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Genetics- Katie > Lecture 24 chapter 23 > Flashcards

Lecture 24 chapter 23 Flashcards

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Biology 101 flashcards
1
Q

Benign tumor

A

the tumor remains localized

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2
Q

malignant tumor

A

tumor cells invade other tissues

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3
Q

Metastasis

A

the tumor cells induce secondary tumors

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4
Q

Cancer

A

abnormal proliferation of cancer cells produces a tumor that crowds out normal cells

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5
Q

genetic evidence for cancer

A
  • carcinogens
  • chromosomal abnormalities
  • inheritance
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6
Q

clonal evolution of tumors

A

tumor cells acquire more mutations that allow them to become increasingly more aggressive in their proliferate properties

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7
Q

Knudson’s multistep model of cancer

A

requires several mutations

- 2 hit hypothesis

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8
Q

Hallmarks of cancer

A
  • genomic instability
  • metabolic stress
  • evading immune surveillance
  • sustained angiogenesis
  • tissue invasion and metastasis
  • activated growth signalling
    0 evading cell death and senescence
  • limitless replicative potential
  • DNA damage and DNA replication stress
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9
Q

Factors contributing to cancer

A
  • tobacco use
  • obesity
  • alcohol
  • UV radiation
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10
Q

oncogenes

A

mutated, dominant-acting stimulatory genes that cause cancer
- need a single hit to be activated

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11
Q

proto-oncogenes

A

responsible for basic cellular functions in normal cells; when mutated, they become oncogenes

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12
Q

tumor suppressor genes

A

mutated recessive-acting inhibitory genes that are inactive

- need a double hit to be inactivated

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13
Q

loss of heterozygosity

A

a gross chromosomal event that results in loss of the entire gene and the surrounding chromosomal region

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14
Q

p53

A 
regulates cell division 
- many types of cancer 
- nearly 50% have a mutation 
most common mutations in all of cancer
-
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15
Q

control of the cell cycle

A

cyclin-dependent kinases (CDKs), cyclins

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16
Q

G1-to-S transition

A

retinoblastoma protein (RB)

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17
Q

G2-to-M transition

A

mitosis-promoting factor (MPF)

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18
Q

mutations in genes that control the cycle of cell division

A

signal- transduction pathways

  • signals trigger a cascade of intracellular reactions producing a specific response
  • Ras protein
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19
Q

Ras signal-transduction pathway

A

conducts signals from growth factors and hormones to the nucleus and stimulates the cell cycle
- mutations in this pathway often contribute to cancer

20
Q

Lynch syndrome

A

called hereditary nonpolyposis colorectal cancer is an inherited disorder that increases the risk of many types of cancer, particularly colorectal cancer
- mutations in any of these genes prevent the proper repair of DNA replication mistakes

21
Q

epigenetics associated with cancer

A
  • alterations to DNA methylation or chromatin structure are seen in many cancers
  • –hypermethylation or hypomethylation
  • reversible and not a mutation
22
Q

changes in chromosome number and structure are often associated with cancer

A

chromosomal instability is a general feature of cancer cells

  • deletions, inversions, and translocations
    ex. a reciprocal translocation between chromosome 9 and 22 causes chronic myelogenous leukemia
  • aneuploidy
23
Q

Burkitt lymphoma

A

caused by a reciprocal translocation between chromosomes 8 and 14

24
Q

follicular lymphooma

A

tranlocation between chromosome 14 and 18

  • lead to deregulation of BCL2 expression in tumor cells
  • places the BCL2 gene next to the Ig heavy chain locus, making it constrictively active
25
Q

BCL2

A
  • encodes an integral outer mitochondrial membrane protein that blocks the apoptotic death (so cells fail to die) of some cells such as lymphocytes and allows them to propagate exponentially
  • an important anti-apoptotic protein and is this classified as an oncogene
26
Q

retroviruses cause cancer by

A
  • mutating and rearranging proto-oncogenes
  • inserting strong promoters near proto-oncogenes
  • human papilloma virus and cervical cancer
27
Q

microRNAs and cancer

A

microRNAs are ubiquitous small non-coding RNA molecules that function in RNA silencing and post-transcriptional regulation of gene expression

  • implicated in the pathogenesis of diffuse large B-cell lymphoma and their target genes
  • bind to the 3’ noncoding end…cell know not supposed to have dsRNA so chop it up
28
Q

Antibody therapy for cancer

A
  • monoclonal Abs target cancer cell-specific Ags and induce an immunological response against the target cancer cell
  • a toxin, radioisotope, cytokine or other active conjugate can be coupled to the Ab as well
29
Q

direct tumour cell killing

A

can be elicited by receptor agonist activity, such a Ab binding to a tumour cell surface receptor and activiating it leading to apoptosis
- can be mediated by receptor antagonist activity; such as ab binding to a cell surface receptor and blocking dimerization, kinase activation and downstream signaling , leading to reduced proliferation and apoptosis

