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BIOL 360 > Topic 9 - Cancer > Flashcards

Topic 9 - Cancer Flashcards

1
Q

can we have individualized cancer therapy?

A

yes. CAR T-cell therapy –> take blood from patient to get T cells, make CAR T cells in lab that can recognize and kill cancer cells, inject back into patient

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2
Q

how come CAR T cells work for some but not others?

A

specific members of the gut microbiome can influence efficacy

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3
Q

what is most common cancer in females?

A

breast cancer

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4
Q

does age play a role in likelihood of cancer diagnosis

A

yes. risk increases with age

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5
Q

are men or women more likely to develop cancer

A

in younger populations and really old populations women are, but other than that men are more likely

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6
Q

what are the most common cancer types among age groups?

A

leukemia, thyroid, breast, lung and bronchus, colorectal

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7
Q

why are new cancer cases increasing each year?

A

because of the growing and aging population

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8
Q

what does TNM stand for?

A

tumor, node, metastasis

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9
Q

how is T ranked as part of TNM

A

size from 1-4 (1 smallest)

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10
Q

how is N ranked in TNM

A

extension to lymph nodes 0-3

0 is less

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11
Q

how is M ranked in TNM?

A

has cancer spread (metastasized) to other parts of the body?

0 (no) or 1 (yes)

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12
Q

what are the stages of cancer 0-4?

A 
0 = abnormal cells that may develop into cancer
1 = cancer relatively small and contained in origin organ
2 = larger but still in same organ
3 = large and may have spread into surrounding tissues and lymph nodes in area
4 = spread through blood or lymphatic system to distant site
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13
Q

why are cervical cancers mostly detected at stage 1 while lung cancers are mostly detected at stage 4?

A

because cervical cancer is screened for every 5 years

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14
Q

what are reasons why stomach, larynx, cervix, and lung cancers may have decreased?

A

decrease in smoking and increase in vaccinations

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15
Q

what are reasons why stomach, larynx, cervix, and lung cancers may have decreased?

A

decrease in smoking and increase in vaccinationswh

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16
Q

how come liver and melanoma have increased?

A

environmental factors - sun/ ozone

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17
Q

what is Koch’s postule and how does it relate to heliobacter pylori experiment

A

how to prove bacterium is causing disease!

someone who won nobel prize proved heliobacter pylori caused stomach cancer through these principles –> had to drink it himself since it didn’t work in mice.

now many stomach cancers can be treated with antibiotics!

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18
Q

T or F. Bacteria and viruses can cause cancer?

A

TRUE

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19
Q

what are carcinomas?

A

arise from epithelia
most common in humans
example: skin
carcinogenesis is linked to mutagenesis

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20
Q

what are sarcomas?

A

arise from connective tissue or muscle cells

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21
Q

what are leukemia and lymphoma?

A

derived from blood cells and cancer of the lymphocytes

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22
Q

chemical carcinogens and radiation can lead to what problems in cancer?

A

can lead to local changes in nucleotide sequences that can lead to problems

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23
Q

what causes tumor growth?

A

imbalance of proliferation and apoptosis

change in ability to differentiate can lead to accumulation of proliferating cells as well

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24
Q

what makes cancer cells so dangerous

A

they reproduce without normal restraints on growth and division
invade and colonize other tissues

25
Q

difference between a benign and malignant tumor

A

benign is non cancerous

malignant is cancerous –> eventually forms metastasis and cannot be removed via surgery

26
Q

how does metastasis form

A

cells grow as benign tumor in epithelium and eventually work their way into capillaries

can adhere to blood vessel walls and/ or escape blood vessels to form metastasis elsewhere in the body

27
Q

barriers to metastasis and whether or not they are easy to overcome

A

escape from parent tissue (difficult)
travel through circulation (easy)
colonization of remote site (difficult)

28
Q

why is it difficult for metastasis to colonize remote site?

A

not used to the new environment

29
Q

how is cell hierarchy important in regards to cancer?

A

in normal cells: stem cells divide and some differentiate into specialized cells

in cancer tissue: some stem cells have indefinite self renewal and others are limited –> not all cancer cells are capable of maintaining metastasis

30
Q

is one single mutation enough to cause a tumor?

A

no. need to accumulate more than one

31
Q

do tumors only have one variety of cell types?

A

No, they have multiple. Both regular and cancerous types – fibroblasts, pericytes, etc.

32
Q

why does cancer occur so “infrequently” if genes are somewhat likely to develop a mutation?

A

cancer development requires a large number of independent rare accidents to happen in a single cell

cancer is progressive accumulation of mutations in a single cell lineage

need at least five mutations usually to get a tumor

33
Q

Genetic changes are heritable changes. What kinds of abnormalities in DNA segments can lead to cancer

A

base substitutions, insertion or deletion of bases, rearrangements, changes in copy numbers of DNA segments

34
Q

what are epigenetic changes

A

environment can cause changes that affect the way genes work

35
Q

are epigenetic changes heritable?

