Lecture 24 Flashcards Preview

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Flashcards in Lecture 24 Deck (43):
1

Which gene encodes for an essential component of a cells cytoskeleton? A single nucleotide mutation at a highly conserved proline position in this gene in pancreatic tumors.

Paladin

2

When a tumor remains localized it is called:

A. Malignant tumor
B. Benign tumor
C. Metastasis
D. None of the above

B. Benign tumor

3

When tumor cells induce secondary tumors it is called:

A. Malignant tumor
B. Benign tumor
C. Metastasis
D. None of the above

C. Metastasis

4

When tumor cells invade other tissues it is called:

A. Malignant tumor
B. Benign tumor
C. Metastasis
D. None of the above

A. Malignant tumor

5

T/F: Cancer can come from a single mutation.

False, multiple mutations required to produce cancerous cells. (Multi step model of cancer)

6

Which theory explains that tumor cells acquire more mutations that allow them to become increasingly more aggressive in their proliferation properties?

A. Multi step model of cancer
B. Clonal selection of tumors
C. Clonal evolution of tumors
D. A and C

C. Clonal evolution of tumors

7

Which of the following are genetic evidence for cancer?

A. Inheritance
B. Chromosomal abnormalities
C. Carcinogens
D. All of the above

D. All of the above

8

Which of the following is likely the initiating event/primary hallmark of hereditary cancer?

A. Genomic instability
B. Oxidative stress
C. Proteotoxic stress
D. All of the above

A. Genomic instability

Oxidative stress and Proteotoxic stress are secondary hallmarks

9

Which of the following is likely the initiating event/primary hallmark of sporadic cancer?

A. Tumor surpressor inactivation
B. Deregulation of growth regulating genes
C. DNA damage
D. B and C

B. Deregulation of growth regulating genes

Tumor surpressor inactivation and DNA damage are secondary hallmarks

10

Sequence of events in Sporadic cancer

A. Deregul. growth-regulating genes; DNA damage/replication stress; Genomic instability/selective pressure for tumor suppressor p53 inactivation
B. Genomic instability/selective pressure for tumor suppressor p53 inactivation; Deregul. growth-regulating genes; DNA damage/replication stress
C. Deregul. growth-regulating genes; DNA damage/replication stress; selective pressure for tumor suppressor p53 inactivation

A.

11

T/F: Certain cancers often found in specific parts of the world.

True

12

Which type of cancer is caused by environmental factors more so than any other cancer?

A. Pancreatic
B. Testicular
C. Lung
D. Brain
E. B and C

C. Lung

13

What is being explored as possible treatments for cancer with not much success?

Molecular biology (gene targeting)

14

T/F: All cancers are heterogenous and do not have shared lesions within pathways.

False, Although cancers are heterogenous, there are many shared lesions within pathways.

15

State terms for the following definitions

1. Mutated recessive-acting inhibitory genes that are inactive
2. Mutant, dominant-acting stimulators genes that cause cancer
3. Responsible for basic cellular functions in normal cells; when mutated, they become oncogenes
4. Gross chromosomal event that results in loss of the entire gene and the surrounding chromosomal region

1. Tumors suppressor genes
2. Oncogenes
3. Proto-oncogenes
4. Loss of heterozygosity

16

Which of the following is true of the differences in the ways tumor suppressor genes and oncogenes contribute to cancer?

A. Oncogenes need single dominant allele to be inactivated; TSGs need two recessive alleles to be activated
B. Oncogenes need single dominant allele to be activated; TSGs need two recessive alleles to be inactivated
C. Oncogenes need two dominant alleles to be activated; TSGs needs one recessive allele to be inactivated
D. Oncogenes need a double hit to be activated; TSGs need a single hit to be inactivated

B. Oncogenes need single dominant allele to be activated; TSGs need two recessive alleles to be inactivated

17

T/F: Mutation in an important cellular process is likely to cause cancer.

True

18

Why are people that are heterozygous for a tumor suppressor gene predisposed to cancer?

Loss of heterozygosity:

- Loss of wild type allele
- Uncovers mutant allele
- Mutant/inactive allele expressed ---> Loss of Tumor suppressor activity

19

What is the gene that regulates cell division and is responsible for many types of cancer?

A. APC
B. BRCA1
C. NF1
D. p53
E. A and D

D. p53

20

Mutations in cell cycle genes can cause cancer. Match the molecules with their functions:

1. Control of cell cycle
2. G2 To M transition
3. G1 to S transition

A. Cdks, cyclins
B. Retinoblastoma protein
C. Mitosis-promoting factor, cyclin B

1. A. Cdks, cyclins
2. C. MPF, cyclin B
3. B. RBP

21

What is used to edit genes and create designer immune cells programmed to hunt out and kill drug resistant leukemia?

CRISPR

21

Which is true of Ras signal-transduction pathway?