30
Q

immune-mediated tumour cell killing

A

can be carried out by the induction of phagocytosis; complement activation; Ab-dependent cellular cytotoxicity
= genetically modified T cells being targeted to the tumour by single-chain variable fragment
- T cells being activated by ab0mediated cross-presentation of ag to Dcs and inhibition of T cell inhibitory receptors such as CTL associated ag 4 or CTLA-4

31
Q

Rituximab

A

chimeric monoclonal Ab against the protein CD20, which is primarily found on the surface of B cells

  • destroys B cells and used to treat disease which are characterized by excessive numbers of B cells, overactive B cells, or dysfunctional b cells
  • includes many lymphomas, leukemias, transplant rejection, and autoimmine disorders
32
Q

The cancer Genome Atlas

A

laying the foundation for personalized cancer care

  • will ID the genomic changes in more than 20 different types of human cancer
  • help us understand what turns a normal cell into a cancer cell by comparing DNA from normal and cancer tissue
  • are certain areas of the genome commonly affected in several types of cancers
    • often affect genes that control pathways in cells that cause cells to divide and survive when they normally would die
  • specific changes- also called signatures- allow us to tell one type of cancer from another
  • -signatures help doctors IF specific types of cancer, which many respond differently to various treatments or have a different prognosis
33
Q

How does the multistep model of cancer explain the observation that sporadic case of retinoblastoma usually appear in only one eye, whereas inherited forms of the cancer appear in both eyes?

A

retinoblastoma results from at least two separate genetic defects, both of which are necessary for cancer to develop. in sporadic cases, 2 successive mutations must occur in a single cell, which is unlikely and therefore typically affects only one eye. in people who have inherited one of the two required mutations, every cell contains this mutation, and so a single additional mutation is all that is required for the cancer to develop. given the millions of cells in each eye, there is a high probability that the second mutation will occur in at least one cell of each eye, producing tumors in both eyes, and inheritance of this type of retinoblastoma

34
Q

Why are oncogenes usually dominant in their action, whereas tumor-suppressor genes are recessive?

A

oncogenes have a stimulatory effect on cell proliferation. mutations in oncogenes are usually dominant because a mutation in a single copy of the gene is usually sufficient to produce a stimulatory effect.
- tumor suppressor genes inhibit cell proliferation. mutations in tumor suppressor genes are generally recessive because both copies must be mutated to remove all inhibition

35
Q

What would be the most likely effect of a mutation that causes cyclin B to be unable to bind to CDK?

a. cells pass through the G2/M checkpoint and enter mitosis even when DNA has not been replicated
b. cells never pass through the G1/S checkpoint
c. cells pass through mitosis more quickly than unmutated cells
d. cells fail to pass the G2/M checkpoint and do not enter into mitosis

A

d. cells fail to pass the G2/M checkpoint and do not enter into mitosis

36
Q

Ras proteins are activated when they

a. bind GTP
b. release GTP
c. bind GDP
c. undergo acetylation

A

a. bind GTP

37
Q

Which type of mutation in telomerase is associated with cancer cells?

a. mutations that produce an inactive form of telomerase
b. mutations that decrease the expression of telomerase
c. mutations that increase the expression of telomerase
d. all of the above

A

c. mutations that increase the expression of telomerase

38
Q

hypermethylation is thought to contribute to cancer by

a. inhibiting DNA replication
b. inhibiting the expression of tumor-suppressor genes
c. stimulating the translation of oncogenes
d. stimulating telomerase

A

b. inhibiting the expression of tumor-suppressor genes

39
Q

Chronic myelogenous leukemia is usually associated with which type of chromosome rearrangement?

a. duplication
b. deletion
c. inversion
d. translocation

A

d. translocation

specifically between chromosome 9 and 22
- philadelphia chromosome

40
Q

Where was pancreatic cancer locus mapped to?

A

Chromosome 4

41
Q

What as the most highly expressed gene in tumors compared to normal tissue?

A

Palladin

a single amino acid change that segregated with the cancer
- all family members had a Serine instead of a Proline

42
Q

What % of pancreatic cancer is fatal?

A

85%

43
Q

What hallmark of Cancer is the origin in hereditary cancers?

A

the establishment of genome instability

–> leads to the establishment of all the other hallmarks

44
Q

What hallmark of Cancer is the origin in sporadic cancers?

A
  • Deregulation of growth-regulating genes may be the initiating event

–> leads to DNA damage and DNA replication stress, which, in turn, lead to genomic instability and selective pressure for tumor suppressor p53 inactivation

45
Q

What are the 3 mechanisms that Rituxan induces B-cell destruction?

A

1) ADCC: attracts NK cells, T cells and macrophages which are involved in recognizing and killing Ab-labeled target cells leading to lysis
2) CDC: binding of the Ab recruits complement proteins, which punch holes in the cell membrane, flooding the cell and leading to cell lysis
3) apoptosis: binding of the antibody signals the cell to self-destruct

Genetics- Katie (15 decks)

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