A

I think so

36
Q

what are the two types of mutations we see

A

driver mutations

passenger mutations

37
Q

what are driver mutations?

A

dominant. help drive development of cancer –> confer growth advantages
mutations of cancer genes
lead to deregulation of cell biological processes
interfere with DNA repair, cell cycle arrest, etc.

38
Q

what are passenger mutations

A

large majority of mutations
do not confer growth advantages
meaningless mutations
–> can become meaningful in right situtation

39
Q

how do carcinogens become harmful to humans?

A

metabolic cells can make them more reactive molecules

main environmental causes of cancer are a product of highly industrialized life…

40
Q

how do we identify mutagenic reagents?

A

AMES test

mix bacteria with test compound and liver extract

41
Q

when detecting cancer, what types of abnormalities in chromosome number and structure can we look for?

A

inter- and intra-chromosomal rearrangements
copy number changes
amplified regions
ex: Philadelphia chromosome has translocation between arm of chromosome 9 and 22

42
Q

what are the two cancer critical genes?

A

oncogenes

tumor suppressor genes

43
Q

differences between oncogenes and tumor suppressor genes

A

oncogenes
- overactivity mutation, gain of function, single mutation event turns normal gene into oncogene, dominant cancer genes (most like this)

tumor suppressor gene
- underactivity mutation, loss of function, require mutation of both alleles, recessive

44
Q

what types of mutations can lead to oncogenes?

A 
deletion or point mutation in coding sequence
gene amplification
chromosome rearrangement
change protein coding regions
regulatory DNA sequence changes
Methylation
45
Q

example of oncogene situation

A

mutation of epidermal growth factor receptor can make it active even in absence of EGF

–> consequently becomes oncogenic –> greatly overproduces protein

46
Q

what types of mechanisms cause tumor suppressor gene mutation

A

can happen in any order and can involve genetic and epigenetic changes

genetic:
lose good copy, chromsome deletion, mitotic recombination event, deletion, point mutation, epigenetic changes (not transcribed anymore)

epigenetic:
DNA methylation and packaging of genes into condense chromatin form

47
Q

how do we identify oncogenes?

A

oncogene should be hyperactive

add it and see if a normal cell line turns into a cancerous cell line

48
Q

what is the Warburg effect and how is it used to identify cancer?

A

cancer cells have altered sugar metabolism

normal cells oxidize all glucose to produce ATP

cancer cells

  • only small fraction of glucose is used for ATP production
  • has greatly increased rate of glycolysis and lactate production
  • 10% of products from glycolysis go directly towards tumor growth
49
Q

how do we identify tumor suppressor genes with Rb genes?

A

hereditary Rb (one mutated Rb copy)

  • much more likely to get cancer because only have one good copy of gene
  • people with inherited mutations usually develop multiple tumors in both eyes

non-hereditary retinoblastoma

  • very rarely both copies of Rb genes will be inactivated
  • get cancer
50
Q

microarrays for identifying cancer genes

A

fluorescently label the isolated DNA from tumor and normal tissue to observe deletion or amplification or other events

51
Q

Sequencing for identifying cancer genes

A

getting more popular because getting cheaper!
human genome was fully sequenced in 2000 so it is template for PCR primer design
amplify and sequence coding exons
sequence cancer genomes (whole gene families and coding exons)
sequence transcriptome

52
Q

oncogenes and tumor suppressor genes from cancer genome sequencing

A

oncogenes: found that the same nucleotide change is repeatedly found among the missense mutations in a gene (missense mutations = change amino acids)

tumor suppressor genes
- found primarily mutations that abort protein synthesis by creating stop codons prematurely (truncating mutations)

53
Q

how does IMATINIB (Gleevec) prevent progression of chronic myeloid leukemia (CML)?

A

IMATINIB binds to ATP binding pocket of hyperactive oncogenic kinase (Bcr-Abl or Philadelphia chromosome)

prevents kinase from transferring phosphate group onto target protein

preventing leukemia!

54
Q

which types of anticancer drugs end with “nib”

A

drugs that are small molecules

55
Q

which types of anticancer drugs end with “mab”

A

drugs that are antibodies

56
Q

why is multidrug treatment awesome!

A

there should be no cell carrying a whole set of rare mutations that would confer resistance to several different drugs

57
Q

how does immunological therapy work?

A

inject antibodies that target and deliver poison to cancer cells!
- antibodies on protein x and PD1

treatment overcomes the immunosuppressants environment by using specific antibodies that prevent tumor cells from engaging with inhibitory receptors on the t cells
- get active t cell response that will kill the cancer cells

58
Q

humans vs elephants

A

elephant blood very sensitive to DNA damage and undergoes a lot of apoptosis
elephants have 20 copies of p53 gene whereas humans only have one

(p53 gets phosphorylated by Mdm2 if there is DNA damage and can then go on to inhibit activity of Cdk - so S phase is paused if something is wrong)

59
Q

ways to detect cancer genes

A 
chromosome abnormalities
tissue cultures
hereditary cancer
microarrays
exons
transcription sequencing

BIOL 360 (9 decks)

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