A. Conducts signals from growth factors and hormones to nucleus
B. Stimulates cell cycle
C. Mutations contribute to cancer
D. Activate cAMP
E. All of the above
F. A, B, and C
G. B, C, and D

F. A, B, and C

22

Lynch syndrome (HNPCC) is an inherited disorder rear increases the risk of many types of cancer, especially colorectal cancer. Mutations in which type of genes cause this disorder?

A. DNA repair
B. Telomeres
C. tRNA
D. More than one of the above

A. DNA repair

23

Why is early detection key in treating colorectal cancer?

- Colorectal cancer develops by sequential mutations following the tumor progression model
- Polyp > benign tumor > oncogene rac activation > benign tumor growth > loss of p53 >malignant tumor develops > loss of anti-metastasis gene > cancer metastizes
- Gets worse and worse

24

Which type of mutations in telomerase could be associated with cancer cells?

A. Mutations that produce inactive from of telomerase
B. Mutations that decrease expression of telomerase
C. Mutations that increase expression of telomerase
D. All of the above

C. Mutations that increase expression of telomerase

Telomerase builds telomeres which protects chromosomes in order to continue replication for cell proliferation

High telomerase - telomeres stick around cannot degrade DNA for apoptosis

25

T/F: Alterations to DNA methylation or chromatin structure are irreversible.

False, Alterations to DNA methylation or chromatin structure are reversible. There are NOT mutations in DNA seq they are epigenetic changes.

26

Which of the following is/are seen in many cancers?

A. Hypermethylation
B. Hypo methylation
C. Chromatin remodeling
D. A and B
E. All of the above

E. All of the above

27

T/F: Chromosomal instability is a general feature of cancer cells

True

28

What is caused by a reciprocal translocation between chromosomes 8 and 14?

Burkett lymphoma

29

Which of the following contribute to chromosomal instability seen in cancer cells?

A. Deletions
B. Inversions
C. Translocations
D. Aneuploidy
E. All of the above

E. All of the above

30

Which of the following is true of follicular lymphoma?

A. Chromosomal translocation deregulates Bcl2 expression causing low levels of Bcl2 and thus increases apoptosis
B. Chromosomal translocation deregulates Bcl2 expression causing high levels of Bcl2 and thus failure of apoptosis
C. Single nucleotides change deregulates Bcl2 expression causing low levels of Bcl2 and thus failure of apoptosis
D. Chromosomal translocation upregulates Bcl2 expression causing high levels of Bcl2 and thus increased apoptosis

B. Chromosomal translocation deregulates Bcl2 expression causing high levels of Bcl2 and thus failure of apoptosis


Bcl2 = anti-apoptotic protein ---> without it...cells proliferate when they should die

31

Why is Bcl-2 considered an oncogene?

Bc it is anti-apoptotic

32

What can cause cancer by mutating and rearranging proto-oncogenes or by inserting strong promotors near Proto-oncogenes or inactivating tumor suppressors?

Retroviruses

33

What is a novel approach that is currently being used to develop treatment for melanoma?

Immune systems ability to promote or halt cancer progression

Checkpoint ab treatments
Other immune treatments

34

Why are miRNAs implicated in pathogens is of some cancers?

miRNAs are non-coding RNAs involved in post-translational regulation of gene expression

Epigenetics/genetics/transcriptional mechanisms can decreases miRNA levels and thus mRNA is not regulated and cells divide and prolif uncontrollably

35

What is most frequently mutated gene in human cancer?

p53 - tumor suppressor

36

p53 function includes:

A. Apoptosis
B. Inhibition of angiogenesis
C. Genomic stability
D. Tumor suppression
E. A, C, and D
F. All of the above

F. All of the above

37

How do monoclonal Abs fight cancer?

Target cancer cell specific Ags and induce immunological response against target cell

38

Which of the following is a type of Ab therapy for cancer?

A. Direct tumor cell killing
B. Immune-mediated tumor cell killing
C. Vascular and Stromal cell ablation
D. A and B
E. All of the above

E. All of the above

39

_________ is a monoclonal Ab against _______ and is used to destroy _________ to treat lymphomas, leukemias, transplant rejection, and autoimmune disorders.

1. Rituxan
2. CD-20
3. B cells

40

Which of the following ways can Rituxan mediated the killing of B cells?

A. Abs label target cells and attract NK cells, macrophages, and T cells to kill B cells
B. Binding of Ab recruits complement proteins leading to cell lysis
C. Ab binding signals apoptosis
D. All of the above
E. none of the above

D. All of the above

41

Which research program aims to identify genomic changes in 20 different types of cancer to help us understand how a normal cell turns into a cancer cell? It has already helped determine that there are signatures that allow us to distinguish between types of cancer and that there are certain areas of the genome commonly affected in several types of cancer.

Cancer genome atlas (TCGA)

42

Why is there a project studying golden retrievers for cancer?

- Golden retrievers - popular, highly inbred
- Less genetic variation - vulnerability to cancer
- Help dogs and can learn things to help humans