.
5. oxygen.
6. ionizing.
7. caspases.
8. endonuclease.
In the figure below, which of the following are A to E likely to represent?
chronic lymphocyte leukemia; melanoma; medulloblastoma; microsatellite instability (MSI)-positive colorectal cancer; MSI-negative colorectal cancer. 
(37) VerifiedA) medulloblastoma (pediatric tumor)
B) chronic lymphocyte leukemia (liquid tumor)
C) MSI-negative colorectal cancer (adult solid cancer)
D) melanoma (mutagen-induced)
E) MSI-positive colorectal cancer
As a cancer develops the mutation rate accelerates. How does that happen?
(35) VerifiedThe average rate of mutation in human cells is low (about 10-6 per gene per cell) and the majority of cancer-causing mutations are recessive at the cellular level, so that both alleles need to be mutated. Cancer might therefore be expected to be highly improbable: the chance that any cell would receive successive mutations, often in both alleles, at several cancer-susceptibility loci would normally be vanishingly small. Cancer nevertheless is common, and altered expression at a few cancer- susceptibility loci can be sufficient. One major explanation is that early driver mutations greatly increase the probability of later mutations in two ways, as listed below.
1) The first way is by giving the cell a growth advantage. If cells with a driver mutation have an increased growth rate, they will produce more progeny than other cells and will produce an expanded target of mutant cells, thereby increasing the probability of a subsequent mutation (see Figure 10.4A).
2) The second, and most important, way of increasing the probability of later mutations in cancer is by destabilizing the genome. Chromosome instability is a feature of most tumor cells, producing grossly abnormal karyotypes with abnormal numbers of chromosomes and frequent structural arrangements that can activate oncogenes or cause a loss of tumor suppressor genes. In some cancers, a form of global DNA instability occurs-it is caused by mutations in key DNA repair genes and can result in greatly elevated mutation rates. Mutations in genes that regulate epigenetic modifications result in additional epigenetic instability that can result in altered expression at cancer-susceptibility loci. Additionally, some types of epigenetic change cause genome instability.
As cancer cells evolve they acquire distinguishing biological characteristics. Describe five of them and for each give examples of how the biological capability can be acquired.
(32) Tumor recurrence is a major problem in cancer gene therapy. Why should tumors recur so readily?
(23) Which, if any, of the following statements is incorrect or very likely to be incorrect?
a) Epigenetic dysregulation is essentially a universal feature of tumors.
b) Epigenetic dysregulation in cancer cells always arises as a result of mutation at a chromatin modifier locus.
c) There is an overall increase in DNA methylation across the genome of cancer cells but with local DNA hypomethylation at the promoters of a few hundred genes.
d) Epigenetic dysregulation may sometimes initiate tumorigenesis.
(36) Give three examples of mechanisms that explain the evolution of drug resistance in tumors.
(27) Illustrate how some tumor suppressor genes are non-classical in the sense that they preferentially acquire missense mutations.
(39) Not all cancer-susceptibility genes make proteins - some make noncoding RNAs. Give two examples of miRNA genes that act as cancer-susceptibility genes and explain how they are involved in cancer.
(43) There are two fundamental classes of cancer gene in our cells. What are they and what distinguishes them?
(31) What is meant by targeted cancer therapy? Illustrate your answer with reference to treatment for chronic myeloid leukemia.
(37) Not all cancer-susceptibility genes make proteins - some make noncoding RNAs. Give three examples of cancer-susceptibility genes that make long noncoding RNAs and explain how they are involved in cancer.
(28) Loci for previously unknown tumor suppressor genes have been mapped to specific chromosomes and specific chromosome regions by screening for loss of heterozygosity. Explain what is involved.
(29) Cancers develop as a result of natural selection operating at the cellular level. What is meant by this, and if there is strong selection pressure on cells to evolve into cancer cells, why do we not all succumb to cancer?
(30) Defective mismatch repair can occasionally occur in some other types of tumor, but it is particularly common in colorectal cancer. Why should that be?
(38) Tumor suppressor genes have been classified into caretaker, gatekeeper and landscaper categories. What is meant by these categories? Illustrate your answer with examples for the first two categories.
(34) Illustrate how some tumor suppressor genes are non-classical in the sense that they can make a significant contribution to tumorigenesis after losing just one allele.
(30) 
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